A SYSTEM OF MEDICINE. EDITED BY J. RUSSELL REYNOLDS, M.D., F.R.S., >71 FELLOW OF THE ROYAL COLLEGE OF PHYSICIANS OF LONDON ; FELLOW OF THE IMPERIAL LEOPOLD-CAROLINA ACADEMY OF GERMANY ; FELLOW OF UNIVERSITY COLLEGE, LOND. ; PROFESSOR OF THE PRINCIPLES AND PRACTICE OF MEDICINE IN UNIVERSITY COLLEGE ; PHYSICIAN TO UNIVERSITY COLLEGE HOSPITAL ; EXAMINER IN MEDICINE TO THE UNIVERSITY OF LONDON. WITH NUMEROUS ADDITIONS AND ILLUSTRATIONS, BY HENRY HARTSHORNE, A.M., M.D., FELLOW OF THE COLLEGE OF PHYSICIANS OF PHILADELPHIA ; FORMERLY PROFESSOB OF PRACTICE OF MEDICINE IN MEDICAL DEPARTMENT OF PENNSYLVANIA COLLEGE, AND PHYSICIAN TO THE EFISCOPAL HOSPITAL OF PHILADELPHIA ; LATELY PROFESSOR OF HYGIENE IN THE UNIVERSITY OF PENNSYLVANIA, AND PROFESSOR CF HYGIENE AND DISEASES OF CHILDREN IN THE woman's MEDICAL COLLEGE OF Pennsylvania; etc. IN THREE VOLUMES. VOL. II. DISEASES OF THE RESPIRATORY AND CIRCULATORY SYSTEMS. PHILADELPHIA: HENRY O. LEAS SON & CO 18 8 0. Entered according to Act of Congress, in the year 1879, by HENRY C. LEA, m the Office of the Librarian of Congress. All rights reserved. COLLINS, PRINTER. CONTENTS OF VOL. II. PART II.-Continued. LOCAL DISEASES, OB AFFECTIONS OF PABTICULAB OBGANS OB SYSTEMS'OF OBGANS. DISEASES OF THE RESPIRATORY SYSTEM. A. DISEASES OF THE LARYNX:- DISEASES OF THE LARYNX, by Morrell Mackenzie, M.D. t ri . PAGE I. Primary Diseases ... 17 Acute Laryngitis ... 17 Definition .... 17 Synonyms .... 18 Etiology . • . .18 Symptoms .... 18 Diagnosis .... 19 Pathology .... 19 Morbid Anatomy ... 20 Prognosis . . . .20 Treatment .... 20 Varieties .... 21 Chronic Laryngitis ... 22 Definition .... 22 Synonyms .... 22 Symptoms .... 22 Diagnosis . . . .23 Pathology . . . .23 Prognosis .... 23 Treatment .... 23 Varieties .... 24 Morbid Growths ... 25 Definition . . . .25 Synonyms . . . .25 History .... 25 Symptoms .... 25 Diagnosis .... 27 Pathology .... 27 Morbid Anatomy... 27 Prognosis .... 28 Treatment .... 28 Neuroses 29 Diseases of the Motor System 29 Bilateral Paralysis of Ad- ductors . . . .29 PAGE Primary Diseases- Unilateral Paralysis of Ad- ductors .... 30 Bilateral Paralysis of Ab- ductors .... 30 Unilateral Paralysis of Ab- ductors .... 31 Spasm: Laryngismus strid- ulus .... 32 Diseases of the Sensory Sys- tem 35 II. Secondary Diseases in Acute Af- fections .... 36 In Smallpox . . .36 In Measles ... 36 In Scarlatina ... 37 In Erysipelas ... 37 In Typhus and Typhoid . 37 Secondary Diseases in Chronic Affections.... 38 Laryngeal Phthisis . . 38 Definition .... 38 Synonyms.... 38 Causes .... 38 Symptoms.... 38 Diagnosis . . .39 Pathology .... 39 Prognosis .... 41 Treatment ... 41 Syphilis 42 Secondary (Edema ... 43 Appendix on the Use of the La- ryngoscope .... 43 III IV CONTENTS OF VOL. II. CROUP, by William Squire, L.R.C.P. Lond. PAGE Definition 46 Synonyms 46 Ilisto.ry 46 Etiology 48 Symptoms ..... 53 Diagnosis 56 Page Pathology 60 Morbid Anatomy .... 61 Prognosis 63 Treatment 63 Varieties . . . . . .70 B. DISEASES OF THE THORACIC ORGANS EMPHYSEMA OF THE LUNGS, by Sir William Jenner, Bart., M.D. Lond., D.C.L. Oxon., F.R.S. Interlobular, Extra-Vesicular, or Extra-Alveolar .... 71 Pulmonary Vesicular Emphysema . 71 Definition, Causation ... 71 Varieties 76 Acute Vesicular Emphysema . 76 Chronic Local Emphysema . 77 Pulmonary Vesicular Emphysema- Large-lunged Vesicular Emphy- sema 78 Small-lunged Vesicular Emphy- sema 85 Complications .... 87 Treatment 90 Appendix 92 Symptoms of the Paroxysms . . 93 History 96 Varieties 97 Causes 98 ASTHMA, by Hyde Salter, M.D., F.R.S. Diagnosis 99 Prognosis 100 Pathology 101 Treatment 102 PHTHISIS PULMONALIS, by J. Hughes Bennett, M.D., F.R.S.E. Pathology of Tubercular Phthisis . 108 Histology, Chemistry, and general Pathology of Tubercle . . 108 Morbid Anatomy of Phthisis Pul- monalis Ill Causes 115 Natural progress .... 119 Theory of its Production . . 120 Symptoms 122 Acute 122 Pathology of Tubercular Phthisis- Chronic, Gradual . . . 123 Hemorrhagic .... 124 Bronchitic .... 125 Laryngeal .... 125 Pneumonitic .... 126 Diagnosis 127 Prognosis 130 Treatment 132 CANCER OF THE LUNGS, by Hermann Beigel, M.D. Literature 144 Pathological Anatomy . . . 145 Symptoms 146 Diagnosis 149 Prognosis and Treatment . . 151 PNEUMONIA, by Wilson Fox, M.D., F.R.C.P. A. Acute Pneumonia . . . 153 Definition .... 153 History 153 Etiology 154 I. Acute Primary Pneumonia . 162 Symptoms .... 162 Complications . . . 184 Variations in its Clinical As- pect . ... 185 Pathology .... 187 Morbid Anatomy . . 187 Pathogenesis . . . 197 Acute Pneumonia- Diagnosis .... 200 Prognosis .... 204 Treatment .... 208 II. Secondary and Intermittent Pneumonia . . . 217 Catarrhal Pneumonia . . 217 Broncho-Pneumonia ; Lobu- lar, Disseminated, or Ve- sicular Pneumonia . .218 Etiology .... 219 Symptoms .... 220 CONTENTS OF VOL. II. V PAGE Acute Pneumonia- Pathology and Pathogenesis . 223 Diagnosis .... 229 Prognosis .... 230 Treatment .... 231 Other forms of Secondary Pneu- monia 233 Appendices to Articles on Acute Pneumonia .... 235 A. On the Pulse in Acute Pneu- monia .... 235 B. On the Retention of Chloride of Sodium in the System, and its Presence in the Sputa .... 236 C. On the Granular Appearance of Lung .... 237 PAGE Acute Pneumonia- D. On the Origin of Exudation and Cell-products in In- flammation . . . 238 E. On the Treatment of Pneu- monia by Venesection .• 238 III. Interlobular Pneumonia . 243 B. Chronic Pneumonia . . : 244 Synonyms .... 244 Definition .... 244 History 244 Pathology .... 257 Symptoms and Physical Signs 260 Diagnosis .... 264 Prognosis .... 265 Treatment .... 267 SYPHILITIC AFFECTIONS OF THE LUNG, by Wilson Fox, M.D., F.R.C.P 270 BROWN INDURATION OF THE LUNG, by Wilson Fox, M.D., F.R.C.P. Synonyms 274 History 274 Pathology . . . . .274 Symptoms 276 Treatment 276 CIRRHOSIS OF TIIE LUNG, by H. Charlton Bastian, M.D., F.R.S. Nature and History . . . 277 Pathological Anatomy . . . 281 Pathology 285 Etiology 294 Details of Five Cases . . . 296 Symptoms 298 Physical Signs 301 Prognosis...... 304 Treatment 304 APNEUMATOSIS, by Graily Hewitt, M.D., F.R.C.P Definition 306 History 306 Pathological Anatomy . . . 307 Etiology 310 Symptoms 314 Prognosis 316 Diagnosis 316 Treatment 317 BRONCHITIS, by Frederick T. Roberts, M.D. Acute Catarrhal Bronchitis . . 318 Natural History . . . .318 Causes 318 Symptomatology .... 320 Acute Idiopathic Bronchitis . . 321 Capillary Bronchitis . . . 322 Bronchitis in connection with the Exanthemata .... 324 With Blood Diseases . . . 324 With Chronic Lung and Heart Diseases 324 Mechanical Bronchitis . . . 325 Duration and Termination . . 326 Diagnosis 326 Prognosis and Mortality . . 327 Pathology 328 Mechanical Bronchitis- Morbid Anatomy.... 328 Treatment 329 Chronic Bronchitis .... 332 Causes 332 Symptomatology .... 332 Diagnosis 334 Prognosis 334 Pathology 334 Morbid Anatomy .... 334 Treatment 335 Plastic or Croupous Bronchitis . 337 Symptoms 337 Diagnosis 338 Prognosis 338 Treatment 338 VI CONTENTS OF VOL. II. PLEURODYNIA, by Francis PAGE Pathology 339 Diagnosis 339 Prognosis 339 Treatment 340 E. Anstie, M.D., F.R.C.P. PAGE Definition 339 History 339 Symptoms 339 Etiology '339 PLEURISY, by Francis E. Anstie, M.D., F.R.C.P. Definition 340 History ...... 340 Etiology ...... 341 Clinical History .... 342 Pathological Anatomy . . . 347 Diagnosis 349 Prognosis 350 Treatment 351 Definition 358 History 358 Symptoms 358 HYDROTHORAX, by Francis E. Anstie, M.D., F.R.C.P. Pathology 358 Diagnosis 359 Treatment 359 Varieties' 360 Clinical History .... 360 Diagnosis 361 PNEUMOTHORAX, by Francis E. Anstie, M.D., F.R.C.P Prognosis 361 Treatment 362 DISEASES OF THE ORGANS OF CIRCULATION. A. THE HEART:- WEIGHT AND SIZE OF THE HEART, by Thomas B. Peacock, M.D., F.R.C.P. Of the Healthy Heart . . . 363 Of the Diseased Heart . . . 367 POSITION AND FORM OF THE HEART AND GREAT VESSELS, by Francis Sibson, M.D., F.R.S. Front View after Death . . . 370 Front View during Life . . . 400 Side View after Death . . . 416 Side View during Life . . . 418 Back View after Death . . . 422 Back View during Life . . . 422 Notes from Pirogoff and Braun . 427 Malpositions of the Heart- Vertical Displacement . . 437 Lateral Displacement . . . 443 Forward Displacement . . 451 Backward Displacement . . 451 LATERAL OR PARTIAL ANEURISM OF THE HEART, by Tuomas Bevill Peacock, M.D., F.R.C.P. Aneurism of the Left Ventricle . 452 Aneurism of the Left Auricle . . 460 Aneurism of the Valves . . . 460 ADVENTITIOUS PRODUCTS IN THE HEART, by Thomas Bevill Peacock, M.D., F.R.C.P. Tubercle in the Heart, and Tuber- cular Pericarditis.... 462 Cancer 464 Simple and other Cysts . . . 465 Entozoa 466 Fibrinous Deposits: Syphilitic Af- fections of the Heart . . . 468 Fibro-cartilaginous and Osseous De- generation ..... 469 Polypoid Growths .... 470 CONTENTS of VOL. II. VII PNEUMO-PERICARDIUM, by J. Warburton Begbie, M.D. . 472 PERICARDITIS, by Francis Sibson, M.D., F.R.S. PAGE Clinical History of Pericarditis as it occurred in the Author's Practice in St. Mary's Hospital . . .474 Rheumatic Pericarditis . . .474 Sex, Age, and Occupation . . 475 The Affection of the Joints . . 488 The Degree of the Joint Affection during the Acme of Effusion . 490 Time in the Hospital . . . 491 Occurrence of previous Attacks . 491 Time of the first Observation of Friction-sound in relation to the Pericarditis and the Joint Affec- tion 492 The Presence or Absence of Endo- carditis 493 Progressive Changes in the Organs 496 Over-action of the Heart and of the Limbs as Causes of Rheumatism with Heart Affection . . .497 Pain 500 Irregularity and Failure of the Heart 505 Difficult and Quickened Respiration 507 Difficulty in Swallowing . . . 508 Loss of Voice 509 Effects on the Pulse .... 509 Fulness of the Veins . . . 509 Appearance of the Face . . . 510 Condition of Face when Effusion at its Acme 513 Affections of the Nervous System . 513 PAGE Affections of the Nervous System- In Rheumatic Pericarditis -with high Temperature . . . 514 In Endocarditis with high Tem- perature . . . . 519 High Temperature without In- flammation .... 520 In which Temperature was not Observed 525 Coma 527 Delirium 527 Temporary Insanity, Melancholia, and Hallucinations . . . 529 Chorea, Choreiform and Tetani- form Movements . . . 532 In Pericarditis without Rheuma- tism or Bright's Disease . . 534 The Physical Signs of Rheumatic Pericarditis .... 539 Percussion 542 Prominence over the Region of the Pericardium .... 547 Position of the Impulse . . 548 Vibration or Thrill . . . 555 Auscultation .... 556 The Character and Tests of Peri- cardial Friction Sound . . 582 Physical Signs of Pericarditis in Bright's Disease . . . 593 Pericarditis, neither Rheumatic nor from Bright's Disease . 596 Treatment of Pericarditis . . 602 ADHERENT PERICARDIUM, by Francis Sibson, M.D., F.R.S. Anatomical Description . . . 608 Physical Signs 609 I Clinical History .... 612 ENDOCARDITIS, by Francis Sibson, M.D., F.R.S. Anatomical Appearances . . 618 Clinical History in Rheumatism . 620 Clinical History in Chorea . . 651 Clinical History in Pyaemia . . 654 Clinical History in Bright's Disease 654 Clinical History in Valvular Disease 655 Pathological Evidence of Endocar- ditis in Cases of Valvular Disease of the Heart .... 655 Treatment 659 CARDITIS, by W. R. Gowers, M.D. . . .661 HYDROPERICARDIUM, by J. Warburton Begbie, M.D. . 663 ANGINA PECTORIS AND ALLIED STATES: INCLUDING CERTAIN KINDS OF SUDDEN DEATH, by Professor Gairdner, M.D. General Description . . . 665 Diagnosis 670 Causes 673 Illustrations of sudden death without pain 675 Pathology 686 Treatment 697 VIII CONTENTS OF VOL. II. DISEASES OF THE VALVES OF THE HEART, by C. Hilton Fagge, M.D., F.R.C.P. PAGE History 706 Description and Anatomy . . 707 Etiology 713 Effects 722 PAGB Diagnosis 749 Prognosis 752 Treatment 755 ATROPHY OF THE HEART, by W. R. Gowers, M.D. Definition 759 History 759 Varieties 760 Causes 761 Pathological Anatomy . . .761 Symptoms ..... 762 Diagnosis 762 Prognosis 762 Treatment 762 Synonyms 763 Definition 763 History 763 Varieties 764 Causes and Pathology . . .764 HYPERTROPHY OF THE HEART, by W. R. Gowers, M.D. Pathological Anatomy . . . 772 Symptoms 776 Diagnosis 781 Prognosis 782 Treatment 783 Synonyms 786 Definition 786 History 786 Varieties...... 786 Causes ...... 787 Pathological Anatomy . . . 793 DILATATION OF THE HEART, by W. R. Gowers, M.D. Consequences 794 Symptoms ...... 796 Diagnosis 799 Prognosis 800 Treatment 800 FATTY DISEASES OF THE HEART, by W. R. Gowers, M.D. Fatty Overgrowth .... 804 History 805 Causes . . . ' . . . 805 Pathological Anatomy. , . 805 Symptoms 806 Diagnosis 807 Treatment 807 Fatty Degeneration . . . 807 Synonyms 807 Definition 807 History 807 Varieties 808 Etiology ..... 808 Fatty Degeneration- Pathological Anatomy. . . 811 Consequences .... 815 Symptoms 815 Course and Terminations . . 818 Diagnosis 819 Prognosis . .... 819 Treatment 820 Rupture of the Heart . . . 820 Symptoms ..... 822 Diagnosis ..... 822 Prognosis 822 Treatment 823 FIBROID DISEASE OF THE HEART, by W. R. Gowers, M.D Synonyms 823 Definition 823 History 823 Etiology 823 Pathological Anatomy . . . 824 Consequences 824 Symptoms 824 Diagnosis ..... 825 Treatment 825 B. ASSOCIATED ORGANIC CHANGES MEDIASTINAL TUMORS, by R. Douglas Powell, M.D., F.R.C.P. Varieties, Etiology .... 826 Age 828 Sex 828 Symptoms 828 Physical Signs 828 Diagnosis 831 Prognosis...... 833 Treatment 833 CONTENTS OF VOL. II. IX C. DISEASES OF THE VESSELS THE DISEASES OF THE AORTA, by E. Douglas Powell, M.D., F.R.C.P. PAGE Aortitis 834 Aortic Endarteritis, Atheroma . 835 Etiology 836 Symptoms 836 PAGE Aortic Endarteritis, Atheroma- Duration 837 Treatment 837 ANEURISM OF THE THORACIC AORTA, by R. Douglas Powell, M.D., F.R.C.P. Aneurism at the Sinuses . . . 838 Symptoms 838 Diagnosis 838 Aneurism beyond the Valves . . 838 Etiology 839 Age 842 Sex 842 Symptoms 842 Physical Signs .... 845 Aneurism beyond the Valves- Diagnosis 848 Prognosis 851 Treatment 852 Spontaneous Rupture of the Aorta . 856 Narrowing of the Aorta . . . 856 Diagnosis 858 Prognosis 858 ANEURISM OF THE ABDOMINAL AORTA, by William Murray, M.D., F.R.C.P. Anatomy 859 Etiology 862 Symptoms 863 Treatment 867 DISEASES OF ARTERIES, by John Syer Bristowe, M.D., F.R.C.P. Inflammation, Arteritis . . .870 Degeneration, Atheroma . . 872 Changes of Dimension . . . 875 Enlargement, Dilatation . . 875 Changes of Dimension- Aneurism 875 Contraction and Occlusion . . 880 DISEASES OF VEINS, by John Syer Bristowe, M.D., F.R.C.P. Inflammation, Phlebitis . . . 880 Degeneration 883 Concretions 883 Adventitious Growths . . . 884 Changes of Dimension . . . 884 Enlargement .... 884 Occlusion S86 CARDIAC CONCRETIONS, by John Syer Bristowe, M.D., F.R.C.P. Anatomy 887 Etiology 889 Symptoms and Effects . . . 890 THROMBOSIS AND EMBOLIA, by John Syer Bristowe, M.D., F.R.C.P. General History .... 892 Obstruction in Arteries of Heart, Spleen, Liver, Kidneys, Brain . 895 Obstruction in Arteries of the Limbs 896 Obstruction of Pulmonary Arteries 896 X CONTENTS OF VOL. II. DISEASES OF THE PULMONARY ARTERY, by R. Douglas Powell, M.D., F.R.C.P. PAGE Atheroma 898 Dilatation, Aneurism . . . 898 Narrowing 899 Symptoms, Cyanosis . . . 899 PAGE Murmur over the Pulmonary Artery 901 Pulmonary Artery within the Lung 901 DISEASES OF THE CORONARY ARTERIES, by R. Douglas Powell, M.D., F.R.C.P. Atheroma, Calcification . . . 903 Thrombosis 903 Aneurism 903 [HAEMOPHILIA, by Henry Hartshorne, A.M., M.D.] . 904 INFLAMMATION OF THE LYMPHATIC VESSELS, by J. Russell Reynolds, M.D., F.R.S. • . .906 Index 909 List oe Chief Authors referred to in Each Article .... 925 LIST OF CONTRIBUTORS TO VOL. II. Francis Edmund Anstie, M.D., F.R.C.P. ; Senior Assistant Physician to the Westminster Hospital, and Lecturer on Medicine in the Westminster Hospital Medical School. Henry Charlton Bastian, M.A., M.D., F.R.S., F.L.S.; Professor of Pathologic Anatomy in University College ; Physician to University College Hospital. James Warburton Begbie, M.D., F.B.C.P., Edinburgh; Professor of the In- stitutes of Medicine in the University of Edinburgh. Hermann Beigel, M.D., M.R.C.P. Bond.; Physician to the Metropolitan Free Hospital, and to the Skin Department of Charing Cross Hospital. J. Hughes Bennett, M.D., F.R.S.E. ; Professor of the Institutes of Medicine in the University of Edinburgh. J. Syer Bristows, M.D. Bond., F.R.C.P. ; Physician to St. Thomas's Hospital; Lecturer on Medicine, St. Thomas's Hospital Medical School. C. Hilton Fagge, M.D., F.R.C.P. Bond. ; Senior Assistant Physician to Guy's Hospital. Wilson Fox, M.D., F.R.C.P.; Physician Extraordinary to Her Majesty the Queen ; Holme Professor of Clinical Medicine in University College; and Physician to University College Hospital. William Tennant Gairdner, M.D., F.R.C.P., Edinburgh; Professor of the Practice of Physic in the University of Glasgow. William R. Gowers, M.D. Bond., Assistant Professor of Clinical Medicine in University College ; Assistant Physician to University College Hospital, and to the National Hospital for the Paralyzed and Epileptic. Henry Hartshorne, A.M., M.D., lately Professor of Hygiene in the University of Pennsylvania, &c. W. M. Graily Hewitt, M.D., F.R.C.P. ; Professor of Midwifery in University College, and Examiner in Midwifery to the University of London; Obstetric Physician to University College Hospital. Sir William Jenner, Bart., M.D., D.C.L., F.R.S.; Physician in Ordinary to Her Majesty the Queen, to II. R. II. the Prince of Wales, and Physician to Uni- versity College Hospital. Morell Mackenzie, M.D.; Physician to the Hospital for Diseases of the Throat, and to the London Hospital. William Murray, M.D. Durh., F.R.C.P. Lond.; Consulting Physician to New- castle-upon-Tyne Hospital for Sick Children. XI XII LIST OF CONTRIBUTORS TO VOL. II. Thomas Bevill Peacock, M.D. Edinburgh, F.R.C.P. Load. ; Physician to St. Thomas's Hospital. R. Douglas Powell, M.D. Lond., F.R.C.P.; Assistant Physician to the Middle- sex Hospital; Physician to the Hospital for Consumption at Brompton. J. Russell Reynolds, M.D. Lond., F.R.C.P., F.R.S.; Consulting Physician to University College Hospital; Emeritus Professor of Medicine at University Col- lege ; Physician to Her Majesty's Household. Frederick T. Roberts, M.D., B.Sc.; Assistant Physician to University College Hospital, and to the Hospital for Consumption, Brompton. Hyde Salter, M.D., F.R.S., F.R.C.P. ; Physician to the Charing Cross Hospital. Francis Sibson, M.D., F.R.C.P., F.R.S. Lond. ; formerly Lecturer on Medicine, and Physician to St. Mary's Hospital. William Squire, L.R.C.P. Lond. A SYSTEM OF MEDICINE. LOCAL DISEASES (continued). DISEASES OF THE RESPIRATORY SYSTEM. A. Diseases of the Larynx. § I. Primary Diseases of the Larynx. Acute Laryngitis. Chronic Laryngitis. Morbid Growths. Neuroses. Diseases of the Motor System. Paralytic Affections. Spasmodic Affections, Laryngismus Stridulus. Diseases of the Sensory System. ? II. Secondary Diseases of the Larynx. In Acute Affections ; the Exanthemata. In Chronic Affections. Laryngeal Phthisis. Syphilitic Disease of Larynx. Appendix, on the Use of the Laryngoscope. § III. Croup. DISEASES OF THE LARYNX. By Morell Mackenzie, M.D. In order to facilitate the treatment of this subject, Diseases of the Larynx have been divided into Primary and Second- ary. The first includes all those con- ditions in which the larynx is the part first affected, and where the disease is generally, though not necessarily, of a purely local character. The second em- braces those conditions where the laryn- geal affection is a complication of a pre- viously developed (acute or chronic) morbid state of the system. The pri- mary affections are the inflammations, the morbid growths, and neuroses ; the secondary are the occasional phenomena met with in the acute exanthemata, in phthisis and in syphilis. The classifica- tion is based on convenience. The limits allotted to this article forbid my occupy- ing space by defending the arrangement, or by anticipating and explaining away any possible charge of apparent incon- sistency in carrying it out. SECTION I. PRIMARY DISEASES OF THE LARYNX. Acute Laryngitis. Definition. - Inflammation of the lining membrane of the larynx, in which the vessels of the submucous areolar tis- VOL. II.-2 17 18 DISEASES OF THE LARYNX. sue may or may not participate, charac- terized by dysphonia, or aphonia, dys- pnoea, and stridulous breathing, cough, slight pain in the larynx-generally re- ferred to the pomum Adami, and increased on pressure externally-and dysphagia. There is generally high constitutional fever. Synonyms.-Latin-Cynanche Laryn- gea, Angina Laryngea, Angina Epiglot- tidea ; French-Laryngite, Catarrhe Lar- yngien ; German-Katarrlische Kehlkop- fenziindung; English - Inflammation of the Larynx. Laryngitis is by some sub- divided into Mucous Laryngitis (the Laryngite muqueuse of the French), and Submucous, or (Edematous Laryngitis {Laryngite oedemateuse). Causes.-(ct) Predisposing.- That re- laxing habits predispose to the disease is rendered probable by the fact that resi- dents in towns are more liable to it than those living in the country (Niemeyer); and of the former, those engaged in in- door occupations are much more sus- ceptible than those much exposed to the weather. At the Hospital for Diseases of the Throat, laryngitis is much more often met with among tailors, shoemakers, porters, and people thus engaged, than among coachmen, cab-drivers, policemen, and others who are constantly exposed to the most inclement weather. Previous inflammation, and of course repeated pre- vious attacks, render the part particularly prone to be affected. Males are more liable to it than females, and adults than children ; but it proves far more fatal to the young; more than four-fifths of the mortality occurring before the tenth year. (b) Exciting. Causes.-Cold draughts of air, whether inspired or bearing on the neck externally, exposure of the body in general to cold, and especially allowing the feet to remain wet and cold for any length of time, are circumstances which in some people may give rise to the dis- ease. Violent functional efforts (in giving the word of command, preaching, sing- ing, &c.), and straining the parts in cough- ing, are not uncommon causes of it. Dusty air and irritating vapors ought, perhaps, to be considered as the traumatic causes ; they are both probably some- times concerned in the production of the disease, without even the patient being aware of their operation. The catarrhal form of the disease is often propagated from the nares, and oedematous inflamma- tion sometimes from the pharynx. Ex- tension of the disease occasionally takes place from below, the bronchial tubes being first affected ; but the opposite se- quence more often takes place, the laryn- geal disease passing off with the occur- rence of bronchitis. Symptoms.-The approach of the dis- ease is generally insidious, and a slight catarrh may suddenly become a most serious affection. (a) Subjective Symptoms. - The patient complains at first of a slight dryness or soreness of the throat, or he may have nothing more than a feeling of roughness, or a tickling sensation with disposition to cough, or there may be a sense of con- striction about the throat, and slight diffi- culty of swallowing; but the period at which this symptom supervenes, as well as its degree, depends on the part of the larynx first and most affected ; in other words, it occurs at an early period, and is greatest when the epiglottis or ary-epi- glottic folds are much affected, and later, and to a less degree, when the more inter- nal parts of the larynx are attacked. In severe cases all the true laryngeal symptoms become greatly aggravated. There is often a sensation as if a foreign body were lodged at the part, the breath- ing becomes extremely embarrassed, and the patient feels great anxiety about get- ting his breath. In fatal cases, the rest- less agony of impending suffocation gen- erally gives -way at last to a comatose state. (6) Objective Symptoms. - (1) Vocal.- There is generally dysphonia in the early, aphonia in the later, stages. The cough is at first clear and shrill, then harsh and croupy, finally aphonic. It is generally frequent, and often paroxysmal. Its ex- act character and variations, however, depend on the particular part of the larynx which is affected. (2) Respiratory.-The inspiration is at first a little prolonged and wheezing, afterwards very much lengthened and ac- companied with stridor. In the later stages there is a kind of groan in expira- tion. In addition to these sounds mucous rales can generally be heard on ausculta- tion over the larynx. As the calibre of the larynx becomes contracted from oede- matous infiltration and spasmodic ap- proximation of the vocal cords, the pa- tient expends all his energies on the respiratory process. Sitting up in bed he desperately clutched the bed-clothes, and in his violent efforts to get breath, the shoulders are seen to rise and the whole chest to heave. (3) Laryngoscopic Signs.- In the early stages, and in mild cases, the mucous membrane is merely seen to be of a bright red color; the hyperremia is, as a rule, diffused, though sometimes there may be distinct injection of the vessels. In severe cases oedema soon appears, the parts affected being seen to be red, swollen, and semi-transparent. When the epiglottis is acutely inflamed, it fre- quently presents the appearance of a raised ridge in the median line, with two DIAGNOSIS-PATHOLOGY. 19 large tumors on each side ; the valve is in fact folded upon itself, and only its upper surface is visible. This condition occludes the view of the larynx. When the ary-epiglottic folds are attacked, their shape becomes very irregular; the venti- cular bands are sometimes seen to be in a highly turgid state, and in this case they eclipse the vocal cords. If the latter are visible, they are of a bright red color, slightly swollen, especially posteriorly; their sharp free edge is rounded, their mobility is impaired, and on inspiration their normal action is occasionally seen to be reversed, the glottis tending to become closed instead of open. been known to occur in seven hours.1 It is rare for the symptoms to remain serious after the fifth day, unless a kind of chronic oedema sets in. The disease may termi- nate in any of the following ways:-(1) Spontaneous resolution may occur. (2) Resolution may be brought about by ther- apeutics. (3) The acute symptoms may pass away, and chronic congestion remain. (4) Death may take place very suddenly, from the combined effects of oedematous swelling and spasm of the glottis, less sud- denly from the former cause acting alone, or slowly, and often preceded by delirium from the effects of exhaustion and imper- fectly aerated blood. (5) Threatened suffocation may be averted by the opera- tion of tracheotomy. Diagnosis.-In very young children it is impossible to distinguish between acute laryngitis and croup; but, where the laryngoscope can be used, the presence or absence of false membrane can of course be ascertained at once. Even with this instrument, however, the essential nature of the morbid process cannot always at any early period be ascertained, as the apparently simple inflammation may be an early stage of the plastic form of dis- ease.2 Laryngismus stridulus differs by its very sudden accession, by its generally occur- ring during sleep, by its passing off and leaving the child in an apparently normal condition as regards the laryngeal symp- toms and respiration, and by the absence of constitutional fever. Spasm of the glottis in adults is easily differentiated by the general symptoms, and still more so by the employment of the laryngoscope. Pathology. -The disease is essentially a simple inflammation of the mucous mem- brane, and submucous areolar tissue of the larynx ; the danger of the disease being in proportion to the extent that the last- named structure participates in the mor- bid process. When the deeper tissues are affected, the products of inflammation ac- cumulate beneath the lining membrane and cause the tumefaction which in this situation is attended with such imminent risk. When the inflammatory process is superficial, its effects are of less impor- tance. The character of the secretion be- comes altered, being at first clear and gummy in character, and afterwards con- taining an increased quantity of pus cor- puscles. There is partial destruction and imperfect formation of the normal epithe- lial structure, but the process scarcely ever leads to ulceration. The danger is not due to the oedematous swelling alone, but also to the spasm of the glottis which [Fig. 1. (Edema of Glottis, a. Tongue, b. Mouth of Larynx, e. Trachea. From a specimen in the cabinet of Dr. Gross.] (4) Miscellaneous Symptoms.-The laryn- geal secretion is generally very scanty, tenacious, and difficult to expectorate; in favorable cases, where the disease is pass- ing off, it may become thick, purulent, and abundant. In the early stages, >though not generally till a few hours after the local symptoms have manifested them- selves, there are signs of inflammatory fever; the tongue is white and furred, the tip and edges being generally red. The pulse is frequent and hard, the skin hot, and the face flushed. At a later stage the constitutional conditions resemble that of hectic, the skin under the immense respiratory efforts being bathed in perspi- ration, and the pulse small, feeble, fre- quent, and irregular. The countenance is of an ashy pallor, the lips purple, and the eyeballs protrude from the dark halo which surrounds them. Course and Termination.-The acute stage seldom lasts more than three or four days, and I have seen a case terminate fatally in twenty-four hours. Death has 1 Dr. Wood, Pract. Med. vol i. p. 780. 2 See article "Croup." 20 DISEASES OF THE LARYNX. the infiltration causes-partly by reflex action, partly by direct irritation of the adductor muscles of the vocal cords. oedema present; and though tracheotomy remains as a last resource, there is always a risk of the disease extending down the windpipe, so that both bronchitis and pneumonia often supervene. [Fig. 2. [Fig. 3. (Edema of Glottis.] Morbid Anatomy. - The superficial appearances, a few hours after death, re- semble those described under the head of Laryngoscopic Signs. In children, the mucous membrane is generally slightly softened, and of a bright red color. In adults, on the other hand, the redness seldom remains after death, as in those cases which prove fatal the activity of the morbid process is in the submucous tissue. The product of the inflammatory process is generally of a serous character, but it may be sero-purulent, or may even be of the nature of what is called "healthy pus." In the latter case, the condition is that of diffused abscess: circumscribed abscess-as far as I am aware-never oc- curs as a sequel of acute inflammation of the larynx. The effusion, however, is much more frequently of the serous cha- racter. It generally collects in those parts where the areolar tissue is most lax : thus the epiglottis and the ary-epiglottic folds are the parts which are both the most fre- quently distended, and which become the most swollen; next to them the ventri- cular bands (false vocal cords) are most commonly affected ; the vocal cords may be a little tumefied, but they are rarely swollen to any extent. The muscles are often saturated with the serous fluid. If the patient survives the acute stage and dies from other causes, the parts previ- ously swollen and oedematous,present a pe- culiarly sodden and shrunken appearance. Prognosis.-In giving an opinion as to the danger, the age of the patient is the most important consideration. In early life, that is, before the development of the larynx has taken place at puberty, the disease is always attended with great danger. As regards adults also, a very serious opinion must always be given. The danger depends on the amount of i Acnte (Edema Glottidis ; exposed from behind.] Therapeutics.-If the case come un- der observation at a very early period, it is really quite impossible to tell whether the disease is a simple catarrh of the larynx, or is likely to turn out a violent inflammatory affection. Under these cir- cumstances a system of rational expect- ancy must be adopted ; a warm, moist and uniform temperature enforced, and gentle diaphoretic and mild purgative medicine administered. The same kind of treatment cannot be carried out in the case of children as where the patients are adults. The fol- lowing will be found useful for the latter class of patients :-In the early stage, and in slight cases, an inhalation of hot steam, or steam impregnated with the volatile principles of benzoin, or hop, or conium, may be used. The following forms will be found ser- viceable :- 1. ]$. Tinct. benzoin, comp. fl. dr. j ad fl. dr. ij: to be added to a pint of water at 150° F., and inhaled (from a quart jug with a nar- row neck, or from a special inhaling ap- paratus) for ten minutes every three or four hours. 2. I). 01. lupuli iq xv. Mag. carb. lev. gr. x. Aquas ad fl. oz. iij. M. A teaspoonful in a pint of water at 150° F., and used as No. 1-for five to eight minutes, three times a day. The addition of a scruple of camphor to three ounces of any of the foregoing will be found useful, if a rather more stimulating effect is de- VARIETIES. 21 sired. The juice of conium in the follow- ing form is often beneficial:- 3. ff. Succi conii fl. dr. ij. Sodae carb. gr. xx. Mix and add to a pint of water at 150° F., and use as No. 1. Or- $. Conise gr. | to gr. Sp. vini rect. fi. dr. j. Mix and add to a pint of water at 150° F., and use as above. Where there is much pain, or tendency to spasm, chloroform (ten to thirty drops) may be added once or twice at intervals of five minutes during the inhalation. These remedies can be used alone or in combination. If crescent inflammation of the pharynx accompanies the laryngeal hypersemia, the local action of guaiacum administered in the form of lozenges will often prove most beneficial. If, however, the disease makes head under this treatment, and the parts are acutely inflamed, without being oedematous, an attempt may be made to restrain the crescent inflammation by the application of a strong solution of nitrate of silver (60 gr. ad 1 fl. oz.), or perchloride of iron (120 gr. ad 1 fl. oz.); or chloride of zinc (30 gr. ad 1 fl. oz.); or chloride of aluminium (gr. 60 ad 1 fl. oz.). Solutions of nitrate of silver, still largely employed by the pro- fession, have not proved more serviceable in my hands than the mineral astringents, whilst they more often cause spasm and nausea. Inhalations of atomized liquids may be tried, and among these tannin (5 gr. ad 1 fl. oz ), ferri perchloridi (3 gr. ad 1 fl. oz.) are most likely to do good. If the inflammatory process is not arrested by the action of these remedies, the oede- ma, which is almost sure to supervene, should be treated by free scarification with the aid of the laryngoscope, and a properly constructed laryngeal lancet. Should this treatment, however, be im- possible or ineffectual, and should the dyspnoea be of a threatening character, tracheotomy must not be delayed. In these cases the result of the operation is especially favorable. General blood-let- ting, leeching, blistering, mercury, and an- timony, were the most weighty remedies of the profession twenty years ago; but they cannot be put in the balance against the topical treatment which the laryngo- scope renders possible. Non-depressant emetics, however, such as sulphate of zinc (20 gr. to 30 gr.), sulphate of copper (5 gr. to 10 gr.), in plenty of warm water, are sometimes useful where there is much oedema ; and leeching and blistering may be conveniently resorted to by country practitioners who have not the opportu- nity of applying remedies with the aid of laryngoscopy. Treatment of Children.-As it is impos- sible to distinguish between infantile la- ryngitis and croup, the treatment must in effect be the same for each disease.1 In addition, however, to the treatment re- commended by Mr. Squire, scarification, as described below, may sometimes be performed with the greatest advantage. Varieties.-Acute inflammation has been here described in its most complete and severe form ; but it can easily be un- derstood that congestion of the larynx, or Subacute Laryngitis, may come on very suddenly, remain for a few days, and pass away without any further development. The hoarseness which often accompanies faucial catarrh is due to this cause, the vocal cords being in this case the part of the larynx most affected. The symptoms either give way, or the disease assumes the character of chronic laryngitis. Traumatic Laryngitis may, perhaps, be considered as belonging to the province of surgery ; but it is desirable briefly to call attention to that form which occurs to children from swallowing boiling liquids. Children of the poorer class are often al- lowed to drink tea from the spout of the teapot, and when left alone they attempt the same feat at the boiling kettle. In- stant inflammation of the pharynx and orifice of the larynx sets in, and in two or three hours, or even sooner, the epiglottis becomes greatly swollen and oedematous. Scarification, first recommended by Lis- franc,2 and since by Busk,3 Tudor, and others, is the most rational treatment. The age of the patient generally renders the use of the laryngeal mirror out of the question; but the fauces should be illu- minated as in laryngoscopy. In children, under these circumstances, the swollen and oedematous epiglottis can be seen in an erect posture at the back of the tongue. It may be scarified with a gum lancet, or a curved, sharp-pointed bistoury, which should be quite blunt (or covered with strips of plaster) up to within two or three lines of its extremity. Emetics either be- fore or after scarification are often useful. The pressure which the'act of retching exercises on the oedematous tissue, per- haps proves beneficial in consequence of the mucous membrane rupturing, and allowing the aqueous matter to escape. A strong solution of nitrate of silver or of some other mineral astringent may some- times arrest the crescent inflammation before oedema has taken place. The local abstraction of blood is recommended by some, and Dr. Bevan4 has reported four severe cases successfully treated by appli- cation of leeches to the margin of the sternum, an emetic followed by a cathar- 1 See article "Croup." 2 Journal G6n£ral, Ann^e 1825. 3 Lancet, August 13, 1859. 4 Dub. Quart. Journ. of Med.., Feb. 1860. 22 DISEASES OF THE LARYNX. tic, two grains of calomel every half hour, and mercurial inunction. Scarification, however, fairly and fully carried out, ought to supersede all other treatment. Tracheotomy, from which a priori the most satisfactory results might be antici- pated, is not a very successful operation in these scalded throats but nevertheless recourse must be had to it when other reme- dies fail, and the dyspnoea threatens death. Chronic Laryngitis. Definition.-Chronic inflammation of the lining membrane of the larynx charac- terized by hoarseness or loss of voice and generally by more or less cough. Synonyms.-Latin-Laryngitis chron- ica ; French-Laryngite chronique ; Ger- man-Der chronische Katarrh der Kehl- kopfschleimhaut. For other synonyms see " Laryngeal Phthisis," which disease was formerly confused with chronic laryn- gitis. Causes.-The causes of the disease are the same as those indicated under the head of Acute Laryngitis, to which dis- ease it often proves the sequel. The chronic forms of inflammation, however, more frequently extend from the pharynx, and the effects of continuity of texture are often seen in chronic alcoholism and the abuse of tobacco. It is also more fre- quently caused by functional excesses. The great and sudden development of the larynx which takes place at puberty in males, is often attended by a mild form of laryngitis - the so-called "cracked voice" of boys being always associated with marked congestion of the vocal cords. There seems also to be a rare constitu- tional condition, where there is a tendency to chronic inflammation of many of the mucous canals. Four such cases have come under my notice ; the patients were all men over fifty years of age. I have at present a gentleman under my care suffer- ing from chronic laryngitis, slight thick- ening of the walls of the lower third of the oesophagus, gastro-intestinal derange- ment, and chronic cystitis. The influence of age and sex is very marked, adult males being by far the most common sufferers, and children the rarest. Symptoms.-Subjective.-The patient's sensations are not generally very vivid, a tickling feeling being generally "all that is complained of; in some cases, however, a pricking or burning pain is felt. The congestion of the vessels and perhaps the presence of an altered secretion causes in some cases a frequent desire and effort to clear the throat. Objective.-(1) Vocal.-Impairment of function is the most characteristic symp- tom of the disease. It varies in degree from slight modification in tone, to com- plete loss of voice. It is characteristic also of this form of hoarseness in the early stage, that it is most marked when there has been rest of function for some time. Thus a person with slight chronic conges- tion may be extremely hoarse on attempt- ing to speak after being silent for some time, but the voice may become almost normal after the function has been exer- cised for a few minutes. The improve- ment probably depends on the quickened capillary circulation, and stimulated nerve-force of the part. It has its anal- ogy elsewhere. In dysphonia, dependent on feeble approximation of the vocal cords on the other hand, the voice is strongest when first exercised, and gradually be- comes weaker as it continues to be exer- cised. Sometimes the voice is clear and natural in its ordinary tones, and the dis- cordance is only observed when powerful exertions are made (as in singing, acting, public speaking, &c.). The cough is gen- erally rather frequent, but it may amount to nothing more than a hawking or "hem- ming" noise, and sometimes it is almost altogether absent. On the other hand, it may be the most troublesome symptom. (2) Respiratory.-The respiration is not materially affected, though moist rales can usually be heard over the larynx. (3) Laryngoscopic Signs.-The congest- ed condition of the lining membrane of the larynx is at once apparent on using the laryngoscope. The hypersemia may be general or partial. The following is the order of frequency in which the rau- cous membrane over the different parts is affected :-First, the capitula Santorini; secondly, the ventricular bands ; thirdly, the epiglottis; fourthly, the vocal cords, and least frequently the ary-epiglottic folds. The redness generally fades off gradually into the healthy colored mem- brane, but injection of the minute vessels is sometimes apparent on the epiglottis and vocal cords. On the former the in- jection is generally arborescent, on the latter the arrangement of the vessels is usually linear, along the attached side of the vocal cord. Sometimes one vocal cord is seen to be bright red, whilst the other is of its usual white color, and the conges- tion may even be limited to a small por- tion of a cord. Sometimes the anterior half or third of the cord, sometimes the posterior portion, is affected ; or even a section of the whole length of a cord may be injected, whilst the rest remains of a normal color. In the latter case it is always the outer attached portion of the cord which is congested. Small pellets of mucus are often seen sticking to different parts of the laryngeal membrane ; and in 4 See Med. Times and Gaz., vol. xix. p. 366; and Brit. Med. Journ., Jan. 14, 1860. CHRONIC laryngitis. 23 cases of long-standing disease, the larynx has the appearance of being very much dilated and covered with secretion; on the other hand, the membrane may look dry and glistening. It is often noticeable that on attempted phonation, the vocal cords do not thoroughly approximate the congestion of the membrane interfering with the action of the muscles. Miscellaneous Symptoms.-The varying character of the expectoration may be in- ferred from what has been already stated, but it may be observed that it is seldom abundant, unless the laryngeal affection is complicated with bronchitis. The con- stitution does not generally suffer, but there is occasionally some sympathetic irritation. Course and Termination.-The tendency of the disease when once fully established is to remain stationary, or the symptoms may disappear for a short time, and then recur. The disease in old people is al- ways complicated with chronic bronchitis, and the symptoms of the later affection mask and outweigh in importance the morbid phenomena dependent on the chronic laryngeal disease. The principal danger is from chronic oedema coming on, but this is an exceedingly rare complica- tion. In some cases, especially between the ages of twenty and forty, persistent chronic laryngitis appears to predispose to the development of phthisis, but it is difficult to tell how far the laryngeal hy- persemia is concerned as a cause, and how far as a consequence. Diagnosis.-An accurate opinion can only be formed by a careful laryngoscopic examination. It is of the first importance to observe whether there be thickening or not; and in the former case to notice carefully whether there be merely inflam- matory tumefaction, oedematous infiltra- tion, or tuberculous exudation. In oedema the swelling is generally of a bright color, and has a characteristic transparent appearance ; in phthisis, on the other hand, the thickened parts are generally of a dull color-though the sur- face may be congested, and the swelling generally presents the appearance of a solid tumor (see "Laryngeal Phthisis"). In all cases of chronic laryngitis of some months' standing, the lungs must be most carefully examined, the history of the pa- tient and that of his family closely inves- tigated, and his general condition inquired into, before a decided opinion as to the nature of the disease is given. Pathology and Morbid Anatomy. -The disease is essentially a chronic in- flammation of the lining membrane of the larynx, in which the vessels of the areolar tissue participate very little. Enlarge- ment and tortuosity of the small vessels is found in cases of long-standing conges- tion, and occasionally, but very rarely, di- latation of the laryngeal canal takes place. Prognosis.-The disease never termi- nates fatally, unless some complication arises ; on the other hand, it is often dif- ficult to cure, especially in old people. Therapeutics.-Local remedies are the most important agents in the treat- ment. These are commonly called "caustics," but their action seems rather of an astringent character. Any of the following may be used:-Ferri per- chlor. (60 gr.), ferri persulph. (60 gr.), ferri sulph. (120 gr.), cupri sulph. (10 gr.), zinci chlorid. (30 gr.), zinci acet. (5 gr.), zinci sulph. (10 gr.), aluminis (30 gr.), alum, chlor. (60 gr.), dissolved in an ounce of water or glycerine. The latter vehicle, through its denser consistence, is better adapted for keeping up a prolonged action on the part. The chloride of zinc solution is the remedy which I most fre- quently employ; but provided that the application is made accurately and suffi- ciently often, it really matters very little which solution is used. The application should be made daily for the first seven days, every other day the second week, twice in the third week, and so on-grad- •ually lengthening the interval between the application. This is a general rule, but it must be modified according to cir- cumstances. In cases where there is ex- cessive secretion from the larynx (laryn- gorrhoea) the local application of turpen- tine sometimes does good, though these cases are very troublesome to treat. On the other hand, where there is long-stand- ing hypersemia, with diminished secretion -where the mucous membrane looks dry and shining-the remedy which I have found most successful is carbolic acid (from half a drachm to a drachm of the pure white carbolic acid to an ounce of glycerine). These local remedies can be best applied with the aid of the laryngo- scope-the laryngeal mirror being held in the left hand and a camel's-hair brush (fixed to a slender rod of aluminium at an angle of about 95° or 100°, and fastened in a wooden handle) in the right hand. Those who do not employ the laryngoscope should hold the patient's tongue well out, in such a position that the posterior wall of the pharynx can be seen, and should then pass the brush down between the latter and the base of the tongue. In this way the remedy is likely to reach the desired destination: the old method of pressing down the tongue with a spat- ula and using a flexible sponge probang could only end in failure. Instruments of the syringe character are quite unneces- sary for the application of remedies to the larynx, and they give rise to more irrita- 24 DISEASES OF THE LARYNX. tion than a simple brush. Powdered sub- stances likewise cannot be recommended •-they are, as a rule, either inert or inju- rious. Great benefit is, however, some- times derived from inhalation-either of steam impregnated with some stimulating volatile principle, or of atomized liquids of an astringent character. For the steam inhalations the following formulas will be found useful:- L- 01. pini sylvest. fl. dr. ij ad fl. dr. iij. Mag. carb. lev. gr. lx to gr. xc. Aquae ad fl. oz. iij. Mix. A teaspoonful to be added tc a pint of water at 150° F., and inhaled for five minutes twice or three times daily. R. Creasote, fl. dr. iij. Glycerine, fl. dr. iij. Aquae ad fl. oz. iij. Mix. A teaspoonful to a pint of water at 150° F. as above. R. 01. juniperi Aug. tq,xx. Mag. carb. lev. gr. x. Aquae ad fl. oz. iij. Mix. A teaspoonful for each inhalation as above. To either of these the addition of a scruple of camphor is often serviceable after the mixture has been used for about a week. For spray inhalations the following in- gredients are most to be recommended : the proportions given are always for one ounce of water; and the quantity to be used each time should be from two fluid drachms to half an ounce of the solu- tion :- Alum, 10 to 20 grains. Tannin, 1 to 20 grains. Perchloride of iron | to 2 grains. Ditto, 2 to 10 grains (in hemorrhage). Sulphate of zinc, 1 to 6 grains. Chloride of zinc, 2 to 10 grains. It is almost unnecessary to observe that the voice should be exercised as little as possible. For singers, actors, clergymen, and others whose occupations require them to use the voice much, rest of the vocal organ is of the utmost importance. When complete silence cannot be en- forced, the least possible exertion should be made in speaking-the patient should, in fact, whisper. All direct sources of irritation must of course be removed. Thus, if the uvula is much elongated, it must be amputated before a radical cure can be effected. As the pharynx is almost invariably more or less affected, astrin- gent lozenges will be found very useful. Tannin, rhatany, and kino may often be prescribed in this form with great ad- vantage.1 Change of climate is often very beneficial. Generally speaking, a warm dry atmosphere suits best, but providing there is no humidity the temperature is not so important. Thus, in parallel cases, I have seen equal benefit follow from a short residence in Algiers and a few weeks spent at Cromer or Margate. The warm relaxing climate of the south coast is generally injurious; but cold winds, especially those of an easterly character, often give rise to subacute inflammation. The waters of Ober-Salzbrunnen and Ems (source Kranzchen) are especially recommended by Niemeyer, who observes, that "'the influence of these waters, so manifestly favorable in many cases, can- not be explained by physiology. " Weil- bach, Eger, Kissingen, and Marienbad are recommended by other German writers, whilst French physicians praise the waters of the Pyrenees. Where suit- able atmospheric conditions cannot be selected, the patient must wear a respi- rator, when the weather is at all cold and damp, and must protect the neck and body generally by warm and suitable clothing. Medicines and hygienic treat- ment may be necessary in some cases, and must vary according to circun> stances. Varieties.-(1) Chronic Glandular Lar- yngitis. (2) Phlebectasis Laryngea. (1) Chronic glandular laryngitis is a variety of chronic inflammation in which the minute racemose glands are princi- pally affected. The credit of first noticing it is generally given, in this country and in America, to Dr. Horace Green of New York, but according to French writers it was described by Professor Chomel (Gazette Medicale, April, 1846) at least six months earlier. It has many synonyms: thus we have dysphonia clericorum (mal de gorge des ecclesiastiques, clergyman's sore-throat), angine glanduleuse,* laryn- gite granuleuse (ou granduleuse), follicu- lar laryngitis, follicular disease of the pharyngo-laryngeal membrane, and tuber- cular sore-throat. As the glands of the larynx are all of the racemose variety (Kblliker), the term follicular laryngitis is obviously incorrect, and glandular laryn- gitis designates the condition more accu- rately. The causes of the affection are the same as those which gave rise to sim- ple inflammation. The French, indeed, consider that it is of an "herpetic" na- ture, but this term is used in such a vague way by French authors, that it really has no definite meaning. The morbid pro- cess of the larynx often results from an extension of the disease from the pharynx, in which situation the follicles are princi- pally concerned ; it may, however, origi- nate in the larynx and afterwards reach the pharnyx. The disease is not peculiar to the clergy, nor is the chronic laryngitis, from which they often suffer, as a rule, of the glandular character. The disease 1 These lozenges have been prepared for me by Messrs. Bullock and Reynolds, 3 Hano- ver Street, who will be happy to give the formulas to any practitioner. MORBID GROWTHS. 25 might with equal truth be called "coster- monger's sore-throat." It is often asso- ciated with indigestion, but whether there is any causative relation between these conditions is uncertain. The symptoms are the same as those of simple chronic laryngitis, but perhaps milder-weakness of voice, fatigue after speaking, a con- stant inclination to clear the throat and swallow the saliva, or perform an act of deglutition, being the principal morbid phenomena. With the laryngoscope the enlarged orifices of the glands may some- times be seen on the epiglottis and the posterior part of the vocal cords as pale specks on the congested membrane, or as small red circles on the pale membrane ; the other laryngeal appearances do not differ from simple laryngitis, except that the approximative action of the vocal cords is more often feeble and imperfect. Constitutional debility was thought by Dr. Green to be a characteristic phenome- non, but there is very often no general weakness or evidence that the system at large is at all affected. As regards the pathology of the disease, it may be re- marked that it is essentially a disease of the secretory system, the normal secretion of the minute racemose glands, instead of being clear and transparent, becoming thick, white, and opaque. The morbid process is essentially mild, but very chronic, in character. The treatment should be the same as that recommended for simple chronic laryngitis. Solutions of the crystals of nitrate of silver (from two to four scruples of the salt to an ounce of distilled water) were strongly recommended by Green, and since "by other writers, but they do not seem to me to act more beneficially than other min- eral astringents. The sulphuretted waters of the Pyrenees, especially of Les Eaux Bonnes, are viewed by the French as almost specific in their action ; and sev- eral patients that I have sent there have derived undoubted benefit from the use of those waters, where the voice remains weak after the glandular disease has been cured. Benzoic acid lozenges often act very beneficially as nervo-muscular stimu- lants. (2) Phlebectasis laryngea,1 or venous congestion of the larynx, is an extremely rare affection. It may depend on general or local causes ; that is to say, it may oc- cur "in persons affected with a morbid preponderance of the venous system" (Hasse), or may be due to a local strain. The symptoms are generally slight; some alteration in the voice, an uneasy sensa- tion in the larynx, and perhaps a more or less frequent cough, being the principal morbid phenomena. The laryngoscopic appearances may be thus described :-In mild cases, when the disease is very lim- ited, extremely fine dark vessels may be running along the upper border of the ventricular orifice : in more severe cases there is less regularity in the distribution of the distended veins, which may be ob- served on the ventricular bands, vocal cords, and arytenoid cartilages. Cases have come under notice in which streaks of blackened mucus adhering to the larynx have been mistaken for varicose veins. This error needs only to be mentioned to be avoided. This condition of the larynx, independently of the inconvenience it oc- casions, is probably attended with some danger, as it most likely predisposes to passive oedema. The disease should be treated by the application of strong as- tringents ; and of these a saturated solu- tion of tannin in glycerine is the best. Constitutional remedies of a tonic and in- vigorating character should also be used. Morbid Growths. Definition.-New formations,whether of simple or malignant character, appear- ing as distinct tumors, projecting from the mucous membrane of the larynx, and more or less separated by a line of de- marcation from the tissue from which they grow. Synonyms. -Latin-Polypus Laryngis; French-Polypes du Larynx; German - Kehlkopfpolypen Neubildungen im Kehl- kopfe ; English-Polypus of the Larynx, Warty Growths, Warts, New Formations, Excrescences, Cancerous Growths, &c. Natural History.-Causes.-Benign growths in the larynx are probably almost always dependent on local hyperemia, and therefore their primary causes must be sought for under the head of Laryngitis. Chronic inflammation of persistent cha- racter but low degree is, probably, the condition most favorable to their develop- ment. Tn young children the disease is often attributed to an attack of croup, and it probably does originate sometimes in this way. The presence of a warty growth in the larynx, however, produces symp- toms closely resembling, and very likely to be mistaken for, those of croup. Nei- ther syphilis nor phthisis are predispo- nents. The evolution of cancerous growths in the larynx (as elsewhere) is dependent on laws of development which are not understood. Symptoms.-(a) Subjective.-The early symptoms are very vague, as the chronic laryngitis which precedes the new for- mation causes the same sensations (see Chronic Laryngitis). Patients occasion- 1 This disease was first described by the author in the Lancet, July 6, 1862. 26 DISEASES OF THE LARYNX. ally complain of a feeling of something striking in the throat, and when the growth is pedunculated there is some- times the sensation of a body moving about in the larynx. This, however, is quite the exception. Even in cases of true cancer there is seldom much pain. Difficulty of swallowing is generally pres- ent, if the growth attain to any size- especially if it affects parts concerned in deglutition or projects into the food-tract. Where the growth is large, shortness of breath is experienced. (6) Objective Symptoms.-(1) Vocal.- The voice is generally, but not necessarily, hoarse. Dysphonia is more common than aphonia. Small warts more often destroy the function than the larger and polypoid varieties (Czermak). The voice has sometimes a kind of paroxysmal or inter- mittent character, being one moment al- most normal, and at the next very hoarse, or even quite suppressed. (2) Respiratory.-The breathing is em- barrassed if the tumor is large, and there is sometimes stridulous breathing. The extent to which the respiration is affected bears a direct relation to the respective sizes of the growth and the laryngeal canal. On auscultation, moist sibilant rales may be heard over the larynx, and a val- vular murmur has been described as being very characteristic of the presence of a morbid growth (Ruble): it is not, how- ever, to be depended on. The cough varies in character and in frequency in different cases, and sometimes is of a croupy character. (3) Laryngoscopic Signs.-With the lar- yngoscope, the disease is generally at once revealed. The appearances vary according to the pathological nature of the tumor. Papillomata, which are the most common of all benign growths, vary in size from a grain of mustard to a wal- nut-their most common size being that of a large split-pea. These growths have generally a mammillary, lobulated, or cauliflower configuration. They are gen- erally of a lighter color than the surround- ing mucous membrane,and most frequently grow from the vocal cords. They are generally sessile and multiple. Fibrous tumors are seldom seen of such small size as those of papillary character, and they are also much less common. They vary in size, from a split-pea to an acorn, and have usually a smooth surface. They are generally single and pedunculated, and in seven of the fourteen cases that have come under my notice, the growth sprang from the vocal cords, and was confined to those parts. Fibro-cellular tumors are comparatively rare, and represent only about 5 per cent, of all benign laryngeal growths. They sometimes attain the size of a cherry, but are generally smaller. They are invariably pedunculated, gene- rally sessile, and usually of a pale color. Cystic tumors are seen as round egg-like projections, and as they usually give rise to some local irritation, they are them- selves red and surrounded by a hypersemic area. The other kinds of growth are too rare to require a special description. In cancer there is generally irregular thick- ening of some parts, and destruction of others. The former process usually pre- cedes the latter. Destructive ulceration is most characteristic of epithelial cancer; and thickening of the encephaloid variety. The epiglottis and ventricular bands (false vocal cords) are the most common seats of true cancer. In encephaloid cancer the parts are often so much displaced that there is difficulty in recognizing them. The epiglottis may be pushed completely on one side, and an ary-epiglottic fold or ventricular band may be so much swollen and inflamed as to cover the parts situated below, on the opposite side of the larynx. Growths, especially small ones, on or about the vocal cords, are apt, as Turek first pointed out, to give rise to functional paralysis of one of the vocal cords. (4) Miscellaneous Symptoms.-Occasion- ally the presence of a morbid growth is proved by the patient coughing up parti- cles which can be examined microscopi- cally. Sometimes the growth rises out of the larynx, and can be seen when the mouth is widely opened.1 In children it is sometimes possible to introduce the finger into the larynx and feel the growth ; but the small size and soft structure of these warty productions make it almost impossible thus to distinguish them. The expectoration is generally increased and altered slightly in small benign growths -very much in the case of larger ones and in cancer. Where the growth is small and benign, constitutional symp- toms may be, and generally are, altogether absent; but where the tumor is so large as to interfere seriously with respiration, the system at large is likely to sympa- thize : in some of these cases there is irri- tative fever, whilst in others the constitu- tional symptoms are more those of hectic. In the case of true cancer, the characteristic cachexia is present. Course and Termination.-In the case of non-malignant growths, the symptoms generally develop themselves slowly, tak- ing several months for their evolution; after attaining a certain degree of severity, they often remain stationary, unless some complication, as oedema or spasm of the glottis, occurs. The latter condition is likely to supervene if the growth is large ; and it gives a paroxysmal character to the 1 Horace Green on Morbid Growths in the Larynx, p. 62; and Rayer, Maladies de la Peau, tome ii. p. 422. MORBID GROWTHS. 27 symptoms. The advanced symptoms are those of impending suffocation. Epithelial cancer usually gives rise to more distress- ing local symptoms ; there is more expec- toration, and deglutition is often difficult and painful. In encephaloid cancer the symptoms progress more rapidly, the fatal termination usually taking place within a few months of its first appearance. This, however, is not always the case.1 The patient sinks from the combined effects of gradual suffocation, slow starvation, and the intrinsic nature of the disease. Diagnosis. - Tumors in the larynx cannot well be mistaken for any other disease, if a laryngoscopic inspection can be made. The possibility of eversion of the ventricle must not, however, be for- gotten. The tubercles of syphilis are seen as irregular whitish prominences on the congested mucous membrane - the posterior wall of the larynx being their most common site. The thickening of laryngeal phthisis is not so great as that of true cancer, nor has it the defined cha- racter of the benign kinds of growth. It is not quite so easy to distinguish between the benign and the malignant epithelial growths. The former, however, are more strictly defined, and never (unless quite accidentally) ulcerated, whilst in the lat- ter there is generally irregular thickening from interstitial exudation, and frequently ulceration. The microscope cannot be relied upon for differential diagnosis should particles be expectorated, or re- moved during life with the aid of the laryngoscope. Several cases have come under my notice where the histological features were decidedly those of cancer, whilst the clinical history was of a totally opposite character. The laryngoscopic appearances and constitutional symptoms furnish much more important indications in relation to the differential diagnosis of the various kinds of growth than the microscopic examination. Pathology.-The non-malignant kinds of tumor are essentially local productions -the result of a perverted nutritive pro- cess in which growth is excessive and de- velopment imperfect. Hence the forma- tion of tissues of abnormal size and mor- bid structure. They are probably always associated in their origin with local hy- persemia. In the case of malignant growths, in addition to the local changes, there are constitutional influences in ope- ration which will be found fully described elsewhere. Morbid Anatomy. - The benign growths found in the larynx are Papillo- mata, Fibromata, Fibro-cellular Tumors, Cystic Tumors, Sarcomata, and Lipo- mata, and they are here enumerated in their order of frequency. The malignant growths belong either to Epithelial or Encephaloid varieties. Papillomata are by far the most com- mon of laryngeal growths, three-fourths of all the benign cases being of this na- ture. The papillary growths, "in their general form and arrangement, have many points of resemblance, but on the enlarged scale, to the papillse, which in various localities constitute natural pro- jections from free surfaces, more espe- cially from the skin and mucous mem- branes. Their basis substance is formed of connective tissue, which is continuous with that which normally exists in the part; whilst the free surface is covered by an epithelium, which may vary in thickness and its number of layers ac- cording to the seat of the tumor. Blood- vessels and even nerves enter into the in- terior of the papillae. These papillary growths vary in size from a pin's-head to a cherry, and may even attain a larger size ; but after reaching a certain magni- tude their growth sometimes ceases spon- taneously. They grow rather quickly, especially in their early stages. To the naked eye they have a rough lobular laminated appearance, and they are gen- erally soft and even friable to the touch. Dr. Andrew Clark has kindly made mi- croscopic examinations of many of the growths of this kind, which I have re- moved during life with the aid of the laryngoscope. He has described them generally as "consisting of more or less perfect connective tissue, clothed with many layers of epithelium." In some of them " enlarged racemose glands, the ter- minal vesicles of which were filled with minute nucleated cells and granular mat- ter," were observed. Dr. Andrew Clark thus described one case:-"The growth was found to consist of two sets of parti- cles, one membranous, the other warty or obscurely papilliform. The membranous portions consisted of from twenty to thirty layers of scaly epithelium, surrounded and penetrated by a confervoid growth. The epithelial cells composing the layers were polygonal, flattened, nucleated, and easily affected by weak alkalies and acids. The nucleus of each cell was oval, ab- ruptly defined, rather large in proportion to the containing cell, in most cases sur- rounded by a clear halo, and in some 1 Lectures on Surgical Pathology. By James Paget, F.R.S. 3d edition, p. 591. For an elaborate description of these growths, the reader is referred to Virchow's Krank- heiten Geschwiilste, vol. i. p. 334 et seq. This eminent pathologist regards Papillomata as a sub-order of his large division of Fibromata, 1 See specimen No. 28, Series xxv., in the Museum of St. Bartholomew's Hospital. 28 DISEASES OF THE LARYNX. showing signs of division. The papillary portion consisted of simple outgrowths of nucleated connective tissue, and rudely- formed bloodvessels, clothed with numer- ous layers of scaly epithelium, similar to those already described. Some of the pa- pillae exhibited large vacuoles or spaces filled with colloid matter, which in one or two instances had burst through the cov- ering epithelium." Papillomata show a greater disposition to recurrence than other growths. Fibromata.-The fibrous tumors of the larynx, like those occurring elsewhere, are found to consist of bundles of white fibres diverging and interlacing in various directions. They seldom attain a larger size than a hazel-nut, and when removed show no disposition to recurrence. Fibro-cellular Tumors of the larynx are comparatively rare. Their growth is rather slow, but they sometimes attain a huge size. "They consist," says Mr. Paget, " of delicate fibro-cellular tissue, in fine undulating and interlacing bun- dles of filaments. In the interstitial liquid or half-liquid substance, nucleated cells appear imbedded in a clear or dimly gran- ular substance."1 Unlike the mucous polypi of the nose, they exhibit no dispo- sition to recurrence. Cystic Growths are still more uncommon in the larynx. I have only met with two cases-both situated on the epiglottis. They are, however, occasionally found near the ventricular orifice. They contain a thick, white, semi-fluid sebaceous mate- rial, which on microscopic examination is found to consist of epithelial cells under- going fatty degeneration, with perhaps a small amount of the proper secretion of the glandulse. When thoroughly emptied they show no disposition to form again. The other kinds of benign tumors, such as Lipomata, Vascular Tumors, Hydatids, &c., are too rare to require a special de- scription in an article of this kind. Cancer.-Under Cancer we must con- sider the two kinds which are found in the larynx. These are (1) malignant epi- thelial, and (2) encephaloid. (1) Malignant epithelial. Though considered with ref- erence to other morbid conditions of the larynx, epithelial cancer is not common; as compared with many other situations, the larynx must be regarded as a favorite site. The epiglottis is the part most fre- quently attacked and next to it the ary- epiglottic folds. It often gives rise to large ragged ulcerations. The disease may be primary, or consecutive to disease in adjacent parts-the pharynx, oesopha- gus, or thyroid gland. Cancer in the larynx is seldom secondary, in the sense that the term is generally employed by pathologists. (2) Encephaloid cancer is less common than the epithelial variety, but, like it, it is often consecutive. It is characterized by its greater tendency to induce interstitial exudation and conse- quent thickening, and perhaps by its lesser proneness to ulceration. As al- ready remarked, it often produces consid- erable displacement. In addition to the different forms of morbid growth here described, others are said to have occasionally existed in the larynx. Ryland quotes a case of " hyda- tids" in the ventricle of the larynx, from Andral, which gave rise to the symptoms of a foreign body at that part.1 The same author speaks of "cartilaginous tumors" in the larynx, and gives several illustrations of supposed tumors of this sort. There is no reason why enchon- droma should not be developed in this part, but it is exceedingly rare, and has not been observed by any pathologist of note. Erectile tumors are described as occurring in the larynx, by Rokitansky. Prognosis.-The prognosis as regards a fatal termination depends on the nature of the growth, and as regards recovery of function, on whether the growth can be removed. Cases of true cancer of course, always prove fatal: whilst the other kinds of tumor ought never to do so. Therapeutics.-Small growths not giving rise to functional disturbance, and showing no disposition to increase in size, need not be interfered with; but where the neoplasm is large, and where it shows a disposition to grow, it should, if possible, be removed with the aid of the laryngo- scope. This removal may be effected by evulsion, for which various instruments are suitable. Most to be recommended are forceps of different lengths and open- ing in different directions; thus, for a growth on the ventricular band, a pair of short forceps opening in the lateral direc- tion is required, whilst for a growth on or below the vocal cords a much longer for- ceps, and opening in the antero-posterior direction are indicated. My tube-forceps are very useful, especially if the larynx is small. Ecraseurs are not, as a rule, to be recommended, but Stoerck's ecraseur, which has a rigid metal loop protecting the wire, is, however, often serviceable. No force should be used in the evulsion of growths. Where they cannot be removed without undue effort, crushing of the growth will often cause atrophy. In some cases, the base of the growth may be incised with the laryngeal lancet; or if the tumor be too large for this method, forceps having a cutting edge may be em- ployed with perfect safety and with the best results. Galvano-cautery, on ac- 1 Op. cit. p. 456. 1 Ryland, Diseases of the Larynx, p. 226. NEUROSES of the larynx. 29 count of the pain it generally causes, and the risk of subsequent inflammation, can- not be recommended. Caustic solutions I have not found to be of any service ex- cept in those cases where the growths, small in size and symmetrical in situa- tion, are of the nature of condylomata. In these cases the tumors possess but a very feeble organization, and are often dispersed by the application of caustic or astringent solutions. Should the growth be very large and threaten suffocation, and should severe spasm be induced by attempts at removal through the upper opening of the larynx, the operation of tracheotomy should be performed ; the neoplasm may be after- wards removed, either with the aid of the laryngoscope or by division of the thyroid cartilage. In cancer, relief can some- times be obtained by the inhalation of simple hot steam, or steam impregnated with various sedative principles, as re- commended in the treatment of Acute Laryngitis. I have seen a few cases in which removal of a malignant growth, situated so as to seriously impede respira- tion and deglutition, has been attended with very great temporary relief. One such case is reported in Pathological Transactions, vol. xxi. p. 53. Neuroses (Nervous Affections of the Larynx). Under this head are included-(1) Dis- eases of the Motor System, and (2) Dis- eases of the Sensory System. DISEASES OF THE MOTOR SYSTEM. This division embraces-first, Paral- ysis of the Muscles of the Vocal Cords ; and secondly, spasm (or Spasmodic Ap- proximation) of the Muscles of the Vocal Cords. The varieties of paralysis are so numer- ous, and their nature so different in differ- ent cases, that it is better to consider them separately under the following heads : (1) Paralysis of the Adductors of the Vocal Cords ; (2) Paralysis of the Ab- ductors of the Vocal Cords. These may again be divided into (a) unilateral and (6) bilateral paralysis. Bilateral Paralysis of the Adductors of the Vocal Cords. Definition.-A condition in which, owing to the non-approximation of the vocal cords on attempted phonation, there is loss of voice. Synonyms. - Latin - Paralysis Glot- tidis, Aphonia Paralytica, Aphonia; French - Aphonie ; German - Kchlkop- flahmung ; English,-Functional Aphonia, Hysterical Aphonia, Aphonia. Causes.-Debility and hysteria are the most frequent causes of this condition ; it often, however, originates in congestion, and remains after the hypersemia has passed away. The rare cases of inter- mittent aphonia dependent on malarious influences, which have been reported,1 probably belong to this category. I have once seen it caused by extensive cerebral disorganization from a tumor at the base of the brain. Symptoms.-The condition is seen with the laryngoscope, on directing the patient to attempt to produce some vocal sound, -that is, to try to say "ah" or "e;" the vocal cords may not move, or may ap- proach each other only very slightly-in all cases remaining distinctly apart. As the vocal cords remain at the side of the larynx, the condition might be called " bi- lateral paralysis with lateral fixture." The laryngeal mucous membrane is gen- erally pale. The voice, of course, is always suppressed. It is only the volun- tary action of the adductors of the vocal cords which is impaired ; the involuntary or reflex movements, especially those of a forcible character, are not generally affected. Thus, coughing and sneezing are usually accompanied with sound, show- ing that the cords approximate. In laugh- ing, however, where the expirations are much less forcible, especially in feeble people, there is often no sound. In other words, these patients do not laugh, but only smile, the term "laughter," strictly considered, being an audible manifesta- tion. The constitutional condition is such as has been already indicated under the head of the Causes of the local phe- nomena. Pathology. - The pathology of the disease probably consists in the "nerve- force" being feebly or imperfectly evolved, or not directed in the proper channel: there is no lesion here. The muscles, which are paralyzed, are the crico-arytse- noidei laterales on both sides, and the arytsenoideus proprius. Prognosis. - The prognosis is very favorable in almost all cases. Treatment.-The treatment consists in the use of local remedies which tend to excite approximation of the vocal cords. Stimulant solutions were formerly recom- mended, but faradization is a far more effective remedy. One pole should be ap- plied over the thyroid cartilage externally, 1 Valleix, Bulletin de Therapie, 1843. 30 DISEASES OF THE LARYNX. the other one to the vocal cords. My "laryngeal electrode"1 will be found very useful. With it, I have cured aphonia of eight, and even ten years' standing. The instrument has been also successfully used by other laryngoscopists, both in this country and on the Continent. The pa- tient's health may generally be benefited by constitutional (tonic) remedies. Unilateral Paralysis of the Adductors of the Vocal Cords. Definition.-A condition in which, owing to one of the vocal cords not being drawn to the median line on attempted phonation, there is loss of voice. Causes.-The condition may be caused by local injuries, may occur in chronic toxaemia (lead and arsenic), or may be due to cerebral disease, or pressure on the pneumogastric or its recurrent branch. It is difficult to say whether its occur- rence as a sequel of diphtheria is due to the first or second cause. Symptoms.-The condition is seen with the laryngoscope. On attempted phona- tion one vocal cord remains at the side of the larynx, whilst the other is drawn to the median line. The condition may be described as "unilateral paralysis with lateral fixture." The mucous membrane covering the affected cord is generally congested. There is aphonia or dyspnoea, and usually an absence of constitutional symptoms. When the paralysis is com- plete, or even much marked, the acts of coughing, sneezing, and laughing are always altered in character, and often unaccompanied by sound : indeed, a modi- fication of the natural cough or sneeze is sometimes one of the earliest symptoms of the condition. When the unilateral paralysis is accompanied with loss of power of the same side of the tongue and palate, it indicates serious cerebral dis- ease near the nucleus of the spinal acces- sory nerves.2 Pathology.-As regards the patho- logical anatomy, I may observe, that in the only case of this disease-a case of seven years' standing, which I have ex- amined after death, there was consider- able atrophy of the crico-arytsenoideus lateralis on the affected side. The ary- trenoideus proprius did not seem to suffer. The disease is probably often due to in- flammatory exudation, either of a simple or dyscrasic character, into the substance of the muscle. When the pneumogastric nerve or its recurrent branch are pressed upon, the abductor muscle is always so much more affected than its antagonist, that the function of the adductor seems to be little affected. Prognosis.-The condition not being in itself dangerous, and being generally due to local causes, need not, as a rule, give rise to serious apprehensions. If there is evidence, such as paralysis of other parts, to show that the disease is due to cerebral causes, the prognosis is, however, serious. It is always very diffi- cult to cure. Treatment. - This should be the same as that recommended for bilateral paralysis of the adductors ; it is not, how- ever, generally so successful. When re- sisting the action of my ordinary elec- trode, the "No. 3 laryngeal electrode," by means of which one pole can be passed into the larynx and the other into the hyoid fossa, so that the current passes through the crico-arytaenoideus lateralis, may be employed. Constitutional reme- dies may be used with advantage in cases of chronic toxaemia. Bilateral, Paralysis of the Abductors of the Vocal Cords. Definition.-A condition in which, owing to the vocal cords not being drawn aside (but remaining fixed near the me- dian line) in inspiration, there is great dyspnoea and stridulous breathing, with- out much alteration in the character of the voice. Causes.-The causes of this condition are generally cerebral, but morbid influ- ences which affect both pneumogastric or both recurrent nerves may give rise to it. In a case of ex-ophthalmic goitre, I once saw it caused by an enlarged and con- stricting thyroid gland, which passed round the trachea and pressed on both recurrent nerves; scrofulous deposit in the bronchial and cervical glands, espe- cially in children, is apt to give rise to it. In cancer of the oesophagus, when the de- posit affects the anterior wall of that tube, both the recurrents may be involved. It is, however, most commonly caused by central disease of the nervous system. It sometimes depends on simple degenera- tion of the muscles, without there being any evidence of implication of the nerves. The condition is fortunately very rare. Symptoms. - On making a laryngo- scopic examination, the vocal cords do 1 Made by Mayer, 59 Great Portland Street, W. 2 See Dr. Hughlings Jackson's valuable Il- lustrations of Diseases of the Nervous System. Lond. Hosp. Reports, vol. i. p. 361, and vol. ii. p. 330. PARALYSIS OF ABDUCTOR OF ONE VOCAL CORD. 31 not separate at all on inspiration. There is a slight interval between them, which alters very little, except in forced expira- tion, as when the vocal cords approximate completely. As the vocal cords always remain near the median line in this form of paralysis, it might be called "bilateral paralysis with central fixture." The vocal cords are generally slightly con- gested. The voice is usually but little affected, but it may be rather harsh: if the patient does not move at all, the res- piration may be little affected; the least exertion, however, brings on dyspnoea and stridulous breathing. The cough is croupy. The condition is in itself apt to produce constitutional symptoms-such as wasting and febrile excitement; and it is often accompanied by paralysis of other parts, or by the cachexia of the dis- ease which indirectly causes it. In chil- dren, it produces the symptoms of laryn- gismus stridulus, and Dr. Ley considered that laryngismus was always of a para- lytic nature, and always due to the same cause-namely, pressure on the recurrent nerves. True laryngismus depends on other causes which operate in an opposite way.1 The paralysis of the abductors of the vocal cords, which produces symp- toms of laryngismus, is found in children of a more advanced age than those who are attacked by the ordinary form of la- ryngismus-that is, by spasmodic laryn- gismus ; of course, however, the paralytic form may also occur to the youngest in- fants. It differs also, inasmuch as the symptoms do not completely pass away; exacerbations may occur, but there is always a certain amount of constant stridor and dyspnoea. Pathology and Morbid Anatomy. -The pathology of the disease has, to a certain extent, been discussed in consid- ering its etiology. The disease consists essentially in a loss of power of the ary- teenoidei postici, the powerful abductors of the vocal cords, and is dependent on the interception or non-generation of the nerve current which, through the medium of the pneumogastric and it branches, supplies those muscles in the normal state. In the case of a patient under the care of Dr. Hughlings Jackson in the London Hospital, where I had diagnosed bilateral paralysis of the abductors during life, these muscles, when examined by Mr. Rivington after death, were found to be greatly atrophied. There is probably, generally, also atrophy of the nerve struc- ture. Prognosis.-The prognosis is very se- rious both on account of the immediate danger of suffocation implied by the con- dition, and from its being sometimes an indication of some very serious disease elsewhere, either in the brain or along the trunks or branches of both pneumo- gastric nerves. The condition is in itself highly dangerous ; for though the simple action of the adductors (the abductors being paralyzed) is not generally suffi- cient to close the glottis completely, the addition of a little inflammatory swelling or cedema would soon bring about that state. Treatment.-The operation of tra- cheotomy should be performed without delay, to save the patient from dying of suffocation. The operation would be likely to exercise a favorable effect on the cerebral disease, for the indirect influence of the exceedingly narrowed glottis (through the respiratory system) on the cerebral circulation must be highly inju- rious. I cannot recommend any medical treatment either of a local or general character. Unilateral Paralysis of the Abductor of one Vocal Cord. Definition.-A condition in which, owing to one vocal cord not being drawn aside (but remaining near the median line) on inspiration, there is some dys- pnoea and stridulous breathing, without much alteration in the character of the voice. Causes.- The causes which lead to paralysis of one abductor are the same as those which produce the bilateral form of paralysis, but the condition now under consideration is more often due to peri- pheral causes ; that is to say, to pressure on one pneumogastric or one recurrent nerve. Aneurisms of the arch of the aorta by pressure on the left recurrent nerve not unfrequently produce this kind of paralysis of the left vocal cord and in the year 1866 a case of aneurism of the right carotid occurred in my practice, in which the right vocal cord was paralyzed. Cancer- ous tumors occasionally involve the pneu- mogastric or its branches, and the stru- mous glands along the trachea may do so likewise. In malignant stricture of the oesophagus, when the disease affects the anterior wall of that tube, one of the re- current nerves is occasionally affected. Symptoms.-The condition can be ob- served with the aid of the laryngoscope ; on directing the patient to inspire, the affected vocal cord is not drawn to the 1 See Spasm of the Vocal Cords, p. 448. 1 Med. Times and Gaz., January, 1864, and Pathol. Transactions, vols. xvii., xix., and xxi. 32 DISEASES OF THE LARYNX. side as in the normal state; its inner edge, however, is not quite in the median line. The vocal cords are generally congested. The condition may be described as " uni- lateral paralysis with central fixture." There is stridulous breathing and dys- pnoea on the slightest exertion, but the last two symptoms, as might be expected, are not quite so severe as where both cords are affected. The constitutional symp- toms vary with the different conditions which give rise to this form of paralysis, but this kind of glottic obstruction gene- rally after a time causes symptoms of irri- tative fever. Pathological Anatomy.-The im- mediate nature of the disease and condi- tion of the nerves and muscles is the same as that which is found in bilateral paral- ysis with central fixture, but here the dis- ease only affects one side. In several cases which I have brought before the Pathological Society of London,1 the mus- cle of the affcted side has been seen to be completely wasted-only a few of its inner and lower fibres remaining, whilst its fellow on the opposite side was healthy and well nourished. In some of these cases the left recurrent nerve has been so completely incorporated in a cancerous or an aneurismal tumor, that its course (after entering into the tumor) could not be traced. Prognosis.-The condition is generally indicative of very serious disease else- where, and the most unfavorable opinion should be given as to the prospects of the case. Treatment.-There is generally little to be done towards the cure of the disease: tracheotomy should be performed if the symptoms of suffocation are at all urgent. Varieties.-In addition to the more palpable forms of paralysis which on the one hand produce aphonia, and on the other lead to suffocation, there are certain states in which loss of power is manifested, by the inability to produce certain notes in singing. Here the crico-thyroid or thyro-arytenoid muscles-muscles, the ac- tion of which, though generally supposed to be antagonistic, is probably, in point of fact, co-ordinate-are generally at fault. The limits of this article render a detailed handling of this difficult subject impossi- ble ; but for further details the reader is referred to my pamphlet on the subject.2 The prognosis, as regards cure, must de- pend on the age of the patient, the dura- tion of the condition, and the natural character of the voice (whether it be tenor or bass). The treatment must sometimes be stimulant (electricity, astringent solu- tions, &c.), at other times sedative. Spasm {or Spasmodic Approximation) of the Muscles of the Vocal Cords. Definition. - A condition in which there is sudden temporary complete or in- complete approximation of the vocal cords, characterized in I he former case by arrest of the respiratory movements and apnoea, in the latter by stridulous inspiration and dyspnoea. Synonyms.-Latin-Laryngismus stri- dulus, Laryngitis stridula, Spasmus glot- tidis, Cynanche stridula, Cynanche tra- chealis, spasmodica, Asthma Koppii, Asthma Millari, Asthma intermittens in- fantum, Asthma thymicum; French- Laryngite striduleuse, Faux croup, Pseu- do-croup nerveux, Spasme de la Glotte ; German- Kehlkopfkrampf, Stimmritzen- krampf (Cerebral Croup, Pseudo-Croup); English-Millar's Asthma, Crowing In- spiration, Child-crowing, Spasm of the Glottis, Spasmodic Croup, Spurious Croup, Cerebral Croup, &c. &c. Causes.-The causes of spasm of the vocal cords are involved in a considerable amount of obscurity, and there is evidence to show that many influences may be con- cerned in its production ; hence it is not surprising that the etiological features concerning it should have undergone vari- ous changes and modifications. The causes may be divided into (1) cen- tral, and (2) peripheral-the latter being subdivided into (a) direct, and (6) reflex. 1. The disease was at one time consid- ered to be always dependent on cerebral disease, or at least on a disordered state of the functions of the brain,1 and this view, which has been assailed in various ways, seems to be again gaining ground. Numerous cases are on record, where other admitted symptoms of cerebral dis- ease manifested themselves before the oc- currence of laryngeal spasm. Limited congestion or interstitial exudation of serous fluid, near the origin of the pneu- mogastric nerves, is probably the condi- tion of the brain which is concerned in the production of this phenomenon. In many cases, however, the structural alter- ation of the brain, if present, is of too delicate a nature for detection, and still more frequently a morbid condition of that organ is produced by the sudden apnoea. Hence, even when the brain is the pri- mary seat of the disease, it is impossible 1 Pathological Transactions, vols. xvii., xix., and xxi. 2 Hoarseness and Loss of Voice. Churchill, 1868. 1 Commentaries on Diseases of Children, by Dr. John Clarke. LARYNGISMUS STRIDULUS. 33 to speak with certainty as to the nature of the morbid condition. The cerebral affection is probably often dependent on a dyscrasic state. A rachitic condition of the bones of the skull has frequently been noticed. Out of ninety-six cases of laryngismus exam- ined by Lederer, there was craniotabes in ninety-two.1 The experience of Sir Wil- liam Jenner and Dr. Wiltshire is of a similar character.2 It has been suggested that the thickness of the cranial bones in rickets allows pressure to be exercised on the brain in the occipital region, when the child lies on its back (Elsiisser); but it is more probable that the rachitic dyscrasia is accompanied by morbid changes of a nutritive character in the structure of the brain itself. Scrofula has also been regarded as an active predisposing cause of the disease (Marsh). Sometimes an attack is brought on by tossing the child in the air, and it still more often comes on in sleep. These facts have been adduced by some as an evidence of the cerebral nature of the dis- ease ; but it must be remembered that both in sleep and in sudden movements of the body the function of respiration not less than the cerebral circulation is modified, and that the spasm of the glot- tis may originate in either process. Dis- ease of the cervical portion of the spinal cord sometimes gives rise to it (Marshall Hall). In cases of disease of the brain or medulla, external pressure applied over these parts has been known to cause laryn- gismus. Hydrocephalus exists in some cases ; and mental emotion-especially terror and rage-occasionally gives rise to the spasm. 2. (a) Direct pressure on the recurrent or pneumogastric nerves by enlarged and tuberculous cervical and bronchial glands has since Dr. Ley's time been regarded as a cause of laryngismus, but in these cases the cause is probably (as Dr. Ley con- ceived) "paralysis of the dilators of the glottis." Enlargement of the thymus gland was at one time, especially in Ger- many, considered the essential cause of laryngismus,3 but at present its influence is considered to be of a very exceptional character. In so far as these causes ope- rate by producing paralysis of the abduc- tors of the vocal cords they belong to the last section of neuroses, but they probably often cause spasm of the adductors by obstructing the venous circulation through the neck, and thus giving risp to cerebral irritation. (6) Amongst the reflex causes of spasm we have those acting directly on the larynx and those operating at a distance. Attacks not unfrequently come on whilst the child is sucking, or rather swallowing, and there can be little doubt that the cause here is the passage of liquid into the larynx. Spasm produced by dangling the child in the air is probably caused by the impression of a current of air on the glot- tis. Amongst the reflex causes of laryn- gismus which act at a distance, there is the irritation of teething, the presence of indigestible food or helminthoid parasites in the alimentary canal, and the impres- sion of currents of cold air on the integu- ment. It sometimes supervenes on the cure of a protracted diarrhoea or a chronic skin affection, but these causes probably act by setting up cerebral irritation. It has been noticed by Sir William Jenner1 that the mother's health has an important influence in the production of rickets, and Kopp has made precisely the same obser- vation with regard to laryngismus. Here there is another link towards the chain of association which Sir William Jenner has attempted to establish between these two morbid conditions. The greater liability of the male sex, which occurs in other laryngeal diseases, holds good here. The disease is most frequent between the ages of six months and two years. Symptoms,-The age of the patient de- stroys the value of subjective symptoms, but those of an objective character are sufficiently marked. The following is the common history of a first attack. A child put to bed, apparently in its ordinary state of health, wakes up suddenly at about midnight with difficulty of breath- ing, inspiration being accompanied by a crowing noise similar to that heard in croup. After two or three of these strid- ulous inspirations, the frightened child bursts out crying and in a few minutes is fast asleep again, as if nothing had oc- curred. This description does not apply to every case. The child may have been peevish and fretful for a few days before, may have suffered from loss of appetite, and may have been restless at night, or a slight "catch" in the breath may have been previously noticed. The first attack may come on at any other time, but it most frequently occurs during sleep. The next day the child may be quite well, and there may be no further return of the symptoms, but it often happens that an- other attack comes on about the same hour the following night. The second attack is generally more severe than the first, both in its character and duration. In severe cases, indeed, the paroxysms are of a most urgent kind and of the most frequent occurrence. A severe fit of 1 Riihle, Kehlkopfkrankheiten, p. 201. Berlin, 1861. 2 See art. Rickets, vol. i. p. 472. 3 Kopp, Denkwiird. in der arzt. Prax. Frank., 1820. vol. n.-3 1 Op. cit. 34 DISEASES OF THE LARYNX. laryngismus may be thus described : the | breathing suddenly becomes greatly em- barrassed, each act of inspiration being much prolonged and accompanied by a harsh stridor : suddenly the sound ceases, the glottis is completely closed, and the respiratory movements of the chest are suspended. The flush which first lit up the countenance gives way to pallor and afterwards to lividity. The eyeballs roll, the veins of the neck are turgid, the fin- gers close on the thumb, which is bent in the palm, and the hands are flexed on the wrist; spasm likewise affects the feet, the great toe is drawn away from the other toes, and the foot is flexed and rotated slightly outwards. These so-called "car- po-pedal" contractions are probably some- times accompanied with great pain. The disease, indeed, may partake of the cha- racter and assume the form of epilepsy. Notwithstanding the severity of the par- oxysm just described, the patient may survive it, the apneea being succeeded by stridulous breathing, and by relaxation of the spasmodic contractions of the feet and hands ; but when the symptoms are of the dangerous character just described, the paroxysm is sure to be quickly followed by others-in one of which the child dies. The severity of the attacks varies between the mild paroxysm which has been de- scribed as occurring at the commencement of the disease, and one sufficiently intense to cause death. The spasm is character- ized by its sudden occurrence and by its complete remission, as a rule by the entire absence of febrile irritation, and by the progressive severity of the spasm, as re- gards recurrence, duration, and intensity. Some of the associated symptoms of laryn- gismus may likewise be present, such as hydrocephalus, a rachitic condition, or enlargement of the thymus body. Diagnosis.-The non-febrile and dis- tinctly intermittent nature of the affection differentiates it from true croup, and its own distinctive characters from all other diseases. Pathology. - The pathology of the disease has been considerably encroached upon in considering its causes, but there still remains something to be said con- cerning its nature. There are two points on which it appears to me necessary to insist: these are (1) that in all cases there is an altered state of the nerve-centres; and (2) that the immediate cause of the phenomena of the stridulous inspiration and apnoea is spasm of the adductors of the vocal cords. The facts which point to an alteration in the brain substance (whether recognizable or not) are first, that both sides of the body (both vocal cords) are affected; secondly, that the various causes (such as dentition, indi- gestion) are not only often in operation without the production of laryngeal spasm, but when they do give rise to that symp- tom they necessarily act through the brain ; thirdly, that frequently other ad- mitted symptoms of cerebral irritation, such as the carpo-pedal contractions, are present. That the disease depends on spasm of the adductors of the vocal cords appears probable for the following rea- sons :-(1) The other phenomena are those of spasm (carpo-pedal contractions). (2) Complete closure of the glottis never takes place under physiological conditions, and therefore it is improbable that the simple action of the adductors of the vocal cords could cause complete closure of the glottis (the action of the abductors being in abey- ance) ; in support of this view I may ob- serve that in three cases of paralysis of the crico-arytenoideus posticus which have come under my notice, the inner edge of the affected cord was not adducted to the median line. (3) The total remission of so urgent a symptom points to its cause being of a spasmodic nature ; there being, as far as I am aware, no instance of com- plete paralysis of a truly paroxysmal cha- racter. Prognosis.-The prognosis depends on the character of the paroxysm and its sup- posed cause. The cases mainly dependent on reflex causes (dentition or irritation of the alimentary canal) generally do well, whilst those due to direct pressure, and those mainly caused by cerebral irritation are more frequently fatal. Thymic asth- ma is especially dangerous, and if there is evidence (such as considerable enlarge- ment of the gland) to show that the spasm is of that character, the most unfavorable opinion must be given. The length of the intervals between the paroxysms is a good prognostic guide-the longer the in- terval the better the chance of recovery. Treatment.-The treatment must be twofold: first, to relieve quickly the spasm of the glottis; secondly, to attack the source of the disease. The immediate treatment generally falls to the nurse or mother. The little patient should be raised and placed in a sitting posture, and then he may be slapped on the back, cold water may be dashed in the face, and ammonia or strong acetic acid held to the nose. These measures are often success- ful by giving rise to violent expiratory actions ; but remedies calculated to re- lieve spasm are equally successful. The warm bath may be used and emetics given directly there is a sigri of the stri- dor-when the paroxysm is on, the child will not drink. A favorite remedy in Ger- many, and one that is highly successful, is tickling the fauces with the finger or a feather until vomiting is produced. De- DISEASES OF THE SENSORY SYSTEM OF THE LARYNX. 35 pressing enemata, such as tobacco, have likewise been recommended, but their use is attended with considerable danger. The ordinary rules for the treatment of disease apply here; that is to say, gentle reme- dies should be used in mild cases and those of a more powerful character in dangerous ones. Putting the lower part of the child's body in a hot bath and dashing cold wrater in its face is a simple and sometimes successful plan. The in- halation of chloroform is a very valuable remedy, but of course must be used with great care, and cannot safely be employed by non-professional persons. If the child appears to be sinking from the apnoea, the trachea must, of course, be opened, and artificial respiration resorted to. Indeed this should even be adopted by the prac- titioner, should he arrive shortly after the apparent extinction of life. Some prac- titioners recommend the use of antispas- modic remedies (whether animal, vegeta- ble, or mineral) between the fits. As regards the fans et origo mali, the most suitable treatment will be found detailed in the various articles in these volumes which treat of scrofula, rickets, hydro- cephalus, dentition, parasites, &c. En- largement of the thymus must be treated by the application of leeches (according to the age and strength of the patient), and afterwards by counter-irritation. Varieties. - The ordinary kinds of laryngismus, according to my views, are essentially due to spasm of the adductors of the vocal cords, but that variety which is caused by pressure on the pneumogas- tric or recurrent nerves is due to paralysis of the abductors. It has been treated of in the last section of neuroses; and differs from ordinary laryngismus, in the ways there indicated. It appears to me that Dr. Ley was right as to the cause of the symptoms of a certain form of laryngis- mus, but mistaken in regarding a rare variety as a typical example. This view explains the very opposite opinions which have been held concerning the etiology and pathology of the disease. I have thought it more convenient to treat spasm of the glottis as an infantile affection, but it must be borne in mind that it sometimes occurs to adults. Wo- men are generally the subjects of it; and it is commonly regarded as an hysterical phenomenon. In one case, however, that came under my notice, there were no symptoms whatever of hysteria, the strid- ulous inspiration being so much wrorse during sleep, that the patient, a woman in the London Hospital, was obliged to be placed in a separate room, on account of keeping the other patients awake. In this case, though the rest of the mucous membrane was much congested, the vocal cords were perfectly healthy. The case recovered under the local treatment re- commended under the head of Chronic Laryngitis.1 The treatment should he the same as that advised for children, though inhala- tions of sedative and anaesthetic vapors may here be employed with advantage. Spasm of the glottis, dependent on the In- halation of poisonous gases and the im- paction of foreign bodies in the oesophagus, requires the most prompt treatment; if not immediately relieved, laryngotomy or tracheotomy should be performed without delay. One form of spasm of the vocal cords is that met with in hooping-cough -the essential phenomena of this com- plaint being a series of short, rapid, and violent expirations, followed by a pro- longed stridulous inspiration-the disease which will be found treated in detail else- where.2 The laryngeal cough, sometimes met with in hysterical women whose lar- ynx is seen with the laryngoscope to be perfectly healthy, is also due to a spas- modic tendency of the adductors of the cords, the spasm only occurring in expira- tion ; and the same may be said of the sharp ringing cough which occasionally affects children, and is usually looked upon as of a reflex nature. The nervous laryngeal cough of adults is as difficult to treat as most hysterical complaints. I have found the most satisfactory results follow from the use of warm sedative and antesthetic inhalations; but the results are often disappointing. Lasegue report- ed a case successfully treated by bella- donna ;3 but in a severe case that came under my care, atropine was given till its full physiological effects were produced, but without relief of the cough. Dr. Har- ley has reported a case4 in which valeri- anate of zinc effected a cure. DISEASES OF THE SENSORY SYSTEM OF THE LARYNX. Hypercesthesia. Increased sensibility occurring inde- pendently of inflammatory disease or structural alteration of the tissues of the larynx, is undoubtedly a rare morbid con- dition, but it may occur either in an in- termittent form or without any periodic character. A case of the former kind is reported by Dr. Gerhardt,5 and a few of the latter have fallen under my notice. Several cases have also been reported by Dr. Handfield Jones.6 Neuralgic cases 1 Med. Times and Gazette, Nov. 15, 1862. 2 Vol. i. 3 Archives Generates, May, 1854. 4 Med. Times and Gazette, vol. ii. p. 116. 5 Virchow, Archiv xxvii. Heft 1 and 2. 6 Med. Times and Gazette, May 2, 1863. 36 DISEASES OF THE LARYNX. should be treated on the ordinary princi- ples which regulate the therapeutic man- agement of such cases. The inhalation of hot sedative vapors and ansesthetics does good in cases of a non-intermittent character; and the internal use of nar- cotics is also indicated. Some of the morbid phenomena already referred to under the head of Motor Affec- tions (such as pertussis and nervous lar- yngeal cough), may be due to increased sensibility of the mucous membrane of the vocal cords-the hyperaesthesia manifest- ing itself in reflex action. Anaesthesia. Although there is great difference be- tween the sensibility of the glottis in dif- ferent people, anaesthesia rarely occurs as a distinct morbid affection. Disease affecting the origin or trunks of the pneumogastric nerves or their supe- rior laryngeal branches, would be likely to diminish the sensibility of the larynx in proportion as the function of the nerves was interfered with.1 Romberg has ob- served that in cholera there is impaired sensibility of the mucous membrane of the larynx.2 Some morbid phenomena of a functional character, such as a vocalist's inability to produce certain notes which previously could be easily formed, are probably in some cases (where the larynx appears healthy) due to impaired mus- cular sensibility. SECTION II. Secondary Diseases of the Larynx in Acute Affections. smallpox. The laryngeal affection may be a mild papular or pustular eruption of the mucous membrane, or it may be a severe inflam- matory disease accompanied by the pres- ence of false membrane. The former, as a rule, causes little or no inconvenience ; the latter is often fatal. In the year 1863, through the courtesy of Mr. Marson, the author of the able article on Smallpox (vol. i. p. 127), I was enabled to examine several patients in the Smallpox Hospital, with the laryngoscope. In one patient laboring under severe purpuric smallpox, I found ecchymotic spots on the under surface of the epiglottis, and on the mu- cous membrane over the arytenoid carti- lages. In a convalescent case, there was a distinct pustule on the edge of the epi- glottis ; in another case, in which the entire body was covered with pustules, the larynx appeared perfectly healthy ; and in another similar case there were no pustules, but there was a marked conges- tion of the mucous membrane ; in another case, the upper surface of the epiglottis was covered with pustules. Riihle, who in a bad epidemic of smallpox, in Greifs- wald, in 1856-57, made no less than fifty- four post-mortems, observes,1 "Although I have seen here and there pustule-like elevations, I nevertheless consider the essential peculiarity of the laryngeal affec- tion to be of a croupous or diphtheritic inflammation." Dr. Riihle further ob- serves, that, as "out of the fifty-four cases there was not a single case in which the larynx and windpipe were in a normal state, he cannot but attribute a certain proportion of the mortality to the laryn- geal affection." Pathological examples of the diphtheritic complications of smallpox are to be found in the museums of St. Thomas's and St. Bartholomew's Hospi- tals, and in other collections. In two in- stances, I have known permanent paralysis of the adductor of a vocal cord follow smallpox : in both, the larynx was affected at the time, and it is probable that the affection was of the diphtheritic character. As regards treatment, it may be observed that in the pustular form of the diseases interference is unnecessary, and that in the diphtheritic form it is almost useless : in the latter case, however, the local treatment elsewhere recommended for primary diphtheria can be adopted. MEASLES. In this disease the affection of the larynx may be either a simple catarrh, or a severe croupous affection. The catarrhal form of laryngitis may occur before the eruption appears, a day or two after the rash has come out, or when it is beginning to decline. It is more common than the croupy form of disease ; and though occasionally the in- flammation runs high, it is seldom of any importance. In some epidemics, catar- rhal laryngitis comes on when the erup- tion has almost disappeared.2 In these cases, there is generally obstinate hoarse- ness. In a number of Professor Hebra's patients in the General Hospital atVienna, in different stages of measles, Dr. Stofella3 found a highly injected condition of the mucous membrane of the larynx in almost all the cases which he examined laryngo- scopically. 1 Op. cit. p. 247. 2 Bohn, Konigsberg Mediz. Jahrbiicher, 1858. 3 Wien Medizin. Wochenschrift, Nos. 18, 19, 20, 1862. 1 Ilufeland's Journ. der pract. Heilkunde, Feb. 1853. 2 Ibid. Feb. 1832. TYPHUS AND TYPHOID. 37 The croupy or diphtheritic form of in- flammation, observes Dr. West, "seldom begins until the eruption of measles is on the decline, or the process of desquama- tion has commenced. Its appearance is most frequent from the third to the sixth day from the appearance of the eruption, but it oftener occurs at a later than an earlier period."1 The treatment should be similar to that recommended for pri- mary croup, but it must always be borne in mind that the secondary disease is of a less sthenic type. SCARLATINA. The affection of the larynx in these cases may be either an acute oedema of the glottis or a croupous inflammation: they are, fortunately, both rare complica- tions. The oedema which sometimes oc- curs in scarlet fever may be dependent on the debility which exists during the con- valescence of severe febrile complaints, or may be due to the renal affection which sometimes follows scarlatina. The croupy inflammation of the larynx, though not common, is peculiar to some epidemics. Goupp described an epidemic in Wurtemberg, in which, in the greater number of cases, croupy symptoms ap- peared from the third to the fourth day of the illness; in some cases death took place before the exanthem appeared.2 It has been observed, that in diseases of the larynx dependent on, or associated with, scarlatina, there is a great tendency to the ulcerative process. A specimen (No. 36, series W), in the Museum of St. Thom- as's Hospital, supports this view. The larynx was taken from an adult patient, who died of scarlatina: there is a very thin layer of lymph covering the mucous membrane of the larynx, and the right arytenoid is laid bare by a large ulcer. The treatment of the plastic form of in- flammation should be such as is recom- mended for diphtheria, viz., the internal use and local application of the persalts of iron, a highly nourishing diet, and the free use of alcoholic stimulants, well di- luted. The practitioner must always have tracheotomy in view. In oedema, this operation is also likely to be neces- sary, but scarification should be first tried. ERYSIPELAS. In erysipelas of the head and neck there is always more or less congestion of the mucous membrane of the larynx; and even when the erysipelatous inflamma- tion is seated on the limbs, there is some- times sympathetic or concomitant inflam- mation of the larynx. It sometimes, though less frequently, occurs in hospital gangrene.1 It may result in an acute oedema, which rapidly tends towards a fatal termination. The symptoms of the disease are, difficulty of swallowing, hoarseness or loss of voice, and pain ; the latter is increased on pressure. Dr. Seme- leder has examined five cases with the laryngoscope; in four of them the ery- sipelas affected the face, and in these he found inflammatory redness and swelling of the epiglottis and larynx down to the vocal cords, though there was no dyspnoea or dysphonia. The inflammatory symp- toms in the larynx disappeared gradually with the desquamation of the skin ; and in one case a relapse of the cuticular affection was accompanied by a recur- rence of laryngeal inflammation. In the fifth case-erysipelas of the lowrcr extremi- ties - there was no hypersemia of the larynx. The poison of erysipelas some- times confines itself to the larynx, the skin being free from inflammation ; at other times it passes from the larynx to the external parts. Cases are on record, at least, which tend to support these views.2 The treatment should be active, and such as has been recommended in ordi- nary inflammation and oedema of the larynx. TYPHUS AND TYPHOID. In typhus there is nothing character- istic about the laryngeal affection; con- gestion of the mucous membrane, plastic deposit on its surface, gangrenous inflam- mation, and oedema, being conditions which arc all occasionally met with. The ulceration is generally of the most de- structive character, and whilst it often involves a large surface, it frequently penetrates deeply and exposes the car- tilages. It is generally at the posterior parts of the larynx, that is, at the under part, in the prone position of a patient with low fever, that the disease is most frequently found; and it is commonly thought to be caused, at least in part, by hypostatic influences. The cricoid car- tilage is frequently seen to be denuded, and of a blackish-gray color, and there is frequently a corresponding discoloration of the opposite wall of the pharynx. In typhoid the same conditions are met with as in typhus ; but there seems to be a greater liability to oedema, the ulcerative process more often appears to originate in a typhous deposit, - " laryngo-typhous being, as it were," says Rokitansky, "the completion of abdominal typhous ;" and 1 Diseases of Infancy, p. 236. 3 Riihle, op. cit. p. 243. 1 Ryland, Diseases of the Larynx, p. 8. 2 Ibid. pp. 73 to 77. 38 DISEASES OF THE LARYNX. it is said that the cartilages often become independently diseased, i. e. become dis- eased without the superjacent tissues being primarily affected. So many con- ditions of the larynx are met with which tend to lead to destruction of the car- tilages, that it seems unnecessary to re- sort to the theory that these structures become independently diseased. If in cases where the cartilages are affected the patient survives the fever, the pathologi- cal changes described at page 39 take place, and the case runs the course of laryngeal phthisis. Dr. Wilks has espe- cially called the attention of the profes- sion in this country to the ulceration of the larynx occurring in typhoid.1 Treatment.-In these cases, where subjective symptoms are often altogether absent, and those of an objective charac- ter are to a great extent masked, the dic- tates of rational medicine should lead us to be prepared by surgical interference (tracheotomy) to prevent death from lar- yngeal obstruction, rather than to attempt to control or oppose the disease. Secondary Diseases of the Larynx in Chronic Affections. LARYNGEAL PHTHISIS. Definition.-Chronic thickening and ulceration of the larynx, usually occur- ring consecutively to pulmonary phthisis, but sometimes being present before there is any evidence of lung-disease. There is hoarseness or loss of voice, often dys- phagia and dyspnoea, with persistent in- crease of temperature, and continuous wasting of the body. Synonyms.-Latin-Phthisis laryngea, Laryngitis chronica, Tuberculosis laryn- gis, Laryngophthisis, Ilelcosis laryngis; French-Phthisie laryngee ; German - Kehlkopftuberculose ; English - Laryn- geal Phthisis, Throat Consumption. Causes.-The causes are the same as those which give rise to other laryngeal affections (such as exposure to cold, func- tional excesses, &c.), plus a special con- stitutional condition, either inherited or acquired, through which cell-proliferation takes place in the submucous tissues. In ordinary chronic laryngitis the rapid evo- lution of imperfect cells takes place at the free surface, but in laryngeal phthisis the interstices of the tissue are the seat of de- posit. Although Niemeyer has done good service in so decisively combating the idea of the tubercular origin of all forms of phthisis, and in pointing out the catar- rhal and intlanimatory nature of many cases of that disease, there can be no doubt that a disposition to low interstitial inflammation is often inherited, or, at any rate, congenital. The feeble texture is excited to chronic inflammation and cell- proliferation by very slight exciting causes. By the Vienna school, the cell-prolifera- tion was called an "exudation," and probably, in a large number of cases, the deposit is more of this nature than that of a true growth; the weak constitution which gives rise to it was called "a dia- thesis." Our views on phthisis are now undergoing a great change, but however unimportant a role tubercle may play, that there exists a diathetic predisposition to low inflammatory action cannot be de- nied. Laryngeal phthisis is often hered- itary, and it frequently attacks several brothers and sisters; as in other laryn- geal affections, males show a greater pro- clivity to it than females. Numerous cases of laryngeal phthisis have come under my inspection, where the most experienced stethoscopists have been unable to discover a trace of lung- disease ; but on the other hand, I must admit that I have only three times met with cases of laryngeal phthisis in the dead subject without finding correspond- ing pulmonary disease. Symptoms.-Subjective.-There is no- thing characteristic about the subjective symptoms: they resemble those met with in chronic laryngitis, except that, owing to the thickening of the tissues, the act of deglutition is more often performed with difficulty. Pain is sometimes expe- rienced in swallowing, but it more often happens that the act is difficult-violent coughing coming on from a little food getting into the larynx; sometimes the drink is violently ejected through the nares. The difficulty of swallowing is most extreme when the epiglottis is much thickened; but it also generally occurs when the ary-epiglottic or inter-arytenoid folds are much swollen. Objective. - (1) Vocal.-Dysphonia, or aphonia, is always present; hoarseness being generally the symptom of the early stages, complete aphonia of the later. The aphonia is, of course, generally de- pendent on structural changes, but it may occur at the commencement of the disease from functional causes (weakened approx- imative action of the vocal cords, and feeble action of the expiratory muscles). The cough varies in different stages. Sometimes the disease is ushered in with violent and frequent paroxysms of cough which nothing can alleviate; sometimes it is only an occasional dry tickling cough; it is generally aphonic in the later stages of the disease. 1 Transact. Pathol. Soc. vol. ix. p. 34, and vol. xi. p. 14. LARYNGEAL phthisis. 39 (2) Respiratory.-The respiration is at first little affected, but afterwards it be- comes embarrassed, and inspiration is often stridulous ; mucous rales can gen- erally be heard over the thyroid cartilage and trachea. In the last stage the dys- pnoea is so great that tracheotomy occa- sionally becomes necessary. (3) Laryngoscopic Signs.-In cases of pulmonary phthisis pallor of the mucous membrane is often noticed, and Dr. Sem- eleder regards amemia of the larynx, where there is no other cause for its ex- istence, as of some prognostic value with regard to phthisis. Congestion of the mucous membrane is generally the cause of the hoarseness in the early stages of laryngeal phthisis. At this period there is nothing to distinguish the condition from ordinary chronic laryngitis; when, however, exudation takes place, the ap- pearance is characteristic. The ary-epiglottic folds look like two large, solid, pale, pyriform tumors, the large ends being against each other in the middle line, and the small ones directed upwards and outwards. The surface is, as remarked, generally pale, but there may be accidental congestion. The inter- arytenoid fold is absorbed in these swell- ings, which interfere with the action of the arytenoid cartilages, and thus prevent the approximation of the vocal cords. Sometimes the swelling only affects the ary-epiglottic fold of one side, and at first the projection of the cartilages of Wris- berg and Santorini interfere with the dis- tinctly pyriform shape of the tumors, but when developed they are pathognomonic of the disease. The condition described is really only chronic oedema of the ary- epiglottic folds, but when once fully es- tablished it is as certain to terminate fatally as a case of acute tuberculosis or encephaloid cancer. Its course is, of course, not so rapid as that of the dis- eases mentioned, but the end is similar. The epiglottis is not unfrequently thick- ened ; sometimes it is so much enlarged as to prevent an inspection of the parts below. Its shape is often somewhat tur- ban-like, the normal contour and surface marks having completely disappeared. In addition to the thickening, the epiglot- tis is in fact often rolled backwards on itself, so that the free edges cannot be seen in the laryngeal mirror; in other cases, where they are visible, the cartilage is often exposed from ulceration. Thick- ening and ulceration of the posterior part of the ventricular bands (false vocal cords) can sometimes be seen, but disease may make considerable progress in this part without coming into the field of vision. Ulceration of the vocal cords is not unfre- quent, the most common situation being at the processus vocalis, the junction of the cartilaginous and ligamentous portions. (4) Miscellaneous Symptoms.-The la- ryngeal secretion varies greatly both in quantity and quality, and probably de- pends more upon the condition of the bronchial tubes and lungs than upon that of the larynx. The constitutional symp- toms are those of pulmonary phthisis. The course of the symptoms varies with the site of the disease, the progress being most rapid when the epiglottis is affected, and generally much slower when the ary- epiglottic folds are the parts implicated. The termination is nearly always fatal where thickening has taken place to any considerable extent. Diagnosis.-Where the characteristic pyriform swellings of the ary-epiglottic folds are present, it is impossible to mis- take the disease ; but where the thicken- ing is not of such a defined character, the diagnosis is not quite so clear. The only conditions which are likely to give rise to an error are acute oedema, and syphilitic thickening. In acute oedema, the rapid occurrence of the disease and the trans- parent character of the swelling differen- tiate it, and in syphilis the thickening is not considerable, whilst the ulcerative process is more active. Pathology.-It is difficult to investi- gate the pathology of laryngeal phthisis, because of the close mutual interdepend- ence of the conditions of the larynx and lungs. As the result, however, of careful observation with the laryngoscope in a great number of cases, the ordinary course of events appears to me to be as follows : -1st. There is chronic hypersemia, gene- rally of a higher degree but more limited extent than is met with in ordinary chronic laryngitis. 2dly. Thickening of the tissues takes place, the kind of thick- ening varying in different parts; thus, the epiglottis and vocal cords appear to become infiltrated with a semi-solid mate- rial, whilst the ary-epiglottic folds be- come distended by a simple serous exuda- tion ;1 the thickening of the ventricular bands (false vocal cords) is generally of the solid character, but is occasionally serous. 3dly. Small ulcers form; these afterwards coalesce and produce larger ulcers (the secondary tubercular ulcers of the larynx of Rokitansky). The small primary ulcers, which are frequently first seen at the posterior extremity of the ven- tricular bands and on the under-surface of the epiglottis, when watched with the laryngoscope, often appear to commence in the minute racemose glands. Subse- 1 In 14 of the 274 cases of oedema of the glottis collected by Sestier (Traite de l'Angine oedemateuse; Paris, 1852), the patients suf- fered from "chronic laryngitis with pulmonary tubercles." 40 DISEASES OF THE LARYNX. quently the ulceration spreads to other parts; sometimes, however, the ulcerative process commences in the vocal cords- destruction of epithelium often occurring some time before the dense structure of the cord itself is affected. In other words, when the cords are first attacked, denuda- tion of epithelium precedes deposit in the tissues. The actual loss of substance which takes place in laryngeal phthisis is not generally great, but chronic disease of the cartilages is frequently found when the disease has existed for a few months ; and it apperrs to me that Dr. Addison's dictum that "inflammation constitutes the great instrument of destruction in every form of phthisis" is true in this in- stance. Tubercle appears to play a very secondary part, if any part at all. As regards the relation of laryngeal phthisis to pulmonary phthisis, as already ob- served, I do not consider that the laryn- geal affection is caused by the disease of the lungs. As a rule, the pulmonary dis- ease precedes the affection of the larynx ; but still, numerous cases occur in which congestion and thickening of the larynx with hoarseness and cough are found be- fore any disease of the lungs can be de- tected either by auscultation or microsco- pic examination of the sputa. On the other hand, in the progress of the disease, evidence of pulmonary disease becomes manifest, and I have only met with three cases in which on post-mortem examina- tion laryngeal phthisis was present with- out any disease of the lungs. As an al- most invariable rule, cavities are found in the lungs, or at least breaking down of lung-tissue. Morbid Anatomy.-On examining the larynx of a patient who has died from laryngeal phthisis, there is commonly found great thickening of the submucous tissues of the larynx, with ulcers varying in size from a pin's point to a shilling. The small ulcers are most commonly found on the under-surface of the epiglottis ; the larger ones at the root of the epiglottis, the posterior extremity of the ventricular bands, and at the processus vocalis. Some- times the ulcerative process is limited to the minute glandulse, and under these cir- cumstances the mucous membrane pre- sents a worm-eaten appearance. Tubercle is said by Rokitansky' to be deposited in the form of gray granulations in the sub- mucous areolar tissue, or to be infiltrated as yellow caseous matter beneath the mu- cous membrane-the true tubercular de- posit being rarely found except over the arytsenoideus muscle and the subjacent arytenoid cartilages. Rokitansky does not consider the thickening of the epiglottis to be of the true tubercular character. I have never seen the gray granulations re- ferred to, and the deposit in the tissues has appeared to me to consist of a serous fluid with a few compound granule cells, and with molecular and granular matter. This debris may or may not be tubercular, but even at this period it may be of more than historical interest to remark that though Louis' found ulceration of the larynx in one-fourth of his cases of pul- monary phthisis, he did not consider that tubercle was ever deposited in the tissues of the larynx. The proportion of cellular elements varies in different cases and in different parts ; in the ary-epiglottic folds they are generally very scarce or alto- gether absent. Pus is sometimes found diffused through the tissues, but rarely circumscribed, unless it be under the peri- chondrium of the cricoid cartilage. Caries of the Cartilages- or, as it is com- monly called, necrosis of the cartilages-far more often results from laryngeal phthisis than from all other diseases together, and it may be regarded as one of the common sequelae. The death of the cartilages is generally believed, and probably with truth, to originate in inflammation of the perichon- drium. After death that membrane is not unfrequently found to be separated from the cartilage by a quantity of pus, and ossification of the cartilage generally precedes its death. The cartilage, with the exception of its more or less ossified condition, may present almost a healthy appearance, or it may be of a dark gray or even black color. The presence or ab- sence of discoloration seems to depend on whether there is a communication (through ulceration of the tissues) be- tween the cartilage and the atmosphere. In those cases where there is ulceration, their surface, and sometimes even their entire thickness, is discolored. Sometimes the cartilages are found to be increased in volume, and still more rarely they are completely atrophied. The latter condition is figured by Ruble.2 The necrosed condition of the cartilages is generally associated with the presence of serum or pus in the adjacent parts of the larynx ; the muscles are soaked in the morbid fluid, and the areolar tissue irregu- larly distended by it. The etiological re- lations between the sero-purulent effusions and the necrosis of the cartilages are of a doubtful, and probably of a varying, cha- racter ; in some cases the former seem to depend on the latter, while in others the opposite relation appears to exist. Some- times the effusion occurs in the parts ex- 1 Pathol. Anatomy, Sydenham Soc. Trans- lation, p. 33. * Louis on Phthisis. 2 Op. cit. Plate I. LARYNGEAL phthisis. 41 ternal to the larynx, especially when the cartilages near the surface externally (such as the anterior parts of the thyroid and cricoid) are affected, and there a laryngeal fistula may be produced. Ac- cording to my experience, the arytenoid cartilages are the most frequently affected, next to them the cricoid, and then the thy- roid cartilage; it is, however, commonly stated that they are affected in the follow- ing order of frequency : first the cricoid, secondly the thyroid, and thirdly the ary- tenoids. Prognosis.-The prognosis is of the most unfavorable character. Where the epiglottis is much thickened, the progress of the case is generally rapid ; on the other hand, when the disease is limited to the ary-epiglottic folds, its course is usually chronic. The result of carefully watching with the laryngoscope, during the last ten years, a great number of cases of laryngeal phthisis, has convinced me that when once thickening to any extent has taken place, that is, when once the disease is fully established, nothing cura- tive can be effected by treatment. Out of several thousand cases, I have only seen two patients recover. Of course, how- ever, suffering may be mitigated, and life prolonged. Therapeutics. - The plan recom- mended for chronic laryngitis sometimes gives relief-the application of mineral astringents, by diminishing the irritability of the mucous membrane, often relieving the troublesome cough. Hot and ames- thetic inhalations likewise sometimes com- fort the patient; and in cases accom- panied by excessive expectoration, I have seen the secretion completely controlled by the inhalation of an atomized solution of tannin (gr. v. ad fl. oz. j.). It is important to bear in mind that there is a tendency to death in three ways -first, by suffocation, the calibre of the laryngeal canal becoming greatly dimin- ished ; secondly, by inanition, the dys- phagia being caused by the thickening of the epiglottis and other parts concerned in the act of deglutition ; thirdly, by the marasmus, which is a characteristic fea- ture of the constitutional malady; and fourthly, by the combined effect of these influences. The fatal termination may, therefore, be postponed by the perform- ance of tracheotomy, when that operation becomes necessary ; by feeding the patient with an cesophageal1 tube, when normal deglutition cannot be effected ; and by the employment of suitable remedies (medi- cinal and hygienic) against the constitu- tional debility. It is unnecessary to make any remarks concerning the operation of tracheotomy, as the conditions which ren- der its performance necessary are suffi- ciently evident. With regard to the use of the oesophageal tube, however, a few observations are called for. The dyspha- gia, it must be borne in mind, is due more to the act of deglutition being imperfectly performed from non-closure of the larynx by the epiglottis, than by the obstruction in the food tract, caused by the thickened epiglottis. It is from food "going the wrong way," not from the fact of its being prevented passing down the gullet, that the difficulty in swallowing arises. Hence there is generally very little difficulty in introducing the oesophageal tube, espe- cially if it be provided with a duck-billed extremity, and be employed with the aid of the laryngoscope. The fatal termina- tion of phthisis is, of course, much accel- erated if the supply of food is to a great extent cut off; and I may observe, that I have prolonged life for many weeks by giving a patient food and stimulants in this way. Alcoholic liquids, which the irritability of the throat would not allow to pass, can be readily introduced into the system by this method. Nutritive ene- mata can be employed instead of the oeso- phageal tube, but the results have ap- peared to me much less satisfactory. Where the patient can swallow a little, but experiences difficulty in doing so from the food occasionally entering the larynx, he should be directed to take nothing but thick liquids. A little arrowroot may be used for giving a proper consistence to the fluids. By thickening the drink (in the way directed) it will be much less likely to pass, beneath the edges of the epiglot- tis, into the larynx. It is also well to direct the patient to take the drink at a draught-to gulp it down, so to speak-• not to sip it. This mode of procedure makes the act of deglutition continuous instead of intermittent, and under these circumstances the passage of food into the larynx is much less likely to occur. Preventive treatment is the only plan which can be adopted with satisfactory results : congestion of the larynx, there- fore, in phthisical persons must be treated with the greatest diligence. The most proper local treatment should be adopted ; complete rest of the vocal organ enforced ; 1 This instrument, which has been pro- vided for me by Messrs. Khrone and Sesse- man, consists of a gum-elastic catheter, about 12 inches long, which is connected with an ordinary pear-shaped India-rubber bottle (provided with a tap) by a bayonette joint. The tube is first passed just beyond the larynx, then the bottle (previously filled with a nutritive fluid) is attached, and the fluid injected. The feeding can be effected with a common catheter and an ordinary In- dia-rubber injecting bottle, but this plan does not answer so well. 42 DISEASES OF THE LARYNX. and, above all, suitable atmospheric con- ditions, if possible, obtained. A warm, dry , and uniform temperature is the grand desideratum. SYPHILIS. The laryngeal phenomena of syphilis differ at different epochs of the constitu- tional disease, and must therefore be con- sidered separately. In secondary syphilis, condylomata are the most characterized conditions, but chronic hypersemia (with- out the mucous tubercles) and superficial ulceration are often met with. Condylo- mata, occurring in the larynx, present a similar appearance to those found in the pharynx and elsewhere; that is to say, they are raised patches of the mucous membrane. An elaborate article has been published by Gerhardt and Roth1 on the subject, and by these observers they are described as being papillary formations, uneven, whitish, smooth or jagged promi- nences, variously situated in the larynx and of various size and extent. These morbid projections were found most fre- quently on the vocal cords, on the inter- arytenoid fold, and in those situations which by friction become mechanically irritated. Gerhardt found these condylo- mata present in 20 per cent, of the pa- tients suffering from secondary syphilis. This proportion, however, has not been found by other observers. In fifty-two cases of well-marked secondary syphilis, which I was kindly permitted to examine at the Lock Hospital in the year 1803, condylomata were only found in two cases, that is to say in less than 4 per cent. Gerhardt's cases, forty-four in num- ber, were in the Venereal Department of a General Hospital, and therefore may well be compared with those at the Lock Hospital. The difference is very remark- able. At the Hospital for Diseases of the Throat we constantly meet with condylo- mata of the larynx, Tint the proportionate frequency of laryngeal condylomata in the constitutional complaint of course cannot be ascertained at this institution. The inter-arytenoid commissure and the epiglottis are the parts which I have most frequently observed to be affected. In addition to the condylomata of secondary syphilis, superficial ulcerations of a lim- ited extent are also occasionally met with ; there is also sometimes very obstinate congestion of the mucous membrane, but it is impossible to tell whether the latter condition is due to the syphilitic dyscra- sia. As regards the treatment, there is little to be said ; the condylomata rapidly disappear under local treatment of a stimu- lating character, and probably often spon- taneously. In the cases reported by Ger- hardt this condition was removed by a mercurial course ; the superficial ulcera- tions may be cured by the common astrin- gent solutions. In tertiary syphilis, rapid, deep, and ex- tensive ulceration is the characteristic morbid condition of the larynx. The ulcerative process frequently destroys the mucous and submucous tissues to a very considerable extent, and the muscles and perichondrium are sometimes attacked.1 The ulcerative process is often associated with an oedematous tendency ; in the lat- ter case, the laryngeal oedema seems often to occur as an extension of disease from the pharynx. Even when the ulcerative process is arrested, however, the danger does not cease; for the cicatrices often undergo a degree of contraction which greatly interferes with the calibre of the larynx. Numerous cases of this sort have come under my notice, and there are many pathological specimens which illus- trate it.2 The epiglottis is peculiarly prone to be affected by syphilitic ulcera- tion. Whilst ulceration is attacking the epiglottis, great dysphagia is generally experienced; but when the ulcers are healed, swallowing can generally be ef- fected without trouble, even though nearly the whole valve is destroyed. When the walls of the pharynx are also ulcerated, there is danger of the edges of the epiglot- tis uniting with the pharynx. This con- dition gives rise to one of the most serious forms of dysphagia. In these advanced stages syphilitic gummata are sometimes formed, not only in the tongue and pharynx, but in the muscles and submucous tissues of the larynx. These generally soften and ulcer- ate. The later forms of syphilitic ulcera- tions should be treated constitutionally with iodide of potassium. Five, ten, or in some cases twenty grains may be given with advantage, in combination with am- monia. By largely diluting the medicine with water, its effect is increased, and it does not irritate the throat in being swal- lowed. The ulcerated surface should be touched every day with the solid nitrate of silver. For this purpose a piece of aluminium wire, suitably curved, and coated with fused nitrate of silver, should be used. The ulcerative process, though of the most active character, is almost always very tractable under this treatment; in no stage of the disease does it appear to me to be necessary or desirable to use mercury. The chronic laryngitis some- 1 Specimen No. 38, W Series. St. Thomas's Hospital. 2 Guy's Hosp. Mus. No. 1655-90, and St. Thomas's Hosp. Mus. No. 22, W Series. ' Virchow, Archiv, Bd. xxxi. 1861, Hft. 1, §7. ON THE USE OF THE LARYNGOSCOPE. 43 times met with in syphilitic persons (asso- ciated as it generally is with chronic bronchitis) resists every kind of treatment. SECONDARY CEDEMA. (Edema may occur as a sequel of Bright's disease, and possibly as the re- sult of cardiac or venous obstruction. Dr. Fauvel has applied the term aphonie alhuminitrique" to the laryngeal oedema occasionally met with in renal disease, but Dr. George Johnson - an acknow- ledged authority on diseases of the kidney, and an accomplished laryngoscopist-is of opinion that, "Dr. Fauvel has consider- ably overestimated the frequency and im- portance of oedema of the larynx as a result of Bright's disease."1 Though I have seen a great number of cases of laryngeal oedema, I have never met with it as a complication of renal disease, but that it may occur is shown by the history of a specimen2 in Guy's Hospital, and by the report of cases under the care of Dr. Rees and Dr. Barlow. (Edema is often the consequence of necrosis of the carti- lages, and has been referred to under the disease (Laryngeal Phthisis) in which that morbid process most frequently takes place. It also sometimes occurs, as al- ready shown, in the exanthemata : here it is more probably the result of low in- flammatory action than of simple dynamic causes. The treatment should be the same as that recommended for acute laryngitis. APPENDIX. ON THE USE OF THE LARYNGOSCOPE. This instrument, constructed for ob- taining a view of the interior of the larynx during life, consists of two parts-(1) a small mirror fixed to a long slender shank, which is introduced to the back of the throat; and (2) an apparatus for throw- ing a strong light (solar or artificial) on to the small mirror. For this purpose either (ci) a second (larger) mirror, which reflects the light from a lamp or the solar rays on to the throat-mirror, may be used; or (6) the luminous rays from a lamp may be collected and thrown directly on to the smaller mirror, by means of a lens placed in front of the flame. The former method is called "illumination by reflection;" the latter, "direct illumination." History. - Various independent at- tempts to examine the larynx have been made at different times by different prac- titioners. Levret, a distinguished French physician, as far as bibliographical re- search at present goes, seems to have been the first to invent a laryngeal mirror. This occurred in the year 1743. In the beginning of the present century, Bozzini contrived a Laryngoscope, which to a cer- tain extent complied with the conditions contained in the above definition; but being clumsily constructed, it could not be used effectively. In the year 1825, an unsuccessful attempt to inspect the glottis [Fig. 4. Laryngoscope.] was made by M. Cagniard de Latour; and a few years later, in 1829, Dr. Benjamin Guy Babington exhibited, at the Hun- terian Society of London, a Laryngoscope which, excepting that a hand-mirror was used instead of a concave circular reflector attached to the operator's head, closely resembled the modern instrument. In later times,3 Senn, Bennati, Baumes, Lis- ton, Warden, and Avery made attempts or suggestions towards obtaining a view of the larynx during life ; but it was left for M. Garcia to lay the foundation of a method of examination, which, through the genius and perseverance of Professor Czermak, at once reached a high degree of perfection. The employment of the Laryngoscope in practical medicine dates from a paper published by Czermak in 1858.1 The Laryngeal Mirror.- The throat- mirror should be of glass backed with a coating of silver (not amalgam, as this is much more readily damaged by heat), mounted in German silver, and fixed at an angle of about 120° to a slender shank or rod about four inches in length of the same material. The shank of the mirror is fixed into a hollow wooden or ivory 1 The Laryngoscope, 1864. 2 No. 179, 650. Lancet, Sept. 5, 1863, vol. ii. p. 277, and vol. i. Feb. 27, 1864. 3 For further historical details see the au- thor's treatise "On the Use of the Laryngo- scope," chap. i. 3d edition (Longmans and Co.) 1 Wien Medizin. Wochenschrift. 44 ON THE USE OF THE LARYNGOSCOPE. handle, about three inches in length and a quarter of an inch in thickness. A lar- yngeal mirror, the reflecting surface of which is about four-fifths of an inch in diameter, will be found convenient in most cases ; where the distance between the uvula and posterior wall of the phar- ynx, however, is great, the largest size mirror, about one inch in diameter, an- swers best; in the case of children, a mirror about half an inch in diameter should be used. Circular mirrors cause the least inconvenience, but where the tonsils are very large, oval or ovoid mir- rors can be most easily employed. Illumination by Reflection.-For throw- ing a strong light on to the laryngeal mirror, and thus into the larynx, it will be found most convenient to employ a circular and slightly concave mirror about three inches and a half in diameter, and having a focal distance of about twelve or fourteen inches. When the solar rays are reflected into the throat, the surface of the mirror should be plane. The mir- ror should be attached in some way to the operator's head, and may be worn either opposite one of the eyes (Czermak), in front of the nose and mouth (Bruns), or on the forehead (Johnson, Fournie). I follow Czermak's plan. The reflector may be attached to the operator's head either by a spectacle-frame (Semeleder)- and in this case the upper half of the rim of the eye-piece of the spectacle-frame may be conveniently removed-or by a frontal band (Kramer). The mirror should be connected with its support by a ball-and-socket joint. In making an ex- amination after the manner of Czermak, the reflector should be perforated by an oblong hole, the long diameter of which should correspond with the long diameter of the eye. Any lamp that gives a bright steady light answers the purpose perfectly well. A moderator, paraflin, or argand gas- burner will each be found convenient. My "Rack-movement1 Lamp" is perhaps the most convenient illuminating appa- ratus that exists. It is now employed at most of the London hospitals, and is very suitable for the private consulting-room. For strengthening the light a lens may be employed, and various lamps and lan- terns have been contrived for the purpose. The " light-concentrator," which forms a part of my rack-movement lamp, will be found useful in Laryngoscopy, for, whilst excluding the lateral rays, it collects all those which can possibly be conveyed to the reflector. Direct Illumination.-The best mode of using direct light is that employed by most of the French laryngoscopists. The lamp, provided with a lens on the side facing the patient, is placed on a table about a foot wide and three feet long. The observer sits on one side of the table, and facing him on the other side is the patient. The lamp, provided with a strong lens on the side of the patient, and screened towards the practitioner, is placed on the table between them. In operating, the practitioner has one arm round each side of the lamp. The method employed by Stoerk and Walker, in which direct light (strengthened by a glass globe of water acting as a lens) is thrown on to the laryngeal mirror, is less perfect on account of the lateral deflexion which the rays un- dergo after impinging on the laryngeal mirror. For demonstrating to a class, the oxy-hydrogen light,1 as employed at the Hospital for Diseases of the Throat, is the most perfect arrangement. Method of Examination.-The patient should sit upright, facing the observer, with his head inclined very slightly back- wards. The observer's eyes should be about one foot distant from the patient's mouth, and a lamp burning with a strong clear light should be placed on a table at the side of the patient, the flame of the lamp being on a level with the patient's eyes. The observer should now put on the spectacle-frame with the reflector at- tached, and, directing the patient to open his mouth, should endeavor to throw a disk of light on to the fauces, so that the centre of the disk corresponds with the base of the uvula. When the observer has gained dexterity in throwing the light, the patient should be directed to open his mouth widely, and to put out his tongue ; and the operator should hold the protruded organ between the finger and thumb of his left hand, previously enveloped in a soft cloth or towel. In thus keeping the tongue out, the greatest gentleness should be used, as the em- ployment of force, by exciting reflex ac- tion, only defeats the object in view. Holding the laryngeal mirror, previously warmed over the lamp (to prevent the condensation of the breath on the sur- face), like a pen in the right hand, the operator should now introduce it to the back of the throat, its face being directed downwards and kept as far as possible from the tongue. The posterior surface of the mirror ought to rest slightly on the base of the uvula, which should be gently pushed rather upwards and backwards towards the posterior nares. The plane of the mirror should form an angle of about 45° with the horizon. Where the tongue forms an arched prominence at the back of the mouth, the patient should be directed to inspire deeply, or to produce some vocal sound ; these acts cause an elevation of the uvula, 1 For a description of the apparatus, see Medical Times and Gazette, July 24, 1859. 1 Made by Mayer and Meltzer, 59 Great Portland Street. ON THE USE OF THE LARYNGOSCOPE. 45 and thus facilitate the introduction of the mirror. It is better to introduce the mirror several times, and keep it in situ only a few seconds, than to allow it to remain in the mouth too long, and thereby produce an irritation which prevents fur- ther examination at the same sitting. When the epiglottis is large and pendent, the mirror should be introduced lower in the fauces, and more perpendicularly than is usually suitable. The Laryngeal Image.-In some cases, on introducing the laryngeal mirror, only the epiglottis may be visible, with per- haps just the tips of the capitula San- torini at the posterior part ; whilst in others the ary-epiglottic folds, the ven- tricular bands, the vocal cords, the small cartilages above the glottis, the cricoid cartilage, the rings of the trachea (and, perhaps, even the bifurcation of that tube), can be seen with perfect distinct- ness. The appearance of parts is shown in the annexed drawings:-• mirror occupies when in situ (that is to say, at an angle of 45° with the horizon, the foot of the page being farthest from the observer). The only inversion which takes place in the formation of the image is in the anterior posterior direction ; the part which in reality is nearest to the observer, the anterior insertion of the vocal cords, becoming farthest in the im- age, and the posterior commissure, which in reality is farthest from the observer, becoming nearest in the image. With regard to the lateral and vertical relations of parts, no inversion takes place. That which is on the right side of the larynx (the right vocal cord, for instance), ap- pears on the right side of the mirror, and that which is on the left side of the larynx on the left side of the mirror ; in the same way the part which is highest in the larynx (the epiglottis) is highest in the mirror, and the parts lower down (the arytenoid cartilages) are at the lower part of the mirror. It is only when the image is transferred to paper, and be- comes a drawing, that its symmetrical character can give rise to mistaken no- tions concerning inversion. It is necessary to make a few remarks on the normal color of the different parts. The epiglottis is of a dirty pinkish hue on the upper surface; its lip (or free edge, and the immediately adjacent under sur- face) is of a decidedly yellow color ; whilst the cushion (and rest of the under sur- face, when visible) is invariably bright red. The ary-epiglottic folds are about the same color as the mucous membrane of the gums, the cartilages situated in them being of a somewhat deeper tint. 77ze ventricular bands are of a bright color, being of about the same shade as the mucous membrane lining the lips. The vocal cords should be pearly white, like the conjunctiva of a child. The cricoid cartilages and tracheal rings are of a yel- low color, and the mucous membrane between them bright red. The Introduction of Instruments within the Larynx.-In applying local remedies to, or operating on, the larynx, by the aid of reflected light, as the right hand is required for the instrument used, the laryngeal mirror should be introduced with the left hand. In this case, the pa- tient must hold his own tongue out. Infra-glottic Laryngoscopy. - In some cases, after tracheotomy has been per- formed, and where a tube is worn, valu- able evidence may be derived by intro- ducing a minute mirror, with its face directed obliquely upwards, through the fenestrated canula. On account of the size of the mirror, it is necessarily made of steel; and as both its size and material cause it to cool very rapidly, a coating of glycerine will be found convenient for neutralizing the effects of the condensation of the water contained in the expired air. Fig. 5. laryngoscopic Drawing, showing the Vocal Cords drawn widely apart, and the position of the various parts above and below the Glottis during quiet in- spiration. ge, glosso-epiglottic folds ; u, upper surface of epi- glottis ; I, lip of epiglottis ; c, cushion ot epiglottis ; u, ventricle of larynx ; ac, ary-epiglottic told ; clK, cartilage of Wrisberg; cS, capitulum Santorini; com, arytenoid commissure ; vc, vocal cord ; ven- tricular b i nd ; yu, processus vocalis ; cc, cricoid car- tilage ; t, rings of trachea. Fig. 6. Laryngoscnpic drawing, showing the approximation of the Vocal Cords, aud the position ol the various parts, iu the act of vocalization. fl, fossa innominata; hf, hyoid fossa; ch, cornu of hyoid bone ; cW, cartilage ot' Wrisberg ; c7, capitu- lum Santo ini; a, a ytenoid cartilages ; com, aryte- noid commissure ;pv, processus vocalis. But to properly understand their rela- tion, this book should be held at the same inclination as that which the laryngeal 46 CROUP. CROUP. By William Squire, L.R.C.P. Bond. Definition.-An inflammation of the larynx and trachea in children, com- mencing in the air-passages and often ex- tending into the bronchi. It induces thickening of the mucous membrane and an altered secretion which may become either membranifbrm or purulent. There is frequent, sharp, harsh, ringing cough ; difficult breathing, with loud, shrill in- spiratory sound ; altered voice, at first hoarse, afterwards whispering, or extinct; fever, loss of appetite, thirst, and little or no difficulty of swallowing. Synonyms. - Cynanche Trachealis, Cullen; Suffbcatio Stridula, Home; An- gina Inflammatoria Infantum, Russell; Acute Asthma of Children, Millar; Cy- nanche Stridula, Crawford ; Angina Tra- chealis, Johnstone ; Angina Polyposa seu Membranacea, Michaelis; Hives, Benja- min Rush ; Cynanche Laryngea, Dick ; Angina Membranacea, Goel'is ; Tracheitis Infantum, Albers; Laryngo-tracheitis, Blaud ; Laryngite striduleuse, Guersant; Spasmodic Laryngitis, Charles Wilson; [Spasmodic and Pseudo-membranous Lar- yngitis, G. B. Wood.-II.] Name.-Croup and Roup (hreopan, Anglo-Saxon, Clamare) were the names popularly applied to the disease when it was first investigated by Home; at the commencement of the present century they were equally in use in the neighbor- hood of Edinburgh. The latter once had a wider range, having been used by Knox as a verb signifying to cry hoarsely, and Burns has " roupet" in the sense of hoarse as from a cold ;* since then, however, it has disappeared from our literature, and Croup, which before Home's inquiry was as strange to England as to the rest of Europe, has been the world-wTide designa- tion of the characteristic group of symp- toms attending impediment to the entrance of air into the windpipe. It is somewhat remarkable that even in those countries where the disease is not infrequent, it is rarely distinguished by a proper name ; Braune in Germany, and Hives in Amer- ica, being the only examples of which I am aware. Strypsiucka in Sweden has more the signification of quinsy or suffoca- tion, and was not popularly applied to this disease when Rosen wrote ; our own "strangles," "closing," "chock," or "stuffing," have neither been generally used nor definitely applied. History.-How large a share Croup has had in the various anginas or cynan- ches enumerated in the earlier stages of the history of medicine, it is impossible to define; in the subdivision of those terms by Boerhaave, there is evident in- tention of including it, and there is evi- dence that it was so included by our English physicians, from Sydenham to Mead. As Home remarks: "Probably it has existed, more or less, in all ages, for the same productive causes must have operated formerly as they do at present." There are other systematic names un- der which cases of this disease have also been included, such as the "suffocative catarrh" of Ettmiiller, and the "tussis convulsiva puerorum" of Willis; though the first of these names is now restricted to capillary bronchitis, and the second to hooping-cough, yet there is a clear refer- ence to Croup in the pages of Ettmiiller. The first evidence of Croup noticed by Baillou was in an epidemic of hooping- cough in Paris, 1576,' and the first men- tion of it by name in this country begins with the distinction between it and hoop- ing-cough drawn by Dr. Patrick Blair,2 in a letter to Dr. Mead, dated Cowpar of Angus, July 6th, 1713, wherein he says: "The tussis convulsiva, or chink-cough, is also some years epidemical and be- comes universal among children; as is a certain distemper with us called the Croops, with this variety, that whereas the chink-cough increases gradually, is of long continuance, seizes in paroxysmes, 1 John Jamieson, D.D., an Etymological Dictionary of the Scottish Language. Edin- burgh. 4to. 1808. The Moeso-gothic hrop-jan is here given as the root of many words, signifying outcry, as croak, rout, hoop; also of the Teutonic roep-en and the Icelandic hroop. In the northern counties of England roopy and ropy are still used for hoarse, and the latter word is some- times heard in the southern counties in the same sense. 1 Baillou, Epid. Ephem. Lib. ii. pp. 197 and 201. 2 Observations in the Practice of Phys etc. London, 1718. HISTORY. 47 and the patient is well in the interval; this convulsion of the larinx, as it begins so it continues, so violently that unless the child be relieved in a tew hours 'tis carried off within twenty-four, or at most forty-eight hours. When they are seized they have a terrible snorting at the nose and squeaking in the throat, without the least minute of free breathing, and that of a sudden; when perhaps the child was but a little time before healthful and well. The most immediate cure is instant bleed- ing at the jugular, either by the lancet or leeches ; when the most urgent symptoms are gone, then emetics or the like are ad- ministered at discretion." The distinction is not always attended to, as even Huxham,1 writing "de per- tussi puerorum," speaks of an acrid hu- mor sometimes attacking the larynx. Dr. Russell2 gives us an account of the disease observed by him in connection with the epidemic of malignant angina then prevalent, from which, however, he is careful to distinguish it. He says:- "I have observed it is most apt to seize children from two years old to eight or ten, but chiefly the younger sort." He details the leading symptoms, and re- marks that the whole "fistula pulmona- lis" becomes inflamed. Home's essay3 is founded on the obser- vation of cases where no epidemic com- plications prevailed. In a careful and most philosophical inquiry into the causes of the symptoms before him, he deter- mined their dependence on the pathologi- cal changes in the larynx and trachea, and regarded the disease as an acute in- flammation. Millar,4 who practised at the same time in the south of Scotland, and had similar cases of Croup under his observation, re- marks upon, but gives undue prominence to, the spasmodic element in the parox- ysm of the disease. Further attention is called to Millar's views by the publica- tion in England of a letter from Dr. Rush,5 of Philadelphia, and a discussion commenced, which has continued to our own day, in which the true nature of Millar's cases is not always remembered. The latter half of the last century and the beginning of the present are remark- able for the numerous outbreaks of epi- demic angina recorded in different coun- tries and places. In the midst of an epidemic at Cremona, Ghizi had described the case of a child dying of laryngeal com- plication, and attempted to set up a dis- tinction between it and the pharyngeal form of the epidemic. The cases recorded by Starr, in Cornwall, occur in his de- scription of an epidemic of this kind, and it is probable that Bussell's were not wholly isolated. Home, careful lest the distinct inflammatory disease which he had constituted should be confounded with an epidemic disorder of so different a nature, drew a distinction at the very commencement of his inquiry between his own observations and those recorded by Russell; yet fresh outbreaks of the epi- demic, its liability to spread to the air- passages, and its severity towards chil- dren, tended to their confusion. One effort to avert the fatal mistake that ensued-and it is the only one-is recorded in the treatise of Dr. Johnstone the younger, of Kidderminster.1 He quotes from Home the "two very differ- ent situations of the suffocatio stridula; the former more inflammatory and less dangerous; the latter less inflammatory and highly dangerous : in the former the pulse is generally strong, the face red, drought great, and they agree -with evacu- ations ; in the latter the pulse is very quick and soft, great weakness, tongue moist, less drought, great anxiety, and evacuations hasten death." Dr. John- stone contends that these are not merely two stages of the same disease, but that the latter applies to that complication of the epidemic which has been observed in all its records from the earliest times, and that it was occasioned by the same epi- demic cause, and required the same sus- taining plan of treatment that his father adopted. Unfortunately, though argued with learning and experience, these views did not prevail; the name of Croup was ap- plied to the epidemic complication, and the treatment laid down by Home for the one disease was very energetically em- ployed against the other. The divergence of opinion tended to stimulate the collec- tion of facts bearing on the subject. The accounts of epidemic Croup, though gene- rally referring to the disease now known as diphtheria, doubtless comprehend some cases of simple Croup ; some of our own accounts of Croup probably include cases of diphtheria. It was to illustrate the tracheal complication of the epidemic that both the great concours on Croup were in- stituted at Paris ; yet the prize essays of 1 Huxham, Obs. de Aere et Morbis Epidem. Lond. 8vo. 1793. P. 77. 2 Russell, Dr. Richard. CEconomia Naturae in Morbis acutis et Chron. Glandularum. 8vo. bond. 1755. P. 72. 3 Home, Francis, M.D., &c. An Enquiry into the Nature, Cause, and Cure of Croup. 8vo. Edin. 1765. 4 Millar, Observations on the Asthma and Hooping-Cough. 8vo. bondon, 1796. 5 Rush, on the Spasmodic Asthma of Chil- dren. 8vo. bondon, 1770. 1 Johnstone, J., M.D. A Treatise on the Malignant Angina, to which are added some Remarks on the Angina Trachealis. 8vo. Worcester, 1779. 48 CROUP. MM. Vieusseux and Jurine, of Geneva, and of Albers, of Bremen, are among the most valuable contributions to our know- ledge of Croup as an independent disease; and, though the tendency in France has since been to restrict the term Croup to one of the accidents of diphtheria, yet the opposite view has in that country been maintained with great ability by MM. Bricheteau, Desruclles, Emangard, and especially in the valuable original work of M. Bland, of Beaucaire.1 A similar controversy, arising under conditions more allied to those of our own country, has been continued in Northern Germany since the time of Wichmann of Hanover, starting from a line of distinction being drawn between its spasmodic or inflam- matory nature ; the treatise of Goelis of Vienna2 is, however, sufficiently compre- hensive. In America the "Observations on Cynanche Trachealis," published in the first volume of "Medical Inquiries and Observations," by Dr. Benjamin Rush, will ever stand as one of the clear- est and most practical accounts of the dis- ease. In our own country we have the careful study of Cheyne,3 enriched, as it is, by the admirable pathological draw- ings from the hand of Sir C. Bell: it forms a worthy sequel to the work of Home, conceived and executed in the same spirit, from observations made in the same local- ity at no great distance of time. We have also the matured experience of the same author, gained in Dublin and its neighbor- hood, published thirty years later in the "Encyclopaedia of Practical Medicine." Dr. Charles Wilson of Edinburgh has pub- lished in the Edinburgh Journal of Medi- cine for 1855-56, a philosophical review of the whole subject. [The opinion that membranous laryn- gitis or tracheitis, "true croup," is a dis- tinct disease from diphtheria, has been supported in America by Drs. G. B. Wood, A. Flint, J. Lewis Smith, Fordyce Barker, and others. Dr. J. F. Meigs con- tends against it. Besides those above- named, abroad, C. West, Virchow, Nie- meyer, Oppolzer, and Letzerich may be cited as favoring the doctrine of the non- identity of the two disorders. Croup is a sthenic localized inflamma- tion, whose causation is connected always with some exposure to cold, wet, &c.; it is never epidemic. Diphtheria is a gene- ral disease, usually epidemic and asthenic in type; the local inflammation in it is secondary to the constitutional affection. In Croup the false membrane is a solidify- ing exudation upon the surface of the mu- cous membrane ; in diphtheria it involves its substance also. Croup is not attended by albuminuria, nor followed by paralysis; both occur not unfrequently with diphthe- ria. Extension of the pseudo-membra- nous deposit into the bronchial tubes is rare in diphtheria,not uncommon in Croup; while the commencement of the deposit in the region of the tonsils and pharynx in diphtheria, and in the trachea or larynx in Croup, is a matter of familiar obser- vation. A table is given in Meigs' and Pepper's treatise on the Disease of Children, which shows that, after diphtheria had, about 1860, become recognized as, at that time, a new disease in Philadelphia, the mor- tality from it added for several successive years more than 300 to the deaths in each year in that city, while the deaths from Croup continued to number, annually, as before, from 200 to over 400.-II.] Etiology.-The collection of facts which go to make up our history of Croup is sufficiently extensive; but, besides the uncertainty as to their true bearing which we see in some of them, others are drawn from too limited an area, or considered in too restricted a relation to come before us in their true value. I have therefore availed myself of the kind permission of Dr. Farr, to consult the careful reports prepared un- der his direction in the office of the Regis- trar-General for England. These reports extend over a period of twenty-five years; they contain particulars of nearly 95,000 deaths from Croup; and therein the locality of occurrence, the season, the sex, and age at the time of death, are readily investi- gated. I have also referred to reports for Scotland, extending over seven years and including 6982 deaths registered as Croup. Croup is specially a disease of childhood, occurring most frequently from the first to the seventh year, and rarely happening, after the tenth. In a hundred deaths from Croup, we may estimate 13 as oc- curring in the first year of life, 25 in the second, 22 in the third, 16 in the fourth, 11 in the fifth, and 12'3 in the succeeding five years, while the deaths beyond ten years of age may be represented by 0'7, the remaining fraction. The proportion of deaths from Croup to one hundred deaths from all causes, registered at each age, is 0'65 in the first year, 3'25 in the second, 6'5 in the third, 8'0 in the fourth, 7'0 in the fifth, and 3'5 for the five follow- ing years together. The proportion for the first and second year of life would be raised to above 1 and 4 respectively,, if the deaths at these ages registered under the head of Laryngitis were included; some considerations, hereafter to be given, tend to raise the proportion for the first 1 Nonvelles Recherches sur la Laryngo- Tracheite. Paris. 8vo. 1823. 2 De Rite Cognoscenda et Sananda Angina Membranacea. 8vo. Vienna. 3 Essays on the Diseases of Children. Es- say II. Cynanche Trachealis. Edin. 4to. 1801. ETIOLOGY. 49 and second years and to diminish the already small proportion registered as occurring beyond ten years of age. In Scotland the proportion registered for the first year is 1'5 ; something over 1 per cent, for the first six months, and for the second six months exceeding 2 per cent. ; though the actual number dying from this cause in the first half-year of life is but little below, and in some years has exceeded, the number of deaths in the second. The annual average number of deaths from Croup in England is near upon four thousand ; and, though this number is somewhat below the returns for the majority of the last ten years, and in excess of the greater number of any of the preceding ten years, yet the propor- tion to deaths from other causes has always been very nearly one in the hun- dred, somewhat above this for the last ten years, a little below it for the preceding ten, again above this proportion for all the preceding years that are registered ; the first of these years, 1838, being as high as 1'30. The lowest proportion was 0'869 in the year 1853 ; the high proportion of 1'335 occurs for the first time in the year 1850; the highest proportion reached is 1'40 in the exceptional year 1858. In Scotland the proportion to other deaths is from 1'5 to 1'8 per cent. ; the annual number of deaths is close upon one thou- sand. Dr. Burke, of Dublin, kindly pro- vided me with the results of the first com- plete registration for Ireland, which shows that in the year 1864 the whole number of deaths from Croup was 1926, and the pro- portion to deaths from other causes 2'05. More boys than girls die of Croup ; this fact is obvious over whatever period or district our inquiries extend : the differ- ence is striking, and by frequent notice has been brought more prominently for- ward than the corresponding fact in the history of some other diseases chiefly fatal in childhood. More boys than girls are born, in a proportion somewhat greater than one in every fifty children, or, to give the result of a very extended exami- nation,1 there are 511'75 males and 488'25 females in every 1000 births; it appears that of this number 83'71 males and 65'74 females die within the first year, after which the death ratio of the two sexes for the next ten years is nearly equal: still there are a larger number of males than of females living at this period, and the deaths of females from all causes are to those of males as 87 to 100 in the first five years, or as 88 to 100 in the first ten years: now the deaths from Croup are so nearly in this proportion, and of late years have so often shown a difference so much less than this, that a doubt might be enter- tained as to whether any difference in the liability of the sexes really existed. A comparison between the deaths from all causes of each sex for each year, with the deaths from Croup at each year, sex with sex, shows a difference of excess on the side of the males so constant, that it is rare to meet with an exception, but at the same time so slight that it can only be considered a characteristic of the dis- ease in the aggregate, corresponding with the results of pneumonia and tubercular meningitis, rather than with the more characteristic zymotic diseases, and con- trasting with those of diphtheria and hooping-cough, where the excess of deaths is greatly on the side of the females. Some of the results of the preceding in- quiry are brought together in the follow- ing table:- Deaths from Croup at each year of age. 1st year. 2d year. 3d year. 4th year. 5th year. 5th to 10th year. All ages beyond. To 100 deaths from Croup . . 13- 25- 22- 16- 11- 12-3 0-7 To 100 deaths from all causes 0-65 3-25 6-5 8-3 7-5 3-5 Males 0-7 3-5 6-7 8-5 7-7 3-7 Females 0-6 3-0 6-3 8-1 7-3 3-4 The influence of climate upon Croup is generally admitted. Cases considered trivial in some parts of France are fre- quently fatal in Korthern Germany, and what in our variable climate excites alarm is regarded with reasonable hopefulness on the continents both of Europe and America. A combination of cold and moisture with rapid alternations of tem- perature, together with some endemic or epidemic influence, has to be admitted. In South America, Buenos Ayres, with its large river, affords frequent instances of Croup ; and in some of the large towns of Australia, with their defective sanitary arrangements and large infantile mor- tality, Croup was not unknown years be- fore the first appearance of diphtheria. The high mortality in Scotland is not greatest in its most northern extremity ; i English Life Table, with an Introduction, by W. Farr, M.D., F.R.S. London, 1864. Table III. p. 24. VOL. IL-4 50 CROUP. the mortality from Croup in the northern counties of England is generally over 1 per cent. ; but this is equalled and often exceeded in the warm southwestern pro- montory of Cornwall, with Devonshire and Somerset. The western shores of England, receiving the Atlantic moisture, show a higher mortality from this disease than the eastern. South Wales has the high rate of 1'5 per cent. This is not so much owing to its mountainous interior, as to its large mining population and the defective sanitary state of its large towns. The highest rate for England is in the populous districts of Lancashire and Che- shire ; and here there can be no doubt that a dense town population, the child- ren specially living under defective sani- tary conditions, causes Croup to be par- ticularly fatal. That it is not merely the combination of cold and moisture, may be shown by the returns from the south- western corner of Scotland, Wigton and Dumfries, the latter conterminous with our Northumberland and Cumberland, and with a rainfall1 exceeding that of any part of England. Though the tempera- ture is sometimes very low, it is more equable than that of many parts of our island, and the mortality from Croup, generally below 1 per cent., is sometimes as low as 0-5. The classical Croup dis- tricts of Scotland still retain their pre- eminence ; they are not confined to the west coast of Scotland : the eastern coast is deeply indented by the sea, and not only do deep valleys of clay extend from these firths, but their shelving shores leave a great expanse of ooze uncovered at every tide; and during the easterly winds, which here prevail for three months of the year with great bitterness, the characteristic cases of Scotch Croup occur. This part of Scotland forms an isthmus, only thirty miles in width, in the vicinity of which, and of the penin- sula formed by the eastern firths, Croup is most fatal, the mortality often exceed- ing 2 per cent. As high a rate is found for Ireland, where imperfect drainage, unreclaimed bog, and a large expanse of inland water add to the influence of the Atlantic in causing a remarkable hu- midity of climate. The influence of season is illustrated by the quarterly reports for London; an average of the ten years from 1844 to 1853 gives the number of deaths from Croup in each quarter as follows : first quarter, 95; second quarter, 81; third quarter, 68," fourth quarter, 92'5; the greatest fatality being in the winter and spring; the greatest variation is found in the second quarter; the third quar- ter has the lowest number, and shows the least variation ; the fourth quarter generally shows a considerable increase on the third, or warm quarter of the year : this was less marked than usual in the year 1852; for while the deaths in the third quarter showed a tendency to increase, being as high as 74, there were only 76 in the fourth quarter, the unpre- cedented mildness of the season doubtless being the cause of this arrest ; the two usually cold months of this quarter, November and December, averaging throughout a temperature of 6° higher than had ever been known during the past eighty years. In the next year severe cold set in before the end of Janu- ary ; in February, the temperature was below the average on most days, there was snow every day ; the second week in March was warm, the end of the month cold with snow ; the summer was vari- able, cold, and wet; double the usual quantity of rain fell in July ; there was line weather in August only. Again, from October 21st to November 8th, the temperature rose to 5'3° above the aver- age, at other times it had been below, and November and December were remark- able not only for low temperature, but also for a density of fog and depth of snow hardly ever exceeded in London. The mortality from Croup in each of the four quarters in this year was : first quar- ter, 93; second, 79; third, 72 ; fourth, 130; and 145 in the first quarter of the next year, 1854, the weather continuing to be cold. The weekly returns for this period show a correspondence between mortality from Croup and temperature. In the winter quarter of 1852, the weekly numbers for November are, 3, 5, 8, 5 ; in the corresponding 'weeks of 1853, they are, 7, 13, 8, 12 ; the high number occur- ring on fall of temperature in the second week of that month. In the previous March there was a rise of temperature in the second week : the weekly numbers for this month were, 15, 8, 2, 10 ; and in the next year, 1854, there are 21 deaths from Croup returned in one wreek in Feb- ruary. Cold, however, may determine the incidence, but not the prevalence of Croup. In most diseases of the respira- tory organs, the greatest fatality is seen in the coldest seasons. The proportional mortality in this class mounts from 11 per cent, in 1852 to 13.5 in 1853, and hooping- cough from 1*8 to 2'3 per cent., while Croup decreased from 0'99 to 0'86 per cent. ; the whole number of deaths from Croup being less in 1853 than it had been for several years. A further illustration of the influence of season and the relation between Croup, the diseases of the respiratory organs, and prevailing epidemics, is afforded by the years 1859,1860,1861. The quarterly re- 1 At Waiilock Head, in Dumfrieshire, there was an estimated rainfall of 80 inches in the year 1861. ETIOLOGY. 51 turns of the mortality from Croup in Lon- don for these three years are as follows:- 1st Quarter. 2d Quarter. 3d Quarter. 4th Quarter. 1859 132 103 80 81 1860 117 80 105 169 1861 236 190 170 252 In the first of these years the summer and autumn were fine and hot. June had a daily excess of 3° of temperature ; in July the mean temperature was 68°, and on the 13th and 18th of that month the thermometer reached 93°; part of October and November was cold, but it was warm at Christmas. The next year, 1860, pre- sents a remarkable contrast to this; a cold period commenced in June : of the three following months, Mr. Glaisher in his re- port1 says, " The weather, during the past quarter has been very remarkable for con- tinued low temperature, frequent rain, large amount of cloud, little sunshine, and bad weather generally ;" the winter that followed was one of the coldest on record, the thermometer being as low as 6° Fahr, in London on Dec. 6th-7th, and at Not- tingham it fell to 8° below zero, or 40° below the freezing-point of water; a rapid thaw set in on Dec. 30th, and though there was severe cold in January, the re- mainder of the winter was more remark- able for rapid changes of temperature than for continued cold. In 1861 the spring was variable, but the summer and autumn unusually hot and dry : in June the ther- mometer was 82°, and on August 12th it was 89'5 ; the years 1770, 1811, and 1831 only had as warm an October ; with the exception of a cold week in November, the warm weather continued up till Christmas. In the cold season of 1860, diseases of the respiratory organs ad- vanced from 13'7 to 16'4. Hooping-cough, however, did not increase, and laryngitis observed a considerable decrease. Croup also decreased from 1'29 to 1'05. During the high temperature of 1861 bronchitis decreased, hooping-cough was on the in- crease, laryngitis and Croup continued the same. The London quarterly reports give similar evidence. Diseases of the respi- ratory organs increased from 15' to 20" bronchitis, from 8* to 10-; pneumonia, from 5* to 6'7; laryngitis and Croup were 0'4 and 0'7 respectively in the wrarm season of 1861; when the former diseases were declining to their usual standard, the latter made their most rapid increase in London. Laryngitis is also approximated to Croup in the time of year in which it is most fatal. The proportional mortality in London from diseases of the respiratory organs is, for each quarter- Diseases of the Respira- tory Organs . . . 25* 15- 10- 20* Bronchitis .... 15* 5' 9- 10* Pneumonia .... 9* 6' 5* 8' Laryngitis . ... 0'6 0'5 0'3 0'4 Croup 0-9 1-0 0-6 0-8 There is a strong contrast between Croup and bronchitis as to the time of year at which each is most fatal; the dif- ference is less marked between it and pneumonia, probably from a larger pro- portion of its victims being among the young ; there is a close correspondence between laryngitis and Croup in this re- spect, and the table shows also the in- creased proportion in which they have latterly appeared in London.1 Eighty- five per cent, of the mortality from laryn- gitis is among children ; and in the great increase in the deaths from this cause during these three years, viz. from 260 in 1859 to 386 in 1861, there are 42 of the smaller number, and about 50 of the in- creased number of these deaths that oc- curred beyond the tenth year. One of the influences bearing upon the mortality of Croup is that of associated epidemics. In the year 1853, when deaths from Croup were few, the mortality from diseases of the zymotic class was 20 per cent., or nearly at its lowest. Smallpox was on the decline ; measles reduced to 1'1 per cent., having been 2'3 in 1851; and scarlatina, though less than it had been, was still 3'7 per cent. From this time an increase is observable in the num- ber of deaths from Croup. In 1854 the mortality from measles was again over 2 per cent. ; scarlatina was over 4 per cent, in this year and the next; and though in 1856 it fell to 3'6, and measles to 1*8, and epidemic diseases generally did not ex- ceed one-fifth of the mortality, yet a new epidemic disease, allied to scarlatina and closely associated with Croup, was devel- oping in England : many of its first vic- tims were registered under this head ; and Croup, which was 1 -05 per cent, in 1855, rose to 1'34 and 1'27 per cent, in the two following years. The year 1857 was un- usually hot ;2 1858 was an epidemic year ; 1 The deaths from these causes in London for each quarter average for 1850-53: Croup, 92, 78, 62, 94; Laryngitis, 68, 61, 34, 43. For 1859-61: Croup, 161, 124, 115, 134; Laryngitis, 110, 74, 47, 68. Before 1845 it was not usual to separate infantile laryngitis from Croup. The average quarterly returns of death from laryngitis for the five years 1840-44 were 7, 9, 6, 10 ; for the subsequent five years, 47, 38, 25, 44; the returns under the head of Croup showing at the same time a diminution. 2 " The temperature was 20 above the ave- rage of the preceding 17 years ; the wind, in- 1 Remarks on the Weather during the Quarter ending Sept. 30, 1860, by James Glaisher, Esq., F.R.S., in Registrar-General's Report. 52 CROUP. diseases of this class constituted more than one-fourth of the general mortality ; diphtheria had not been separated in the registers, and the returns under the head of Croup and scarlatina were increased, the one by a thousand, the other by more than ten thousand, and their proportional numbers to 1'4 and 6'8 respectively. In the next year Croup is 1'3 and scarlatina 4'5 per cent., diphtheria appearing as 2'2 per cent. In the next two years, 1860 and 1861, the mortality from epidemic diseases is reduced to less than one-fifth of the whole, scarlatina and measles are about 2 per cent., and diphtheria 1*25. Croup is again 1 per cent. In 1861 the number of deaths from diphtheria is at its lowest, that from Croup a little higher than in 1860. The increase was chiefly at the end of the year, and was almost con- fined to London and Lancashire; the deaths in this part of England were more by 2000 in the last quarter of the year than in either of the two previous winter quarters; in Manchester they rose from 1682 to 2123, and other large towns in this district show a similar increase. In London the chief coincidence is that of the increase in the mortality from scarla- tina from 467 in the third quarter to 1145 in the last. In the corresponding quarter of 1860 it was 602. Hooping-cough and fever were on the increase in these dis- tricts, and from this time the commence- ment of an epidemic period may be dated. The year 1862 was cold, wet, and un- healthy ; the mortality from Croup is again 1'3 per cent. ; from hooping-cough, 2'8 ; from other diseases of the respiratory organs, 15'6; scarlatina is increased to 3'4 and diphtheria is 1T3 ; zymotic dis- eases generally have increased to 21'2 ; the whole mortality during the year being very great. It is to some general causes acting un- favorably upon the health of children, rather than to the influence of a particu- lar epidemic, that these variations in numbers are to be attributed. Croup, indeed, seems to hold a place interme- diate between diseases of the zymotic class and those of the respiratory organs. Diseases of the zymotic class generally show a greater mortality among females than males. Croup differs from them as a class in this respect. Hooping-cough exemplifies this point of difference in the greatest degree ; Measles, though often followed by Croup, shows no periodical coincidence with it, except in the time of year at which it is most prevalent, cold appearing to increase the fatality of both; Scarlatina is distinguished by being least fatal in the spring ; while Smallpox is not modified in its violence by either season or climate. Whenever these diseases have increased there has been an increase, at least, in the fatality of Croup, and the same is noticeable with respect to Diph- theria. This differing from the preceding diseases in its liability to recurrence, and to some extent corresponding with Croup, is distinguished, as to these general char- acteristics, by showing a greater mortal- ity among females ; by being when least epidemic, like scarlet fever, most fatal in the autumn and winter ; and when most epidemic, like smallpox, by a progression independent of season and climate. Croup differs from diseases of the re- spiratory organs in its periods of greatest mortality, and widely from some of this class as to prevalence at different periods of life ; the whole class agrees with Croup in showing a greater mortality of males than of females, and the effects of climate and season are always obvious in both. One disease of this class, infantile laryn- gitis, has been specially commented upon, to set forth its contrast with the class, and its affinities to Croup, and to show by the intimate correspondence of the two in every particular by which they can be compared, that this form of disease should not be considered, from the absence per- haps of one anatomical character, as in any way different from Croup, nor here- after be classed apart. Croup has also some relations to dis- eases of the constitutional class. In the severer forms of local inflammations, in- dividual susceptibility is concerned ; and besides a predisposition, induced either by previous illness or by the causes exam- ined, some constitutional infirmity may predispose, and it is noticeable that this source of disease is more apt to come out in the first decade of life among males, and just after that period in females. Croup affects children of certain families, and certain children of some families, more than others ; it is said that those of a florid complexion are often more liable. We see in a family some suffer much under infantile disorders that affect others but slightly, without knowing why. Not only is the tendency to spasm hereditary, but to local congestion, at particular ages. Where there is no diathetic peculiarity, some aberration from health is a usual predisposing cause. There are other causes, such as sudden changes of dress, the impression of cold air after heating exercise, even residence at the sea-side, which may influence the frequency, though not the fatality, of Croup. Children who have suffered an attack are specially liable to a recurrence on exposure to any of these causes, and the recurrent attack is not always the least severe. stead of moving at the average rate of 110 miles a day, passed over London at the rate of 81 miles during the 53 weeks. The rain- fall was 21'4 inches."-Registrar-General1 s Twentieth Annual Report, p. xliii. SYMPTOMS 53 Symptoms.-The symptoms of Croup follow quickly upon the cause which ex- cites them ; the first indication is often mere hoarseness in the tone of voice or cry, the child is feverish, and either dull or fretful; is thirsty, and drinks without difficulty ; the tongue has a white fur, and is red at the tip and edges ; there is some heat and dryness of the skin, and a check to the secretions generally ; an occasional short dry cough may be noticed, and a little harshness of breathing. The more characteristic symptoms generally come on at night; during the first sleep the cough is noticed to be sharp and harsh, with that peculiar croupy clang which, when once heard, is always easily recog- nized ; this may be repeated at some in- tervals without rousing the child froA sleep; the heat and dryness of the skin are now more marked, the pulse is fre- quent and strong, and the breathing loud and difficult, when some repeated clang- ing cough, with shrill-drawn breath, wakes the child in a fright struggling for breath. He starts up, is flushed and hot, the eyes staring, the conjunctivae red, a hissing sound accompanies every inspira- tion, and is very marked and loud after the short dry sounding cough ; it is evi- dent that insufficient air enters the chest, although the respiratory efforts are great; the circulation is now also highly excited, the turgescence of the face and neck in- creases, and the color deepens, the child puts its hand to its throat as if to remove obstruction, speech becomes impossible, and soon, as if in despair, muscular effort relaxes and air begins to enter the chest more freely. The paroxysm may come on within a few hours of exposure, and sometimes, though rarely, before the usual symptoms of ingress have been noticed ; it may begin at any hour, but most frequently at night, and is seldom delayed beyond thirty-six hours from the commencement of the illness ; it may last but a few min- utes, or be prolonged with varying in- tensity for more than an hour; its first accession is nearly always followed by a remission, more or less complete, some- times so perfect that the most careful ex- amination is required to ascertain the presence of the disease, and to prevent a fallacious confidence following too closely upon the first alarm. Its intensity also varies much; but however slight in de- gree, it occasions an acceleration of pulse, an increased heat and redness of the sur- face, especially of the face, also an injec- tion of the conjunctival vessels not ex- isting before, and which will probably subside if the paroxysm be not too soon repeated. The temperature as taken in the axilla has been found at 100°, with the first pre- monitory symptoms ; by the second day, or at night, it will rise to 102°, possibly to 103°, coincident perhaps with the earlier paroxysms, but not with the severer at- tacks which may follow : indeed, the tem- perature is generally less on the third day, and will subside by the fifth unless pul- monary complication have arisen. A high temperature at the very onset may point to one of the exanthemata ; its per- sistence to diphtheria. It is important to consider whether the patient is being seen shortly after such an attack ; for if seen before, or at some time after a first slight attack, there will be neither redness of conjunctiva nor coryza, and even though sneezing or some catar- rhal symptoms have preceded, there will be no defluxion from the nose; the skin will be dry and harsh rather than hot; the urine will be found to be in small quantity and of a high color, with no marked sediment. The pulse is quick and hard ; the respiration is accelerated, but, though disturbed and somewhat op- pressed or wheezing during sleep, it is not much altered in frequency ; and, unless there be already some implication of the lung, or the presence of some other dis- ease, it will not have a ratio of more than one to three, nor of less than one to four pulsations. The most valuable indication of the presence of the disease, even in this early period, is drawn from the respiratory sounds and movements. The voice may attract attention, the cough will soon give the trumpet-note of alarm, but, without the impeded respiration and its physical signs, their indication is not conclusive ; they may even be absent during some temporary lull in the symptoms, and then is the favorable moment for a careful aus- cultation. The inspiratory sound is pro- longed, and, instead of the ordinary blow- ing murmur, there is a sibilant tubular sound, high in pitch and of a metallic quality, constituting a prolonged harsh stridor ; the expiratory sound is also pro- longed, but is low in pitch ami harsh, the respiratory murmur is weak, especially in the anterior and upper part of the chest, and is masked by the tracheal siffle ; this is very marked over the larger bronchi, but is not always enough to conceal the presence of a certain amount of mucous and sibilant rhonchus in some of the smaller bronchi posteriorly; there is no dulness on percussion, not even over spots where the murmur is altogether absent. The respiratory movement may also be noticed to be deficient in this stage, and when exaggerated during dyspnoea, to be inefficient; the supra-clavicular spaces are depressed during inspiration and though the diaphragm may descend well, the in- tercostal spaces will not bulge, nor will the walls of the chest be fully expanded. The cough is sure not to be long quiet, 54 CROUP. and its short, dry, abrupt character at- tracts notice ; it is not, strictly speaking, a hoarse cough, there is no deficiency in body of sound, and it is high in pitch ; a shrill inspiration accompanies each effort; during the paroxysm the cough will be fre- quent, and it is then the sign most worthy of attention. Our further investigation of the state of the respiratory organs must at this time be limited to inspection of the front of the chest, and percussion at the back; when the attack is over, during sleep, or after vomiting, ausculta- tion can be satisfactorily accomplished. The condition of the whole extent of the body should now be examined, to re- mark the absence of spasmodic contrac- tion of the thumbs or toes, the presence or absence of a rash on the skin, of oedema of the extremities or of the face and neck, and the degree of warmth and tone of color of these parts as compared with the body generally ; the last point is to be specially noted, so that any variation in the depth or tone of color in these parts and in the face and lips may be readily appreciated. The sides of the neck are to be examined for enlarged glands ; those at the outer border of the sterno-mastoid are always palpable, but it is important to note that the glands at the angle of the jaw are not enlarged. An early oppor- tunity must be taken for a full and clear inspection of the inside of the mouth and throat. There may be some redness of the soft palate, sometimes oedema of the uvula; the pharynx will be either of a pallid red or of a brighter pink hue ; there will be a remarkable absence of free secre- tion, and no speck of adherent exudation visible in any part of the pharynx or ton- sils : some enlargement of the tonsils has been noticed, and if it be sufficient to press forward the anterior arch of the palate a slight irregularity of outline will be occasioned, but the membrane is con- tinuous, of uniform color, and smooth. Before this inspection is ended, the tongue should be sufficiently depressed to bring the epiglottis into view ; the vivid red- ness and turgescence of its apex contrasts strongly with the surrounding textures, and indicates the condition of the sub- jacent orifice. The disease attains its height by the end of the third day at the latest, but the intensity of the attack may hasten the stages of its advance, and death may oc- cur within forty-eight hours of its com- mencement. The characteristics of this second period are high vascular excite- ment, and an ever-increasing difficulty of respiration ; the cough is now almost in- cessant, or frequently recurring in shocks of convulsive violence; there is no free secretion ; a little viscid phlegm, clear or muco-purulent, may sometimes be ex- pelled, or an opaque mucus be seen in the lower part of the pharynx. Pain is complained of in the front of the larynx, or nearer the top of the sternum; the voice may become whispering or sup- pressed from the effort to speak being evidently painful; the stridulous inspira- tions are louder and more continuous, the labored and sonorous breathing being audible at a distance ; and now, though the thirst is great, deglutition is not al- ways easy, in some cases, from imperfect closure of the glottis, the liquid provoking great dyspnoea ; in others the urgency of the dyspnoea itself not permitting the effort. Even at this stage, if the attacks of dyspnoea have neither been too severe nor too frequent, and air sufficient to maintain life be yet admitted to the tongs, the pulse will steadily maintain its force and frequency; there will be great heat of surface and profuse perspiration, especially on the face and forehead, which parts will be of a bright red color; the veins of the neck and temples may be- come distended and dark, and the face and lips at times purple, but if they quickly assume a brighter tint it may not be too late for the disease to take a favor- able turn. The first evidence of this is a change in the character of the cough; it becomes lower in tone and less dry, not less in force nor much less in frequency, but becoming moist, and gradually effect- ing the expulsion of some thick semi- opaque mucus in which not unfrequently small whitish opaque flakes are discerni- ble. At the same time the sibilant in- spiration is neither so loud nor so per- sistent; it is still heard before each cough, and it will be audible during sleep or on first waking; the voice at times regains its natural quality, at others is only hoarse or dissonant in its higher tones; the accessions of dyspnoea are rare and less marked, the febrile excitement sub- sides, a more equable perspiration is maintained, the urine becomes abundant and frequently affords large deposits of urate of ammonia and sometimes of oxa- late of lime; the soft palate, tonsils, and pharynx become paler and less tumid ; a loose muco-purulent secretion is often seen in the gullet; the tongue is less red, less furred, and more moist: thirst dimin- ishes, and appetite returns; the harsh tracheal siffle will have been replaced by some mucous rales, the normal respiratory murmur will be everywhere restored dur- ing this favorable progress, and, if unin- terrupted, three days may suffice to es- tablish convalescence. A persistence of irritability in the air-passages may greatly delay this, and a further extension of dis- ease to the lung endanger it altogether. Auscultation here again becomes the only basis of confidence, as upon the subsi- dence of the more urgent signs, others, less obvious but not less important, may SYMPTOMS. 55 be discovered ; it may be found that there are parts of the lung to which air is not admitted; that there is an accumulation of mucus in the bronchi, or an amount of bronchitis, with the development of sub- crepitant rhonchus, that will seriously im- pede recovery. An extensive capillary bronchitis, or the existence of pneumonia, will not only be indicated by their special characters, and by the acceleration of the pulse-respiration ratio, but also by the general symptoms ; the signs of laryngeal obstruction have diminished, but the res- piration is as much embarrassed ; there is less effort, but there is no relief; and the disease advances to its close as surely and even more hopelessly than if its ad- vance had been unbroken. The third stage is that of apnoea and rapidly advancing exhaustion: it may come on in the manner just described, but more frequently is the direct sequence of the more urgent symptoms of the sec- ond stage, which, when about to lead to this result, present some additional note- worthy particulars. The tracheal siffle is accompanied by " tremblotement, " a laryngo-tracheal mucous rale with a trem- ulous character heard in both expiration and inspiration, or a click either constant or occasional, may also be heard through the stethoscope and whatever the char- acter of the rale or siffle, it now becomes audible over the trachea in expiration. The voice is whispering or completely suppressed, the cough stifled, powerless, or altogether absent; it may, however, recur in some paroxysm of dyspnoea and afford temporary relief by the chance ex- pulsion of some membranous shreds. The hand may at times be directed to the mouth or throat as if to remove some ob- struction, but the paroxysms become more urgent and without remission, there is restless tossing of the body and limbs on the bed, consciousness is im- paired, and voluntary power much dimin- ished ; the respiratory efforts may con- tinue for a time to be violent, loud stridor marks both the expiration and inspira- tion ; with the latter act the larynx is seen to be forcibly drawn towards the sternum, the supraclavicular and inter- costal spaces sink, and though the abdo- men descends, the epigastrium recedes; the head is thrown back, the lower jaw fixed, the mouth partly open, the alse nasi dilated and depressed; the veins of the neck and temples are distended and dark, the eyes starting, and the face livid ; the pulse becomes either too rapid or too weak to be counted, the temperature falls and the perspiration becomes cold and clammy, the neck and even the extremi- ties may be swollen as well as the face, and assume a leaden color, or the whole surface becomes of a marble-like pallor, the features are set, the eyes lose their expression, oscillate in the orbits, become distorted and fixed. Sometimes the whole body is bent backwards, and death has been known to occur at the moment of an inspiratory effort. Suffocation is every moment imminent, but frequently an ap- parent calm in the more violent symp- toms precedes death, a gradually decreas- ing quantity of air is entering the lungs, the whole chest is flattened and much diminished in fulness and capacity; the countenance, though not livid, no longer retains its florid hue-it becomes shrunk- en, dusky, or pallid ; complete stupor sets in, the limbs become flaccid, the surface cold ; the pulse is small, weak, and fre- quent ; the eyes are dull and sunken ; the respiration becomes gasping and irreg- ular, the pulse intermitting, and both soon cease. The whole duration of the disease, advancing uninterruptedly to its fatal termination, rarely exceeds five days. The division into the three stages of in- gress, full development, and termination by apnoea, is an arbitrary one ; the limits of each cannot be defined, nor is there any natural line of separation; whenever apnoea is commencing, the third stage has arrived, and this may be suddenly fatal, even though the first stage seems unac- complished ; so also in the second stage the signs of increasing obstruction in the trachea may be undeveloped, and yet the third stage have set in and be gradually advancing. [No allusion is made in the above ac- count to a class of cases familiar to Amer- ican practitioners, designated by Condie and others as Spasmodic Croup, or sudden Night-Croup. This is quite a different affection from laryngismus stridulus, with which it has been confounded by some writers. It often occurs without any pre- monition, in children, in the middle of the night; the child being awakened from sleep by difficulty of breathing, attended by a short, barking cough. This, although alarming, is, under proper treatment, never, or almost never, fatal. All the symptoms, and the manner of their relief (by relaxation and secretion), point to a combination, in the pathology of this affection, of pre-inflammatory congestion of the laryngeal and tracheal mucous membrane with spasmodic narrowing of the glottis. Intermediate between this and mem- branous or "true" Croup, is Catarrhal Croup, or Croupal Catarrh (alluded to on a subsequent page under Diagnosis). In the latter, the symptoms are those of an ordinary acute bronchial attack, except that the cough has a barking sound, much t1 A mucous rale sufficiently tremulous to be audible without the stethoscope, is usually a very favorable sign.-II.] 56 CROUP. most marked at night; and often, in the night, croupal difficulty of breathing comes on. Under suitable relaxing treatment, these croupal symptoms will seldom recur for more than three nights; but, if ne- glected, or undue exposure occurs, the disorder may pass into the form of true membranous Croup, with all its dangers. The common proclivity, in children at least, to anginose symptoms at night, is hard to explain. It is, nevertheless, a fact, that the commencement of a hoarse barking cough, with difficulty of breathing in the daytime, and, equally, its continu- ance through the day after beginning in the night, are much more serious in prog- nostication than when such symptoms are entirely nocturnal. A day-time barking cough, with fever, should always receive prompt and careful attention.-II.J Diagnosis.-Numerous causes affect- ing the glottis and larynx, modifying their special functions, and interfering with the entrance of air into the lungs, give rise to croupal symptoms that are to be distin- guished from Croup. Spasm of the glottis is readily excited in infancy ; irritation of the gums, or of the stomach, or an undue excitability of the nervous system, will suffice for its production without either local congestion or general febrile action. It is often first noticed as the child starts out of sleep with a stridulous or crowing inspiration checked or interrupted by the spasm; the head is thrown back and fixed, the chest motionless and the face livid; in some convulsive action a little more air may enter the chest, when in a few sec- onds the spasm yields sufficiently for ex- piration to be effected, perhaps to be suc- ceeded by another crowing inspiration or by a more free entrance of air, and the at- tack terminates in a fit of crying; the breathing then regains its natural charac- ters, no signs of stridulous inspiration remaining. An attack of this severity is seldom the first to which the patient has been subject, but it is likely to be repeated on the slightest cause of excitement or alarm ; the crowing inspiration will not always be heard ; there may be only mo- mentary holding of the breath or acts of involuntary deglutition; it sometimes is induced by the act of swallowing or of suckling ; or it interrupts a fit of crying, the loud and long expiratory sounds of that act being replaced by a short faint sound, and inspiration becomes long and noisy, instead of being short and free ; an expression of alarm is fixed on the face, which becomes red and turgid, and the spasm may either pass rapidly into natural crying, or there may be more serious cause for alarm. The breath may be held for a half a minute, the spine arched backwards and rigid, the thumbs bent inwards on to the palm of the hand, the great-toes sepa- rated from the others, and both fingers and toes strongly flexed. Where the con- vulsive proclivity is marked, and some persistent irritation not in the windpipe keeps up cough which might mislead, this bending in of the thumbs is a valuable aid in the diagnosis. In the slighter cases the attack being accompanied by crying rather than cough, and the tone of the cry being natural, would almost suffice to distinguish these cases of child-crowing, or laryngismus stridulus, from Croup. Dr. Clarke,1 who describes this condition accu- rately, remarks that "it has sometimes been called chronic Croup, but it is very different from Croup, and is altogether of a convulsive character." Some cases of this kind have been de- scribed by Franks and Kopp, in Germany, as thymic asthma. The enlarged thymus is only one of the signs of a persistence of the infantile condition, among others a quickness of the pulse and respiration, and even the infantile ratio between these acts of 3 to 1 may be noticed : nor are these attacks limited to the earlier months of infancy, but may be continued into the fifth year; their abrupt commencement and termination, the freedom of respira- tion in their intervals, and a concomitant derangement of the child's health not of a febrile character, in which slighter symp- toms of the same kind occur, the tempera- ture often being considerably below the healthy standard, separate all cases of this kind from Croup. Foreign bodies entering the glottis2 pro- duce croupal symptoms which are distin- guished from Croup by the absolutely sudden manner in which a child, probably in perfect health at the time, is seized ; it may be during a meal, or with a known object in the mouth which has disap- peared while about to speak or at play, and not during sleep or at night. There is one kind of foreign body, however, which may find its way into the glottis during sleep, and that is an ascaris lum- bricoides from the stomach ; several in- stances of this are on record. It might seem possible that matters vomited during sleep should be drawn into the windpipe ; this has happened to adults, but rarely if ever to children. The dyspnoea from any of these causes, if not suddenly fatal, is as violent at the first moment as at any sub- sequent time. There may be remissions from the foreign body descending into the bronchus ; in this case the sound of the 1 Commentaries on some of the most impor- tant Diseases of Children, by John Clarke, M.D. Part I. p. 88. London. 8vo. 1815. 2 A case is recorded in the 1st volume of the Med. Times and Gaz. for 1853, p. 126, of a fruit seed, three-fifths of an inch long and one-fifth in circumference, passing the glottis of a child two years and one month old. DIAGNOSIS. 57 voice or of the cough would be clear, and there would be no tracheal siffie, while the signs of obstructed respiration, more frequently found on the right, must always point out the site of the foreign body : when it is in the larynx or trachea it gives rise to constant dyspnoea, with loud expi- ratory bruit as well as the stridulous in- spiratory sound. The ingress of acute Croup has been attributed to a possible accident of this kind, the alarm occasioned by the sudden onset of dyspnoea having made the mother or nurse oblivious of the premonitory cough; taking the stetho- scopic signs and general course of the symptoms together, the diagnosis need not long remain doubtful. When boiling water or chemically irritating fluids have been swallowed, there is no room for doubt, and the state of the mouth, phar- ynx, and nares, confirms the history; the whole course of the resulting lesion differs only from Croup in its sudden commence- ment and in its cause. Injury to the larynx from without is a possibility that suggests a careful exam- ination of the integuments of the neck for any appearance of injury, or of subcuta- neous emphysema: the outline of the larynx should be traced; its mobility noted, as also whether there is marked tenseness, swelling, or tenderness, in its immediate neighborhood ; these last char- acters, with a limited extent of redness of the skin and loss of elasticity at the spot, might indicate deep-seated abscess. There are other chronic affections which in their exacerbations may simulate Croup. Polypus, or growth from the mucous membrane in the interior of the larynx, may occasion croupal dyspnoea, which be- sides its chronic history is accompanied with stridor, both in inspiration and in expiration. Tumor causing mechanical obstruction of the trachea is rare in chil- dren. Spasm of the glottis may be occa- sioned by tumors, enlarged glands, or abscess, implicating the recurrent nerve ; post-pharyngeal abscess may not only cause obstruction, but serious injury to the windpipe ; it is generally a sequel to other diseases, and" is therefore more likely to be met with in secondary Croup, of which it may not only be a complica- tion but a cause ; a digital examination of the posterior wall and sides of the pharynx would give the necessary information of its progress where inspection is unsatis- factory. Even in acute disorders, and especially in the more urgent and sudden cases of dyspnoea, the pharyngeal surface of the glottis should be examined by touch, whereby an unsuspected cause of obstruc- tion may be at once detected and removed. The interior of the mouth and throat should be inspected in all cases ; without this the nature of the diseased action can- not be evident, and by it alone it can often be determined that some disease other than Croup is the cause of the symp- toms. The physical examination of the chest must never be neglected; where Croup is present it is the chief means of tracing its progress, and, as pointed out by Dr. Williams, the first sign of the dis- ease, even at the onset, may be detected by the stethoscope, and by the same aid some of the diseases liable to be mistaken for Croup are most easily recognized. Catarrh in young children, with a pro- clivity to spasm, may occasion a hard ringing cough, attended by sibilant in- spiration in the early part of two or three successive nights ; the respiratory surfaces are now the source of the irritation excit- ing this spasmodic cough. In stronger or older children the same local affection sometimes induces a passing hoarseness or aphonia, and a short harsh cough which is husky rather than dry, and is neither frequent nor spasmodic, unless it be slightly so during the first sleep, and then even sibilant inspiration may be audible ; but this again disappears, the breathing is free, there is no acceleration of the pulse, and any heat of skin soon yields to perspiration : the illness has commenced with well-marked catarrhal symptoms; the cough is at times heard with a moist sound, or is attended with secretion, and auscultation furnishes the signs of incipi- ent bronchial catarrh ; these are well de- veloped on the second day, and become more extended ; they are uninterrupted by the siffle of laryngeal obstruction, which no longer even obscures the normal breath-sounds. Hooping-cough often has the frequency, more rarely something of the tone, of the cough of Croup on its first commencement, but as it progresses the cough is attended by a shrill inspiration which differs in character from that accompanying the cough of Croup only by the sonorous qual- ity constituting the hoop; the cough is also worse during the first half of the night, and occasions suffocative fits of dyspnoea ; these are produced differently from those of Croup, and are more directly the effects of the cough, which consists of short expiratory efforts rapidly succeeding each other, no inspiratory action inter- vening. Thus a turgescence and lividity of countenance is caused, which rapidly disappears after free inspiration is accom- plished ; it is at once obvious that sufficient air is received into the chest during the inspiration, as the sonorous quality would seem to indicate, while the perfect relief to the child, the gentle play of the chest walls, and their rounded form offer a suf- ficient contrast to the dyspnoea of Croup. Moreover, at the period of the illness when the hoop is developed, the cough has al- ready existed some days with precedent 58 GKOUP. catarrhal symptoms ; the more persistent dyspnoea of severe hooping-cough comes on still later, but whether in its earlier symptoms or later elfects, it is in the more distant air-tubes that the signs of disease are detected, and not at their commencement. The hoop is, moreover, only an occasional phenomenon, while in Croup the stridor continually increases and becomes unintermitting. In measles a ringing cough, and dys- pnoea resembling that of Croup suffi- ciently to mislead, sometimes accompany the catarrhal symptoms of invasion ; the cough may have exactly the tone of Croup, but the stridulous inspiration is less marked, and both will sooner become catarrhal. The febrile condition is simi- lar, so that unless the presence of measles is expected, or its signs just apparent, there may be no guide as to the nature of the affection but the character of the throat-redness ; this is in patches of dusky red instead of being uniformly bright. The croupy condition induced by the in- gress of measles subsides when the rash is well out; it is however liable to recur- rence, from various and often slight causes, for some time after the original disease has entirely disappeared. Diphtheria implicating the air-passages produces the effects of Croup, with very similar symptoms ; these, though they do not supply the main elements of the diag- nosis, afford many points of difference ; they are the sequel of a more general or a more prolonged diseased action, and may not appear till after three or four days, or even a week, of illness : their mode of development is most varied ; sometimes they have not attracted atten- tion until the dyspnoea is unintermitting ; sometimes at their very beginning they will embarrass the respiration and excite the circulation to a degree that completely alters the features which had up to that time marked the disease ; at others, in the intervals of dyspnoea, though the respiration is not free, the child will take food, resume its play, and either seem cheerful and excitable, or indifferent to its danger. Though the croupal symp- toms may show an exacerbation during the first half of the night, they are as frequently first noticed at other times ; they are neither so paroxysmal in their commencement, nor so dependent on the urgency of the cough. An excess of suffo- cative difficulty may not occur so early as in Croup, but when it has occurred there will not be so complete a remission as after the first paroxysm of Croup; the impeded respiration, with signs of laryn- geal and tracheal obstruction in both ex- piration and inspiration, may be detected before any severe distress has been thereby occasioned. Early notice is often given by a hoarse cough, which has a muffled rather than a ringing sound, and by an unpleasant tone of the voiee, which is husky rather than hoarse, or it is nasal in tone, or croaking and deep, but much sooner becomes whispering or perma- nently extinct. Where the more general characters of diphtheria are well marked, its epidemic prevalence known, a contagious influence traced, or some days of illness have pre- ceded the attack, there will be little diffi- culty in rightly estimating the nature and cause of these additional symptoms, and none if the few days of previous ill- ness have been under observation, so that the special products of diphtheria and the asthenic tendency of that disease have been recognized. Where the phenomena of dyspnoea are those first presented to our notice, it will not be possible to ar- rive at a diagnosis from them, unaided by inquiry as to the history of attack; whatever the character of the dyspnoea, and however recent or even sudden the attack, if severe illness have recently been recovered from, or if there is the history of only a short illness that seemed to be passing off, it may not be diphtheria, but it is probably idiopathic Croup ; while if there have been two or more days of illness immediately preceding the first croupy symptoms, if on one day there have been dulness or debility and refusal of food, if one night's extreme restless- ness unattended by cough, with excita- bility or irritability, headache, vomiting, an unusually free action of the bowels, or even a very free secretion of urine, coryza, and congested or glistening conjunctiva, delluxion of glairy fluid from the nostrils, or stoppage of one or both of them, creamy moist tongue and difficult or pain- ful deglutition, the presence of diphtheria may be inferred ; there will then be greater enlargement of the lymphatic glands of the neck, and especially of those at the angle of the jaw ; these may be so full as to render a free inspection of the mouth difficult, yet the enlarged tonsils, and the unequal congestion of the soft palate, will give further confirmation, even if no patch of diphtheritic deposit come into view. The fullest and clearest inspection pos- sible of the mouth should be obtained ; one spot of diphtheritic deposit brought into view clears up all doubt in this most important matter; it may be below or behind the enlarged tonsil, or almost hid- den in the angle of the soft palate and uvula, or completely concealed by the uvula or velum ; it may only just be com- mencing in the follicles of the tonsils, or may have already cleared from their sur- faces, leaving only the mark of its attach- ment, or a faint indication within the substance of the mucous membrane. When extensive deposit in the fauces in- DIAGNOSIS 59 vades the larynx by continuity, a glance is sufficient to confirm what the general aspect of the patient would suggest, and from the greater enlargement of the lym- phatic glands a very limited inspection is often all that can be obtained; there would in such cases probably be consider- able fetor of the breath, and secretions escaping from the mouth without effort to expel or restrain them. But the im- plication of the larynx is as frequently effected by new centres of deposit as by continuity of advance, and there are not wanting cases of diphtheria to show that the diseased action may commence in the air-passages ; in these cases the careful record of the mode of ingress-the attack being recent, this is more easily obtained with accuracy-and the consideration of the concurrent symptoms must be mainly depended upon, bearing in mind that it is in these cases where the excitement of the circulation and general heat of surface are most likely to mislead ; the pulse, however bounding, quick, or full, is not strong or hard, and the breathing, though disturbed, is not accelerated proportion- ately with the pulse ; indeed, during the development of diphtheria the respiration generally has a ratio of less than one to four pulsations ; any precedent vomiting, diarrhoea, or diuresis, with loss of sleep, loss of appetite, or difficulty of swallow- ing, powerfully aid the diagnosis ; while an inspection of the fauces is of the greatest importance, as some of the ap- pearances are the same whether the first product of the disease be deposited there or not. In diphtheria some part of the pharynx is sure to become the seat of the disease, and to show unequal redness and turges- cence at some points before the deposit occurs; or if the first patch have sepa- rated from the tonsil, these signs would indicate fresh deposit elsewhere ; and while it is rare for the larynx to be the part first attacked, it is very frequently invaded by extension from these new cen- tres of deposit. The aryteno-epiglotti- dean folds are often the points from which such extension proceeds, and cannot at this time be brought into view ; or some point near the posterior nares may be im- plicated, and be therefore quite out of sight; in these cases a glairy or yellowish mucus in streaks along the back of the pharynx, or collected in some quantity in the gullet, will give indications of the dis- ease : probably other isolated patches may appear either in the nares, on the lips, or even the eyelids ; the lymphatic glands are always enlarged, and the deglutition is or has been difficult. In making the discrimination between diphtheria and Croup it is necessary to detect the phe- nomena which are the earliest to appear, and those which are most easily ascer- tained, but not to neglect others which may confirm the diagnosis. The occur- rence of epistaxis, or of blood in the ex- pectoration, or of well-marked pieces of false membrane in the matters cleared from the throat with specks of blood on one surface, would point to diphtheria. The presence of albumen in the urine is conclusive in the diagnosis, and may sometimes be detected in the pale urine passed at the commencement of the at- tack, though frequently not appearing till a later period. Paralysis of some of the muscles of vocalization, deglutition or of motion, is equally distinctive of diphthe- ria. Finally, a prolonged convalescence and a less tendency to recurrence not only confirm the diagnosis, but complete the distinctions between diphtheria and Croup. Smallpox is sometimes attended by a consecutive affection of the larynx and trachea simulating Croup; about the seventh day of the eruption a little hoarse- ness, some hard cough, dry at first, but soon with expulsion of tenacious mucus, characterize a secondary Croup, the result of the specific lesion of the larynx and trachea, which is rapidly fatal. Measles gives rise to secondary Croup, only distinguishable from idiopathic Croup by its more asthenic character, and by its having been preceded by the specific dis- ease. It does not come on till the rash is disappearing and the cough which attend- ed the eruption is subsiding ; there is fre- quently an aphthous condition of the mouth at the same time. We may here infer a specific action on the mucous membrane similar to that exciting pneu- monia under the same conditions. Some cases of secondary Croup are subsequent to the pneumonia of measles ; these1 and many of those occurring earlier are really owing to diphtheria attacking a patient debilitated by the primary disease : diph- theria may also complicate measles. Scarlet fever may possibly excite croupal symptoms by extension of the specific in- flammation of the throat to the larynx ; more frequently some general turgescence of tonsils, submaxillary lymphatic glands and the parts about the throat excite croupy paroxysms. Croup secondary to scarlet fever is later in its appearance. The majority of these cases of secondary Croup are complications with diphtheria, and in the few which survive recurrence is rare. Erysipelas is sometimes attended by croupal complication ; here the dysphagia is extreme, and the epiglottis is swollen, red, and erect. (Edema of the glottis may follow con- tinued fever or other prolonged illness ; the consequent dyspnoea comes on in the 1 Archives Generates de Medecine, tome vi. p. 466. 60 CROUP. night; and may be rapidly fatal; but if a remission occur there is neither the same degree of sibilant respiration nor the cough of Croup, there is but little dys- phagia, and the epiglottis is neither red nor swollen. Inflammation of the tongue or mouth, either from the effects of mercury or other causes, may extend to the larynx. In all these cases there is the existence of the previous disease, and the affection is of the asthenic type; some of the latter are rare in children of the age at which we expect Croup. Hysteria may come on in a subject young enough to render it important to exclude the possibility of its being Croup, so closely may it simulate the leading fea- tures of the disease. Dr. Cheyne relates a case so deceptive, that he was induced to order bleeding for its relief. This close correspondence is more liable to occur in one who has been the subject of Croup in childhood; but then, though the attacks may have been numerous up to eight or nine years of age, there has been an im- munity for the past three or four years. Cough with occasionally a croupy sound is first heard, and the attack generally comes on towards night: the cough is loud and peculiar, and tile respiration be- comes soon noisy both with inspiration and expiration, the head is thrown back, the hands clutch at the throat, the face becomes red and swollen, the eyelids are closed and puffy, and the pupils dilated. The dyspnoea may be of some continu- ance, but is not really so extreme as it may seem ; the auxiliary muscles of res- piration are not called into service ; there is no drawing in of the supraclavicular spaces, nor sinking of the epigastrium; the respiratory murmur may be weak, but is everywhere audible; there is no tracheal sitfle heard by the stethoscope placed at the top of the sternum; the voice may be harsh and produced with difficulty, but is not much altered : a con- clusion will be arrived at by conjoining these particulars with an observation of the general attitude, the arching back- wards of the body, the tossing of the limbs, the age and sex of the patient, the absence of definite complaint, the im- paired volition of hysteria, and the spas- modic muscular actions, the most obvious of which will probably be the grating of the teeth. In these cases, whatever other disordered functions may be associated with the attack, it is necessary to be satis- fied that it is not owing to local irritation, and that there is no appearance of dis- ease in the fauces. and this, not of the superficial or catar- rhal kind, but such as affects profoundly its texture, nutrition, and secretion. The determining cause of this, as of other more deeply-seated inflammations, it is difficult to estimate. What in one sub- ject may excite but a passing irritation, in another sets up a definite course of dis- eased action, its phenomena modified by the conditions of the part in which it is developed. The vital importance of the parts which are here the seat of the dis- ease, the special endowment of the glottis and larynx, and some peculiarity in their structure and development, determine the phenomena of Croup. At the time of puberty the larynx rap- idly increases to one-half more, or to double its previous calibre, according to sex ; an increase in the capacity of the trachea has been going on for some time, but during childhood the air tube and its orifice are remarkably small; at this pe- riod the mucous tissue is capable of as much distension from turgescence of its vessels, and even of more swelling from submucous infiltration than accompany the inflammatory process in adults: hence a certain condition of the lining mem- brane might become a dangerous obstruc- tion to the entrance of air in the one case, and not offer an alarming impediment in the other. The existence of submucous cellular tissue as far as to the vocal cords, conduces to this possibility. The upper part of the larynx is also finely organized for the exclusion of any foreign or irrita- ting particles from the air- passages; its muscles are spasmodically excited directly these irritants from without come into contact with the mucous membrane cov- ering them. In this disease, the irritant cause is from within; no sooner is the congestion of the membrane sufficient to interfere with the normal state of its sur- face, than a source of irritation is pro- vided which cannot fail to induce the vio- lent action of the muscles beneath: at first, probably, it is not so much the swell- ing as the dryness of the membrane, from check to its natural secretion, which is concerned in the causation of the spasm ; the hoarse voice indicates turgescence of the mucous membrane as far as to the vocal cords ; the tone of the cough and the in- termitting laryngeal siffle show that swell- ing is not great, and that spasm is an in- tegral part of the seizure. The further effects of the inflammatory action are very evident, whether its intensity be confined to its first site, or be extended further along the air-passages ; in the first case inflammatory products are formed both beneath and upon the mucous membrane, in the second they are accumulated on the surface, and in either the results are commensurate with the symptoms, and Pathology.-Croup is essentially an inflammation of the mucous membrane at the commencement of the air-passages, MORBID ANATOMY. 61 afford a sufficient explanation of the re- sulting apnoea. A very small amount of exudation, added to the swelling and spasm of the larynx, may not only be fatal, but produce symptoms of greater urgency than would ensue from a considerable accumulation in the trachea, and yet few traces remain after death to show that the passage of air was precluded. In the trachea all in- flammatory exudation must be found upon its surface, and may there remain with less obstruction to respiration than is pos- sible in the larynx, though not without offering a further impediment to the en- trance of air into the chest; the power of the cough is thus lessened, and it is fur- ther diminished by the imperfect closure of the swollen glottis, while the secretions of the surface over which the inflamma- tion extends are altered, so as to be less easy of detachment until the inflamma- tory action yields, by which time all ex- pulsive power may be lost, so that albu- minous concretions in the air tubes are a frequent post-mortem appearance, and are often remarkable in the trachea; it does not necessarily follow that the inflamma- tory action has been more intense at this part, still less that this has been its start- ing-point. The symptomatic fever which accompa- nies the disease often has its sthenic cha- racter modified at an early period by the imperfect aeration of the blood ; an early indication of this is afforded by the cere- bral phenomena: some of the symptoms most distressing to witness are not those most felt by the sufferer; movements at first instinctive become imperfectly co- ordinated, and with the impairment of consciousness purely convulsive; the bend- ing backwards of the head in the latter stages is not most frequently observed when the trachea is most obstructed, but is referable to convulsive action; and spasm may be the immediate cause of death. Whether respiration be thus sud- denly stopped, or more gradually abol- ished, the actual termination of the dis- ease is always by apnoea. Morbid Anatomy.-Intense redness of the mucous membrane is persistent after death; swelling is seldom found, though sometimes the aryteno-epiglottid- ean folds are considerably distended, so as to diminish the upper opening of the larynx. Swelling may also be noticed at the base of the epiglottis, in the sacculus laryngis, and at the superior vocal cords and ventricles of the larynx ; the mucous membrane is not much thickened, and has rarely undergone softening ; sections of the mucous folds sometimes discover serum, sero-purulent fluid, or even pus beneath ; pus has also been found dis- seminated between the muscles and car- tilages of the larynx ; the surface of the membrane has not lost much of its smooth- ness or polish; small patches of semi- transparent lymph occur, or a soft whitish exudation rests on some parts of the sur- face or fills the ventricles, or, in its place, viscid mucus or pus may be found on the [Fig. 7. False Membrane In Trachea.] upper edge of the glottis or filling the laryngeal pouch. Ulceration of the sur- face is rare, especially in acute cases ; Dr. West has observed it in one case of idio- pathic Croup not of the most sthenic type, and more frequently in cases of secondary Croup ; in one such case he records1 "an uneven granular appearance of the larynx, and ulceration of the epiglottis. " In some cases of Croup secondary to measles, small aphthous ulcerations may occur above the rima glottidis coexistent with true aphthae of the mouth ; no deposit in the pharynx or slough of the tonsils is found in true Croup. Dr. Cheyne remarks2 that " in other diseases inflammation and incrus- tation, extending from the fauces to the larynx, may often be observed, but in genuine Croup, as it exists in Scotland and Ireland, never." The formation of false membrane, more or less continuous, is a usual result of the inflammatory pro- cess in Croup ; its most frequent situation is in the trachea, but its presence is not so invariable as to make it pathognomonic ; in some cases shreds of lymph, or striae of viscid mucus, or vivid redness only, are found in the trachea; in others a soft curdy lymph, or pus, is present in some 1 Lectures on the Diseases of Infancy and Childhood, by Charles West, M.D. 2d edi- tion. 8vo. Lond. 1852. P. 220, note. 2 Cyclopaedia of Practical Medicine. Arti- cle, Croup, by J. Cheyne, M.D. London, 1833. Vol. i. p. 499. 62 CROUP. quantity and extends into the bronchi. Where a more fibrinous exudation com- pletely fills the trachea, it is separated from its surface by a layer of pus or of muco-purulent secretion, some of which may be found on both sides of the lower part of the false membrane, but it is less abundant and more viscid at its upper part. The false membrane may extend into the bronchi; its transition to a soft and less tenacious substance is so gradual that it may become at any point indistin- guishable from the muco-pus covering the surface, which seems to be undergoing the same inflammatory process. The false membrane of Croup differs from that formed during the specific inflammation of diphtheria, both in its chemical and physiological relations; it is not simply fibrine, but consists of effused lymph in which the presence of albumen can always be chemically demonstrated : microscopi- cally it is a mass of cystoid corpuscles ; it is not the result of an interstitial change in the substance of the mucous membran e, but an exudation from its vessels and glands, so that the structure of the mem- brane producing it remains singularly free from pathological injury. This point has liet,' who represent the French school, in applying the terms Croup and pseudo- membranous laryngitis only to cases of diphtheria, remark "that the mucous membrane beneath the false membrane presents very various conditions - it is sometimes perfectly healthy; this is a fact we have ourselves established. '' And again, alluding to the number of cases of severe Croup on record where mere shreds of false membrane were found in the larynx and trachea, an instance of which they themselves observed, they ask, "May there not yet be a disease which presents so great a similitude to Croup that it has been confounded with it by most authors, and in which there is found after death either no alteration in the mucous mem- brane of the larynx, or a simple inflam- mation, without swelling enough to oblite- rate the air-passages ?" It is such a disease that we mean by Croup ; and while in young children sim- ple turgescence of the mucous membrane conjoined with spasm may be too soon fatal for the special products of inflam- mation to be found, and in others these products collected near the base of the arytenoid cartilages and in the sacculus laryngis may occlude the glottis at an early period of the disease; yet a more or less continuous membranous exudation may in other cases completely fill the trachea, and eyen extend into the bron- chi ; whether it is ever so closely identi- fied with the mucous structure, or so purely fibrinous as is the special product of diphtheria, will require further ob- servations to decide. In some cases the false membrane rapidly forms again after expulsion. Sir Thomas Watson relates a case2 where after tracheotomy it was com- pletely re-formed in six or seven hours : the rapidity of its formation indicates a developed specialty rather than an orig- inal intensity of inflammation, and nu- merous instances prove that the most vigorous antiphlogistic treatment has no effect in retarding its development, while in some acutely inflammatory cases of Croup going on to their fatal termination, no false membrane has been expectorated, and pus only has been found in the wind- pipe. The bronchi show more or less trace of inflammation in their whole extent: in the upper tubes a wflfitish concrete exu- dation is often developed, and sometimes presents sufficient tenacity to be removed entire from one or two divisions; the smaller ramifications are often filled with opaque mucus but slightly aerated. Pneu- [Fig. 8. False Membrane of Croup. From a Specimen in Dr. Gross's Cabinet.] arrested the attention of many of the ob- servers of Croup. Albers, of Bremen, records the absence of all traces of inflam- mation of the subjacent mucous mem- brane in some of his cases, and considers that the plastic exudation being accom- plished, the inflammation not only dimin- ishes but probably ceases altogether. Ue notices also cases of another kind, and it is probable that two classes of disease were before him. MM. Barthez and Ril- 1 Traite des Maladies des Enfants. Paris. 8vo. 1843. Vol. i. pp. 320 and 336. 2 Lectures on the Principles and Practice of Physic. 4th edition. Vol. i. p. 856. PROGNOSIS TREATMENT. 63 monia both lobar and lobular frequently coexists, and vesicular emphysema is gen- erally present in some part of the lung. The heart may contain dark blood, both to the hopeful conjecture of Dr. Wood, of Philadelphia, that one case in fifty only is fatal. The mortality estimated by Jurine, of one in ten, is probably nearer to what we experience ; where it has been placed as high as one-half, two-thirds, or four- fifths, cases of diphtheria are included; nor is it surprising that the most fatal complication of a very fatal disease should be thus mortal when, under a misconcep- tion of its nature, the course of treatment pursued has been such as would endanger the result of uncomplicated diphtheria.1 The inherent fatality of secondary Croup is also increased by subjecting it to the course of treatment required in uncom- plicated cases, and the favorable prospect of some of these is sometimes in jeopardy from the too prolonged use of tartar emetic. The slightest cases of Croup furnish grave cause for anxiety; for some of the most severe there is a hope in re- serve, faint though it be, which is offered in few other acute diseases. Early treat- ment has a great effect on the favorable result of even the most severe cases. The most active treatment will often be of the least avail in the advanced stages. The signs of a favorable progress are a softening in the tone of the cough, a diminution in the frequency and severity of the attacks, with a more free entrance of air into the chest, a less distress of breathing in the intervals, a return of the voice towards its natural tone, a loose or moist sound with the cough, and the pos- sibility of a comfortable repose. This change in the symptoms must be continu- ous for twenty-four hours, and no lung complication present itself, before confi- dence is warrantable. If the paroxysms be more frequent and more violent, and there be no diminution of the dyspnoea, or an increased restless- ness in the intervals ; if the voice be sup- pressed, and the cough less powerful or absent; if the expansion of the lung be reduced till the chest walls seem retracted or flattened, there is no hope of a favor- able change taking place; and even if death be not sudden, it will come on more slowly, but not the less surely, with evi- dences of disordered consciousness and coma : where this stage is reached, though from some unexpected relief air has been again admitted into the lung, and some of the functions of life are resumed, and even continue for a time, recovery is scarcely possible. Treatment.-Few diseases are so de- pendent for their relief on the prompt and careful adoption of a thoroughly antiphlo- gistic treatment at their very commence- [Fig. 9. False Membrane of the Bronchial Tabes.] in its right cavities and in the left auricle, and the venous trunks and sinuses are similarly distended; there may be con- gestion, but there is no fibrinous deposit found in the liver, spleen, and kidneys. The brain may show congestion of its ves- sels or slight serous effusions within its ventricles. Numerous enlarged lymphatic glands are found beneath the thyroid on each side of the trachea; sometimes lymph has been effused both in this situ- ation and between the sterno-hyoid and sterno-thyroid muscles. Prognosis.-We have no data from which to judge the proportion the mor- tality from Croup bears to the number of the attacks. The fully formed disease is one of the most fatal to which childhood is liable, and the younger the sufferer the less favorable the prognosis. Were every case considered as one of Croup, in which hoarseness of voice and peculiarity of cough lead to the prompt and careful adoption of the means necessary to ward off the disease, we might under the most favorable hygienic conditions come near [1 When positively membranous, however, Croup is fatal in a considerable majority of cases.-H.] 64 CROUP. ment as is true idiopathic Croup. Unless the first threatening symptoms have re- ceived all the attention they demand, a free abstraction of blood may be indispen- sable in checking its progress. The in- duction of vomiting in the early stages is often the most effective means of arrest, and one that must be resorted to in all stages of the disease but the last. The air to be respired will require its tempera- ture elevating and made equable by day and night, and aqueous vapor should be diffused therein. The warmth of the sur- face and the application of warmth exter- nally must be attended to, and diluents only allowed to be taken. The exclusion of every possible irritant, as well as moderating the degree of irrita- tion already existing, are of the utmost importance, either in preventing the pro- gress of the threatened malady, or in favoring its arrest and subsidence. However urgent the symptoms, atten- tion must first be directed to their course and development, and their cause ascer- tained ; before our special remedies are employed steps can be taken to secure those general aids which are indispensa- ble. There must be a fire in the room, and a large quantity of hot water in read- iness for a bath must be prepared ; mean- while some hot water can be brought to the bedside, sufficient perhaps for the im- mersion of the child's arms ; the steam from it may be of some service, or sponges wrung thoroughly dry from it and repeat- edly applied to the throat will afford some relief; the nurse or chief attendant upon the child must be retained in the room not only to assist in these measures, but to afford the necessary information as to the commencement of the attack and its antecedents, while at the same time the degree of embarrassment of the breathing, the state of the pulse, of the cervical glands, and of the surface generally, can be noted. An emetic should be in readi- ness, either the ipecacuanha wine, or the antimonial wine, or both ; a combination of the two in equal proportions is well suited for the earliest stages, or a mixture of twelve grains of powdered ipecacuanha with a drachm of syrup, or of mucilage, and three drachms of water, will be of the same strength as the wine ; an aqueous solution of the tartarized antimony of any strength can be made by means of hot water ; some of this solution, containing at least a grain of antimony, must be added to the above mixture, the half of it given early to excite vomiting, and the remainder in less than half an hour, if that action has not commenced. In this Interval an inspection of the throat should be obtained, and care must be taken to make it thoroughly efficient; a good light is required ; if artificial light is needed, three candles cemented together will afford it; the child must be well se- cured in the nurse's lap, the head resting against her shoulder-sudden movements of the head, arms, or feet, must be guarded against, and by passing a firm unyielding instrument, or the broad handle of a tablespoon, to the back of the tongue, it can be depressed and at the same time brought forward so as to show the epi- glottis. This inspection may be conve- nient before the first emetic dose is given, and if any doubt exist as to the nature of the attack, would then be advisable; whenever it is accomplished the diagnosis is complete, and the activity of the means employed can be proportioned to the severity of the disease, the stage at which it has arrived, and the condition of the patient. [In simple spasmodic "night croup," the prompt use of ipecacuanha alone, in powder, syrup, or wine, will often suffice to produce the needful relax- ation and secretion. For a child four years old, 15 or 20 drops of the syrup of ipecac, may be used, to be repeated in a quarter of an hour unless relief to the breathing occurs. Vomiting is not in it- self necessary, but the relaxant should be pushed until this follows, or until the res- piration becomes soft and free. Ipecac- uanha has the great advantage of doing no harm (simply acting as a mild purga- tive) if it should not be rejected by the stomach. The old remedy, " Hive Syrup, " is objectionable, and, with young chil- dren, unsafe, on account of its containing tartar emetic. A certain number of cases of night croup exhibit, in the recurrence of attacks, a predominance of the nervous element over the hypersemic, so as to call for such remedies as assafoetida, hyoscyamus, or musk, in combination with ipecacuanha, and, if needful, with sinapisms and the warm bath.-IL] Before repeating the emetic it will be advantageous to make use of the warm bath : this should be of a temperature of 98° or 99°, and maintained at the higher degree of heat, or even raised two or three degrees above it by the gradual ad- dition of hot water ; a warm blanket must be in readiness to envelop the child on removal, and hot towels to dry the sur- face completely. The air of the chamber should be raised to a temperature some- what over 65°, and never allowed to fall lower ; it can be made moist by placing a kettle of boiling water on the fire with a tin tube fixed to the spout, or a long roll of paper, to convey and diffuse the steam. After the action of the emetic there will generally be great relief to the distress of breathing, and quiet sleep will follow. It is now the time to listen attentively to the breathing; however complete the relief afforded by the emetic or the warm bath may be, the patient must be seen during TREATMENT. 65 sleep, or visited again at night, not only to see that the improvement continues, but for the purpose of noting the state of the respiration ; the stethoscope should be applied to the side of the neck or to the top of the sternum to ascertain the cha- racter of the tracheal bruit, to the upper part of the chest in front and to the lower part of the side or back, in aid of other observations as to the degrees of freedom with which the air is entering. If the result be satisfactory, it may be sufficient to prescribe ten grains of alkaline citrate of potash, or five grains of chlorate of potash, to be given every four hours, freely diluted with water or with milk and water, and a grain or two of calomel for its aperient action, which may be aided if necessary by castor oil in the morning ; it is better to produce this effect by giving three or five grains of calomel at once, should the child have gone through a severe paroxysm of dyspnoea. If there be persistence of the febrile symptoms, of the cough, or of any laryngeal quality in the breathing, half-drachm doses of anti- monial wine must be given with each dose of the saline, or a smaller dose at more frequent intervals, taking care with young children that it is given less frequently as the symptoms subside, and that it is omitted altogether as soon as relief is ob- tained. The emetic must always be at hand, so that in cases of a threatened paroxysm its full effect may be again in- duced. It is to be borne in mind that the paroxysm has a tendency to recur even when the disease is not advancing, and that the recourse to the warm bath may afford such relief as to enable the air to be drawn in again either with freedom or with lessening signs of obstruction. The attack, when treated early, is not unfrequently arrested ; the patient re- quires to be carefully watched, that any return of the croupy symptoms may re- ceive timely attention ; however favor- able the progress, the child should be confined to bed for two or three days, the diet being gradually increased; the temper- ature of the room is to be maintained dur- ing this time, and great caution exercised before allowing the patient to leave it, the chest symptoms meanwhile being anxiously observed. Where the season is cold, or unusual susceptibility has been induced by repeated attacks of Croup, it may be necessary to restrict the patient for ten days or a fortnight to an apart- ment wherein the air is artificially moist and warm. In the more severe cases a tent should be formed over the child's bed, to which steam can be admitted from the long spout of the kettle, which, filled with boiling water and placed behind the bed, can be kept hot by a spirit lamp or other means ; the temperature within can be regulated from 70° to 75°, but at times it may be raised tQ 80°, and a larger quan- tity of steam be admitted with advantage. Calomel should be given from the first, and repeated frequently in small doses, interrupted occasionally for the repetition of the emetic ; a grain, or half a grain of calomel, combined with the quarter or eighth of a grain of ipecacuanha, accord- ing to the age of the patient, is to be pre- scribed every two hours ; if the bowels become disturbed, it can be persisted with in diminished doses until its charac- teristic effect on their secretions is obvi- ous, nor is it then to be entirely discon- tinued. Antimony has great power in moderating the intensity of the first stage of the inflammation; it may, therefore, be used alone to cause vomiting, and as it will be necessary to repeat it with this object, it is better not to give it in fre- quent small doses, which, by inducing in the system a tolerance of its influence, render its emetic effect less easily ob- tained ; for the same reason it is not to be the only emetic employed; where it is of service its good effect is soon observ- able, and can be secured by giving it in small doses with other emetics. In the later stages of the disease it is entirely inadmissible. [Alum, introduced as an emetic in Croup by the late Prof. C. D. Meigs, of Philadelphia, appears sometimes to have decided efficacy in unpromising cases, when false membrane is being deposited. It is much less harsh than antimonial preparations. Dr. James, of New York, has reported1 a case of membranous croup in a child two years old, almost moribund, in which the hypodermic injection of grain of hydrochlorate of apomorphia was fol- lowed by vomiting, with ejection of a tracheal cast of membrane, and recovery. -II.] In some cases, the necessity for blood- letting has to be considered in the earliest stages of the treatment: in certain dis- tricts, where the subjects of the attack are well nourished, and living much in the open air, the early abstraction of blood has been found by experience to be a main element in the favorable issue of the illness; there are also certain cases where the attack is of such severity that the influence of the emetic is better aided by the loss of blood than by the use of the warm bath. In these cases the bleed- ing should be practised before the action of the emetic has commenced, and the blood should be withdrawn rapidly, so that the system may at once feel the effect of the loss; the external jugular vein affords the requisite flow most readily ; it may be obtained from the VOL. II.-5 P N. Y. Med. Record, April 26, 1879.] CROUP. 66 arm, except in young children, and with them leeching is not so efficient a sub- stitute as might be expected. The youngest children bear the loss of one or two ounces of blood better than absti- nence from food, or the eflects of depress- ing medicine ; for a child of four or five years of age, bleeding to the extent of three or four ounces will suffice, either for present relief or for a cheek upon the advance of the disease; it is to be remem- bered that in the cases where it is most indicated, neither of these objects will be attained by this remedy alone ; even where the immediate relief is great, in a few hours there will be a return of most of the symptoms which generally indicate its employment, and these will require for their control many of the means al- ready mentioned, probably with the aid of local bleeding. General bleeding is only of service in the early stage of the disease, it is not to be repeated ; loss of blood is only allowable while there is heat of skin, florid hue of face and lips, and firmness, as well as fulness of pulse, but these conditions do not of themselves de- mand it; it is to be sparingly resorted to among town populations ; it is seldom ad- visable where the attack accompanies any marked deterioriation of health ; and it is contra-indicated in almost all cases of secondary Croup. Local bleeding by means of leeches is of great service wherever the disease is pro- gressing towards its full development; the relief thus obtained is often very great, and may be afforded more than once if other considerations do not render such means of relief unadvisable; the influence of even a moderate loss of blood in this manner may either favor the subsidence of the disease, or the specific action of calomel upon its products,. while in con- junction with the warm bath it may often replace with advantage the too frequent repetition of antimony. Leeches are best applied over the mastoid processes, or a little lower on the neck if a larger number are to be used or a free afterflow from their bites is desirable; in the former situation these can be readily closed by means of dry lint aided by pressure if re- quired, in the latter they can be covered with a linseed poultice. External warmth to the neck and chest is useful; it can be applied wfithout the necessity of frequently disturbing the child, by cloths wrung out of hot water and covered with warm towels or by oil- silk and handkerchiefs, or by small bags containing heated bran, which can be ac- commodated to the child's changes of position. Care should be taken that no part of the surface is chilled, and dry, warm flannels should be from time to time applied to the body, legs, and feet. Counter-irritation is of doubtful effi- cacy,' the application of tincture of iodine to the sides of the neck is of some service, and acts more beneficially when it is cov- ered with water-dressing. Linseed poul- tices, not too moist, with which a little mustard is mingled, may be usefullv ap- plied to the back of the neck and shoulders, or even to the legs ; where signs of bron- chial irritation are found at any part of the chest, or there is less expansion at one part than another, the advantage de- rived from having that part covered with a large simple linseed poultice is very great; if the other symptoms are favor- able, it may be sufficient to use stimulat- ing friction over these parts three times a day when the poultice is changed. A blister may be required for more serious pulmonary implication, but must be strictly limited to a particular spot, and should be so dressed with cotton-wool as to give rise to no ulterior pain or discom- fort. Opiates are to be avoided; sleep is needful, and will naturally happen while the disease is within safe limits, then the easy respiratory movement and increasing roundness of the chest present a strong contrast to the flattening and retraction observable during restlessness and excite- ment ; sleep will continue while that normal condition of the chest is main- tained, if not, it is soon interrupted, and there would be danger in its being artifi- cially prolonged. The strength is to be carefully guarded during the necessary contest with disease, and requires early support; milk and fari- naceous food as well as whey and barley- water, are soon necessary ; if the attacks of dyspnoea have been severe, beef-tea or chicken broth may be given early ; if dis- tasteful, or tending to excite spasm in deglutition, they are to be given in small quantities by tne rectum. The various meat essences, prepared after Liebig's formula, are very serviceable, as they contain the restorative salts of the flesh without any of the protein compounds re- quiring gastric digestion. Alcoholic stimulants are injurious, until the primary obstruction to respiration is overcome, and some pulmonary complica- tion is the source of danger. The stimu- lant expectorants are often required, and when repeated emetics are indicated in the decline of the disease a stimulant should be combined; ammonia, or the ammoniated tincture of valerian, may be added to the wine of ipecacuanha given for this purpose ; the tincture of lobelia may also be cautiously used as an adjunct, but not if there be much obstructing secre- tions; senega is here of the greatest value, [' At an early stage, a sinapism applied over the sternal region may be decidedly use- ful.- H.] TREATMENT. 67 either in large, repeated doses as an emetic, or in combination with ammonia and squills as an expectorant ; for this pur- pose, when the occasion arises, a grain of carbonate of ammonia with two or three minims of tincture of squills and a dessert- spoonful of infusion of senega may be given every two or three hours, as pre- scribed by Dr. West, mixed with a very little milk and sweetened with treacle or coarse sugar; the infusion of senega should be made with an ounce to ten ounces of boiling water, or of double the pharmaco- poeial strength, and its pungency shielded as above, or by the addition of glycerine ; it may be freely given for its emetic effect, after the first urgency of the attack has subsided, and it may be aided in its action by the addition of ipecacuanha wine and of tincture of squills. When emetics are most beneficial, care must be taken so to regulate their employment as not to inter- fere with the necessary absorption of nourishment from the stomach, as sus- taining the integrity of the vital powers is an important element in calculating the hopes of a final recovery. From a very early period in the treat- ment of Croup, from the earliest if the disease has made some progress before treatment has commenced, the necessity for affording relief by the operation of tracheotomy has to be carefully consid- ered, and steadily kept in view ; at any moment the best judged means of treat- ment may be rendered nugatory by threat- ened suffocation, and whenever this is im- minent tracheotomy is to be performed. However insidiously the condition of apnoea may come on, if it be advancing and its course unvaried by temporary im- provement, unless we are satisfied that the cause of apnoea is in the pulmonary tissue itself, and not chiefly in the primary air-passages, no period of the disease, nor the surrounding conditions of the patient, scarcely even the age of the sufferer, should determine us to withhold this chance of life. The extension of the dis- ease beyond the point at which the trachea is to be opened does not prevent the suc- cess of the operation; actual inflammation or consolidation of the lung, which would preclude recovery, will have been ascer- tained in its course, and can be determined by physical examination of the chest at any period; any extension short of this cannot be so determined when the distress of breathing is at its height. Where a certain extension seems probable, the operation is not always contra-indicated ; the admission of air restores vitality to the system, and affords a mechanical aid in expelling the morbid products, thus tend- ing to prevent further change in the lung itself. The surrounding conditions that are essential in undertaking tracheotomy are the same that are necessary for the successful treatment of cases where this extreme means of relief is not demanded; some approach towards securing these can be made, whatever the social state of the patient. The treatment is not to be dis- continued after the urgent signs of distress are obviated by tracheotomy; and though there be now no longer need for some of the medicines, greater attention is, if pos- sible, required in regulating the state of the air to be respired. The most frequent cause of death after the operation, next to the use of too small a tube, and the risk of its becoming obstructed by secre- tions, is extension of the disease to the lung ; this is the natural termination of the disease, whenever the state of the trachea allows it to run its course. The age of the patient has hitherto been closely connected with the success of tracheotomy; the unfavorable result of this operation among young children has seemed to be from the difficulty at this period of life of counteracting the asthe- nic tendency of the disease for which it has been chiefly practised; some results of this operation at different ages are given by M. Andre,1 when Interne at the Ilopital des Enfants Malades, from which it appears that, while of the cases beyond six years the recoveries are one-half, they are not one-fourth of those under that age, and of six cases under two years old there was not one instance of recovery. Most of the statistics relating to trache- otomy are drawn from cases of diphthe- ria, so that analogical deduction from them is unsafe ; they show, however, one uniform result that is doubtless applicable to the disease and to this climate, that the relative proportion of cures increases with the frequency with which the opera- tion is attempted. Dr. Buchanan of Glas- gow has operated2 twenty-six times with nine recoveries ; of eleven cases operated upon by Dr. Cruickshank during two years in a wild country district in Scot- land, eight were successful.3 Mr. Spence1 of Edinburgh has published some most interesting and instructive reports of cases of Croup, in eight of which he performed tracheotomy with three recoveries. The facts brought together by Dr. Fuller5 in his valuable paper on tracheotomy in Croup, and the improvement in the tra- 1 On Tracheotomy in Croup, by M. Andr^, Bulletin de Therapeutique. Paris, 1857. Tome ii. p. 471. 2 Tracheotomy in Croup and Diphtheria (additional cases),by George Buchanan, A.M., M.D. Glasgow, 1866. 3 The Science and Practice of Medicine, by W. Aitken, M.D. Vol. i. p. 587. (Third Edition.) London, 1864. 4 Edinburgh Medical Journal, 1860, p. 693. 5 Medico-Chirurgical Transactions, vol. xi. p. 50. London, 1857. 68 CROUP. cheal tube, recommended by him and M. Gendron de 1'Eure, contribute powerfully to this conclusion. The want of success with children under three years of age in this country ought not to discourage the operation. Mr. Henry Smith1 details two instances, one a child of eleven months, and the other two years, wherein the dif- ficulty of maintaining free the opening into the trachea seemed the only obstacle to recovery. It is somewhat remarkable that in the first three successful opera- [Fig- 10. Purham's Canula and Pilot.] tions in this country for this disease no tracheal tube was used: two of these cases are recorded in the 3d and 6th vol. of the Medico-Chirurgical Transactions; the third was by Mr. Carmichael of Dub- lin, in 1820,2 who maintained the opening for a week by the aid of tin retractors on the edges of the external wound. One of Dr. Buchanan's most urgent cases was brought to a successful termination with- out the use of a tube.3 Dr. Wood, in his treatise on the Practice of Medicine, 5th edition, vol. i. p. 865, mentions three cases in which Dr. Pancoast, of Philadelphia, "removed a small piece of the trachea itself, thereby superseding the necessity of the canula, and avoiding irritation from that sourcetwo of these were successful. The fear of subsequent nar- rowing of the trachea renders this objec- tionable ; passing a ligature through each edge of the tracheal wound might keep it open with safety for a short time; or a piece of wire bent like an eye-speculum, as made for me by Coxeter, might be used to separate the edges. No tube with less than a quarter of an inch diameter is suf- ficient to carry on respiration ; at a year old such a tube cannot be introduced into the trachea ; it would not be tolerated at two years old, so that at these ages other means must be looked for to secure a pas- sage for the air : if it should prove that in a certain class of cases the mere opening of the trachea is sufficient, and that re- covery is frequently possible without the introduction of the tube, then there would be room to hope for success even in the youngest children. [In Dr. J. Solis Cohen's monograph on Croup and Tracheotomy,4 statistics are given of this operation in different countries. Those from Ameri- can sources include 325 cases of trache- otomy, with 84 recoveries ; or rather more than 1 success for 4 operations. Bouchut, Bergeron, and Barthez have reported not very different results in France. In eight London Hospitals (to 1859) 170 operations were recorded,1 with 57 recoveries. The most favorable results for a considerable number of cases appear to have been those of Trousseau, in Paris. In private practice he is reported as having had, be- tween 1851 and 1854, 24 operations, with 14 recoveries. Trousseau advocated early operations ; the prognosis of which is no doubt better than that of those postponed until a moribund state is reached. In this country, the uncertainty of the opera- tion itself, and the possibility of the false membrane being detached so as to allow recovery without operation, have made it generally difficult to avoid postponing it until a very late stage. All statistics show particularly unfavorable results from tracheotomy with patients under two years of age. In regard to the operation itself, Trous- seau, C. West, and R. W. Parker2 particu- larly urge the importance of cleaning out the trachea, with a feather or otherwise, before inserting the tube. Besides its not being too small, the tube should have a curve not too great; imitating rather (to use Parker's language) the Gothic than the Roman arch. If, afterwards, the inner tube should be found to be dry, West and Parker advise spraying into it a solution of sodium bicarbonate, ten to twenty grains to the ounce of water, from time to time. -II.] One great cause of non-success from this operation has been owing to cases of diphtheria being mistaken for Croup. The striking difference in the character of the two diseases, and in the treatment they require, struck me forcibly during the ob- servation of some cases at the Hopital des Enfants Malades, under the care of Trousseau, in the summer of 1850; the want of success in the earlier operations 1 Medical Times and Gazette, 1853. Vol. i. p. 244. 2 Transactions of the King and Queen's College of Physicians, Ireland. 3 Glasgow Medical Journal, January 1st, 1862. [4 Philadelphia, 1874.] [> Med. Times and Gazette, Oct. 15, 1859.] [2 Lancet, Nov. 30, 1878.] TREATMENT. 69 at that institution may partly be attri- buted to such cases being treated as Croup in our sense of the word. The favorable result in some cases recorded by Dr. Con- way Evans1 may be attributed to his recognition of their true relation in this respect. During the period 1850-53, but few of the croupal affections that came under my notice at the Marylcbone In- firmary were cases of diphtheria ; during the last ten years the majority of cases in London requiring tracheotomy have been cases of this kind. For the operation a good light is indis- pensable ; also, two assistants, one of whom may be the nurse, but two in addi- tion are preferable ; an unyielding cushion to support the shoulders, so that the head may rest well back upon the table beneath. An incision not less than an inch and a half in length is to be made exactly in the middle line; three ink-spots on the skin may be made to indicate this, and further, to avoid any superficial vein, the skin should be pinched up on both sides, and transfixed with the knife cutting out- wards. Each layer of fascia is to be di- vided on a director, the knife-edge always being turned from the sternum, the isth- mus of the thyroid is to be pulled upwards by a blunt hook, and the cellular tissue at its inferior border parted by the di- rector, with as little use of the knife as possible ; nevertheless the trachea should be bared over the line at which it is to be opened ; the edges of the external wound are to be held apart by blunt hooks or wire retractors; small sponges affixed to stems are useful; all hemorrhage is to be restrained before the trachea is opened; a sharp hook may be used to fix the tra- chea, or it may be seized below with the artery-forceps. I have seen no sharp- pointed director suited for perforating the trachea and guiding the knife securely; having the thyroid drawn well up and shortening the knife in the hand with the edge directed upwards suffices to enter the trachea safely and to secure a well- placed opening. The expanding forceps or dilator is a useful aid in the introduc- tion of the tube. However retracted the chest walls, some escape of air and mucus generally follows the knife, and then a full inspiratory action restores at once the normal outline of the chest; if respira- tion have ceased, it would be desirable by means of a tube to make suction from the trachea before commencing artificial in- flation of the lungs or the auxiliary respi- ratory movements. Chloroform has been used safely in this operation on several occasions, but it may be better in some cases to abstain from any addition to [Fig. 11. Bryant's Canula. A. Pull length. B. Shortened.^ already existing causes of apnoea, al- though it much facilitates the operation.2 The tube introduced should always be the spring-sided, bivalve one ; the inner tube should have an opening in its upper con- vex surface, as used by Liston ; after a time a valve fitted to one of this kind, as recommended by Mr. Thomas Smith,8 to admit of inspiration through it, and of expiration through the larynx, is a valu- able addition ; the collar recommended by M. Trousseau advantageously inter- venes between the outer extremity of the tube and the skin. [It is important, after tracheotomy, for the atmosphere breathed by the patient to be warm and moist. Some practitioners assert the advantage, in all cases of seri- ous croup, whether operated on or not, of maintaining a temperature around the patient of 90° or 95° Fahr., kept in a high degree of humidity by the generation of steam. Inhalation of the vapor of lime- water, and of that of a solution of lactic acid, is reported to promote the dissolu- tion of the membranous exudation. Such remedies are, at least, safe and worthy of trial.-H.1 After the operation free use is to be made of nutrient and remedial enemata ; liquids can sometimes be swallowed with ease, at others they require always to be given in the form of sop. Secondary Croup requires support or 1 Edinburgh. Medical Journal, 1860. Vol. v. p. 400. [2 Ether is undoubtedly safer for this use.-H.] 3 The Obstacles to the Re-establishment of Natural Respiration after the Performance of Tracheotomy, by Thomas Smith, F.R.C.S. A paper read before the Medico-Chirurgical So- ciety, June 27th, 1865. 70 CROUP. stimulation from the first; no emetics more depressing than ipecacuanha wine are available for repetition ; this one an- swers very well when they are only re- quired to meet the nocturnal remissions, at other times this interferes too much with the desire for nourishment; small doses of sulphate of copper in solution, as proposed by Hoffman, act well as an emetic on repetition ; in some cases alum, as recommended by Dr. Meigs of Phila- delphia, teaspoonful doses of the powder being given in honey or syrup every ten or fifteen minutes; it is rarely necessary to give the second dose, and the emetic effect may be obtained several times a day without exhausting the patient. An occasional dose of calomel is of service; there is no necessity for the continuous use of mercury, and its full influence is prejudicial. Great benefit often results from the administration of full doses of perchloride of iron. Salines are only ad- missible when Croup complicates the early stage of measles; at other times and in the other exanthemata the mineral acids are better adjuncts. The air to be re- spired need not to be kept as warm and moist as in primary Croup, but there must be the same care as to its purity. Close attention is to be given to the state of the fauces ; local applications are of service here both as a stimulus to the mucous membrane near the entrance of the larynx, and for the removal of the mucosities which offer some impediment both to res- piration and deglutition. If nourishment and wine are not readily swallowed, nu- trition is to be supplemented by the injec- tion per rectum of small quantities of beef-tea, to which a little brandy must occasionally be added. Varieties.-There is great difficulty in defining the varieties of Croup that have been described : the greater number of them depend either on the inclusion of other diseases, or on a misapprehension of the nature of this; the terms spasmodic and nervous have been applied to the most acute inflammation of the trachea, as well as to spasm of the glottis; while pseudo-membranous, inflammatory, or as- thenic have probably included more cases of diphtheria than of Croup, Catarrhal Croup has been applied to all these varie- ties when they fortunately have had re- covery as their one common result. Croupal catarrh may exist independ- ently, the inflammation being superficial and, under favorable circumstances, rap- idly passing off: stridulous laryngitis, as used by M. Bretonneau, may be taken as its type; though not requiring the most energetic treatment, it must never be neg- lected. The temperature of the patient here affords the most valuable indication of the gravity of the disease. In merely spasmodic attacks there is little or no ele- vation of temperature. The stridulous laryngitis or false Croup of M. Guersant includes many of the slighter cases of Diphtheria as well as of Croup ; he has remarked1 the frequency with which it occurs among the upper classes of Paris rather than among the poor, and that it is sometimes observed in connection with exudation on the fauces,2 a complication which he justly considers as " fort embar- rassante pour le diagnosticthese cir- cumstances prevent the terms False Croup and Catarrhal Croup from being considered equivalent. Epidemic Croup is strictly diphtheria ; when that disease prevailed epidemically in England at the end of the last century, any fresh outbreak of it was so spoken of; an outbreak at Chesham, in Buckinghamshire, in 1793, carefully de- scribed by Mr. Rumsey, leaves no doubt on this point ; sometimes on its appear- ance in a fresh locality it was simply called Croup, and the word excited as much ter- ror then, as diphtheria has again given us reason to associate with the disease it now designates. [Allusion has been made above to the subdivision of croupal affections into three varieties, besides the laryngo-tracheal lesion of diphtheria. A sufficiently com- plete classification of the disorders in which laryngeal dyspnoea occurs as a lead- ing symptom, may be the following :- Laryngismus Stridulus ; Spasmodic Night Croup ; Croupal Catarrh; Pseudo-membranous Laryngitis ; Laryngeal Diphtheria.-H.] 1 Archives Generates de Medecine, tome xvii. Croup et Pseudo Croup. M. Blache, p. 493. 2 Ibid. p. 507. diseases of the respiratory system.- Continued. B- Diseases of the Thoracic Organs. 1. Emphysema. 2. Asthma. 3. Phthisis. 4. Cancer. 5. Acute Pneumonia. 6. Chronic Pneumonia. 7. Syphilitic Affec- tions of the Lung. 8. Brown Induration of the Lung. 9. Cirrhosis. 10. Apneumatosis. 11. Bronchitis. 12. Pleurodynia. 13. Pleurisy. 14. Hydrothorax. 15. Pneumothorax. EMPHYSEMA OF THE LUNGS. By Sik William Jenner, Bart., M.D. Lond., D.C.L. Oxon., F.R.S. Definition.-Relative excess of air in a part or the whole of the lungs. The relative excess of air may be the result of increase in the quantity of air in the vesicles, of diminution in the solid tissues of the lung, or of the presence of air in lung structures which in health do not contain air. Pulmonary Emphysema may be divided into- 1. Interlobular, extra-vesicular, or ex- tra-alveolar Emphysema. 2. Vesicular or alveolar Emphysema. This division, first made by Laennec, has been adopted by all subsequent writers on the subject. Interlobular, Extra-Vesicular, or Extra-Alveolar Emphysema. Definition. - Air in the connective tissue of the lung. The connective tissue of the lung is seated chiefly, at least, between the lobules and under the pleura. The air in extra- vesicular Emphysema occupies the meshes of this connective tissue. When air is present in the connective tissue between the lobules, it accumulates in small bubbles of tolerably equal size, separated from each other by bands of tissue, so that the surface of the lung looks as if streaked or crossed by rows of small beads. When air is m the sub- pleural tissue it forms air-blebs, sometimes of very large size. Air may be formed after death in the connective tissue of the lungs by decom- position ; it may be generated there during life by gangrene ; and it may be extrava- sated into the same tissue in consequence of rupture of the normally air-containing structures of the lung. When formed by decomposition after death, the gas is usually seated in the interlobular tissue ; when generated by gangrene, in the sub- pleural tissue; and when extravasated from the air-vesicles, it commonly occu- pies both situations. Air extravasated into the connective tissue of the lung occasionally finds its way into the posterior mediastinum, and thence into the subcutaneous tissue of the neck, face, trunk, &c. Rupture of the normal air-vesicles may be the result of injury inflicted from with- out, or of the pressure of the air on their inner surface during violent expiratory efforts made when the glottis is closed, e. g. during cough and parturient efforts. The distension of the air-vesicles by in- spiratory efforts is never great enough to cause their rupture. Interlobular Emphysema is a condition of little importance. When the air finds its way through the connective tissue of the posterior mediastinum into the subcu- 71 72 EMPHYSEMA OF THE LUNGS. taneous tissue, the air is quickly absorbed, and in a few days no trace of the Emphy- sema is to be detected. With the exception of the cases in which the air reaches the subcutaneous tissue, the diagnosis of pulmonary extra-vesicular Emphysema is impossible, and even in these cases there are no pulmonary signs or symptoms to indicate the existence of the local lesion. Should the existence of extra-vesicular Emphysema be ascertained, no treatment is needed. Pulmonary Vesicular Emphysema. Definition.-Increase in the capacity and size of the air-vesicles of the lungs. Pulmonary Vesicular Emphysema is a very common, and frequently a grave disease. Causes of increase in the capacity and size of the air-vesicles.-All forms and de- grees of Pulmonary Vesicular Emphy- sema have their origin either in destruction of the partitions between the air-vesicles, or in over-distension of individual air- vesicles. In the former case, two or more air-vesicles are, by the primary lesion, thrown into one; in the latter, each air- vesicle is, by an over-distending force, increased in capacity and size. It is improbable that nutritive changes in the tissue of the walls of any hollow viscus ever lead directly to expansion of its cavity. But changes in the walls of a hollow viscus may weaken their resisting power and so favor the expansion of its cavity ; and again, changes in the walls of a hollow viscus may cause a dilatation to be permanent, which otherwise would have been temporary. Changes in the walls of a hollow viscus, which strengthen their resisting power, may, at the same time, weaken their con- tractile power. Walls so changed may resist a dilating force longer than healthy walls, but should the dilating force be sufficient to stretch them, the dilatation of the cavity they inclose is permanent. The walls are indeed stronger, but then the cavity is more likely to suffer perma- nent dilatation. The causes of increase in the capacity and size of the air-vesicles of the lungs are then divisible into :- 1. The forces which determine their over-distension ; 2. The conditions which favor their over-distension; 3. The conditions which render their over-distension permanent; 4. The lesions of structure by which two or more vesicles are thrown into one. Although this division should always be kept in view when considering the causes of Pulmonary Vesicular Emphy- sema, it will be better, in an article such as this, to consider the causes included in the second and fourth divisions inci- dentally, as occasion arises, when treating of the causes included in the first and third divisions. Determining causes of over-distension of the air-vesicles.-Pressure of air on the in- side of the air-vesicles is the force which directly causes their normal expansion ; increase in that pressure is the immediate cause of their over-distension. Excess of pressure of air on the inside of the pulmonary air-vesicles (of the whole or of a part of the lung) may be brought to bear, (a) By excessive expansion of the chest- walls ; (6) By normal expansion of the chest- walls, when disseminated portions of the lung are shrunken, and no longer admit air; (c) By unequal compression of the lung at the moment when there is impediment to the free escape of air from its air-con- taining parts. (a) In health, inspiration is effected by muscular effort, ordinary expiration chiefly by the elasticity of the thoracic parietes and of the lung textures. The muscular effort of inspiration overcomes the resistance to the entrance of the air into the air-vesicles, offered by the elas- ticity of the lungs and of the walls of the thorax; the muscular effort ceasing, the elasticity of these parts is sufficient to ac- complish the ordinary expiratory act. The elasticity of the ribs and of their cartilages diminishes considerably as age advances, while in a large number of cases the muscles of inspiration continue as powerful as, and are sometimes more powerful than, in early life. The result of inspiratory expansion of the chest being constantly accomplished by the action of the muscles undiminished in power and activity, and of expiratory diminution of the chest being constantly performed incompletely and imperfectly by thoracic parietes, the elasticity of which is diminished, is gradual expan- sion of the chest-walls, increased capacity of the chest, and dilatation of the air- vesicles of the lungs. The capacity of the chest not being reduced to its normal size during expiration, the inspiratory effort is made on a chest retaining too much air in the lung-vesicles, and thus, especially if there be repeated and powerful calls on the inspiratory power, as from cough or great muscular effort, the result is con- siderable over-distension of the air-vesi- cles.1 In the same way lessened elasticity of 1 Dr. G. Budd, in a paper on Pulmonary- Vesicular Emphysema, published in the Med.- Chir. Soc. Trans, for 1840, clearly pointed out the part which loss of elasticity of the lung plays in the production of Emphysema. PULMONARY VESICULAR EMPHYSEMA. 73 the lungs from age-degeneration, or other cause, without loss of power in the mus- cles of respiration, leads to increase in the capacity of the thorax, and over-dis- tension of the air-vesicles. The excessive expansion of the thorax, and therefore the dilatation of the air-vesicles in this, as in the last case, is determined by ex- treme muscular inspiratory action-the necessary result of deficient ordinary ex- piratory power.1 Another cause of increased expansion of the thorax has been described by Freund. He says that persons of all ages, from twenty years upwards, the well-nourished as much as the withered and decrepit, are liable to a chronic dis- ease of the cartilages of the ribs, which results in their hypertrophy and increased firmness and rigidity, and in diminution of their elasticity. As this increase in the size of the cartilages takes place in all directions, the ribs and sternum are separated from each other more than they are in health: the ribs being forced out- wards and upwards, and the sternum for- wards and a little upwards. The capacity of the thorax is thus (Freund says) in- creased, and the lungs proportionately over-distended. It has been contended by later writers that Freund exaggerated the frequency at least of this affection ; that he supposed changes in the cartilages resulting from their stretching to be the primary affection-in fact, that he took the effects of the action of the determining cause for the determining cause itself. For the capacity of the thorax to be in- creased under the conditions named by Freund, the diaphragm must continue to be at the termination of ordinary expira- tion on as low a level as in health. Usu- ally, however-and perhaps always when the cartilages lengthen-they bend so as to form an angle, with its concavity up- wards, about their centre. (b) It is evident that if disseminated portions of lung are from any pathological condition diminished in size and no longer admit air, and that if, at the same time, the chest-walls expand during inspiration to the same amount as in health, the air- admitting vesicles must be over-distended in proportion to the number of cells into which no air enters, and the degree to which the airless vesicles are diminished in size. Thus, in certain cases of bron- chitis, disseminated lobular collapse is common. The collapsed lobules are smaller in bulk than are the air-contain- ing lobules-their vesicles admit no air during inspiration. The necessary result is, that if the chest-walls expand to the same degree as before the establishment of collapse, and so inspire an equal quan- tity of air, the capacity of all the air-ves- icles still pervious must be increased.1 (c) If a lung removed from the body be moderately inflated, and the bronchus leading to it be tied, and then the sub- stance of the organ be compressed at one part, over-distension of the air-vesicles of the uncompressed part is produced. Should the compressed part be large, and the compression considerable, even rup- ture of the air-vesicles of the uncom- pressed part may result. Under the con- ditions supposed, air is forced from the compressed parts of the lung into the air- admitting structures of the uncompressed parts of the lung.2 The conditions essential to the over- distension of the air-vesicles here present are :- (a) Inflation of the lung. (6) Closure of the natural passage for the escape of air from the lung. (c) Unequal pressure on the lung. (d) Unequal support of different parts of the lung. During violent cough and great muscu- lar effort, these essential conditions are fulfilled :- (a) Preparatory to cough and to great muscular effort, a deep inspiration is taken, i. e., the lungs are inflated. (6) Then the glottis is closed, i.e., the air is prevented escaping by the natural channel. (c) Then, by the action of the expira- tory muscles, the lungs are strongly com- pressed, and an examination of the struc- ture of the thoracic walls at once shows that the compression must be unequal. (d) Examination of the structure of the walls of the chest also shows that the sup- port offered to the lungs by those walls is very different in degree at different parts.3 Again, when blowing a wind instru- ment the chest is expanded to its utmost, and then the chest-walls compress the in- flated lungs-the air cannot escape as freely through the instrument as through the open glottis, and the mechanical effect is over-distension of the air-cells of the least compressed and least supported parts 1 This point has been excellently well brought out by Dr. W. Gairdner. 2 This expiratory theory was first advanced by Mendelssohn, in a very able paper, " Der Mechanismus der Respiration und Circula- tion," 1845. The writer of this article was unacquainted with Mendelssohn's paper when he advanced the same theory in 1857, and so far as he knows the existence of Mendels- sohn's paper was unknown in this country, and rarely, if ever, referred to abroad till Biemer's article appeared in 1867. 3 For details on this point see the author's paper on the Determining Causes of Pulmo- nary Vesicular Emphysema, in the Med.-Chir. Soc. Trans. 1857. 1 See p. 75. 74 EMPHYSEMA OF THE LUNGS. in proportion to the impediment to the escape of air and the force with which it is attempted to drive the air forward. The over-distension of the air-cells thus effected will be in proportion to the amount of inflation of the whole lung, to the firm- ness with which the glottis is closed, or the smallness of the aperture of the wind instrument, or other obstacle to the free escape of airto the extent, degree, and difference in the force of compression ex- ercised on the several parts of the lung at the same moment; and to the deficiency of support afforded to the less compressed parts by the thoracic parietes. The greater and the more extensive the com- pression of one part of the lung, and the less the compression of the other, the greater will be the distension of the air- cells in the less compressed part; and the less the imperfectly compressed parts are supported by the thoracic parietes, the greater will be the distension of their air- vesicles. It would at first sight appear that the over-distension of the vesicles should be in all cases limited to the less compressed and the less supported parts of the lungs, but on further examination it will be seen that this opinion is erroneous. Thus, if from some change in the walls of the chest or of the air-vesicles, the latter continue over-distended after the force which di- rectly determined their over-distension has ceased to act, or in other words, if there be permanent dilatation of the air- cells, then the size of the chest and of the lungs is permanently increased. The portions of lung corresponding to the intercostal spaces are less compressed and less supported just before violent ex- piration than are the parts immediately under the ribs themselves. Now with every increase in the size of the lungs, or thorax, or both, the relative positions of the lungs and ribs are changed. As the chest enlarges, the ribs assume a more horizontal position, the lower intercostal spaces become wider, and their support- ing power by so much diminished. By these changes in the lungs and in the chest-walls their relative positions are being constantly shifted, and fresh por- tions of the lungs are being constantly brought to correspond to the ribs and to the intercostal spaces, &c., and thus, ulti- mately, the air-vesicles of the whole lung may be over-distended. But when the air-vesicles of the whole lung are thus over-distended, the dilatation of the vesi- cles at the apex and margin of the lung is in excess of the dilatation of the vesicles of other parts. Strong expiratory effort, while there is impediment to the free es- cape of air from a part or whole of the lung, is now admitted to be the most com- mon efficient determining cause of over' distension of the air-vesicles. Pulmonary Vesicular Emphysema is very common in horses, and for this rea- son, viz., that they are constantly making powerful muscular efforts with closed glottis. No one who watches a horse draw a heavy load up a short steep incline on a damp cold day can doubt this. While making the effort, the horse holds its breath, having previously inflated its lungs-no sooner, however, does the ani- mal cease its eflbrt than the glottis is opened and the air suddenly expressed from the lungs. The degree to which the air was compressed during the powerful effort (and the consequent strain on the less compressed and less supported part of the lung) may be judged by the distance to which, and the sudden violence with which, the cloud of breath-vapors is seen to be driven forth. Permanence-securing causes, or the condi- tions which render over-distension, or in- crease in the capacity and size of the air- vesicles of the lungs permanent.-Whatever destroys the partitions between adjacent air-vesicles, and whatever permanently diminishes the ordinary or habitual respi- ratory power, must, to a like degree, be a permanence-securing cause of increase in the capacity and size of the air-vesicles. The permanence-securing causes, there- fore, are :- 1. Direct injury to the elasticity of the walls of the air-vesicles ; 2. Permanent diminution of the power of supporting or compressing the lung, at any one part, during violent expiratory efforts; 3. Changes in the structure of the pa- rietes of the thorax, which permanently diminish their elasticity, and therefore their ordinary or habitual expiratory power; 4. Chronic changes in the structure of the lungs, which permanently diminish their elasticity, and therefore their ex- piratory power; 5. Atrophy of the septa between the air-vesicles of the lungs, by which two or more vesicles are thrown into one. 1. If the forces which expel the air from the air-vesicles, viz., the elasticity of the thoracic parietes, and the elasticity of the walls of the air-vesicles, are at the termination of over-distension of the vesi- cles in a state of health, then the force determining their over-distension ceasing to act, the air-vesicles return to their natural size; but if, as very rarely hap- pens, the air-vesicles have been very greatly over-distended, or kept for a very long time over-distended, or have been very repeatedly over-distended, then the elasticity of the walls of the air-vesicles may be permanently injured, and the over-distending force ceasing to act, they 1 Dr. Budd's case. PULMONARY VESICULAR EMPHYSEMA. 75 do not recover their normal dimensions. They are under the circumstances sup- posed permanently over-distended. The elastic structures of their walls have been directly injured by the over-distending force. So great even may be the force by which their over-distension has been ef- fected, that the partitions between adja- cent vesicles may be destroyed, and two or more vesicles thrown into one; or even, as has been previously mentioned, the destruction may have reached further, and air have been extravasated into the interlobular tissue. 2. The observations of Ziemssen on a case in which there was loss of muscular power in the four upper intercostal spaces, proves that this loss may be a cause of Vesicular Emphysema. In Ziemssen's case, during violent expiratory effort, these intercostal spaces no longer affording their normal support to the lung were forced outward so much as to stand above the level of the ribs. When the muscles of either intercostal spaces were stimu- lated to contract by faradization, then the bulging during expiratory efforts of that intercostal space ceased, thus proving that want of muscular contraction at any part during expiratory effort is a cause of over-distension of the air-vesicles of the lung at that point; and if the want of support be permanent, then certainly the over-distension will be permanent. 3. The degenerations of the ribs and cartilages incident to age diminish their elasticity, and consequently diminish the expiratory power of the chest-walls. If, as was previously pointed out, the inspira- tory muscles act perfectly when the ex- piratory force resulting from the resilience of the ribs and cartilages is diminished, dilatation of the thorax, over-distension of the air-vesicles, and enlargement of the lungs are determined. As age-degeneration is a permanent lesion, the loss of elasticity resulting from it is permanent; the dilatation of the thorax, over-distension of the ait-vesicles, and the enlargement of the lungs, is per- manent. Age-degeneration of the ribs and their cartilages is, with perfectly act- ing inspiratory muscles, therefore a per- manence-securing cause of Large-lunged Vesicular Emphysema. The disease of the cartilages of the ribs described by Freund, once established, is permanent, and therefore, the over-dis- tension of the air-vesicles due to the ex- pansion of the chest resulting from it, is also permanent. 4, 5. Whatever changes in the lungs diminish their elasticity, to the same de- gree render permanent the over-distension of the air-vesicles determined by any of the forces previously enumerated. Diminished elasticity of the lung may be the consequence of those changes in texture which result from repeated or long-continued congestion. After a part has been the seat of long-continued or of repeated congestion, it is, if an organ, in- durated and toughened ; if a tissue, tough- ened and thickened. If death occur long after the outset of the congestion, then a certain amount of wasting of the original structures is found to have taken place. In some cases, certainly, these changes are due to the formation among the nor- mal anatomical elements of the part, of imperfectly developed connective, fibrous, or fibro-cellular tissue. All degenerations of texture incident to age are attended by more or less loss of elasticity.1 The degenerations incident to age,2 as they affect the lung, may be divided thus:- («) Atrophy, or waste of all the anatom- ical constituents of the lung, with general diminution in its size. As the partitions between the air-vesicles atrophy, two or more vessels are thrown into one. This form of atrophy has been supposed to be preceded by fatty degeneration. (5) Thickening of the fibrous element of the lung, with more or less waste of some of its anatomical constituents. When the subject of this form of degeneration the size of the lung is often increased, and it may be considerably so. In this latter form of age-degeneration there is, at the outset at least, no atrophy of the inspiratory muscles; while in the former, the muscles on the outside of the chest are wasted and pale, and the dia- phragm is thin, lax, and in folds. In both, the ribs and cartilages are the seat of degenerative changes attended by loss of elasticity. So, also, when the ribs and cartilages lose elasticity from age-degeneration, the lungs rarely preserve their normal elasti- city ; they too, commonly, like the ribs and cartilages, are suffering from age- degeneration. The conjunction of diminished elasticity of the lungs and of the parietes reduces the ordinary or habitually employed expi- ratory force to a minimum. Now, this 1 Diminution of elasticity is one of the most marked effects of the changes in nutrition in- cident to advancing age, e. g., of the skin, giving the aged look ; of the arteries, causing them to become tortuous or S shaped, at first when the part in which they are placed is shortened, as in flexion of the limbs, and then permanently ; of the intervertebral car- tilages, of the elastic structures in the sole of the foot, the joints, the bones, &c. 2 Those changes of nutrition which are the characteristics of age, and in fact constitute old age, may occur, generally or locally, at an unusually early age. Thus, one man grows prematurely old as regards his jaws, another as regards his hair, another as re- gards the heart, &c. 76 EMPHYSEMA OF THE LUNGS. being the case, if the muscles of inspira- tion and of expiration retain their nor- mal power, then frequent cough, habitual straining at stool, moving heavy weights, climbing hills, blowing wind instruments, or other causes of repeated and powerful inspiratory efforts, followed by violent ex- piratory compression of the inflated lungs, with impediment to the escape of air, will be followed by great and permanent in- crease in the size of the thorax, and cor- responding over-distension of the air-vesi- cles. Changes in the lung, attended by loss of elasticity, said to be independent of age and of congestion, have been described by various authors. M. Villemin thinks that the true ana- tomical structure of the walls of the air- vesicles is a network of capillary vessels, with a nucleus filling each intercapillary mesh, and elastic fibres on the inside of the vesicles crossing over the capillaries and intercapillary nuclei. "In Pulmo- nary Vesicular Emphysema," M. Ville- min says, "the nuclei in the meshes of the capillary network hypertrophy, com- pression and atrophy of the capillaries fol- low ; then the enlarged nuclei undergo fatty degeneration; they fall from their places in the walls of the air-vesicles, de- struction of the elastic tissue and of more capillaries occurs; apertures are formed between adjacent vesicles, and finally, two or more vesicles are thrown into one." "There is then," M. Villemin says, "a first stage of Emphysema, a true hy- pertrophy of the elements of the vesicular membrane ; from this there naturally re- sults an extension of that membrane, and an increase in the capacity of the vesi- cles." It does not, however, necessarily fol- low, even though M. Villemin's anatomi- cal observations be correct, that there is an increase in the size of the lung, as he supposes, because the wralls of the air- vesicles are lengthened; for they might, under such circumstances, be folded on themselves. Moreover, the accuracy of these observations has been doubted. The so-called intercapillary nuclei are said by some observers to be epithelium on the inside of the air-vesicles. "Changes in the nutrition of the lung," Freund says, "necessarily follow on the changed conditions of the respiratory movements due to the lengthening of the rib-cartilages, and these changes are at- tended by loss of elasticity, and the other changes in the walls of the air-vesicles which follow on their continued over-dis- tension." Dr. Waters while admitting that his in- vestigations do not enable him to say what is the nature of the degeneration which leads to Emphysema, and that his microscopical researches on this point have yielded no results, adds, " I do not entertain the slightest doubt that the dis- ease in its severer' forms is of a constitu- tional nature." Varieties of Pulmonary Vesicular Em- physema.-As over-distension of the air- vesicles may occur in perfectly healthy lungs, and in lungs the seat of any of those pathological changes which impair their elasticity, and as, moreover, the dila- tation may affect the air-vesicles of the whole, or of a great part of the lung, or may be limited to the air-cells of a small part of the lung, Pulmonary Vesicular Emphysema has been divided into varie- ties. The various forms of Pulmonary Vesic- ular Emphysema may be described under the four following heads :- Acute Vesicular Emphysema. Chronic Local Emphysema. Large-lunged (or Ilypertrophous) Em- physema. Small lunged (or Atrophous) Emphy- sema. Although perfect and uncomplicated specimens of each variety are common, cases of Pulmonary Vesicular Emphysema are frequently seen in practice and in the dead-house, in which these several varie- ties are conjoined in the same lung, and, again, cases which cannot at the time when they come under observation be re- ferred absolutely to the one or the other group. The reasons for this are manifest when the etiology and the pathology of the affection are considered. Acute Vesicular Emphysema.-By Acute Pulmonary Vesicular Emphysema is signified acute over-distension of pre- viously healthy air-vesicles. The part of the lung, the air-vesicle of which are over-distended, is puffed up, is paler than it should be; the vesicles them- selves, seen through the pleura, are mani- festly larger than natural. The pallor is due solely to the excess of air in the vesi- cles stretching their walls, and so sepa- rating the capillaries further than should be from each other. The meshes of the capillary network on the walls of the air- vesicles are widened. Acute Vesicular Emphysema may be produced by too much air being drawn into the over-dis- tended air-vesicles by inspiratory effort; or by too much air being driven into the air-cells of parts of the lungs by extreme compression of other parts by expiratory efforts, while the escape of the air by the natural outlet is prevented or retarded, e. g., by closed glottis, narrowing of the trachea or bronchi. Both these forces conspire to determine the occurrence of acute over-distension of the air-vesicles in acute bronchitis. In that disease disseminated collapse, and the consequent diminished bulk of lung CHRONIC LOCAL EMPHYSEMA. 77 and increased desire for breath, lead to violent inspiratory efforts and over-dis- tension of the pervious air-vesicles ; while the frequent and violent expiratory efforts with closed glottis (preparatory to cough), determine over-distension of the air-vesi- cles of the less compressed and less sup- ported parts of the lung. When the ribs are greatly softened, as in some cases of rickets, the anterior mar- gin of the lungs is the seat of Acute Vesic- ular Emphysema. The over-distension of the air-vesicles is produced partly by the compression of the lung at a little dis- tance from its margin by the recession during inspiration of the ribs at their junction with their cartilages, but chiefly by the great advance of the sternum and rib-cartilages during inspiration, these parts being thrust forward by the impress- ing ribs. In Acute Pulmonary Vesicular Emphy- sema, the rule is that the air-vesicles re- sume their normal size as soon as, or very soon after, the over-distending force ceases to act. The walls of the air-vesicles and the adjacent tissues being healthy, they contract to their normal dimensions. In comparatively rare cases, the over- distension is so great, so long-continued, or so frequently repeated, that the over- stretched walls of air-vesicles are injured, their elasticity is impaired, and the air- vesicles continue permanently larger than they should be. It is in this way that severe and pro- longed hooping-cough in children appears to produce Chronic Pulmonary Vesicular Emphysema. The over-distension espe- cially affects the air-vesicles of the apex and anterior margin of the lungs, the air being forced into those parts during the violent expiratory efforts which precede the cough. Symptoms.-If widely spread, and ex- treme, Acute Pulmonary Vesicular Em- physema causes increased resonance of the chest; the symptoms due to the lesion are masked and altogether lost in those proper to the disease to which it is secondary. It requires no special treatment. Chronic Local Emphysema is char- acterized by extreme permanent over-dis- tension of a few vesicles. The large vesi- cles are formed by the coalescence of sev- eral smaller. The largest may be as large as a poulet's egg, are not unfrequently the size of hazel-nuts, though more commonly not larger than peas. In the same group, vesicles are often found varying in size from a pin's head to a hazel-nut. The walls of these large vesicles are never healthy; they are thick, opaque, wanting in elasticity, and vessels of some size frequently ramify on the larger. Threads composed of obliterated bronchi, the remains of vessels or of lung tissue,, cross the cavity of the larger vesicles. Sometimes these vesicles communicate with a small bronchus ; at others the bronchus leading to them is occluded. The most common seat of Chronic Local Emphysema is the apex of the lung, then the anterior margin, and the margin of the base of the lung. At the apex, the Emphysema is often conjoined with the remains of old tubercle. The pathology and mechanism of the production of Chronic Local Emphysema is best studied as it occurs at the apex of the lung, when that part is the seat of obsolescent or of calcified tubercle. When tubercles obsolesce or calcify at the apex of the lung, a considerable por- tion of lung-tissue in their vicinity is usu- ally the seat of chronic congestion and exudation of lymph. This portion of lung loses its porosity, becomes tough, in- elastic, and puckered, i. e., irregularly con- tracted. Here and there, however, por- tions of the lung-textures are damaged, not destroyed, so that some air-vesicles still admit air. In health the inspiratory and expira- tory force are at a minimum at the apex. But during expiratory efforts with closed glottis, as in severe cough, the air is driven from the more compressed parts into the little compressed apex, and thus the vesi- cles still pervious to air are over-distend- ed ; and, as their walls have, from the previous changes in the tissues of the apex of the lung, lost much of their elas- ticity, the over-distension is permanent. Every paroxysm of cough must add to their dilatation. The diminution in size of the apex assists, as a permissive cause, in the production of extreme Chronic Local Emphysema at the apex. Thus in proportion to the loss in the elasticity of the air-admitting textures, to the frequency and the violence of the ex- piratory efforts with closed glottis, and to the permanent diminution in the size of the apex, will be the degree and the rapid- ity with which Local Emphysema at that part will be established. The anterior margin of the lung, the margin of the base, the anterior inferior angle of the superior lobe of the left lung, are, like the apex, very imperfectly com- pressed and supported during expiratory efforts, and so air is forced powerfully into the vesicles of those parts; and should the texture there be damaged at any time so as to diminish its elasticity, the result will be great dilatation of a few vesicles. The margins of the lungs are thus some- times fringed with large vesicles. Chronic Local Emphysema is always a secondary lesion. Its formation at the apex is the consequence, not the cause (as some have fancied) of the obsolescence of tubercles. Coincident with the obsoles- 78 EMPHYSEMA OF THE LUNGS. cence is damage to the air-admitting tex- tures of the lung, and it is that damage which renders the Chronic Local Emphy- sema with large vesicles possible. Symptoms.-The development of Em- physema at the apex of the lung, when that part is the seat of chronic consolida- tion with contraction, diminishes the de- pression of the shoulder, and of supra- and infra - clavicular regions, and increases the resonance of the same parts; the di- lated vesicles often projecting above and surrounding the solid textures. The di- latation of the vesicles may be so exten- sive and considerable as to cause supra- clavicular bulging either permanently or during cough.* It is unattended by other symptoms. Treatment.-From the nature of the lesion, it will be understood that no treat- ment is required. Large-lunged Vesicular Emphy- sema.-By this name it is proposed to designate those cases in which there is over-distension of the air-vesicles of the whole, or of a large section of one or of both lungs, great increase in bulk of the lungs, or of the affected part of the lungs, and corresponding increase, local or gen- eral, in the capacity of the thorax. The term Hypertrophous Pulmonary Vesicu- lar Emphysema has been used to describe the same set of cases.2 General Large-lunged Vesicular Em- physema is a very serious disease. The symptoms directly due to it are grave; the diseased conditions dependent on it for their origin are very frequently fatal. Thus a large proportion of cases of heart disease have their starting-point in Large- lunged Vesicular Emphysema. It rarely occurs in a marked form be- fore the middle of life, and it more com- monly affects those disposed to accumula- tion of fat in the subcutaneous tissue and internal parts. Lungs, the subject of this form of Vesicular Emphysema, are larger and drier than healthy lungs.1 The parts uncolored by pigment are paler than healthy lung. The lungs overlap the pericardium to a considerable extent, and meet above it even to near the top of the sternum; they have a down-cushion-like feel, and retain the impression of the fingers. When the thorax is opened they contract less than healthy lungs do under like circumstances. Large-lunged Vesicular Emphysema is, in the great majority of cases, "preceded by attacks of bronchitis, by congestion of the lungs, by dry winter cough, or by chronic bronchitis ; that is to say, by dis- eases having as immediate consequences toughening and thickening of the tissues of the lung,2 and severe cough ; in other words, diminished elasticity of the lungs, and powerful expiratory efforts with closed glottis. By far the most common determining cause then of the over-distension of the air-vesicles in Large-lunged Vesicular Emphysema is powerful expiratory effort with closed glottis; and the most common permanence-securing cause is the changes in the texture of the walls of the air-vesi- cles resulting from excess of blood in their capillaries. The next most frequent determining and permanence-securing causes of Large- lunged Vesicular Emphysema are dimin- ished ordinary or habitual expiratory force, dependent on age-degeneration of the bones and cartilages in the thoracic parietes, without loss of full muscular in- spiratory power, occurring alone, or more commonly conjoined with thickening of 1 The bulging part is resonant and cannot, therefore, be confounded by a tolerably care- ful observer with the prominence of the same part due to distension of the veins during severe cough. 2 Large-lunged is by far the better of the two names, because it involves the expression of no opinion in regard of disputed facts. Many observers regard Pulmonary Vesicular Emphysema as atrophic from its outset-no matter how it originates. And it must be admitted that even when the disease has been hypertrophic when first established, the lungs may be greatly wasted in regard of their essential anatomical constituents before death. And again, in some cases of Large- lunged Vesicular Emphysema, as in those in which the occurrence of the disease is deter- mined, and its continuance secured, by in- crease in the capacity of the chest from age- degeneration of the ribs and cartilages with- out diminution in the power of the respira- tory muscles, the wasting and rarefaction may not be preceded by hypertrophy of any anatomical constituent of the lung. 1 When Vesicular Emphysema follows on bronchitis, congestion of the lungs, and simi- lar pathological conditions, the lungs, at the very outset of the disease, weigh more than in health, and would continue to do so were it not for the waste of the normal anatomical constituents of the lung-blood, bloodvessels -epithelium, or intercapillary nuclei-which follows on over-distension of the air-vesicles, and on the lesions which secure the perma- nence of their over-distension. 2 To comprehend the relation between bron- chitis, the changes following it in the walls of the air-vesicles, and the frequency with which bronchitis supervenes on Pulmonary Vesicular Emphysema, it must be remem- bered that the blood of the bronchial arteries is returned to the heart chiefly through the pulmonary veins, and that many good ob- servers affirm that the bronchial mucous membrane is in great measure nourished by the blood of the pulmonary artery, and that anastomoses exist between the finest divisions of the bronchial and pulmonary arteries. LARGE-LUNGED VESICULAR EMPHYSEMA. 79 the tissues and diminished elasticity of the lungs-changes also due to age-degen- eration. As bronchitis, winter cough, and con- gestion of the lungs are common at ad- vanced periods of life, i. e., at the period of life when, without loss of muscular in- spiratory power, age-degeneration of the bones and cartilages of the thorax and of the lungs is common, it is manifest that violent expiratory efforts with closed glottis, habitually defective expiration, and therefore excessive inspiratory dila- tation, changes in the lung due to conges- tion, and changes in the lung-tissue due to age-degeneration, must in a very large number of cases conspire to produce Large- lunged Vesicular Emphysema. Fig. 13. Fig. 12. Fig. 12 shows increase in the thickness of the wails of the air-cells. Magnified two dia- meters. A portion of the above magnified 400 diameters. The changes which occur in the texture of the lung, in consequence of continued congestion, have been admirably described and figured by Rokitansky. When the lung is congested, as from disease of the left side of the heart, an in- crease in the quantity of the connective tissue occurs, the walls of the air-vesicles are thickened, the parenchyma appears thicker and swollen and unusually re- sistant. On section of the lung, the margins of the lung-vesicles are thicker than in health, and the cavity of each vesicle more visible than it should be, because its thickened walls prevent collapse. Some- times the cavity of each vesicle is in- creased, and the lungs are larger than they should be; in other words, the sub- stance of the lung is toughened and thick- ened from the formation of tissue, and enlargement of the lung, with dilatation of the vesicles, follows when any of the determining causes of over-distension of the air-vesicles come into action. But, however produced, permanent over-distension of the air-vesicles is fol- lowed by various pathological changes in their walls. Some of these changes are the direct mechanical result of their over- distension ; some are the result of degen- erative changes in the structures thus mechanically injured ; some of defective nutrition consequent on the injury in- flicted on the capillaries of the walls by their stretching; some of altered nutrition due to the alterations in structure ; some are due to the pathological states to which the permanence of the over-distension is owing. So that when the disease is far advanced, and has existed for some time, not only are individual air-cells enlarged, but the partitions between many are per- forated ; between others they are reduced to mere ridges; at places they have alto- gether disappeared; and at places they are greatly, though it may be irregularly, thickened by imperfectly constituted fi- brous tissue formed in and about the nor- mal structures. And so, ultimately, atro- phy of some structures is conjoined with increase in size and thickness of others; and rarefaction and condensation may affect adjacent parts of the same lung. If a portion of lung in an advanced stage of Vesicular Emphysema be in- 80 EMPHYSEMA OF THE LUNGS. flated, dried, and then cut across, the cut surface appears to be made up of spaces varying in size from a millet-seed to a hemp-seed, while near to the apex and margin of the lungs may be a few much larger spaces. These spaces or small cav- ities are separated and intersected by septa and by threads of very variable de- grees of thickness. pulmonary artery distributed on the walls of the air-vesicles are first stretched in proportion to the over-distension of the vesicles, and then, the over-distension continuing, some of the stretched vessels give way and are obliterated. The passage of blood through the capil- laries lengthened by stretching must be attended by increased friction, in propor- tion to the lengthening and narrowing of the vessels. Destruction of the capillaries diminishes the number of channels through which the blood can pass, and so impedes, in propor- tion to the number of capillaries torn, the passage of the blood from the right to the left side of the heart. Impediment to the flow of blood through the lungs is the cause of the greater number of the primary and sec- ondary symptoms of Large-lunged Vesic- ular Emphysema. The several causes of impediment to the flow of blood through the lung and their modes of action are- 1. Deficient extent of chest-movement in ordinary respiration ; especially defi- cient ordinary or habitual expiratory movement: 2. Violent expiratory efforts with closed glottis; by the pressure brought to bear on the heart and great vessels, as well as on the air in the anterior of the air-ves- icles, and so on the capillaries in their walls: 3. Diminished resistance from loss of elasticity of the lung; by disturbing the normal proportion borne by the pressure of the air on the inner to that on the outer chest-walls : 4. Lengthening of the pulmonary capil- laries ; by increasing the friction : 5. Destruction of pulmonary capillaries', by diminishing the channels for the pas- sage of the blood from the pulmonary ar- tery to the pulmonary vein. As the establishment of an efficient col- lateral pulmonary circulation is anatom- ically impossible, any impediment to the flow of blood through all, or nearly all, the pulmonary capillaries, must have as direct result impediment to the escape of blood from the right ventricle. The first effect of difficulty to the pas- sage of blood through the pulmonary capillaries must be, in accordance with general laws, increased efforts, and so hypertrophy of the walls of the right ven- tricle ; increased pressure on the inside of the right ventricle, and so dilatation of its cavity. At the outset, the impediment to the onward passage of the blood may at parts of the lung be trifling, compared with the impediment at other parts; in such case these parts suffer from the increased blood- pressure, become hypersemic, and, it may be, oedematous. Fig. 14. Section of lung in an advanced state of Chronic Ve- sicular Emphysema. (From Rokitansky, Lehrbuch der Pathol. Anatomie. B. iii. 1861.) Black pigment accumulates in consid- erable quantity on the inner surface of the dilated vesicles, and amid the fibrous and other solids. This black pigment owes its origin in part to the conversion of the luematin in the partially destroyed capillaries into melanin. When the whole of both lungs are em- physematous, the changes just described are much more advanced at the margins and apices than they are elsewhere; and, as a rule, they are more advanced at the base of the left than they are at the base of the right lung; these being, in the great majority of cases, the parts first to suffer in Large-hinged Vesicular Emphy- sema, because they are the parts least compressed and least supported during expiratory efforts with closed glottis. Effect of over-distension of the air-vesicles on the circulation.-The capillaries of the LARGE-LUNGED VESICULAR EMPHYSEMA. 81 The impediment to its onward passage is soon felt by the blood in the right auri- cle, and in the whole systemic venous sys- tem, of which the right heart is merely the terminus. When the auricle and ven- tricle are dilated, the right auriculo-ven- tricular orifice is dilated, and the result of increase in its circumference, without corresponding increase in the size of the tricuspid valve, is incompetence of the valve to close the dilated opening, and regurgitation of blood during the ven- tricular systole, from the right ventricle to the right auricle, and veins opening into it. But the impediment to the flow of blood through the pulmonary capillaries is not only followed by over-distension of the venous system, but ultimately the blood passes from the systemic capillaries into the veins with difficulty, and so an impedi- ment arises to the escape of blood from the arteries, and from the left side of the heart, which is merely the head of the general arterial system. That such impediment to the escape of blood from the arteries does exist when there is strong impediment to the flow of blood through the lungs, is manifested by placing the finger on an artery when a patient suffering from General Pulmonary Vesicular Emphysema coughs violently ; the artery instantly becomes full and tense, and, for the second of violent expiratory effort, ceases to pulsate. Over-filling of the capillaries of an organ or tissue with retardation of the flow of blood through them never continues for any length of time, and is never repeated frequently without inducing changes in the structure of that congested organ or tissue. The changes of the several organs, re- sulting from mechanically-induced conges- tion, are considered at length in the arti- cles on diseases of special organs. Only such changes of special organs as give rise to the more important symptoms in bad cases of Large-lunged Pulmonary Vesicu- lar Emphysema will be here considered. Speaking generally, if an organ be the seat of mechanically-induced intermitting congestion, the earliest result is increased nutrition and enlargement of the organ. When the dilatation of the capillaries has reached a certain degree and becomes permanent, then wasting of the structures of the part with increase in connective tis- sue, especially of imperfectly formed con- nective tissue, may result. The formation of the latter may precede, and greatly preponderate over the wasting of the natural structures of the part. A large number of free granules, of olein and protein, are found among the proper anatomical elements of the part almost from the very commencement of the con- gestion ; and fatty degeneration of the normal structures frequently precedes their disappearance. The parts that especially suffer in Large- lunged Vesicular Emphysema are- The Heart.-First and most certainly, the heart. The first effect of the impediment to the passage of the blood through the lungs is increase in the muscular tissue of the right side of the heart; then follow accu- mulation of blood in the ventricle, and some dilatation of its cavity. The right auricle next suffers in the same way, and soon the whole venous system : the veins of the heart suffering over-distension in common with the other veins. Mechanically-induced congestion of the walls of the heart, with increased action of the organ, leads not only to hypertro- phy, but ultimately to induration and toughening of the walls. When these changes have occurred in its muscular tissue, the heart loses its power of close contraction, and permanence of the dila- tation produced by the pressure of the blood on its inner surface is the result. Free granules of olein and protein are found between the muscular fibres ; and, after a longer or shorter time, fatty de- generation of the damaged muscular tissue follows. When distension of the veins has reached a certain point, the blood escapes from the systemic capillaries with difficulty, and increased action of the left ventricle follows. As the walls of the left side of the heart suffer from the same mechani- cally induced congestion as the walls of the right side, when impediment to the escape of blood from the left ventricle is established, its walls and cavity experi- ence, though in a less degree, the same changes in texture, &c., as the right side of the organ, viz., hypertrophy, indura- tion, toughening, and permanent dilata- tion. The Liver.-1The radicles of the hepatic vein, then the terminal twigs of the portal vein and finally its radicles, suffer conges- tion from the same cause as the systemic capillaries, i. e., from the impediment to the escape of blood from the inferior vena cava. In consequence of the impediment to the circulation, the liver is first enlarged from mere congestion, and in this stage a variety of "nutmeg liver" is found after death. When the congestion has continued for some time, the organ is more or less en- larged, indurated, and toughened, and free granules of olein and protein infiltrate all its tissues ; then its natural structures waste, especially, it is said, the cell ele- ment, and a certain amount of granular atrophy is the final result. Ascites very rarely occurs before the hepatic structure is organically injured, VOL. IL-6 82 EMPHYSEMA OF THE LUNGS. and rarely to any great amount from those changes only which follow directly from the impediment to the circulation here considered. The Kidneys, in common with other organs, suffer congestion in cases of ex- treme Large-lunged Vesicular Emphy- sema. This extreme congestion is evidenced during life by the presence of albumen, and sometimes of blood, in the urine. The kidney suffering from mechanically- induced congestion is at first larger, dark- er, and moister than in health. Granules of olein and protein are scattered through all its structures. After a time, indura- tion and toughening of the organ follow. A slight amount of granular atrophy of the previously enlarged kidney is the ulti- mate result. The Connective or Cellular Tissue through- out the body suffers from its mechanically- induced congestion. Its texture is tough- ened and thickened, and serosity is effused into its meshes. Anasarca is one of the earliest conse- quences of over-filling of the venous sys- tem from impediment to the flow of blood through the lungs. The anasarca is fre- quently attributed to the regurgitation of blood through the right auriculo-ventricu- lar orifice ; but both the regurgitation and the anasarca are really due to a common cause, i. e., to the state of the pulmonary capillaries. As a rule, however, before over-distension of the veins is so great as to relieve itself by letting out serosity into the cellular tissue, the pressure on the in- side of the right ventricle and auricle is sufficient to dilate the auriculo-ventricu- lar orifice to such an extent that the tri- cuspid valve is incompetent to its closure, pulsation in the jugulars is perceptible, and the anasarca is then erroneously at- tributed to a tricuspid regurgitation, as it is often called. Blood and General Nutrition. - Nie- meyer has pointed out that congestion of the venous system from mechanical im- pediment to the onward flow of blood through the lungs, or right heart, cannot exist without causing impediment to the escape of its contents from the thoracic duct. To this Niemeyer attributes the deficiency of fibrine and of albumen in the blood in cyanosis dependent on mechani- cally-induced over-filling of the venous system, and to it he also attributes the general emaciation which occurs in ad- vanced cases of Pulmonary Vesicular Emphysema. The Vessels of the Lungs.-In the last stages of the disease, after the left ventri- cle has suffered hypertrophy and dilata- tion, secondary lesions of the lung not unfrequently occur-thus the lungs may become greatly congested, and oedema of the lungs or congestive pneumonia follow. The mechanical impediment to the flow of blood through the pulmonary capillaries has told back through the systemic capil- laries on the left side of the heart, and so on the radicles of the pulmonary veins. Sy mptoms of Large-lunged Vesicular Em- physema. - The chief direct symptoms of Large-lunged Vesicular Emphysema are :- (a) Increase in the size of the thorax; (b) Increase in the resonance of the thorax, and prolonged expiration ; (c) Shortness of breath. (a) The lungs are larger than in health, and the capacity of the thorax is in pro- portion to the size of the lungs. The increase in the circumference of the thorax is effected chiefly by diminution in the natural obliquity of the ribs. By this alteration in the direction of the ribs, the lower intercostal spaces are very considerably widened. The sternum is carried forward. The lower latero-dorsal bulging of the thorax is increased. The enlargement of the circumference of the chest thus gained is made still greater by posterior curvature of the low- est cervical, the dorsal, and upper lumbar part of the spinal column. The patient stoops, he grows round-shouldered and round-backed.1 Increase in the capacity of the thorax from above downward is produced by lowering of the diaphragm. At the ter- mination of expiration in extreme cases of Large-lunged Vesicular Emphysema the diaphragm lies very low, so that it is not in contact with the inner surface of even the lowest rib. When the air-vesicles of the upper half of the lungs are the first to suffer over- distension, or are much more affected than are the air-vesicles of the lower part of the lung, the upper part of the thorax is dis- proportionately larger. When the deter- mining cause of the over-distension has been violent cough from bronchitis, then the disproportion in size between the upper and lower part of the thorax is sometimes increased by imperfect expan- sion of the lower part of the lungs; the condition of the bronchial mucous mem- brane and the contents of the bronchial tubes preventing the free and ready en- trance of the air into the air-cells of these parts of the lung. The increase in the capacity of the tho- rax is determined by the forces which determine the over-distension of the air- vesicles, viz., by repetition of full inspira- tory efforts, expiratory efforts with closed 1 Whenever the depth of the chest, from before backwards, requires to be increased, e. g., in dilatation of the heart-effusion into the pericardium-the patient instinctively rounds his back and elevates his shoulders. LARGE-LUNGED VESICULAR EMPHYSEMA. 83 glottis, and diminished elasticity of the thoracic parietes, or of the lungs, or more commonly of the two conjoined. (6) Of the physical signs, after those furnished by inspection of the thorax, by far the most constant and important in regard of diagnosis is increased resonance on percussion - clear full sound. The abnormal clearness on percussion is due to the relative increase in the quantity of air in the chest, and to the tension of the chest-walls. As the large lungs overlap the heart, the region of precordial dulness is dimin- ished, and, as the diaphragm is flattened, the hyper-resonance extends posteriorly even to the twelfth rib, and in front often as low as the margin of the thorax, even on the right side, the liver lying alto- gether under the abdominal parietes. Expiration is, in extreme cases, consid- erably prolonged in consequence of the diminution in the resilience of the chest- walls and lungs, and of the large size of the latter. At the same time, the inspi- ratory murmur is short and feeble. But when this form of Pulmonary Vesicular Emphysema is limited to a part of the lung, the only physical signs are local bulging and hyper-resonance. (c) Shortness of breath is always present in Large-lunged Vesicular Emphysema. At first, the shortness of breath is only felt on exertion; the patient cannot mount a hill as he did. Then, when walking on level ground, he requires to stop, from time to time, to take in breath - he breathes too frequently, and pants a little; or it may be that he " suffers with his breath" after a full or an indigestible meal, when the descent of the diaphragm is impeded by a distended stomach. However the shortness of breath is in- duced, the subject of Large-lunged Vesic- ular Emphysema is, from a very early period, conscious that his " wind" is no longer what it was. As the disease advances, the shortness of breath is experienced on the least ex- ertion, e. g., ascending a few steps, or a gentle slope ; and finally, even when sit- ting on a chair. The patient is always panting. By the altered position of the ribs and the diaphragm, a considerable increase in the capacity of the thorax is, as has been shown, obtained; but it is obtained at the expense of the inspiratory capability. The chest-walls are constantly expanded, and when the disease is far advanced, the capacity of the chest may be greater at the termination of expiration, than, in the normal condition of the lungs and chest-walls, it should be at the termina- tion of inspiration. As Dr. C. J. B. Wil- liams has tersely expressed it, "Breath is taken as it were on the top of breath." The lowering of the diaphragm may be so considerable, it is said, as to cause its physiological action to be reversed. In place of increasing the capacity of the thorax by its contraction, the diaphragm may draw, it has been said, the lower ribs inwards, and so diminish to a slight extent the capacity of the lower part of the chest at the end of inspiration. The diaphragm may be forced down- wards by the expiratory efforts, which determine over-distension of the air-cells, but it probably never lies very low till the elasticity of the lungs is considerably im- paired. The great natural agent in effecting the ascent of the diaphragm, after it has been lowered by its own contraction, is the elasticity of the lungs. The muscles re- lax at the termination of inspiration, and the diminution in the size of the lungs re- sulting from their resilience greatly aids in determining the passive ascent of the diaphragm. When the lungs, from loss of elasticity, no longer diminish in size as much as they should, at the termination of inspiration, the ascent of the diaphragm is less than it should be, and it begins to act at the commencement of each inspira- tion from a lower and lower level; conse- quently, the increase in the capacity of the thorax obtainable by its contraction is always lessening, till finally, it is per- haps just possible that its normal physio- logical action may be, as above stated, reversed.1 When the ordinary muscles of inspiration are, in consequence of the per- manent expansion of the chest, unable to dilate it sufficiently to take in a proper supply of air, all the extraordinary mus- cles of inspiration are habitually employed in breathing; hence the muscles of the neck, back, &c., capable of aiding inspi- ration, are, after a time, considerably hy- pertrophied, the shoulders are raised, and the enlargements of the muscles of the neck, the scaleni especially, give a pecu- liar breadth to the neck. Imperfect aeration of the blood result- ing from the damaged state of the pulmo- nary capillaries, and the changes which take place in the walls of the air-vesicles 1 The common cause of recession of the lower part of the chest during inspiration is some impediment to the free entrance of the air into the lungs, and the pressure of the external air for this reason being brought to bear with undue force on the outside of the thorax by the powerful action of the inspira- tory muscles. The lower parts of the chest- walls are there most yielding, and are there- fore pressed inwards by the weight of the atmosphere. On this and other points con- nected with the deformity of the chest in Pulmonary Vesicular Emphysema, the reader is referred to Dr. Sibson's elaborate and most able paper in the thirty-first volume (1848) of the Medico-Chir. Soc. Trans., "On the Movements of Respiration in Disease." 84 EMPHYSEMA OF THE LUNGS. after they have been long over-distended, add greatly to the shortness of breath; while the dilution of the air taken in at each inspiration by the large quantity of residual air left after expiration, must still farther distress the breathing by in- terfering with aeration of the blood. The shortness of breath, then, in un- complicated Large-lunged Vesicular Em- physema, is due to the small extent of movement of the chest-walls, including the diaphragm, during respiration, to the impurity of the air in the thorax at the termination of inspiration,1 to the state of the capillaries of the pulmonary artery, and to the structural changes in the sub- stance of the walls of the air-vesicles. If bronchitis in any form, or asthma, supervene, the distress of breathing is greatly increased ; and in some cases in which the distress of breathing has been unusually great, fatty degeneration of the heart has been found after death (Vir- chow). General description of the symptoms in a case of advanced Large-lunged Vesicular Emphysema. - The thorax is barrel- shaped; the antero-posterior, lateral, and vertical diameters are increased; the sternum is arched ; the lower cervical, dorsal, and upper lumbar spine is curved, concavity forward ; the ribs are too hori- zontal; the intercostal spaces are widened, and but little, if at all, depressed below the level of the ribs ; the posterior bulg- ings on either side of the vertebral column are greater than they should be ; the costal angle is larger than in health, and as the diaphragm is flattened and the lower part of the sternum is forced for- ward, at the same time that both lungs are enlarged, the heart is at once less covered than in health by the sternum, thrust downwards by the forces that over- distended the air-vesicles, and carried downwards by the contraction of the dia- phragm, and can, in consequence, be felt and seen beating below the ensiform car- tilage. The heart, and especially the right ventricle, is dilated, and hypertro- phied-its impulse is heaving, and its dilatation and hypertrophy render the epigastric pulsation very perceptible. The shoulders are raised, and the mus- cles of the neck and shoulders, especially the sterno-cleido-inastoidei, the scaleni, the omo-hyoid, and the trapezii, stand prominently out. The fossa behind the clavicle is fre- quently deepened; when,.however, there is excess of emphysema above the level of the first rib, there may be post clavicu- lar bulging. Under all circumstances, when the patient coughs there is undue prominence, or bulging even of the post- clavicular fossa, and of the intercostal spaces, the air being forced from the more, to the less compressed and supported* parts by the expiratory efforts preceding the opening of the glottis. The neck is broad from hypertrophy of its muscles, and its veins are unduly promi- nent. As the obstruction to the circula- tion increases, the veins of the neck pul- sate synchronously with the beat of the right ventricle, and fill from below when emptied by the pressure of the finger. The whole venous system is manifestly dilated, the larger veins of the upper ex- tremities have a knotted appearance from over-distension just above their valves, the hemorrhoidal veins are enlarged, thickened, &c., and often bleed-it may be to the great relief of many of the dis- comforts from which the patient is suffer- ing. The face has a coarse, bloated, dusky, and, on exertion, even livid aspect; the alae of the nose, and the lips, espe- cially the lower lip, are thickened. The eyes are prominent, the conjunctivae in- jected, occasionally yellowish, and the eyelids puffy-drowsiness, mental dulness, and headache are common symptoms. Emaciation is sometimes very consider- able. The legs are oedematous, or the whole cellular tissue the seat of anasarca. Orthopnoea is often present, because in the recumbent position the extraordinary muscles of inspiration can have only im- perfectly supported points, in place of fixed points, from which to act; and again, because the weight of the body in the recumbent position interferes with the expansion of some part of the chest-walls, and the position and weight of the ab- dominal viscera with the descent of the diaphragm. In this stage of the disease the urine frequently contains albumen, and now and then blood and blood-casts of tubes. The abdomen generally is fuller than natural. The spleen and liver are in- creased in size, and the latter organ is frequently so much depressed by the de- termining cause of the distended lungs, by the enlarged and distended heart, and by the flattened diaphragm, that its upper convex surface can be distinguished by eye and touch through the "abdominal walls. When from supervention of bronchitis, or other cause, the impediment to the 1 Although the capacity of the chest is greater in Large-lunged. Vesicular Emphyse- ma than it is in health, spirometrical observa- tions show that its vital capacity, as measured by the quantity of air that can be expelled after deep inspiration, is diminished. The residual air must therefore be much greater than it should be. Speaking of the difficulty of breathing in Emphysema, Magendie (Le- mons, 1825, tome i. p. 169) observes: "The tissue of the lung has lost some of its elas- ticity, and no longer reacts with -sufficient force on the air which has penetrated into its parenchyma." small-lunged vesicular emphysema. 85 pulmonary capillary circulation is tempo- rarily increased, the liver and spleen may be proved, by percussion and touch, to be larger than before, and to resume their former size, as the circulation through the lungs becomes freer, and the mechan- ically-induced congestion is in conse- quence lessened. The pulse in Large-lunged Emphysema is often small and weak, from the small quantities of blood which pass through the lungs and therefore into the left ven- tricle. The urine is, speaking generally, that of imperfect respiration, and of conges- tion of the kidneys and liver. At times it is very abundant, pale, clear, and of low specific gravity ; at others it is scanty, high-colored, and loaded with lithates, which as the urine cools form a heavy brickdust-like sediment. This deposit is not in all cases due merely to the con- centration of the urine, there may be an absolute increase in the quantity of uric acid. Owing to the imperfect aeration of the blood there is a scanty supply of oxy- gen distributed through the system, hence the products of tissue metamorphosis are in a lower stage of oxidation, and uric acid is formed to some extent in place of urea. Parkes thinks it is only when bron- chitis is superadded to Emphysema that there is such deficient oxidation as to lead to excess of uric acid in place of urea. J. C. Lehmann, in a carefully-observed case, found the urine after each attack of diffi- culty of breath deficient in urea and very acid. It contained oxalic acid and allan- toin. To this Parkes objects, that in Lehmann's case bronchitis complicated the Emphysema, and refers to a case of uncomplicated Emphysema so severe as to cause cyanosis and constant dyspnoea, observed by Ranke and himself, in which very little uric acid and a full quantity of urea were present in the urine. Biemer says, after quoting the observations of Lehmann and Ranke, that he has more often been able to detect small quantities of bile pigment in the urine. A trace of albumen may, when the dis- ease is far advanced, be constantly pres- ent in the urine; the quantity being in- creased with every increase of the impedi- ment to the flow of blood through the lungs. When the congestion of the kid- neys is suddenly greatly increased, or at- tains, even slowly, an extreme degree, the urine contains blood and blood-casts of tubes. Much albumen, with little evi- dence of impediment to the flow of blood through the lungs, renders it probable that organic disease of the kidney is present. It is not uncommon for the symptoms to be very trifling for some years, and then for a year or more, to see the graver symptoms only when the patient has an attack of bronchitis ; with the cessation of the bronchitis the oedema of the legs, the albumen in the urine, and the jugular pulsation frequently disappear. The over- distended heart and veins having their walls, as yet, to any serious degree, un- damaged, contract nearly to their normal dimensions, when the extra impediment to the flow of blood through the lungs, due to the acute attack, has passed away. But the improvement is only for a time, another attack of bronchitis renews the serious symptoms, and after one or more such renewals, they are permanently established. The variations in severity of the chief symptoms of Large-lunged Vesicular Em- physema may be summed up thus: the increase in size of the thorax varies from that obtained by a slight diminution in the natural obliquity of the ribs, or trifling local bulging, to the utmost expansion of the chest-walls: the hyper-resonance on percussion, from slightly increased clear- ness to the fullest clear sound; the pro- longation of expiration, from an amount difficult to appreciate, to that in which it considerably exceeds in length the inspi- ratory sound. The impediment to the flow of blood through the lungs varies, from just enough to give, when the pa- tient coughs, undue prominence to the great veins of the neck, to sufficient to cause hypertrophy and dilatation of the right side of the heart, jugular pulsation, and knotting and enlargement of all the superficial veins, anasarca, albuminuria, enlargement of the liver and spleen, dila- tation of the systemic capillaries and ar- teries, hypertrophy and dilatation of the left side of the heart, and finally organic changes in the structure of all the organs in the body, and of the connective tissue generally. The shortness of breath varies from a mere " touch in the wind" to ina- bility to move without great distress of breathing. The imperfect aeration of the blood va- ries from just sufficient to cause a slightly dusky hue of the lips on exertion, to enough to give the patient the purple or leaden hue of cyanosis. When Large-lunged Vesicular Emphy- sema is limited to a lobe or part of a lobe, as not unfrequently happens, then local fulness or bulging, and hyper-resonance with trifling shortness of breath, are com- monly the only evidences of the disease. Small-lunged (or Atropiious Pul- monary) Vesicular Emphysema.- After Large-lunged Vesicular Emphy- sema has lasted some time, and the over- distension of the vesicles is extreme, a certain, it may be considerable, amount of wasting of the tissues of the lung en- sues ; ami thus a form of Atrophous Em- physema is established. 86 EMPHYSEMA OF THE LUNGS. But in the variety of Emphysema desig- nated Small-lunged or Atrophous Pulmo- nary Vesicular Emphysema, atrophy of the lung-tissue is the primary disease, or it supervenes on trifling primary over-dis- tension. Small-lunged Vesicular Emphysema is confined to persons well past middle-life. Those who suffer from it are commonly thin. Withered-looking, shrivelled, old persons frequently have their lungs dam- aged by this form of Emphysema. It is a far less troublesome and less grave af- fection than is Large-lunged Vesicular Emphysema. In primary general Small-lunged Vesic- ular Emphysema the whole of both lungs suffer. There is waste of tissue, true atrophy. In some cases fatty degenera- tion has been said to precede absorption, or the final disappearance of tissue. In this form of Emphysema the sepa- rate vesicles are not dilated ; but the par- titions between adjacent vesicles with their pulmonary capillaries and other structures disappear or are reduced to mere threads, and two or more vesicles are thus thrown into one. No over-dis- tending force is necessary to determine the increased capacity of the vesicles. Lungs the subject of this disease are smaller, lighter, and drier than are healthy lungs. They would, from the destruction of the capillaries, be pale, but the pallor from this cause is commonly concealed by the large amount of black pigment spread through them. They weigh much less than healthy lungs, be- cause they have lost much of their natural structures. The air-vesicles are large, but the lungs themselves are small. The division between the superior and inferior lobe is more vertical than in health. The elasticity of the lungs is in a great measure lost-there is no resilience in them-they pit on pressure, and the pit remains. Their small size, their light- ness, and the very small space into which they may be compressed are often most remarkable. They are occasionally so much wasted, that, on opening the tho- rax, they sink back at once toward the spine and posterior part of the thorax. When the lungs and air-passages are in health, death takes place at the termina- tion of expiration. On opening the tho- rax, healthy at the moment of death, and permitting the pressure of the air to bear on the outer surface of the lungs, there is at once a slight diminution in their size. This diminution is due to the elasticity of the lungs. Before the opening of the tho- rax the complete elastic contraction of the lungs was opposed by the pressure of the air on the inner surface of the air- vesicles. In Hypertrophous Pulmonary Vesicu- lar Emphysema the resilience of the lungs is diminished, hence when the thorax is opened there is less contraction of the lungs, and therefore less separation of the lungs from the chest-walls, than there is when the lungs and air-passages are healthy. The quantity of solid tissue constituting the walls of the air-vesicles, <fcc., and the irregular thickening of that tissue, prevent any mere collapse of the lungs. When the lungs are in a state of ex- treme Atrophous Vesicular Emphysema, they have not only lost in a great meas- ure their elasticity, but a large quantity of their solid tissues has disappeared. The consequence is that, when the thorax is opened, and the pressure of the air on the internal and external surfaces of the lung is equalized, although little or no diminution may occur from its resilience, the weight of the lung may be sufficient to cause it to fall in like an inflated bag of wet paper. If the subject of extreme Atrophous Pulmonary Vesicular Emphysema suffer from cough, then Local Emphysema with large vesicles is frequently superadded to the General Atrophous Emphysema. The elasticity of the lungs being diminished, the vesicles of the parts least compressed and least supported during expiratory efforts being permanently and greatly over-distended, atrophy of their walls throws several air-vesicles into one, and air being forced into the large cells so formed may lead to their extreme dilata- tion. For reasons previously assigned, these vesicles are found at the margins and apex of the lung. Coincidently with the occurrence of the changes in the textures of the lungs which constitute Atrophous Vesicular Emphy- sema, the ribs and their cartilages expe- rience degenerative changes by which their elasticity is diminished, but at the same time also the inspiratory muscles shrink and lose strength. The chief direct symptoms of Small- hmged or Atrophous Pulmonary Vesicular Emphysema are-(1) shortness of breath; (2) diminution in the size of the thorax. Shortness of breath in Small-lunged Emphysema is never felt to any notable degree, unless the patient makes exertion, and as the disease usually occurs in the aged, or in those wasted from other chronic diseases, persons indisposed and incapable of moving quickly, exertion sufficient to cause distressing shortness of breath is rarely made. Primary Atrophous Vesicular Emphy- sema is commonly attended by general waste,'and is therefore accompanied by waste of blood as well as of tissues; so that the capillary pulmonary vessels, al- though reduced in number, still suffice for the passage of the diminished quantity of blood. SMALL-LUNGED VESICULAR EMPHYSEMA. 87 Again, the lungs being small, the expi- ratory power is enough to drive out the air, and the play for inspiration is consid- erable. The patient, in place of, as in Large-lunged Vesicular Emphysema, al- ways " taking in breath on the top of breath," in Small-lunged Vesicular Em- physema inspires from the bottom of his breath. The chest in Small-lunged Vesicular Emphysema is diminished in capacity, and all its diameters are less than in health. The diminution in the antero- posterior and lateral diameters is obtained by a great increase in the obliquity of the ribs. The upper intercostal spaces next the sternum are widened and depressed below the level of the ribs. So obliquely placed are the lowest ribs, that their car- tilages almost reach the crest of the ilium, and the intercostal spaces are lost, the ribs themselves really touching. The cartilages between the ribs and sternum, as the ribs become abnormally oblique, bend so as to form an obtuse angle. Res- piration is short, the thorax moves as a whole in inspiration, and the expiratory recoil follows quickly. The inspiratory murmur is short and feeble-the expira- tory not prolonged. From the loss of elasticity in the ribs and cartilages, and the imperfect tension of the chest-walls, the resonance on percussion may be even less than in health, although the solids in the chest are diminished. As the lungs are small, the heart is less covered than it should be, and so the extent of precordial dulness may be increased, and that, al- though the heart itself may be partaking of the general atrophy. As Atrophous Emphysema is usually accompanied by waste of blood, and as the general mus- cular power of the patient forbids active exercise, there is commonly in Small- lunged Emphysema not only little distress in breathing, but no damming back of the blood in the right ventricle, over-disten- sion of the venous system, dropsy, or hypertrophy, or dilatation of the heart. Complications of Pulmonary Vesicular Emphysema.-The frequent conjunction of bronchitis and Pulmonary Vesicular Emphysema has been admitted from the time the latter was recognized as a special disease. Laennec considered the Emphy- sema to be in all cases the consequence of bronchitis, and especially of that form of bronchitis which was designated dry catarrh. And Louis, while denying the relation of the two diseases as cause and effect, admitted the frequency of their co- existence. It is now established that bronchitis is the most common cause of the direct pro- duction of Pulmonary Vesicular Emphy- sema, and also that Emphysema may be developed independently of bronchitis; and that when so established, the subjects of Emphysema are very prone to suffer from bronchitis. So that although, as a rule, bronchitis is the cause of Pulmonary Vesicular Emphysema, it may be the con- sequence ; and the Emphysema, in rare cases, may be unaccompanied from first to last by bronchitis. One cause of the frequency with which bronchitis supervenes on Pulmonary Vesi- cular Emphysema is, that when a part of the lung only is emphysematous, and the passage of the blood through the capilla- ries of that part is consequently impeded, hypersemia of the non-emphysematous tissues is the necessary result-the blood passing into the vessels of the part which offer it the least resistance. Chronic general catarrhal bronchitis, with much violent cough and little expec- toration, is the most common complication of general Large-lunged Vesicular Em- physema. Acute capillary bronchitis is one of the most common causes of death in the same form of the disease. If the heart be, as it so often is, dilated and hy- pertrophied, then the acute capillary bron- chitis is usually attended with much con- gestion of the substance of the lung. Chronic bronchitis with profuse purulent expectoration is less common in Large- lunged than it is in Atrophous Pulmonary Vesicular Emphysema. When the puru- lent discharge is considerable, the so- called amyloid degeneration of various organs is said to occur pretty frequently. In this case, amyloid degeneration is con- nected with the profuse suppuration and not with the Pulmonary Vesicular Em- physema. Dilatation of the bronchial tubes is com- mon in all forms of Pulmonary Vesicular Emphysema. In severe Large-lunged Vesicular Em- physema, it is common to find an excess of fluid in the pericardium after death. It is only when congestion and oedema of the lungs have complicated the disease that an excess of serosity is found in the pleurse. The subjects of Large-lunged Vesicular Emphysema frequently suffer from dis- turbance of the digestive organs. The liver is loaded with blood, and the bile formed is thick and dark. The walls of the stomach are congested, and ultimately thickened. The result is notable disturb- ance of the stomach digestive processes. The patient suffers from visible distension of the epigastric region, and also from a sense of weight and fulness in the same part, especially after food, altogether dis- proportionate to the quantity and the quality of the food taken. Elatulence and acidity of stomach are troublesome symptoms. The distension of the stomach is fre- quently so great as very decidedly to in- tensify, by the impediment it offers to the descent of the diaphragm, the habitual 88 EMPHYSEMA OF THE LUNGS. dyspnoea. The derangement of the stom- ach is also a not infrequent exciting cause of asthma. Spasmodic asthma is a very common complication of Pulmonary Vesicular Em- physema, especially of the large-lunged form of the disease. Attacks of extreme difficulty of inspiration supervene sud- denly in the early morning, or at uncer- tain times, on the habitual shortness of breath. In addition to attacks of ordi- nary spasmodic asthma, the subjects of Pulmonary Vesicular Emphysema often suffer for weeks together from increased dyspnoea, out of all proportion to any catarrhal bronchitis which may happen to be present. This dyspnoea is, in a great measure at least, due to spasm of the bronchial muscular fibres.1 Phthisis. - One of the most marked anatomical characters of congenital tu- berculosis, i. e. of an inherited disposition to the deposit of tubercle, is the small size of the lungs. It is by no means un- common for a deposit of tubercle to take place in the apex of such lungs, and then for the tubercle to obsolesce or to calcify. The subjects of these changes frequently live to an advanced age. Chronic solidi- fication with contraction of the apex of the lung, much black pigment in the solid tissue, and Local Emphysema with large vesicles, frequently follow the obsoles- cence or calcification of the tubercles. After passing middle life, the subjects of these lesions frequently become affected with general Atrophous Pulmonary Ve- sicular Emphysema, rarely, if ever, with Large-lunged Vesicular Emphysema. Subsequently, the solid tissue of the apex of the lung may undergo molecular disin- tegration, and a cavity be formed ; death, in such cases, is said to have occurred from tubercular consumption, when, in- deed, there are no tubercles present. This is a form of senile phthisis. Headache and drowsiness are common consequences of Large-lunged Vesicular Emphysema. These symptoms are due to congestion, the consequence especially of the mechanical impediment to the pas- sage of blood through the lungs, aided in some cases by the imperfect aeration of the blood, and by those changes in the coats of the vessels so commonly seen in the subjects of the disease here considered. The veins and arteries, from changes in their walls, partly due to the congestion of their rasa vasorum, lose some of their normal reactive force, and hence the pres- sure of the blood on the inside of their walls leads here, as elsewhere, to their permanent dilatation. After death, we find not only increased capillary vascu- larity and excess of serosity in the meshes of the pia mater, but the arteries and veins in the same structure manifestly larger than they should be. Diseases which in their progress are fre- quently complicated with Pulmonary Vesic- ular Emphysema.-All diseases accompa- nied by severe cough, by diminution of the whole or part of a lung, or by impedi- ment to expiration, are accompanied by over-distension of the air-vesicles. All diseases or changes in nutrition at- tended by damage to the elasticity of the lung, render permanent what would other- wise be transient over-distension of the air-vesicles. Winter cough, catarrhal, and other forms of bronchitis, are undoubtedly the diseases most frequently conjoined with Pulmonary Emphysema. Disease of the left side of the heart, by damming back the blood in the lungs, and so inducing changes in their texture, leads to permanent dilatation of the air-vesicles when their over-distension has been once determined by cough, &c. Pneumonia is sometimes attended by Acute Vesicular Emphysema of the air- admitting vesicles, but as the walls of the over-distended vesicles are healthy, and their over-distension is neither extreme nor of long duration, they return to their natural size when the pneumonia sub- sides. After solidification has passed away, the textures of the lung damaged by the pneumonic exudation may be the seat of permanent Chronic Emphysema. When one pleura contains sufficient fluid to render the lung altogether useless, the opposite side of the thorax expands more than it should, and is for the time larger than in health, and its air-vesicles are enlarged in proportion to the degree of the expansion of the side. Should the impervious lung be, from long compres- sion or other cause, so damaged as never again to admit any quantity of air into its vesicles, then permanent over-distension of the vesicles of the opposite lung is the consequence. It rarely happens that the distension of the air-vesicles in this case is sufficient to interfere with the capillary circulation on their walls, or to induce atrophy or other serious changes of the vesicular septa. In chronic phthisis, the bases of the lungs very frequently suffer from vesicular emphysema ; this is especially likely to happen when there has previously been dry pleurisy with adhesions at the same point. Hyper-resonance of the bases of the lung is, therefore, frequently conjoined with tubercular dulness of the apices. The expiratory efforts of cough are the determining cause ; the damage inflicted 1 It is possible that in many cases asthma precedes Pulmonary Vesicular Emphysema, and the violent efforts to inspire are the de- termining causes of the Emphysema, and that in this as in so many other cases the effect has been mistaken for the cause. SMALL-LUNGED VESICULAR EMPHYSEMA. 89 on the textures by the pleurisy is a com- mon cause of the permanence of the over- distension. The Vesicular Emphysema in this and similar cases, when tolerably limited in extent, is not attended with notable disturbance of respiration or cir- culation. It must, it is true, add a little to the shortness of breath, and a little to the impediment to the circulation through the lungs, but these additions are insig- nificant in comparison with the primary disturbances of respiration and circulation resulting from the original disease. Dis- eases attended by incomplete occlusion of the air-passages frequently have, as con- sequence, over-distension of the air-vesi- cles of the whole or of part of the lung. In accidental occlusion of the larynx, Acute General Vesicular Emphysema is frequent. Thus, in tlie case of a woman, who in a state of drunkenness choked herself by thrusting the food with her finger from the over-full pharynx into the larynx, the lungs were the seat of ex- treme General Acute Emphysema. In such cases, supposing the obstruc- tion to be at first incomplete, the sufferer does what he would do if the obstacle were removable-he makes the deepest possible inspiration, and then coughs. The violent expiratory effort drives the air into the less compressed and supported parts. The local obstacle to the escape of air being irremovable, causes an excess of air to be retained in the lungs. A second deep inspiration follows, and so finally general over-distension of the air-vesicles is established. The full normal distension of the lungs with air may be mistaken for Acute Gen- eral Emphysema, if death occur while the lungs are distended by a deep inspira- tion, and a foreign body in the larynx prevent the expulsion of the air from the lungs by the natural death-expiratory act. In croup, the false membrane in the larynx may, in rare cases, act for a short time as a valve, admitting the air to pass into the lung, but opposing its escape, and so cause Acute Vesicular Emphysema. In croup, again, pulmonary lobular col- lapse and lobular pneumonia are both common, and, when present, some of the Acute Vesicular Emphysema found after death may be secondary to those lesions of structure. But more commonly than in either of the modes just enumerated, the Acute Vesicu- lar Emphysema found after death in croup is produced during the expiratory efforts of coughing ; that it is so produced is proved by the situations it occupies, viz., those parts of the chest which in these cases are seen during life to recede during inspiration, and to advance during expiration. In hooping-cough, Vesicular Emphy- sema is a constant result of the violent expiratory efforts of that disease. When the over-distension is extreme, and is frequently repeated, the elasticity of the walls of the vesicles may be diminished, and then a certain amount of over-dis- tension remains a permanent lesion. As bronchitis is a frequent complication of hooping-cough, disseminated lobular col- lapse may in some cases aid to a slight extent in the production of the Vesicular Emphysema. Hereditary nature of Pulmonary Vesicu- lar Emphysema.-Jackson' found that 18 of 28 subjects of Pulmonary Emphysema were born of parents one of whom was affected with the same disease ; while of 50 non-emphysematous patients 3 only came of emphysematous parents; and Niemeyer remarks, "I have known at least one family in which, without catarrh preceding, all the members for three gen- erations suffered from emphysema." These facts afford some support to the theory that Pulmonary Vesicular Emphy- sema is hereditary. But Pulmonary Vesi- cular Emphysema is far too common a disease for Jackson's few oft-quoted ob- servations, or for solitary badly stated facts, such as that of Niemeyer, to prove, or even to render it highly probable that it is really hereditary. If the cases be excluded in which the disease owes its origin to inherited pre- disposition to bronchitis, heart disease, asthma, premature age-degeneration, &c., the facts adduced in support of the hered- itary nature of Pulmonary Vesicular Em- physema will be reduced to an insignifi- cant figure. It is not denied that the disease may be hereditary, but it is with- out question in the writer's mind that the evidence adduced in support of its being hereditary in the sense in which tubercle and cancer are hereditary, is altogether insufficient for the proof. Diseases of the lungs to which Pulmonary Vesicular Emphysema indisposes.- Pneu- monia with exudation of lymph, croupose pneumonia as it has been called, rarely occurs in the emphysematous parts of a lung. The destruction of the capillary vessels which occurs in Chronic Vesicular Emphysema, is supposed to afford a cer- tain degree of exemption from this form of inflammation. Although a streak or two of blood in the sputa is not uncom- mon in the bronchitis from which emphy- sematous patients suffer, hemorrhage in quantity from emphysematous lungs is said to be rare. Those suffering from Atrophous Vesicular Emphysema alone enjoy a practical immunity from pneu- monia and from hemorrhage. Tubercle has been said to be excluded by Pulmonary Vesicular Emphysema. 1 Quoted by Louis. 90 EMPHYSEMA OF THE LUNGS. No doubt active congestion of a part accompanies the formation of tubercle, and active congestion rarely affects the emphysematous parts of a lung, and to the same extent Vesicular Emphysema of the lung indisposes to the deposit of tuber- cle. It is to the wasting of the vessels in Emphysema of the lung that the immu- nity, so much as it is, from tubercle is due. The blood in Pulmonary Vesicular Em- physema is less fully aerated than in health. To this venosity of the blood, Rokitansky attributes the infrequency of tubercle in the subjects of Pulmonary Vesicular Emphysema. Uis theory, how- ever, is opposed by facts. Treatment of Chronic Pulmo- nary Vesicular Emphysema.-The treatment of Pulmonary Vesicular Em- physema may be divided into Curative, Palliative, including the treatment of its direct consequences, and Preventive. Curative Treatment. -Some therapeu- tists have supposed that, by the lengthened administration of small doses of strych- nine, and others, that by the skilful em- ployment of electrical power, permanent contraction of the walls of the dilated air- vesicles may be obtained. But, although powerful agents for exciting muscular contraction, neither strychnine nor elec- trical action have any influence in restor- ing or increasing the elasticity of a tissue. In Chronic Pulmonary Vesicular Emphy- sema, it is the elasticity of the walls of the air-vesicles which is damaged. Experi- ence, as might have been anticipated, has afforded no evidence in support of the value of the drug or the battery in the cure of Pulmonary Vesicular Emphy- sema. Again, some therapeutists have placed persons suffering from Chronic Pulmo- nary Vesicular Emphysema in a chamber supplied with condensed air, in the hope that the breathing of the condensed air would cure the disease. Others have alleged that great attention to diet, and the administration of iron, and other blood, nervine, and stomach tonics, will, by improving the nutritive powers, cure the disease. But, if it be remembered, that to cure Chronic Pulmonary Vesicu- lar Emphysema of severity sufficient to cause trouble to the patient, is not only to renew the elasticity of the walls of the air-cells, but also to restore the stretched vessels to their normal length and to their natural tone, to repair the apertures in the walls of the air-vesicles, and to replace the torn and otherwise destroyed capilla- ries by healthy vessels, it will be at once admitted that the cure of Chronic Pulmo- nary Vesicular Emphysema is impossible. Persons suffering from Emphysema have been greatly relieved by breathing con- densed air ; but the relief, as might be anticipated, has been temporary only; and while attention to diet, &c., is of no avail to cure the disease, it is of great im- portance in staying the progress of the dis- ease and relieving distress. Preventive Treatment.-The great fac- tors of Pulmonary Vesicular Emphysema being- Excess of pressure of air on the inside of the air-vesicles, Age degenerative changes of the parietes of the thorax, Changes of the texture of the lung, from excess of blood in it. Age-degenerative changes of the lung, in order to prevent the disease and to stay its advance when established, care must be taken to guard against these, its deter- mining and permanence-securing causes. Catarrhal, and all other forms of bronchitis being beyond question the most frequent exciters of the Pulmonary Vesicular Em- physema, the prevention of these diseases is of the very highest importance. To secure immunity from bronchitis, and to prevent its recurrence, clothing must be adapted to the season, and it is necessary that cold and wet, especially fog and cold winds, be avoided. A mild climate has a marked influence in preventing the attack of bronchitis, to which so many are sub- ject during the winter in this country, lienee it is most important for those whose lungs are the seat of Vesicular Emphy- sema, to spend the winter in a mild, and not too dry air. When chronic or subacute bronchitis is present, the freer the secretion from the bronchial mucous membrane, and the less violent the cough, the less likely is Chronic Emphysema to follow. Expectorants and opiates combined are the great medicinal agents. The expectorants selected when the cough is dry, should be those that pro- mote secretion; when the secretion is abundant, those that favor its expulsion. Violent and irritative cough-that is, cough out of all proportion to the matter to be expectorated, should be restrained by sedatives: Opium, belladonna, stra- monium, conium, and prussic acid, are the chief sedative agents in this class of cases. These drugs are more efficacious when given with little water, and in a small quantity of mucilage and syrup. Seda- tive inhalations are particularly useful. The sedative should be placed on the sponge of Maw's inhaler, and the steam of hot water passed through the sponge. Chloroform vapor exhibited in this way is sometimes very serviceable. When the secretion from the bronchial mucous membrane is too abundant and purulent, the mineral acids, quinine, iron, especially the tincture of the sesquichlo- ride, and cod-liver oil, are invaluable ; as is also the inhalation of mild stimulants, TREATMENT OF CHRONIC PULMONARY VESICULAR EMPHYSEMA. 91 e. g., iodine diffused in small quantity through the room. In these cases, a change to dry sea-air is often very serviceable. All efforts which try the muscular powers, as carrying heavy weights, are injurious. All exertions which induce panting, or oblige the person to stop fre- quently to recover his breath, are calcu- lated to inflict permanent injury. Rapid walking, hill climbing, and violent exer- tions of all kinds, are to be carefully avoided. Walking exercise should, as much as possible, be limited to level ground. Many an old gentleman has been hur- ried to his grave by attempting to follow the birds as he did in his early days, and by striving to improve his health by active exercise, It is a great gain for length of life to take old age pleasantly. Those predisposed to the disease and, a fortiori, subjects of Pulmonary Vesicular Emphy- sema, should never attempt to play wind instruments. When urging these points on a patient, it must never be forgotten that the per- manence-securing cause being established, every single over-distension of the air- vesicles permanently increases their size. The increase on each occasion is indeed insignificant; but as every repetition of the over-distension adds to that previously existing, it follows that, should the over- distension be frequently repeated, a con- siderable amount of dilatation must be the ultimate result. All the foregoing means which are of importance in preventing the occurrence of the disease, are practically still more important as preventing its increase when established. Many a man whose wind was merely touched, has become dropsi- cal, &c., by attempts to renovate himself, by endeavors to climb, hunt, and shoot as he did before his "wind" began to go. Old age has commenced on his chest; he is but between fifty and sixty, and he won't admit the existence of it. He strives against its inevitable consequences, and dies from the effects of the struggle years before he would have done had he shunned the contest. All measures which oppose the super- vention of the degenerative changes of age, are to be sedulously employed, with the hope not only of specially retarding age-degeneration of the lungs and thoracic parietes, but of the body generally. Diet, carefully regulated exercises, and, of drugs, iron and cod-liver oil, especially the former, are among the most potent means for effecting the object in view. Palliative Treatment.-The distress from which the subjects of Large-lunged Vesi- cular Emphysema suffer, is due- 1. To shortness of breath ; 2. To congestions of distant organs pro- duced mechanically by the impediment to the flow of blood through the pulmonary capillaries ; 3. To the abnormities of blood which result from the functional and structural changes of the liver and kidneys espe- cially, consequent on their congestion. 1. The remedies for the shortness of breath vary according to its direct cause. Having regard to the treatment, the causes of shortness of breath may be summed up thus :- (a) Organic changes in the walls of the thorax, in the walls of the air-vesicles, and in the capillaries in the walls of the air-vesicles, and dilution of the air received into the air-vesicles at each inspiration, by the excess of air retained in them at the termination of expiration. Breathing condensed air, it appears pro- bable, temporarily relieves the distress of breathing due to the dilution of the air. Whether it does more than this is doubtful. (6) Catarrhal and other forms of bron- chitis.-For the shortness of breath aris- ing from these affections, expectorants which both favor free secretion and ex- pectoration are the great remedies. Ipe- cacuanha and carbonate and muriate of ammonia, squills and senega are the most potent remedies (see art. Bronchitis). (c) Asthma.-Free secretion and expec- toration from the bronchial mucous mem- brane, affords the most efficient relief in continuous shortness of breath from this complication. Ipecacuanha, squill, am- monia, and senega alone, or combined with sedatives and antispasmodics, are the agents best calculated to attain the desired end. It must not be forgotten that disturb- ances of the digestive organs, the liver, stomach, and bowels are common in Large-lunged Vesicular Emphysema, and are also frequent exciting causes of attacks of spasmodic asthma in that disease. (d) Congestion of the liver, accumula- tion of flatus in the stomach and bowels, and loaded bowels by interfering with the descent of the diaphragm, are common causes of shortness of breath. It is in consequence of this that a full dose of blue pill, or calomel and colocynth, followed by a brisk, warm, saline aperient, so often affords marked relief to the dys- pnoea of Large-lunged Vesicular Emphy- sema. Blue pill occasionally, aromatic saline antacid aperients, taraxacum with soda, or nitro-hydrochloric acid with aromatics, and attention to diet, are the means best calculated to ward off shortness of breath from these causes. 2. In treating the congestions of organs, two objects have to be kept in view. 1st. To remove the impediment to the flow of blood through the lungs. 2d. To relieve directly the local conges- tions. 92 EMPHYSEMA OF THE LUNGS. The impediment to the flow of blood due directly to organic changes in tlie walls of the air-vesicles and in the pulmonary capillaries, is irremediable. Catarrhal and other forms of acute and chronic bronchitis increase the impedi- ment to the capillary circulation through the lungs : and, therefore, to relieve those affections, is to relieve the congestion of the venous system. Free secretion and expectoration from the bronchial tubes, is the most efficient agent for affording re- lief in these cases. Violent cough again impedes the flow of blood through the lungs, and so pro- duces congestion of the venous system. Sedatives, therefore, by checking cough, become means of relieving local conges- tions. Free secretion from the kidneys, liver, and intestinal mucous membrane, relieve the local and general over-distension of the capillaries and veins of those organs, resulting from impediment to the flow of blood through the lungs. Of diuretics, the ordinary salts of pot- ash, with small quantities of iodide of potassium, are, as a rule, the most effica- cious. This class of remedies should be preceded by one or more doses of blue pill, with squill and digitalis. It is common for diuretics not to act till the tension of the venous system has been, to some extent, taken off by other means. Hence should diuretics fail when first given, aperients may be employed, and their use be followed by diuretics with advantage. Blue pill, and other cholagogues, fol- lowed by hydragogue aperients, such as cream of tartar with jalap, effect the desired object by promoting a full flow of secretions from the liver and intestines, and so especially relieving congestion of the portal radicles and terminal branches. A natural relief is occasionally afforded to a congested organ by spontaneous hemorrhage from it. Cerebral congestion is relieved by epistaxis ; congestion of the lungs by hsemoptysis; of the liver and intestines, by hsemorrhoidal bleeding ; of the kidneys, by hannaturia; of the sto- mach, by hsematemesis. The blood thus lost may not only relieve the vessels of the organ from which it escapes, but the venous system generally. When congestion of an organ is extreme, the application of dry-cups, or the removal of a small quantity of blood by cupping- glasses, is sometimes very useful. When the distension of the whole venous system is extreme, the removal of a little blood from the arm gives marked and sudden relief when judiciously performed. The stomach dyspeptic symptoms are due chiefly to congestion of the stomach following on congestion of the liver. They (are best treated by occasional doses of mercurials, saline aperients with mineral acids, and mustard poultices to the epi- gastric region. These remedies may be followed by small doses of strychnine, and light aromatic bitters. Aromatics, with alkalies, afford tempo- rary relief to the sense of distension and weight. 3. The congestion of the kidneys is sometimes accompanied by the retention of urinary elements in the blood, conges- tion of the liver by slight jaundice, and finally by organic diseases of these organs and then all the abnormities resulting from those diseases follow. For the special treatment of the condi- tions of blood dependent on the diseases of the liver and kidneys, see the article on those diseases. Here it is only necessary to say that the treatment before recommended for the relief of the congestion of these organs, is that best calculated to secure the removal from the blood of the elements retained in it. In cases of Atrophous Pulmonary Ve- sicular Emphysema, the great object is to support the failing general powers. Iron is one of the most important tonics in this class of cases. A moderate supply of stimulants is useful. When accompanied with profuse puru- lent expectoration, mineral acids, espe- cially the sulphuric, with small doses of quinine, tincture of the sesquichloride of iron, cod-liver oil, and mild sea-air, are the great remedial agents. Stimulating inhalations are sometimes serviceable. WORKS CONSULTED. Laennec, Traitfi de 1'Auscultation mediate et des Maladies des Poumons et Coeur. Paris: 1826. Magendie, Lemons, 1825. Tome i. Louis, Recherches sur 1'EmphysMne des Poumons. M&noires de la Soci€t£ d'Observa- tion. Tome i. Paris: 1837. Dr. G. Budd, Remarks on Emphysema of the Lungs. Med.-Chir. Transactions, 1840. A. Mendelsohn, Der Mechanismus der Respiration und Circulation. Berlin : 1845. Dr. Sibson, On the Movements of Respira- tion in Disease. Med.-Chir. Trans., vol. xxxi. 1848. Dr. Gairdner, On the Pathological States of the Lungs connected with Bronchitis and Bronchial Obstruction. Edin. Monthly Jour- nal, 1851. Ranke, II., Beobachtungen und Versuche uber die Ausscheidung der Harnsaure. Mu- nich : 1858. Parkes, On the Urine. London: 1860. Donders, Beitrage zum Mechanismus der Respiration und Circulation in gesunden und krankheiten Zustande. Zeitschrift fiir Rat. Med., 1853, p. 287. Freund, Der Einlluss der primaren Erkrank- ASTHMA: SYMPTOMS OF THE PAROXYSMS. 93 ungen des knorpeligen Thorax auf Entste- hung gewisser Lungen Krankheiten. Wiirzb. Verhandl. 1859. Ziemssen, Ueber die Pathogenese des sub- stantiven Lungen-Emphysems. Deutsche Klinik, p. 157, 1858. Biermer, Lungen-Emphysem. Virchow's Handbuch der Pathologie und Therapie, vol. v. Rokitansky, Lehrbuch der Pathol. Anato- mie, Bd. 3, 1861. Dr. A. T. H. Waters, Researches on the Nature, Pathology, and Treatment of Emphy- sema of the Lungs, 1862. Niemeyer, Ueber Emphysem der Lunge. Berlin. Med. Wochenschrift, 1864. Villemin, Recherches sur la Vesicule pul- monaire et 1'Emphyseme. Archives Generates de Med., Oct. and Nov. 1866. Hourmann et DSchambre, Archives Gen- erales, 1835. Rainey, Medico-Chirurg. Soc. Trans., 1848. Rossinol, Rech. anat. sur 1'Emphyseme, 1849. ASTHMA. By Hyde Salter, M.D., F.R.S. Definition.-Asthma may be defined as dyspnoea of peculiar urgency and vio- lence, generally paroxysmal and recur- rent, often periodic, not necessarily at- tended by cough or expectoration, accom- panied usually by dry rales, and compati- ble with easy and healthy respiration in the intervals of the attacks. The History of Asthma may be divided into the History of the Paroxysms and the General History of the Disease. A. Symptoms of the Paroxysms.- Before the attack itself sets in, it is not at all uncommon for the asthmatic to be aware that it is impending, by certain premonitory symptoms with which his experience has made him familiar, and of which it has given him the infallible in- terpretation. It is, however, more com- mon for there to be no distinct premoni- tory symptoms, but for the first slight traces of the attack to be the only warn- ing of its approach. When premonitory symptoms do occur, they are generally such as are referable to the nervous sys- tem ; as, for example, an unusual buoy- ancy of spirits and mental excitement, or depression, lethargy, and an irresistible sleepiness. One very common symptom is profuse diuresis, the patient passing, some hours before the attack, a large quantity of clear pale urine, almost as white as pump-water-identical, in fact, with what is called nervous water, or hysterical water. Asa rule, however, as has been mentioned, the patient has no warning, no sign whatever to guide him ; and this is one of the peculiar features of Asthma, and imparts to it that uncertainty and ever-possible nearness which makes it so disqualifying a disease and one so destructive of the engagements of life and the duties of an active career. It always threatens because it never threatens. Nay, more, from the time at which it is most apt to occur-the early morning-the pa- tient has not even the warning of the in- itiatory symptoms, but sleeps through them till he is awoke to find himself with the attack full upon him. He goes to bed every night uncertain whether his next return to consciousness may not be among the full developed horrors of the asthmatic struggle. The Initiatory Symptoms, when they are not slept through, and when they show themselves by day, consist in a faint development of the characteristic dyspnoea of Asthma-a slight sense of constriction across the chest, a short dry cough, a ten- dency to wheeze, and an indisposition to exertion. The asthmatic's friends notice that he walks about with his shoulders higher than usual; and he complains of flatulent distension which makes the girth across the epigastrium greater than usual, so that he unbuttons his waistcoat to give himself ease and room. This is not a mere sensation, the circumference of the chest is really considerably increased, and the patient usually attributes it to distension of the stomach with wind. No doubt, in many instances, there is a large develop- ment of gas in the stomach at the com- mencement of an asthmatic paroxysm ; but in the great majority of instances this increased girth of chest and abdomen is probably due to that enlargement of the cavity of the chest which always accom- panies the asthmatic state, and is a part of it, of which more will be said by and by, and which enlarges the girth of the chest by the elevation of the fibs, and of 94 ASTHMA. the abdomen by the depression of the dia- phragm. These initiatory symptoms may hang about for some time, even for some days, before they culminate in an attack, the asthmatic creeping about with a gradually increasing sense of constriction across the chest, a more perceptible wheeze and a greater and greater incapacity for exer- tion. At other times the paroxysm is at once so fully developed that it can hardly be said to have any initiatory symptoms at all. There is nothing more uniform in Asthma than the time at which the at- tack is apt to come on. In nineteen cases out of twenty, this is in the early morning, from two to four o'clock. So uniform is this, that it is the exception to find it otherwise. Each case, as a rule, has its own particular time: one will always be awoke at two, another at three; and so unvarying is the time, that the patient often knows exactly what o'clock it is by his asthma waking him. There are, however, two circumstances that vary the time : one, the hour at which the patient goes to bed-the earlier this is, the earlier does the attack come on ; and the other, the intensity of the exciting cause-the more powerful this is, the ear- lier is the attack likely to follow it: thus a supper in a favorable air may bring on the Asthma at three o'clock; in an unfa- vorable air as early as one. Occasionally the Asthma will remain in abeyance as long as sleep lasts and develop itself im- mediately after waking ; but this is rare. A not at all uncommon time for the at- tack to come on is about two hours after dinner. In some, it always appears on getting into bed at night. There cannot be a doubt that the part of the four-and- twenty hours the most free from it is the forenoon, from breakfast to luncheon or early dinner; many asthmatics who suffer more or less at all other times are free then. When the paroxysm is fully developed, the appearance of the patient is very char- acteristic. He sits in a fixed position, un- able to move, generally leaning forward with his hands or elbows planted on some- thing in order to raise his shoulders; some- times he stands, leaning over some piece of furniture, finding this position easier than sitting : kneeling up in bed, leaning over the pillows, or kneeling on the floor against a bed or chair, is, in many cases, the easiest position. He is pale, or, if very bad, dusky in complexion; the shoulders are raised, the back rounded, and the sweat often pours off the face from the violence of the respiratory efforts. These efforts are so great that the body is quite convulsed by them, the shoulders are thrown up, the head thrown back, and the mouth opened at each inspira- tion; and all the muscles mediately or immediately connected with the chest thrown into violent action. The patient cannot bear anything tight around his body, all his clothes must be loosened; all curtains drawn around him, all by- standers crowding about him, seem to increase his sense of suffocation. Some- times he will sit by an open window the whole night in the coldest weather, so great is the desire for fresh air; he feels as if death was impending, as if his chest were bound with iron, and as if the only thing that would give him relief would be to cut it open. The extremities are often cold, especially the lower extremities, although the perspiration may be running from the face at the same time ; the pulse is small and quick. If the patient is stripped and the chest watched, it will be seen that, although the respiratory efforts are so violent, there is very little real movement, the muscles tug at the ribs, but the ribs refuse to rise -they strive to compress them, but they refuse to subside. Although violent the respirations are not often hurried, not exceeding the natural number; but al- though the number may be natural, in every other respect the respiratory rhythm is disturbed ; the inspiration is short and jerky; the expiration inordinately long, often wound up with a sudden pumping out of the last quantities of the expired air ; and there is no post-expiratory rest. On listening to the patient's chest, everything seems lost in loud musical rales of high pitch, and mostly sibilant; among these is also often heard sonorous rhonchus. These sounds are multitudi- nous, of all pitch, and utterly discordant, squeaking, chirping, mewing, whistling, cooing, snoring, and fifty other sounds. They are almost invariably louder at ex- piration, and sometimes confined to it. The typical sounds of Asthma are of this dry character; occasionally, however, moist rales are heard either from the Asthma being complicated with bron- chitis, or from the attack approaching its termination, when mucus is being poured out. But there is one auscultatory phenome- non in Asthma, which, although negative in its character and apt to be overlooked, is far more important and significant than these noisy manifestations of bronchial stricture ; it is the almost complete or total absence of the respiratory murmur: this is not only not heard because it is drowned by the other sounds, but because it is really, for the time being, in abey- ance; for even when the musical rales are absent, as they sometimes are, the res- piratory murmur is equally defective. The reason of this absence of respira- tory murmur is that the bronchial spasm prevents the air reaching the recesses of SYMPTOMS OF THE PAROXYSMS. 95 the lungs in sufficient quantity to generate it. The more severe the Asthma, the more complete is the loss of the respira- tory murmur, and no sooner docs the spasm yield than the normal sound is reinstated. Not unfrequently, the physical signs of Asthma, above described, are partial in their distribution, the respiratory murmur is not totally absent but crops up tolera- bly clearly here and there ; the sibilant and sonorous rales, too, are patchy-some parts of the chest, especially those where the respiratory murmur is best heard, be- ing free from them. There can, I think, be but one inter- pretation to this patchy distribution of the physical signs of Asthma; namely, that the Asthma itself has a patchy dis- tribution-that the tubes are in some parts affected, in others free. In those parts where, from the absence of spasm of the tubes, the access of air is free, we often hear a respiratory murmur of strongly-marked compensatory character, the inrush of air remarkably clear and loud. This is just what might be ex- pected, and depends upon the whole of the violent inspiratory efforts being spent upon those parts of the lung where the absence of bronchial spasm renders its in- flation possible. There is yet another fact to be observed; namely, that the physical signs of Asthma change their seat with considerable rapid- ity : we may hear a patch of sibilus or rhonchus one minute, and the next it may be gone; we may find complete absence of respiratory murmur, and in a quarter of an hour, in the same place, it may be quite audible. In fact, for no two con- secutive hours does the asthmatic chest present the same physical signs at the same place. This fugitiveness and migra- tion of the normal and morbid sounds show that the bronchial spasm itself is constantly changing its seat, that con- stricted tubes are constantly becoming re- laxed, and patulous ones contracted. Occasionally, the physical signs show that the Asthma is lateral, confined to one lung, or nearly so, the rales will occupy one lung and normal breath-sound the other. The patient himself is sometimes quite aware that only one of his lungs is affected, and knows which it is. In most of those cases in which Asthma is thus restricted to one side, it always occurs more or less on the same side. In such cases there is probably some organic cause, such as emphysema or bronchitis, for its localization. Percussion, during a paroxysm of Asth- ma, is always exaggeratedly resonant; in this, the chest distension, and the loss of respiratory murmur, the conditions bear a striking resemblance to emphysema : in one respect, however, besides the tempor- ary duration of these signs, there is a marked contrast; in emphysema, the intercostal spaces are not depressed, even in strong inspiration, while in Asthma they are drawn in to an extraordinary degree; and not only the intercostal spaces, but all yielding parts bounding, or lying contiguous to, the chest cavity, as the supra-stcrnal and supra-clavicular fossse, and the scrobiculus cordis. The surface in these situations is literally sucked in at each inspiration, and nothing more strikingly suggests than this appear- ance the real nature of the difficulty in asthmatic breathing, nothing more strik- ingly proves that it must depend on a condition which temporarily renders the lung incapable of following the inspira- tory enlargement of the chest wall. Before the paroxysm ceases there is commonly some expectoration. In many cases the fit never ceases without it, and not until the expectoration is established will the spasm give way, however long it may be delayed. It is this circumstance that has given rise to the theory that the material discharged has been the cause of the preceding attack, and that the violent respiratory efforts are merely the mechan- ism which nature adopts to get rid of it. This was Bree's theory, and expressions frequently used by patients show that such an idea is still very prevalent. They say, " If I could once get the phlegm up, the spasm would give way." No doubt, the phlegm, when there, is a source of irritation and an additional cause of dys- pnoea, and no doubt, if it were discharged, the patient would be, pro tanto, under better circumstances. No doubt, too, in many cases, the spasm will not give way till the expectoration takes place, but only because the expectoration will not take place till the spasm begins to yield. Till that takes place, the mucus is locked up behind the constricted tubes, and can- not be discharged partly because its channel of egress is too narrowed, and partly because sufficient air cannot be introduced behind the constricted tubes to produce efficient cough. That the pituitary theory of Asthma-the theory of a material irritant present in the secre- tion of the tubes-is incorrect, is shown by the fact that there are many cases in which there is no secretion first or last, the chest sounds being dry throughout, and the spasm going off without any ex- pectoration. And even in the cases where the attacks always terminate with more or less spitting, they begin dry. At first there is no cough, and nothing but a dry wheeze; by and by, to the wheeze, rattling is added, and cough begins to ap- pear, and before the paroxysm is over moist sounds may be heard all over the chest, and the couch may be incessant. The mucus has evidently been gradually 96 ASTHMA. developed as the attack has progressed. In fact, the spasm is the cause of the secretion, and not the secretion the cause of the spasm. This is not at all inconsist- ent with the discharge of the secretion, when once formed, being attended with relief. The material itself is peculiar and very characteristic. True asthmatic septum, where there is no bronchitis, consists of . little pellets of gray pearly mucus, like pieces of tapioca, or very firm arrowroot. It is free from pus, free from either stringy or watery mucus and not frothy. Barely, another material is expectorated during the attack-blood. In most in- stances where this occurs it is only char- acteristic of the severest paroxysms ; in some few cases I have known every attack attended with more or less blood-spitting. It is generally small in quantity, in streaks and patches ; sometimes it amounts to a profuse hemorrhage. It evidently de- pends upon the rupture of the over- distended bronchial venules and capil- laries, due to the congestion into which they are thrown by the partial asphyxia of the asthmatic paroxysm. The duration of a fit of Asthma is a thing about which there is no rule-it may be over in a few minutes, it may last many weeks. But though there is no rule for the disease there generally is for the case; each case has, as a rule, its own length of attack although the uniformity may not be rigid. A very common length is for the attack to begin at three or four o'clock in the morning, and be over by breakfast time, or gradually clear off at nine or ten o'clock in the morning. In many cases, the attack involves a single day, never more or less. From two or three days is not an uncommon duration. In some cases, the duration is complex, each attack extending over many days and consisting of a succession of shorter paroxysms with easy breathing between ; and then, the bout being over, many months may be passed before another at- tack occurs. This is especially the case in those instances in which the Asthma is due to some cause that occurs at distant intervals, such as hay Asthma. Here the asthmatic state will last, more or less, throughout the whole of the grass-flower- ing season, although consisting through- out that time of short paroxysms, each not lasting above an hour or so, and per- I haps confined to the night. The method of termination of an attack depends very much upon two circum- stances : one, the length of time the attack has lasted ; and the other, whether it yields spontaneously, or in obedience to remedies. If the attack has lasted long it is always slower and more protracted in its departure; for the lungs are left so congested that it may be days before their circulation can resume the condition it was in before the fit. For the same rea- son, the expectoration after a prolonged attack is more profuse and continues longer. Again, if an attack is left to die out by itself, its departure is often tedi- ous, and it may show many partial re- missions before it takes its final leave. If, however, some powerful influence is brought to bear upon it, it may yield almost instantaneously-the patient may be one minute struggling for breath and the next without a trace of dyspnoea, as for example where the Asthma is suddenly arrested by some violent emotion, as fear, or where it yields to the influence of some powerful depressant, as tobacco. Unless the paroxysm has been of very short du- ration it generally leaves the patient with a sense of clogging and stillness at the chest; he feels himself more than usually incapable of exertion, and is easily wind- ed : this gradually gets less and less, and in a day or two may have completely passed away. The expectoration often continues for several days after the attack is quite gone ; at first, it occurs through- out the day, is then confined to the morn- ing, and finally ceases altogether. There is one peculiarity in the state of the asthmatic after the paroxysm that is especially worthy of remark, and that is the diminution of the asthmatic tendency that he then experiences-the almost cer- tain immunity, for the time being, from a repetition of the attack. There are many things that he dare not do at other times without the certainty of bringing on a paroxysm, that immediately after an at- tack he may do with perfect impunity. It seems as if each fit were a sort of "clearing shower," as if the tendency to fall into the asthmatic state accumulated in the intervals, and was, so to speak, discharged by the paroxysms. Certainly the fact, which we frequently see in Asth- ma, that the longer the time that has elapsed since the last attack the more particular must the asthmatic be in not exposing himself to the ordinary exciting causes of his disease, and the more sensi- tive of their influence does he become, is compatible with this idea. We see just the same thing in epilepsy. B. Such is the history of an asthmatic paroxysm. But, besides the features of a paroxysm, there are certain points in the history of the disease that deserve notice. Of these I will especially advert to three : -First, the periodicity that the disease so frequently exhibits ; secondly, the change of phase that time impresses on many cases; and thirdly, the influence which sex and age appear to exercise on the lia- bility to the disorder. 1. Periodicity.-That Asthma is mark- edly periodic no one who has watched it VARIETIES OF ASTHMA. 97 can doubt. Although in some instances there appears to be no particular interval at which the attacks are apt to occur, yet, in the majority of cases, the interval is well marked, and in many, minutely and singularly regular. This is one point, among many others, that vindicates for Asthma a place among the neuroses. But while each case preserves its own periodicity with more or less regularity, there is no particular period for Asthma itself; for, while in one case the attacks will occur regularly at the same time every night, in another they will occur once a month, in another once a year. So regular is the time of recurrence in some cases that the asthmatic knows ex- actly when to expect an attack. The periodicity of Asthma is clearly divisible into two kinds, intrinsic and extrinsic. Of the former, which is the only true essen- tial periodicity, we see examples in those cases in which the attack comes on after the same interval irrespective of external circumstances. Of the latter we see ex- amples in those cases where the regular return of the attack is simply due to the regular return of the exciting cause. The period in the last cases is almost always that of some natural interval. Thus the annual periodicity of hay fever is of this kind ; so is the monthly periodicity of hysterical Asthma, and the diurnal pe- riodicity of cases in which sleep and the recumbent posture induced the attacks. Indeed, in any case in which the perio- dicity affects some natural interval I should suspect that it was extrinsic, and dependent on the periodic recurrence of the exciting cause. Thus, in all cases in which the attack comes on every Satur- day, or every Sunday, or every Monday morning, I believe the attack is due to something having a weekly recurrence, something in which Saturday and Sunday differ from other days-a suspension of the usual employment; difference of food, or the time of taking it ; sleep after food ; the taking of supper. That the periodic- ity of such cases is not inherent or essen- tial is shown by the fact, that if the ex- citing cause is made to recur at irregular intervals the attacks become correspond- ingly irregular, and all periodicity is lost. 2. Change of Type by Time.-It is not at all uncommon to see the features of a case change considerably as time advances, and ultimately differ very much from what they were at first. And there is a certain type of change that commonly ob- tains, so that it is possible in any given case to predict what the effect of time will probably be. As a rule, the attacks are the most violent in the early history of a case, and gradually becomes less and less severe. It is very common for patients to say, " I never have those awful attacks now that I used to have, they seem to have quite left me." But while the at- tacks become milder they often become more frequent, so that a monthly periodi- city may be exchanged for a weekly, or diurnal one. At the same time, another change is generally going on-the breath- ing in the interval is getting less and less free ; certain slow organic changes are gradually being impressed on the lungs by the repetition of the attacks, by which their functional integrity is increasingly impaired; so that while at first the attacks are severe and distant, and the breathing in the interval like that of a healthy per- son, after a time the paroxysms become so slight and frequent, and the breathing so embarrassed, even at its best, that there can hardly be said to be any distinct at- tacks, and the disease has ceased to be paroxysmal. 3. Age and Sex.-It is a commonly re- ceived opinion that Asthma is a disease of advanced life. Nothing can be more erroneous. It is confined to no age ; and so far is it from being peculiarly a disease of the old, that I find a larger number of cases take their origin in the first ten years of life than in any subsequent equal period. During youth, from ten to twenty, few cases originate ; but, from that time up to fifty, the asthmatic tendency regularly in- creases. From that time forward, fewer and fewer cases take their origin. No doubt, many old people are asthmatic; but that is simply because many asthmatic people reach old age. It must be borne in mind, too, that with respect to old people the word "Asthma" is very loosely used : three-fourths of the "Asthma" of old people are due to chronic bronchitis. Men are liable to Asthma, in relation to women, in the proportion of two to one. C. Varieties of Asthma.-All cases of Asthma fall, I think, under one of two main divisions-Idiopathic or Primary, and Symptomatic or Secondary. Idio- pathic Asthma is the inherent and essen- tial form of the disease that occurs inde- pendent of and uncomplicated with any other affection. The best marked, most typical, and characteristic cases, and I may add the most severe are of this kind. In these cases we generally get consider- able intervals between the attacks, those intervals being marked by perfect freedom of breathing, and the attacks by a regu- lar periodicity. There are many points of resemblance between this variety of Asthma and epilepsy. Both of them affect the same nervous temperament, both of them are markedly periodic, and in both each paroxysm seems to act as a sort of thunderstorm, and to discharge, or work off, some particular state which consti- tutes the liability to the condition, and which accumulates in the intervals, and VOL. II.-7 ASTI1MA. 98 reaches its maximum immediately before the fit. So close a relation, indeed, exists between this form of Asthma and epilepsy, that I have seen two or three well-marked cases in which the one kind of fit took the place of the other. Most examples of Asthma in the young are of this idiopathic type. Symptomatic or Secondary Asthma may be sub-divided into three varieties- peptic, bronchitic, and cardiac-that is to say, Asthma may have its origin in stom- ach derangement, in an inflamed condi- tion of the bronchial mucous membrane, and in heart disease. Each of these varie- ties has something peculiar in itself, de- pending generally on the nature of its cause. Thus peptic Asthma is apt to come on two or three hours after taking food, may be entirely regulated by dietetic rules -brought on at any time, or kept off in- definitely at pleasure-according to what is eaten, and when. It is remarkably in- dependent of the other recognized causes of Asthma, and is (through the stomach) more amenable to treatment, and more hopeful, than any other form. Bronchitic Asthma, perhaps the commonest of all, is distinguished from all other varieties by certain well-marked characteristics. It is only caused by the causes of bronchitis, especially cold. As a rule, the patient never has Asthma without bronchitis, and never has bronchitis without Asthma, so that we generally have really a complex condition to deal with, although the bron- chitic element may sometimes be so slight as hardly to be detected. There is gene- rally in these cases an abundant expecto- ration and a good deal of cough and moist breath sounds. Such cases are often very intractable, and from this reason, that we have two diseases to treat-bronchitis and Asthma : the bronchitis is intractable be- cause it is so greatly aggravated by the Asthma, and the Asthma is intractable because its exciting cause, the bronchitis, abiding, any remedies that are brought to bear upon it are rendered inoperative or merely of transient efficacy. Indeed it so happens, that in one element of treatment, air, that which is best for the bronchitis is often worst for the Asthma, and vice versol. Thus many of these cases lose their asthmatic tendency in London, where the bronchitis alone survives; while if you send them to the Mediterranean for the cure of the bronchitis, the asthmatic tendency is so much increased, that they are worse than ever, so that they have the alternative of bronchitis at home or Asthma abroad. Being dependent on the causes of bronchitis, such cases are gene- rallyworse in the winter; indeed, in many of them, the Asthma occurs only in the winter. I think most of the cases in which Asthma occurs every morning are of the bronchitic kind, the reason being that the inflamed condition of the bronchial mu- cous membrane constitutes an ever-present exciting cause, which, in a person with the asthmatic tendency, only requires sleep and the recumbent posture in order to bring it into activity. The third va- riety, the least common of all, is Cardiac Asthma, or Asthma complicating heart cases, and depending upon the heart dis- ease. A great deal that goes by the name of Cardiac Asthma is not Asthma at all; it is simply cardiac dyspnoea, unattended with any bronchial spasm. Now and then, however, a heart case is met with in which paroxysms of true Asthma occur, attended with wheezing, prolonged expi- ration, and other characteristic signs of Asthma. In these cases, I have no doubt that the immediate exciting cause of the Asthma is the pulmonary congestion pro- duced by the heart disease. This last variety, and bronchitic Asthma, when the bronchitis has become chronic, may be classed together as "organic" Asthma ; the peptic variety and the idio- pathic, as non-organic. D. Causes of Asthma.-The causes of Asthma may be divided into two classes-those affecting the air-tubes pri- marily and directly, and those applied to some remote part. Of those that are brought to bear directly upon the air- tubes there are three kinds: first, things inhaled ; secondly, some offending con- dition of the blood; and, thirdly, an in- flamed condition of the mucous membrane of the air-tubes. There is an endless variety of mate- rials which, when respired, will produce Asthma in those possessing the asthmatic tendency, and they produce it no doubt by virtue of that morbid sensitiveness of the bronchial mucous membrane in which the Asthma in these cases essentially con- sists. Some of these materials are such as will produce a certain amount of Asthma in many people, such as the smell of a lucifer-match, pitch, smoke, pungent vapors. Some are rendered asth- matic by dust, some by fog and damp. Particular smells will at once bring on Asthma in some people, such as that of flowers-roses, for example, and privet. The commonest vegetable emanation hav- ing this effect is hay-this form of Asthma being well known as Hay Asthma, and a part of that curious disease, Hay Fever. In some people animal emanations have a similar effect: some are at once ren- dered asthmatic by the presence of a cat, some cannot go near a stable, or even ride behind a horse, or go near those who have been riding; some the effluvium of rabbits renders asthmatic ; some, guinea- pigs ; some cannot go near a poulterer's shop where there are hareskins; some have their Asthma brought on immedi- DIAGNOSIS OF ASTHMA. 99 ately if they go to a menagerie ; and some suffer immediately if a dog comes near them. A more subtle influence is that arising from change of weather, or par- ticular winds, some persons being ren- dered at once asthmatic by an easterly wind. A more subtle influence still is that arising from locality. Almost all asthmatics are influenced to a certain de- gree by the air they breathe, but to many it is the one thing that regulates their Asthma. Some are best in a dry air, some in a moist, some high, some low, some inland, some by the seaside. In some there is only one place that will ren- der them asthmatic, in others there is only one place at which they are free from Asthma; in some the peculiar character of air that offends is well known; in some it is utterly inscrutable. In some so slight is the peculiarity of air that will determine the supervention of Asthma, that they may be perfectly well in the front of the house, but cannot sleep at the back. As a rule, a dry air is worse for Asthma than a rather moist one, the air of a high locality than a low. Yet the most constant circumstance noticed in respect to air, is the superiority of urban air over that of the country. So common an incident is this, that it becomes an im- portant element in treatment-many a case of Asthma is at once cured by living in a dense quarter of some smoky and crowded city. The cases in which I am inclined to think Asthma is brought on by an offend- ing condition of blood, are cases in which it is apt to come on a little time after the ingestion of certain articles of diet. Cases in which people are asthmatic about two hours after a meal (a very common cir- cumstance) are of this kind. In some only certain articles of diet will give rise to the Asthma, as wine, beer, sweets ; in some only what upsets the digestion ; in some any food whatever. My reason for thinking that it is the condition of the blood circulating in the respiratory organs after the absorption of these ingesta, that produces the bronchial spasm, and not the irritation caused by the presence of food in the stomach acting on the gastric periphery of the pneumogastric nerve, is the time at which the Asthma comes on. If it were the presence of the food in the stomach that caused the Asthma the symptoms would appear immediately on taking it, whereas it is not until a couple of hours afterwards, at about the time when the results of digestion are enter- ing the circulation, that the difficulty of breathing comes on. Moreover, the rapid- ity with which the Asthma will super- vene varies as the rapidity with which the ingesta are absorbed; thus, after wine, which is rapidly taken up, the Asthma will quickly make its appearance. Inflammation of the bronchial mucous membrane is one of the commonest cauess of Asthma, perhaps the commonest of all, especially in people in advanced life. Such cases are really complex cases, being bronchitic as well as asthmatic ; indeed the bronchitic may be said to be the fun- damental and essential part of them, and their essential treatment is the treatment of the bronchitis. Take care of that and the Asthma will take care of itself. The only difference between such cases and cases of ordinary bronchitis, is that the bronchitis happens to occur in individuals in whom bronchial spasm is easily in- duced. The immediate excitants of the asth- matic paroxysm to which I have already referred are such as act directly on the bronchial tubes ; but there are some that produce bronchial spasm by application to some remote part. Such causes always act, I believe, through the nervous sys- tem ; and they may either act through the organic nerves or the ccrebro-spinal. We see an example of the former in cases where Asthma is at once produced by a loaded stomach, or a loaded rectum: of the latter, where Asthma is at once pro- duced by cold feet, &c. In both these classes of cases the exciting cans* is ap- plied to the periphery of the nerves on which it acts ; but this need not be the case, for sometimes, the irritant is applied to a nervous centre. Asthma, for ex- ample, has been known to be produced by organic disease of the brain; and that very common occurrence, the production of Asthma by violent emotion, is another example of the same thing ; only here the irritant applied to the centre is psychical and not physical. In speaking of the causes of Asthma I must not omit to mention those which lay the foundation of the asthmatic tendency. Perhaps the largest group of causes of this kind are conditions affecting the vascu- larity of the bronchial tubes, such as measles, hooping-cough, bronchitis. In many cases the sole predisposing cause appears to be some inherited peculiarity. E. Diagnosis of Asthma.-It is of the utmost importance to be able to recog- nize Asthma with certainty, because there are several diseases with which it might be, and often is, confounded, and, because the treatment of these diseases and of Asthma is of the most opposite kind. The three forms of dyspnoea with which Asthma is apt to be confounded, are bron- chitis, emphysema, and heart disease. From bronchitis, Asthma may be distin- guished by its sudden access, and often equally sudden departure, by the absence of cold as a necessary cause, and frequently by the absence of expectoration and of moist sounds. Moreover, when expec- 100 ASTHMA. toration does occur, it is of a different kind; in bronchitis it is often purulent, in pure Asthma never. Again, the action of remedies distinguishes the two dys- pnoeas: the intensest asthmatic dyspnoea will often suddenly, almost instantaneous- ly, yield to certain remedies; in bronchitis this is not the case ; if the dyspnoea is se- vere, so as to be at all commensurate with Asthma, it always takes some time to subside. From emphysema, Asthma may be dis- tinguished by the paroxysmal character of the dyspnoea, by its violence, and by the absence of any dyspnoea whatever in the intervals. In emphysema, the cause of the difficulty of breathing is organic and unchanging, and, therefore, dyspnoea is never completely absent, and varies in amount only in proportion to the degree to which respiration is taxed. The pres- ence or absence of the physical signs of emphysema will also, of course, materially aid the diagnosis. The dyspnoea that Asthma is the most apt to be confounded with, and which it most resembles, is that of heart disease. The two resemble one another in that they arc both paroxysmal, both intense, both apt to occur at night, both compati- ble with organic soundness of lung, and both intolerant, though not exactly in the same way, of the recumbent position, of exertion, and of sleep ; moreover, in both of them the respiration may be perfectly normal between the attacks. It is not wonderful, therefore, that with so many points of resemblance, the two should some- times be confounded. There is, however, no real difficulty in distinguishing them. In cardiac dyspnoea there is generally an absence of the characteristic signs of nar- rowing of the bronchial tubes, universally present in Asthma, such as wheezing, prolonged expiration, suppression of respi- ratory murmur, &c. The length of the attacks, too, is different, the asthmatic paroxysm being commonly longer than the time reached by an attack of cardiac dyspnoea. ) F. Prognosis of Asthma.-This va- ries greatly in different cases, in some being unqualifiedly favorable, in some unqualifiedly unfavorable, and in some doubtful; it is principally influenced by the following considerations :- 1. The presence or absence of an organic cause.-If the Asthma is manifestly de- pen^ent on some organic cause, in its na- ture irremediable and irremovable, it is manifest that the resulting Asthma must be itself incurable. If, for example, it depends upon inveterate bronchitis it is clear that all treatment can be merely palliative, and that a final cessation of the Asthma can never be expected. If, on the other hand, the circulatory and respi- ratory organs are found to be perfectly sound, then, quoad this circumstance, the prognosis is favorable ; for, though the absence of organic disease does not make the final cessation of the Asthma certain, it makes it possible ; in other words, the absence of organic disease makes the prognosis negatively favorable though not positively so. 2. Age has great sway in influencing the prognosis of Asthma; the younger the individual the more probable is ulti- mate recovery : an asthmatic child of ten will probably lose his Asthma, an asth- matic man of forty will probably not; an asthmatic man of sixty you may say, will certainly not ; in an asthmatic youth of twenty it would be difficult to say, as far as the circumstance of age goes, on which side the probabilities would lead. The reason for this fact appears to be, that Asthma has much more commonly an or- ganic basis in advanced life than in early life, that the tendency of Asthma to lay the foundation of organic change is much greater in advanced life than in early life, that the loss of a constitutional peculiarity is much less probable in advanced life than in early life. 3. The frequency and severity of the at- tacks very much influence the prognosis ; for, if the attacks are very severe and very frequent, the lungs are unable to re- cover in the intervals from the injuries inflicted by the attacks, and certain or- ganic changes are probably and speedily induced. If, on the other hand, the at- tacks are light, and the intervals between them long, the lungs are able perfectly to recover from the temporary derangement produced in them by the paroxysms ; and such a case may go on for an indefinite time without the development of any or- ganic changes. 4. The state of the patient in the inter- vals is of great importance in influencing our views as to prognosis. If the lungs and heart appear to be anatomically and functionally sound, if the breathing is perfectly natural and free, and there is no wheezing, cough, or expectoration in the intervals, the prognosis is infinitely more favorable than if the reverse is the case. Persistent difficulty of breathing in the intervals of the attacks is a very bad prognostic sign ; indeed, I think the state of the respiration in the intervals of the attacks is of more importance than either their frequency or severity. 5. Lastly, the history of the case often greatly influences our prognosis, because the past often implies the future; if we find that the tendency of the case-the direction it appears tor be taking-is to- wards an alleviation of the symptoms, the attacks becoming lighter or less fre- quent, or in any way mitigated, we have strong warrant for a favorable prognosis ; PATHOLOGY OF ASTHMA. 101 if, on '.he other hand, the attacks have been becoming more frequent, more easily in- duced, more violent, or protracted, or in any way aggravated, then a favorable issue becomes exceedingly improbable. G. Pathology of Asthma. - Our views respecting this must be greatly in- fluenced by our views of the immediate condition in Asthma. My belief is that the immediate and essential condition of the asthmatic paroxysm is a state of con- traction of the bronchial tubes. What proof have we of this ? In the first place, the sudden induction and remission of the asthmatic paroxysm is consistent with its depending on muscular spasm; in the second place, there is abundant proof that the air in the lungs is locked up, and can neither be got in nor out: there is evi- dently plenty of air in the chest, percus- sion is even hyper-resonant; the patient is as unable to drive air out as to draw it in, can neither inspire nor expire, cannot discharge breath enough to whistle or blow out a candle, or blow his nose. The muscles of respiration tug and labor to fill and empty the chest, but the chest walls remain almost immovable: the inspira- tory muscles cannot raise them, the ex- piratory cannot depress them. On listen- ing to the chest we find corroborative evidence of the stagnation of the air. The respiratory murmur is in a great degree lost. This absence of respiratory sound, accompanied by violent respiratory effort, is one of the most striking and suggestive of the facts of Asthma. How can we explain it, except by supposing that there is some bar to the ingress and egress of air; and what can this bar be, unless it is spasm of the bronchial tubes ? It can- not be inflammatory thickening of the mucous membrane lining them ; for the sudden, almost instantaneous, establish- ment and remission of the dyspnoea is in- compatible with this. It cannot be mu- cous plugging of the tubes ; for the attack will often come and go without any ex- pectoration whatever. But we have still more positive and precise evidence of cir- cumscribed narrowing of the air-tubes in the musical sounds that are present in asthmatic breathing. This symptom has all the certainty and precision that char- acterize physical phenomena, and shows that the air-tubes are the seat of constric- tions that throw the air passing through them into vibrations, and convert them into musical instruments ; and since these musical sounds are multitudinous the points of constriction must be many ; and since they are constantly varying in local- ity and character, the constrictions of the tubes must be undergoing similar change. Lastly, the effects of remedies and their nature tell the same tale, and point to muscular spasm as the immediate essen- tial condition. The most powerful reme- dies of Asthma are what are called cere- bro-spinal depressants, such as emetics, tobacco, &c.-remedies whose direct effect is to relax muscular spasm. If, then, the immediate condition is muscular spasm, the presumption is, that the primary and essential condition is an affection of the nervous system; with very few exceptions we may lay it down as a rule that perturbed muscular action points not to the muscular system, but to the nervous. What proof have we, then, that the nervous system is involved in Asthma? Some of the most striking proofs of this are derived from the nature of the causes of Asthma ; and many of these not only show that the nervous system is the real seat of the morbid action, but they show also what portion of the nervous system is involved. The most numerous of the causes of Asthma are what may be called respired irritants, noxious materials of whatever nature contained in the inspired air. It is manifest that these can only be appreciated by the perceptive nerves dis- tributed to the bronchial mucous mem- brane, and that they can only give rise to bronchial spasm by the irritation which they produce being propagated to the bronchial ganglia, and by them reflected to the motor filaments distributed to the muscular wall of the bronchial tubes. This, then, is the nervous circuit involved in these cases-extremely short, but still a distinct nervous circuit. In other cases an undigested meal will produce Asthma ; here the nervous circuit is longer, and in- volves the gastric branches of the vagus as its afferent portion, and the pulmonary as its efferent. In other cases a loaded rectum, or uterine irritation, may be the cause of the paroxysm; here the circuit is still longer. In other cases, the sud- den application of cold to the surface may at once induce bronchial spasm ; here the circuit involves the cerebro-spinal as well as the ganglionic system of nerves. In other cases, some sudden emotion may at once throw the patient into a paroxysm of Asthma ; here there is no true circuit, no reflection, but the stimulus is propagated direct from the centre to the periphery. There are other circumstances that point equally clearly to the nervous nature of Asthma. The action of many remedies is not explicable on any other hypothesis. For example, emotion will not only cause Asthma, but it will cure it, and in the most sudden and complete way. Nervous stimulants, such as coffee, strong forms of alcohol, &c., are very powerful remedies ; and nervous sedatives, such as stramo- nium, are among the best known and most efficient of our means of relief. The view that the nervous system is essentially engaged in the asthmatic state, does not negative the fact that the foun- 102 ASTHMA. dation of Asthma may be laid, and the asthmatic tendency determined, by some- thing organically affecting the respiratory organs. All who are familiar with Asthma must have observed that it frequently takes its origin in childhood from measles, or hooping-cough, or bronchitis. Now, these are diseases disturbing the vascular condition of the bronchial mucous mem- brane ; but a morbidly vascular mucous membrane is a morbidly sensitive mucous membrane, and, therefore, a mucous mem- brane whose irritation is likely to produce, through the nerves supplied to it, spasm of the muscular wall of the tube which it lines, just as we see spasmodic stricture of the urethra apt to occur in gonorrhoea. H. Treatment of Asthma.-There are two things that the physician has to do-two problems suggested to him-in the treatment of any case of Asthma: one is to relieve the attacks when they occur, and the other is to prevent their occur- rence ; in other words, one is the treat- ment of the paroxysm, and the other the treatment of the disease. Of these two the latter alone deserves the name of cura- tive treatment, the former is merely pal- liative. I shall first consider the treat- ment of the paroxysms. On being summoned to a patient in an asthmatic paroxysm, the first thing that the physician has to do, is to remove any exciting cause, and to place the patient in the most favorable condition. If an offending meal or some error in diet ap- pears to be the exciting cause, an emetic should be at once given ; if a loaded rec- tum, a purgative should be administered, &c. ; if smoke or dust, or any vegetable or animal emanation, is the cause of the attack, this cause should be immediately removed; free ventilation should be se- cured, and the crowding and officious ministrations of friends should be forbid- den. The sufferer should not be made to speak; everything should be done for him, and done without the necessity of his requesting it. The position in which he is placed will make a great difference to him, not only to his comfort, but to the abatement of his symptoms. The best position to put the asthmatic in, as a rule, is sitting in a chair and leaning for- ward on something in front of him, so as to raise his shoulders. Sometimes he ■will find leaning on something in a stand- ing posture the easiest position; but, generally, standing involves too much exertion. Sitting at a table and leaning forward so as to rest the elbows on it, or resting the elbows on the arras of an arm- chair, or kneeling up in bed, or kneeling on the floor and resting the elbows on the side of the bed or a chair, are positions that give the greatest relief. I have known one patient who elevated the shoulders by placing under them two short crutches which rested on the side of her chair. The great object is, in some way or other, to raise the shoulders, and the advantage of doing so by these me- chanical means is that it saves the mus- cles the labor and fatigue of so doing. The reason why it is necessary that the shoulders be in some way raised, is that the inspiratory muscles passing from the shoulders down to the chest wall may act with greater power as elevators of the ribs. Having then placed his patient under the most favorable circumstances for the abatement of the spasm, the physician has next to select the remedies that he will employ. This selection is very much influenced by the patient's experience. From the constitutional nature of Asth- ma, and its persistent character, it is rare to see a patient in his first attack. The great majority of asthmatics that one sees are habitual sufferers from their disease, and have generally some knowledge, often a very accurate one, of the remedies that best suit their case. But in this there is the greatest variety, and the experience of one person would be no guide to the treatment of another. Indeed, the beha- vior of Asthma to remedies is marked by the most extraordinary uncertainty and caprice ; that which is the most valuable in one case is inert in another; in some there are many things that will give re- lief,-the only question being which is the quickest and the most complete ; in other ca^es all remedies are alike powerless. The remedies of the asthmatic parox- ysm may, I think, be divided into three classes :-Direct Depressants, Sedatives, and Stimulants. Depressants.-I have already spoken of the value of emetics for the purpose of evacuating the stomach of unwholesome or undigested contents. No doubt, in this way, by the removal of an exciting cause, the paroxysm may often be re- lieved. But emetics also relieve Asthma very efficiently as depressants, quite independently of their emetic action. I maybe asked, "How do I know that it is as depressants, and not as evacuants of the stomach, that emetics give relief?" For two reasons : first, because they will give the same relief when the patient has an empty stomach ; and secondly, because the relief comes on when the first sense of nausea is experienced, and before any vomiting has taken place ; in a moment, at the first sensation of faint sickness which gives warning of the approach of vomiting, the spasm will suddenly yield, and the patient pass into a state of tran- quillity and ease. If this condition could be produced and kept up without giving rise to vomiting I think it would be just as well for the asthmatic, provided that TREATMENT OF ASTHMA. 103 vhe paroxysm was not kept up by a loaded stomach. The emetic that I have most commonly given is ipecacuanha powder, in twenty-grain doses ; it generally acts in a quarter of an hour; a tumbler of warm water should be taken before its first action and after each act of vomiting. I have lately thought the ipecacuanha wine preferable to the powder, from its action being sooner over ; the powder, I think, sometimes sticks to the surface of the stomach, and keeps up a teasing and lingering retching. With a view to pro- duce nausea, short of vomiting, I some- times give ipecacuanha lozenges, directing the patient to take one at short intervals till a slight sense of nausea is experienced, and to return to the lozenges as soon as this passes off: this plan is often quite successful. Tobacco.-As this is one of the most powerful depressants, so it is one of the most powerful remedies in Asthma. In those unaccustomed to its use, and in whom, therefore, its full physiological effects are most developed, it is almost impossible for the asthmatic paroxysm to resist it. If I were asked to name a remedy on which I should place the greatest reliance in subduing the most obstinate asthmatic spasm, I should say tobacco in those unaccustomed to it. I believe that the death-like collapse that it produces is something before which Asth- ma must go down. From this potency it is in obstinate cases a most valuable remedy, but it has three disadvantages: in the first place, it is peculiarly distress- ing-the sensation that it produces is as near like the worst form of sea-sickness as possible, perhaps a little worse ; in the second place, it sometimes produces alarming, if not dangerous symptoms; and in the third place, it is in a large class of asthmatic patients, adult males, inoperative in consequence of its habitual use. It should always be given with great care, and tentatively, especially to those who have never before tried it; and the mildest forms should be chosen. Like ipecacuanha, tobacco relieves Asthma in- dependently of the vomiting it may pro- duce. By careful management and expe- rience, smoking may be carried just far enough to give rise to a sense of faintness and slight nausea, without its passing on to vomiting at all. Another remedy, very efficacious, very commonly used, and very like tobacco in its action, is the Lobelia inflata. I find that different authorities have a very dif- ferent estimate of the value of this remedy; and I myself am conscious that I have a much higher opinion of it than I had some years ago. The fact is, I now give it in a way that I believe tests its power much more fairly than the ordinary way in which it is administered; this is the plan recommended by Dr. Elliotson, of giving it in gradually increasing doses at short intervals, till its physiological effects are manifested. I generally start with twenty minims of the ethereal tincture, and tell the patient to repeat the dose every half-hour, making it five minims larger each time, till some slight nausea and feeling of faintness is experienced. By this plain the efficacy of the drug is fairly tested ; by the ordinary plan of giv- ing the patient fifteen or twenty drops every three or four hours, its value is not tested. I have on many occasions known as much as forty or fifty drops reached before any feeling of nausea was produced, and before the Asthma was relieved ; but with the nausea came the relief. I should never feel the slightest confidence that Lobelia was valueless as a remedy, in any given case in which it had been adminis- tered in the ordinary way. I have many times, by changing the method of its ad- ministration, obliged patients to reverse their verdict of it. When a patient has found out his maximum dose, I advise him on the next occasion to start with that dose ; it saves him the trouble and loss of time of gradually working up to it. Sedatives.-The relief obtained in Asth- ma from this class of remedies, no doubt depends on their rendering the nervous system less irritable and less susceptible to sources of disturbance, and the pres- ence of sources of irritation less likely, therefore, to issue in the production of spasm. Some of them appear to act lo- cally, on the nervous system of the lungs alone, but most of them on the general nervous system. Those that experience has shown to have the most value in Asthma, are: tobacco, in sedative doses, stramonium, datura tatula, belladonna, conium, hyoscyamus, ether, and chloro- form ; and lastly, the fumes of burning nitre paper may be mentioned in the same category. Tobacco, smoked in the ordinary way, is certainly of great service to many asth- matics. By its habitual use, they keep themselves much freer from attacks than they are without it, and are constantly able to check the asthmatic tendency when it shows itself. If at any time a little wheezy they resort to their pipe or cigar, and soon experience its soothing effects ; the breathing quiets down and becomes clear, and they are soon them- selves again. Many asthmatics have told me that they are sure that, if they left off smoking, their asthma would soon be- come troublesome; and that, as long as they smoked, they may do many things with impunity that, without their tobac- co, would be sure to bring on their symp- toms. But, while very useful in this way, I do not think that it is equal to the sub- ASTHMA. 104 duing of a severe attack, unless pushed to what may be called a poison dose ; and then it ceases to be a sedative and be- comes a depressant. The two species of datura-the D. stra- monium and the D. tatula-certainly de- serve a very high place among the reme- dies of Asthma : they are however of very variable efficacy in different cases; and that is the probable reason why different observers entertain such different opinions of their value ; some thinking very iiighly of them and some regarding them as next to worthless. I find, in my own prac- tice, that in the majority of cases they do some good, and in many are the one sov- ereign remedy. I have had some cases that I may say have been completely cured by them, and others in which, though they have not effected a final cure, the disease has, under their continual use lost all its horrors. It does not, however, do to speak of them together as if their ope- ration was always alike. In most cases they differ in their effects; in some, one being the most powerful, in some the other. In some cases one will be com- pletely successful, while the other is per- fectly inert. Seeing that they not only belong to the same class of remedies, but are merely different species of the same genus, this diversity of their action is very extraordinary. Of the two, I think the tatula is the more powerful. I have, however, met with many cases in which it has been powerless where the stramo- nium has always given relief. They may be given in two ways-either by smoking the leaves in a pipe or cigar, or else inter- nally as tincture, or extract; though I doubt if in these two ways exactly the same agent is given. I doubt whether the combustion in smoking does not pro- duce something that did not before exist, as in the case of tobacco-smoking. Nev- ertheless it is certain that in both ways the daturas are of value. When smoked they are best used with one of two objects, or both-either habitually, at stated in- tervals-say night and morning-with a view of keeping off the attacks and mak- ing them less likely to come on ; or hav- ing them always in readiness to fly to on the least approach of an attack, so as to ■check it at once and prevent its develop- ment. This latter plan often answers very well. The patient fills his pipe and puts it by the side of his bed over-night, with the means of lighting it, and when he wakes towards morning with the first traces of his Asthma upon him, he at once lights it and smokes away, the dyspnoea ■subsiding with each whiff that he draws ; so that in a few minutes he is able to put it out, and lie down and go to sleep again. This is the story of many asthmatics, and they would rather not' go to bed at. all. than do so without their stramonium by their side. Internally I often give, something with advantage, the extract of stramonium in a pill. I give it in a quar- ter of a grain dose generally, combined with an eighth of a grain of belladonna, and two or three grains of extract of co- nium. This pill, taken at bedtime, has sometimes the effect of preventing the de- velopment of the attack during the night; it guards the patient through the critical time, and tides him over it. But I must say that I think stramonium taken inter- nally has not that general utility that it has when smoked, and I have known it quite useless in patients, who, when they have smoked it, have found it very effica- cious. Conium and hyoscyamus are sedatives that doubtless have some value in Asth- ma, and are very commonly employed; but, in the majority of cases, the relief they give is but slight and temporary, and they are not remedies on which re- liance can be placed. I think I have seen them most efficacious when given in com- bination, in the form of tincture, with chloric ether. Of belladonna I have made an extensive trial since this article was first written, and I am satisfied of its great value in many cases. In not a few its employment has resulted in a complete and apparently permanent cure. I gen- erally give it in the form of the tincture at bed-time, increasing the dose each night, until the asthmatic tendency ceases to show itself, or until, without such re- sult, the physiological effects of the drug are well marked. [Iluchard, after care- ful experimentation,1 asserts that the most intense paroxysms of Asthma may be promptly relieved by hypodermic in- jections of morphia. lie describes the influence of this remedy, also observed in other forms of dyspnoea, in the following words: "Morphia makes one breathe freely."-II.] Chloroform.-There is, perhaps, no dis- ease in which the wonderful power of chloroform is more shown than in Asth- ma. I have never seen a spasm that it failed to subdue. The worst of it is that its operation is often evanescent;-as soon as its physiological effects pass off, its remedial effects disappear too. This, however, is by no means always the case, the cure frequently remaining permanent after the stupefying effects of the agent have quite passed off. And even where the Asthma does return, it is no slight thing to be able to suspend its horrors for a time, and to give the sufferer a short respite. It has certain disadvantages that would induce me not to place it among the first remedies that I would try, but to keep it rather as a last resort [' London Medical Record, March 15, 1879.] TREATMENT OF ASTHMA. 105 when everything else has failed:-in the first place, it is, as we know, not entirely devoid of danger; in the second place, it is often not safe to trust it in the patient's hands or those of his friends, and, there- fore, can only be used in the presence of the medical attendant; in the third place, its habitual use is very apt to generate a liking for it, and to pass into a kind of dram-taking. I have seen two or three painful cases of this kind that make me always unwilling to begin its use, just as I am unwilling to begin the habitual use of opium in any chronic malady. Tn those rare cases in which Asthma never comes on during sleep it is of great value as in- ducing sleep. I have known ten drops in this way cure an attack and give the patient a good night, simply by just put- ting her off to sleep. I do not think that any amount of asthmatic dyspnoea is any reason against giving it, or constitutes in any degree an element of danger-sup- posing, that is, that the Asthma is pure, and that the dyspnoea is neither cardiac nor bronchitic. In either of these cases the dyspnoea, being organic and not of a nature which the chloroform would re- move, would constitute a serious embar- rassment: whereas the asthmatic dys- pnoea would cease to exist, and therefore cease to be any source of danger, in just such proportion as the intluence of the chloroform was established. Nitre Paper.-This is, perhaps, now one of the best-known and best-established remedies of Asthma, as it is one of the most uniformly successful. So generally is it efficacious, that it is always a matter of surprise to me when an asthmatic tells me that it does him no good. I am not certain of the category in which I ought to place it, and I class it among sedatives, and am inclined to think that it acts as one, chiefly on account of the strong so- porific influence that it exercises. It affects not only the patient in this way but the bystanders. On the very day that I am writing this, a lady has com- plained to me that she finds it almost im- possible to administer the nitre fumes to her husband, on account of the irresisti- ble sleepiness with which it overwhelms her; and I have mentioned in my work on Asthma the case of a lady who burnt the paper every night of her life in bed, but always had to wake her husband up, as soon as the fumes had relieved her breathing, because they made her so help- lessly drowsy that she feared she might fall back while the paper was still burn- ing, and set the bed on fire; she always did fall back asleep before the process was over, and her husband always had to take charge of the embers. What are the exact products of the burning of nitre paper I do not know, nor of those products what may be the remedial one, or ones. This is a subject that still waits investigation. The papers may be made by the patient (by dipping ordinary blotting-paper, white or red, into a warm saturate solution of saltpetre), or bought at any. chemist's. The papers should be kept in a dry place, so as always to be fit for use. When em- ployed, a piece about six or eight inches square should be torn off and lit at one corner. As the ignition fizzes along the edge of the paper, white fumes arise which are to be inhaled. I do not think it ne- cessary or advantageous that the actual smoke itself should be drawn into the chest, but the air in its immediate neigh- borhood which is impregnated with it. It is a good plan to burn the paper in a small room, or confined space, so as to get the air thoroughly charged with the fumes: a cupboard, or closet, or four-post bed, with the curtains close drawn, an- swers very well; I have seen a patient make use of a large carriage umbrella for this purpose. There are two ways in which the paper may be advantageously used :-one habitually at stated periods, as a preventive, as, for example, every night and morning; and the other when the Asthma shows itself, with a view to its immediate relief By using it in the former way, patients may often prevent the development of any attack for a long period. For example, many persons burn the paper every night in their bedroom on going to bed, and retire to rest with confidence and with the certainty of im- munity through the night; whereas, if they go to sleep without first impregnat- ing the air of their bedrooms with the nitre fumes, they are as certain to be dis- turbed with their Asthma. Others, with a view to its use in the latter way, always carry some nitre papers about with them wherever they go, and if their asthmatic symptoms appear burn a piece, and in a few minutes are relieved. Such pa- tients never go to bed at night without having some of the paper by their bed- side, that, if their Asthma disturbs them at night, they may immediately resort to their remedy. So rapid are its effects often in these cases, so complete is the relief, and so drowsy do the combined ef- fects of the previous dyspnoea and the nitre paper render the patients, that they have not time, as I have already men- tioned, to put the still burning paper in a place of safety before they fall back asleep. Stimulants.-This is a class of remedies whose action is very different from, one may almost say opposite to, the action of those I have just mentioned, but which nevertheless exercise a most powerful in- fluence over the asthmatic state. Among these, coffee is perhaps the best known, and the most generally efficacious. I find, in the majority of cases of Asthma 106 ASTHMA. that come before me, that coffee has been tried, and that it has given relief. It should be made as strong as possible, cafe noir, taken as hot as it can be swallowed, without either milk or sugar. It should also always be taken upon an empty stomach; coffee taken with food not only does no good, but does positive harm, by impeding the process of digestion. 1 have known more than one case, as I have mentioned elsewhere, in which coffee made in the ordinary way, and taken im- mediately after dinner, had a strong ten- dency to induce Asthma, although, taken in the way I have above described, it had a very powerful beneficial influence. Alcohol, in its various forms, is another remedy of this class, that my experience during the last few years has induced me to think highly of as a remedy for Asth- ma. In many cases it does not do much good, but in some it has a most powerful effect, and these I have noticed are fre- quently cases in which all other remedies have failed. In such cases I should cer- tainly, if for this last reason alone, recom- mend its use; in any case where other remedies answered I do not think I should, on account of the many manifest objections there are to the habitual use of the stronger forms of alcohol. I have ob- served that it seems of little use unless given hot and strong-about half spirit and half boiling water; this circumstance seems to make more difference than the kind of spirit, or the actual quantity taken. Some asthmatics prefer brandy, some whisky, some gin ; but in all, how- ever small the quantity of spirit taken, it must be hot and concentrated. The worst of this remedy is that it is so apt to be- come habitual, and to require to be given in larger and larger doses. While speaking of stimulants, I think I ought to mention the curious and striking remedial effect that sudden emotion has in Asthma. There is nothing that sus- pends the asthmatic state so completely and so immediately. At once, without any gradual subsidence, the patient will pass from the most violent paroxysm to a state of perfectly free and unimpeded breathing. And this is the case not only in emotional temperaments, but in all kinds of people, of both sexes, and at all ages. The emotion may be pleasurable or painful, but it must be intense, and I think it acts more powerfully if it is sud- den. Did the length of this paper permit, I might relate some very curious and in- teresting cases in illustration of this point, but I must content myself with merely mentioning the fact. And surely, if it were w'anted we could not have a more striking or convincing proof of the nervous nature of Asthma; I should myself want nothing more to establish this theory of the disease than this single therapeutical fact. I have hitherto been speaking exclu- sively of the treatment of the paroxysms. But a very important part of the treat- ment of Asthma, indeed the only radical treatment of the disease, is the treatment in the intervals-that which is directed to the prevention of the attacks altogether. This is the only treatment that deserves the name of curative ; the treatment of the paroxysms is but palliative. There are, I think, three forms of treat- ment that have for their object this final cure of the disease by the prevention of the paroxysms. The first, the treatment by air-that is, by locality ; the second, dietetic treatment and the regulation of the digestive organs; and the third, treat- ment by the avoidance of the excitants of Asthma, such as hay, animal emanations, &c. These different plans of treatment are applicable to different classes of cases; but if we examine them closely we shall see that they all really belong to one kind of treatment, that they all essentially consist in the avoidance of the provoca- tives of the attacks ; their applicability depending upon what, in each particular case, is the special exciting cause. Treatment by Air.-It has long been known to those who have either observed or experienced Asthma, that locality ex- ercises a most remarkable control over the disease-that there are certain airs in which the asthmatic cannot breathe, and that there are certain other airs in which he enjoys a sure immunity from his mal- ady ; that, in fact, his being an asthmatic or not depends entirely on where he lives: if he lives in the one place, he is constantly suffering, but he might live twenty years in the other and never have an asthmatic sensation. There are some circumstances with regard to this curious fact that are constant, and worthy of note. In the first place, the effect is immediate; let the asthmatic be suffering ever so severely, he no sooner arrives at the air that, in his case, is curative, than he is at once relieved. In the second place, the effect is invariable for each particular case; there is nothing irregular or haphazard about it; the same thing may be repeated twenty times, and always with the same result; so much is this the case that the asthmatic knows he may calculate on it with the greatest safety. I have men- tioned elsewhere the case of a gentleman who, let him be suffering ever so much at Cambridge, would accept an invitation to a dinner party in London, knowing that as soon as he arrived in town he would be well. And this may go on for a life- time, and is as noticeable in the produc- tion as in the cure of Asthma. A person may have an attack of Asthma on going to a particular place; twenty years after he may revisit that place, and he will again be attacked. Again, the effect is PHTHISIS PULMONALIS: DEFINITION. 107 permanent; as long as the patient resides in the curative air, he is free from his disease, if it is for the rest of his lifetime, but only so long as he resides there ; for the remedy does not eradicate the asth- matic tendency; the patient has only to be exposed to the same influences as be- fore to have all his old symptoms return upon him in their original force, and that after any lapse of time during which they have been suspended. Another noticeable point in most cases is the inscrutable cha- racter of the atmospheric peculiarity on which this influence depends, and very often its extreme slightness: the fact only is known that in such an air the Asthma never appears; but what is the peculiar character of that air, or in what respect it differs from another in which the pa- tient cannot breathe, neither the asthmat- ic, nor his friends, nor his medical advisers, can even guess. But while the effect of locality is con- stant for each particular case, the expe- rience of one case is not the slightest guide for another ; on the contrary, there is the utmost diversity and contrariety with regard to this circumstance in differ- ent cases. The air that is a certain cure to one is death to another. One patient is best in the country, one in town ; one is best in an elevated position, one in a low one ; one is relieved by a relaxing air, one by a bracing ; one is best at the sea- side, one inland. But though there is this uncertainty and irregularity, yet on the whole, on the average, there are cer- tain rules as to what is curative. Thus, in the great majority of cases, an urban air is the air that cures, and of a city air that seems to be the best which is the most urban-the densest and smokiest. As a rule the air of a low situation is better than that of a high one, and a re- laxing air than one that is bracing. In some cases there is one place, and only one where the Asthma manifests itself. In such cases the circumstance has gene- rally been discovered by accident-the asthmatic has suddenly been seized, soon after his arrival at some place that he never visited before, with strange and alarming symptoms which have turned out to be Asthma. These symptoms may never again appear except on a return to the same locality. It is, however, much commoner for there to be many places where the Asthma is apt to occur, and only one, or but few in which the asthmatic tendency seems to be in abeyance. Treatment by food is the sovereign and final treatment of all those cases in which the Asthma is produced, and only pro- duced through the stomach. There are many cases in which a late dinner, or a supper, is sure to bring on an attack, but in which nothing else will. In such cases the patient has only to abstain from food after an early dinner, and he will see no more of his Asthma for such time as he keeps up such abstention, if it is for the term of his natural life. Such a person may cease to be an asthmatic at pleasure -that is, he ceases to be an asthmatic in esse, not in posse; for immunity so obtained does not destroy the asthmatic tendency: let him at any time break through his rules and his Asthma will immediately reappear. Treatment by the avoidance of special pro- vocatives is, as I have already mentioned, but the application to other cases of the same principle as the treatment of peptic cases by dietetic rules. Some patients always have Asthma brought on by hay, some by the smell of flowers, some by emanations from particular animals, such as cats, or dogs, or horses. Such persons have merely to keep themselves out of reach of the especial exciting causes, and they may elude their disease for any length of time. The radical treatment of bron- chitic Asthma belongs to the same cate- gory, and consists essentially in the treat- ment of the bronchitis. Place such a patient under such circumstances as pre- clude the bronchitis, and with the cause you preclude the result; send such a case to Australia, and there is an end of his Asthma, because there is an end of his bronchitis. PHTHISIS PULMONALIS. John Hughes Bennett, M.D., F.R.S.E. Definition.--By the term Phthisis or Consumption (from to waste or consume) has been understood from the earliest times a disease characterized by wasting or emaciation of the body. The cultivation of morbid anatomy having determined that this condition was fre- quently dependent upon the deposition of 108 PHTHISIS PULMONALIS. little grains or nodules of a peculiar sub- stance in the lungs, these received the name of tubercles. Thus the terms tu- bercle, tubercular disease, or tuberculosis, gradually came to be regarded as synony- mous with Phthisis, which may now be said to comprehend all kinds of disease essentially connected with or dependent upon pulmonary tubercle. It is this important morbid condition which we propose to describe in the pres- ent article, under the general heads of Pathology, Symptoms, Diagnosis, Prog- nosis, and Treatment. I. Pathology of Tubercular Phthisis. The pathology of Phthisis involves a consideration of the histology, chemistry, and general pathology of tubercle-of the morbid anatomy of the disease-of its causes-of its natural progress-and of the theory of its production. Histology, Chemistry, and Gen- eral Pathology of Tubercle.-The term tubercle literally implies a little swelling, and in this sense it still serves to distinguish a class of skin diseases. As applied to the peculiar deposits so fre- quently found in the lungs and other organs, it now means not only those pro- ducts when they present a tubercular form, but when they are infiltrated in masses, or exhibit appearances wholly opposed to the original signification of the word. At present, by tubercle is under- stood a peculiar morbid deposit, some- time gray, but more frequently of a yel- lowish color, varying in size, form, and consistence, which sometimes softens, and causes ulceration in the surrounding tex- tures, but which at others dries up, be- comes cretaceous or calcareous, and pro- duces induration and cicatrization. The ultimate structure of tubercle varies according as it is soft or hard, or as it has been recently or for a long time deposited. If we mix a minute fragment of yellow, tolerably soft or cheesy, tubercle with a drop of water, and crush it be- tween glasses, so that it may be tho- roughly broken up, and capable of being examined with a magnifying power of 250 diameters linear, it may be seen to con- sist of a number of irregular-shaped bodies, and of numerous molecules and granules. The bodies are called tubercle corpuscles, and approach a round, oval, or triangular form. Their longest diameter varies from the four-thousandth to the [Fig. 15. Acute Phthisis.-Showing one of the alveoli filled with fibrinous exudation and leucocytes, and some cellular infiltration of the alveolar wall. X 200. (Green.)] two-thousandth of an inch. They are solid, having a distinct external outline, and have embedded in them generally three or more granules and molecules, varying in size from a point scarcely mea- surable to the six-thousandth of an inch in diameter. Acetic acid causes partial solution and transparency of these bodies. Ether and alcohol produce little chancre. Ammonia and liquor potassse cause them to break down and dissolve witn varying rapidity. The molecules and granules differ greatly in various specimens of tu- bercle, sometimes being very minute, and at others half the size of the corpuscles themselves. Chemically, they may be albuminous and partially soluble in acetic acid-fatty when they are soluble in ether and potash-or mineral when they are dissolved by the mineral acids. The corpuscular and molecular ele- ments of tubercle are always present, but PATHOLOGY OF TUBERCULAR PHTHISIS. 109 in different proportions. Generally speak- ing, in indurated or gray tubercle there are few molecules, and the corpuscles are so compressed together as to be scarcely distinguishable. On the other hand, in soft tubercle the molecules are numerous, and the corpuscles easily separable. The more tubercle softens and becomes difflu- ent, the more the relative amount of the molecular element increases. In chronic tubercle, and especially when it has undergone the cretaceous or calcareous transformation, the elements described become mixed with hard, gritty particles of earthy salts. These are of irregular form and size, and are large and numerous in proportion as the tubercle is more and more calcareous. They are often associated with crystals of choles- terine, and not unfrequently with black pigment granules and masses. When tubercle is converted into a mass of stony hardness, a thin section of it presents an irregular granular appearance, made up of a congeries of minute earthy particles without any distinct form. Tubercle corpuscles may be associated with pus and granule cells, as well as those peculiar to glandular organs or mu- cous surfaces. From pus corpuscles they are readily distinguished by the action of acetic acid, which in them causes no [Fig. 16. Acute Phthisis.-A transverse section of a terminal bronchus (air-passage) and the surrounding alveoli. Showing the lobulated character of the pulmonary consolidation, b, cavity of bronchus containing a little mucus, v, a bloodvessel. X 50, reduced X- (Green.)] granular nucleus to appear. From the fibre or plastic cells found in recent lymph they may be separated by their irregular form, smaller size, and the absence of primitive filaments. With the granule cell they can scarcely ever be confounded on account of its large size, brownish ap- pearance and granular structure. From gland or epithelial cells they are distin- guished by their smaller size and the ab- sence of nuclei. Cancer cells also are at once recognized by their size, trans- parency, and oval nuclei. The only ele- mentary structures resembling tubercle corpuscles are those constituting the re- ticulum of cancer and the disintegration of fibro-nucleated growths. The former, although often, even to the naked eye, resembling tubercle, and under the micro- scope composed of irregularly-shaped nuclei, and numerous molecules, result- ing from the histolysis of cancer, are almost always associated with the more recent cell-forms of that growth, while the fragments or presence of fibres serve to distinguish the latter. It should be remembered that all forms of exudation, and many kinds of growth, at an early period of development, present a molecu- lar and nuclear structure throughout, and might by inexperienced histologists be confounded with tubercle. A careful con- sideration of all the circumstances con- nected with tubercle, and of the distinctive structures associated with it, however, will seldom deceive the skilful observer.1 Tubercle has been made the subject of special chemical analysis by numerous chemists, from which the following con- clusions may be drawn : 1. That it con- sists of an animal matter, mixed with certain earthy salts. 2. That the relative proportion of these varies in different specimens of tubercle. That animal mat- ter is most abundant in recent, and earthy salts in chronic tubercle. 3. That the animal matter consists principally of al- bumen, occasionally mixed with a small amount of fibrin. Fat also exists to a slight degree, and becomes more abundant [' See article on Scrofula, vol. i.] 110 PHTHISIS PULMONALIS. as a constituent as the disintegration of tubercle progresses. 4. The earthy salts are principally composed of the insoluble phosphate and carbonate of lime with a small proportion of the soluble salts of soda. 5. That very little difference in ultimate composition has yet been de- tected between tubercle and other albu- minous compounds. From the preceding structural and chemical facts tubercle must be regarded as a morbid product, having a very low degree of vital power, seldom proceeding beyond an imperfect degree of nuclear formation, and having a constant tendency to fatty or mineral degeneration. It as- sumes four forms:- 1. Miliary Tubercle, when the morbid deposit is scattered throughout an organ, or on the surface of a membrane, in iso- lated grains like millet seeds. Some- times they are sprinkled indiscriminately throughout a tissue ; at others, they are in groups or clusters more abundant in one part than in another. Occasionally they are minute, of grayish-color, semi- transparent, and hard to the feel-the so- called gray granulations of Bayle. More [Fig. 17. Section of lung from a case of somewhat Chronic Phthisis. Showing the thickening of the alveolar walls by a flbro-nucleated adenoid-like tissue ; together with an accumulation of epithelial cells within the alveolar artery. The latter are undergoing retrogressive changes. X 200. (Green.)] frequently they are of a yellow color, about the size of a millet or mustard seed, and of soft consistence, so that they can be easily crushed between the fingers. In consistence they may vary greatly, being sometimes hard, or, as they are then called, crude, or they may be so soft as to resemble cheese and cream. They may have undergone the cretaceous or cal- careous transformation, and still preserve their miliary form. 2. Infiltrated Tubercle occurs in diffuse masses, varying in size from that of a bean to that of the entire organ affected. Thus a lymphatic gland, or the lobe of a lung, may present a uniform deposition of the substance throughout its whole ex- tent. Between these two extremes every variety in extent of deposition may be observed, masses being frequently formed by the agglomeration or condensation of miliary tubercle. Like it, also, this form of the deposit may be gray or yellow, crude or soft, and undergo the cretaceous and calcareous transformation. 3. Nodular and Encysted Tubercle.-This form of tubercle exists in rounded, isolated masses, varying in size from that of a small pea to a bean. It may present all the characters of the other forms, but is fre- quently seen to be surrounded by a cap- sule, more or less dense, of fibrous tissue. 4. Cretaceous and Calcareous Tubercle.- This form of tubercle is distinguished by its white appearance, and its putty-like, gritty, or stony consistence. All these forms of tubercle run into one another, and may exist in the same indi- vidual, and often in the same organ, es- pecially in the lungs. They indicate no further essential difference in the nature of the deposits than is concerned with its amount and extent, its hardness or soft- ness, its color-whether white, yellow, gray, or black, or its being recent or old -miliary and infiltrated tubercle being generally new, while encysted and cal- careous tubercles are always chronic. In the last the animal matter has been ab- sorbed, while the mineral matter remains to form a concretion. Great discussion has taken place as to whether tubercle is peculiar to any par- ticular elementary tissue, and as to how it is produced. Like all forms of exuda- tion, it may occur in every vascular tex- ture, and readily coagulates in the minute spaces between or outside the textural elements immediately external to the vessels. Of this we may easily be satis- MORBID ANATOMY OF PHTHISIS PULMONALIS. 111 fied by studying its special histology in various organs. With regard to its mode of production, tubercular matter is first separated from the bloodvessels as a fluid exudation, forming by its coagulation a molecular blastema. The molecules of which it is composed then aggregate or melt into each other to produce the tubercular cor- puscles. These, if compressed together and formed slowly, constitute the indu- rated dense granulations described by Bayle: but if separated by the soft mo- lecular matter, produce the more common yellow miliary tubercles. The idea that these bodies are invariably the result of [Fig. 18. Chronic Phthisis.-Showing the new interlobular fibroid growth surrounding and encapsulating a degene- rated and caseous portion of the consolidated lung. X 50, reduced (Green.)] cell-proliferation originates from the erro- neous hypothesis maintained by Virchow and his followers, viz., that all morbid products are derived from cells. In their attempts to maintain this view, they have mistaken the occasional enlargement and proliferation of fibre cells in areolar tissue first described by Lebert, as fibro-plastic cells, for tubercular granules, which they describe as the essential elements of the lesion. It is not in the pleura or peri- toneum, however, where such fibrous growths are occasionally seen, that the real manner in which tubercle is formed can be well observed, but in the lung, where the disease is most common and best characterized. There, all observa- tion demonstrates that it originates in a molecular exudation, which, in conse- quence of diminished vital power, seldom passes beyond the nuclear stage of growth. It is this low type of hysto-genesis that communicates to the exudation those es- sential characters which form the founda- tion of tubercular or phthisical disease. Morbid Anatomy of Phthisis Pul- monalis.-Although tuberculization of the lungs is a constant and essential ele- ment of Phthisis, it rarely, if ever, hap- pens that the disease proceeds to a fatal termination without affecting other or- gans. Nothing, also, is more common to find, during the examination of dead bodies generally, than that the lungs are often the seat of tubercle to a greater or less extent, although during life the pres- ence of the disease has never been sus- pected. So common, indeed, is this lesion, and so many have been the able investi- gators of the alterations it produces in the various organs of the body, that all the anatomical facts connected with it may be said to be thoroughly known. We shall notice the morbid changes observed in cases of Phthisis in the different parts of the frame, seriatim. The Lungs.-These are the organs in which, according to the researches of Louis, tubercle is sure to be discovered, if it occur in the body at all. This law, though now known to admit of some ex- ceptions, especially as regards tubercular peritonitis, is still so generally true as to be one of the most valuable generaliza- tions ever arrived at in pathological science. To the same distinguished phy- sician we are indebted for another fact of no less importance, viz., that when tuber- cle occurs in the lungs it attacks the 112 PHTHISIS PULMONALIS. apices of those organs first. The excep- tions to this law are so few as in no way to invalidate its great practical value. These vary in size from a pea until they involve nearly the entire lung. There may be one or several. They may be iso- lated or anfractuous, that is, communi- cating with one another. If recent, the internal walls are irregular and rough; but if chronic, the ulcerative process has dissected out the fibrous tissue, leaving irregular bands stretched across the inte- rior, composed of bloodvessels, the bron- chi, or indurated fibrous tissue. When very chronic, the interior is lined with a smooth membrane. These cavities may be filled with air and fluids in varying proportions ; the latter being viscous, purulent, occasionally sanguinolent, and not unfrequently ichorous, of a dirty- green color and offensive odor. These changes in the lung may be associated in varying proportions with many other le- sions to which the organ is subject. Pleuritic adhesions by means of fibrous lymph, are very common ; the pleura?, at the apices of the lung, often being united to each other by a dense, tough substance which renders their separation impossible. Bronchitis, in all its forms and stages, may exist together with more or less em- physema, dilated bronchi, and collapse of the lung. There may be pneumonia or extravasation of blood, involving varying amounts of lung tissue. There is a disease frequent in coal- miners, called carbonaceous lungs or Black Phthisis, in which there is no tu- bercle, but a deposition and infiltration of lamp-black or carbon in a finely molecular form, and which gives rise to cavities and disorganization of the pulmonary tissue, also commencing at the apex. It is ac- [Fig. 19. Apex of Lung affected with. Tubercular Pneumonia.] The morbid changes found in the lungs of those who die laboring under Phthisis Puhnonalis vary according as the disease is acute or chronic, as it is advancing or retrograding, and as it is associated with other lesions. In acute cases miliary and infiltrated tubercles are more or less gene- ral in one or both lungs. The deposit is generally soft, and frequently diffluent, causing ulceration and irregular anfrac- tuous cavities. The intervening pulmon- ary texture is often engorged with blood, is more or less pneumonic, while the bronchi are loaded with purulent matter. The acute disease in many respects re- sembles anatomically gray hepatization of the lung, and like it is more frequently most developed in the lower lobe. . In chronic Phthisis, constituting the vast majority of cases met with, all the forms of tubercle previously described are met with. The tubercle is most abundant at the apex, but may invade the greater portion of one or both lungs. In the latter case, it will most often be observed that one lung is more affected than the other, so that an examination of them displays all stages, either of the onward or retro- grade progress of the dis- ease ; these, although often associated together in very chronic cases, are so distinct- ive anatomically as to require a separate description. The appearances of the lung during the onward progress of the disease are-1. The pres- ence of miliary tubercle to a greater or less extent. 2. The softening of this tubercle, so that it readily breaks down under the finger or a current of water, and forms small cavities or irregular ulcerations communicating one with another. 3. The existence of distinct ulcers, excava- tions, or cavities, as they are named. [Fig. 20. Apex of Tuberculous Lung.] companied by black spit, and is generally fatal.1 The retrograde progress of the disease 1 See the author's Clinical Lectures, 5th edit. "On Carbonaceous Lungs," p. 756. MORBID ANATOMY OF PHTHISIS PULMONALIS. 113 is characterized anatomically first, by the horny induration and cretaceous or calca- reous transformation of the tubercular matter; secondly, by puckerings and cica- trices of the lung tissue ; and thirdly, by contractions, loss of substance, and more color. Occasionally, also, linear and radiating cicatrices indicate the disap- pearance and closure of pre-existing ulcer- ations. Sometimes, however, tubercular cavities, instead of closing and forming cicatrices, remain permanently open and filled with air. They are lined by a smooth membrane, and al- most always communicate with a bronchial tube. In this condition we discovered, in 1842, in such a case, associated with pneumotho- rax fungi growing in the infiltrated matter lining the chronic cavities, and have found them frequently in similar excavations since then.1 At other times the bronchial tubes are permanently dilated, by the contraction and induration of the pulmonary tissue between them. This occurrence, conjoined with the other lesions referred to, gives rise to that condition described by Dr. Corrigan as cirrhosis of the lung.2 The various alterations now de- scribed may be associated with other lesions, especially chronic adhesions of the pleurae, emphy- sema, chronic bronchitis, and dense pigmentary deposits. Not unfre- quently it may be observed that whilst one portion of the same lung presents a marked example of the retrograde progress of Phthisis, another portion as decidedly shows the progressive changes. In such a case the former indicates tolerably well the older and more chronic transformations of the pulmonary tissue. It would thus appear that there is noth- ing essentially destructive or necessarily fatal in Phthisis, and that in all stages of the disease it may be checked, and enable the individual affected to live many years subsequently, and die of old age or other disorders. Attention to morbid anatomy in recent times is demonstrating that this occurs far more frequently than was for- merly supposed, and is due not only in many cases to the spontaneous efforts of nature, but in not a few to the direct interference of art.3 This latter termina- tion, however, is materially interfered [Fig. 21. Pulmonary Caverns. From a specimen in the cabinet of Dr. Gross.] or less induration of the organ. It may be observed in about one-fourth of all those who are examined after death in our public hospitals, that the apices of the lungs contain one or more masses, vary- ing in size from a millet-seed to a coffee- bean, of cretaceous or calcareous matter. That these masses were originally tuber- cle cannot be doubted by those who have had any experience in post-mortem ex- aminations, the more so as in various cases such tubercle, whether in the mili- ary, infiltrated, or nodular form, may not unfrequently be seen to present the vari- ous stages of induration and horny hard- ness, approaching towards the calcareous substance. Such hard masses if dug out and allowed to dry, indeed, become creta- ceous, the animal matter having shrunk away, leaving the mineral substance un- altered. In old persons above seventy years of age, it has been shown by Roger and Boudet that the presence of these concretions in the lungs increases to the extent of from one-half to four-fifths of all those examined. If these concretions or masses of indur- ated tubercle occur at the surface of the lungs, the pleurfe covering them and sub- jacent tissue are frequently drawn in and puckered. If they occur deeper, they are surrounded by indurated pulmonary texture, more or less tinged of a black 1 Description of a Cryptogamic Plant found growing in the sputa and lungs of a man who labored under pneumo-thorax. Trans, of Royal Soc. of Edinburgh, 1842. 2 See Dublin Medical Journal, vol. xiii. 1838; Laennec, vol. i. p. 201; Reynaud, M6- moires de l'Acaddmie, tome 4me; Cruveilhier, Anatomie Pathologique, livraison 32, planche 5, fig. 3; and the author on Pulmonary Con- sumption, 2d edit. Case 3, p. 57. 3 See the author's work on Pulmonary Consumption, in which several such cases are recorded, and the post-mortem appear- ances figured,-Figs. 21 to 26. VOL. II.-8 114 PHTHISIS PULMONALIS with should other organs participate in the disease; and the morbid changes ob- served in them, therefore, next demand our attention. rarely that tubercle is deposited in the heart or pericardium, but when this does occur, it takes place in the nodular form. The heart, however, is very liable to be- come atrophied, and smaller than usual. In lingering cases of the disease, with ex- treme emaciation, it may be found after death not larger than a duck's egg. The bulk appears to be adapted to the dimin- ished amount of blood in the body, and the little work it has to do. Alimentary Canal.-Very rarely ulcera- tions may exist in the pharynx, but en- largement of the follicles is common. The oesophagus and stomach are organs which are remarkably free from tubercular dis- ease ; but, according to Louis, the mu- cous membrane of the latter viscus is liable to softening, mammillation, and attenuation, in the majority of cases. In the small intestine the glands of Peyer are very liable to enlargements and ulcer- ation, especially in its lower third. The enlargements are owing to the deposition of tubercle in and around the solitary and aggregated glands, often accompanied by considerable redness and vascular conges- tion. It presents the miliary or granular forms, although occasionally it may ex- hibit small nodules the size of peas. Tubercular ulcerations of the small intes- tines are common in the last stages of Phthisis, and occupy the scat of the soli- tary and aggregated glands. In the first case they are rounded, with abrupt or tuberculated margins, with a yellowish or dirty-gray base. In the latter case they are oval in form, running transversely round the gut, so that they are readily distinguished from typhoid ulcerations, the long axis of which is in the opposite direction. Their margins are smooth, sometimes tuberculated; the base sunk, and covered with a purulent or dirty- grayish substance. Above the ileo-colic valve the ulcers have a tendency to run into one another and produce an ulcerated surface, more or less broad, surrounding the gut. These ulcers occasionally are so deep as to perforate the intestine. Similar tubercular granulations and ulcers may also be found in the large intestine. Peritoneum.-In rare cases the intesti- nal ulcerations perforate the bowel, almost always giving rise to fatal peritonitis. Not unfrequently, however, chronic ad- hesions exist, to a greater or less extent, on the peritoneal surface outside these ulcers, uniting coils of intestines to one another, or to the abdominal walls. Chronic tubercular peritonitis may also occur when the intestines are covered and agglutinated together by coagulated exu- dation. studded throughout with miliary tubercle. This lesion, though it may ac- company Pulmonary Phthisis, may, some- times, exist as a primary and independent disease. [Fig. 22. Cicatrix at apex of Lung, from arrested. Tuberculosis.] The Pleurae.-We have already pointed out that during the whole progress of Phthisis the pleuree, as well as every other part of the lung, are apt to be af- fected. This, however, may not only be exhibited by adhesions more or less dense, but not unfrequently by the deposition of tubercle in a miliary or infiltrated form, the latter of which assumes a laminar or stratiform character. Effusions and exu- dations into the pleural cavity may also occur, giving rise to more or less hydro- thorax and empyema. Further, the pul- monary pleura may be ulcerated and communications take place with tubercu- lar cavities, or with the bronchial tubes, in which last case pneumo-thorax is the result. The Trachea and Larynx.-The trachea .and larynx are very commonly the seat of 'congestion and ulceration in cases of Phthisis. In the mucous membrane of the former the ulcerations are frequently ■small, numerous, and round, as if dug •out with a small point; at others, they .are larger, deeper, and lay bare the carti- laginous rings. In the larynx they are generally irregular, varying greatly in size, and sometimes involving both vocal cords and the ■whole interior of the organ. Their edges are occasionally studded with indurated tubercles, and sometimes there is thickening with oedema of the cellular tissue, tending to close the glottis. In chronic cases of laryngeal ulceration, which is often called Phthisis laryngca, caries and necrosis of the cartilages may occur. The Bronchial Glands.-It is seldom in cases of chronic Phthisis that the bron- chial glands escape being affected with tubercle, which assumes the infiltrated form, and causes in these considerable •enlargement. On section they may be almost colorless, but they are sometimes more or less loaded with black pigment. Heart and Pericardium.-It is very CAUSES OF PHTHISIS PULMONALIS. 115 Mesenteric and other Lymphatic Glands. •-These are very liable to be enlarged in Phthisis, when they may present greater or less induration and enlargement, ac- cording to the recent or chronic condition of the disease. Tubercle usually is pres- ent in them in the infiltrated form, at first yellow, cheesy or soft, afterwards white and indurated, and, in a few cases, cre- taceous and calcareous. Liver.-In children the liver is not un- frequently the seat of miliary and infil- trated tubercles, but in the adult this is very rarely observed. More commonly the organ is enlarged, a result previously supposed to be owing to fatty degenera- tion, but now known to depend upon a peculiar albuminous transformation known as the waxy disease, from its re- semblance to beeswax. In this condi- tion it may be so enlarged as to weigh eight or ten pounds. It presents a pecu- liar density to the feel, a pale fawn or yel- low-brownish color; and on section the cut edges, when held up to the light, are semi-translucent. We were the first to examine this disease of the liver micro- scopically in 1845, and found the hepatic cells to be condensed together, shrivelled, colorless, and of peculiar transparency, with the nucleus absent, or evidently dis- appearing. 1 It has been supposed by some to be related chemically to starch, and therefore called amyloid degeneration. But it is never changed blue on the addi- tion of iodine, although we have found that like certain other forms of albumin- ous compounds it possesses the property of fixing colors, such as the reddish-brown tint of iodine, or the peculiar pigments of indigo and carmine. Spleen and Kidneys.-Both these organs, like the liver, in early life may become subject to tubercular deposits in the mili- ary form, which in the adult are very rare. The kidney further is liable to ex- tensive tubercular deposits, causing ab- scesses, or what is known as scrofulous pyelitis. Like the liver also, it is com- monly affected in Phthisis with the waxy degeneration, causing induration and en- largement of its substance, and the same translucent albuminoid degeneration of the cells and vascular elements. Other textures and organs.-In the fore- going summary we have only shortly al- luded to the morbid changes most com- monly found in cases of Phthisis. It should be understood, however, that al- most every vascular tissue in the body may, under particular conditions, be sub- ject to tubercular deposits in conjunction with the disease of which we are treat- ing, and thus, in special cases, the bones, muscles, the brain and its membranes, skin, the bladder, testes, &c. &c., may be occasionally involved. Causes of Phthisis Pulmonaeis.- The various circumstances which predis- pose to Phthisis have been most anxiously investigated. All we can venture to offer in this place is a very general summary of the numerous researches undertaken in connection with this subject. Age.-Phthisis is not a disease that is common in early infancy or in advanced age. It is more frequent during child- hood and youth, although cases may be seen in many persons of middle age, as well as among young children. Prom the returns of the Brompton Hospital for Consumption, it would appear to be most frequent between the ages of twenty and thirty. Age unquestionably greatly in- fluences the progress of Phthisis, the acute being most common in young, and chronic in elderly persons. We should not forget, however, that Phthisis in advanced life is frequently the termination of a prolonged case, which commenced many years pre- viously. Sex.- It is generally supposed that Phthisis is more common in females than in males, but this does not appear to be an invariable rule. It is certainly not the case in the Royal Infirmary of Edin- burgh, Dr. Home having pointed out that in the years 1833, '34, and '35, 185 cases were males, and only 112 females. The same excess of males laboring under the disease has prevailed in that institution ever since, as in the years 1843 to 1846 in- clusive there were-males 356, females 217; and in the latest reports for the year 1865 the numbers are-males 126, females 64. Hereditary tendency.-Instances are not uncommon in which members of the same family are observed to become affected one after another with Phthisis, on arriv- ing at a certain age. This, however, may depend not so much upon weakness in- herited from parents, as it does upon a vicious method of rearing the infants and children of certain families. We have seen the children of many families become phthisical, in whom no hereditary taint could be traced, and have frequently pointed out, in the clinical wards of the Royal Infirmary, that, among the six or eight cases of Phthisis then present, not one could be traced to hereditary causes. Although, therefore, there can be no doubt that weakness in parents is a cause of weakness in the offspring, we are of opin- ion it is by no means so general or in- fluential a source of Phthisis as is usually supposed. Vitiated atmosphere.-This has been con- cluded to be a powerful cause of Phthisis by numerous authors, and there can be no 1 See the author's Clinical Lectures, 5th edit. Case clxi. p. 731. Also remarks on the waxy degeneration, Idem, p. 249. 116 PHTHISIS PULMONALIS doubt that the habitual breathing of de- oxidized or impure air must greatly im- pede nutrition. Among the poor there can be little difficulty in attributing its effects to close or overcrow'ded rooms, in which they work and sleep. Among the higher classes this is not so obvious a cause, although Baudelocque, in support of this his favorite theory of the origin of tubercles, accused them of lying in bed too long, and said that the children slept with their heads under the bedclothes. Climate.-It is an undoubted fact that Phthisis is more frequent in temperate climates than in very cold or very warm ones. It is by no means common in Rus- sia and Canada, notwithstanding the long continued cold, nor does it prevail among the nations of the tropics. These last, on the other hand, are pecularly liable to Phthisis on coming to Europe. Some favored spots are stated to be free from Phthisis ; among these, it has been re- cently pointed out by Drs. Macrae and M'Coll, are the islands of Lewis and Mull, among the western isles of Scotland. Dr. Iljaltelin has informed me that Iceland enjoys a like immunity. Contagion and Infection.-Several of the older writers were of opinion that Phthi- sis was contagious and infectious, an opin- ion still widely disseminated in certain countries, more especially Spain and Italy. We have too frequently seen the death of a phthisical patient in Italian hotels give rise to the most extortionate demands for the pretended destruction of bedding and furniture, all of which should be firmly resisted. It has occasionally been ob- served that Phthisis in a wife or husband has been followed by the appearance of the disease in the husband or wife. The frequency also with which young women become phthisical after pregnancy has given rise to the idea that they may have been infected by the opposite sex through the uterus. These ideas have received no support from the profession. In 1865, however, it was announced by M. Ville- min1 that the cause of tubercle was a virus, and that he had succeeded in inocu- lating it in healthy rabbits, by inserting gray granular tubercle below incisions in their skins. These experiments appear to have been carefully performed. They have been successfully repeated by Le- bert, and also by others, with varying re- sults. The experiments of Drs. Andrew Clark,2 Wilson Fox,3 and Burdon Sander- son4 have further shown that not only tubercle but a variety of other morbid products, and even local irritation of the tissues, may produce deposits in the glands, lungs, and various organs in rab- bits, and especially in guinea-pigs. Thus the introduction of a seton produced them in one case, and pieces of putrid muscle in no less than four out of five inocula- tions. 1 These facts show that the lesions described as tubercle are analogous to the secondary deposits occurring in pyaemia, and which are known to result from the poisoning of the blood by absorption and injection into it of putrid fluids, but they in no way support the hypothesis that Phthisis Pulmonalis is contagious or infec- tious. But we shall again allude to this matter under the head of Theory of the Production of Phthisis. [The controversy in regard to the com- municability of Phthisis has not yet been set at rest. Amongst the most careful experiments upon the subject appear to have been those of Tappeiner, of Meran, in the Tyrol.2 He caused dogs to breathe for several hours daily the air of a cham- ber which had been impregnated, by means of an atomizer, with a mixture of phthisical sputa with water. After a pe- riod varying from twenty-five to forty-five days, all but one of eleven animals so treated were found, upon being killed, to have miliary tuberculization of both lungs ; most of them having the same de- posit also in the kidneys, and some in the liver and spleen. Microscopical examina- tion accorded with the naked-eye appear- ances. Dr. Max Schottelius, becoming ac- quainted with these experiments, repeat- ed them, with important variations. In a number of instances he impregnated the air to be breathed not with tubercular sputa, but with those of simple bron- chitis ; in other like experiments, with brain, cheese, and cinnabar. Bronchitic sputa produced tuberculosis in the ani- mals so exposed as often as did the sputa of phthisis. Cheese had a less frequent effect; pulverized brain still less; and cinnabar the least of all, but still produc- ing some tubercles in the lungs. These investigations only confirm the conclusion above stated by Dr. Bennett, that the causation of tuberculosis by an introduc- tion of material into the system from without is not specific; since other mat- ters besides tubercle can produce the same effects. Still, this does not finally dispose of the subject. The question whether there is or is not a specific contagium of tubercle, as there is of syphilis or smallpox, has much of pathological interest. But the paramount inquiry for the physician is, 1 For a good summary of M. Villemin's views and experiments, see Edinburgh Medi- cal Journal for February, 1867, p. 756. 2 Medical Times and Gazette, 1867. 3 On the Artificial Production of Tubercle in the Lower Animals. 4to. London, 1868. * Tenth Report of the Medical Officer of the Privy Council. London, 1868. 1 Wilson Fox, op. cit. p. 5. [2 Lancet, Nov. 23, 1878.] CAUSES OF PHTHISIS PULMONALIS. 117 can Phthisis, whether specific or not, ever be communicated ? Drs. W. II. Webb1 and E. Holden,2 in papers upon this topic, give references showing an affirmative opinion in regard to this question to have been expressed by Galen, Cullen, Heberden, Morgagni, Laennec, Andral, Bright, Addison, Cop- land, Drake, Dickson, Budd, Walshe, Beale, Bowditch, Flint, Stille, Da Costa, and others. Dr. Holden obtained, in answer to cir- culars of inquiry, two hundred and fifty replies from leading physicians in various parts of the United States. Of these, one hundred and twenty-six affirmed their belief in the communicability of consump- tion. Seventy-four gave a negative an- swer ; and fifty were in doubt upon the subject. The evidence which has produced this affirmative conviction in so many minds is of a simple character. A man or wo- man, previously in excellent health, and without inherited predisposition to con- sumption, nurses a wife, husband, sister, or friend, through a fatal attack of Phthisis; and then, after a few weeks or months, sickens and dies of the same dis- ease. Coincidence is, of course, apart from communication, a possibility; and the effect of long, anxious watching, prob- ably with much confinement in a close atmosphere, must not be ignored. Some cases, however, have a more striking appearance. Take, for example, the following :-3 " The only two midwives practising at Neuenberg, a healthy little town of 1300 inhabitants in 1875, were R. and S. Of these, the woman S. was undoubtedly the subject of Phthisis, with abundant puri- form expectoration. In the first case de- scribed, Dr. Reich extracted the child by turning. While his attention was en- gaged with the mother, he noticed that, owing to some difficulty in the child's breathing, the nurse S. sucked the mucus from the infant's mouth, and also endeav- ored to promote respiration by blowing into its mouth. For the first three weeks the child progressed well, but then its health failed, and within three months of its birth it died of well-marked tubercular meningitis, initiated by symptoms of bron- chial catarrh. In May and June follow- ing two more children died of the same disease. These three cases had been at- tended by the nurse S. • Dr. Reich's at- tention being thus attracted, he found, on investigation, that between the 4th April, 1875, and the 10th May, 1876, seven chil- dren, in addition to the above three, had died (all within the first year) of tuber- cular meningitis, although in no case was there any history of hereditary tubercu- losis ; that all these cases had been at- tended by the woman S., while of all the cases attended by the other midwife, R., not one had died of this disease, nor had any manifested in any way indications of any tubercular form of disease. The du- ration of the illness varied from eight days to three weeks; whereas of the ninety-two children who died in their first year during the nine years from 1866 to 1874, only two died of tubercular me- ningitis; and similarly, among the twelve infants who died in 1877, there was only one such case, and its parents were tuber- culous. The midwife S. herself died of Phthisis in July, 1876. It was ascer- tained that S. had been frequently in the habit of sucking mucus from the mouth of infants, and also of caressing and kiss- ing them." On the other hand, as Dr. A. Stille re- marks, " if Pulmonary Phthisis were often conveyed by contagion, the cases ought to be of daily occurrence, since the dis- ease is the most frequent of all mortal diseases." Dr. Cotton,1 of the Brompton Hospital for Consumptives, and Dr. Mac- Cormac,2 of Dublin, have argued strongly against the idea of communicability. Prom the statistics of the Brompton Hos- pital, collected by Drs. Cotton and Ed- wards, it has been shown that of the many nurses and others engaged in that institution during twenty-one years, but one nurse and one servant died of Phthisis. Especial care seems to have been taken, in the Brompton Hospital, in regard to ventilation and other hygienic conditions. Dr. Cotton's expression is, that "a resi- dence in the consumptive hospital, and long-continued working in its wards, is a very good way, indeed, not to catch the disease." In the most cogent instances cited in favor of contagion, the person ap- pearing to contract Phthisis from another has been one who, for weeks or months together, slept in the same room, often in the same bed ; besides being in the same apartment also for a great part of every day. Thus not only the injurious effect of "rebreathed air" (MacCormac) was felt, intensified usually by shutting up windows, &c., to keep out the cold, but the inhalation of air exhaled from dis- eased lungs was almost constant. " Con- tinuous molecular change" (Snow) may be easily supposed in this way to occur; through the introduction into healthy lungs of minute particles of disintegrated f1 Amer. Journal of Med. Sciences, April, 1878, p. 426.] [2 Amer. Journal of Med. Sciences, July, 1878, p. 145.] [3 Reich, in Berliner Klinische Wochen- schrift. Sept. 18, 1878.] [* Brit. Med. Journal, 1872, vol. ii. p. 239.] [2 On Consumption; London, 1865.] 118 PHTHISIS PULMONALIS. lung tissue, given out in the breath of a phthisical patient, and not removed by ventilation. From the foregoing considerations, the following conclusions may be derived :- 1. Tubercle is not a specific morbid pro- duct, and therefore in no strict sense can Phthisis be called a contagious disease. 2. Exposure to the atmosphere breathed by consumptives is not attended by clan- ger, so long as good ventilation is main- tained. 3. Inhaliiig the breath of patients far advanced in Phthisis, in close rooms, and for long periods together, has been, in some instances, followed by the develop- ment of the disease in persons previously healthy. 4. Therefore, we should always advise that no healthy person shall sleep in the same bed ■with a consumptive; nor, if avoidable, in the same room, unless am- ple ventilation is maintained.-II.] Occupation.-Phthisis is unusually com- mon among the workers in certain trades, more especially stonemasons, grinders and polishers of steel, dressers of flax and fea- thers, cotton carders, china scourers and potters, tailors, sempstresses, straw-plait- ■ers, lace-makers, silk-workers, and iron ana coal miners. On the other hand, cooks, butchers, tanners, tallow-chandlers, and soap-boilers, enjoy to a great degree an immunity from the disease. In the first class of cases the inhalation of foreign particles into the lungs excites local irri- tation, which proves injurious to the res- piration, and deteriorates the constitu- tion ; or the result is occasioned by the combined operations of sedentary employ- ments, impure atmosphere, exhaustive work, and bad food. In the second class of cases there are good wages, and, as a concomitant, good food, while a constant contact with oil is supposed to offer an additional explanation of the fact. Humidity has been supposed to exercise a considerable influence in the production of Phthisis. Magendie thought he had produced tubercle in rabbits by confining them in damp cellars. Baudelocque points to numerous localities, such as morasses, houses surrounded by ditches, and so on, where the disease is rife. It is also com- mon in Holland, and other countries lia- ble to damp fogs and an atmosphere satu- rated with moisture. Phthisis has been shown to prevail in the damp soils of the United States by the careful investiga- tions of Dr. Bowditch, of Boston, U. S., and of England by those of Dr. Buchanan.1 On the other hand, in elevated dry re- gions it is said to be comparatively rare. In the Seventh Annual Report of the Reg- istrar-General for Scotland, it is pointed out that for every 100,000 inhabitants there died annually from consumption 206 persons in Leith, 298 in Edinburgh, 310 in Perth, 332 in Aberdeen, 340 in Dun- dee, 383 in Paisley, 399 in Glasgow, and 400 in Greenock. In these towns, there- fore, the death-rate is diminished in pro- portion to the dryness of the site. Diet. - Of all the causes producing Phthisis and tubercular diseases gener- ally, a low diet, or imperfect assimilation of food, is the most obvious and unequiv- ocal. Among the lower orders we observe this to be the case in all large cities, among the ill-fed and half-starved poor, in orphan and foundling institutions, and whenever from any cause the food of the people is rendered scarce or dear. In the higher classes we observe it following the system of nourishing infants by hired nurses, or bringing them up by hand, and in early childhood from a pampered in- dulgence in indigestible or non-nutritious substances. Not unfrequently it results from allowing weak children to reject the fatty constituents of food. Most of the other causes to which we have referred will be found on examination to have in- fluenced the economy, by diminishing ap- petite, and impeding digestion and assimi- lation of food. Other diseases.-It has frequently been observed that Phthisis follows attacks of previous diseases, which by either affect- ing the lungs, or strongly depressing the system, and not unfrequently by both, appear to have caused the disease. Thus it has followed pneumonia, bronchitis, measles, and hooping-cough in persons previously healthy. Want of appetite and dyspepsia in the young are fertile sources of Phthisis. Indeed, all disorders ■which permanently lower the strength in the young, and interfere with the nutri- tion so necessary at that period of life for developing the growth of the body, may be regarded as a cause of tubercle. The weakness resulting from parturition and prolonged lactation in feeble women is a striking example. For the same reason it occurs in some rheumatic and gouty persons. Predisposition.-Seeing that none of the causes mentioned invariably produce the disease, and that striking exceptions may be cited of persons who exposed to one or all of them have yet escaped the malady, the difficulty has been attempted to be got rid of by recourse to predisposition. In the same manner that many persons ex- posed to fever or smallpox are not affected, or that certain plants only grow on par- ticular soils or patches of ground, so it is said there must be a something super- added to other causes in tubercular cases, which is called predisposition. It is un- necessary to enter upon the subtle argu- ment which has thus been raised, and 1 Tenth Report of the Medical Officer of the Privy Council, 1868. NATURAL PROGRESS OF PHTHISIS. 119 which appears to us, in the present state of science, as reasonable as is the calcula- tion of chances concerning the probability of escape to any particular soldier who exposes himself to the fire of an enemy. In neither case is it predisposition nor chance, but rather the operation of fixed laws, which it is not given to us as yet to recognize, or regarding which we cannot so calculate as to avoid their operation. It may be observed, especially among the lower classes, that vitiated air, hu- midity, want of cleanliness, bad diet, drunken habits, and a variety of debili- tating causes, all concur apparently to produce the effects, so that it becomes very difficult to attribute the disease to any one especially. In the higher classes two causes more especially are found, viz. an hereditary taint, and improper nutri- tion. On looking at the whole train of causation, it seems to me certain that they may all converge in mal-assimilation or deficiency of food. As far as the strength of the economy and constitution of the blood are concerned, it matters little whether deficient vitality be caused by the food being deficient, or, if abund- ant, its not being digested; or again, if digested, its being deteriorated in the lungs by noxious gases, by inoculation of morbid matters, or by constant conges- tion, the result of tissue irritation. As a general conclusion we hold to the belief that the great cause of tubercle is weak- ness of constitution, or diminished vital power, however produced; a theory which has the merit of teaching mankind to avoid all causes which may exhaust the frame, and to establish as remedies every- thing that can communicate to it strength and vigor. Natural Progress of Phthisis.- The commencement of Phthisis may be said to be established as soon as it is dis- tinctly shown that tubercles exist in the lung. This period, however, is generally preceded by more or less deterioration in the general health, indications of debility, and impoverishment of nutrition. It is true there are many individuals in whom the deteriorating process is so gradual, that this change has not been observed either by themselves or their friends, but it is seldom that such will escape the ob- servation of the experienced physician. At other times the impaired health is caused by some exhausting malady of a general character, or of one especially affecting the chest. It sometimes happens that the first obvious departure from health is a hemorrhage coming from the lungs. It is under these or other exhausting cir- cumstances that a matter is exuded in a fluid state from the capillaries of the lungs, which collects and coagulates in such por- tions of the pulmonary texture as offer least resistance. Although a small por- tion may insinuate itself between the ele- mentary textures of the organ, it will principally pass into the air-vessels, so as to obstruct the entrance of air. A miliary tubercle may in this way block up from three to twenty of these air-vesicles. The amount of isolated tubercles so formed in the lung, their aggregation and union to- gether giving to the morbid product the appearance of infiltration, somewhat im- pedes respiration and the functions of the pulmonary organs, according to the extent of the morbid product. Their presence, also, by irritating the pulmonary nerves, gives rise to the frequent dry cough so common in the early stage of the disease. The tubercular matter having coagulated, constitutes a foreign solid body, which can only be removed by being again broken down and so rendered capable of being either absorbed or excreted. Thus the miliary or infiltrated forms, whether gray or yellow, after a time soften-a process which may commence at any part of the mass, and gradually affect the whole. This softening is a disintegration or slow death of the tubercular exudation, con- stituting true ulceration, which is more or less extensive, according to the amount of the morbid deposit. When recent, the pulmonary tissue in the immediate neigh- borhood is more or less congested, but when chronic it is thickened and indu- rated, often forming a capsule, which sur- rounds the hardened tubercle, or a mem- brane lining an excavation. The other neighboring tissues are also necessarily involved. The pleurae are thickened, the bronchi sometimes loaded with tubercle, at others obliterated by pressure, the bloodvessels are congested, ruptured, and ultimately impervious, and the nerves compressed and irritated. As the ulcera- tive process extends, the elementary struc- tures of the lung are more and more de- stroyed, the excavations become larger, more numerous, and unite with each other, until at length the pulmonary or- gans can no longer perform their func- tions. In most cases, however, before this is arrived at, tubercle appears in other parts of the body, producing com- plications, under the united effects of which the strength is exhausted. It is only in rapid or acute cases of Phthisis that the ulcerative tendency of the tubercular exudations pursues an uni- formly destructive progress. In chronic cases this is frequently checked, and for a time slumbers, the symptoms improving and the patient exhibiting temporary signs of recovery. These arrestments of the disease may be of greater or less dura- tion ; and there can be no doubt that they are permanent in a far greater num- ber of persons than is generally supposed. Indeed, while the more extended cultiva- 120 PHTHISIS PULMONALIS. tion of morbid anatomy in recent times has demonstrated the frequency of creta- ceous and calcareous concretions at the apices of the lungs, as well as of pulmon- ary cicatrices, physical diagnosis and more careful observation have shown in the living, that corresponding with the disappearance of symptoms and physical signs the health has improved, and ulti- mately been permanently restored. We are satisfied that there is no period in the history of the disease in which permanent arrestment may not take place, although, of course, it is far more common when it is limited in extent, and confined to one lung. The facts we have seen and re- corded on this subject, however, show1 that individuals with extensive cavities and disease on both sides may, under favorable circumstances and with appro- priate management, ultimately recover. Theory of the Production of Phthisis.-It is not our intention to en- ter into an account, descriptive and crit- ical, of the numerous views which have been held in past times as to the essential nature of Phthisis. It will be sufficient ro speak of the two theories which are now being discussed, and of the reasons which induce us to adopt the one and to reject the other. The first theory sup- poses an altered condition of blood, origi- nating in a perversion of nutrition. This perversion, as we have seen, has been considered by some to be owing to vitiat- ed air, by others to imperfect assimilation of food, and by others to an hereditary taint. It has also been shown experi- mentally, that it may be caused in the lower animals by inoculation of various morbid matters. All these, and indeed other causes, may originate or co-operate in diminishing the vital power of the in- dividual, and directly or indirectly pro- duce weakness, feeble digestion, and an impoverished blood. It is when in this condition that any accidental irritation of the lungs, often inappreciable and unde- tectable, causes a limited congestion here and there in the pulmonary organs, which terminates in more or less exudation of the liquor sanguinis. This exudation coagulating causes the miliary and infil- trated forms of tubercle previously de- scribed, which partaking of the dimin- ished vital power of the organism, instead of being transformed into the pus charac- teristic of a similar exudation in a healthy person, produces the small, irregular, and imperfect bodies called tubercle corpus- cles. Instead of cells, which are rapidly produced, broken down, and absorbed as in pneumonia, we have numerous mole- cules and bodies resembling ill-formed nuclei. In short, we have a chronic exu- dation, in which the vitality is so lowered that it tends to disintegration and to pro- duce the lowest kind of organic forms,- i. e., molecules, granules, and nuclei. The second theory is one which, instead of ascribing tubercle to an exudation froin the blood, of low vital power, regards it as the result of increased cell development and multiplication of the included nuclei. According to this view tubercular matter is a new growth, which when we consider that it sometimes reaches the size of an apple, as in the brain, would demand for its production increased rather than di- minished nutrition. Notwithstanding the desire of those who support an exclusive cell theory to trace tubercle as well as every morbid product to some cell trans- formation, the most careful and repeated investigations of histologists have failed to do so. According to Virchow, how- ever, upon isolating the constituents of a tubercular mass "either very small cells provided with one nucleus are obtained, and these are often so small that the membrane closely invests the nucleus, or larger cells with a manifold division of the nuclei, so that from twelve to twenty- four or thirty are contained in one cell; in which case, however, the nuclei are always small and have a homogeneous and somewhat shining appearance."1 This description of small nuclei in the interior of cells, and the appearances figured as constituting the structure of tubercle, have, so far as we are aware, never been confirmed by any experienced histologist. Tubercle is so common a morbid product that if such indeed were its constitution, it ought to be seen at once ; but our most anxious and repeated efforts have failed to discover it, nor does there exist a sin- gle preparation anywhere capable of demonstrating it. Cells containing many nuclei are very rare, associated with tubercle, and when they do occur are evidently dependent on the occasional irritation of texture which is produced around the morbid products-they are a result and not a cause. As a matter of fact, therefore, not to speak of the theo- retical improbability of a disease originat- ing in weakness commencing with in- creased power of vital development in the pre-existing tissues of the organism, this theory must lie rejected. In support of this last theory it is fur- ther maintained by Virchow and his fol- lowers, that the term tubercle should be limited to the minute, indurated granula- tions which, as Lebert originally pointed out, are the result of increased nuclear growth in the fibrous tissues-what he denominated fibro - plastic corpuscles. The larger so-called tubercular infiltra- 1 See my work on Pulmonary Consumption, Cases 1, 2, 21, 22, &c. 1 Virchow, by Chance, p. 476, and fig. 140. THEORY OF THE PRODUCTION OF PHTHISIS. 121 tions of morbid anatomists and practical physicians they regard as chronic or, as they call them, cheesy exudations. Dr. Burdon Sanderson proposes that tubercle should be called an "adenoid growth,"1 and it may be granted that a mass of molecules and tubercle corpuscles, such as we have described, in a fibrous tissue, may present a vague resemblance to one of Peyer's glands. But a slight considera- tion must show that these distinctions are more verbal than real. It is not the oc- casional, scattered, and rare indurated granulation with which we are so much concerned as the extensive, chronic mor- bid deposit. Transferring or limiting the term tubercle to the accidental granule, and calling the general and essential mor- bid product chronic inflammation, or ade- noid growth, constitutes no real advance in pathology. What we have from the first maintained is that we have to do with a tubercular exudation, which differs from an inflammatory and cancerous exu- dation in its low vital energy and dimin- ished power of transformation into cell forms ; and that this is the essential ele- ment of Phthisis Pulmonalis. Two re- cent French admirers of Virchow's doc- trines have proposed to separate ordinary Phthisis, from granular tubercle of the lungs, under the name of Tubercular Pneumonia,2 and Niemeyer suggests for the term Phthisis, Chronic Pneumonia.3 These propositions, while they indicate an essential agreement with the doctrines contended for in this article, offer no real advantage. It is not the name we attach to a morbid state, but a clear comprehen- sion of the morbid state itself, which is of real importance. It is now many years ago that we pointed out the existence of a true vesicular pneumonia, which to the naked eye resembled scattered grains of yellow tubercle, but which under the microscope was composed of desquamated epithelial scales and pus-cells, mingled with fine molecular matter.4 That a pneumonia may be vesicular, lobular, or lobar, is now agreed upon by every path- ologist, and the same forms dependent on the extent and seat of the exudation may be observed in tubercular deposits. Satisfied then that tubercle is essentially a coagulated exudation, we have next to ask, why such exudation is not rapidly transformed into pus-cells, as occurs in an acute pneumonia ? The reply is, in con- sequence of the deficient strength and want of vital formative power in the or- ganism. If it be further asked, on what that deficient energy, in its turn, is de- pendent ? the answer is, that in conse- quence of impeded nutrition, or other causes, the blood is rendered so abnormal, that its fluid constituents when exuded are incapable of supporting cell forma- tion. But it must not be forgotten that as the blood is continually undergoing changes, now receiving and then giving off new matters, it never remains the same for many hours together. An exu- dation at one period may abound in ele- ments which do not exist in it at another. Hence why we find all kinds of interme- diate formations in the textures in tuber- cular cases, and why the exuded matters associated with the lowest form of morbid formation may be occasionally mingled with the higher. A cancerous growth, however, is very rarely met with in con- junction with tubercle. When we next come to inquire what is the nature and essential cause of that altered nutrition which so modifies the blood, that when its fluid portion is ex- uded it should constitute tubercle, we must inquire in what manner the diges- tive processes are primarily impaired. And here we must remember that all food essentially consists of albuminous, fatty, and mineral constituents, which are re- duced in the alimentary canal to a fluid condition by the mechanical triturating action of the teeth, jaws, and stomach, as well as by the chemical solvent action of alkaline and acid juices. An observa- tion of the peculiar dyspepsia which so frequently accompanies tubercular disease will satisfy the observer that it depends upon excess of acidity in the alimentary canal, which favors the solution of the albuminous and mineral matters, but is opposed to the emulsionizing of fat. It has consequently been attributed by Dr. Dobell to diminished secretion from the pancreas. In youth the indisposition to eat fatty substances is well marked, and among the ill-fed poor it is fat which is the most costly ingredient of food.1 In either case it is the non-assimilation of the fatty elements of food and their di- minution in the blood, while the albu- minous elements are comparatively in excess, that gradually interferes with nu- trition ; the molecular basis of the chyle is impoverished, the elementary molecules so necessary for the formation of healthy blood corpuscles are diminished, the liquor sanguinis consequently is poor in fat and rich in albumen, the entire growth of the constitution, as a result, is affected, and its powers rendered weak; lastly, when exudations do occur, more especially in the lung, they are of an albuminous char- 1 See Edinburgh Medical Journal, Novem- ber, 1869, p. 386; and Eleventh Report of the Medical Officer of the Privy Council, plate 5, fig. 3. 2 Herard et Cornil sur la Phthisie, 1867. 3 On Pulmonary Consumption ; Sydenham Society's Translation. 4 Clinical Lectures, 5th edit. p. 689. 1 See Report by Dr. Edward Smith. PHTHISIS PULMONALIS. 122 acter, exhibit slight power of transforma- tion into cells, and only produce that slow abortive nuclear material which is called tubercle. Such is the theory of Phthisis we consider most consistent with all the recognized facts connected with the origin and progress of the disease, the correct- ness of which is still further supported by what is now knowm, 1st, of the chemical constitution of the food, and the trans- formations it undergoes in the body; 2dly, of the relations which exist between di- gestion and the working powers of the individual; and 3dly, as we shall subse- quently see, by what experience has taught us of its successful treatment. II. Symptoms of Phthisis. From what has been previously said under the head of Morbid Anatomy of Phthisis it must be apparent that the symptoms which it presents will not only have reference to alterations in the func- tions of the lungs, but to those which may arise from disease in other organs. We must further consider that its onset may be insidious and scarcely perceptible, or on the other hand startling from its vio- lence or acute character ; that its progress may be rapid, slow, or irregular, and its termination ushered in by various phe- nomena not unfrequently of a very com- plex character. Notwithstanding, to the pathologist who has carefully studied the morbid anatomy, natural progress, and theory of the disease, the symptoms and physical signs of Phthisis will enable him to determine the morbid condition pres- ent in the great majority of cases with an exactitude and certainty of which the modern cultivators of medicine may well be proud. Premonitory Symptoms. - Before any one can positively state that tubercle ex- ists in the lung, there generally occur symptoms indicative of diminished gen- eral health, and of deteriorated constitu- tional vigor. In many cases it is observ- able in young persons that they are not good eaters, dislike fatty substances, are capricious with regard to food, become thin, pale, weak, and liable to dyspepsia, complain of indigestion and irregularity of the alvine discharges, and to the ob- servant eye are at once recognized as individuals ill nourished and liable to tubercular disease. This condition, how- ever, is often not noticed by the parents or friends, who regard it as only natural to youth, or to the circumstance that they eat so little. On other occasions it creates apprehension and alarm, the physician is consulted, who, however, can detect no pulmonary disease or pulmo- nary symptom of any kind. If, in addi- tion to the above plicnomena, the indi- vidual complains of chills, cold feet, occasional perspiration, quick pulse, ren- dered more frequent at night, the general condition is one highly favorable to the occurrence of Phthisis. In adult persons the premonitory symp- toms are most commonly lassitude, inca- pacity for following the usual employment, diminution of appetite, with or without indigestion, and a sensible falling off in flesh. Various diseases may manifest themselves, such as gouty or rheumatic attacks, influenza, bronchitis, fever, dys- entery, and others, which leave the indi- vidual in a debilitated state. There may now come on considerable haemoptysis, although an examination of the lungs reveals no sign of tubercle ; or an attack of pneumonia may appear, which if treated by lowering remedies may usher in the disease. Occasionally the skin of the face becomes gray, and a haggard and worn expression is communicated to the countenance. Pregnancy and lactation in weak females frequently introduce Phthisis, as, indeed, may everything that calls too strongly for exertion of the vital powers in weak and predisposed persons, or that causes vitiation of the blood. It is in this respect that the recent experi- ments of Clark, Fox, and Sanderson, previously referred to, indicate how Phthisis may follow suppuration or irri- tating diseases of texture, and how if oc- casioned in one organ it may spread to others. It is when the constitution is thus en- feebled that Phthisis appears in its acute or chronic forms. Acute Phthisis.-This form of the dis- ease, commonly called "galloping con- sumption," is generally distinguished not only by its rapid progress, but by the febrile symptoms which accompany it. There are frequent chills, followed by great heat and sweating, red tongue, nausea, loathing of food, vomiting, and diarrhoea. There is a rapid pulse, at first of good strength, but soon becoming feeble, dyspnoea on slight exertion, cough, profuse expectoration, sometimes tinged with rusty-colored blood. Occasionally the expectoration is trifling. There is great exhaustion, rapid emaciation, rest- lessness, and, before death, wandering of the mind and delirium. On percussion one or both lungs exhibit unusual dul- ness, which rapidly extends and becomes more intensified. It is sometimes most marked at the base. On auscultation there are at first dry, bronchial sounds, and prolonged expiration, 'which soon pass into moist rattles, loudest with in- spiration. The crepitations are now transformed into mucous rales more or less coarse, frequently accompanied with dry, bronchial murmurs and pleuritic frictions. The extent of these signs in- SYMPTOMS OF PHTHISIS. 123 dicates the area of lung-tissue involved, while the amount of increased vocal reso- nance points out the density of tubercular and pneumonic exudation infiltrating the lungs, or the anfractuous softening and excavations produced. These acute symptoms occur occasion- ally in most cases of Phthisis, and indi- cate the period when exudation is being rapidly deposited in the lungs, or on the pleurfe. In many cases they constitute attacks supposed to be the result of hav- ing "caught cold." Then they decline, and are absent for varying periods. The greater the number of these attacks, the more rapid is the progress of the disease ; and when they are continuous, it pro- duces that form of it denominated acute Phthisis. Such cases may prove fatal in a period varying from two or three weeks to a few months. C hronic Phthisis.-In the vast majority of cases the progress of Phthisis is slow, often coming on imperceptibly, and too frequently exciting little attention until it is far advanced. I have known the only daughter even of a medical man slowly pass through all the stages of the disease, the cough and expectoration failing to attract special notice in the family until three weeks before death, when on ex- amination by a physician large cavities were detected. At other times it is ushered in by well-marked disease, such as pneumonia or bronchitis, and in some instances the first symptom observed is hemorrhage. These different modes of onset in the disease we regard as suffi- ciently important to merit a separate description. Gradually-developed Phthisis.-The first symptom which appears is cough; at first, however, so slight as scarcely to attract attention, and attributed to tran- sient exposure to cold, or tickling in the throat. It may be observed, however, to be persistent, and of a dry, hacking character. Sometimes the cough is ac- companied with pains in the shoulders, tightness in the chest, slight dyspnoea on exertion, together with all the other symptoms described as premonitory. On percussing the chest no dulness can be detected at this early period; but on auscultation there may frequently be detected feeble respiration under one clavicle, and, during forced inspiration, harshness of the breath murmur, with prolongation of the expiration. After a variable time expectoration follows the cough ; at first consisting of transparent, frothy mucus in small quantity, but soon becoming opaque and purulent, and often streaked with a little blood. The cough and expectoration now become gradually increased, and all the other symptoms which have preceded or accompanied them are intensified ; the failing appetite is more marked, the quickened pulse and feverish excitement more evident, and the general weakness, falling oft' in flesh, pallor, and languor make progress. A period, sooner or later, arrives when on careful percussion a sensible dulness may be detected under one clavicle. On aus- cultation over this dulness, either there is increased harshness of the breath-sound on taking a deep inspiration with pro- longed expiration, or a slight crepitation may be discovered during some parts of the inspiratory act. Increased vocal resonance, also, is present over the dull portion of lung. The various symptoms and signs enumerated characterize what many authors regard as the first stage of the disease. The physical signs now assume marked importance in the history of the case, in- dicating, in the majority of instances, with great exactitude, the extent of the tuber- cular deposit, and the changes which it undergoes. The area over which dulness can be detected by percussion gradually extends from the apex downwards, until it occupies one-third, one-half, or even a greater portion of the lung. Dulness may appear at the summit of the other lung, and all the signs observed on the one side may follow on the opposite one. The crepitation on inspiration also extends, and, at first very fine, gradually becomes larger and coarser, until a loud, mucous rattle is established. The vocal reso- nance, which at first is only slightly in- creased, becomes louder and louder, until at length decided bronchophony is pro- duced. During the occurrence of these changes in the physical signs, the cough becomes more frequent and prolonged, especially early in the morning, the ex- pectoration is more abundant, and at length consists of dense, purulent masses, some of which sink in water. These also may, from time to time, be streaked with blood, or even slight hemorrhage from the lungs may occur. There is now generally visible emaciation of the body, consider- able debility, indisposition to take exer- cise, dyspnoea on exertion, and especially on going up an ascent. The tongue is red, often glazed, and occasionally anae- mic. There is anorexia and nausea, or the appetite is much diminished, and very capricious. The night sweats are often distressing; there is thirst, quick pulse, and not unfrequently marked fever at night. Sometimes diarrhoea may super- vene, which invariably accelerates the progress of the disease. At others there may be various complications, such as at- tacks of laryngitis, pharyngitis, bronchitis, pleuritis, pneumonia, all of which produce increased weakness, and aggravate the sufferings of the patient. These occur- rences characterize what have been termed the second stage of the disease. 124 PHTHISIS PULMONALIS. The further progress of Phthisis is now characterized by the formation of excava- tions in the lungs, which arc distinguished by loud, moist rattles, passing into gur- gling or splashing sounds, if the cavities be large and contain fluid, or by loud, bronchial blowing, and rarely amphoric breathing, if they be dry. Percussion with the mouth open sometimes elicits a clear tone over such cavities ; at others a peculiar chinking or cracked-pot sound. On speaking there is a shrill vocal reso- nance, called imperfect pectoriloquy; and occasionally the words uttered seem to come out of the chest, and strongly strike the ear through the stethoscope, a sign termed perfect pectoriloquy. Together with the signs of a dried cavity are fre- quently coarse creaking sounds, indicating the existence of chronic adhesions. At the same time dulness, and the other signs audible in the second stage of the disease, arc more or less extended over one or both lungs. The cough is now very harassing and prolonged, and often so violent as to occasion vomiting, and it disturbs sleep at night. There is more or less dyspnoea, and occasionally, if the lung be extensively diseased, orthopnoea. The expectoration is greatly increased, con- sisting of nummular masses of dense, pur- ulent matter, often containing portions of infiltrated lung, which rapidly sink in water. Sometimes it is greenish, ichor- ous, and of offensive odor. In very chronic cases, on the other hand, with dry cavities, the expectoration is trifling, and brought up with considerable diffi- culty. Haemoptysis is now a more com- mon symptom, and may vary in amount from a few teaspoonfuls to twenty ounces, or even more. Such attacks invariably cause great alarm, and produce exhaus- tion in proportion to the amount of blood lost. The patient frequently complains of pain in the thorax, which in very chronic cases is often severe, ushering in, more or less, flattening of the chest, that may now occur to a greater or less extent. As the disease extends, and the cavities enlarge, the strength of the patient de- clines, the appetite is lost, and it becomes difficult to eat anything. Hectic fever appears, there is a pink blush on the cheeks, rapid pulse, occasional rigors, profuse sweating at night, and extreme emaciation. Sometimes the vital powers slowly decline, and at length become ex- tinct ; at others, a colliquative diarrhoea appears, which more rapidly closes the scene. These symptoms constitute the third and last stage of the disease. In the majority of chronic cases the progress of the disease is not uniform, but subject to numerous interruptions, and even long pauses in which there is decided amendment, with great amelioration and even absence of symptoms But the phys- ical signs, though they become modified, still indicate the existence of organic le- sion. Not unfrequently, however, such pauses and ameliorations are continued for a long period, and in many cases may [Fig. 23. Diurnal range of the Temperature in Hectic Fever.- (Finlayson.)] usher in a permanent arrestment of the disease. In such cases the expectoration gradually ceases, and the cough becomes dry. This, in its turn, becomes less fre- quent, and at length disappears. Auscul- tation indicates that the moist rattles are converted into dry blowing or bronchial murmurs. Coarse friction sounds appear, and indicate adhesions and cicatrizations. Dulness on percussion and increased vocal resonance remain, and, although seldom altogether got rid of, become more and more circumscribed, leaving sometimes only a trace behind to indicate the pres- ence of disease. In severe cases the sub- clavicular regions of the chest are retract- ed ; dense pleuritic adhesions are formed, which circumscribe the movements of the thoracic walls ; but healthy respiration is heard in such portions of the lungs as were unaffected. Under such circum- stances, although full vigor of body is not restored, life is continued, and enjoyed for an indefinite period, and death ulti- mately caused by circumstances altogether independent of the pulmonary lesion. Hemorrhagic Phthisis.-The peculiarity of this form of Phthisis is that it com- mences with haemoptysis more or less vio- lent. I have now seen several cases in which individuals who imagined them- selves to be in very good health, and in whom, on the most careful inquiry, no- thing but some slight dyspepsia or falling off in appetite could be discovered, were suddenly seized with hemorrhage from the lungs. From that moment their general health began to give way, and Phthisis was developed, of which they died. I remember the case of an exten- sive sheep-farmer in the south of Scot- SYMPTOMS OF PHTHISIS. 125 land, who walking home one afternoon- as he thought in the possession of perfect health-was seized in the road with bleed- ing from the lungs. I saw him a few days afterwards ; and failed to detect, either from his external appearance, general symptoms, or physical signs, the slightest evidence of pulmonary disease. Never- theless in a few weeks he became pale and languid, cough appeared, and on his again visiting me a peculiar roughness, or what some call a dry crackling, was distinctly audible at the apex of one lung. He spent the following winter in the south of France ; but, notwithstanding every care that could be exercised, he died of Phthisis at the end of three years. So many cases of this kind have come under my notice, that I have no hesita- tion in regarding it as a peculiar form of the disease, in which tubercle is deposited in such a manner as in the first instance to induce degeneration and rupture of a considerable-sized vessel in the lung. The loss of blood so occasioned from one or more attacks assists in developing the disease, which subsequently progresses in the usual way. Occasionally such hemor- rhages may occur several times before tubercle deposit has spread so as to be recognizable by physical signs. Not long ago I saw an Australian who for upwards of two years had several such attacks, and who only on reaching this country, in the month of November, when I ex- amined him, had cough developed, with the incipient harshness of respiration. This form is most common in adults, and is generally fatal, although I have seen a few instances in which, after a time, it was permanently arrested. It is allied to that class of cases in which at any period of the disease hemorrhage makes its appearance, and is recurrent. Bronchitic Phthisis. -■ This form of Phthisis is more common in the young than in adults, and manifests itself in bronchitis, which attacks the apex of one or both lungs. It is a common sequence of severe attacks of influenza, hooping- cough, measles, or other diseases in which the bronchi are affected, in weak persons. They do not readily throw off the pulmo- nary affection, are very liable to colds ; dyspnoea is readily excited by unusual ex- ertion ; they complain of a sense of tight- ness or constriction about the chest, which, on being examined physically, is quite resonant on percussion ; but there is harshness of the inspiratory murmurs on taking a forced breath, with prolonga- tion of the expiration, without increase of vocal resonance. In short, there is slight bronchitis at the apex, which, how- ever, is permanent, or if it disappear for a time shows a great tendency to return. Occasionally there is wheezing, more or less sibilation, and great dyspnoea on exertion, with cough, expectoration, and slight haemoptysis. For a long time the general health exhibits no further evi- dence of disease ; but at length frequent cough and expectoration appear, weak- ness, failing appetite, emaciation, and the usual symptoms of Phthisis. In some cases the ordinary physical signs are also manifested, but in others I have known death occasioned without the production of dulness on percussion, increased vocal resonance, or other distinct signs of tuber- cular consolidation. In such cases, from first to last, bronchitis appears to be the only lesion while the patient wastes away and dies, although on inspection of the lungs afterwards they will be found to contain more or less tubercle. In 1845 I ■was consulted in the case of a young lady eleven years of age, who, after a violent and prolonged attack of hooping-cough, complained of dypsnoea on exertion, and cough. There was no dulness on percus- sion, and on auscultation there was harsh- ness of inspiration, and slight prolonga- tion of expiration at the apices of both lungs, especially on the right side. Under this affection she labored for eight years, in all other respects enjoying tolerable health, when the appetite began to fail, purulent expectoration became continu- ous, and all the symptoms of Phthisis were manifest. She died early in 1855, never having exhibited any of the phys- ical signs of Phthisis, the disease appar- ently being structurally one of bronchitis and emphysema. On examination after death, however, I found circular patches of miliary tubercle, about three-quarters of an inch in diameter, irregularly scat- tered through the pulmonary tissue on both sides, together with emphysema.1 I have since seen several similar cases, and am satisfied that bronchitis developed in weak young persons, especially when it appears at the apex of the lungs, is a frequent prelude and accompaniment of Phthisis, communicating to it a peculiar character, which has frequently led to much error in determining the nature of the disease. This form of Phthisis is allied to all those cases in which bron- chitis, in its various phases, constitutes a leading feature of the disease. Laryngeal Phthisis. - This distressing form of Phthisis is from an early period accompanied by a tickling in the larynx, which seems to be the origin of the cough. The voice becomes weak and hoarse, and not unfrequently there is more or less pain on deglutition. On inspection of the fauces and throat, follicular disease or great dryness of the mucous membrane is common. Sometimes the laryngeal dis- ease completely masks the pulmonary 1 See the author on Pulmonary Consump- tion, 2d edit. Case xvi. p. 70. 126 PHTHISIS PULMONALIS. lesion, causing a hoarse rough murmur on inspiration, which renders the physical signs at the apex of the lung inaudible, so that unless marked duhiess is distin- guished by percussion, it may be over- looked. Ultimately the voice is lost from destruction of the vocal cords by tubercu- lar ulceration. Deglutition becomes dif- ficult, and vomiting readily excited by reflex actions through irritation of the laryngeal, pharyngeal, and glosso-pharyn- .geal branches of the eighth pair of nerves. Under these circumstances emaciation makes rapid progress, all the symptoms of ulcerative laryngitis being added to those of Phthisis. (See Laryngitis.) Pneumonitic Phthisis. - I have now watched a considerable number of cases in which unquestionable Phthisis has originated in an acute pneumonia at the apex of the lungs, which, instead of dis- appearing in the usual way, has become chronic. Under such circumstances the dulness on percussion and bronchophony remain, the summit of the lung is consoli- dated, the general health, instead of ral- lying, remains weak, cough and expecto- ration become troublesome, while loud mucous and gurgling rattles arc gradually formed in the lung, indicating the exist- ence of cavities. Sometimes the consoli- dated lung remains latent for a considera- ble time, the patient in vain endeavoring to restore his original strength. Then an attack of haemoptysis has occurred, which induces him to visit a physician, and it is discovered that the lung is consolidated, and all the signs of Phthisis are more or less apparent. Discussion has taken place as to whether such cases should be denominated chronic pneumonia or Phthi- sis. In my opinion there is no difference between them. The exudation of the pneumonia degenerating, and not being absorbed, is transformed into tubercle, causing softening, ulceration, and de- struction of the lung, in exactly the same way as if Phthisis had been developed from tubercle at the commencement. I have also seen survivors from this form of the disease with flattening of the chest, as in ordinary chronic Phthisis. It must not be overlooked either that in- tercurrent attacks of pneumonia are very frequent during the progress of Phthisis, and that at all times the two diseases ex- hibit a marked tendency to run into one another. This circumstance confirms the truth of the pathology previously given, and unequivocally proves that tubercle is only a low type of exudation from the blood. In healthy persons such exuda- tion is transformed into pus, and rapidly disappears, whereas in individuals who are weak, and whose vital power is low, this process is more or less interfered with, is prolonged, and in extreme cases terminates in Phthisis. This view has recently been adopted by Niemeyer, who is one of those who purpose to call Phthi- sis Puhnonalis a chronic pneumonia, in the propriety of which, as applied to all its forms, I cannot concur. Complications.- Tubercular disease of the lungs is necessarily associated with every lesion occasioned by inflammation and tubercular exudation of the textures of the organ. Indeed it may be said to be made up of exudation disorders, acute or chronic, affecting the air-vesicles, bron- chi, fibrous tissues, and serous coverings of the lungs. Hence the various symp- toms of laryngitis, bronchitis, emphysema, hemorrhage, pneumonia, and pleurisy are more or less mingled together, may super- vene on each other, and occasionally, as we have seen, be so predominant and per- manent as to give peculiar characters or forms to the disease. Occasionally pleu- ritis gives such a character to Phthisis, occasioning local acute or stitching pains. T ubercular cavities in the majority of cases induce thickenings and dense adhesions between the pleura1, but sometimes they may burst or ulcerate through the pleurse, where there is no adhesion, causing pneumo-thorax, associated or not with more or less empyema. In addition, however, to these lesions of the chest, Phthisis may be associated with tubercular deposits occurring in other organs, in which case a train of symptoms will arise dependent upon the local lesion, wherever that may be. Of these the most common, and the most to be dreaded, is tubercular ulceration of the intestines, inducing colliquative diarrhoea, and perhaps perforation of the gut, with fatal peritonitis. In the young, also, we may find the disease associated with va- rious tubercular or scrofulous diseases of the osseous texture, and sometimes of the brain or its membranes. It would exceed our limits to enter upon the innumerable complications which in this manner may arise ; all that is necessary to say is, that there is no tubercular disease of any organ or tissue which may not be found sometimes associated with Phthisis, and which, con- tributing its own special symptoms to the pulmonary ones, increases the general dis- ease and downward progress of the patient. Besides this class of affections, there are others of importance. It is by no means uncommon during the progress of Phthisis to find persons complaining of puffiness of the feet, or face, and on examination of the urine it will be found to contain albu- men. In short, one of the forms of Bright's disease may develop itself, and usually that now recognized as the waxy form. The liver also may enlarge, and add to the distress of the patient by its pressure and bulk. Such increased growth of the hepatic organ will also generally be found to be dependent on a DIAGNOSIS OF PHTHISIS PULMONALIS. 127 waxy transformation of its cells and ves- sels. The spleen may undergo a like al- teration, although its enlargement is more rare. Pericarditis and otlier inflamma- tory diseases may occur-occasionally gout or rheumatism. Cancerous disease, it is now known, may be associated with Phthisis, but it is an occurrence of ex- treme rarity. In chronic cases the prac- titioner must be prepared to meet with a variety of other complications, which, though they may bear no essential or con- stant relation to Phthisis, render the dis- ease more distressing and fatal should they occur. III. Diagnosis of Phthisis Pulmonalis. It has been previously pointed out that Phthisis is preceded by premonitory symp- toms, which indicate diminished health, weakness, or imperfect nutrition of the individual. This condition has been spoken of by some writers as constituting a pretubercular stage of disease. Ail that can be said, in a diagnostic point of view, of this state of health, is that in young and delicate persons it should occa- sion much anxiety, as it may, or may not, terminate in Phthisis, and that it should demand great watchfulness and frequent careful examination, in order that the first positive signs of the disease may be detected. Acute Phthisis.-The diagnosis of this form of the disease is exceedingly difficult, as all the symptoms and signs are identical with those of an acute in- flammation of the lungs. It is only by careful observation of the premonitory symptoms, the existence of a marked hereditary taint, the amount of emacia- tion as compared with the extent of local disease, the continuity of the fever, and the rapid formation of cavities, that we are at length able to pronounce with con- fidence as to the presence of acute Phthisis. In all its essential features the attack is similar to acute pneumonia of the apex, from which in its earliest stages it cannot be separated. As the disease progresses, however, the excessive exhaustion and breaking clown of the lungs establish the nature of the affection, while its rapid progress and the continued fever too cer- tainly indicate its acute nature. In the present day the extreme difficulty of diag- nosis is fortunately not of so much import- ance as it used to be, when such symp- toms led to bleeding, and an antiphlo- gistic treatment. In the course of chronic Phthisis similar symptoms may arise, either from fresh exudation of tubercular matter, or from intercurrent attacks of pneumonia or pleurisy, communicating to the disease for a time an acute character. Chronic Phthisis.-In this, by far the most common form of the disease, it is of the greatest consequence to deter- mine its commencement by the conjoined methods now in vogue. Its progress is capable of being recognized with con- siderable certainty, and the means at our disposal for doing this may be considered under the heads of Pulmonary Symptoms, Pulmonary Percussion, Pulmonary Aus- cultation, Microscopical Examination of the Sputum, and Altered Changes in the Form and Movements of the Chest. Pulmonary Symptoms. - The earliest symptom is cough, which, at first short and dry, resembles the ordinary effort at clearing the throat. Sometimes it is attributed to the chest, but more com- monly is thought to arise from dryness or tickling in the throat. Such a cough too frequently excites little attention, al- though its persistency and defiance of ordinary remedies communicate to it a grave character. After a time the cough is followed by expectoration, at first of a thin mucous fluid, which, however, soon becomes thick and opaque, or is slightly streaked with blood. There is now occa- sionally felt a tightness or constraint, on taking a deep breath, under one clavicle, which, as the disease progresses, becomes painful, especially on coughing. This cough and expectoration, more particu- larly when they follow the premonitory symptoms, and are developed in the man- ner described, are highly characteristic of Phthisis. In the subsequent stage of the disease, the cough becomes more frequent, harassing, and long-continued. The tick- ling in the throat may excite vomiting. The expectoration is more abundant and prevalent, frequently tinged with blood, and forms distinct masses (nummular sputa) generally indicative of excavations, and may be so heavy that, instead of float- ing, it sinks in water. Lastly, it may contain masses of indurated matter, com- posed of portions of tubercular lung, or, in very chronic cases, fragments of creta- ceous or calcareous matter. Early hae- moptysis, as we have seen, is highly diag- nostic of Phthisis, and should always ex- cite grave attention. Should it be soon followed by or mixed up with the other symptoms, the diagnosis is considered more certain. Pulmonary Percussion.-When miliary or infiltrated tubercle occupies a certain number of the air vesicles, careful percus- sion above or under one clavicle elicits slight dulness of the pulmonary note, especially well marked when compared with the clear note on the opposite side. As it is seldom that the disease com- PHTHISIS PULMONALIS. 128 mences at the apices of both lungs at once, this sign is one of great value, and indicates very positively, not only the ex- istence, but very frequently the extent of the disease. The greater the dulness or flatness of tone, the more solid is the por- tion of lung struck; and the further over the chest, anteriorly and posteriorly, the dulness can be produced, the greater is the amount of pulmonary tissue involved. It should not be overlooked, however, that occasionally the disease exists equally on both sides, when diagnosis by means of percussion is always difficult. In the earlier stages, indeed, it is then impossi- ble, and in the later stages, even with large cavities on both sides, I have known the percussion note so equal and clear as to mislead the careless observer. Some- times also, though the lung be greatly condensed, an amount of emphysema an- teriorly communicates clearness on per- cussion : hence the lung should always be examined posteriorly as well as anteriorly, in order to avoid error. On percussing the chest in cases of Phthisis with the mouth open, there is sometimes elicited a peculiar noise, called by Laennec the bruit depotfelb, or cracked- pot sound, which he thought was diag- nostic of a cavity. But I have found this noise could also be produced in cases of pneumonia, in pleurisy with effusion, and even in several healthy chests. Moreover it is often absent when pulmonary cavi- ties arc unquestionably present, and can- not therefore be considered as diagnostic of their presence, unless it be coexistent with other symptoms and signs of Phthisis. When present, it seems to indicate either healthy lungs, with very elastic thoracic walls, or else increased density mingled with confined or compressed air in the thorax. In either case, on striking the chest smartly, the air beneath is forcibly ejected through the bronchi and trachea, producing vibrations which occasion the peculiar sound.1 Pulmonary Auscultation. - The first sounds audible with the stethoscope are prolongation of the expiratory murmur and slight harshness, or a wavy inter- rupted character communicated to the inspiratory murmur. These signs, if clearly marked under one clavicle, follow- ing the premonitory symptoms, and ac- companying persistent hacking cough, can leave no doubt that tubercle is actu- ally present, and the disease pronounced. 'It frequently happens, however, that these signs are so indefinite that, although we may suspect, we hesitate to speak confidently. In all chronic organic dis- eases there must be a period so nicely balanced between health and disease-in which the altered texture is so slightly- altered-that our senses are incapable of appreciating any alteration that may be produced. It is in such cases that every- thing which enables us to determine such delicate signs with greater exactitude be- comes valuable, and I have no hesitation in stating that the differential stethoscope of Dr. Scott Alison has here afforded me the greatest assistance. In several deli- cate young persons, in whom when every precaution and care has been employed we fail to discover any alteration in the pulmonary sounds, an increased intensity in the sound of the carotid artery below the clavicle has afforded valuable indica- tions. It is at this early and uncertain period of the disease that the greatest skill in auscultation and diagnostic powers are required in the physician. As the disease advances, the prolonged expirations and harsh inspirations be- come more marked, and at length a de- cided increase in the vocal resonance of the affected side is audible. This indi- cates considerable condensation of the apex of the lung. If the disease pro- gresses, slight crepitation is audible, at first at the termination of a forced in- spiration, and gradually it occupies the whole of that act. This is diagnostic of tubercular softening. The fine moist rattle now becomes evident, and the in- creased vocal resonance louder, until it amounts to bronchophony. The auscul- tatory signs also extend in area over the chest, preceding the dulness on percussion, and generally appearing in the order in which they were noticed over the apex. At length the crepitation passes into mucous rale. This in its turn becomes coarser and coarser, indicating the existence of greater softening and even of cavities. As these enlarge, gurgling and splashing sounds are heard, especially on coughing, and the increased vocal resonance becomes pealing, and imperfect or perfect pectori- loquy7 is present. These latter sounds are diagnostic of a cavity or cavities. The sounds heard over these vary according to their size, contents, and the condition of the walls. If large, with rigid walls, and partly filled with fluid and partly with air, tinkling or metallic squnds may be heard on coughing or speaking. If al- together dry, amphoric or blowing noises may be distinguished. These last, if per- sistent, indicate that the secretion of pus is arrested, the softened tubercle got rid of, and contraction and cicatrization pos- sible. When in chronic cases of Phthisis dry blowing, combined with friction sounds, can be determined at the apex, it points out that adhesion and contractions of the tuberculatcd pulmonary tissues are taking place. If absence of respiratory murmur 1 See the author on Pulmonary Consump- tion, &c., Diagnostic Value of the Cracked-pot Sound, p. 108. DIAGNOSIS OF PHTHISIS PULMONALIS. 129 exist, it may depend on pleuritic effusion, when dulness on percussion and increased vocal resonance, or segophony, will de- termine the nature of the lesion. But it may be accompanied by resonance on percussion, with a brazen, hollow, or metallic sound on coughing or a forced inspiration ; in which case there is pneu- mo-thorax, and the tubercular cavity has formed a communication with the pleura. In retrograde Phthisis, the ausculta- tory signs disappear in the inverse order to that in which they appear. The moist sounds become dry, and these last dimin- ish in intensity and extent. Friction noises and dry bronchial murmurs are heard, with prolonged expiration, wheez- ing, and sonorous rhonchi indicative of rigid bronchial tubes, conjoined with more or less emphysema. The area of dulness gradually diminishes, but a con- densed mass in the lung generally re- mains for years at one or both apices, giving rise to harsh respiratory murmurs and increased vocal resonance, consti- tuting strong evidence to the judicious observer of the diseased changes through which the lung has passed. Microscopical Emamination of the Spu- tum.-The sputum of phthisical patients, in the great majority of cases, may be found to contain, under the microscope, fragments of the areolar and elastic tis- sues, derived from disintegration of the lungs. They not infrequently present circles and half-circles, indicative of the form of the air-vesicles, and, when pres- ent, offer the most positive proof of pul- monary ulceration. Van der Kolk, of Utrecht, was the first to point out that [Fig. 24. Lung tissue obtained from sputa after digestion in caustic soda. (Drawn by Dr. John Wilson.)] such fragments might be seen with the microscope, at the commencement of the disease, long before percussion or auscul- tation gave any positive signs of its exist- ence. Although such examples are rare, I am satisfied that they do occur, and that the microscopical examination of the sputa under such circumstances enables us to arrive at a clear diagnosis when otherwise there would be great doubt. Drs. Andrew Clark and Fenwick have confirmed this fact by their researches into the structure of phthisical sputum. The latter physician has pointed out that the examination is much facilitated by first liquefying the sputa with a solution of caustic soda, when the fragments of lung tissue are precipitated, and their amounts as well as character readily esti- mated. Altered Changes in the Form and Move- ments of the Chest.-As Phthisis advances, a distinct flattening and sinking in of the thoracic walls below the clavicle may be observed, generally coincident with the formation of cavities and loss of lung substance, of which it is diagnostic. An alteration in the movements of the affected side may be seen even earlier, and may be roughly ascertained by spreading the fingers of both hands like a fan over the two sides of the chest, and bringing the thumbs together at the middle of the ster- num. On a forced inspiration, it may thus easily be seen that the thumb corre- sponding with the affected side moves less. The amount of this movement can be ascertained with great exactitude by means of the stethometer, and compared with that on the opposite side. In addition to the symptoms and signs referable to the chest, there must not be overlooked a variety of circumstances which in conjunction with these will materially assist the diagnosis. Among these are the preceding premonitory symptoms ; the continued impaired appe- tite and disordered digestion ; the aug- menting languor and debility ; the hectic night-sweats ; lustrous eyes ; the hope- fulness and imaginative intellect ; and even the alternations of the disease from better to worse, all of which arc more or less characteristic. Much has been written concerning what is called the differential diagnosis of VOL. IL-9 130 PHTHISIS PULMONALIS. Phthisis, and the means of distinguishing it from other diseases of the chest. But the truth is that a Phthisis necessarily implies the existence of almost every lesion of the lung, the tubercular exuda- tion giving rise to or being accompanied by congestions and inflammations of the plcurie, bronchi, and pulmonary paren- chyma, with all their local signs and general symptoms. Pulmonary hemor- rhage and abscess are common. Emphy- sema, though seldom present in its ad- vanced stage, so as to alter the form of the chest, is common in limited portions of the lung near chronic and retrograde tubercular deposits. Any lesion what- ever, occurring at the apex of the lung in a young person laboring under the pre- monitory symptoms we have described, must be regarded with suspicion. In adults, an acute pneumonia at the apex may go through its natural progress, and leave no trace behind. But if it becomes chronic, a Phthisis may be the result. Indeed there are many cases in which a chronic pneumonia of the apex and Phthisis Puhnonalis may be said to constitute the same disease. Cancer of the lung is a disease of advanced age ; the dulness on percussion is more marked, the tubular respiration and bronchophony are much greater, and moist rattles are scarce or absent. Expectoration is trifling, and, when present, unlike that of Phthisis ; sometimes it resembles currant jelly. The emaciation, night-sweats, and gene- ral aspects afford little assistance. A di- lated bronchus, independent of Phthisis, is rare, but when present is often asso- ciated with bronchitis and asthmatic symptoms, while the physical signs of the cavity are generally best marked at the posterior and middle regions of the chest, rather than at the apex. In advanced cases a pleurisy with effusion or a pneumo- thorax may occur, when the physical signs distinctive of each will readily establish the diagnosis. The great difficulty is to detect Phthisis at its first appearance, and hence everv circumstance that can throw light on its history at this period is important. Ac- cording to Dr. Ringer, the heightened temperature of the body, as determined by the thermometer, indicates the deposi- tion of tubercle for several weeks before physical signs are developed. It is true that a similar increase of temperature occurs in a few other diseases, such as typhoid fever or rheumatism, but their symptoms are readily separable from those of Phthisis. This new method of recognizing the disease at an early stage requires more extended observation before it can be generally adopted. The subse- quent progress of Phthisis admits of being followed by the physician cognizant of its morbid anatomy, and well skilled in aus- cultation, not only with certainty, but in the majority of cases with a degree of ex- actitude that must be regarded as highly honorable to the progress of medicine in modern times. IV. Prognosis of Phthisis Pulmonalis. Phthisis Pulmonalis, up to a compara- tively recent date, was not only regarded as a very dangerous disease, but as one which was uniformly fatal. This idea was supported by the circumstance that before the general introduction of physical diagnosis it was not clearly detectable until it was far advanced, while the merely palliative treatment then in vogue was anything but favorable to recovery. If, notwithstanding, a case here and there did ultimately get well, medical men were more disposed to accuse themselves of an error in diagnosis than doubt the correct- ness of so general a dogma as the incurabil- ity of consumption. Even when at length morbid anatomy unequivocally demon- strated the possibility of tubercular cavities cicatrizing, and of individuals afterwards attaining an advanced age, such an event was regarded as one of extreme rarity, and as occurring altogether independently of treatment. "No fact," says Andral, "demonstrates that Phthisis has ever been cured, for it is not art which ope- rates in the cicatrization of caverns ; it can only favor this, at most, by not oppos- ing the operations of nature. For ages remedies have been sought to combat the disposition to tubercles, or to destroy them when formed ; and thus innumerable spe- cifics have been employed and abandoned in turn, and chosen from every class of medicaments." Even Louis, in his ad- mirable work, while admitting that a cure might rarely take place, points out that in such cases the disease must be limited and the result fortuitous. Hence the ad- mitted occasional recoveries in no way interfered with the general view enter- tained of the unfavorable prognosis of this malady, or stimulated medical men to replace a palliative by a curative treat- ment. At present, so far from Phthisis being considered to be uniformly or even gene- rally fatal, it is admitted that treatment can in a great majority of cases prolong life, whilst in many, the number of which is annually increasing, a complete and permanent cure may be effected. This revolution in our prognosis of the disease is owing-1st, to the facts arrived at by morbid anatomy; 2d, to a more perfect theory or pathology of the disease ; and 3d, to the discovery of cod-liver oil as a remedy. 1. The careful post-mortem examina- PROGNOSIS OF PHTHISIS PULMONALIS. 131 tions now made with such regularity in our large hospitals have demonstrated the frequent occurrence of old condensa- tions, cicatrices, and calcareous concre- tions at the apices of the lungs in persons of advanced age who have died of other diseases. In 1845, I pointed out that in the Royal Infirmary of Edinburgh they occurred in the proportion of from one- fourth to one-third of all the individuals who died after the age of forty. Roger and Boudet had previously shown that at the Salpetriere and Bicetre hospitals in Paris, amongst individuals above the age of seventy, they occurred in one-half and in four-fifths of the cases respectively. There can be no doubt that these cica- trices and concretions indicate the heal- ing and drying up of cavities and softened tubercular matter at some previous period in the life of the individual, and the con- sequent spontaneous cure of the disease in a considerable number of persons. 2. The careful examination of tubercle by means of the microscope demonstrates that it neither originates in nor gives rise to cell formations, but that it consists of an exudation of the blood rendered feeble in vital power by impaired nutrition, and especially by deficiency of primary mole- cules of fat in the blood.1 Hence the encouragement given to our efforts in stim- ulating the nutritive functions, and especi- ally assisting in the increased assimilation of an easily digestible oil, whereby, while the tissues generally are supplied with formative material, the tubercular matter has time to degenerate and be absorbed ; so that any cavities which have been pro- duced may cicatrize. Attempts at cure in this direction have been so eminently successful as to influence our prognosis in a marked manner. 3. It is very much to be doubted, how- ever, whether this pathology would ever have been arrived at, or if it had, whether a successful treatment could ever have been established, unless the therapeutical properties of cod-liver oil had been recog- nized. This animal substance is easily assimilated, is not purgative, and meets all the indications required, while expe- rience has demonstrated that it restores to the emaciated body the nutritive ele- ments it so much requires, and enables it to triumph over the disease. It can no longer, therefore, with truth be consid- ered that Phthisis Pulmonalis is that op- probrium medicines it was formerly con- sidered. Nor should certain charitable institutions any longer refuse to admit such cases on the ground of their incura- bility. In my work on Pulmonary Consumption1 will be found full details of the arrest of the disease in its most advanced stage, the individuals not only being still alive, but having enjoyed excellent health since their recovery, for periods varying from ten to twenty-live years. To the list of cases therein given I could now add many more. Twelve similar cases were recorded by Dr. Quain in 1852,2 and many others may be found scattered in the works of different authors, and in the practice of individual medical men. There can be little doubt that could they be collected it were easy to prove that such examples, instead of being few and far between, arc much more numerous than is generally supposed. It is very difficult, however, to watch for many years in succession the progress and termination of chronic Phthi- sis ; and in hospitals this difficulty is in- creased, as the patients on getting better go out long before the disease is even per- manently arrested. All attempts to in- duce medical men to unite and record their experience on this or any other great question involving the prognosis or treatment of disease have hitherto failed. We are, therefore, limited to the conscien- tious efforts of individuals in our attempt to elucidate this question, which cannot be expected in a matter of such magni- tude and importance to be, at present, of any great avail. Among these, how- ever, I have great pleasure in referring to the accurate method in which Dr. Pollock has recorded his ten years' experience at the Brompton Consumption Hospital.3 Were such method and care more uni- formly practised by hospital physicians, and extended over more lengthened pe- riods, many of the unsolved problems connected with this subject might be elu- cidated. I confidently look to the future as affording means for demonstrating the ratio and conditions under which the prognosis of Phthisis may be determined. In the mean time, I can only express my conviction that its permanent arrestment and cure are, by judicious treatment and hygienic management, becoming every day more frequent and more widely extended. In reference to the prognosis of indi- vidual forms or cases of Phthisis, we must regard acute Phthisis as generally fatal. The difficulty here lies in the diagnosis. Once recognized, however, the persistency of intense fever, with rapid emaciation and formation of cavities, give us little hope of a favorable termination. 1 In making this statement I am fully aware of the observations and arguments of Virchow and his followers, but which, for the reasons previously given, I regard as not only inconsistent with histological and patho- logical research, but as especially opposed to all we know of clinical facts in modern times. 1 Pp. 152 et seq. 2 Lancet, pp. 487 et seq. 3 The Elements of Prognosis in Consump- tion. London, 1865. 132 PHTHISIS PULMONALIS. In the earliest periods of Phthisis, the prognosis should be very guarded, but on the whole encouraging. As a general rule, the more slowly it advances, the less fever and emaciation, and the better the appetite, the more probability exists of an arrestment. In the second stage, the favorable symp- toms are limitation of the disease to one lung, dulness not extensive, and not in- creasing rapidly ; no persistency of moist rattle ; expectoration moderate ; fever tri- fling ; emaciation not great; capability of taking nourishment and a certain amount of exercise. The unfavorable symptoms are continuous fever, quick pulse, hae- moptysis repeated, profuse expectoration, rapid softening of the tubercle, and its deposition in both lungs; bad appetite and impaired digestion ; increasing ema- ciation ; profuse diaphoresis and the ex- istence of unfavorable complications. In the third stage, the favorable signs are the existence of a cavity in one lung ; gurgling or other moist rattles occasion- ally disappearing, and the excavation be- coming dry, with blowing sounds; grad- ual flattening of the subclavicular space, while the other parts of the chest move freely. Further, the disease in the oppo- site lung absent, or if present slight, with- out a tendency to extend ; coarse friction sounds over the cavity; and a general tendency to concentration, density, and fixity of the lesion. The favorable symp- toms accompanying these local changes are, a tranquil pulse, no fever or sweating, emaciation checked, tolerable appetite, and capability of digesting nutriment, di- minished cough and expectoration, power of taking more exercise and gaining flesh, and absence of complications. On the other hand, the unfavorable symptoms are the converse of these, espe- cially cavities on both sides, loud, moist, and gurgling rattles, increasing dyspnoea, profuse expectoration, especially of green- ish or ichorous matter, extreme ema- ciation, anorexia, nausea, vomiting and incapability of retaining or digesting nu- triment, profuse diaphoresis and quick pulse, fever and restlessness at night. If now any serious complication arises, more particularly continued diarrhoea, albumin- ous urine with oedema of the feet or ankles, laryngitis, or pneumo-thorax, &c., &c., death is not very distant. It is very rarely that haemoptysis proves fatal, but should it occur profusely when weakness is extreme, death may be immediate. V. Treatment of Phthisis Pulmonalis. The treatment of Phthisis Pulmonalis, up to a recent period, has been too much governed by a desire to relieve symptoms -in other words, has been more palliative than curative. Unfortunately the reme- dies useful for the former purpose are altogether incompatible for the latter, and ultimately even fail to relieve the func- tional derangements to which they are directed. A study of the pathology of the disease has led us to the conclusion that Phthisis is dependent,-firstly, on impoverishment of the blood ; secondly, on exudations into the lung, which assume a tubercular character; and thirdly, on destruction of the lung, owing to the suc- cessive depositions and softening of these. It follows that, instead of endeavoring to relieve cough or favor expectoration, our chief attention should be directed to im- prove the faulty nutrition, to cause ab- sorption of the tubercular exudation, to arrest the ulcerative process, and, lastly, prevent a recurrence of the disease. The special treatment required in individual cases should be made subordinate to these great ends-at all events should not be opposed to them. We shall therefore con- sider the treatment as general and special: the first directed to favor the removal of the pulmonary lesion ; the second to check occasional symptoms and complications. General Treatment of Piithsis Pulmonalis.-The great indication in the treatment of Phthisis Pulmonalis should be to improve the nutrition of the economy. This does not merely consist in increasing the quantity and improving the quality of the food, but in employing all those means which shall secure-1st, an appropriate diet; 2d, causing its as- similation, and the formation of good blood; 3d, securing the proper purifica- tion of this by the atmosphere ; 4th, see- ing that a proper demand for the addition of new matters to the tissues is created by sufficient exercise ; and 5th, that the effete matters be properly excreted from the economy by the emunctories. All these processes are comprehended in the function of nutrition. We shall most concisely convey our ideas as to the best means of increasing nutrition in phthis- ical cases, under the distinct heads of Diet, Cod-liver Oil, Pure Atmosphere, Climate, Exercise, and Bathing. Diet.-One of the leading symptoms in cases of Phthisis is the diminished, capri- cious, or disordered appetite, and power of taking food. It is true that many cases persistently assure you that they eat heartily, but on careful inquiry they will admit their appetite is easily satis- fied, or that they are small eaters. Even the friends sometimes assert that the pa- tients eat as usual, that they have ob- served no change and so on, the fact being that the nutritive matter actually taken into the economy is far less than it ought to be. So little observation and attention TREATMENT OF PHTHISIS PULMONALIS. 133 do those affected exhibit concerning their own cases, and so anxious do they appear to represent every circumstance in the most flattering point of view, that it is far from uncommon for them to declare them- selves as constantly getting better, up to the moment of their death. I have fre- quently pointed out to my clinical pupils that, in the reports of these cases taken down by the clerk at the bed-side, in an- swer to questions, it has been recorded day after day that the appetite is better and better, while the patients are visibly getting more emaciated, more weak, and at length die. Among the poor and half- starving population, it frequently happens that it is not the appetite or desire for food that fails, so much as the food itself. The result here, however, is the same, viz. that the body is not sufficiently nour- ished, that the tissues disintegrate more rapidly than they can be supplied with new substance, and that the blood is de- ficient in what is so necessary for support- ing health. In all cases of Phthisis Pulmonalis the diet should be generous, consisting of boiled milk, cream, eggs, butter, toasted bread, and all kinds of animal food, and farinaceous puddings. Acid substances and drinks should be as a rule avoided, the tendency to dyspepsia from too much acidity being generally present. After dinner a glass or two of generous wine (sherry) or two or three glasses of sound claret (not acid) may be indulged in. As much variety as possible should be se- cured, and every pains taken by good cooking and superior quality of the viands to tempt the weak and capricious appe- tite. As to quantity, I have never seen any necessity for limiting it. The only difficulty is to take enough ; the which once accomplished, amelioration in all the symptoms may be confidently predicted. It should be remembered, however, that mere eating and loading the stomach, without a proper digestion and assimila- tion, can be of little benefit. In this re- spect individuals differ, some doing best with two or three meals a day, whilst others find that eating more frequently, but less at a time, answers better. In nothing is the constant attendance of a judicious medical man more serviceable than in watching the effects of diet, and observing from its influence on each indi- vidual case how it should be regulated. When fever runs high, the pulse is quick and the tongue furred, there will naturally be no disposition to take solid food. Under these circumstances we should take care that nutritious drinks are regularly administered, especially beef-tea and milk, and seize the earliest opportunity of returning to a more sub- stantial diet. Many may think that in most acute cases, or during an intercur- rent attack of pneumonia, these rules should be departed from. Formerly, in- deed, antiphlogistics and the local appli- cation of leeches were employed ; but it has now been satisfactorily demonstrated that even in acute cases of pneumonia itself, in vigorous constitutions, such practice is injurious how much more, then, would it be so in cases of Phthisis ? Inflammations are now recognized to be diseases of weakness, and we feed them as we do fevers, with the most marked success. When, therefore, attacks of either supervene during the progress of Phthisis, so far from doing anything to diminish the strength of the economy, the most anxious care will be required on the part of the practitioner to counteract, by all the support he can administer, the future exhaustion of his patient. An increase in the quantity and im- provement in the quality of the food may frequently be observed to benefit cases of Phthisis, especially among the half- starved poor; the more so if associated with change of scene, active exercise, or varied employment. The treatment prac- tised at the commencement of this cen- tury by Dr. Stewart, of Erskine, near Glasgow, which consisted in freely ad- ministering beefsteaks and porter, and causing exercise to be taken in the open air, excited considerable attention in its day by the success it occasioned. I have been informed that in America the con- sumptive patient, by eating the bone marrow of the buffalo on the prairies, is at length enabled to hunt down the ani- mal. I have known several young men on large sheep farms in Australia cure their tubercular lungs by eating fat mut- ton and galloping about on horseback. Whenever food rich in fat can be tolerated by the stomach, it will produce like effects, and hence the occasional value of bacon, pork chops, caviare, suet, yolks of eggs, and the produce of the dairy, such as milk, cream, and butter. Cod-liver Oil.-All good food must con- sist of a proper mixture of albuminous, fatty, and mineral principles. The two former, holding the third in solution, after being prepared by the digestive fluids form a molecular fluid-the chyle- out of which the blood is formed. In Phthisis, however, the process of chylifi- cation is impaired ; the fatty constituents of the food are not separated from it and assimilated, or they are deficient, as very commonly results from a dislike to fatty substances. In either case, the blood abounds in the albuminous elements, and when exuded into the lungs, as we have seen, forms tubercle. To induce health, it is necessary to restore the nutritive 1 See the author's Treatise on the Restora- tive Treatment of Pneumonia, 3d edit. 1S66. 134 PHTHISIS PULMONALIS. elements which are diminished, and this is done directly by adding a pure animal oil to the food. By so doing, we form richer chyle and better blood ; we restore the balance of nutrition, which has been disturbed ; respiration is again active in excreting more carbonic acid gas ; the tissues once more attract from the blood the elementary molecules so necessary for their maintenance; the entire economy is renovated, so that while the histogene- tic processes are revived, the histolytic changes in the tubercle itself also are stimulated, and the whole disappears. We have previously seen that food rich in fat will occasionally produce these effects, but then the powers of the stomach and alimentary canal must not have under- gone any great diminution. In most cases, however, the patient is unable to tolerate such kind of food, which is not digested. Under these circumstances, cod-liver oil is directly indicated, by giving which we save the digestive apparatus, as it were, the trouble of separating fluid fats from the food. By giving the oil directly in quantity, a large proportion of it enters the system, unites with the al- bumen, and thereby forms the molecular basis so essential for the chyle. Since the days of Liebig, chemists have generally supposed that albumen forms the basis of the tissues, and is a flesh-former, while fat is necessary for respiration, and by its decomposition furnishes heat. An unac- quaintance with histology is the cause of this error, fat being demonstrably neces- sary for the development and support of muscle and of every tissue. This has re- cently been further shown by the investi- gations into the diet of labdrers by E. Smith, the feeding of animals by Lawers and Gilbert, and the experiments of Haughton, Frankland, Fick, and Wislice- nus. Hence the universal craving and necessity for fat by the vigorous and working man, whilst a dislike to it is a strong symptom of inherent weakness, and an incapability of assimilating it the chief cause of tubercular disease. It was in the years 1840 and '41 that I found cod-liver oil used very generally in the German hospitals in all scrofulous and phthisical cases. In England it at one period had been employed in Manchester, at the beginning of the century, by Drs. Kay and Bardsley, in rheumatism, but had fallen into neglect. In the hospitals of Heidelberg and Berlin, I watched with great care the effects of the oil in several cases of Consumption, and satis- fied myself of its remarkable powers as a nutrient, under circumstances which in British hospitals would have been at- tended with little hope. In the autumn of 1841, therefore, I published a mono- graph containing an account of what was then known of this substance, and recom- mended it especially to my countrymen, both from theoretical and practical grounds, as a valuable remedy in Phthisis.1 The first physician who tried it in the Royal Infirmary of Edinburgh was Dr. Spittai; but so little were druggists ac- quainted with the oil, that I found on visiting his wards that all the patients were taking linseed oil. The same mis- take had previously occurred to Rush, in Berlin. I was therefore obliged to get it made expressly, which, after a time, was done by the Messrs. Parker and Co., oil merchants, Leith-walk, who for many years made the purest cod-liver oil in Great Britain, which they sent over the country at the moderate rate of 16s. a gallon. When in the course of time it was asked for in London, Mr. Jacob Bell, the eminent druggist in Oxford-street, caused a very pure oil to be made from the livers of the cod, which, however, was so expensive, that he dispensed it at the rate of half-a-crown an ounce. I was consequently written to by numerous per- sons in London and elsewhere, and was thus the means of causing hundreds of gallons to be distributed by the Messrs. Parker to all parts of the country. Gradu- ally, its value was generally appreciated throughout Scotland, and was extending in England, when it was tried in the Brompton Consumption Hospital of Lon- don. In 1849, Dr. Williams published a paper, in which, from extensive trial of the remedy, its value and mode of action were confirmed, a result still further sup- ported by the Report of the Brompton Consumption Hospital, published in 1851. Since then the employment of cod-liver oil in Phthisis has been almost universal, and has contributed in no small degree to remove that hopelessness and despair with which the treatment of the disease had been previously accompanied. In 1841, it was unknown in our druggists' shops, except here and there, where it was kept in small quantities for the use of tanners, who, curiously enough, had discovered that it possessed far superior power to all other fatty substances in penetrating and softening leather. At that time the eminent Edinburgh drug- gists, Duncan and Flockhart, did not dispense one gallon in the year, whereas at present they dispense between six and seven hundred gallons annually. A most extensive experience has now amply confirmed the opinion I published regarding it thirty years ago-viz. "That no remedy has so rapidly restored the ex- hausted powers of the patient, improved the nutritive functions generally, stopped or diminished the emaciation, checked the 1 See the author's treatise on the Oleum Jecoris Aselli, &c., 1841; also with Appendix, 1847. TREATMENT OF PHTHISIS PULMONALIS. 135 perspiration, quieted the cough and ex- pectoration, and produced a most favor- able influence on the local disease. Many individuals presenting the emaciation, profuse sweats, constant cough and ex- pectoration, as most prominent symptoms, with a degree of weakness that prevented their standing alone, after a few weeks' use of it, are enabled to get up with ease and walk about, with a visible improve- ment in their general health, and an in- creased amount of flesh." Thus it must be regarded as an analeptic (avaKa^avM^ to repair) or general restorative, being di- gestible where no other kind of animal food can be taken in sufficient quantity to furnish the tissues with a proper amount of fatty material. It is not by a chemical so much as by a histological process that the result is produced. By some, however, it is supposed that the superiority of cod-liver oil over other fatty substances is owing to the iodine, bromine, resin, and other medicaments it contains. But the quantity of these drugs in cod-liver oil is very minute, and it has been abundantly proved that no combina- tion of them given internally has any effect on the progress of Phthisis. Hence the idea of giving a watery extract of cod- liver oil, when the oil cannot be taken, appears to us to be erroneous in theory, and unlikely to succeed in practice. On the other hand, there are so few persons who cannot take the oil when it is abso- lutely necessary, that such preparations need be very seldom employed. I have known many individuals who prefer the brown and apparently nauseous to the light and comparatively pure oil. In all cases, that kind of oil is best that is most readily tolerated by the stomach. Those who at first express dislike to the remedy, by a little perseverance may be made to take it readily; if not, they should try whether it be retained best immediately before, immediately after, or in the inter- vals of meals. The crunching a biscuit, or a lump of sugar on which there has been placed a drop of some essential oil, sometimes removes the difficulty. At others, a little coffee, orange wine, or a bitter, and occasionally slightly warming the oil, so as to render it more fluid, an- swer well. By these or similar methods, it is rare indeed that the oil cannot be taken. [The addition of ether to cod- liver oil has lately been recommended.- II.] Numerous substitutes have been pro- posed for cod-liver oil, such as shark, dugong, and skate oils, cocoa-nut oil, neat's-foot oil, &c. Any of these sub- stances, including cream and butter, so long as they can be assimilated, and do not prove purgative, are beneficial in Phthisis. It will be found, however, that, of all oleaginou s matters known, cod-liver oil is the most generally useful and the best. Dr. Baur, of Tubingen, recom- mended that it should be used externally, but extensive trial has demonstrated what physiology teaches, viz. that the skin, being only slightly pervious to substances from without, cannot be made the vehicle for introducing nutritive matter. Dr. Buist, of Aberdeen, recommended injec- tions into the rectum, but objections to the use of constant enemata in this country are insurmountable, and although useful as a temporary measure, cannot be made available to a sufficient degree for the cure of a disease like Phthisis? What then is really required is not oil added directly to the blood, but oil digested and emulsionized by the pancreatic and other intestinal fluids; a truth which has in- duced Dr. Dobell to recommend that be- fore administration it should be mixed with pancreatic juice. In most cases where there is fever, rapid pulse, and furred tongue, cod-liver oil is no more tolerable than food. Under such circumstances it should not be in- sisted on. It will also be judicious, when taken for any length of time, to intermit its use now and then for a few weeks, and give in its stead a vegetable bitter. By attention to this circumstance, the medi- cal practitioner will easily satisfy himself that in this substance he possesses a most valuable means of prolonging life, and sometimes even of causing permanent cure in Phthisis Pulmonalis, especially when the benefits it confers are conjoined with the other methods of general treat- ment to be noticed. An additional benefit has followed the obvious good effects of cod-liver oil in Phthisis, as stated by Dr. E. Smith, who says : "A prime reason of the good which has resulted from the use of the cod oil is the regular supply of fat to persons who otherwise would not have taken it in due quantity; and a great merit in the intro- duction of it to general use is in having led inquirers to prove the very important part which fat plays in the animal sys- tem, and the real necessity for it which exists in all persons and particularly in the young."1 This observation evidently results from the histology, pathology, and treatment of Phthisis which for so many years we have endeavored to impress upon the profession. Pure Atmosphere.-If it be essential for the purpose of nutrition to supply the blood with those materials which are ne- cessary for building up the tissues and compensating the waste they undergo during their action, it is equally so that such materials should be properly pre- pared and fitted for the purposes to which they are to be applied. Of the various 1 On Consumption, p. 348. 136 PHTHISIS PULMONALIS. processes necessary to this end there can ' be little doubt that that of respiration is the chief, the object of which is constantly to introduce into the blood from the at- mospheric air a certain amount of oxygen, and constantly to give off from the blood to the air a corresponding amount of car- bonic acid gas. If the lungs be feeble or diseased, their action is of course dimin- ished, a circumstance which only renders it the more necessary that no difficulty to oxygenation of the blood should be allow- ed to originate from a deteriorated con- stitution of the ail' itself. But this truth is one which it is exceedingly difficult to impress upon patients, the irritability of whose chests and whose susceptibility to cold induce them to close the doors and windows, and thus prevent fresh air from entering their rooms. Now, while the giving off carbonic acid gas by the lungs makes no impression upon the mass of the atmosphere at large, it soon sensibly de- teriorates the amount of air inclosed in a moderate-sized room, the breathing of which is most destructive to the phthi- sical invalid. Instead of inhaling only oxygen and nitrogen, and expiring car- bonic acid gas and nitrogen, they take in a sensible amount of carbonic acid at each inspiration, which poisons the arte- rial blood, renders it less fit for nutri- tion, and irritates and burdens the lungs, occasions languor, bad appetite, pallor of countenance, and indeed every evil which it should be the aim of the physician to remove. Moreover, good diet and cod-liver oil must be useless un- less a vigorous respiration exists at the same time, as they tend to increase the carbonaceous elements in the frame, which are mostly excreted by the lungs. A proper ventilation of the rooms occu- pied by the patient is therefore absolutely essential, and this rule especially applies to the sleeping room. The majority of mankind spend one-third of their life in sleep, while the invalid often remains in the bed or bedroom much longer. How important then is it to secure a pure breathing air during this period ! It is now twenty-five years since I became convinced of the injury of shut- ting up patients in their rooms during winter, and regulating the temperature, as was formerly the custom. A young man, with cavities in his lungs, who had borne confinement in this way tolerably well for a winter, found it so irksome on a second trial, that on one occasion he went out and walked to the top of Ar- thur's Seat. Instead of being worse, he that day ate his dinner with appetite, all his symptoms were moderated, and under the combined influence of pure air and exercise he not only was better, but ulti- mately worked out a perfect cure, and is now alive in good health. Since then I have had abundant opportunities of satis- fying myself of the great advantages to be derived from securing free ventilation and pure air to consumptives. These points are dwelt on as forcibly as possible, because it must be admitted that, partly as the result of custom or prejudice and partly in consequence of the severity and changeableness of the climate, a good ventilation of the house and sleeping room is, in this country, a matter of extreme difficulty. In all cases, however, it merits the especial attention of the physician. Hence he should regard the position of the house, the nature of the prevailing winds, the windows of the sitting-room, and the place in it occupied by the patient, how the bed is placed in reference to the door and windows, &c. The great end he should aim at is to sur- round his patients with as much pure air as possible, consistent with warmth and ab- sence of draughts, a problem often very difficult to work out. There should be no curtains round the bed, an open fire should burn in the room during winter, in itself an excellent ventilator, the bed should be placed in a position free from the direct draught between the fire and the door or window, and only a moderate temperature permitted, as when in bed the patient ought not to feel cold. In summer good ventilation should be se- cured by letting down the windows an inch or so at the top - an excellent method, first strongly insisted upon by Dr. McCormack, of Belfast, and one which, indeed, is at all times available in this country; unfortunately, abroad, the construction of the windows does not ad- mit of it. The necessity of constantly breathing pure air should prevent the phthisical patient from attending crowded assemblies, tables d'hote, theatres, con- certs, or any amusements where the at- mosphere must necessarily be deterio- rated, and which, being breathed for hours, almost invariably exacerbates the symptoms and increases the malady. It is in consequence of the facility of breath- ing a purer air all day, and the necessary avoidance of crowded and closed rooms at night, that I am persuaded the upper classes of society experience much of the good effects of residing in certain places famed for their climate-the next point we must consider. Climate. - It was formerly supposed warm climates were beneficial for con- sumptive patients, and artificially heated temperatures, cow-houses, and other con- trivances were had resort to, to compass this end. But it will be invariably ob- served that unaccustomed warmth, the excessive heat of summer and autumn, or the climate of India and other tropical countries, is most injurious. Continuous frost and cold are in themselves beneficial, TREATMENT OF PHTHISIS PULMONALIS. 137 but by preventing the individual taking exercise in the open air they are not on that account to be recommended. What is really required is a cool temperate cli- mate, free from great alternations of tem- perature, which should range from 55° to 66° Fahr, during the day, and from 45° to 55° at night. The air should be dry, or with only slight moisture, and a clear bright sun. Such an exhilarating climate, in which exercise can be taken almost daily in the open air during the winter and spring months, is the best for the consumptive patient. It exists to the greatest perfection on the north shore of the Mediterranean, between Cannes and Savona in the western, and between Spez- zia and Pisa in the eastern Riviera. It may also be found in various places on the southeast coast of Spain, especially at Malaga ; on the north African shore, such as Algeria and Egypt, and many other places. In the western hemisphere, suit- able places may be found, especially in the islands of the West Indies, and in Australia the southern shores of Victoria. The native of the British Isles who visits the sheltered nooks of the south European shore between Cannes and Pisa will be struck with the bright sun, clear atmo- sphere, genial yet bracing air, steady temperature, verdure, and brilliant vege- tation which surround him from January to March'-months which at home are characterized by frost, snow, rain, fog, gloom, bleak winds, and a barren vegeta- tion. After this period, however, the picture is reversed. Then a hot and sul- try atmosphere, a scorching sun, an intol- erable glare, innumerable mosquitoes, a brown and burnt-up vegetation exist, while at home there prevail a genial atmosphere, cool breezes, moderate sun- beams, a varying sky, an emerald foliage, and a charming variety of mountain and lake which gives all that can be desired. I do not know a better winter residence for the invalid than some sheltered bay in the western Riviera where, in consequence of the sea being immediately in front of his house, and innumerable little valleys of the Alps close behind it, he can at all times protect himself from wind, from whatever quarter it may blow. Many observations have satisfied me that the still, warm, and moist relaxing atmo- sphere, though of the greatest service in cases of asthma, is injurious to the phthisical invalid. Great care should be taken to avoid sharp winds, and espe- cially east winds. This at Mentone is readily done by walking out of the back door of your house directly into some pro- tected Alpine valley. In this country, however far we go west, it is escaped with difficulty, and as a general rule North Britain more especially should be avoided from January till the end of May. In summer and autumn, on the other hand, I am satisfied that the cool atmo- sphere of Scotland cannot be surpassed in benefit, especially as we find it on the shores of a Highland lake, admitting of every variety of exercise, active and pas- sive, in the open air. Indeed, whatever advantages may result from a well-chosen winter residence, carelessness in fixing on a proper habitation during summer will more than counterbalance the good pre- viously obtained. It is by perseverance in well-doing that the great end of cure is to be arrived at. For winter, the best climate for the consumptive invalid in this country is the south coast, extending from Hastings on the east to Penzance on the west side, in- cluding the several stations of Bourne- mouth, Ventnor, Sidmouth and Torquay. In Scotland, Rothsay, and in Ireland, Cork, are the best stations. To the large mass of persons who cannot avail them- selves of even these advantages, every opportunity should be seized on of going out when the weather admits of it. It is not so much to a foreign climate itself as to the facility it affords for enjoying exercise, and free atmosphere, without the risks that prevail in Great Britain, that the benefit is to be attributed. With proper care, however, much may be done at home, and many cases have been per- manently cured in this country by means of hygienic treatment, conducted on the principles we are now advocating. For summer, the west coast of Scotland; and especially the beautiful bays on the shore of Loch Lomond, near Tarbet, offer the best residence for the consumptive. Here the immediate neighborhood of Loch Long furnishes the visitor with all the advantages of a marine as well as of a fresh-water lake, both which are so situ- ated that the most perfect protection from wind, combined with shade, is close at hand. It cannot be too strongly im- pressed upon the patient that careless- ness in summer too often more than counterbalances the good results that have been obtained in winter. Exercise.-The best stimulant for nutri- tion is appropriate exercise, which by ac- celerating the circulation and respiration, and causing natural wasting of the tis- sues excites the demand for substance to repair it. It will generally be found use- less to give nutriment, even when com- bined with pure air and good climate, un- less by means of exercise, air be forced 1 On this subject I cannot too strongly recommend the perusal of Dr. Henry Ben- net's work, "Winter in the South of Europe," although the views expressed in the text are derived from personal experience, and careful examination of the great advantages referred to. 138 PHTHISIS PULMONALIS. into the lungs in somewhat increased quantity, and circulated by means of the blood throughout the system. And here it is that favored localities are of so much value, by tempting the invalid out of the house, and permitting him to remain there, without encountering cold, wind, rain, or other risks to which he is exposed in this country. All exercise, however, should stop short of considerable fatigue. I say considerable, because some patients are always indisposed to move, and plead weakness and fatigue as incapacitating them from any exercise whatever. Walk- ing, or riding on horseback, are the best kinds of exercise when weakness is not great. Slowly climbing a hill brings all the muscles into action, and is a good stimulant to the respiratory and circula- tory systems. All violent, sudden and unequal exertions should be avoided. Reading or speaking aloud, singing or practising upon some wind instrument, may be permitted in moderation, when the disease is not active, but should never be long continued. As a general rule they are injurious. It is often better to take a little exercise at a time, but fre- quently in the course of the day, and to continue it regularly and methodically, gradually increasing its amount and vary- ing its character as the strength improves. For those who are weak and feel soon exhausted, passive exercise is best, such as in a carriage or in a boat, of course well wrapped up and protected from the wind. In summer, sitting or lying, well supported, in a boat pulled on a Highland lake, while, for occupation, reading, mixed with a little fishing, and the conversation of a pleasant companion-the various tints and outlines of the landscape also serving occasionally to occupy the attention-is perhaps the most salubrious kind of exer- cise for the not over-weakened invalid. For the same reason long voyages at sea are beneficial. I can speak with confi- dence of the three months' voyage to Aus- tralia by the Cape of Good Hope, com- mencing about the end of October. The climate is all that could be wished for, the trade-winds assist the vessel forward, the sea breeze is invigorating, and the life on deck all that could be desired. I have known many persons, very ill on leaving, lose all their symptoms before landing at Sydney or Melbourne. Sultry heat on shore must then be carefully avoided, and the visiting neighboring mountains or Tasmania becomes necessary in summer, in order to avoid the enervating effect of extreme heat. The return voyage should be carefully considered, and the winter at Cape Horn especially avoided. When none of these methods are avail- able, sitting out in the open air should always be insisted on, in a garden, on a balcony, or even at an open window, any- thing being better than remaining shut up in a room from morning to night. In this, as in all other matters concern- ing hygiene, the patient requires to be cautioned and carefully watched. For if some feel disposed to do too little, others imagine they cannot do too much. Un- der the idea that riding was beneficial, I have known a man hire a horse, and gal- lop about until he was so exhausted that he did not recover for a fortnight. Others in foreign hotels have taken rooms at the top of the house to obtain pure air, with- out considering the excessive toil imposed upon them by having to climb the lofty stairs. Others take villas in the neigh- borhood of towns, and are thus led into a daily fatiguing walk greater than their strength will sustain. Again, free expo- sure to the air must be conjoined with avoidance of draughts and cold winds. The rapid motion of a carriage through a dry bracing atmosphere is too much for the invalid, who should proceed slowly. Carelessness and often an unacquaintance with these dangers are constantly pro- ducing mischief, so that the watching and regulating these matters will require all the vigilance of the practitioner. Bathing.-There is no doubt that the relation between the skin and lungs is very intimate, a fact better observed per- haps in Phthisis than in any other dis- ease. When the lung can no longer exhale the large amount of watery vapor which is required, it is separated by the skin as insensible or sensible perspiration. Any sudden cold or chill affecting the skin is at once communicated to the lungs by reflex action, and excites irritation and cough. Now this susceptibility of the skin, so far from being prevented, is fos- tered and increased by constantly living in warm rooms, wrapping up too closely in shawls or furs, warm bathing, oint- ments, &c. &c. What is required is, that the skin should be kept constantly clean, and the epidermis and sebaceous matter that obstructs the orifices of the ducts daily removed by cold bathing whereby the organ is gradually accustomed to the application of a lower temperature, and rendered less liable to be affected by changes in the atmosphere or wind. In the majority of cases also a momentary plunge into the cold bath produces a glow of heat and pleasant feeling of reaction, exciting the capillary circulation of the surface, and relieving congestion in the lungs. When, however, in consequence of weakness, such reaction is not experi- enced, but in its stead, shivering, head- ache, and continued cold, then either a tepid bath should be employed, or the sitz bath, and sponging rapidly only the chest and throat should be practised. There is no better protection against catching fre- quent colds than daily sponging the chest TREATMENT of phthisis pulmonalis. 139 with cold water. The neck and chest, however, should always be covered, the growth of beard and moustache in men encouraged, whilst women should avoid low dresses, and always be prepared with an extra shawl to throw round the should- ers, even in going from one room to an- other through an exposed lobby. Respi- rators are not useful in conveying warm air into the lungs, nature having carefully provided for this, but by acting as extra pieces of clothing, and protecting the skin of the face. An ordinary comforter, and a small shawl held in the hand to be ap- plied to the face on encountering a sudden gust of wind, is a better contrivance. From what has been now stated with regard to the general or hygienic treat- ment of Phthisis Pulmonalis it will, we trust, be apparent that all the means spoken of unite to produce one result, and that no one of them alone can be depended upon. It will be of little use giving good diet or cod-liver oil, unless a pure atmo- sphere enter the lungs so that chyliflca- tion may produce good sanguification, while these in their turn are directly stimulated by exercise and judicious bath- ing. All these operations work together for good, the object being to stimulate the whole nutritive functions, augment appe- tite, gradually increase the strength, ar- rest the onward progress of the disease, and initiate in it that retrograde process formerly described, which shall terminate in health. To arrive at this end, how- ever, a special treatment will be required for each individual case, which we must next proceed to describe. Special Treatment of Phthisis Pulmonalis.-It is to the undue import- ance so frequently given to the special as distinguished from the general treatment of Phthisis that the former want of suc- cess may be attributed. The management of individual symptoms and the adminis- tration of drugs, so far from being the chief, should invariably be the subordi- nate part of our object, and this for the obvious reason that, if nutriment succeed in checking the disease, the symptoms will disappear of themselves. At the same time it must necessarily happen in the course of every case that various symp- toms and complications will press them- selves upon our notice, and their pallia- tion or removal, while still continuing our general efforts at cure, is always a matter of great importance. It is only by study- ing individual examples of the disease, observing the numerous and varied com- binations and indications that each pre- sents, that the difficulties the practitioner has to combat in this way can possibly be understood. I have too frequently seen patients lying in bed, enervated, without appetite, sweating at night, and appa- rently sinking, with a mass of bottles and boxes at the bedside bewildering to con- template-each of these it is imagined has some special symptom or purpose to fulfil -such as lozenges, drops, and mixtures, to relieve coughs ; opiates and sedatives, to cause sleep and diminish irritability; catechu, gallic acid, tannin, and acetate of lead, to check diarrhoea or arrest haemop- tysis ; sulphuric acid, to relieve sweating; chalk and antacids, to combat acidity and dyspepsia; quinine, iron, or bitters, as tonics; wine, to support strength ; cod- liver oil, &c. &c. All these I have seen administered at intervals about the same time, so that the stomach, drenched with drugs, is utterly prevented from perform- ing its healthy functions. Under such circumstances suspending all such sup- posed remedies, or preventing the patient from having recourse to them at will, is often the best introduction to an improve- ment, which the cold or tepid bath, in- sisting on their getting up and going into the open air, has, much to their surprise, tended to increase. It follows that, in all our attempts to relieve symptoms, the utmost care should be taken not to inter- fere with the far more important object of arresting and ultimately curing the dis- ease by general treatment. The various phenomena that present themselves, there- fore, should be managed as follows. Loss of Appetite and Dyspepsia.-These are the most constant and important symptoms of Phthisis, inasmuch as they interfere more than any other with the nutritive processes. If food, or its substi- tute, cod-liver oil, cannot be taken and digested, it is in vain to hope for amelio- ration. Here we should avoid a mistake into which the inexperienced are very liable to fall. Nothing is more common than for phthisical patients to tell their medical attendants that their appetite is good, and that they eat plentifully, when more careful inquiry proves that the con- sumption of food is altogether inadequate, and that they loathe every kind of animal diet. We should never be satisfied with general statements, but determine the kind and amount of food taken, when suf- ficient proof will be discovered, in the vast majority of cases, of the derangement, formerly alluded to, of the appetite and digestive powers. Very commonly also there will be acid and other unpleasant tastes in the mouth, loathing of food, and other dyspeptic symptoms. In all such cases, especially if too much medicine has been already given, the stomach should be allowed to repose itself before anything be administered, even cod-liver oil. Sweet milk, with toasted bread, and small por- tions of meat nicely cooked, so as to tempt the capricious appetite, should be tried. Then ten drops of rhe sp. ammon. aromat., given every four hours in a wine-glassful 140 PHTHISIS PULMONALIS. of some bitter infusion, such as that of calumba or gentian, with a little tinct. aurantii, tinct. cardamomi, or other car- minative. In this way the stomach often regains its tone, food is taken better, and then cod-liver oil may be tried, first in teaspoonful doses, cautiously increased; or other forms of fat, such as pork fat, bacon, suet, or butter, may be tried. Should this plan succeed, amelioration in the symptoms will be almost certainly observed. Nausea and Vomiting.-Not unfrequent- ly the stomach is still more deranged; there is a feeling of nausea and even vom- iting on taking food. In the later stage of Phthisis, vomiting is also sometimes occasioned by violence of the cough, and the propagation of reflex actions, by means of the par vagum, to the stomach. In the former case, the sickness is to be alleviated by carefully avoiding all those substances which are likely to occasion a nauseating effect, by not overloading the stomach, but allowing it to have repose. Here also, in cases where too much medicine has been administered, a suspension of all medicaments for a few days will frequently enable the practitioner to introduce nour- ishment cautiously with the best effect. I have found the following mixture very effectual in checking the vomiting in Phthisis: R. Naphthse medicinalis ; tinct. cardamomi comp. ^j; mist, cam- phorse 5 vij. M. ft. mist., of which a sixth part may be taken every four hours. When it depends on the cough, those remedies advised for that symptom should be given. I have tried emetics for the relief of nausea and vomiting, but with no good result. Cough and Expectoration.-At first the cough in Phthisis is dry and hacking. When tubercle softens or bronchitis is present, it becomes moist and more pro- longed. When excavations exist, it is hollow and reverberating. In every case cough is a spasmodic action, occasioned by exciting the branches of the pneumo- gastric nerves, and causing simultaneous reflex movements in the bronchial tubes and muscles of the chest. The expectora- tion following dry cough is at first scanty and muco-purulent, and afterwards co- pious and purulent. When it assumes the nummular form,-that is, occurs in viscid rounded masses, swimming in a clear fluid mucus,-it is generally brought up from pulmonary excavations. The accumulation of the sputum in the bron- chial tubes is an exciter of cough; and hence the latter symptom is often best combated by those means which diminish the amount of sputum. When, on the other hand, the cough is dry, those reme- dies should be used which diminish the sensibility of the nerves. In the first case, the amount of mucus and pus formed will materially depend on the weakness of the body and the onward progress of the tubercle. Hence good nourishment and attention to the digestive functions are the best means of checking both the cough and the expectoration; whereas, giving nauseating mixtures of ipecacuanha and squills is perhaps the worst treatment that can be employed. There is no point which experience has rendered me more certain of than that, however these symp- toms may be palliated by cough and ano- dyne remedies, the stomach is thereby rendered intolerant of food, and the cura- tive tendency of the disease is impeded. On the other hand, nothing is more re- markable than the spontaneous cessation of the cough and expectoration on the restoration of the digestive functions and improvement in nutrition. When the cough is dry, as may occur in the first stage, with crude tubercle, and in the last stage, with dry cavities, slight counter- irritation is the best remedy, employed in various forms. Opium may relieve, but it never cures. The occasional use of the sponge saturated in a solution of nitrate of silver is frequently of the greatest ser- vice, especially when from irritation of the fauces or" larynx vomiting is occa- sioned. There is a period in the history of chronic Phthisis when the cavities become dry and the sputum inspissated, tough, and difficult to expectorate. The practi- tioner is then frequently asked for some medicine to loosen the phlegm, relieve the feeling of tightness or compression in the chest, and dyspnoea. Under these cir- cumstances, in no case should he resort to expectorants and opiates. The patient should be instructed that these are favor- able symptoms, and indicate healing and cicatrization going on in his chest. In- stead of relaxing, now is the time to per- severe in avoiding palliatives which nau- seate and depress the system. A few drops of sulphuric ether in camphor julep, diminishing alarm, and a little quietude, constitute all the treatment required. [An excellent combination for such cases, which does not nauseate, is of ammonium carbonate, 2 or 3 grains at a dose, with syrup of wild cherry bark, in teaspoonful doses.-II.] Pain.-It is very surprising to what an extent tubercular disease of the lung may occasionally proceed, without causing in- convenience in the chest. Frequently there are sensations of constriction or op- pression, which, however, scarcely excite attention; or from their fugitive character are attributed to any cause but the right one. Occasionally there is a fixed pain in the affected side, which is increased on coughing. This more especially occurs when there is chronic pneumonia or pleu- risy. The best method of relief is to keep TREATMENT OF PHTHISIS PULMONALIS. 141 the parts at rest as much as possible, and apply warm fomentations or a hot poul- tice. Slight counter-irritation with tinc- ture of iodine may also be tried. On the other hand, leeches and cupping, though they may give relief, are opposed to the general principle of supporting the strength, and should be avoided. The same may be said of blisters, croton oil, tartar emetic ointment, and the moxa. I have long satisfied myself that severe counter-irritation is of no real benefit, whilst it produces an amount of suffering that irritates, and frequently does harm. Opiates are also injurious, by destroying the appetite and increasing the perspira- tions. At the same time, if pain be very distressing and long-continued, and espe- cially if it destroy sleep, some anodyne must sooner or later be had recourse to. Under these circumstances I have found chlorodyne derange the appetite, tongue, and stomach less than any other remedy of this class. Recently, chloral in fifteen or twenty-grain doses has seemed to me to act as a pure hypnotic and cause less disturbance to the economy than other remedies. Again, when all curative efforts are obviously useless, and death is approaching, palliatives need no longer be withheld. Then, all hopes of course being abandoned, relief of pain, if it ex- ists, becomes our chief duty. But even then it should be effected with caution and discretion, otherwise the discomfort and increase of other symptoms in the pa- tient will more than counterbalance the temporary benefit obtained. [There is reason for attaching some im- portance to the suggestion of Dr. E. Smith, that small or moderate doses of opium or morphia, given (in advanced cases) through the day as well as at night, may lessen the waste of substance and of energy, the palpable occurrence of which has given rise to the name, consumption. -II.] Diarrhoea. - This is a very common symptom throughout the whole progress of Phthisis, at first depending on the ex- cess of acidity in the alimentary canal, to which we have alluded, but in advanced cases connected with tubercular deposit and ulceration in the intestinal canal. The best method of checking this trouble- some symptom is by improving the quality and amount of the food. The moment the digestive processes are renovated, this, with the other functional derangements of the alimentary canal, will disappear. Hence at an early period we should avoid large doses of opium, gallic acid, tannin, and other powerful astringents, and de- pend upon the mildest remedies of this class, such as chalk with aromatic confec- tion, or an antacid, such as a few grains of carbonate of potash. When, on the other hand, in advanced Phthisis, con- tinned diarrhoea appears, and is obstinate under such treatment, then it may be pre- sumed that tubercular disease of the intes- tine is present, and the stronger astringents with opium may be given as palliatives. Hcemoptysis.-This symptom sometimes appears suddenly, as we have seen, in in- dividuals in whom there has been no pre- vious suspicion of Phthisis, and in whom, on careful examination, no physical signs of the disease can be detected. On other occasions, the sputum may be more or less streaked with blood ; and lastly, it may occur in the advanced stage of the disease, apparently from ulceration of a tolerably large vessel which may be di- lated or aneurismal. In all these cases the best remedy is perfect quietude, and avoidance of every kind of excitement, bodily and mental. Astringents have been recommended, especially tannin, gallic acid, acetate of lead, and opium; but how these remedies can operate, I am at a loss to understand; and I have never seen a case in which their administration was unequivocally useful. Can it be sup- posed that either of these substances can be absorbed into the blood in such quan- tity as to render that fluid more capable of coagulating in the lung where the ves- sel is ruptured ? I have now met with several cases where supposed pulmonary hemorrhage really originated in follicular disease of the pharynx or larynx, and, with the supposed phthisical symptoms, was removed by the use of the probang and nitrate of silver solution. Sweating I regard as a symptom of weakness, and therefore as a common, though by no means a special one in Phthisis. Here, again, the truly curative treatment will consist in renovating the nutritive processes, and adding strength to the economy. It will always be ob- served that, if cod-liver oil and good diet produce their beneficial effect, the sweat- ing, together with the cough and expec- toration, ceases. On the other hand, giving acid drops to relieve these symp- toms, as is the common practice, by add- ing to the already acid state of the ali- mentary canal, is directly opposed to the digestion of the fatty principles, which require assimilation. It should not be forgotten that consump- tive patients, and all those suffering from pulmonary diseases, are especially sensi- tive to cold. The impeded transpiration from the lungs in such cases is counter- balanced by increased action of the skin, which becomes unusually liable to the in- fluence of diminished temperature. Again, cold applied to the surface immediately produces, by reflex action, spasmodic cough and excitation of the lungs. Every observant person must have noticed how cough is induced by crossing a lobby, going out into the open air, a draught of 142 PIITIIISIS PULMONALIS. wind entering the room, getting into a cold bed, &c. &c. The mere exposure of the face to the air on a cold day takes away the breath, introduces cough, and obliges the patient instinctively to muffle up the mouth. The numerous precau- tions, therefore that ought to be taken by the phthisical individual, should be pointed out, especially the necessity of warm clothing, to which large additions should be made on going out into the air. Thus, covering the lower part of the face is important as a means of extra clothing, and not as a means of breathing warm air, as the favorers of respirators imagine. The patient should always sit with his back to the horses or to a steam-engine, and if by accident his shoes or clothes be- come wet, they should be changed as soon as possible. In the house ladies should have a shawl near them, to put on in going from one room to another, in de- scending a stair to dinner, &c. By atten- tion to these minutiae, much suffering and cough may be avoided. Febrile Symptoms.-The quick pulse, general excitement, loss of appetite, and thirst, which are so common in the pro- gress of phthisical cases, are dependent on the same causes as those which induce symptomatic fever in general. Vascular distension, resulting in exudation and its absorption, is proceeding with greater or less intensity in the lungs, and frequently in other organs. This leads to nervous irritation and increase of fibrin in the blood, accompanied by febrile phenomena. The intensity of these is always in propor- tion to the activity of local disease, or to the amount of secondary absorption going on from the tissues, or from morbid deposits. Nothing is more common than attacks of so-called local inflammations in Phthisis, and the careful physician may often deter- mine by physical signs the supervention of pleurisy, pneumonia, or bronchitis on the previously observed lesion, and not unfrequently laryngitis, enteritis, or other disorders. In such cases, nature herself dictates that the analeptic treatment, otherwise appropriate, is no longer appli- cable-food disgusts, and fluids arc eagerly demanded. Under these circumstances, it has been common to apply leeches to the inflamed part, and extract blood by cupping, measures which undoubtedly cause temporary relief, but which are wholly opposed to the plan of general treatment formerly recommended, and to what we know of the pathology of the disease. Every attack of febrile excite- ment is followed by a corresponding col- lapse, and it should never be forgotten that, in a disease which is essentially one of weakness, the patient's strength should be husbanded as much as possible. Hence the treatment I depend on in such circum- stances consists of at first the internal administration of the neutral salts, com- bined with diuretics, in order to favor crisis by the urine. Subsequently qui- nine is undoubtedly advantageous. I have satisfied myself that such attacks are not to be cut short by leeches or cup- ping, and although in many cases, as pre- viously stated, temporary relief is pro- duced, the exposure of the person, and unpleasant character of the applications, the trickling of blood, and wet sponges, as often irritate, and give rise to unneces- sary risk. Still there are cases where topical blood-letting, if it cannot be shown to have advanced the cure, cannot be proved to have done harm; but these cases, as far as my observation goes, are very few in number. In the rapidly feb- rile cases, or the so-called instances of acute Phthisis, mercury has been recom- mended, but has never produced the slightest benefit. Debility.-This is a very common symp- tom of Phthisis from the first, and fre- quently leads the patient into indolence both of mind and body, a condition very unfavorable for the nutritive functions, upon the successful accomplishment of which its removal depends. It is to re- move the weakness that tonics have been administered, but I have never seen qui- nine, bitter infusions, or even chaly- beates, of much service alone, while the continual use of nauseous medicine dis- gusts the patient, and interferes with the functions of the stomach. Neither have I ever been able to satisfy myself that the hypophosphites of soda or of lime, or the syrup of those phosphates and iron, have ever been of service. In all cases, the re- moval of debility is to be accomplished by counteracting the dyspeptic symptoms, giving cod-liver oil, an animal diet, and improving the appetite by gentle exercise and change of scene. Should the practi- tioner succeed in renovating the nutritive functions, it is often surprising how the strength increases, in itself a sufficient proof as to what ought to be the method of removing the debility. I have fre- quently seen patients who have been so weak that they could not sit up in bed without assistance so strengthened by the analeptic treatment, that they have sub- sequently walked about and taken horse exercise without fatigue, and this after all the vegetable, mineral, and acid tonics have been tried in vain. Despondency and Anxiety.-It is impos- sible for the careful practitioner to avoid noticing the injurious influence of de- pressing mental emotions on the progress of Phthisis. Indeed the worst cases are those of individuals with mild, placid, and unimpassioned characters, who give way to the feelings of languor and debility which oppress them. Such persons are most amiable patients-they give no trou- TREATMENT OF PHTHISIS PULMONALIS. 143 ble-anything will do for them-they re- sign themselves to circumstances, and state that they are eating well and getting better up to the last. These are cases of bad augury, for it is exceedingly difficult to inspire them with sufficient energy to take exercise, or to carry out those regu- lations which are absolutely essential to renovate the appetite and the nutritive functions. Such persons are benefited by slow travelling, cheerful society, and everything that can elevate the spirits, and, insensibly to themselves, communi- cate a stimulant to the mental and bodily powers. Anxiety, on the other hand, though it may sometimes depress and in- terfere with the digestive functions, is often a most useful adjunct to the physi- cian. Those who experience it are most careful of their health, sometimes indeed too much so ; but, if once satisfied of the benefit of any particular line of treatment, they pursue it with energy. These are cases of good augury, and most of the permanent cures I have witnessed have been in such persons-medical men, and others acquainted with the nature of their disease, who have exhibited resolution and a noble fortitude, who have bravely struggled against local pain, general de- bility, and nervous fear, and literally fought the battle of life with the greatest success. When the disease has been arrested, all the symptoms have disappeared, and even some degree of embonpoint returned, the patient must still be careful, still consider himself an invalid, and continue to pur- sue the hygienic regulations which have proved so beneficial. These, however, will not materially interfere with his enjoyment of life, or even the pursuit of active business or professional life. Amongst the poorer classes, it will be more difficult to obtain such handiwork or occupation as may not be injurious. In order to live, however, they must ex- change their unhealthy for more healthy modes of life. As a general rule, the dwellers in towns should seek the country, and the inhabitants of rural districts change the scene of their labors-always remembering that it is not mere place that can benefit, but the opportunities it may offer for carrying out that improve- ment in the nutritive functions we have endeavored to show is so necessary. Local Treatment.-It has not failed to suggest itself to medical practitioners that remedies might be useful if applied di- rectly to the lungs. To this end con- densed air, an oxygenated atmosphere, carbonic acid, sulphurous and tar fumes, and all kinds of substances in a gaseous form have been inhaled. Solutions in a state of vapor, or divided into spray, have also been tried. Astringent and other fluids have been injected down the larynx and bronchi. Pulmonary cavities have even been opened from without, and vari- ously treated with a view of causing cica- trization. The result of all these efforts has been-what an intelligent considera- tion of the pathology of the disease might have anticipated-a uniform failure. Statistics.-It is a matter of extreme difficulty to determine with exactitude how the change in the treatment of Phthisis which commenced in 1841, and became pretty general in 1850, has in- fluenced the mortality of Phthisis Pulmo- nalis. In 1852, Dr. Wood, of Philadel- phia, remarks of it, that in that city, during the ten years from 1840 to 1849 in- clusive, the average proportion of mor- tality from Phthisis was 1 in about 0'76 from all causes, or 14'8 per cent., and the same average existed in previous years. Cod-liver oil was then generally used in its treatment, and the mortality sank in this disease during 1850-1 to 1 in 8'33, or about 12 per cent., and in 1851 it was only 11'86 per cent. In 1862, Dr. C. J. B. Williams, in one of the Lumleian lectures delivered to the London College of Physicians, observes that the experience of Louis and Laen- nec gave an average duration of two years' life in Phthisis after it was decidedly de- veloped, but that, since cod-liver oil was introduced, he infers from 7000 cases that the average duration of life has been four years. The registration of deaths in Scotland only commenced in 1855, and offers there- fore no means of comparison, as regards Phthisis Pulmonalis, between the mortal- ity occurring before and after that period. But the English registration of deaths commenced in 1837, and, with the excep- tion of a few years, has continued up to the present time. The following is the result:- Years. Average annual population. Average of total number of deaths. Average of deaths from phthisis. Percentage of deaths from phthisis to total deaths. 37-41 15,720,385 347,070 55,718 16-0 50-54 18,174,011 359,681 50,515 14-0 55-59 19,257,184 425,703 50,187 11-3 60-64 20,196,787 495,531 51,595 10-4 144 CANCER OF THE LUNGS. It would appear from the above table that, taking a five years' average previous to 1841, before cod-liver oil and an ana- leptic treatment were introduced, the pro- portion of deaths from Phthisis was 16 per cent. ; whereas, in the years 1850 to 1854 inclusive, the deaths were 14; in 1855 to 1859, 11'3 ; and in 1860 to 1864, only 10'4 per cent, of the deaths from all causes. It must be observed, however, that a certain number of cases annually are vaguely returned as "lung diseases," and that whilst deaths from Phthisis have diminished, those from pneumonia and bronchitis have greatly increased. Doubt- less exactitude in diagnosis has very much extended among medical practitioners during the last twenty years, whilst it is a matter of common observation that the winter and spring seasons have increased in severity and duration, circumstances which to a certain extent might account for the numerous returns of pneumonia and bronchitis. Without attaching, there- fore, too much importance to the exacti- tude of the results obtained by the Regis- trar-General, all that can be said is, that as far as they can be relied on, they ex- hibit during the last twenty-five years a marked diminution in the mortality of Phthisis Pulmonalis, as compared with the period before cod-liver oil and a re- storative treatment were employed. CANCER OF THE LUNGS. By Hermann Beigel, M.D., M.R.C.P. Bond. Literature.-Hollerius, Op. omnia, De Morb. intern. 1674; Heister, De Asthm. schirr. 1749; De Haen, Ratio medend. Parts v., vi. 1765; Morgagni, Epist. i. xxii. art. 22; lb. Epist. xx. art. 39, 1780; Van Swieten, Comment, ad Aptor. Part ii. p. 797; Bayle, Recherches sur la Phthisie pulmon. Paris. 1810; Langstaff and Lawrence, Med. Chir. Transact, viii. p. 272; Langstaff, Med. Chirurg. Trans- act. ix. p. 297; Andral, Clinique Medi- cale, 1830; Cailliot, Sur 1'Encephaloide, 1833 ; Williams, Diagnosis of Diseases of the Chest, 1835 ; Durand-Fardel, Journal Hebdomad. 1836; Laennec, Traite de 1'Auscultation, 1839; Stokes, Diseases of the Chest, 1837; Strave, De Fungo pul- monal. 1839; Kleffaus, De Caner, pulmon. Groning, 1841; Marshall-Hughes, Guy's Hosp. Rep. 1841; Watson, Lond. Med. Gazette, 1841; John Simon, General Pa- thology, 1850 ; Lebert, Traite des Maladies cancereuses, 1861; and his Anat. Pathol. 1855-1862; Ebermann, De Cancro pul- mon., Petropolis, 1857; Bright, Guy's Hosp. Rep. v. p. 377; Harrison, Dub. Journ. xvii. p. 326; Green, Dub. Journ. xxiv. p. 282; Tiniswood, Monthly Journal, July, 1844; Burrows, Med. Chir. Trans, xxvii. ; Maclachlan, Lond. Med. Gaz., 1843; King, Ibid.; Kohler, Krebskrank- heiten, 1857; Pemberton, On Melanosis, Midland Quarterly Journ. of Med. Sci- ence, May, 1857, p. 129; Bright, Diseases of the Heart, Lungs, &c., 1860; Aviolet, Du Cancer du Poumon, Paris, 1861; Beg- bie. Archives of Medicine, 1861; Bokitan- sky, Pathol. Anat. 1861, vol. iii.; Walshe, Diseases of the Lungs-on Cancer, 1863; Skrzeczka in Virchow's Archiv, vol. xi. p. 179; Virchow's Geschwiilste; Cockle, On Intrathoracic Cancer, 1865; Andrew, Primary Cancer of the Lungs, Transact. Path. Soc. 1865, p. 51; Charles Moor, Re- port on Cases of Cancer, Brit. Med. Journ. 1866, vol. ii. ; Bindfleisch's Pathologische Gewebelehre, Dritte Lieferung, 1868. Cancer of the Lungs is by no means a frequent occurrence. Bayle observed only three cases at the post-mortem examina- tion of 150 individuals who died of phthi- sis. Begin, at 200 dissections, has only twice observed the disease. Herrich and Popp found malignant growths in 68 out of 1171 corpses; but amongst these 68 there were only six cases of Cancer in the Lungs. Recent observations by Dr. James Russell, Dr. Andrew, and others, have, however, confirmed the opinion held by excellent observers, that the lung may not only be the only affected organ, but in secondary cancer be really a place of predilection. Walshe considers "Cancer in the lungs to be particularly common as the secondary development, where the testicle has been the primary seat of the disease ;" whilst Dr. Day, of Stafford, appears strongly in- clined to consider it more frequently a sequence of cancer of bones than of any other primary cancerous development.1 » Med. Tinies, 1866, vol. ii. p. 230. PATHOLOGICAL ANATOMY. 145 The truth is that cancerous affection of the lungs is comparatively common after primary development, both in the testicles and bones, but that other organs may also-though not with equal frequency- be the nidus for primary deposits, which then may be followed by secondary Can- cer in the Lungs. But it must be borne in mind, that the place of primary depos- its sometimes is revealed only at the post- mortem examination, which fact leads us to believe that many cases, recorded as primary Cancer in the Lungs, have been in fact secondary affections, and that the organ in which primary deposits have been formed was overlooked. Concerning the age which seems most liable to be attacked, we learn from Eber- mann that in 72 cases the following rela- tions are recorded:- From 1 to 9 years, 1 individual. " 9 "19 " 1 " " 19 " 69 " 66 " " 69 " 79 " 3 " " 79 " 89 " 1 " It appears, then, from this table, that the disease is rare before the age of 20, when it becomes frequent during a long period. It may be mentioned that of 78 cases in which the sex had been noted, 51 occurred in men ; so that the ratio, there- fore, was eight to three. Concerning the forms in which Cancer of the Lungs may be observed, colloid is extremely rare, scirrhous very rare, but en- cephaloid comparatively common. In fact, some first-rate observers-Bayle, Laennec, and others-consider encephaloid the only species of cancer to be found in the lungs. This form, likewise called medullary carci- noma, which has received its name from the striking resemblance to brain, being thus the prevalent form of Cancer in the Lungs, to which the whole clinical inter- est is attached, it seems but right that, in a work like this on practical medicine, our remarks on Cancer of the Lungs should principally be confined to that form. Pathological Anatomy.-Encepha- loid, as already mentioned, so much re- sembles the medullary substance of the brain, that, for the unaided eye, it would sometimes be difficult to say whether it be brain or pathological growth. Its con- sistence is generally soft, pulpy, and de- pends upon the amount of stroma present, the meshes of which contain the creamy fluid, generally known as cancer juice. The vessels traversing the fungus have but thin walls, which sometimes rupture, and, admixing blood and clot with the medullary matter, give rise to the modi- fication of encephaloid, which has been called Fungus hcematodes. In the early stages of development it is not the extravasation of blood which tinges the growth, but the abundance of very minute vessels traversing the growth, and detectable only by the aid of the mi- croscope. Their walls are very thin and transparent, and easily liable to break. The extravasation extends through the cancerous mass in the same way as it does through the tissue in apoplectic effusions, and the pleural cavity sometimes also contains a clot of pure blood. If, on the other hand, the cancer-cells contain black coloring matter-probably a modification of the coloring matter of the blood-the growth, of course, assumes a dark appearance, and is then called "Cancer, or Fungus Melanodes." Ac- cording to Rokitansky, this species is ob- served only in cases of general cancerous cachexy, or, in other words, as a second- ary form; but Dr. Rogers mentions that it appears also as a primary affection. Of 60 cases of melanosis collected and published by Pemberton,1 the post-mortem appearances were recorded in only 35. Of these 35 cases, 17 exhibited deposits in the lungs ; but there is no practical difference between encephaloid, fungus hsematodes, and cancer melanodes. Secondary Cancer of the Lungs is rarely limited to these organs, but generally in- volves the adjoining parts, as costal pleura, pericardium, heart, diaphragm, bronchi, vessels, and nerves ; or the Can- cer may on the contrary, take its rise in one of these organs, and during its pro- gress involve the lungs. The bronchi may become compressed or filled with cancerous matter and their walls corroded. The arteries, but not the veins, enjoy a certain immunity when traversing a cancerous growth. The glands generally participate in the infil- tration and transformation of structure ; the mediastinal glands particularly may grow into an enormous and highly vascu- lar, cerebriform mass of several (seven) pounds weight,2 traversed by the aorta and pulmonary artery, which may become compressed, and even converted into a very thin, soft, yellow elastic band. I have met with an extremely rare case; the patient was a woman, aged 59 years. She was several times operated on for Cancer in the right breast, but the growth always recurred. Ultimately the lungs become involved and the patient died. At the post-mortem examination, large encephaloid masses were found at the root of the left lung, and both lungs were infil- trated with medullary cancer. But the 1 Midland Quarterly Journal, May, 1857, p. 145. 2 A case under the care of Dr. Rees : Lan- cet, 27th August, 1864. See also Dr. Fr. Braun's "Das Vorkommen des Williamsche Tracheal Tones;" Erlangen, 1861. VOL. II.-10 146 CANCER OF THE LUNGS. mediastinal and a very great number of bronchial glands had been changed into large dark-colored lumps of Cancer mela- nodes. Of the nerves, by their anatomical rela- tions, the vagus and recurrentes are par- ticularly liable to become involved in the process, and to be materially altered. Amongst the cases contained in Dr. Cockle's most elaborate and able work on Intrathoracic Tumors, the one simulating laryngeal phthisis is of particular interest, in which " the cervical portion of the left par vagum was manifestly enlarged."1 The shape in which the heteroplastic growth under our consideration may be found, varies very much from numberless miliary dots to cancerous tumors of twelve or fourteen pounds weight. In other in- stances, the lung may preserve its shape, but its normal tissue be entirely destroyed, or rather replaced by cancerous matter. In other instances again, cancerous patches may be observed with intermedi- ate healthy tissue, or, which is the most common, the different forms coexist- miliary deposits in one spot, nodules or nodes and larger growths in another, while a third part may be infiltrated. As an extremely rare occurrence, which has been observed only a few times, is the form which Rokitansky has called cancer- ous pneumonia, and in which the tissue of the lung may be compressed but otherwise normal, whilst the air cells are filled with detritus, fat globules, and principally with cancer-cells. Such a case has recently been published by Dr. Shrzeczka.2 The diseased lung is generally adherent to the inner surface of the sternum and ribs, or it may be compressed or retracted, entirely uncovering the heart, and most closely agglutinated to every part and or- gan contiguous to it. In cases of com- pression of one lung, the other generally becomes dilated, in order to compensate for the diminished size of the diseased one. In some instances, the cancerous forma- tions are limited to the costal or pulmo- nary pleura ; and often assuming a shape which has been compared to "wax- drops,"-Cruveilhier's "Plaques squir- rheuses"-do not penetrate into the lung- tissue or air-cells, but remain superficial. In other instances, nodular deposits are formed in the very substance of the lung, growing in a centrifugal direction, and breaking through the pleura. If cancerous derangements of other or- igans than the lungs have proved the immediate cause of death, but few-four er five-cancerous spots, of the size of a ;pea only, may be found in the lungs.3 The tumors, of course, undergo the same changes as cancer generally does. The softening begins in the centre, and, advancing towards the periphery, gives rise either to cancerous ulcers or, which is a rarer occurrence, to a cavern filled with puriform, bloody, and putrid juice ; the walls of such a cavity are generally thick, infiltrated with its contents, and are likewise in a state of disintegration. On microscopic examination, the enceph- aloid is seen to consist of two distinct formations, the one being the stroma, forming differently shaped and sized meshes, which consist of fibrous bundles, partly or totally converted into an agglo- meration of fatty molecules. The consistence of the encephaloid de- pends upon the density of the stroma. From these meshes, the other forma- tion, viz. the so-called cancer-juice, can easily be squeezed, and appears as a creamy semi-liquid fluid. The microscope reveals its color, as depending on an abundant amount of spindle-shaped and other cells, which contain one or more large nuclei and blastema. The cells are generally in a state of retrograde formation, or fatty degenera- tion, which causes their contours to ap- pear more distinct. In a still more ad- vanced stage, the cells become completely transformed into an agglomeration of fatty molecules. Symptoms.-Not unfrequently the pa- tient exhibits but slight symptoms, if any, even when the disease is already far ad- vanced. This is particularly the case with secondary, less frequently in pri- mary Cancer, and depends on the nodular formation of the disease ; for these nod- ules being surrounded by normal lung- tissue, permeable to the air, render aus- cultation and percussion useless. Dr. Stokes relates a remarkable case, illus- trating not only the comparative slight- ness of symptoms, but also the rapidity of growth. The patient was under the care of Dr. Little, in Sligo Infirmary.1 A young man was brought in, simply dying from a diseased leg which had been neg- lected. Dr. Little conceived that the only possible means to save life was amputa- tion above the knee, which he did with the happiest result. Hectic fever disap- peared, and in four or five weeks the pa- tient had increased a stone and a half in weight; but he came back shortly, com- plaining of pulmonary irritation, and died in a fortnight after re-admission, when it was found that both lungs W'ere converted completely into cancerous masses. The rapidity of growth in isolated cancerous masses was very singular. Yet, in the majority of cases, there exist symptoms 1 Dr. Cockle, On Intrathoracic Tumors, vol. ii. p. 109. 2 Virchow's Archiv, vol. xi. p. 179. 8 Garrod, in the Lancet of 1867, vol. i. 1 Medical Times, Sept. 1, 1866. SYMPTOMS. 147 enough for the formation of a strict diag- nosis. The symptoms generally met with may be arranged in the following man- ner :- 1. General appearance of the patient.- Cases which run through all stages with- out apparent alteration of the patient's general health, are exceptional. Gen- erally, the health is impaired in one or another way; and if there exists anything in disease which may be called " the habit" of that disease, I should be in- clined to speak of a "cancerous habit." It may, perhaps, be difficult, nay impos- sible, to describe appropriately this habit, but a practitioner's eye trained to observe diseases and to notice even slight altera- tions in the countenance of his patients will surely discover it. There is something inexpressibly pain- ful and anxious in the lineaments of pa- tients laboring under cancerous affections, which is not met with in any other dis- ease. Nor is the characteristic tint of the patient's skin often absent. Rapidly pro- gressing emaciation is another concomi- tant of Cancer; and fever of hectic nature, a rapid, small, irregular pulse, which throbs 100 to 130 times in a minute, gen- erally are present to the last moment of the patient's life. The literature of the disease under con- sideration furnishes us with numerous cases, the course of which has been pre- cisely similar to that of phthisis; colli- quative night-sweats, diarrhoea, exacer- bating fever, copious expectoration. In such cases, errors in diagnosis are not only excusable but unavoidable, and such errors have been committed. The appe- tite is likewise mostly deficient; the natural functions in disorder ; and sleep, either by pain, dyspnoea, or other causes, interrupted or entirely disturbed, and languor and debility take possession of the poor patient. 2. Shape of the thorax.-The thorax may become altered in two directions, being either increased or diminished in bulk. In both instances the alteration may extend over the whole diseased side, or be partial. Enlargement of the thorax will be ob- served, when by heteroplastic growth or effusion into the pleural cavity, pressure is exercised from within upon the chest- walls ; whilst diminution of the volume of the thorax will ensue from decrease of the organs situated within the chest, thus al- lowing the atmospheric pressure and cer- tain muscles to act from without upon the walls of the thorax, in such a manner as to cause loss of its curved shape, and to produce flattening and depression at cer- tain points. The same effect may be brought about by adhesion of the pulmonary to the costal pleura. The alteration may sometimes occasion a difference between the one side of the thorax and the other, amounting to six or eight inches. In other instances, the alteration is but slight and discernible rather by inspection than by measurement. The movement of the thorax during res- piration, depending in a very great meas- ure upon the permeability of the lungs to air, will alter under the same conditions as if the lungs had undergone infiltration by other diseases, or had been com- pressed by fluid or air into the pleural cavity. 3. Auscultation and Percussion.-It need scarcely be mentioned that the physical signs will correspond with, and depend on, the state of the organs contained in the chest. We are aware from the prin- ciples of physical examination, that sepa- rate cancerous nodules, though they may exist in a very great number, do not exer- cise any influence upon the normal res- piratory sound, nor do they materially alter the sound on percussion. The tis- sues surrounding the cancerous nodules lose their contractility, and would give a tympanitic sound, if their tympanic char- acter were not injured by the solid nature of the newly-formed nodules. When the nodules become confluent, and the deposits are large, they of course interfere with normal respiration; and, according to their nature and extension, the normal sounds of auscultation and percussion will be altered. 4. Cough.-Cough may exist and con- tinue in a slight degree, so as to deceive in respect to the real nature of the disease, both the patient and the physician. But the cough may increase, and become so violent as to resemble hooping-cough, and to torment the sufferer day and night. If the disease be confined to one lung, or if one pleural cavity become filled by effused fluid, cough and shortness of breath set in from very evident causes, as soon as the patient tries to lie on the healthy side. Implication of the one or both vagi in the cancerous process will, of necessity, also be followed by frequent distressing cough of a laryngeal character.1 5. Expectoration.-It is in some cases entirely absent, but in others very copi- ous, muco-purulcnt, separating into two or more layers when allowed to stand un- disturbed in a glass or any other appro- priate vessel. The lowest layers fre- quently containing so-called cancer-cells, or masses of Cancer, afford conclusive assistance in forming a diagnosis. When a communication exists between a broken bronchus and cavity, and disin- tegration is going on, the expectorated matter is sometimes unbearably fetid, and contains elastic fibres and detritus of lung- 1 Cockle, loc. cit. vol. ii. p. 106. 148 CANCER OF THE LUNGS. tissue. In case of corrosion of a vessel, haemoptysis sets in, and may possibly im- mediately endanger life. Admixture of small quantities of blood with the sputa is neither a rare occurrence, nor of great importance. In the above-mentioned case of com- munication between a bronchus and a cavern, large cancerous masses, with an admixture of blood, may be expectorated, as has been observed by Andral, Bayle, Hartman, Langstaff, or the sputa consist only of blood, and the expectorated masses are of a dark brownish color, as described by Stokes, Burrows, and others. 6. Pain.-The lancinating pain, which forms a most distressing symptom of cancer in other parts of the body, is hap- pily a comparatively rare occurrence in Cancer of the Lungs. When present, it is by no means restricted to the diseased organs, but extends to parts distant from the original place of affection. This is easily explicable by the anatomical dis- tribution of the nerves, on which pressure may be exercised, or by the compression, embolism, or thrombosis of large blood- vessels, which may prevent proper circu- lation in distant parts, and even cause gangrene. I have observed a very interesting case in a female fifty-two years of age. She had been operated on for Cancer in the left breast. Three years after operation she was suddenly seized with violent pains in the chest, lasting for some hours, disappearing then, and reappearing seve- ral days. The pain was so excruciating, that the patient in one of the paroxysms attempted suicide, but was prevented from committing it. When she was free from pain, she had neither cough nor any other sign of chest-disease. Her previous history, together with her present state, confirmed my opinion on the case as being one of intra-thoracic cancer. About a fortnight before her death, which occurred six months after I had first examined her, she began to cough and to waste away with remarkable rapidity, and three days before death the left lower extremity ex- hibited symptoms which left no doubt that circulation had ceased in it. At the post-mortem examination, both lungs were found studded with small cancerous tumors, the largest of the size of a pea, leaving between them healthy tissue. The root of the right lung was involved in a large cancerous soft mass ; the liver like- wise contained a considerable number of cancer-nodules, and the left iliac artery was entirely closed by a firm thrombus. 7. Dyspnoea and Palpitation of the Heart. -Dyspnoea may exist in a very trouble- some degree even when the physical signs are still insignificant; such will particu- larly be the case when the lungs are filled with miliary deposit. But the same may take place, the lung being but little or not at all affected, when pressure is exercised on those vagus-fibres which are inserted into the lungs. Physiology teaches that such pressure will cause acceleration of the respiratory movements, whilst irrita- tion of those branches of the vagi, which reach the upper part of the larynx, retard these movements. In both instances dyspnoea may be the result, and this again may become the cause of palpitations. These, however, are generally the conse- quence of the implication of the heart or pericardium in the disease, be it indirectly by pressure, displacement, &c., or by di- rect participation in the cancerous depo- sitions. Displacement of the heart by tumors or fluids will, of necessity, alter the action of the heart, which, according to Louis, is smaller in persons dying of Cancer than of any other disease. In such cases it seems to waste in common with the other tissues of the body, and becomes still more contracted from the quantity of the circu- lating fluid being so much diminished. It needs no explanation to prove that degeneration of, or infiltration into, the lungs, compression or closure of the larger bronchi, their being filled with cancerous matter, or the effusion of fluid into the pleural cavity, will likewise be followed by dyspnoea, or-particularly at more ad- vanced stages of the disease-by orthop- noea. 8. Dysphagia is oftener connected with intrathoracic tumors of considerable size than with Cancer of the Lungs. It is al- ways the result of pressure on the oesopha- gus, or of swelling of that organ in conse- quence of pressure. In very rare cases dysphagia may exist as a reflex action, but then it will exhibit a remittent char- acter, whilst it will remain stationary when dependent on pressure; in some cases the symptoms will appear as soon as the patient assumes a certain position, wherein the tumor is allowed to exercise pressure upon the oesophagus. Dr. Cockle's work contains cases illustrating both kinds of dysphagia.1 This symptom may exist in so high a degree, and the compression of the oesophagus may be so complete, as not even to allow fluids to pass, and it may become necessary to feed the patient by nutrient injections. 9. The Voice of a patient suffering from Cancer of the Lung is liable to many alterations. A deep bass may become altered into a high treble, or into hoarse- ness, according to the different causes, viz. pressure on the recurrent nerves, compression of the trachea or direct affection of the larynx by the disease. In more advanced stages of Cancer of the Lung, as well as of tuberculosis, there is 1 Cockle, loc. cit. vol. ii. pp. 107, 144. DIAGNOSIS. 149 scarcely a case in which the voice would not be altered in some way. According to Dr. Cockle, extinction of voice may exist without any sign of obstruction in the larynx, and without either stridor or dyspnoea, being dependent solely on pa- ralysis of the laryngeal muscles, conse- quent on pressure upon the nerves by the cancerous mass within the chest. By means of the laryngoscope, such an affec- tion in our days will be recognized during the patient's life. In a case of complete aphonia, it was observed by Andral at the post-mortem examination, that a can- cerous mass had been exercising pressure on the inferior laryngeal nerves. 10. Contraction of one or both pupils as a symptom of intrathoracic tumor, and as due to interference with the sympa- thetic nerve, was first pointed out by Dr. Gairdner. Though this symptom is not pathognomonic, viz. characteristic either of Cancer in the Lungs, or of intra- thoracic tumor, yet its presence may, in some instances, form a valuable link in the chain of symptomatic evidence. 11. Effusion into one or both pleural cavities is another symptom which is com- paratively more often met with in cases of intrathoracic cancer than Cancer of the Lungs. If present, the lung is often adherent to the vertebra, drowned as it were in the fluid, and compressed some- times to the size of a fist, but may other- wise remain healthy in structure. If the lung-tissue, under these circumstances, is in an infiltrated state, we have a remark- able instance of an organ being infiltrated with a new formation and, at the same time, diminished in size. The effused fluid has generally a lim- pid, yellow appearance, and contains al- bumen. The effusion generally takes place with great rapidity, and when para- centesis has been performed it is replaced in the same manner. A case published by Dr. Begbie, in the "Archives of Medicine," in 1861, is of great interest in respect to the symptoms under consideration. The patient was a quarryman, 50 years of age, who came to the Edinburgh Royal Infirmary, desirous of obtaining advice for what he thought a slight affection of the chest. The symp- toms had become troublesome only ten days before Dr. Begbie saw the patient, who, on being obliged to leave off work, had consulted a medical man in his neigh- borhood. This gentleman ordered some cough-mixture, and applied a mustard- plaster over the chest; but the symptoms became worse. When Dr. Begbie saw the patient, he diagnosed intrathoracic cancer, and, from the 24th of September to the 16th of October, 550 ounces of fluid were drawn from the enlarged chest. The patient eventually died, and primary mediastinal and pulmonary cancer was found at the post-mortem examination. It must be borne in mind that cancer- ous infiltration into the lungs may pro- gress so rapidly as to be mistaken for effusion into the pleural cavity. Mr. Middleton brought such a case under the notice of the Pathological Society of Lon- don, at the meeting on the 14th of No- vember, 1850. During life, several medi- cal men concurred in the opinion that the phenomena which the patient ex- hibited could only be due to effusion into the right pleural cavity. But at the post- mortem examination it was found that very rapid infiltration, and enlargement of the right lung, had taken place. Such cases we must bear in mind, in order to examine thoroughly and very carefully before we decide on performing the opera- tion of paracentesis. 12. Fever is generally moderate, of hec- tic type ; the pulse but little accelerated ; the aid of the thermometer is, however, of great importance, for though the tem- perature may be normal, or but little raised, the daily exacerbation will not es- cape attentive observation. The pulse increases likewise towards evening, and each exacerbation is followed by perspira- tion, which in many cases is. indeed, very profuse and quite as violent as that which occurs in phthisis, and exhausts the pa- tient in an extreme degree. Diagnosis.-Primary Cancer of the Lungs, in the majority of cases, admits of no diagnosis. Physical examination tells us whether or not alteration of the lung-tissues has taken place, whether or not the pleural cavity be filled with fluid or solid ; but we remain ignorant of the nature of that alteration. In rare cases only, a suspicion will arise; but, unfor- tunately, the post-mortem examination will finally show whether our opinion has been justified, or based on wrong conclu- sions. Microscopical examination of the sputa should never be neglected, it being one of the principal means by which the real nature of the disease may sometimes be revealed. "I have seen many in- stances," says Dr. Williams,1 " and others are on record, of ulcerous cavities formed in melanose and encephaloidsolidifications of the lungs, and the expectoration in one case of a black and red, and in the other of a streaky, whitish, sanguinolent, and puriliginous matter, led to a suspicion of the nature of the disease before death." The diagnosis of secondary Cancer gener- ally does not afford such insurmountable difficulties as many believe. Its appear- ance, after primary deposits have been 1 Pathology and Diagnosis of Diseases of the Chest, p. 154; London, 1835. 150 CANCER OF THE LUNGS. made in, and eventually removed from, other organs, will very often serve as a guide for our conclusion. In fact, if after the removal of a malignant growth, pul- monary or bronchial symptoms of any kind appear, it is but wise to suspect them as the beginning of the occurrence of Cancer; at all events let us be on our guard, and not treat these symptoms as if they would occur in persons in whom no signs of cancerous diathesis have ever made their appearance. It is in these cases in which Hutchin- son's much-neglected instrument, the spi- rometer, will afford good services. Indi- viduals from whom Cancer of any organ has been removed, should, after opera- tion, from time to time be measured in respect to the capacity of their lungs. If the amount of air evidently becomes diminished, gradually or suddenly, then we shall seldom be wrong in assuming that cancerous deposits have been made, and respectively are still progressing. But, notwithstanding our greatest care and attention, we shall meet-and that not seldom-with cases in which a strict diagnosis will either prove impossible, or be made only after repeated examination and closely watching the case for a longer period. The diseases which are particu- larly liable to be confounded with Cancer of the Lungs are chronic pleurisy with effu- sion into the pleural cavity, tubercular infil- tration and aneurism. Differential Diagnosis.-1. Chronic Pleurisy with effusion into the pleural cavity. -Though the consistence of encephaloid may be of a semi-fluid nature, yet it will differ in many points from effusion in respect to the symptoms as revealed on physical examination. The area of dul- ness on percussion, in different positions of the patient, never so strictly follows the laws of gravity as in cases of effusion. Another point of importance is, that in chronic pleurisy the area of dulness some- times diminishes, which is particularly the case after much perspiration, or after exhibition of diuretics, or similar medi- cine ; but the Cancer, once formed, will under no circumstances decrease. It is true that, as Dr. Cockle says, "In many cases, mere physical diagnosis is utterly incompetent to decide the ques- tion, inasmuch as chronic pleurisy consti- tutes in itself an integral part of the natu- ral history of intrathorax cancer." But in this instance, viz. when during the cancerous process effusion into the pleural cavity has taken place, we have not any more to decide between Cancer and pleu- risy with effusion ; it is evident that phys- ical examination has contributed its share towards the formation of the diagnosis, ■when it has taught us whether the pleural cavity be filled 'with fluid, solid, or semi- fluid matter ; and in respect to this point, with proper care and attention, we shall always arrive at a satisfactory decision. According to Winterich,1 the vocal fremi- tus in Cancer is oftener present than ab- sent, whilst in effusion the reverse holds good. But, if physical examination in some cases is at a loss to answer the questions proposed for diagnostic purposes, then the history of the case, the general appear- ance of the patient, the rapidity of devel- opment of the cancerous growth, the pecu- liar expression of the patient's face, the peculiar tint of his skin, and perhaps the coexistence of Cancer in other organs, will sufficiently make up for the deficien- cies of physical signs, and place us in a position which will enable us to make the diagnosis certain. 2. Tubercular Infiltration.■-1The physi- cian will only be 'called upon to decide between phthisis and Cancer, when the affection has assumed great proportions. In this case it must be remembered that the latter disease never spreads so exten- sively as the former does, in which the total absence of rhonchi may also be an important sign. Haemoptysis is a com- paratively rare occurrence "in Cancer, but not so in phthisis. The absence of the phthisical habit, the fact that patients, suf- fering from Cancer are not unfrequently in a comparatively good condition, even in advanced stages of the disease, the co- existence of tumors, or the former re- moval of such, together with-sometimes lancinating-pain in the chest, and the microscopical examination of the sputa, ■whereby the product of Cancer sometimes may be found, will afford diagnostical hints. Compression of the oesophagus, displacements of neighboring organs in an extremely high degree, the rare occur- rence of caverns, symptoms of compres- sion of the aorta or vena cava, the not unfrequent limitation of the disease to one side only, are signs frequently met with in Cancer. Diagnosis will become still more diffi- cult or entirely impossible, in cases of co- existence of tuberculosis and Cancer. It was due more particularly to Rokitansky that the opinion became general that tu- berculosis and Cancer exclude each other, i. e. that they never do coexist in the same person. Rokitansky, however, af- terwards altered his opinion, saying that the coexistence of both diseases is merely a very rare occurrence. Other authori- ties hold the same opinion. But many cases have been published, showing that Cancer by no means excludes tuberculo- sis. I refer the reader to Dr. Pollock's 1 Winterich's Krankheiten der Respira- tions-Organe, in Virchow's Patliologie mid. Therap. Erlangen, 1854. PROGNOSIS AND TREATMENT. 151 case,1 published in the " Transactions of the Pathological Society," and to a highly interesting one, recently published by Pro- fessor Friedreich,2 concerning a woman forty-nine years of age, who suffered from primary Cancer of the left lung, with metastatic depositions in the heart, kid- neys, suprarenal capsules, right lung, and pancreas, and from cancerous pleurisy of the left side. At the same time obsolete and recent tubercular enterophthisis and oedema of the brain were found at the post- mortem examination. 3. Aortic Aneurism.-In the course of development of cancerous affections, par- ticularly at the root of the lung, great bulging in the clavicular region may take place, accompanied by pulsation and other symptoms resembling aneurism of the aorta. Here the remark of Stokes is of great value, concerning the contrast be- tween the area of dulness on percussion and the pulsation. But the pulsation itself is of a different character in the two diseases, viz. circumscribed in aneurism, but diffused, not culminating in a particu- lar spot, in Cancer, in which, affection the ordinary signs of aneurism, as murmur or pulsation over the dull part, murmur above the clavicle, or propagated to the vessels of the neck, are also absent. I am furthermore inclined to believe that, in some cases, the sphygmograph will render great service in arriving at a decision, whether a disease be intrathoracic Cancer or aneurism. Gordon,3 Marlin Solon,4 and others, have published very instructive cases, in which Cancer was mistaken for aneurism, and the treatment of Valsalva adopted. But, notwithstanding these au- thorities, I maintain that a careful exami- nation and consideration of all symptoms, together with the history of the case, will seldom fail to result in a strict diagnosis, and to screen us from erroneous conclu- sions. Prognosis and Treatment.-Can- cer of the Lungs is a deadly disease, and, in spite of all medical efforts, leads finally to a fatal end. The first symptoms, as a moderate pain in the chest, difficulty of breathing, a dry cough, &c., sometimes last for years with- out alarming the patient, till more severe and dangerous phenomena make their appearance, and with tremendous speed hurry the patient into the grave. In the present state of our science we have neither means for extinguishing an existent cancerous cachexia, nor for caus- ing deposits to be absorbed, which, once produced, seldom remain stationary for any long period, but go on increasing, destroying the affected tissues, and inter- fering with neighboring organs. In the good olden times, when physi- cians fancied that even a disease like Can- cer would fly before a long prescription, many formulas were in vogue in which arsenic was the principal drug. This remedy was considered a specific, and eminent practitioners speak of it in terms of high commendation. Others again advocated the use of co- nium, bichloride of mercury, the prepara- tions of iron, and a number of other medicaments. But it appears that the efficacy of all these "specifics" became weaker and weaker in the same propor- tion as diagnostic science became strict and exact, and that arsenic and the other drugs effected a cure in those cases only in which a closer examination demon- strated that the case for which it had been applied was not Cancer at all. But, though medical science has not yet arrived at a point to furnish us with means of curing Cancer of the Lungs, we must not rest quiet and leave such pa- tients to their fate. Our profession has other tasks to fulfil where cure is impos- sible, namely, to relieve pain and allevi- ate other bad or dangerous symptoms, and thus to prolong life. In this respect we can act sometimes with very great benefit towards the sufferer. I had a patient under treatment who dreaded the approach of night, this being for him the signal of excruciating pain, restlessness, and torture, during which he incessantly offered prayers to Heaven for his death. Besides deposits on his lungs, there were likewise some in his liver, and the stomach was also affected, and rejected food and medicines as soon as they were taken. When he came under my care, I injected, every night, half a grain of mor- phia hypodermically, and from that time he enjoyed at least good rest at night. Our attention will therefore entirely be directed towards troublesome symptoms, improvement of the patient's nutrition, and keeping up his strength. Hence it becomes evident that bleeding in any shape and to any extent should only be resorted to in cases of pressing emer- gency. Dry-cupping, however, will prove beneficial when dyspnoea becomes trouble- some, in which cases other counter-irri- tants may also be applied to the skin with success. In one case, under my care, a hot bath of a minute's duration gave rest to the much-exhausted patient, while other remedies failed to diminish the dyspnoea. For the relief of pain, connected with Cancer of the Lungs, I can strongly recom- mend the hypodermic injection of mor- phia, beginning with a quarter of a grain, 1 Transactions of the Pathological Society, vol. iii. (1851-52) p. 254. 2 Virchow's Archiv, xxxvi. 4, 1866. 3 Med.-Chirurg. Transact, vol. xiii. 4 Archiv. Gen. de Med. tome xxiv. p. 142. 152 PNEUMONIA. and increasing the dose according to the requirements of the case. In respect to the method of injection and mixing the solution, I refer the reader to my paper "On Hypodermic Injections," which has been published in the "Medical Mirror" of 1866. Cough is another symptom which often resists all therapeutic endeavors. Where medicines can be taken, we should apply narcotics, opium, hyoscyamus, Indian hemp, and similar drugs. But, unfor- tunately in many cases the stomach, either by reflex action or by being also affected by the disease, rejects the drugs, and ren- ders our efforts useless. In these cases I propose the application of atomized fluids, which, indeed, would be the only means by which to introduce medicaments into the system. I refer the readers who are not acquainted with this mode of treat- ment to my work "On Inhalation."1 The patient's strength will appropri- ately be kept up by nutrient, easily di- gestible food, and avoiding everything which could possibly produce a conflux of blood towards the internal organs. In those unfortunate cases in which pressure on the oesophagus prevents the patient from taking solid food, it must, of course, be given as a fluid, and, if necessary, by the aid of the stomach-pump. In the patient's room, a moderate but equal temperature ought to be kept by day as well as by night ; all the natural functions must be regulated as far as pos- sible, and moderate exercise in the open air should be encouraged on fine days, and avoided only when it causes difficulty of breathing. Some physicians advocate cod-liver oil. It may be tried in cases in which it does not at all interfere with the function of the stomach, but it ought to be given up at once if it causes loss of appetite or sickness. Fetid breath, sometimes of unbearable intensity, disgusts not only everybody in the patient's room, but even the patient himself. This disagreeable quality of the breath can be destroyed in a short time, by inhalation of liquor chlori, per- chloride of iron, or creosote. Should one be called upon to give some prophylactic hints to persons de- scended from parents who died of Can- cer, the first care to be taken will be strictly to regulate the diet of such per- sons. Let them take regular exercise and live in mild climates, in places situated as high as possible ; advise them to undertake voyages, or to undergo a course of the so-called "grape-cure" of which many physicians speak in com- mending terms, and which produced very good effects in a case under my own care. The coast of England is a very healthy abode during the summer months for delicate individuals. But for such per- sons as wish to go abroad, Marseilles, Spezzia, Nice, Livorno, Venice, Heligo- land, Kiel, Swinemiinde, and the very pleasant isle of Rugia, could be recom- mended. Places where grapes are methodically used for medical purposes are Meran in Tyrol, Durkheim and Bingen in Ger- many, Krems in Austria, and Presburg in Hungary. The best time at which to send patients there is during the vintage, which is generally in the months of Sep- tember and October. PKEUMOKIA. By Wilson Fox, M.D., F.R.C.P. Synonyms. - Peripneumonia,2 Peri- pneumonia Vera (as opposed to Peripneu- monia Notha, or Capillary Bronchitis) ; Debris Pneumonica, Hoffmann; Fievre Pneumonique, Fluxion du Poitrine (French authors); Pneumonites, auct. var. Varieties and other Synonyms.- Croupous and Catarrhal Pneumonia (Rokitansky and modern German authors). Acute Sthenic Pneumonia-Broncho- pneumonia (English and foreign authors, signifying a similar distinction of origin and course). Lobar Pneumonia-Lobular or Disseminated Pneumonia (signifying ana- tomical differences in the extent and charac- ters of the pulmonary affection). Acute Pneumonia-Chronic or Interstitial Pneu- monia (signifying differences in course and duration, and also in anatomical charac- ters'). Interlobular Pneumonia (an affeo 1 On Inhalation as a means of Local Treat- ment of the Organs of Respiration by means of Atomized Fluids and Gases, by H. Beigel, M.D. London: Hardvvicke, 1866. 2 Grisolle considers that the prefix nt pi is merely expletive. ACUTE PNEUMONIA. 153 tion of the interlobular tissue). Primary Pneumonia-Secondary Pneumonia {sig- nifying differences in origin). Other varie- ties have been termed, according to the origin or characters of the disease- Bilious, Gastric, Typhoid, Latent, Inter- mittent, Hypostatic, Tubercular, Scrofu- lous, Rheumatic, Gouty, Puerperal, Me- tastatic, and Pneumonia Potatorum (Huss). ACUTE PNEUMONIA. Definition.-A disease whose essen- tial anatomical feature consists in the inflammation of the vesicular structure of the lungs, which is thereby rendered im- pervious to air through the accumulation in the interior of the alveoli of the pro- ducts of such inflammation. Clinically it is characterized by pyrexia, which, in the majority of cases, when the disease is pri- mary, commences with rigors ; it is also commonly attended by pain in the side, by dyspnoea, cough, sanguinolent sputa, great physical prostration, and by the physical signs of pulmonary consolidation. Its course, when primary, is usually acute, and tends to terminate favorably by a crisis occurring from the third to the tenth day, but it may prove fatal from the first to the fourteenth day, or at later periods. When secondary to other dis- eases, the termination by crisis is uncom- mon, and its duration is also more pro- tracted ; and under all circumstances of its origin it may, in some instances, lapse into the chronic state. Its immediate cause is uncertain, and it appears in the majority of instances to depend either on an unknown but suddenly produced dys- crasia, or on an alteration in the composi- tion of the blood induced by various dis- eases. In other cases it is produced through the extension to the pulmonary tissue of bronchial inflammation, or it may originate through local disturbances of the pulmonary circulation occasioned by congestion or collapse, or by obstruc- tion through emboli of the pulmonary artery, or it may be caused by mechanical injury to the tissue of the lung. Although the anatomical characteris- tics of Pneumonia can be defined with a certain approach to accuracy, the clinical features of the disease may nevertheless present a considerable diversity of aspect under the varied circumstances of its origin. In some cases variations in the ana- tomical process may be observed corre- sponding with these different features of the disorder, but distinct lines of demar- cation are in this respect very frequently wanting, and the author believes that the anatomical distinction between the " crou- pous"1 and the "catarrhal" forms, on which especial stress has of late been laid, is by no means so sharply defined as some recent writers have maintained. From a clinical point of view, however, the separation of the main types of these two forms of the disease into distinct species has a practical value, and it may therefore be stated that the principal classes to be distinguished are (1) Pri- mary or Acute Sthenic Pneumonia ; (2) Secondary Pneumonia, including most of the catarrhal forms; (3) Interlobular Pneumonia; (4) Chronic Pneumonia. Under the head of Etiology, the relations of the different forms of the acute disease will be treated collectively. History.-In the earlier days of medi- cine, since the times of Hippocrates and Galen (by whom, however, both diseases were recognized), Pneumonia was con- founded with Pleurisy to such an extent that the rusty sputa characterizing the former disease were described as an attri- bute of the latter ; and pleurisy was said to be capable of producing cavities in the lung. Valsalva, Morgagni, Huxham, and Boerhaave gave accurate descriptions of Pneumonia, but still the distinction between it and pleurisy was not com- pletely recognized until the writings of Bichat and Pinel, and the collapse of the lung attending pleuritic effusion was by most other writers mistaken for inflam- mation of its substance.2 The accurate 1 The term "Croupous," introduced by Rokitansky, and largely used in Germany, appears to the author to be in some respects best avoided. It was originally employed by Rokitansky to define a particular form of exu- dation, and in its application to Pneumonia he drew a parallel between this disease and croup of the larynx, attended by false mem- brane. The analogy appears to be an erro- neous one in two aspects, for in the first place the Pneumonia attending laryngeal diseases when false membranes are present is seldom seen in the form recognized as characterizing acute sthenic Pneumonia, but is most com- monly of the type termed Broncho-pneumonia; and, secondly, there is no boundary line of distinction between the forms of the disease characterized by a coagulable exudation in the vesicles, and those where cell-products are mingled with some fluid exudation. The extreme types are, it is true, distinct, but every shade of gradation may be observed between them. 2 According to Pinel, "Nos. Philos." ii. 145-191 et seq., the question of the distinc- tion between these two diseases appears to have given rise to the most animated discus- sion among the writers of the 17th century. The history of the earlier views on Pneumo- nia will be found at length in Grisolle's work on Pneumonia; also in Wunderlich's "Path. Therap.," art. Pneumonie, and in Neumann, " Krankheiten des Menschen," 2e Ed. i. 151 154 PNEUMONIA. clinical separation of the two diseases was finally fully evolved by Laennec. Since his time, the most important advance in the definition of the disease has been that made by Jorg, Bailly, and Legendre in the separation and distinction of the various forms of collapse, or defective ex- pansion from true inflammatory action. The other features of interest in recent researches will be alluded to in their ap- propriate places. Etiology.-On many points in the etiology of Pneumonia the only data at our disposal refer to the disease as a whole, irrespective of any of the special varieties before alluded to. The circum- stances predisposing to particular forms will be, as far as these are known, de- scribed separately. A. Race and Climate.1-Inflammation of the lungs appears, with but few ex- ceptions, to be more commonly associated with climates presenting marked and rapid variations of temperature than with extreme degrees of either cold or heat. Thus in tropical climates it is uncommon during the hot season, and, on the other hand, in some of the expeditions to the North Pole the disease has been almost unknown. It is said also to be very rare in Iceland. Throughout the European continent, below 60° north latitude, it is a very prevalent disease, and the southern portions, including the shores of the Medi- terranean,2 are nearly as liable as the more northern countries. Thus in Copen- hagen the mortality from Pneumonia is 6'3 per 100 of all deaths ; and in Gibral- tar 41 per 1000 soldiers suffer from the disease. In the more tropical climates, elevation above the sea-level increases the frequency of the disease, and it is very common in the high table-lands of Mexico.3 The disease appears to be rare in Egypt, though bronchitis is com- mon in tlie valley of the Nile ; in India it is more common in Bengal than in Bombay. Though equability of tempera- ture appears to confer a certain degree of immunity from the disease, yet there are some remarkable exceptions ; for in Sene- gal, which possesses a variable climate, Pneumonia is rare, while in the Bermu- das, where the temperature is remarkably uniform, it is by no means uncommon ; and it is stated, on the authority of Dr. Farry,1 that Pneumonia and affections of the lungs in general are less common, both in the Northern and Southern States of the Union, than in the central portions where the temperature is more uniform. Oregon and California appear to enjoy a singular immunity from the disease. In certain countries, as in Sierra Leone, the Cape, and the Mauritius, the negro races, at least when employed in military ser- vice, appear to suffer more than the whites ; but it is considered possible that the preponderance of the affection among them is due to their being more exposed to vicissitudes of temperature than the European soldiers, with whom greater precautions are taken. The disease is said to be more common among sailors on land than when at sea ;2 but it may be questioned whether this difference is not in part due to other in- fluences, causing an increased relative frequency on land, such as greater irregu- larity of life and severer exertion. In England, Pneumonia appears, from the returns of the Registrar-General for 1863-4, to rank next after the following main causes of mortality :-Phthisis, bronchitis, scarlatina, old age, and con- vulsions. The frequency, and also the mortality of the disease, however, vary considerably in different years, as is shown by the contrast of 26,052 deaths registered under this head in 1855 when compared with 21,118 occurring in 1867 ;3 and the data of nearly all the large hospitals of the Continent furnish confirmatory evi- dence of the same kind.4 (quoted by Wunderlich). The confusion be- tween Pneumonia and pleurisy was aided by the fact, that before the writings of Bichat the term pleura was limited to the parietal membrane, the visceral portion being con- founded with the tissue of the lung. 1 For a large number of the data under this head, the author is indebted to the writings of Grisolle, "Traits de la Pneumo- nic," and Hirsch, "Handb. der Hist. Ge- ograph. Pathol.," 1864; and also to an elabo- rate statistical work on the Geographical Distribution of Pneumonia, by Ziemssen, "Monatsblatt fiir med. Statistik und offene Gesundheits-pflege," 1857, analyzed at con- siderable length in Canstatt's "Jahresb.," 1857, ii. 119. Many of the data on this sub- ject refer, however, to pleurisy and Pneumo- nia collectively, and this is especially the case with those given in Hirsch's work. 2 Clark on Climate, p. 121. 3 Elevation in cold climates, in some situa- tions, also appears remarkably to predispose to the disease. Thus of the French troops quartered, on Mont Cenis from December to May, one-fourth of the whole number were attacked by pneumonia. (Chomel, Le?. Clin. Med., Ed. Sestier, p. 451.) 1 American Journ. Med. Science, 1841. (Grisolle.) 2 Dr. Wilson's report to the Admiralty gives for 1000 sailors : Short voyages, 29 per 1000; home service, 35'1 per 1000; Mediter- ranean, 31'8. Sailors as a class suffer but little-175 per 24,000. (Le Roy de Mericourt.) These data are quoted from Grisolle. 3 In the last-named year these proportional numbers are 995 deaths from Pneumonia, to 1,000,000 living; and 45,275 to 1,000,000 of deaths. 4 This is especially evident from the statis- tics of Huss, " Behandlung der Lungen Ent- ziindung:" for while the average number of ETIOLOGY. 155 It would appear from Ziemssen's anal- ysis that the mortality from Pneumonia is greater in large towns than in country districts ; but in this respect there are considerable differences in degree between different cities, that of Cork being 0'5 ; London, 1'7; Paris, 2'3; Turin, 3'8; and Algiers, 4'3 per 1000. Ireland seems to suffer to a less degree than most of the European countries. B. Classes and Professions.-There ap- pears to be a general consent that Pneu- monia is more common among the labor- ing than in the wealthier classes of society, and that, among the former, those whose occupation involves the severest exertion and the greatest amount of exposure are the most liable to suffer. In the English army the soldiers suffer more than the officers.1 The disease is more common in the French army than among the civil population.2 C. Seasons.-It may be stated as a gen- eral truth, that in European countries Pneumonia is most common during peri- ods of the year in which there are the greatest vicissitudes of temperature, while either a continuously low or high tempe- rature has much less influence in its pro- duction. Thus, of 2616 cases collected by Huss3 during a period of sixteen years in Stockholm, the spring months, March, April, May, and J une, gave 4'J per cent. ; the winter months, November, Decem- ber, January, and February, yielded 30 per cent. ; and the summer months, July, August, September, and October, 21 per cent. Of the individual months, August and September are those in which the greatest immunity is observed ; but this is nearly equalled by June and July, while April and May show the greatest frequency. Huss states that the relative frequency in individual months in different years corresponds closely to rapid changes of temperature observed in them. Baro- metric variations, independently of the influence of wind, appear to have little or no effect in the production of the disease. The converse, however, appears to hold true of cold winds, and particularly of those from the north and east; and though the effects of these in the produc- tion of Pneumonia have been more ob- served in the aged, and also, though to a less degree, in the young, than in persons of middle life, yet there is a strong proba- bility that their agency is similarly exert- ed at all ages.1 It was stated by Huxham2 that dry cold air was most frequently asso- ciated with Pneumonia of an inflamma- tory type, and that " bastard peripneumo- nies" were most common in damp seasons. Dr. Jackson3 has also shown that in Massachusetts, a damp climate, complica- tions are more common than in drier atmospheres. D. Age must be regarded as an import- ant etiological element in the predisposi- tion to Pneumonia, and it is also one of the conditions most materially influencing its mortality. Some of "the details given by writers antecedent to the researches of Legendre and Bailly are, however, unreliable,owing to the confusion then existing between Pneumonia and collapse of the lungs oc- curring in infancy. Thus Valleix and Vernois4 stated that of 114 newly-born children 113 had hepatization of the lungs. In spite of these doubts, however, there is very little question that Pneumonia is a very frequent disease of early life. Of 186 cases of primary acute (croupous) cases during 16 years was 163'5, these in 1849, 1851, and 1853 amounted respectively to 243, 242, and 203 admitted to hospital; while in 1840, 1841, and 1844, the numbers were only 107, 102, and 97. It will be seen in the section devoted to the prognosis that the mortality of the disease in different years also presents considerable variations; and also that the relative mortality at different seasons by no means corresponds to the fre- quency of the disease at these periods. 1 On the Mediterranean stations the sol- diers suffer from Pneumonia in the proportion of 32 to 42 per 1000 ; the officers in the pro- portion of 14'1 per 1000. On the Canadian stations the proportion of soldiers affected is 43 per 1000, and that of the officers is 10'6 per 1000. (Quoted from Grisolle.) 2 Deaths from Pneumonia in the civil popu- lation of France, 30 per 1000; in the army, 39 per 1000. (Lancereau, Ann. d'Hygiene, 1860, xiii. 269. Valleix.) 3 The amount of statistical evidence on this head is large and conclusive, and the results obtained by all observers agree very closely with those of Huss. For other references see Chomel, "Leo. Clin. Med. ' Pneumonie,'" p. 444; Grisolle, loc. oit., 139; Wunderlich, "Allg. Path. Therap.," Bd. iii., Abth. ii. B., p. 304; Bamberger, "Wien. Med. Woch.," 1857; Roth, "Wiirzb. Med. Zeitsch.," 1860; Hamernigk, "Die Cholera Epidem.," Prag, 1850. Ziemssen, "Die Pleuritis und Pneu- monie im Kinderalter," p. 187, found in Grieswald a rather larger proportion during the summer months than has been noticed by other observers. He attributes this to the cold winds and rapid variations of tempera- ture observed there during this season. More- head, "Dis. of India," pp. 300-303, found Pneumonia in India to be most common in the cold season, and next in frequency in the wet season. During the latter period it is very liable to be complicated by intermit- ten ts. * See for evidence on this subject Grisolle, p. 142. 2 Essay on Fevers, 1757, p. 222. 3 Dr. Sibson, Brit, and For. Rev. 1858, xxii. p. 23. 4 Valleix, Clin, des Malad. des Enfans nouveaux-ngs, 1838, p. 114. 156 PNEUMONIA. Pneumonia in children, recorded by Ziemssen,1 117 occurred in the first six years of life, and only 69 in the succeed- ing ten years. Gunsburg,2 for 5000 cases of Pneumonia, gives the following rela- tive table of frequency at different ages :- earlier periods of life ;* but it becomes apparent first at ages when the occupa- tions of the sexes differ, and when males are more exposed to climatic influences than females. When, however, the con- ditions of life for both sexes are identical, this relative disproportion in great mea- sure disappears.2 Huss has adduced the fact that it is also much less marked in advanced age.3 Females, as it would appear from Gri- solle's data, are somewhat more predis- posed to the occurrence of the disease at the menstrual period. Neither pregnancy nor the puerperal condition seems, how- ever, to create any special proclivity, ex- cept when the latter is complicated by septicaemia. F. Constitution.-Opinions differ whether Primary Pneumonia most commonly at- tacks the vigorous or those in previously bad health. The Hippocratic doctrine was in favor of the former view, which is also supported by Grisolle. Huss, on the contrary, thinks that it is more common in weakly subjects. Dr. Hughes Bennett,4 in 118 cases-84 males and 34 females- found that of the males 27, and of the females 22, were in bad health at the time of the seizure. Huss considers that the fact that robust males are frequently attacked depends in great measure on the greater degree of exposure to external in- fluences to which they are subjected. Chlorotic females seldom suffer. Rickets, on the other hand, appears to produce a predisposition to the disease, for of twenty- four patients dying rickety, Grisolle found Pneumonia in one-half. It is possible that this may be caused by the greater severity of bronchitis and the increased tendency to collapse in these subjects, and also to the fact that collapse of the lung when complicating bronchitis induces a liability to further inflammatory changes. Under Years. Years. u . 11 per cent From 4 to 14 . . 13 66 u 14 " 20 . . 6 66 u 20 " 30 . . 17 66 66 30 " 40 . . 16 66 66 40 " 50 . . 10 66 66 50 " 60 . . 9 66 66 60 " 70 . . 7 66 66 70 " 80 . . 11 66 Lombard has given, further, the follow- ing proportion of deaths from Pneumonia and deaths from other diseases at different ages:- Deaths from Age. all causes. Years. Years. Pneumonia. 274 . . under 1| . 56=4. 310 . . from 1| to 14 . . 70=1. 112 . . " 15 " 19 . 387 . . " 19 " 27 . . 39=^. 766 . . " 27 " 75 . • 46=^- Grisolle's statement may therefore be re- garded as embodying the truth on this question, viz. that Pneumonia (both pri- mary and secondary, lobar and lobular col- lectively) is a disease very frequent in in- fancy, that it is less common from infancy to twenty years of age, that it is compara- tively frequent from twenty to forty, less so from forty to sixty, and very frequent, and also very fatal, after sixty years of age. To this it may further be added, that the Pneumonia of old people and of children approximates more, but by no means exclusively, to the type of catar- rhal, or broncho-pneumonia. E. Sex.-In the Pneumonia of adult life, males are more commonly affected than females in proportions varying from two or three to one.3 This difference be- tween the sexes is not observable in the 1 Ziemssen, in 91 cases of children under four years of age, found that the boys affected numbered 41, and the girls 35. 2 Thus Tolmouche has observed that in prisons the number of individuals of the two sexes suffering from Pneumonia are, compara- tively speaking, equal (Ann. d'Hygiene, xiv. pp. 252-7.) Ruef also (Heidelb. Med. An- nalen, ii. 1836) has noticed a similar equality in the liability of the sexes to the disease when women are employed in outdoor labor. 3 Of the cases between the ages of 16 and 50, the males formed 85*5 per cent., and the females 14'5 per cent.; but of the cases be- tween 50 and 70, the males constituted only 5549, and the females 44*81 per cent. Dinstl also (Oest. Zeitsch. fur prakt. Heilkunde, viii. 1862) found in 1212 cases of Pneumonia, that after aetat. 50 the number of females af- fected was greater than that of the males. 4 The Restorative Treatment of Pneumonia, 1866, p. 24. 1 Loc. cit. p. 155. 2 Klinik der Kreislaufs und Athmungs-Or- gane (Breslau, 1856), quoted from Huss, loc. cit. 3 The proportion of 2 males to 1 female is that given by Grisolle and generally accepted. Of the actual numbers treated by Huss, the proportion was 5 to 1, but it amounted to 3 to 1 when calculated on the total numbers of all cases of males and females admitted to hospital. The proportion in the general hos- pital at Vienna (quoted by Huss) is 1*98 males to 1 female. Huss thinks that the greater disproportion observed in the more northern climate between males and females may be due in part to the greater intensity of climatic conditions to which the former are there exposed. ETIOLOGY. 157 It has been observed that some persons are liable to repeated attacks of the dis- ease-a peculiarity which may either be due to some special but unknown consti- tutional predisposition, or to the fact that previous attacks induce a proclivity to its return. The latter hypothesis is to some degree favored by the fact that the lung first affected is the most liable to suffer in a subsequent attack.1 In 175 cases anal- yzed by G-risolle, 54 had suffered from pre- vious attacks, but of these only two were in females. The period between the at- tacks varied from one month to twenty- five years. Most usually the intervals varied from three to five years ; but these tend to become shorter in proportion as the attacks become more frequent.2 The number of attacks from which in- dividuals have suffered is also very re- markable. Thus Andral3 records a case of a patient who had had fifteen attacks in eleven years, Chomel4 has seen ten re- currences, J. P. Frank5 eleven, and Rust has even recorded twenty-eight attacks in the same individual.6 Intermittent fever also predisposes to recurrence. A patient of Ziemssen's thus affected had four at- tacks in five years, three of which were in the left lower lobe and one in the right upper lobe.7 Difficult dentition predisposes to Pneu- monia in children,8 and also makes the prognosis more unfavorable. Favorable hygienic influences confer a certain de- gree of comparative immunity from the disease. Drunkenness appears to act powerfully as a predisposing cause of Pneumonia, though its effect in imme- diately producing the disease may be re- garded as somewhat doubtful. G. Direct Exciting Causes.-The influ- ence of these in the production of the acute primary disease has been very variously estimated by different observers. Some authorities, and particularly writers of the last century,1 attribute its origin mainly to the influence of a chill-an an- tecedent which others have denied from statistical data. Grisolle asserts that a discoverable cause of this nature could only be affirmed in one-fourth of his cases. Chomel2 and Andral3 express very simi- lar opinions. Ziemssen says that among children a discoverable cause only existed in one-tenth of his cases. In fifty-three cases analyzed by myself, a distinct cause, which when present was always of the nature of a chill, could only be affirmed in sixteen. It must, however, be admit- ted that this is the most common of the discoverable causes, and that the frequent absence of evidence of such an origin is common not only to Pneumonia, but also to many catarrhal affections and further to acute rheumatism, diseases which, to say the least, are very frequently due to this immediate agency. The most prob- able explanation of such cases would ap- pear to lie in the existence of a more extreme constitutional susceptibility, in consequence of which causes so slight as to pass unnoticed at the time of exposure may produce effects which persons less predisposed to suffer from their influence would have escaped. I do not think, as far as my own observation has gone, that the cases excited by a chill can be sepa- rated from the rest and placed in the category of Broncho-pneumonia, for in most of the instances coming under my own cognizance these cases have run as typical a course of acute primary Pneu- monia as those in which no such cause has been discoverable. The indirect evi- dence afforded by the seasons of the year at which Pneumonia is most prevalent, strongly bears out the opinion that vicis- situdes of temperature are among the most important agencies in its produc- tion. They appear to act most strongly 1 In 35 cases of recurrence collected by Grisolle, the return of the disease was noted 25 times in the lung first affected. In the remaining 10 the disease changed sides: Pneumonia of the left lung recurred more frequently than that of the right, in the pro- portion of 16 to 9. This is the more remark- able when it is remembered how much more frequently the right lung suffers from the primary disease. 2 Dr. West of 78 cases in children, found that 31 had suffered from previous attacks. Of these, 21 had been affected once, 4 twice, and 2 four times, and 4 others were said to have had several attacks. 10 of these pa- tients were under 2 years of age; 10 more between 2 and 3, and the remaining 11 were between 3 and 6. Ziemssen, in 201 cases of children, found 19 cases in which the attacks were repeated. Of these, 14 had Pneumonia twice, 3 three times, and 2 four times. In some instances the disease recurred at corre- sponding periods of consecutive years. 3 Clin. MEd. iii. 371. 4 Diet, de MEd. xviii. art. " Pneumonie." 5 Interpretationes Clinicse, Tubings, 1812, p. 96. (Grisolle.) 6 Quoted by Dr. Williams, art. "Pneumo- nia," Cyc. Pract. Med. iii. 406. i Ziemssen, loc. cit. 154. 8 Of 201 cases of Pneumonia observed by Ziemssen, this condition was present in 37. Of these, 16 had Broncho-pneumonia after long-continued bronchitis, and 21 suffered from primary or "croupous" Pneumonia. 1 Pinel (Nos. Phil. ii. 163) defines as the causes of primary Pneumonia: "Impression brusque d'un air froid apres un violent exer- cice, comme la course, la lutte, le chant, les cris, une Equitation rapide contre la direction du vent, une boisson froide lorsqu'on est EchaufFe." 1 Lemons, p. 464. 3 Clin. Med. vol. iii. PNEUMONIA. 158 at the two extremes of life. Cruveilhier1 particularly noticed the injurious effects of cold on the aged in the Salpetriere ; and Hourmann and Dechambre,2 out of 156 cases of Pneumonia in old people, observed 140 in the winter and early spring months, from November to May. Both these writers, and also Cruveilhier, remark upon the injurious effects of north and northeast winds in producing inflam- mation of the lungs in the aged.3 Laennec thought that prolonged expo- sure to cold had more effect than a sud- den chill, but I cannot say that my own experience has led me to adopt this view. Nearly all the cases of Pneumonia which I have observed from traceable causes were owing to a temporary chill, such as a wetting, exposure to draughts of cold air when heated, and similar influences. There can be very little doubt but that Pneumonia, in many instances at least, must depend in great measure on predis- posing constitutional or local conditions, whose nature is unknown, but whose in- fluence is distinct. It is to their influence that the special localization of acute dis- eases arising from general in contradis- tinction to specific causes, is due; and it is also to the greater or less degree in which they predominate, that the rela- tive facility of the production of such diseases may in great measure be at- tributed. Excessive exertion appears to act as an occasional cause. Wunderlich quotes a statement of Barth's to the effect that he had traced this cause in 12 out of 125 cases, and Wunderlich says that he can confirm Barth's experience. Traumatic causes do not easily produce a pneumonia of any extent or severity: the lung appears "to have remarkable powers of recovery from direct injury.4 Injuries and blows to the chest are how- ever occasionally followed by Pneumonia without distinct evidence of direct lacera- tion of the lung.5 The mechanism of such influences appears in some cases very ob- scure. Thus in a case admitted into Uni- versity College Hospital, under Sir W. Jenner, a patient struck his shoulder- blade on rising from a stooping position. He had previously been in apparently good health, though on admission he was found to be suffering from albuminuria, in addition to signs of pleuro-pneumonia on the side struck. Pericarditis also super- vened, and the case proved fatal. The pneumonia was in the lower portion of the upper lobe, and there was also exten- sive pleuritic effusion on the same side, but there was no evidence of mechanical injury to the chest-wall or to the lung. The kidneys were fatty. It is probable that in this case the pre-existing kidney disease acted as a powerful predisposing cause to the pathological conditions found. Pneumonia may, on the other hand, be easily excited by foreign bodies entering the lungs from the bronchi. This condi- tion is said to be not uncommon in those cases of dementia when food finds its way into the bronchi, and where gangrene of the lung is very liable to supervene. Grains of wheat or beards of barley enter- ing the bronchi are also occasional causes of Pneumonia.1 Blood gravitating into the vesicular structure of the lungs in cases of pulmonary hemorrhage may oc- casionally act as an exciting cause,2 and it is thought probable that the dissemi- nated Pneumonia observed in diphtheria and capillary bronchitis may be, in part at least, occasioned by the gravitation or insufflation into the air-vesicles of the fluid secretions of the bronchial tubes. It is very doubtful whether irritating vapors can produce true lobar Pneumonia. They may, however, produce a dissemi- nated form of the disease, resembling closely the "lobular pneumonia" occa- sionally occuring in bronchitis.3 1 Grisolle, p. 146. 2 See Dr. Hermann Weber's, Dr. C. Baum- ler's, and Dr. Sanderson's papers in the Trans. Clin. Soc. iii. This subject is a very wide one, and involves the disputed question whether haemoptysis, unassociated in the first instance with tubercles, can originate a dis- ease running the course of phthisis. I have more than once seen Pneumonia follow haemop- tysis in the course of early phthisis, but I have hitherto regarded it as probable that the haemoptysis may be the result of the conges- tion which precedes Pneumonia acting on the weakened pulmonary vessels. In some cases of phthisical subjects, this appears to be the undoubted mechanism of the haemoptysis ob- served ; but in other cases there is a strong probability that the Pneumonia results from the haemoptysis in the manner described. 3 See Bretonneau, Rech. Infl. Spec. Tiss. Muqueux, Paris, 1826, p. 100. Gendrin (Hist. Anat, des Inflam. ii. 302) says that if an animal be made to breathe chlorine, the lungs are found studded with little solid nodules arising from an exudation into the air-vesicles. Gendrin considered these to be 1 Anat. Path., liv. xxix. 2 Pneumonie des Vieillards, Arch. G6n. 2e S^r., xii. p. 29. 3 The mode of action of these causes will be further considered under the head of Pa- thology. 4 Grisolle, pp. 43-4. 6 See a case quoted by Grisolle, loc. cit. 316, from J. P. Frank, of a porter who had overstrained himself; also Dpchek, " Ab- theilungs-bericht Allgem. Krankenhauz zu Prag;" Prager Vierteljahresch. 1853, xxvii. p. 37-two cases where Pneumonia followed a blow on the chest; also Wunderlich, loc. cit. Bd. iii. Abth. ii. 13; also noted by Mor- gagni, "Epist." ii.; also a case by Andral, "Clin. Med." iii. obs. vii. p. 293. ETIOLOGY. 159 H. Epidemic Causes.-The only positive data on this subject are those afforded during the prevalence of epidemics of in- fluenza. This disease has certainly a con- siderable tendency to give rise to Pneu- monia, which is for the most part of a catarrhal type. Thus Nonat1 observed, during the epidemic of influenza in 1837, that of 300 deaths in the hospital Hotel- Dieu, in Paris, in the month of February of that year, 80 were due to Pneumonia ; and Laserre,2 in La Pitie, observed in three months in 1842, during a similar epidemic, 31 cases of Pneumonia. It would appear, however, that un- healthy conditions of crowding, with bad ventilation, strongly predispose to the disease when other causes, particularly measles, are present ; and some evidence has lately been adduced to show that similar influences may operate independ- ently of the presence of any immediate cause.3 Griesinger1 has stated that in malarial districts Pneumonia has at times a ten- dency to assume an epidemic character. It may be doubted whether, independently of such causes, Pneumonia can be con- sidered as an epidemic due to a specific poison, or whether its greater prevalence at certain seasons, and in particular years, producing an apparent resemblance to a zymotic disorder, has not resulted from some of the atmospheric agencies before alluded to.2 It has been asserted that Pneumonia and "typhus" fever have a tendency to appear simultaneously, and it has hence been concluded that some connection may therefore possibly exist between these dis- eases. This belief is disproved by the returns of the Vienna hospitals, and also by Huss's statistics; though IIuss con- sidered that during the prevalence of these disorders Pneumonia is liable to assume the typhoid form. I. Influence of other Diseases in the pro- duction of Pneumonia.-There appear to be at least six categories under which Pneumonia occurring in the course of other diseases may be classified :- 1. It may be the immediate effect of the poison producing the primary disease, or of the altered composition of the blood thus induced,3 and in this light it is probable that many of the pneumonias occurring in the course of the acute feb- rile diseases should be regarded. 2. It may be the result of accidental products accumulating in the blood, as is identical with some forms of tubercle. It may also be recalled that Cruveilhier pro- duced similar results (to which he attached the same interpretation) by injecting mercury into the trachea. Reitz (Sitzb. K. K. Akad. zu Wien, 1867; Math. Nat. Wissch. Cl. Iv. 3) has varied these experiments by injecting caustic ammonia into the trachea. I have repeated this experiment in a dog. The re- sult was an intensely developed membranous exudation, extending throughout the trachea and smaller bronchi, but becoming more fluid and puriform in the latter. There was no uniform lobar consolidation in the lungs, but these were studded throughout with small yellow spots, solid, not at all prominent, rarely exceeding the size of a pea, somewhat irregular in their outlines, finely granular on section, breaking down in various parts into cavities which in some places attained the size of a hazel-nut. These were filled with a diffluent puriform matter, and when near the surface, they projected like blisters from un- der the pleura by which they were covered. Death had occurred on the third day after the experiment. Dinstl, however (Oest. Zeitsch. Prakt. Heilk. viii. 1862, and Schmidt's Jahrb. 1866), has occasionally seen Pneumonia arise from the inhalation of irritating vapors. 1 Arch, G6n. de Med. 3e Ser. tome ii. 1837, p. 16. 2 Ibid. xv. 1842, p. 130. 3 Thus Dahl, ' ' Norsk Mag. filr Laegevi- denz," xxii. Hft. 6; Virchow's Jahresb. 1868, ii. 95, has twice observed an epidemic of Pneumonia in the prison of Christiania. The first of these was in 1847; the second was in 1866-7, when of 366 prisoners, 62 had Pneu- monia, or one-sixth of the whole number. The servants working outside were equally affected with the prisoners. In other years Pneumonia has been a rare event in the prison. Prof. Boeck, who was consulted by the Government, considered that overcrowd- ing had a great influence in the production of the disease. In the " epidemic" of 1866-7, the weather was very cold during a great part of the prevalence of the disorder, and Pneumonia was common also in the surround- ing district. 1 Infections Krankheiten; Virchow's Hand- buch, Sp. Path. Therap. ii. 43. 2 The descriptions of epidemics of Pneumo- nia are only to be found in older writers, and the nature of the disorder must in some of these cases be considered at least doubtful. Lebert, " Path. Anat." i. 651, says, however, that he has convinced himself of the existence of epidemics of Pneumonia in certain parts of Switzerland. Further information on this subject may be obtained in the following works : Hirsch, loc. cit.; Ozanam, Hist. Med. des Mal. Epid^m., Paris, 1835; Lebecq de la Cloture, Obs. sur les Malad. et Consid. des Epidemiques, Paris, 1776-1778; Max Simon, Etude Pratique retrospective, et compare© sur le Traitement des Epidemiques au 17e Sibcle, Paris, 1859. (Quoted by Lebert, loc. cit.) 3 0. Weber, in addition to other internal inflammations, has succeeded in producing diffuse Pneumonia by injecting the blood of a febrile dog into another healthy one. (Pitha and Billroth's Handbuch der Chirurgie, i. 610.) See also Virchow, Ges. Abhand. 660, et seq. Also Billroth, Archiv fur Klin. Ch.i- rurg. vol. vi. 160 PNEUMONIA. seen in albuminuria, and possibly in dia- betes,-or it may arise from the mechani- cal or infecting inlluence of solid materials formed elsewhere, and conveyed by the blood current to the lungs, as in throm- bosis and in some cases of pyaemia. 3. It may be the secondary result of other diseases affecting the lungs or air- passages, as tubercle or bronchitis. 4. It may be the effect of mere passive congestion, mainly of mechanical origin, arising either from valvular disease of the heart or from weakness of the circulation, aided by defective respiratory movement and dependent position, and in many cases by collapse of lung in the course of some of the acute febrile and also in that of chronic exhausting diseases. 5. It may be the result of a direct ex- tension of diseases affecting other organs, as when abscesses of the abdominal viscera communicate with the lungs. In some cases Pneumonia, secondary to pericar- ditis, may have a similar origin. G. It may be a purely accidental com- plication. In many of the acute febrile diseases no other cause can be assigned for the occurrence of Pneumonia than the pres- ence of a blood poison.1 In others the mechanism is more complex, as in diph- theria and measles, when the effect is probably in part due to the secondary ef- fects of bronchitis or collapse ; and even in some cases of typhoid fever Pneumonia may rise either from embolism,2 or from secondary blood-poisoning resulting from the ulceration of the intestines. The characters also of the Pneumonia arising in the course of other diseases vary considerably. In some, as in measles and hooping-cough, it mainly presents the characters of lobular or broncho-pneumo- nia ; in others, as in variola, the inflam- matory changes may be either lobar, or may be disseminated irregularly through- out the lungs. The appearances in dia- betes may be either those of the acute lobar form, or the Pneumonia may occur in disseminated nodules, tending to un- dergo a necrobrotic or cheesy change, and which appear to be closely allied to. if not identical with, the tubercular process. In albuminuria either the acute lobar form may predominate with firm exudation, or the inflamed part may present a smoother section, together with softer consistence and a more translucent appearance, arising from coexisting pulmonary oedema. Of the acute specific fevers, measles is that most commonly attended by Pneu- monia. The frequency of the latter dis- ease varies, however, in different epidem- ics, and at different periods of the same epidemic and it is a more common com- plication of the disease during childhood than in adult life. Typhoid fever stands next in order of frequency-typhus fever, according to the statement of Dr. Murchi- son,2 involving a minor degree of liability to the disease. In both these diseases, however, the data are somewhat uncer- tain, owing to the liability to hypostatic congestion of the lungs, which is commonly found when they prove fatal. In typhoid fever especially, the Pneumonia tends oc- casionally to assume the lobular and ve- sicular forms of the disease. In scarlatina, Pneumonia is less com- mon during the earlier stages, but is by no means rare when in its later periods it is complicated by albuminuria. In glanders and farcy, secondary Pneu- monia is extremely common. It usually assumes a disseminated form and tends to pass into suppuration, presenting in this respect many features common to pyae- mia.3 Pneumonia is occasionally observed in cases of erysipelas.4 In some cases it ap- pears to be due to secondary blood-poison- ing, and to assume the disseminated form of pysemic Pneumonia.5 In other in- stances, however, it appears to be rather of the nature of an intercurrent phenome- non, and approximates more or less closely in its characters to those of the acute pri- mary disease; and it appears not im- probable that the Pneumonia may, under these circumstances, originate from the 1 Barthez et Rilliet, Mal. des Enfants, iii. 264. These authors observed 65 cases of Pneumonia and lobular Broncho-pneumonia in 167 cases of measles. Bartels (Virch. Arch. xxi. pp. 75-6), in an epidemic in 1860, found Pneumonia or Broncho-pneumonia in 12 per cent, of his cases, but these complica- tions contributed 80 per cent, of the deaths ■which occurred. 2 Continued fevers, p. 184. 3 It is remarkable that, although this is the condition most ordinarily found in the human subject, yet that in the horse these diseases are associated with peri-bronchitis, and in this respect closely resemble tubercle. (Cornil and Ranvier, Manuel Histol. Path.) 1 Stokes, Dis. of Chest, p. 339. 5 See vol. i. art. "Erysipelas," by Dr. Reynolds, p. 321. 1 It has been noticed by Andral that Pneu- monia may appear with the first invasion of the exanthemata, and that its occurrence at these early periods sometimes coincides with an imperfect development of the eruption. In a case of variola he observed, during the invasion, crepitation in both lungs, with a viscous rusty expectoration, which vanished on the appearance of the eruption. I have recently seen a case where crepitation and dulness at the base of the lung disappeared within twenty-four hours after the eruption of variola had taken place. (Cf. Clin. M6d. iii. pp. 409-460.) 2 I have seen a well-marked instance of this, where both lungs contained infarcta surrounded by secondary Pneumonia. ETIOLOGY. 161 same blood-poison as that which gives rise to the erysipelas. It has also been observed to arise by a propagation of the inflammatory action from the skin, ex- tending through the mouth, fauces, and air-passages to the lung tissue.1 In the course of acute rheumatism, Pneumonia is a not very uncommon com- plication.2 In some cases it appears in a form truly metatastic with the rheumatic affection of the joints ;3 but most com- monly the joint affection persists during its continuance. The influence of acute gout in the production of Pneumonia ap- pears to be much less marked than that of rheumatism. Other febrile states associated with dis- ordered conditions of the blood are fre- quently causes of Pneumonia; but at present these cases have not been fully analyzed with regard to the mechanism of its production. Thus the statistics of Mr. Erichsen4 show that it is common after severe surgical operations, 45 per cent, of deaths from these causes present- ing signs of inflammation of the lungs. It also appears to be common in puerperal fever.5 Grisolle states that five-sixths of child- ren affected with gangrene of the mouth suffered from intercurrent Pneumonia. It is also very common in the course of scurvy and purpura. In the latter dis- ease I have seen it assume anatomically the acute primary form. Albuminuria, associated with disease of the kidneys, is again a very common cause.1 Rayer found Pneumonia in one- twelfth of these cases. The collection by Jaccoud,2 of Frerichs and Rosenstein's returns, shows that the affection was found in 52 of 416 cases, or in 12-8 per cent. Dr. John Taylor,3 however, found the frequency of Pneumonia to be 24 per cent. Becquerel,4 in 129 cases of Bright's disease, found Pneumonia in 20 per cent.; but in 100 cases examined by Dr. Bright5 it was only found in 6 per cent. Rosen- stein6 considers that Pneumonia in this disease is nearly as frequent as pleurisy. It has been already stated that Pneu- monia is a very common secondary result of bronchitis. The relation of the two diseases is threefold. In some cases they appear to be due to a common cause, and acute primary lobar Pneumonia may originate simultaneously with a general bronchitis. In other cases it appears to be the result of a direct extension from the bronchi, and under these circum- stances it may appear in the form of "lobular" or "vesicular" Pneumonia; but in other instances the disease thus originating is in the lobar form, and offers no distinctive characters from the primary disease.7 In the third class the Pneumonia is produced by the interven- tion of collapse, the mechanism of which process will be further considered here- after. Bronchitis in the adult, as it would appear from the analysis of Grisolle, often precedes Pneumonia, having been ob- served by him as an antecedent in 76 out of 201 cases, and in 53 of these the catarrh was recent, i. e., it had commenced with- in a month or three weeks before the Pneumonia appeared. Such antecedent bronchial catarrh, according to Grisolle's experience, is less common in the summer months. My own observations would lead me to the belief that bronchial 1 See a case by Gubler, quoted in a thesis by LabbS, "De PErysipele," Theses de Paris, 1858, p. 57. Vulpian, Pneum. Second. 2 Dr. Fuller, in 268 cases of acute rheuma- tism, observed 28 of Pneumonia. Dr. Latham, "Dis. of Heart," i. 161, in 136 cases found Pneumonia in 18. Dr. John Taylor (Med.- Chir. Trans. 1845, vol. x. p. 565) only ob- served it three times in 86 cases. My own observations would lead me to the belief that this complication is not infrequent. I have seen several cases of this class. In the au- tumn of 1865-6, several cases of acute rheu- matism simultaneously admitted into hospital suffered from Pneumonia. 3 Grisolle, p. 173, cites three cases of this kind; one from Andral, "Clin. Med.," iii. 463: and a fourth where, in two consecutive attacks of acute rheumatism occurring at in- tervals of some years in the same patient, Pneumonia appeared and disappeared "eight or ten times, following the same course, and having the same duration as the joint affec- tion." 4 Med.-Chir. Trans, vol. xxvi. 5 Tonnele (Arch. Gen. xxii. 487) found Pneumonia in one-twelfth of the fatal cases of puerperal fever. Grisolle, p. 165, says that perimetritis is associated with septic pleurisy, and not with Pneumonia, while uterine phlebitis is more commonly associated with Pneumonia. 1 Dr. Grainger Stewart (Bright's Diseases of the Kidney) gives the following data of the frequency of Pneumonia in the different dis- eases of the kidney associated with albumi- nuria: acute nephritis, 21 per cent.; con- tracted or cirrhotic kidney, 7 per cent.; waxy kidney, 4 per cent. 2 Le?. Clin. Med. 1867. 3 Loc. cit. p. 565. 4 Serneiotique des Urines, 1841. 6 Guy's Hosp. Rep., 1836. 6 Path. Therap. Nierenkrankheiten, p. 198. 7 Some authors, and Rilliet and Barthez in particular, consider that this form results from extension of the disseminated variety, and they have termed it " Pneumonie vdsicu- laire,' ' or ' 'disseminSe, ' ' or ''lobulaire general- is4e." It does not appear to me that this distinction can be always maintained; and, further, it not infrequently happens that in cases of acute pulmonary pneumonia, in ad- dition to the lobar form, disseminated nodules are found in other parts of the lungs. VOL. IL-11 162 PNEUMONIA. catarrh may not infrequently precede by two or three days the symptoms of inva- sion of Pneumonia. Bronchitis common- ly precedes the Pneumonia of the aged.1 Phthisis is so commonly complicated with Pneumonia, that the latter may, as stated by Dr. Addison, be regarded as the immediate cause of a large proportion of the phenomena of this disease. The question of their mutual relations belongs, however, rather to the subject of Phthisis than to that of Pneumonia. Congestive conditions of the pulmonary circulation are also a common cause of the disease. The influence of cardiac affections in its production is a very im- portant one, and Pneumonia tends to ap- pear in their course in a proportion of from one-third to one-fifth (Grisolle and Dr. King Chambers).2 It is probably mainly to the influence of congestion that the inflammatory changes appearing in collapsed portions of lung are due, and it is not impossible that it contributes in a considerable degree to the Pneumonia complicating capillary bronchitis. The influence also of congestion in the produc- tion of the inflammation of the lungs which attends the later periods of life, when it mainly occurs in the most depen- dent parts of the lung-the hypostatic pneumonia of Piorry-is unanimously ad- mitted.3 Pneumonia being found in a proportion of one-sixth to one-seventh of chronic and cancerous diseases,4 and of one-fifth of chronic diseases of the nervous system.® ACUTE PRIMARY PNEUMONIA. Symptoms.-The invasion of the dis ease is sometimes preceded by prodro- mata, which may exist for one or two days, or even longer,6 before the outbreak of the severer symptoms. They are, however, very frequently wantingwhen present they may exist as before stated, as a slight degree of bronchial catarrh, or in the form of general malaise, chilliness, loss of appetite, headache, pains and aching in the back and limbs, and an earthy or icteric tint of skin.2 In old people the disease may be preceded for one or two weeks by headache and vertigo, epistaxis and lumbar pains.3 Pyrexia of a marked kind is stated to precede sometimes by some days all other signs of the disease, but these cases are exceptional,4 and it may be questioned whether pyrexia in such instances has not been caused by a central but undiscovered Pneumonia. There are not, as far as I am aware, any authentic thermometric observations re- corded of the temperature during the prodromal period,® but Huss states that a slight degree of feverishness is sometimes observed. In a large proportion of cases. exposure to cold. (Grisolle, p. 157.) Zim- mermann (Prager Vierteljabresch. 1852, vol. xxxii. p. 97) gives a case in a young man where the prodromata had lasted a week. It may, however, be doubted how far these symptoms can be regarded as being in any respect special forerunners of the inflamma- tion of the lungs; or whether they are not rather to be considered as symptoms of a bad state of health which predisposes to the dis- ease. 1 Grisolle estimates the frequency with which prodromata are observed in the adult as about one-quarter of all cases. In those to which I have had access the proportion has been 15 out of 53. They are much less commonly observed in children and in old people. Durand-Fardel noted their presumed absence in 20 out of 50 cases (Mal. des Vieil- lards, 470). 2 Andral (Clin. Med. ii. 284, obs. iv.) gives a case of a female who, after drinking largely while heated, was seized with diarrhoea and bronchitis; after ten days the diarrhoea ceased, and signs of Pneumonia then ap- peared. 3 Hourmann et Dechambre, Arch. G^n. 2e Ser. xii. 4 Grisolle, p. 187; Traube, Deutsche Klinik, 1857, p. 22. 6 The only case absolutely bearing on this subject with which I am acquainted is one by Monthus, "Essai sur la Pneumonie Dou- ble." A patient was in the hospital for ab- scess of the foot. Her temperature had been normal throughout. One night she got a chill from a draught of cold air. In the morning she felt ill, and the temperature was 100'4; within a quarter of an hour a rigor supervened. At the commencement of the rigor the temperature was 100'9. During the rigor and for an hour after, the tempera- ture was 105'8, it then fell to and remained at 103'6. On the following day crepitation appeared in the lung, and the temperature was 1040. 1 Dilatation of the bronchi appears to be a very common cause of secondary Pneumonia. Thus Barth (M6m. Soc., obs. iii. 1856) met with Pneumonia in 12 out of 40 cases of bron- chiectasis. Biermer, Theorie Anat, der Bronch. Erweiterung (Virch. Arch, xix.), found it in 12 out of 54 cases ; and Rapp (Verhand, der Wiirzb. Med. Gesellsch.), in 21 out of 24 cases. The Pneumonia thus met with is in some cases lobar, in others lobular. It occasionally passes into gangrene. 2 Med.-Chir. Rev., Oct. 1853. 3 An interesting case of this kind is quoted by Vulpian, "Pneumonies Secondaires," from Rayer, "Mal. des Reins," ii. 293. The pa- tient was obliged to maintain the sitting posture, and the lower portions alone of both lungs were found affected with Pneumonia. 4 Grisolle. 5 Calmeil, Diet, de Med., ii. 196. 8 Such prodromata may last from one to two weeks, or five or six days, and then the Pneumonia may appear after a slight further ACUTE PRIMARY PNEUMONIA. 163 however, the disease commences suddenly and without previous warning, in persons who up to the moment of seizure had felt perfectly well, and it is not uncommon for the invasion to occur during the night after the patient has gone to bed in his usual health. The invasion is most commonly marked by rigors, which are generally of a severe character. They form one of the most constant features of Pneumonia in adults, and their frequency and intensity are greater in this than in almost any other disease, with the exception of intermit- tent fever, pyaemia, and puerperal fever.1 They are, however, commonly absent in most cases of secondary Pneumonia, and also in that succeeding to long-continued bronchitis. The rigor usually only occurs at the commencement of the disease, and it is rarely repeated, though this is some- times observed.2 In some cases it may appear subsequently to other symptoms, such as pain or cough, and in other in- stances it commences suddenly, after ma- laise and a general feeling of illness have existed during some days. When rigors are absent, the invasion of the disease may be evidenced by other symptoms, such as great prostration and pyrexia. In children also it may be marked by symptoms indicating the early implica- tion of the nervous system, such as con- vulsions, vomiting, and headache or de- lirium, which may occur suddenly and without previous warning, or by the milder symptoms of stupor, restlessness, and loss of appetite. In old people sudden pros- tration and a semi-comatose state may be the first symptoms observed.3 Rigors may precede by a period of from twelve to twenty-four hours, or even in some cases, of from three to four days, all other symptoms and local signs of Pneumonia with the exception of Pyrexia.4 More commonly, however, other symptoms oc- cur early, and particularly pain in the side, dyspnoea, oppression of the chest, cough, and rusty expectoration. In some cases the earlier symptoms may be head- ache, or vomiting, or diarrhoeasevere lumbago is also occasionally observed. Of the symptoms indicating the pul- monary affection, pain in the side is one of the earliest and the most constant, and it may be the first symptom noticed, in some cases preceding the rigor.2 It is commonly very acute, and its presence is the cause of great anxiety and distress to the patient. It usually corresponds to the site of the Pneumonia, but exceptions to this are occasionally observed, and it assumes at times the character of lum- bago. Much discussion has arisen as to its cause, but probably in most cases it is to be attributed to concomitant implica- tion of the pleura. It generally continues during the earlier stages of the disease, tending to diminish towards the third or fourth day, but sometimes lasting until the eighth or ninth. It is aggravated by deep inspirations and by cough, and it occasionally coexists with marked tender- ness on pressure : I have observed it to be associated with considerable cutaneous hypereesthesia of the affected side. The other symptoms of the declared disease usually show themselves within twenty-four hours of the invasion, and the aspect of the patient is then to a cer- tain degree characteristic. There is great prostration - a flushed but somewhat earthy or dusky tint of face, tending in some cases to lividity. The skin is pun- gently hot, sometimes dry, but not infre- quently perspiring. The countenance is expressive of anxiety, particularly when pain is present; at other times the ex- pression is dull and heavy. The respira- tion is accelerated, and when pain is severe it is shallow and irregular; and the expansion of the aloe, nasi with the res- piratory act is strongly exaggerated. Dys- pnoea and a great sense of thoracic op- pression are frequently but not constantly present. Speech is rendered difficult and 1 Huss (loc. cit.) observed rigors in 80 per cent, of his cases. They occurred in 145 out of 182 cases observed by Grisolle, and in 110 of these they were the first symptom noticed. Louis observed rigors as the initial symptom in 61 out of 79 cases. I find their entire ab- sence recorded in 9 only out of 53 cases. In 34 they were distinctly present. 2 Louis, Rech. Fievre Typh. ii. 128. 3 In 35 cases of Pneumonia in old people, Durand-Fardel observed the phenomena of invasion to be as follows : In 7, rigors only; in 8, rigors and pain in the side; in 6, rigors and vomiting; in 8, pain in the side alone; and in 6, vomiting alone. Dyspnoea was rare at the outset, and was only observed in 12 out of 50 cases. It was comparatively constant at later periods. 4 This state, when protracted, constitutes the "Febris Pneumonica" of older writers. The term is also applied to some forms of "Latent Pneumonia." 1 Headache occurred among the first symp- toms in 12, and vomiting in 9, out of 53 cases which I have been able to analyze. For the opportunities of making many of these obser- vations I am indebted to the kindness of my colleagues, Sir W. Jenner, Dr. Hare, and Dr. Reynolds, who have allowed me access to the pulmonary cases under their care, and also have permitted me to use their case-books to supplement, when necessary, my own obser- vations. 2 In 201 cases analyzed by Grisolle, pain in the side was only absent in 29. In 182 it appeared within the first twelve hours in 121. In four it only appeared on the third or fourth day, and in two of these latter its in- vasion was marked by the recurrence of an intense rigor. 164 PNEUMONIA. broken by the accelerated respiration, the dyspnoea, the cough, and the thoracic pain. There is a short hacking cough, attended with a labored expectoration of viscous, tenacious, and rusty sputa. The pulse is accelerated, it is full, and occa- sionally resisting, but more commonly it is soft, or small, or dichrotous. The de- cumbency is in most cases dorsal; ortho- pnoea is less frequently observed. Tre- mors and subsultus tendinum mark severe cases, which may also be complicated by convulsions or delirium. The urine is scanty and high-colored. There is com- plete anorexia and great thirst; the tongue is dry and furred, and the lips cracked ; vomiting is sometimes present; the bow- els are usually confined, but diarrhoea is by no means rare. These symptoms may last with unabated or even with increas- ing intensity, for a period varying from the third to the tenth day of the disease, within which time a notable improvement is usually suddenly observed ; the tem- perature falls abruptly, the flush disap- pears and gives way to pallor ; the skin becomes bathed with a profuse perspira- tion ; the pulse and respiration, particu- larly the latter, fall in frequency; the dyspnoea and distress are markedly dimin- ished ; the cough becomes freer and looser, and the rusty sputa ordinarily disappear. In favorable cases the patient at once feels and declares himself better, and the appetite may return immediately; while in severe cases, or in weakly patients, in spite of the fall of temperature, an in- tense degree of prostration, amounting even to collapse, and sometimes ending fatally, ensues. When this crisis has taken place there is usually a rapid and continuous improvement both in the gen- eral symptoms and in the physical signs, which may, however, be occasionally in- terrupted by a relapse and by a return of the febrile condition after an interval of twenty-four, forty-eight, or seventy-two hours. In some cases, however, the crisis is indeterminate, the defervescence of the pyrexia is gradual, and the improvement slow and protracted. In unfavorable cases death may occur from asphyxia or col- lapse within the first ten days, without the subsidence of the pyrexia; or even, as before stated, after the temperature has fallen to the normal standard. The symptoms now enumerated require, however, a more special consideration. Respiratory System.- Accelerated res- piration and dyspnoea are among the most marked phenomena of Pneumonia. The latter is not, however, constant as a sub- jective symptom, and seems to bear, in many cases, no relation to the rapidity of the breathing.1 It is, however, occasion- ally the first symptom observed, especially in secondary pneumonias, and it may exist to an intense degree, producing a sense of impending asphyxia ; in children it occa- sionally occurs in suffocative paroxysms threatening death.1 Its intensity is com- monly but not constantly in proportion to the rapidity of the invasion and of the extension of the disease. It is much ag- gravated by the coexistence of general bronchitis together with the Pneumonia. It has been said to be more intense when the inflammation affects the apex of the lung, but Grisolle has shown that facts do not confirm this opinion. In some cases the sensation of dyspnoea is probably masked by the prostration of the nervous system. The rate of respiration is greatly quick- ened. The number of respirations per minute is seldom less than 30, often 35 to 40, and they may even reach 60 or 70. The acceleration of the breathing is gen- erally proportionate to the extent of lung affected, but this is not invariably the case. It is increased by coexisting bron- chitis, or by any cause interfering with the thoracic expansion, such as preg- nancy. The acceleration of the breath- ing is proportionately greater than that of the pulse, and hence arises the perverted pulse-respiration ratio which is especially insisted on by Dr. Walshe as one of the earliest signs of Pneumonia.2 This per- version may reach the limits of 60 respi- rations to 100 pulsations per minute; or in some cases, when the pulse remains slow, the ratio has been observed of 56 pulsations to 60 or 70 respirations per minute.3 The respiration is commonly more rapid in children than in adults, and in them the anhelation may be extreme and the respiratory movements irregular. In some cases of asthenic Pneumonia the pulse-respiration-ratio may not vary mark- edly from that of health.4 It is not im- probable that the extreme degrees of fre- quency of respiration may in some cases be due indirectly to peculiar states of the nervous system.6 The breathing, in ad- without any sense of dyspnoea. It is possible that in some of these cases the blood is suffi- ciently aerated by the accelerated breathing to prevent the sense of dyspnoea being felt. In some cases, when the respiration is less rapid, the sense of dyspnoea is extreme. 1 Ziemmsen, loc. cit. 2 Dr. Walshe (Dis. of Lungs, Edit. 1860, p. 366) says that the return to the normal ratio may, on the other hand, be one of the first signs of improvement. ® Ibid. « Ibid. 5 Traube (Annalen der Charite, vol. i.) considers that the rapidity of the breathing is in part due to pain, and in part to the high temperature of the blood affecting the ner- vous centres, as it is diminished by the appli- cation of cold. 1 Dr. Walshe says that he has seen patients breathing at the rate of 50 or 60 per minute ACUTE PRIMARY PNEUMONIA. 165 dition to being rapid, is commonly shal- low, particularly when pain in the side is severe. Cough is not only an almost constant, but it is one of the earliest symptoms.1 It is short and hacking, and rarely parox- ysmal, though it sometimes becomes so in children in the later stages of the dis- ease. The violent paroxysms, resembling those of hooping-cough, mentioned by Rilliet and Barthez, are thought by Ziemssen to be more characteristic of Broncho-pneumonia. It is often, on the other hand, less frequent in old people and in children than in adults, and it has been observed in the former, that a cough previously existing, and caused by bron- chitis, has ceased or has become greatly diminished on the invasion of Pneumonia. The cough often ceases when a fatal ter- mination is approaching. The expectoration which attends the cough usually presents characteristic fea- tures, depending on the admixture of blood. This is not, however, always ap- parent at the outset, when the sputa may be frothy and aerated. They soon, how- ever, tend to become peculiarly viscous, adhering with great tenacity to the con- taining vessel, and owing to this quality they are often expectorated with great difficulty. They are at the same time transparent, having various tinges of red- dish-brown or saffron, or they may be of a lighter tint, resembling apricot jelly or barley-sugar. The most common color is that characterized familiarly as "rusty," which aptly expresses their appearance. In rarer cases they may sometimes, in the earlier stages, present a brighter tint, or even a rose color, but this is by no means so strongly marked as in the ear- lier stages of acute bronchitis, though in Pneumonia the sputa of the first few hours are commonly of a brighter red than subsequently, and streaks and specks of blood may appear in them. Dr. Walshe remarks that profuse haemoptysis is com- monly a sign of coexisting tuberculosis. In the cases when I have seen this, the same connection has been distinct. Huss also confirms this observation, but adds that in the Pneumonia complicating heart disease, the sputa may contain an unusual quantity of blood. In other cases the sputa may be more watery, almost diffluent, of a dark purple color, and occasionally offensive. This appearance, familiarly known as "prune- juice," and which probably results, in part at least, from the presence of oedema of the lungs, is commonly considered a sign of gray hepatization; but this con- nection is by no means invariable, for such sputa may coexist with red hepati- zation,2 and may be absent when gray hepatization is found post mortemsputa of this character are, however, to be re- garded as indicative of a grave form of the disease. The sputa which have now been de- scribed may be regarded as almost pathog- nomonic of the pneumonic process in some of its forms, but variations in their char- acters may be sometimes observed, and they are said at times to present a green- ish tint.2 They may also at times exhibit appearances during some days, differing but little from those of bronchitic sputa, and without any blood-tinge which is ap- preciable to the naked eye, but in these cases they are commonly more tenacious and gelatinous than those seen in simple bronchitis.3 In severe cases they may be simply purulent throughout.4 In other instances the viscidity is less apparent, and the prune-juice sputa in particular are often diffluent and watery. The rusty sputa are, however, the most usual form, and they commonly are pre- sent early in the disease, and are among its first symptoms.5 The time of their appearance is, however, often considera- prune-juice sputa preceded all the physical signs of consolidation (Clin. Med. iii. obs. 28, p. 361), and when they coexisted only with red hepatization (lb. obs. 39, p. 392) ; also another case where they appeared on the fourth day, but were replaced on the subse- quent day by ordinary expectoration, the pa- tient proceeding afterwards to recovery (lb. obs. 40, p. 393). Durand-Fardel has also noticed them in the earlier periods of the disease (Mal. des Vieillards, 477). Huss also states that prune-juice sputa are by no means constant accompaniments of gray hepatiza- tion, but that they are common in the Pneu- monia of drunkards, and also in tubercular Pneumonia. 1 See Andral, loe. cit. obs. 24, pp. 350-1. Of two fatal cases of gray hepatization coming under my own observation, this character was not observed in one. In the other the sputa were diffluent, and had the tint of burnt sienna. 2 Grisolle. These have not come under my own observation in the earlier stages. A greenish tint is not uncommon during the period of resolution. When icterus compli- cates Pneumonia, a greenish tint is sometimes observed. (Andral, loc. cit. obs. 55, p. 440.) 3 Sputa of this kind are, however, more common in Pneumonia which is secondary to bronchitis, and particularly in the Pneumo- nia accompanying influenza. 4 Only one such case has come under my own observation. 6 In 191 cases observed by Grisolle, charac- teristic sputa existed on the second day of the disease in 71; they were present in 33 of 53 cases analyzed by myself. Of the cases in which they were absent, 4 were in children, in another the Pneumonia was secondary to albuminuria, and they were absent in one fatal case. 1 In 8-9ths of cases (Grisolle). 2 Cases are recorded by Andral where 166 PNEUMONIA. bly delayed, and they may not be seen until the fifth or sixth day, or even until the twelfth day. In one case coining un- der my own observation, there was not a vestige of expectoration until the tenth day, when the Pneumonia was rapidly approaching resolution, and the amount was then limited to two small rusty masses expectorated on each of two consecutive days.1 When present, they commonly continue through the first five or six days, but they may preserve their rusty tint until the ninth day.2 In some cases, otherwise typical, no expectoration whatever occurs through- out the whole course of the disease. In others the characteristic sputa may be absent during the acute period, and only a moderate amount of bronchitic, or slightly purulent, or pigmented sputa may appear during resolution. In cases of gray hepatization and of abscess of the lung the sputa may be purulent or creamy- looking. When gangrene supervenes they become offensive, and fragments and debris of pulmonary tissue may be found in them. The entire absence of expec- toration is said to be more common in Pneumonia of the apex than in that of the base of the lung.3 Children under six years of age seldom if ever expectorate, but Ziemssen says that he has found the rusty tint in the sputa of infants when vomiting has taken place. They are also often absent or only mucoid in the Pneu- monia of old age,4 and in many cases of secondary intercurrent Pneumonia, and in that complicating delirium tremens. The sputa often cease or fail to be expec- torated when the disease is approaching a fatal termination.5 Both purgation and bleeding diminish or check the expectoration. When Pneumonia complicates other diseases of the lungs, the rusty sputa may be more or less masked by other forms of expectoration present, or they may re- place these. Remak1 first described, as one of the phenomena of Pneumonia, casts of the air-vesicles and of the minuter bronchial tubes, which may be found in the sputa when these are floated in water. He regarded them as pathognomonic of the exudative period, but they are by no means constant.2 Histologically the main elements of pneumonic sputa consist of swollen epi- thelium cells, which have assumed, by imbibition, the spheroidal form ; large mucoid cells, sometimes with double nuclei, and occasionally tinged with im- bibed hsematine; swollen cells of columnar epithelium, occasional granule cells, free oil-globules and blood-disks. Dr. Walshe says that true pus-cells are never found in the rusty sputa of Pneumonia. They may however appear when the disease is approaching resolution, and in this stage large round cells containing granules of black pigment become a very predominant feature, mingled with free nuclei, free pigment-granules, and much granular debris. Chemically the sputa contain mucus and albumen.3 Sugar has been observed in them by Dr. Walshe4 and by Dr. Beale,5 and tyrosine by Griesinger.® They contain, in the earlier stages, a small amount of organic constituents, and an excess of fixed salts7 in proportion to the absence of bronchitis, or to the viscosity of the exudation in the air-vessels. The ab- sence of expectoration in some cases where resolution is very rapid is a remarkable evi- dence of the absorptive power of the lung. 1 Diagnostische und Pathognostische Unter- suchungen, 1845. 2 Biermer says that in 25 cases he failed to find them six times. (Die Lehre von Aus- wurf, p. 52.) 3 Scherer, quoted by Biermer, loc. cit. p. 114. 4 Loc. cit. p. 367. 5 Med.-Chir. Trans, vol. xxxv. 6 Bleuler, Clin. Beobach. fiber Pneumonie, Diss. Inaug. (Zurich, 1865), p. 37. There was no icterus in this case. The patient recovered. 7 Biermer, loc. cit. Beale, loc. cit. In three cases Dr. Beale found the following proportions of fixed salts and of chloride of sodium in the sputa :- In 100 parts of solid matter. 1st case. 2d case. 3d case. Fixed salts . . . 24'78 32'86 20'67 Chloride of sodium 10'12 18'11 12'67 In another fatal case where the sputa con- tained 9'83 per cent, of fixed salts in the solid matter, the blood taken from the heart con- 1 Grisolle questions whether rusty sputa expectorated only during convalescence may not be considered critical. In the case in question they only occurred after the ther- mometric crisis, and their amount is almost invariably too small to permit them to be re- garded as a true critical evacuation. 2 Exceptional cases are recorded where viscous and rusty sputa may continue during longer periods, as in a case by Dr. Stokes, "Diseases of Chest," 361, where a patient with broken ribs continued to expectorate sputa of this character for weeks after the physical signs of Pneumonia had disappeared. Andral also quotes a case where rusty sputa continued to the nineteenth day, lasting nine days after all physical signs had disappeared. (Loc. cit. 526.) 3 Out of 14 cases where the sputa were entirely absent, in 7 the apex was the site. (Grisolle.) 4 Rusty sputa were observed in 17 out of 61 cases of Pneumonia in old people observed by Hourmann and Dechambre, and in 18 out of 50 cases observed by Durand-Fardel. 5 The absence of expectoration may, as suggested by Andral, be sometimes due to ACUTE PRIMARY PNEUMONIA. 167 the serum of the blood, but this excess is reduced during resolution, when the fixed salts are diminished in amount, probably owing to their elimination by the kidneys. Among these salts the chlorides are some- times in excess. In some cases the sputa tend to assume an acid reaction. This was noticed by Dr. Beale, who suggested that it might be due to the pneumic acid discovered by Verdeil, and found by him to be increased in the inflamed lung.1 The true explana- tion would appear to be that afforded by the observations of Bamberger, that they are markedly deficient in alkaline phos- phates when contrasted with the sputa of simple catarrh.2 The expired air, as Nysten and Dr. Walshe have observed, is colder than natural, and the amount of carbonic acid excreted is also diminished.3 The physical signs indicative of the dis- ease commonly make their appearance within twenty-four or forty-eight hours from the symptoms of invasion, but they may be undiscoverable for three or even four days, though probably when their appearance is thus delayed the Pneumonia may be central. In the order of their typical sequence they may be stated to consist of the following signs, corresponding to the anatomical stages of engorgement, hepa- tization, and resolution: among them, however, certain varieties occur :- (1) Altered characters of the respiratory sound, which may be either weaker or harsher than natural, and attended or immediately followed by fine crackling rales. (2) Dulness on percussion, attended by bronchial or tubular or suppressed breath- ing, bronchophony, and increased vocal fremitus, together with diminished respi- ratory movement, chiefly affecting the act of expansion. (3) The return of crepitation, usually in a coarser form;-gradual diminution of percussion dulness, together with the return of the respiratory movements and of the characters of the respiration and of the vocal resonance and fremitus to the healthy standard. (1) The, Congestive Stage.-The indica- tions of this stage are in most cases some- what uncertain. There may, however, occasionally be noticed, even "at an early period, a deficiency of pulmonary tone on percussion, not amounting to absolute dulness, but presenting this character in an increasing degree as hepatization ad- vances. In some cases, however, during the early stages, the percussion note may be distinctly tympanitic. Sometimes, as was first noticed by Dr. Stokes, an in- creased harshness of the respiratory mur- mur may be the first phenomenon ob- served, but this is not constantly present, although it may occasionally be heard at the confines of a part where hepatization is extending. In some cases, however, the respiratory murmur is weakened and loses in clearness and softness, acquiring almost ab initio the character of the "in- determinate" breathing of Skoda.1 The existence of fine crepitation in this stage is less constant; when present its characters may be best described in the terms of Dr. Walshe as occurring "in puffs more or less prolonged, but rapidly evolved, composed of a variable, some- times immense number of sharp crackling sounds, all perfectly similar to each other; conveying the notion of minute size ; dry; coexisting exclusively, except in rare cases, with inspiration; and, once estab- lished, remaining a persistent condition until superseded by other phenomena." The simile introduced by Dr. Williams, between this rale and the sound produced by rubbing the hair between the fingers close to the ear, is so truthful as to have become almost proverbial. For its proper evolution it is often necessary that a full inspiration should be taken. It requires, under these circumstances, to be distin- guished from the rale produced on the first full expansion of a portion of the lung which has been previously in a condition of imperfect action, either from muscu- tained only 2'82 per cent. Healthy pulmo- nary mucus, according to Hasse, may con- tain 18 per cent, of fixed salts, and the mucus of influenza, according to Wright, contains 8'9 per cent. (Quoted by Dr. Beale.) 1 See Gaz. Med. 1851, p. 777; also Robin et Verdeil, Chern. Anat. Phys. ii. 460-1. 2 Wurzburg Med. Zeitsch. ii. Nos. 5 and 6. Bamberger's observations contain the follow- ing interesting facts in relation to the compo- sition of pneumonic sputa:- (a) They contain no alkaline phosphates, while catarrhal sputa contain 10 to 14 per cent, of alkaline earths. (b) In catarrh the soda is to the potash as 31 to 20, while in Pneumonia the soda is to the potash as 15 to 41. (c) Sulphuric acid in catarrh is equal to 3 per cent., in Pneumonia to 8 per cent. (d) At the period of resolution the chemi- cal character of pneumonic sputa approaches the catarrhal type. 3 Walshe, loc. cit. This latter phenome- non is common to many acute diseases. 1 Dr. Walshe, p. 355, states that when congestion is near the surface the respiration is weaker and harsher. When the part af- fected is deeply seated, the intervening healthy pulmonary tissue may give rise to puerile breathing. He has also observed a "fair number of cases in which exaggerated breathing, coupled with febrile excitement and slight pain in the side, were the earliest indications of a central Pneumonia eventually travelling to the surface." 168 PNEUMONIA. lar weakness or from pleurodynia. The latter, however, disappears after one or two deep respirations, while the true crepitant rale is, as above stated, persist- ent. The crepitant rale may often be mingled with sibilant or sonorous rales, or, in other cases, where pre-existing bronchitis passes into Pneumonia, with coarser bubbling rales. The rale is often wanting in children, and both in them and in old people it is commonly coarser and less rapidly evolved than in the Pneumonia of adults. In some cases, however, when the stage of engorgement passes rapidly into that of hepatization, crepitation is not heard, even though the Pneumonia be developed under direct observation.1 Occasionally it may only be heard after bronchial breathing has appeared. The mechanism of the crepitant rale is not yet determined. The two leading theories respecting its mode of production are (1) that it may be produced by air and the viscous exudation matter in the pul- monary vesicles, and (2) that it is due to the expansion of the parietes of the vesi- cles previously agglutinated together.2 In rare cases bronchial breathing may be heard during the congestive stage.3 Vocal fremitus and vocal resonance are increased in proportion to the condensa- tion of the pulmonary tissue, but true bronchophony is not heard. (2) Stage of Hepatization.-The crepi- tant rale last described may disappear at various periods of the second stage, or it may continue throughout its entire course, becoming coarser as resolution advances. The characteristic physical signs of the second stage depend, however, on the filling of the air-vesicles with the pro- ducts of inflammation, by which the part so affected is distended to the degree of medium or full insufflation. In conse- quence of this all further expansion move- ment of the affected part ceases, though thoracic elevation continues, and a cer- tain though not extensive degree of en- largement of the affected side may ensue.1 The distended lung may even encroach on the mediastinum,2 and may occasionally cause a slight displacement of the heart.3 The prominence or obliteration of the in- tercostal depression is, however, not seen to the extent observed in cases of pleu- ritic effusion, although they sink to a less degree than normal during the act of in- spiration. The percussion note over the affected part loses its normal pulmonary reso- nance. In some cases it becomes in the early stages slightly tympanitic in qual- ity, and it may retain this character an- teriorly when the dull note posteriorly indicates complete consolidation of the latter region. Over lung completely con- solidated, the percussion note may be almost toneless, and the sense of resist- ance is greatly increased, though neither of these qualities is so strongly marked as in the presence of extensive pleuritic effusion. Instead of absolute tonelessness the note may, however, be tubular or am- phoric. The tympanitic quality is less common when the consolidation has at- tained its maximum intensity,4 but it sometimes returns during the progress of resolution. In the earlier stages it is often necessary to compare the percussion note on the two sides, in order to detect a slight degree of dulness on that affected. The contrast becomes increasingly marked as consolidation advances. When the Pneumonia affects the base, the upper part of the lung often continues to give excessive or even tympanitic reso- nance ; and a cracked-pot sound may sometimes be elicited here when the chest wall is elastic. The note under the cla- vicle is, however, rarely so markedly am- phoric or tubular as that found in the same situation in cases of pleuritic effu- sion.5 The limits of percussion dulness are sometimes sharply defined, but occa- 1 Walshe, loc. cit. 356. Dr. Walshe states also that "the diagnosis of Pneumonia must be made once in every four or five cases in- dependently of the crepitant rhonchus" (loc. cit. 337). In the writings of Laennec and Andral great stress is laid on the rale. The latter author describes, on the strength of its persistence, a case where the stage of en- gorgement lasted eight days, and ended fa- tally without hepatization. It is probable that this was only a case of capillary bron- chitis. (Clin. Med. iii. 297. obs. viii.) 2 Walshe. Dr. Walshe, however, has ob- served a rale indistinguishable from true pneumonic crepitus in some cases of pulmo- nary oedema. (Loc. cit. p. 123.) 3 Traube (Annalen der Charite, i. 286) says that bronchial breathing may occur during the stage of engorgement when the combined effect of oedema and of swelling of the pulmonary tissue is sufficiently great to expel air from the pulmonary vesicles. 1 This point has been the subject of consid- erable discussion, but the enlargement appears to be settled in the affiimative. Dr. Walshe, however, states that general enlargement of the side is never the resultant of Pneumonia alone. 2 Walshe. 3 Ibid. 4 This is noticed by Skoda, and referred by him to the lung still containing some air-a proposition also maintained by Dr. Hayden (Dublin Journ. 1866, xli.). Dr. Baumler attributes it in some cases to relaxation of pulmonary tissue, in others to a note con- ducted from the larger bronchi. (Deutsch. Arch. Klin. Med. i. 145.) 5 Walshe. ACUTE PRIMARY PNEUMONIA. 169 sionally they are indistinct. In the latter case the percussion note at the margins of the inflamed part may yield a tym- panitic resonance, or may have its natural resonance impaired by a pneumonia ex- tending deeply. Blowing or bronchial respiration pass- ing into tubular and intensely metallic breathing, distinguish this stage.1 These characters usually succeed those of the first period with great rapidity. Grisolle describes, under the title of "bruit de taffetas," from its resemblance to the noise produced by the tearing of linen, an intermediate sound, occasionally heard between the disappearance of the crepi- tation and the supervention of bronchial breathing. The bronchial character is heard first during expiration, but it sub- sequently attends the inspiratory sound also. In some cases, however, when there is no evidence of pleuritic effusion, all res- piratory sound may be completely absent over hepatized lung. The cause of this is uncertain, for post-mortem evidence has shown that it does not necessarily depend on complete exclusion of air from a large tract of lung, since under such circumstances tubular and bronchial breathing may persist, and, on the other hand, respiration may be absent when only a small portion of pulmonary tissue is affected ; nor does it necessarily depend on the obstruction of the bronchi by exu- dation matter.2 In other cases tubular breathing may alternate with absence of respiration.3 The intensity of the bron- chial or tubular breathing appears to de- pend in some measure on the size of the bronchial tubes included within the por- tion of lung affected. The vocal resonance is increased in in- tensity, and is at the same time altered in quality, acquiring the character known as bronchophony. The cough may also acquire a bronchial character. Intense whispering pectoriloquy may be occasion- ally heard.' The heart's sounds are also sometimes heard with undue intensity over the affected lung.2 The vocal fremitus is generally in- creased over the affected side. In com- paratively rare cases, however, this is not observed ; the difference between the two sides may be so slight as to be scarcely perceptible, or the fremitus may even be less on the affected side. In some excep- tional cases, however, vocal fremitus, vocal resonance, and the respiratory mur- mur may all be simultaneously absent,-■ a condition when the diagnosis from a case of pleurisy might present some diffi- culties.3 (See Diagnosis.) In some instances pulsation may be felt over the affected lung. It is a dis- puted point whether this is due to the transmission of the cardiac impulse, or to increased pulsation in the arteries of the inflamed lung.4 The signs now enumerated are most distinct when the inflammatory consoli- dation has reached the surface. When it is seated in the deeper portions of the lung, and the more superficial layers are left unaffected, the physical signs may be comparatively obscure. Laennec thought that crepitation and bronchial breathing could be heard deeply ; and this may sometimes be the case, though instances occur where neither of these signs are distinct. The signs also derived from al- terations in the vocal fremitus, and reso- nance, are usually wanting under these circumstances.5 Where inflammation of the pleura complicates the Pneumonia, friction is commonly heard during its whole course. It may, however, be ab- sent during complete consolidation, owing to entire loss of movement of the hepa- tized lung, and also when effusion is ex- tensive. " When this takes place, the dulness increases in extent, and the re- sistance is greater. Bulging of the affected side becomes more distinct, and displace- ment of the heart occurs if the left side be affected; and sounds of respiration usually become weaker, and the bronchial breathing less distinct; but the intensity of this, and the site in which it is heard, depend on the proportion of fluid present. 1 "The tubular form (of respiration) occurs in perfection in but one condition of lung, that of hepatization; so true is this, that tubular and pneumonic breathing may be used as convertible phrases, but not infre- quently Pneumonia runs its course without having produced true tubular breathing, dif- fused blowing alone being audible." (Walshe, loc. cit. 122.) 2 This view is, however, affirmed by Skoda, who says that the auscultatory phenomena of respiration may be restored after coughing. 3 Dr. Walshe (loc. cit. 360) has traced this in one case to pressure on the main bronchus. Other theories advanced have been that of Grisolle, that it may be due to complete loss of elasticity of the lung; or of Dr. Gairdner, that it is due to collapse from obstruction of the bronchi. 1 Walshe. This, according to my own ob- servation, is not very uncommon. 2 Ibid. 3 Wintrich, Virchow's Handb. vol. v. Abth. i. p. 299. In this case also the bronchi were obstructed by firm exudation matter. The case was mistaken for pleurisy, and paracen- tesis was attempted. There was no fluid in the pleura. 4 The latter opinion is denied by Grisolle, but supported by Graves, Stokes, and Skoda, and admitted as a possibility by Dr. Walshe. 5 This subject will be further alluded to under the head of " Diagnosis." 170 PNEUMONIA. The fremitus is commonly diminished. Bronchophony may also be diminished below the fluid, or may continue at its level, or the vocal resonance may in the latter position assume an aegophonic tone. The period necessary for the evolution of the different physical signs varies. The duration of the initial stage of congestion may, as has been already stated, extend over two or three days, and bronchial breathing and distinct percussion dulness may not appear until the second or even the fourth day, and this appears to be more commonly the case with Pneumonia of the apex. In other cases hepatization may advance so rapidly that a large tract of lung may be consolidated in from twen- ty-four to forty-eight hours, or bronchial breathing may be heard within twelve hours from the period of invasion. The condition of the unaffected lung is usually that of increased functional ac- tivity. In some cases it is hyper-resonant on percussion, and the respiratory mur- mur over it, and over the sound parts of ihe affected side, is of an exaggerated or puerile type. In three cases I have ob- served that bronchial breathing friction, and moist rales were heard over the healthy side where resonance on percus- sion has been perfect, for a distance of more than a hand's breadth extending outwards from the scapula.1 These signs disappeared pari passu with the return of the affected side to a normal condition. The vocal fremitus was not increased over the unaffected side, although a broncho- phonic tone of the voice was conducted for a short distance, but not so far as the bronchial breathing. It seems difficult to explain these phenomena on the theory of consonance, and my own conviction is that they are due to direct conduction. (3) During the stage of resolution the ab- normal physical signs commonly disap- pear in an inverse order to that in which they originated. Improvement is gen- erally first manifested by a reappearance of the crepitant rale. This rale - the rhonchus crepitans redux - is usually coarser and less rapidly evolved than that heard during the progress of hepati- zation ; it tends to pass into a more liquid form-the subcrepitant rale-and occa- sionally it acquires a distinctly fine bub- bling character. In some instances, how- ever, resolution may proceed rapidly without the occurrence of redux crepita- tion. Sibilant and sonorous rales also appear in the affected part, and some- times in other portions of the lung. The dulness on percussion gradually disap- pears ; the tubular breathing diminishes in intensity, it loses its metallic quality, and both it and the bronchial breathing pass into blowing respiration, which finally becomes indeterminate or simply weak. Similar changes occur in the bron- chophonic tojie of the voice, but the vocal fremitus and resonance usually continue intensified as long as the percussion note remains less resonant than natural. The signs which persist the longest are some duhiess on percussion, and the sub- crepitant or fine moist rale, and the latter may often remain during a prolonged pe- riod after the other physical signs have dis- appeared. In some cases, however, when the resolution is very rapid, the redux crepitation may be wanting, and the dul- ness and altered characters of the respi- ration may vanish within twenty-four hours, giving place to a weakened "or in- determinate respiratory sound. Friction also may continue long after the other physical signs have disappeared. Generally, though occasional exceptions are observed, the parts last affected are those in which the signs of resolution first appear. In some instances, however, I have noticed the dulness disappear in irregular patches over the consolidated part. When a whole lung has been con- solidated, the resolution usually com- mences at the apex. If this is not the case the existence of tubercle may be suspected.1 In cases of double Pneumo- nia the lung last affected may first show signs of improvement; but occasionally the resolution of that first attacked may progress, while hepatization is still ad- vancing in the other. (4) The physical signs of gray hepatiza- tion and of diffuse suppuration of the hmg^ present nothing characteristic. Occasion- ally a high metallic bubbling rale, as de- scribed by Stokes, supervenes, while dul- ness on percussion still persists; but I have observed this in a case where, post mortem, the lung was found to be almost entirely in a state of red hepatization. The formation of a circumscribed abscess (a very rare event in Pneumonia not aris- ing from secondary deposits in pyohsemia) is only discoverable by the local signs of the formation of a cavity, together with profuse purulent expectoration, which is often offensive, and in which the elastic tissue of the lung may sometimes be found. Gangrene of the lung - also a rare event in primary Pneumonia - is mainly to be recognized by the signs of a cavity, coupled with the peculiar fetor of the sputa and the expectoration of debris of pulmonary tissue. Circulatory System.-The pulse is almost invariably accelerated, though exceptional 1 Walshe, loc. cit. 372. 2 It may be doubted, whether the latter ought to be described as a separate condition. (See Pathology.) 1 Barthez and Rilliet (i. 460) describe bronchial breathing as being sometimes heard close to the spine on the unaffected side. ACUTE PRIMARY PNEUMONIA. 171 cases occasionally occur, particularly in old people,1 when this is not observed. In adults, in cases of moderate severity it usually ranges from 90 to 1202 pulsations per minute, but it may reach 130 or 140, and in children 160,180, or 200, or it may be so rapid as to be uncountable. The extreme degrees of frequency of the pulse in children are commonly only observed in the earlier periods of life. In some cases the pulse may become notably re- tarded before the fatal issue.3 A pulse above 130, or even 120, is, except in chil- dren, a very unfavorable sign.4 The fre- quency of the pulse commonly, but not always, bears a certain proportion to the acceleration of respiration, and a similar proportion may within certain limits be observed between the frequency of the pulse and the degree of temperature at- tained.5 In characters a pulse of moderate fre- quency is commonly during the earlier periods full, but soft; it may, however, be tense and incompressible.6 These char- acters tend, however, to diminish by the fifth day, when the pulse usually becomes smaller and often acquires a dichrotic character. A rapid pulse is, however, generally both small and weak. A small pulse may at times be associated with signs of distension of the right ventricle, particularly when the Pneumonia is ex- tensive and other signs of defective aera- tion of the blood are distinct, but it may occasionally be observed when these are not marked, and when the distension of the right side of the heart is not demon- strable either by percussion or by in- creased post-sternal or epigastric impulse. It is, however, a priori, extremely prob- able, and it is also confirmed by post-mor- tem observation, that overloading of the right cavities of the heart is the direct result of the obstructed pulmonary circu- lation, and the immediate effect of this will be that a proportionately diminished amount of blood is propelled by the left ventricle into the systemic arteries, though the general injurious effect on the aeration of this fluid is partly compensated for by the increased rapidity of the circulation. The diagnosis may in some cases be aided by the palpation and auscultation of the heart. If the cadiac impulse be strong and the sounds full when the pulse is small, the over-distension of the right ventricle is probably present. In other instances the impulse is weak and the sounds less distinct than natural, and the enfeebled pulse must then be attributed to impaired cardiac power.1 A small pulse may therefore be attrib- uted in many cases to the first-named cause, though enfeebled cardiac innerva- tion has probably in some instances a con- siderable share in its production. A di- chrotous pulse must, however, depend in a greater degree on weakened cardiac power and also on diminished tonicity through impaired innervation of the muscular coat of the arteries. The dichrotous character is often extremely marked about the period of the crisis.2 The heart's action is commonly more accelerated in weakly people, and also by coexisting cardiac disease, so that a rapid pulse in Pneumonia may occasionally draw attention to this previously unsus- pected complication.3 Intermittence of the pulse is sometimes observed in adults ; it is much more com- mon in the Pneumonia of old age, inde- pendently of any discoverable cardiac dis- ease. In children the pulse, when very rapid, is frequently unequal, but not dis- tinctly intermitting. Occasionally, as remarked by Dr. Graves, a murmur may be heard over the heart during the height of the disease, and may disappear during the progress of resolu- tion. I have also observed this in one case; the murmur was systolic, and was limited to the apex. In Dr. Graves's case it was heard over a large extent of the affected side. No satisfactory explana- tion has been offered of this phenomenon. It is difficult to attribute it to polypoid concretions of fibrine, seeing that its dis- 1 Walshe, loc. cit. 2 In a quarter of Grisolle's cases it was, however, below 100. 3 Thus in a case by Grisolle, in an old man, the pulse was only 58 for twenty-four hours before death. 4 Out of 184 cases of recovery, Griesinger observed a pulse of 120 to 150 in fifty-four patients above the age of 15. Twenty-seven patients, having a pulse of this frequency, died. Hence nearly one-third of all the pa- tients above 15 under Griesinger's care with a pulse above 120, died. The dangerous sig- nificance of this symptom rises to an extreme with advancing age. (Bleuler, loc. cit.) 5 Ziemssen, loc. cit. 217. Griesinger, loc. cit. 8 It may seem superfluous to point out the fallacy which may arise from rigidity of the arteries from calcification in advanced life, but this condition requires constantly to be remembered in estimating the "strength" of the pulse in acute disease- 1 See some excellent critical remarks on this subject in M. Jaccoud's Clin. Med. The test proposed by M. Jaccoud of " radial recur- rence, i. e. of the blood finding its way back by the collateral circulation to the radial ar- tery when compressed superiorly, is, I believe, fallacious as an evidence of cardiac power. It may be observed in the weak and dichro- tous pulses of advanced phthisis. 2 For sphygmographic tracings of different varieties of the pulse in Pneumonia, see Ap- pendix A. 3 Traube, Symptom en der Krankheiten der Respirations-Organe, p. 31. 172 PNEUMONIA. appearance was not attended by any of the phenomena of embolism. Evidences of impeded circulation through the lung are also observed in the cyanotic tint of the lips, and less com- monly of the fingers (though this is some- times seen in children), and also in the occasional distension of the jugular veins,1 which may sometimes pulsate ; a similar pulsation has been seen to extend to more distant parts of the venous system.2 Epistaxis is sometimes observed. It may be one of the earliest symptoms, or it may appear among the phenomena of the crisis. I have observed it under both sets of circumstances, but not so fre- quently as has been noticed by some authors. The condition of the blood will be de- scribed under the pathology of the dis- ease. Digestive System.-1This also participates in the general pyrexial state. Thirst is marked, and the appetite is lost. The tongue varies in appearance; sometimes it shows but little alteration, but usually it is coated with a thick creamy fur. In severe cases it tends to become dry and brown, and sordes form on the teeth, and the lips are dry and cracked. Difficulty of deglutition is occasionally observed in old people.3 Vomiting has been already stated to be an occasional symptom of the invasion. I find this recorded in eight out of fifty- three cases, most of whom were adults; it is much more common in children, oc- curring, according to Barthez and Rilliet, in one-half, and according to Ziemssen in three-eighths, of all cases of Pneumonia. It usually ceases after the first or second day, but it may sometimes continue throughout the pyrexial period, and even subsequently.4 I have known a case in which erysipelas followed Pneumonia, and where vomiting continued during three weeks, and placed the patient's life in considerable danger. Diarrhoea is also an occasional symptom of the invasion, though not so frequently so as vomiting, with which, however, it may coexist. It rarely continues un- checked throughout the case, except in very young children ; it sometimes ap- pears at the period of the crisis or during resolution.1 When the gastric symptoms are severe, they have given rise to the description as a special variety of a gastric or bilious form of Pneumonia (in which, however, the complication with icterus is not included). This variety, which was first described by Stoll, has been the subject of much dis- cussion, and it appears to be a very ill- defined one. A certain number of cases, indeed, occur in which the symptoms of gastro-duodenal, or enteric catarrh, are very distinct. I have met with three or four such; but all gradations can be ob- served between these and the more ordi- nary symptoms evincing participation of the digestive tract in the disturbance oc- casioned by acute pyrexia. When the condition is a marked one, the complexion is more opaque and earthy than usual. There is greater prostration, and often the headache is more than com- monly severe. The tongue is much load- ed, nausea is present, or vomiting may persist throughout. The epigastric region is sometimes tender. Constipation is pre- sent in some cases, diarrhoea in others, and the latter often appears towards the crisis. Huss found this form of compli- cation most frequent in the summer months.2 The ordinary state included under this term does not appear to exer- cise much influence on the mortality of the disease, though cases presenting its more decided features are usually pro- tracted in their course. Nervous System.-Headache has been already spoken of as an almost constant symptom. It may be very severe, and in such cases it is greatly aggravated by the cough. It usually, however, tends to di- minish after the first three or four days. Delirium is also common,3 but except in patients of dissipated habits, in whom it may assume the characters of delirium tremens, it is rarely violent. It may, however, occasionally appear in so sud- 1 Grisolle (loc. cit. 257) thinks that this may be occasionally due to pressure by the hepatized lung. It has been observed by him on the affected side in Pneumonia of the apex, and he cites Bouilland as having simi- larly seen distension of these veins limited to the affected side. 2 Stokes (loc. cit. 331), quoting from Graves, says that the pulsation was seen in the back of the hand. Graves (Clin. Med. ii. 41) says head. (Query a misprint.) 8 Wunderlich, Abth. iii. B. ii. 363. 4 Louis (Fifevre Typh. ii. 465) records gas- tric symptoms, pain or vomiting, in 17 out of 24 cases of Pneumonia which died, and in 23 out of 58 which recovered. In many, these symptoms occurred late in the disease, and it may be questioned whether they were not in part due to antimonial treatment. 1 Diarrhoea appears to have been very com- mon in Louis's cases, amounting to one-third. 2 Huss found gastro-intestinal catarrh in 5 per cent., "acute enteritis" in a little more than 1 per cent. 3 Its frequency is variously estimated by different observers. Louis and Andral stated it at nearly 20 per cent.; but others-Grisolle, Briquet, and Huss-have shown that it does not appear in more than from 8 to 12 per cent. It often, however, occurs to a slight degree at night, and hence may fail to be no- ticed. Grisolle says that it is more common in males than in females, in the proportion of 21 to 6. ACUTE PRIMARY PNEUMONIA. 173 den and severe a form as to be mistaken for acute mania (Grisolle),but most com- monly it exists only as a calm wandering, or as an incoherent talkativeness. Huss remarks, contrary to some previous state- ments on this subject, that delirium is not especially common in Pneumonia of the upper lobes, but that it is most liable to occur when a large tract of lung is af- fected- either in the single or double form. Under these circumstances, Huss attributes its appearance to cerebral con- gestion. In the Pneumonia of old people it is particularly common. Huss says that it is most frequent in patients who have been bled. It usually occurs during the height of the disease, and commonly makes its appearance at the time of the evening exacerbation of the pyrexia; it rarely continues more than four or five days. I have known it to make its first appearance in the prostration following the subsidence of the fever.1 In other cases I have observed it to commence im- mediately before the crisis, and to con- tinue subsequently. Both of these events are, however, rare-the period succeeding the crisis being more commonly charac- terized by a subsidence of pre-existing nervous symptoms. Its appearance in a marked form is a sign of danger, and is indicative either of the prostration of the patient or of the severity of the disease. Grisolle says that three-fourths of his patients presenting this symptom died; but the treatment by bleeding to which they were subjected must be taken into account in estimating this degree of mortality which certainly is not corroborated by my own expe- rience, and though the symptom tends to occur in a large proportion of fatal cases, others may preserve a perfect intelligence to the last moments of life. The delirium, in fatal cases, tends to pass into an im- perfect coma. A comatose condition in- dependently of delirium is sometimes ob- served ; it is most common in old people and in children,2 and in the former there may be a complete prostration of the men- tal faculties, extending even to a failure in the pronunciation of words.3 In drunkards Pneumonia is so con- stantly associated with nervous disturb- ance as to have led Huss to describe a special form, the Pneumonia Potatorum. The delirium may assume the form of active delirium tremens, with sleepless- ness, delusions, and noisy talkativeness, associated with tremors of the limbs and uncertainty of pronunciation-symptoms which may sometimes appear with the first invasion of the disease ; or in weak- ened patients, the subjects of chronic alco- holism, the state may be one of profound prostration and stupor, alternating with a low muttering delirium. In both these forms the general signs of Pneumonia may be indistinct or may be masked by the nervous symptoms, though in the first class the invasion may be sudden and acute, and attended with rigors. Pyrexia is, however, present in both varieties, and is a valuable clue to the mischief in the lungs. Tremors are not uncommon in weak- ened patients independently of delirium. Convulsions are rare and quite excep- tional in the adult. They are, however, very common in children,1 particularly under five years of age, in whom they often attend the invasion of the disease, and they are specially prone to occur if dentition is advancing or difficult. In other cases they occur towards the fatal termination. They are sometimes gen- eral and epileptiform; sometimes they appear only in the form of spasm or rigid- ity of one limb, or of some of the mus- cles of the face or the eyeballs ; occasion- ally also a stiffening of the muscles of the neck, passing into opisthotonos and a tetanic state, has been observed.2 I have known a state of partial paralysis to re- main subsequently in the limbs affected.3 When the convulsions are general, and occur in the earlier stages of the disease, they are seldom repeated; but if this is the case, they generally end in a fatal coma. Partial convulsive movements may, however, recur more frequently. In other cases in children the cerebral disturbance may resemble those seen in the earlier stages of tubercular meningitis, being marked by prostration, headache, delirium, and strabismus - symptoms whose deceptive character is further in- creased by attendant constipation. Bar- thez and Rilliet state that these symptoms 1 The observations of Heintze (Arch, der Heilk. 1868) appear to show that the occur- rence of delirium in Pneumonia is not spe- cially connected with excessive elevation of temperature. In the cases observed by him it was much more frequent in cases of Pneu- monia of the upper lobe than in that of the lower, in the proportion of 40'17 per cent, of the former to 25-5 of the latter. As regards season, it was more common in the cooler than in the hotter months of the year. 2 Grisolle relates a case of a young adult who remained perfectly insensible without movement for twenty-six hours, but finally recovered. 3 Hourmann and Dechambre, loc. cit. 1 Barthez and Rilliet give to the affection of the nervous system in children the title of " Pneumonie C6r6brale," which they subdi- vide into "Pneumonie Eclamptique" and " Pneumonie MeningSe." 2 Weber, Path. Anat, des Neugeboreneu und Sauglinge, ii. 61. These symptoms were attended by inflammatory changes in the cerebro-spinal arachnoid sac. 3 This, according to Barthez and Rilliet, is very rare. 174 PNEUMONIA. are, however, rarely accompanied by the automatic cries, by the sighing respira- tion, the grinding of the teeth, or by the expression of indifference, and by the rapid changes of color which characterize tubercular meningitis. Ziemssen, how- ever, remarks that all these may be ex- ceptionally observed, and that the coma may be so deep as almost to simulate death.1 The collective appearance of this group of symptoms is fortunately of ex- treme rarity in the Pneumonia of chil- dren. Disturbances of vision occurring sud- denly, with undue sensitiveness to light, a false coloring of surrounding objects, and associated with a dilated condition of the pupils, have been occasionally ob- served. In these cases ophthalmoscopic examination has revealed undue disten- sion of the veins of the retina ; these symptoms disappeared soon after the reso- lution of the Pneumonia.2 Deafness was observed in one case by the late Dr. Hil- lier,3 and this symptom may at times add to the difficulty of diagnosis from typhoid fever. It does not, however, appear to be a common complication.4 The urine is diminished in quantity and increased in specific gravity during the acute period of the disease. The de- crease in water may reduce the amount passed to little more than one-half the normal quantity. At the same time the excretion of urea is vastly augmented, amounting sometimes to 85'5 grammes or 1326 grains in twenty-four hours,5 though usually the amount varies between 35 and 55 grammes (761 and 858 grains).6 This large amount of excretion necessarily rep- resents destruction of tissue, for it is found at a period when very little food is taken. It usually reaches its height dur- ing the pyrexial period, increasing daily in amount until shortly before the crisis, though differences are observed in the period at which the maximum is attained. After the crisis, in spite of an increase of food, the amount may fall within one or two days, to or below the normal standard. In other cases an excess may be passed for some days during the period of resolu- tion,1 and the normal amount may only be attained on the fourteenth day. The uric acid is also increased, and probably to a greater proportionate degree than the urea, and generally during the pyrexial period. It may reach at the crisis the amount of 37'7 grains,2 or even the enormous amount of 103 grains3 ex- creted in twenty-four hours. Like the urea, an excess may continue to be passed for some days after the pyrexia has dis- appeared.4 Large deposits of urates tend to occur during the whole period of the disease. The sulphuric acid also appears to be slightly increased ; the phosphoric acid is lessened, and the free acidity is said to be diminished.5 The chloride of sodium is markedly diminished, and sometimes its excretion is entirely suppressed during the height of the disease, even when hydrochloric acid or chloride of sodium is taken internally.6 The hydrochlorate of ammonia continues in some cases to be excreted. The chloride of sodium reappears during resolution, and may for some days after be passed in excessive amounts, showing that it has been retained in the system ; and the ex- cess of chlorides may persist in the urine after that of the urea has ceased.7 1 Dr. Parkes (loc. cit.) says that he has found 50 or 60 grammes per diem during the period of resolution. 2 On the tenth day. Zimmermann, Prager Vierteljahresch. 1852, vol. xxxvi. p. 118. The average normal amount appears to be from 6 to 9 grains daily. 3 Huss, loc. cit. p. 47. This amount must be regarded as very exceptional, as would appear from other analyses given by the same author. 4 Dr. Parkes considers that this may proba- bly be due to some of the uric acid being re- tained in the system, owing to its being less easily got rid of than "the diffusible urea." Zimmermann (loc. cit.) for the case quoted above gives the following averages :- Grain? per diem. Stadium Increment! . ... 15 Crisis 37'7 Stadium Decrementi (21 days- average) .13'5 First 7 days of Stadium Decrementi 21'26 Second 7 days " 11'9 Third 7 days " 8'29 5 For these statements the author is in- debted to Dr. Parkes's work. Huss, how- ever, says that both these acids are dimin- ished, at least in the form of their salts. 6 For the chief investigations on this point see Redtenbacher, Zeitsch. der K. K. Gesellch. der Aerzte zu Wien, 1850, by whom the dis- covery of this peculiarity was first announced; and Dr. Lionel Beale (Med.-Chir. Trans, xxxv.), by whom this subject was further investigated; also Dr. Parkes, loc. cit. 7 For remarks on the relative excretion of 1 In a case where this was observed by Ziemssen, the coma ceased with the crisis on the fifth day. 2 Sichel, Gaz. des Hopitanx, June, 1861. Seidel, Deutsche Klinik, 1862, p. 269. 3 Dis. of Children, pp. 40-42. 4 Griesinger (Bleuler, loc. cit.) met with it five times in 228 cases. 5 Parkes on Urine, 271. There will be found here a complete list of authors who have investigated this subject. 6 The estimates of the normal amount of urea vary considerably. The normal daily average for an adult man under ordinary conditions of life may probably be regarded as 500 grains. ACUTE PRIMARY PNEUMONIA. 175 Bigler has found that iodide of potassium, when given internally, is also retained in the system during the height of the dis- ease, but that during resolution it is ex- creted by the urine.1 In some very exceptional cases the urea and uric acid appear to be retained in the system during the febrile period, even when there is no albuminuria, and are ex- creted in large quantities during conva- lescence, forming a sort of pseudo-critical discharge.2 Dr. Parkes states that these patients are more liable to diarrhoea during convalescence, and that possibly some elimination of the retained matters may then take place by means of the in- testinal mucous membrane. Patients pre- senting these phenomena of retention are also liable to a more protracted conva- lescence than those whose urinary excre- tion is large throughout the disease. During convalescence the amount of wrater passed is increased, but that of the urea tends to fall below the normal amount, while the chlorides, as before stated, are commonly increased in quantity. Albuminuria, usually slight in amount, is a more frequent complication of Pneu- monia than of almost any acute disease, except typhus.3 It is found commonly during the height of the disease, more rarely during convalescence, but it may appear for the first time as late as the twenty-third day. In most cases it must be regarded as one of the general phe- nomena of the disease, due probably to the kidneys being affected by the same cause which sets up the inflammation in the lungs. Its presence is also indicative to a certain degree of the intensity of the cause, for cases in which it occurs are generally more severe in their character and more fatal in then' issue than those in which it is not found.4 It is very common also in the Pneumonia which appears as part of the general phenomena of some morbid blood poison, as in diphtheria and other conditions, to which further allusion will be made (see Pathology). It is very commonly attended with epithelial casts, and sometimes with blood in the urine. Bile pigment is not infrequent. The biliary acids are less common. Pibrine and cystine have also been found. The vesical mucus is increased, and the urine tends to decompose early (Dr. Parkes). I have observed retention of urine in one case associated with severe cerebral symp- toms. The skin is pungently hot, but many variations are observed with respect to perspiration. It may appear shortly after the rigor, and subsequently give place to a dry pungent heat, or the skin may be dry until the crisis is attained, or perspira- tions may continue throughout the entire course of the pyrexial period. Andral thought that sweating was a favorable sign, but I have observed it more than once in fatal cases, and even in those where the temperature has not been markedly elevated. Profuse sweating usually attends and follows the crisis. Louis remarked that sudamina were rare in Pneumonia.1 They have been abundant in three of the cases which I have observed ; a few also may often be seen when sweating is copious. Herpes is a very common complication.2 It most usually appears on the face, and particularly about the lips and angles of the mouth, but it may occur occasionally in other situations.3 I have seen a tonsil- litis having the characteristic appear- ances of the herpetic form appear on the fifth day of a Pneumonia. It seldom ap- pears before the third or fourth day, but I have known an eruption which from the description I concluded to be herpes pre- cede the Pneumonia by a period of some weeks, the patient remaining out of health in the interval. It may also appear dur- ing the crisis, and, in rare instances, during convalescence.4 The face, as has been stated, is flushed, the chlorides in the urine and sputa, see Ap- pendix B. 1 Beitrage zur Statistik der Pneumonie; Wien Med. Woch. 1858, No. 48 (Canstatt's Jahresb. 1858). 2 Parkes, loc. cit. 3 Parkes, loc. cit. Dr. Parkes quotes the following statistics. He found it in 6 of 13 cases, or in 46'1 per cent.; Finger in 15 of 33, or in 45'4 per cent.; Becquerel in 9 of 21, or in 42.'8 per cent.,-collectively represent- ing 30 cases of albuminuria out of 67 cases of Pneumonia, or a ratio of nearly 45 per cent. Metzger, however, did not find it once in 48 cases. In 32 cases which I have analyzed, it was found 10 times, or in rather more than 31 per cent.; Martin Solon and Ziemssen each found albumen only twice in 24 cases. 4 In seven non-albuminous cases, Dr. Parkes met with only one death ; while in five where albumen was present during the height of the disease, three died. Of the ten cases in which I find albuminuria to have been pres- ent, five died, but in one of these the disease of the kidneys was probably of old standing. Griesinger (Bleuler) found albumen in the urine in 63 out of 121 cases. Of these, 42 re- covered and 21 died. In 22 cases where the amount of albumen was considerable, 8 died. 1 Fifevre Typh. ii. 111. 2 Ziemssen observed it in half of the cases of children under his care. Geisler ("Ueber die prognostiche Bedeutung des Herpes bei der Pneumonie," Arch, der Heilk. 1861, ii.) found it in 43'2 per cent, of 421 cases in Wunderlich's wards. In cases under my own care it has been less frequent than this. 3 Thomas has observed it around the anus. (Arch, der Heilk. viii. 478.) 4 Six days after the resolution of the fever. (Thomas, ib.) 176 PNEUMONIA. particularly over the malar bones.1 The flush may be bright in tint, or it may tend to a cyanotic or violet tinge, particularly in children. With the flush there is, however, usually an opacity or earthy tint of the skin around the eyes and lips. In rare cases the whole surface of the body may be of a bright-red tint, so as even to give rise to the suspicion of the presence of one of the eruptive fevers.2 The flush tends to disappear with the progress of the disease ; occasionally, and particularly in children, and sometimes in old people, there may be an earthy pallor throughout, which may be attended with a bluish tinge of the eyelids. Pallor of the face is most commonly observed dur- ing the crisis. The temperature3 of the body in Pneu- monia has only been made the subject of accurate thermometric observations with- in the past twenty years, though many of the more important facts bearing on this subject had been previously stated by earlier observers.4 It is, however, to Von Baerensprung,5 Traube,6 Zimmer- mann,7 Wunderlich,8 Thomas,9 and Ziems- sen1 that we owe the revival of observa- tion and most of our accurate knowledge on this subject.2 One of the most marked features of Pneumonia,3 which is almost sufficient to distinguish it from other diseases, is the sudden and considerable rise of tempera- ture which marks its invasion, and which, with some exceptions, is then maintained, with slight morning remissions and even- ing exacerbations, throughout its course until a crisis occurs. The rise of tempe- rature during the rigor is common to most diseases in which this phenomenon occurs,4 but its subsequent maintenance at a very high standard during the suc- ceeding first hours and days of the disease is limited to a small class of inflammatory affection. An instance of this has been already given. I have known a case in which the temperature had reached 105° within a few hours of the first feeling of illness, although the usual rigor was absent; and others may be quoted from different ob- servers who have had an opportunity of witnessing the earliest phenomena of inva- sion. Thus Zimmermann5 relates a case where, after prodromata of a week's dura- tion, the temperature within three hours after the initial rigor reached 102° and within twelve hours it attained the height of 104°. Thomas6 observed a tempera- ture of 105° within nine hours of the inva- sion ; Ziemssen, within four hours after the initial vomiting in a child, found a temperature of 102'5°; within twelve 1 Unilateral Hushing of the cheek on the affected side, and attended with a higher temperature than on the opposite side, was described by Gubler (Union Med. 1857) as very common in Pneumonia and also in other pulmonary affections, and was attributed by him to the implication of the pulmonary branches of the sympathetic plexus. Other observers, as Barthez and Rilliet, have con- troverted this opinion, and have shown that the cheek on the side opposite to the affected lung may show an excess of hyperaemia. Jaccoud (loc. cit. p. 28) observed in an attack of Pneumonia in his own person, that a local flush, attended by a disagreeable sensation of heat in the cheek on the side opposite to the affected lung, preceded the Pneumonia for twenty-four hours, during which time, with this exception, he felt in perfect health. The Pneumonia then commenced suddenly with rigors. He states that he has met with five similar instances. 2 Barthez and Rilliet (loc. cit. i. 522). 3 In all ensuing statements on this subject, the temperatures quoted will be those of Fahrenheit's scale. Quotations from other ob- servers have been reduced to this standard. 4 Thus Donne (Arch. G6n. de Med. 1837) observed a temperature of 1030, and Roger, in a more extended series of researches (Arch. Gen. de M6d., Ser. iv. vol. vi.) stated that Pneumonia had a higher temperature than almost any other disease, and that in the majority of cases this exceeded 1040 Fahr. 6 Muller's Archiv, 1851-2. 6 Annalen der Charity, i.; Ueber krisen und kritischen Tagen. i Various writings in "Med. Zeit. des Vereins fur Heilkunde im Preussen," spe- cially in "Prager Vierteljahresch." 1852. 8 Various papers in "Archiv fur physiol. Heilkunde;" "Das Verhaltniss der Eigen- wiirme im Krankheiten." 9 Archiv fur Heilkunde, 1864-5. 1 Pleuritis mid Pneumonic im Kindesalter. 2 Among English authors the most valuable observations are those by Dr. Parkes, Med. Times, 1866; by the late Dr. Waters, St. Barth. Hosp. Rep. vol. ii.; Dr. Compton, Dublin Quarterly Journal, xlii.; Dr. Grim- shaw, ib. 1866; and Dr. Maclagan, Edinb. Med. Journal, 1869. 3 Grisolle (loc. cit. 163) says that in some cases the course of Pneumonia is apyrexial throughout, though the physical signs and rusty sputa are present. Grisolle's statement is made apparently irrespectively of thermo- metric observations. Wunderlich, however, repeats the statement (Eigenwarme im Krank- heiten, p. 337). Such cases must, however, be excessively rare, and require data as to the day of the disease upon which they came under observation. The majority of cases in hospital practice are rarely admitted before the third day, and it must be remembered that even at this early period the temperature may in some cases fall from a pyrexial height to the normal standard. I have never seen a case of Pneumonia unattended by pyrexia tree from this suspicion. 4 This was observed by De Haen, in Inter- mittent Fevers, Rat. Medendi, Ed. 1761, i. 117. 5 Prager Vierteljahresch. 1852, xxxvi. p. 97. 6 Archiv fur Heilk. 1864. ACUTE PRIMARY PNEUMONIA. 177 hours this had reached 104-6°, and within twenty-four hours the temperature was maintained at 103'5°. The highest temperatures are most commonly observed on the second or third day of the disease, but exceptions to this rule are not infrequent. In some in- stances the maximum temperature, pre- ceded by a very sudden rise of from one to two degrees Fahr, above the previous average, may occur immediately before the crisis. The highest recorded tempe- ratures in cases ending favorably are 106'7° in the rectum1 (Ziemssen), and 107° (Kocher), but they rarely exceed 105° or 106°. In fatal cases, however, there may be a considerable rise before death, as to 106'9°, 108'9° (seventh day), or even to 109'4° (fourteenth day-Thomas2); a slight post-mortem rise is also occasion- ally observed. In the fatal cases which have come under my own observation this ante-mortem rise has not been noticed, but in most of these the temperature had been only moderate throughout. The higher temperatures, according to my own experience, are however, rather the ex- ceptions than the rule.3 In the majority of cases it has seldom exceeded 104°, and a large number run their course without the temperature of 103° being attained. As a general rule the milder cases are those in which the pyrexia is least, but cases may end fatally in which the tem- perature has barely exceeded 102°. In old people especially, in whom Pneumonia is comparatively the most fatal, the tem- perature is very commonly lower than in adults. After the invasion the pyrexia generally runs a certain definite course, with a series of regular daily exacerbations and remis- sion, which commonly occur respectively in the evenings and mornings, represent- ing in this respect, though with some irregularity, an exaggeration of the nor- mal diurnal variations,4 and which ac- cording to their relative extent have given rise to various classifications.1 Usually the daily course is that the morning tem- perature from 6 to 9 A. M. is the lowest, but it seldom falls more than 1° or 1'8° Fahr, below that observed in the evening, and the temperature at these periods of remission never, or only in the most ex- ceptional cases, reaches the normal stand- ard. In the forenoon or early in the afternoon the fever again increases, com- monly reaching its maximum intensity early in the evening, or sometimes even at mid-day.2 From this point the tem- perature falls towards midnight, when a second slight exacerbation occasionally occurs, which does not however reach the same height as that of the afternoon.3 Subsequently to this the temperature con- tinues to sink during the night until an early hour the following morning, from which a gradual rise takes place, culmi- nating in the exacerbation of the succeed- ing afternoon. In very rare cases the rise of temperature takes place early in the morning, when the highest temperature is observed, under which circumstances the corresponding remission is noticed at mid-day, or a continuous fall takes place until the evening. During the course of the acute disease the morning remissions and evening ex- acerbations maintain in typical cases a very uniform standard of temperature until the period of the crisis is attained, unless fresh extensions of the pneumonic process occur, when a sudden increase of the temperature may be usually observed. In the earlier periods of the disease or during the stadium incrementi a more 1 Those proposed by Thomas and Wunder- lich are as follows :- (a) A subcontinuous course, with daily variations of from f° to -|O Fahr. (6) Subremittent, with daily variations of to 1'5° Fahr. (c) Remittent, with variations from 1'5° to 2'50 Fahr. (d) Intermittent, a very rare form, with complete apyrexial periods in the daily course. There is a form of Pneumonia described as accompanying intermittent fever where there also appear to be complete apyrexial periods corresponding to the type of the fever. 2 This occasional irregularity renders a mid-day observation on the temperature ne- cessary in all cases when scientific accuracy is required. In fact, unless frequent obser- vations are made, the period of the maximum elevation of temperature may escape observa- tion. 3 This second exacerbation may sometimes be anticipated; that is, when the afternoon exacerbation occurs early, a rapid fall may take place until early in the evening, and the second rise may take place early in the evening instead of at midnight. 1 This was observed on the sixth day in a child who at the time was sweating profusely. 2 This terminal elevation of temperature is sometimes preceded by a marked remission. It is sometimes gradual, extending over a pe- riod of from twelve to twenty-four hours, but it may take place very rapidly, i e., within six hours. The temperature has been known to rise on the supervention of severe brain symptoms from 101'70 to 108'7°, or 7 degrees Fahr. 3 Out of twenty-seven cases whose tempera- ture has been carefully taken throughout, in one only was a temperature of 105'8° attained on the sixth day, the crisis occurring on the eighth day. Griesinger (Arch, der Heilkunde, i.), out of seventy-two cases, only observed the temperature higher than 103° Fahr, in nineteen. 4 See Von Baerensprung, Muller's Archiv, 185], pp. 160 et seq.; Ib. 1852, p. 251. VOL. II.-12 178 PNEUMONIA. marked remission may occasionally occur, and may even be repeated more than once. This is followed in some cases by an intenser exacerbation, but in others the temperature of the succeeding rise falls below the average standard of the case. When an exacerbation of the fever follows this remission, it is also frequently attended by an extension of the pneumo- nic process or by a secondary inflamma- tion of some other organ.1 The pyrexia tends to subside abruptly by crisis or gradually by lysis, the resolu- tion by crisis being however the most usual form, and the rapidity with which this takes place in typical cases is again almost peculiar to this disease. Ther- mometric phenomena of the crisis may commence either at the period of the morning remission or of the post-meridial exacerbation. If at the former, the tem- perature, which on the preceding evening may have maintained its previous height, is found on the following morning to have fallen to the normal or nearly to the nor- mal standard, and the succeeding exacer- bation on the following evening is less by 1 or 2 degrees Fahr, than those previously observed. From this period a gradual fall of temperature ensues, and within forty-eight hours from the commencement of the crisis it has usually reached the limit of health, or it may have fallen be- low it, and after this no further elevation ensues.2 The extent of the fall of tem- perature is sometimes very remarkable when the fever has been severe, amount- ing even to 9'7° Fahr, in sixty hours.3 This is sometimes intensified by the fact that when the fever has been high and the patient is weak, and in children par- ticularly, the temperature may sink dur- ing the critical defervescence to 1°, 2°, or 2'5° below the normal, and may continue at this low point for forty-eight or seventy- two hours. I have observed in a child a temperature of 96'5° (axilla) with a cold skin and profuse perspiration maintained in spite of artificial warmth for forty- eight hours. Such cases in children, how- ever, do not commonly end unfavorably. Variations in the phenomena of the crisis are, however, not uncommon. Some- times immediately before it occurs the temperature may rise to a higher point than those previously observed. In other cases, for twenty-four or forty-eight hours previously, both the morning and the evening temperature may show a lower range before the final rapid decline takes place. In some, again, the crisis is marked rather by successive falls of tem- perature during the periods of remission, those of exacerbation maintaining during twenty-four or forty-eight hours the same height as before, but finally participating in the decline-a course which may be regarded as presenting simply a modifica- tion of the ordinary rhythmical progress of the disease. Sometimes, after the crisis has distinctly appeared, the fall of the temperature is suddenly checked, and a temporary ex- acerbation may occur, attended by a ces- sation of the critical perspiration and by a return of the restlessness and of the other febrile symptoms. For some days after the disappearance of the fever there is also a tendency to tem- porary trivial exacerbations from slight causes, such as a meal or a slight exer- tion ; but these, within certain limits, do not interrupt the progress of convales- cence.' The course of the fever is, however, subject to other variations, which are due commonly to the progressive invasions of other portions of the lung or of the oppo- site lung, and the crisis may be disturbed by a relapse. The former may occur while the fever is still present. They are often marked by an increased intensity of the succeed- ing exacerbations, which may give the pyrexia a remittent type. Relapses most commonly occur within the first three or four days succeeding to the crisis.2 I have, however, known a relapse take place as late as the sixteenth day, when the temperature had been natural since the eighth day.3 They are marked by a sudden rise of temperature from the normal oi' subnormal standard previously attained. The duration of the pyrexia in these relapses is, however, commonly shorter than that of the pri- mary attack, usually terminating within three or four days ; but cases are recorded where even a third relapse has ensued.4 1 Monthus (loc. cit.) remarks that the apy- rexial period following an attack of double Pneumonia is marked by a rather higher temperature, and more readily shows slight subsequent exacerbations than when the Pneumonia has been unilateral. 2 Monthus, loc. cit. 206. 3 The duration of the pyrexia in the second attack was only two days. 4 See a case by Ziemssen, p. 186, of Pneu- monia of the upper lobe. The maximum temperature of the original attack was 102° Fahr. On the ninth day the temperature fell to normal. On the tenth day there was a return of the fever with invasion of the 1 Kocher, Behandlung der croupiisen Pneu- monie mit Veratrum Preparaten ; Wurzburg, 1866. 2 Griesinger (Bleuler, loc. cit.) found this rapid fall of temperature in 112 out of 146 cases. The normal temperature was reached within twelve hours in 37 cases; within twenty-four hours in 32 cases ; within thirty- six hours in 43 cases. In 41 cases the fall of temperature was more gradual. 3 Ziemssen, loc. cit. 211. ACUTE PRIMARY PNEUMONIA. 179 It is therefore very important to maintain thermometric observations for some days after the normal temperature has been attained-the more so as relapses with in- vasion of other portions of the lung are seldom attended with a return of the initial rigors, and the increased tempera- ture may give the first indication of the extension of the disease. In other cases the temperature falls by a gradual lysis, which, in some cases that I have observed, has only reached the normal standard on the twelfth or four- teenth day. In a third series, again, the crisis is in- complete, and the course of the pyrexia is protracted. There is very often noticed on one of the days intervening from the seventh to the tenth inclusive, a marked fall both of the morning and evening tempera- ture ; but this does not reach the normal, and on the succeeding days pyrexia per- sists, though not usually at its previously high standard. A slow defervescence then ensues which may be protracted over two or three weeks, and is attended with a somewhat irregular course of the tempera- ture-that in the morning being often nearly normal, while in the evening it may be on some days 100° and on others 102° Fahr., occasionally rising to 103° or 104°, and on the succeeding evening it may again only be 100°. These cases are generally attended with a protracted dis- appearance of the physical signs-the consolidation and bronchial breathing with fine rales lasting, together with the pyrexial state, for three weeks or a month, but gradually disappearing and ending in perfect recovery.1 The circumstances determining a more protracted course of the pyrexia are not always clearly discoverable. Cases where bronchitis passes into Pneumonia, and which belong rather to the clinical cate- gory of broncho-pneumonias, often evince this tendency ; but I do not think that this peculiarity is sufficient under all cir- cumstances to remove a case in which it is observed from the category of the pri- mary form, as it is occasionally seen when the mode of invasion and the earlier course are typical of this condition ; and it must, therefore, I think, be regarded as a somewhat exceptional variation. The eases in which I have observed this course are most commonly those which are accompanied by an extreme degree of gastric catarrh, or when the Pneumonia attacks persons of weakly constitutions, or those of previously dissipated habits. In some cases also where bleeding has been practised the recovery has been slow.2 A very widespread opinion now exists that venesection tends to retard convalescence. The presence of tubercle or the tubercular diathesis appears also to protract the course of acute Pneumonia. Such patients may in many instances recover entirely from the inflammatory consolidation, but in others the resolution is imperfect, and the disease, although in rare instances, 1 In one case under my own observation, a boy aged 15, previously in good health, got chilled. Pneumonia supervened with rigor on the following morning; admission on the third day of disease with well-developed Pneumonia of the lower two-thirds of the right lung, and severe gastric catarrh. Tem- perature on fourth day, 105°; on the eighth day it fell to 990; on the ninth and tenth days it was 990 and 98'40; On the eleventh day it rose to 100° without any discoverable increase of the Pneumonia. It then fluctuated between 100° and 102°, reaching to 103° on the fourteenth day, and only fell gradually to the normal on the thirty fifth day. The physical signs only completely disappeared by the sixtieth day. 2 This was the case in that by Zimmermann before quoted. The case was peculiar in its course. The temperature on the first day was 1040 in spite of VS to 2 lbs. and repeated on the second day to 14 oz. Up to the third day there were only the physical signs of congestion, but the respiration was slightly bronchial in one place. On the third day there was a distinct remission in the morning (99'80), but followed by an evening exacer- bation to 105'80. On the fourth day, rusty sputa, dulness, and bronchial breathing ap- peared in the lung. A second imperfect crisis occurred on the ninth day, with a subsequent elevation of temperature on the tenth, reach- ing 1030 on the seventeenth day, and with irregular intermissions maintaining a tem- perature of 100O to the twenty-fifth day. middle lobe, and with a temperature of 104'90. On the fourteenth day a second remission of the pyrexia took place, followed on the fif- teenth by a return of the fever (temperature 102'7), and with invasion of the lower lobe. The final crisis and permanent recovery oc- curred on the eighteenth day. In another case by the same author, with Pneumonia of the left lower lobe, the crisis occurred on the fifth day. On the sixth there was a severe return of the fever, followed on the eighth day by the physical signs of consolidation of the right upper lobe, while the resolution of the lung first affected continued unimpeded. The final fall of temperature began on the eleventh day and continued through the twelfth, when convalescence was re-established. Grisolle says that relapses occurred with him in the proportion of once in 28 cases. Briquet met with 16 instances in 92 cases. Grisolle quotes a case in which three consecutive relapses took place, the last being on the twenty- seventh day. Commonly the course of the relapse is shorter than that of the first attack, rarely lasting more than three or four days. In the case, however, quoted, each attack lasted nine days, and the last was very se- vere. (There is some confusion in Grisolle's statement with respect to the duration of the relapses.) 180 PNEUMONIA. passes into the condition of a chronic tubercular Pneumonia.1 Pneumonia of the apex is said by Ziemssen and Bleuler to tend to maintain a high temperature during a longer pe- riod than that of the base,2 and that in non-tubercular patients, though the pro- tracted course may give rise to the sus- picion of this complication. This, how- ever, is not invariably the case, for I have known the crisis to occur in a well-marked case of Pneumonia of the apex as early as the fourth day. Ziemssen thinks that such cases may be distinguished from tu- bercular Pneumonia by the constantly maintained high temperature; but my own experience would show that this sign cannot be relied on, since I have observed that the elevation of temperature in cases of protracted simple Pneumonia is not always continuous, while it may be so in some cases of tuberculosis and of tubercu- lar Pneumonia. The coexistence of pleuritic effusion certainly tends in some cases to render the thermometrical crisis incomplete and to protract the period of defervescence. It also, as might be expected, delays the disappearance of the physical signs ; the complication with pericarditis has a simi- lar influence in the crisis. Ziemssen re- marks that neither pleurisy nor pericar- ditis, when occurring in the course of Pneumonia, has any necessary tendency to raise the temperature above the stand- ard of the individual case. The period of the crisis has been a sub- ject of considerable discussion and of careful thermometric observation. The recognition of this tendency has been common to many observers, and it was pointed out by Laennec. Andral3 thought that the seventh, fourteenth, or twenty- first days were the most common periods of its occurrence-supporting the doctrine of special critical days advanced by Hip- pocrates. Grisolle disputed this opinion. Traube (Ueber krisen und kritischen Ta- gen) has again revived it, and has asserted that in acute diseases, and especially in Pneumonia, the crisis usually occurs on the third, fifth, seventh, ninth, or eleventh days, and that therefore it has a prepon- derating tendency to appear on uneven days. This, however, has been denied by different observers, whose observations show that the crisis is by no means so constant on the uneven days as Traube believed, but that in a large proportion of cases, amounting respectively to 20 and 25 per cent, and collectively to 46 per cent, of the whole number, it tends to oc- cur on the fifth and seventh days.1 The cases of which I possess sufficiently accurate thermometric observations give very similar results, though in smaller numbers. Out of twenty-seven cases end- ing favorably, a distinct thermometric crisis occurred in eighteen, and two more were admitted on the fifth and eighth days respectively with the physical signs of Pneumonia, but with a normal tem- perature, which was maintained subse- quently. These, therefore, may justly, I think, be added to the above, making the proportion of cases terminating by crisis, as compared with those not thus ending, as twenty to twenty-seven. The following were the days2 in which a crisis was observed :-On the fourth day, one case; on the sixth, one ; on the seventh, six ; on the eighth, two ; on the ninth, four; on the tenth, two; and on the eleventh day, two cases. The period of complete defervescence varied from twelve hours (four cases) to seventy-two hours (one case). In the remainder it 1 The days of crisis observed by Wunder- lich (Spec. Path. Therap. Abth. iii. B. ii. p. 334), Ziemssen (loc. cit. 174), Thomas (Arch, der Heilk.), and Bleuler (loc. cit.) may be best expressed in a tabular form:- Crisis, Number of Cases. Day of disease. Wun- derlich. Ziems- sen. Thomas Bleul.r Total. 1st 0 0 0 0 0 2d 0 0 2 0 2 3d 10 9 6 6 31 4th 11 3 6 13 33 5th 14 31 11 22 78 6th 14 5 5 26 50 7th 19 35 10 32 96 8th 4 4 4 24 36 9th 3 9 0 12 24 10th 0 0 2 6 8 11th 0 8 0 1 9 12th 0 0 0 3 3 13th 0 3 0 1 4 14th 0 0 0 0 0 75 107 46 146 374 1 This course is, however, very rare in the acute primary disease. Most of the forms of tubercular Pneumonia run the course of catarrhal or broncho-Pneumonia. 2 See a case by Ziemssen (loc. cit. pp. 180-2) of Pneumonia of upper lobe, in a child aged nine months. The pyrexia lasted thirty- one days, and the physical signs only disap- peared three weeks after the subsidence of the fever. Bleuler (loc. cit. p. 19) states that of the cases observed by him and Gries- inger when the inflammation affected the apex of the right lung, in one only did the fall of temperature occur before the sixth day, and in three-fourths of these cases it took place after this date, while in more than half the cases of Pneumonia of the base deferves- cence ensued from the third to the fifth day. 3 Clin. Med. iii. 516. 2 I have reckoned the day of invasion as the first, the next day as the second day. ACUTE PRIMARY PNEUMONIA. 181 varied from twenty-four to forty-eight hours. Two other cases terminated by gradual lysis, one on the twelfth and another on the fourteenth day, the temperature grad- uaPy falling to the normal. In five others the duration was pro- tracted without complications, which would account for the persistence of the pyrexia, except in one instance, where there was considerable pleuritic effusion. In this case an imperfect crisis took place on the tenth day, but the temperature re- mained elevated until the forty-sixth day. Of the remainder three recovered per- fectly, though the pyrexia only ceased on the twenty-fourth, thirtieth,1 and thirty- fifth days respectively.2 In the fourth there was, however, a suspicion of tuber- culosis. The Pneumonia, which had in- vaded the whole right lung, and which was complicated with pleurisy, resolved imperfectly, and occasional pyrexia re- mained until the eighty-first day. As far as I have observed, I do not think that cases where the temperature is much elevated, i. e. above 104°, necessa- rily have a longer duration than those in which the pyrexia is less marked. The pyrexia in the former may end rapidly by an early crisis, and in the latter its disap- pearance may sometimes be considerably protracted. My own observations would also tend to confirm Thomas's opinion that the extent of lung affected does not necessarily delay the appearance of the defervescence, though cases supporting the contrary opinion, which has been ad- vanced by Ziemssen, may sometimes be met with. Together with the disappearance of the fever, the aspect of the patient markedly changes. The flush disappears, and pro- fuse sweating is almost constantly ob- served.3 The face may be pallid and sunken, and, as before stated, the general condition may be one of such intense col- lapse as to lead to immediate fears of a fatal issue, which indeed sometimes oc- curs at this period.4 The pulse becomes small and often dicrotous, and generally falls in frequency. It seldom, however, attains the normal standard, and is liable to irregular exacerbations for some days later, quite irrespective of any correspond- ing variations of temperature. Children particularly may be for hours partially unconscious and almost incapable of being roused, with a cold skin bathed in colli- quative perspiration.1 A catarrhal flow from the nose is sometimes also observed, in children at this period simultaneously with the perspiration. The respiration at the same time falls in frequency. The pain in the side, if this has persisted up to the period of the crisis, disappears or is much relieved. The cough becomes looser; the expecto- ration loses its tenacity, and the rusty character diminishes, though it may not finally disappear until some days later. In its further course and during the reso- lution of the Pneumonia the sputa gradu- ally assume a bronchitic character. The most marked appearance is, however, that of black pigment, which takes the place of the rusty tinge of blood, and the early appearance of which is a favorable sign. The amount of this pigment in some cases, when the resolution is retarded, is some- times very considerable : I have seen the sputa during many days almost black from its presence. Other phenomena are occasionally ob- served, some of which have been regarded as truly critical, that is to say, as in part conducing to the fall of temperature ; others, however, must be looked upon as accidental, or as a result of the subsidence of the fever. Among the former, whose influence in really producing a fall of tem- perature must be considered doubtful, are hemorrhage and diarrhoea. Hemorrhage is occasionally observed in the form of epistaxis, more rarely as hsematuria, and occasionally it proceeds from the bowels.2 Diarrhoea is more common,3 but it must be remembered that the crisis may take place without any of these events, and their appearance is as a whole decidedly exceptional, the only constant critical dis- charge (with the exception of the changes in the amount of the urinary secretions) being that from the skin. Erysipelas is mentioned as an occasional critical phenomenon.4 1 An excellent and life-like description of this condition is given by Ziemssen, loc. cit. 167. 2 I have only seen one case of this nature. 3 Huss, p. 53, says that diarrhoea most commonly occurs on the seventh day in cases of Pneumonia characterized by severe gastric disturbances, but that the convalescence of such cases is usually protracted. 4 Grisolle quotes from Serres a case of a pa- tient who had several attacks of Pneumonia, each terminating in an attack of erysipelas. I have only seen one such case. The erysipe- las appeared three days after complete defer- vescence, and the resolution of the Pneumonia and the subsequent recovery of the patient were greatly protracted. 1 This case was a man of dissolute habits. An imperfect crisis took place on the ninth day. The general symptoms were very se- vere, with profuse puriform sputa after the second week, giving rise to strong suspicions of gray hepatization. 2 This case has been already alluded to (see note, p. 179). There was in this case an imperfect crisis. 3 Herpes also may appear as a critical phe- nomenon at this time. 4 I have seen two cases of this nature. 182 PNEUMONIA. When the nervous system has been pro- foundly implicated during the pyrexial period, the symptoms of such disturbance also commonly disappear during the crisis. Delirium or extreme restlessness usually pass, particularly in children, into quiet sleep. In adult persons, and especially in those of dissipated habits, this may not be the case ; I have seen symptoms closely resembling delirium tremens persist during forty-eight hours after the normal temper- ature has been reached and maintained. The physical signs of the disease may begin to improve coincidently with the disappearance of the fever.1 The com- mencement of the resolution, however, is more commonly observed after the first twenty-four or forty-eight hours of the apyrexial period. In some cases it is so rapid that all the physical signs of the disease may have totally disappeared in twenty-four hours from the first appear- ance of improvement.2 I have seen this in one case where the whole lower lobe has been implicated, and it may occur without any marked increase of the ex- pectoration, or even when this has been scanty and quite insignificant in quantity. Indeed it may be said that, generally speaking, the proportion of exudation re- moved by expectoration must be small in comparison with the whole amount pres- ent in the lungs. Commonly, however, the course of resolution is more protracted. Grisolle states that all the physical signs had only completely disappeared in 37 out of 103 cases who left the hospital between the twentieth and the fifty-fifth days. Dr. Stokes gives the following results of 24 cases, dating from the commencement of resolution. In nine the physical signs had disappeared at the end of a week ; in nine more at the end of fourteen days; in five at the end of three weeks; and in one they lasted a month. In 26 cases of which I have notes of the total3 disappearance of the physical signs, their duration after defervescence was as follows:-In one case, two days, in three, three days ; in one, four days ; in one, five days ; in one, six days; in three, seven days; in one, nine days; in nine, from ten to fifteen days ; in five, from twenty to twenty-five days; in one, from twenty to thirty. Two other patients left the hospital with phy- sical signs still remaining on the twenty- fourth and eightieth days.1 In some of the cases of longer duration the Pneu- monia was complicated with pleurisy, and when much effusion has been present some dulness at the base may remain al- most indefinitely, as I have seen in one or two cases not included in this list. The coexistence of tubercles may also indefi- nitely protract the resolution. Patients whose health has been previously bad are also liable to a retarded resolution ; but this is not always observed. The same tendency has been noticed in cases where the defervescence is not marked by a crisis, or only by an imperfect one.2 Dr. Stokes has observed that retraction of the chest walls may follow an attack of Pneumonia. This has been disputed by Grisolle and Woillez; but Dr. Walshe has seen it take place when the Pneumo- nia had been unattended by liquid effu- sion into the pleura. I have also observed it in one of the cases of protracted Pneu- monia before mentioned.3 The recovery of strength and of flesh is generally very rapid. The appetite often returns almost with the cessation of the pyrexia. Wachsmuth observed in a pa- tient whose loss of weight in four days degree of oedema, particularly in the lower portions of the lung. 1 Bleuler (loc. cit.) gives the following pe- riods of resolution in 150 cases: One day, 5 cases ; two days, 2 cases ; three days, 4 cases; four days, 21 cases; five days, 21 cases; six days, 30 cases; seven days, 13 cases; eight days, 11 cases; nine days, 5 cases; ten to fifteen days, 18 cases ; fifteen to twenty days, 6 cases; more than twenty days, 7 cases, among which were included 3 cases of Pneu- monia on the right upper lobe. 2 Ziemssen remarks that in cases where the crisis is early, resolution may be short, but my own experience has not confirmed this. 3 In a boy in whom the pyrexia and physi- cal signs lasted together sixty days (see note, p. 179), there was observed when he left the hospital some flattening inferiorly of the right (the affected) side. One month later, when he presented himself for examination, the measurements were: At nipple-right side, 12 inches; left, 12 inches. At sixth rib- right side, 11 inches ; left, 11 j inches. There was also some procidentia of the shoulder on the right side. The amount of effusion pres- ent here was throughout extremely small, but some dulness still remained at the right base, attended with weak breathing. 1 Grisolle states that the improvement in the physical signs may precede the disappear- ance of the pyrexia. Grisolle's statement appears, however, to be made independently of thermometric observations. I have never seen a case where this occurred before a marked form of temperature, and it must be remembered that Grisolle regards a rapid pulse as one of the phenomena of the fever. It has been already stated that the pulse may remain rapid after the fever has subsided. 2 Ziemssen gives a case of a child where the physical signs had disappeared before the end of the eighth day of the disease. 8 This includes the final disappearance of all rales as well as dulness and bronchial breathing. Crepitation or fine moist rales may, as has been before stated, often persist for days, or even weeks, after all other signs have disappeared. Probably the weakened resistance of the vascular coats leaves, during a lengthened period, a tendency to a certain ACUTE PRIMARY PNEUMONIA. 183 amounted to a daily average of 24 oz. in the twenty-four hours, and in whom the loss of weight continued for forty-eight hours after the crisis, that in the succeed- ing four days nearly 2 lbs. were regained.1 I have repeatedly observed that from 7 to 14 lbs. may be gained in weight during the first few weeks of convalescence. An attack of acute Pneumonia is sel- dom succeeded by secondary diseases, ex- cept in patients liable to tubercle. Ziems- sen has observed in children that oedema of the lower extremities may be caused by a pure hydrsemia, independently of albu- minuria, which, however, is sometimes present to a slight degree. Dr. Walshe has observed the same phenomenon asso- ciated with coagulation in the veins. Gubler2 and Macario3 have each ob- served instances of general paralysis fol- lowing Pneumonia, but these cases are fortunately rare. The termination of Pneumonia is not, however, always favorable. It may end fatally or it may give rise to local abscess or to gangrene of the lung, or finally it may pass into a chronic state. In some cases, which may prove fatal during the acute stage, the pyrexia may persist to the last, and may, as before stated, increase rapidly towards the close of life. In others, however, no elevation of temperature occurs, and it may even sink to normal before the fatal termina- tion : I have seen in one case, in a patient aged 62, death occur after the crisis had taken place forty-eight hours previously, and in whom during the first portion of this period the symptoms might on the wrhole have been considered favorable. Most commonly death ensues during the acute period of the disease, when it is usually preceded either by intense pros- tration or by extreme dyspnoea. The pulse becomes small and extremely rapid and dicrotous, and the respiration is commonly greatly accelerated. Expecto- ration becomes difficult, or ceases, while large coarse metallic rales are heard in the trachea and larger bronchi, and fine and medium-sized rales indicative of oede- ma of the lung, extend over the non-con- solidated portions. The face becomes livid, the extremities cold, and the skin is often bathed in profuse perspiration, which is colliquative when the temperature is low. A semi-comatose state supervenes towards the last, but in some instances intelligence is preserved to within a few minutes of the fatal issue. In children, coma or convulsions are very common. In old people death may often take place suddenly and unexpectedly.1 Sometimes, particularly in children as described by Ziemssen, death may occur at a later stage. The fever does not main- tain the high standard of the earlier periods of the disease, but persists together with the physical signs. The pulse re- mains accelerated, the skin becomes in- tensely pallid ; emaciation, reducing the patient to the extremest degrees of maras- mus, progresses rapidly ; and the patient dies in the third or fourth week. In other cases there is observed an incomplete remission, followed by a return of the fever, and the patient gradually sinks in the course of the second week. Some cases, however, presenting these characters lapse into a more chronic stage ; the fever and physical signs may persist during many weeks, but the for- mer may subside, while the lung remains permanently consolidated with signs of dilatation of the bronchi.2 No special condition of the lung is necessarily associated writh a fatal termi- nation in the earlier periods of the dis- ease, but the red or gray hepatization, or even diffuse suppuration, may be found in different cases under circumstances which are otherwise apparently similar. The termination in abscess is very rare. Huss says it only occurs once in fifty or sixty cases, and usually only in patients of bad constitution. According to this author, it is most commonly met with in males over forty years of age, and he states that it was more common when bleeding formed part of the treatment than it has proved since this was aban- doned by him. The period of this termi- nation, as determined by profuse purulent expectoration, has varied, according to Grisolle, between the fifteenth and twenty- eighth days. Profuse expectoration may continue for three months subsequently. The site of the abscess is usually at the apex; one case, however, has been re- corded by Dr. Stokes, where a cavity in the midst of pneumonic tissue was found at the base of the lung. The signs of this condition have been already described.3 Cases in which it occurs usually run a protracted course, though death ordi- narily, according to Grisolle, takes place before the thirteenth week. Pyrexia per- sists, and the expectoration, which is at times intermittent, consists of large quan- tities of puriform matter. The pyrexia tends to assume the character of hectic 1 Zur Lehre von Fieber, Arch, der Heilk. 1865, p. 236. In this case the temperature had been very high, 106TO, and the defer- vescence was gradual after the crisis. 2 Arch. GAn. 1860-1. 3 Graz. M6d., Par. 1858. Huxham says: "I have seen in some cases (though few in- deed) a complete paraplegia." (On Fevers, p. 183.) 1 Cruveilhier, Path. Anat., Liv. xxix. 2 These cases will be again considered un- der the head of Chronic Pneumonia. 3 See ante, p. 170. 184 PNEUMONIA. fever, but from the rarity of the disease thermometric observations are wanting. Epiaciation progresses as long as the fever remains, and many cases end fatally, sometimes with the signs of pyohsemia, in other instances by rupture of the abscess into the pleural cavity, and occasionally by sudden suffocation resulting from the filling of the bronchi with pus. Others, however, progress more or less completely to recovery ; in these the abscess cavity may either cicatrize, or it may remain patent but completely quiescent, and re- vealed only by physical signs more or less distinctly indicating its existence.1 The termination in gangrene is almost equally rare with that in abscess, and Grisolle has even doubted whether it is a cause or a consequence of the latter. Some well-authenticated instances are, however, recorded, and it appears that an epidemic constitution may at times pre- dispose to its occurrence.2 It commonly appears late in the disease ; but it has been seen as early as the fifth day (Huss). In fifty-three cases of which I possess observations, I have found two instances of gangrene,3 and in both these it was irregularly diffused through scattered spots of pneumonic infiltration. Its site, according to Huss's observations, is most commonly in the lower lobe, and it has almost invariably occurred in exhausted constitutions. Gangrene is much more common in tubercular Pneumonia. Its physical signs have been already de- scribed. In addition to these its advent is usually marked by a sudden and in- tense prostration of strength, with a rapid weak pulse and sunken countenance. The characteristic sputa are, however, the only positive signs, when developed suddenly in the course of a primary Pneu- monia. It appears to be almost invari- ably fatal. Complications of Pneumonia.- Some of these affecting the kidneys and nervous system have been already de- scribed. Others, however, deserve men- tion.4 Laryngitis, though not mentioned by Huss, is an occasional complication. Gri- solle quotes Serres as having collected the histories of ten cases, and Dr. Walshe says that oedema of the glottis may be one of the causes of a fatal termination. Bronchitis is a more frequent complica- tion. Grisolle says that it has occurred in one-fourth of his cases, that it is seven times more common in males than in females, and that it is most frequent in the winter months. It affects both lungs, though it sometimes appears in excess on the affected side. Its intensity varies greatly in individual cases. Its presence, when general, however, increases the dyspnoea and the lividity of the face. It also renders the sputa more abundant and the cough more frequent. It is seen from Huss's tables that it tends (at least when severe) to increase the mortality of the primary disease.1 Pleurisy is also very common. There are, indeed, very few cases of Pneumonia reaching the surface of the lung in which the visceral pleura is not implicated. Effusion, according to Grisolle, occurs in about 15 per cent. The amount of fluid is commonly in inverse ratio to the extent of lung implicated. Its signs are naturally, almost invariably, found at the base, what- ever the site of the Pneumonia. Its in- fluence on the pyrexia and on the progress nia. The following table from Huss gives a relative estimate of the frequency of other complications, and of their influence on the mortality. This table appears to include cases of both catarrhal and acute primary Pneumonia ; but while some chronic diseases are mentioned, the omission of others, as can- cer, is remarkable. Huss, however, does not treat of the secondary Pneumonias compli- cating other diseases. Recov- eries. | Deaths. | Total. Per ct. of deaths. Pleuritis 92 12 104 11-53 Bronchitis capillaris, acute . 120 20 140 14 28 Bronchitis chronica. 36 6 42 14-28 Emphysema pulmonum . 20 6 26 23 07 Tuberculosis pulmonum 24 12 36 33'3 Pericarditis .... 10 12 22 54-54 Endocarditis .... 1 3 4 75 Phlebitis after bleeding . 0 2 2 100 Valvular disease of heart 16 7 23 30-43 Meningitis cerebralis 0 2 2 100 Erysipelas faciei 11 1 12 8-33 Catarrhus intestinalis . 110 13 123 10-56 Enteritis et entero-colitis, acute 31 6 37 16-21 Colitis chronica 0 2 2 100 Icterus 21 2 23 8'69 Bright's disease 20 26 52 50 Acute articular rheumatism . 20 2 22 8-69 Intermittent fever . 60 6 66 909 Chlorosis 20 5 25 20 Delirium tremens . 144 36 180 20 Chronic alcoholism . 12 4 16 25 Total .... 774 185 959 1 Of 20 cases, Huss states that 12 died, 4 recovered completely, and 4 only partially. A case of cicatrization of a supposed pneumo- nic abscess has been recorded by Dr Stokes. 2 Hughes (Guy's Hosp. Rep. 2d Ser. vii. 1848) found 28 cases of gangrene in 200 post- mortem examinations of Pneumonia. At one time it was noted that several cases of gan- grene appeared during the prevalence of an epidemic of influenza, and that as many as six cases occurred in one week. 3 See also notes to Section on the Morbid Anatomy of Pneumonia, "Gangrene." 4 Under this head I only propose to treat of such complications as may appear sec- ondarily to or simultaneously with Pneumo- 1 The inclusion of cases of Broncho-pneu- monia in Huss's statistics must, however, be remembered. VARIATIONS IN ACUTE PNEUMONIA. 185 of resolution has been already considered. Unless very considerable in amount, or when occurring on the site opposite to the pneumonic lung, it does not very materially modify the mortality. Un- der the latter circumstances, however, it may dangerously lessen the respiratory surface. Pneumothorax has been men- tioned as an occasional complication ; but its existence is very doubtful, and is en- tirely unsubstantiated by post-mortem evidence. Probably the tympanitic note occasionally heard over the non-consoli- dated parts has given rise to error in this respect. Pericarditis, though a less common event, is a very dangerous complication. Huss's statistics show that it proves fatal in more than half the number of cases affected. In some cases it appears to originate in the same cause as the Pneu- monia, or it may be caused by a direct extension of the inflammatory affection- (it may, however, occur, and apparently with about equal frequency, in pneumonias of the right and left side)-or, finally, it may in some cases be due to secondary septic effects resulting from the absorp- tion of inflammatory products in the lung.1 Its influence on the pyrexia and on the phenomena of resolution have been already described. The evidence of other cardiac lesions secondary to Pneumonia is but slight, but in some cases there appears to be a ten- dency to the formation of fibrinous con- cretions in the cavities of the heart. Icterus.-A slight icteric tinge of the conjunctiva is by no means uncommon. Distinct jaundice is also an occasional complication.2 It may in some cases be produced by congestion of the liver, arising from the impeded circulation in the lungs ; in others it is probably due to coincident gastro-duodenal catarrh. It is more com- mon in the summer than in the winter months. It appears to be more frequently associated with Pneumonia of the right than with that of the left lung; but it must be remembered that the former is much more liable to be affected. The theory of its production by direct exten- sion of the inflammatory action from the lung to the liver is now generally con- sidered untenable.3 I have met with one case in which icterus preceded the attack Pneumonia; it usually, however, fol- lows the invasion of the disease. Accord- ing to Grisolle, the liver can very rarely be felt to be enlarged.1 Gastric symp- toms, and particularly nausea and vomit- ing, tend to accompany this condition. Parotitis is a rare complication, but it is one whose appearance seriously in- creases the gravity of the prognosis. Most of the cases of Pneumonia in which it occurs prove fatal.2 Grisolle states that its progress is very rapid, and that it tends to pass into suppuration or gan- grene. In the former case, the pus may burrow deeply among the muscles of the neck, or may open into the external ear. The pus is, however, usually infiltrated, so that but little escapes on incision. It appears to be most common in advanced life. The only case in which I have met with it was in a girl aged fourteen.3 In rare cases an inflammatory condition of the joints occurs in the course of Pneu- monia. Grisolle reports four such. In all these the joint affection was multiple, but it was not migratory. Three of these cases proved fatal. In the only one ex- amined the joints contained pus, and Gri- solle considers it probable that the affec- tion was septic in its nature, since in all the fatal cases the lung was found in a state of suppuration. In one case, a pa- tient of Dr. Reynolds, a man of dissipated habits, effusion came on in the knee-joint on the day after the crisis, attended with a slight rise of temperature. The Pneu- monia resolved perfectly, but the swelling of the knee became chronic.4 Variations in the Clinical Aspect of Acute Pneumonia. Many of these, depending on the sever- ity of the coincident affection of the di- gestive or of the nervous system, have been already described. Three classes, however, deserve some mention, viz., lung. In these cases, however, the right and lower lobes were affected with equal fre- quency. 1 Andral reports a case (Clin. M^d. iii. p. 441, obs. Iv.) of icterus accompanying Pneu- monia, where the hepatic region was painful and resistant. The stools were natural, though all the tissues were stained with bile. Post-mortem, the liver was found softened, and of a deep red color. The biliary passages were free ; and bile could easily be expressed from the gall-bladder into the duodenum. 2 Two such cases are related by Behier, Conferences de Clinique M&licale. 3 This case has already been referred to as an instance of Pneumonia passing into gan- grene. 4 This patient was transferred to the surgi- cal wards, and I am unable to trace his sub- sequent history. 1 Dr. Parkes, Clinical Lecture, Med. Times and Graz.,1860 ; i. 187. 2 It occurred in 7 per cent, of Grisolle's cases, in less than 1 per cent, of 237 cases analyzed by Roth, Wiirzb. Med. Zeitsch., i. Nos. 3 and 4. Cvostek (Canstatt's Jahresb. 1867) met with icterus in the proportion of 21 per cent, of 147 cases, and the mortality in these cases was 23'8 per cent. The average mortality of the whole number of these cases was 16'8 per cent. 3 Out of 20 cases observed by Grisolle, 16 were associated with Pneumonia of the right 186 PNEUMONIA . Latent Pneumonia, the so-called Typhoid Pneumonia, and Pneumonia assuming an intermittent type. Latent Pneumonia.- The class of Latent Pneumonia is an ill-defined one, and in many cases in children the accom- panying cerebral affection may mask the ordinary symptoms of the disease. It is very rarely that in vigorous adults the inflammation of the lungs does not present characteristic clinical features, but in old people many of these are often absent. In cases also where Pneumonia is secondary to other diseases, the chief symptoms may be altogether wanting. In old people the disease maybe only re- vealed by prostration, headache, and de- lirium, and none of the usual phenomena of invasion may be present. Cough also and expectoration may be entirely absent, or the latter may fail to present the char- acteristic rusty tint, and may be transpa- rent and viscous, or simply puriform. Subjective dyspnoea is also less frequent, though some acceleration of the respira- tion and the perversion of its normal ratio to the pulse rarely fail to be ob- served. The flushed face is also less frequent in the aged than in adults, and the coun- tenance is often pale, earthy, and sunken. The skin may be dry and hot, but it may fail to communicate to the hand the pun- gent feeling of heat sometimes described ; or it may be relaxed and perspiring throughout. Fever is, however, almost always present, though seldom ranging so high as in adults and in children. Its presence is, however, a valuable indica- tion for a careful investigation of the chest, since Pneumonia is one of the few febrile affections to which elderly people are liable. The disease, however, may be so entirely latent that its presence in a state of gray hepatization may only be revealed post mortem after a sudden and unexpected death.1 The Typhoid Form oe Pneumonia is very common in elderly people, and might be described as a sub-variety of the Latent form. Its occurrence, judging from my own experience, must be rare in this country, though some of the severer, and particularly of the fatal cases, tend to assume towards their close some of the characters described. Dr. Stokes, how- ever, has found it more common in Dub- lin. It has also been described by Hux- ham as occurring in scorbutic patients, in whom it is often associated with dysen- tery, attended by bloody stools. Huss remarks that it occasionally occurs spo- radically, but only in those who have been exhausted by toil, want, or other de- pressing influences. It is very doubtful whether the reported epidemics of this character have been pure Pneumonia, or not rather typhoid fever.1 Many of the cases in which Pneumonia occurs as a complication of other diseases tend to assume this type,2 but it may occasionally be met with as the primary disease. It may be described as a form of Pneumo- nia marked by intense prostration and by the signs of profound depression of the nervous centres. Its invasion is often gradual; the initial rigor may be slight or nil, and pain in the side may be absent or slight; the cough and sputa are often present at the outset, but the latter may be merely viscous, or may present the characters of prune juice. Stupor, alter- nating with a constant low muttering de- lirium, and associated with tremors and subsultus tendinum, with a fixed but vacant expression of countenance, and with complete abolition of senses of sight and hearing, and also in some cases of the faculty of speech, are its most promi- nent features. The tongue is dry and brown, and sordes form on the teeth. In- continence or retention of urine are some- times observed. The pulse is small, but markedly accelerated. Sloughs may form on the more prominent parts. These symptoms may continue through the whole course of the disease, which usually ends fatally on the tenth or twelfth day, or later. The course in cases of recovery is commonly protracted, and resolution is very slow. Wunderlich describes, as a variety of Pneumonia, a class of cases attended with early breaking down of lung-tissue (Jau- chige Pneumonie), which present a great resemblance to the typhoid form. The sputa are fetid and of a dirty color. The fever is high, and prostration sets in early. Sweating is profuse, and there is a tendency to colliquative diarrhoea. Their course is protracted, and they tend to a fatal termination. When recovery 1 This would appear to be the case in the epidemic quoted by Grisolle, as described by Torchet, at Noyers, M^m. Acad. Imp. 1838. 2 Dr. Stokes (loc. cit. p. 339) describes va- rious forms: (1) As a complication of "En- teritis, or Gastro-Enteritis (2) As a compli- cation of true typhus ; (3) Occurring in cases of bad erysipelas; (4) Occurring in cases of diffuse cellular inflammation ; (5) Occurring in cases of delirium tremens from excess ; (6) As a consequence of phlebitis ; (7) As appa- rently the sole disease. 1 Hourmann et Dechambre, Pneumonie des Vieillards (Arch. Gen. de M^d. 2e S^r. xii. 37). These authors state that of 49 cases of Pneumonia in old people uncomplicated by disease of the heart or brain, 21 were latent. It is almost always latent when occurring in old people with cardiac or cerebral affections. See also Cruveilhier, Anat. Path. liv. xxxii. PATHOLOGY. 187 take'; place the fever subsides, and the sputa lose their fetid odor and peculiar color, and become simply purulent. I have seen one fatal case of this kind asso- ciated with dysentery, and with sloughs in the mucous membrane of the stomach.1 Some forms of Pneumonia occurring sec- ondarily to dilatation of the bronchi are very prone to assume this character. INTE RMITTENT PNEUMONIA. -Among the inhabitants of malarial districts the symptoms of Pneumonia, and in particu- lar the pyrexia, often assume an intermit- tent type. The invasion is commonly attended with rigors, followed by pyrexia and sweating; but with these symptoms of ague the physical signs of Pneumonia may simultaneously make their appear- ance. In some cases, after the first twen- ty-four hours the fever ceases, and during the apyrexial period a marked improve- ment is said to take place in the physical signs: the dulness diminishes and the rales disappear, while the respiration over the affected part may be merely weak, or may in some cases retain the bronchial character. A second invasion, however, occurs with increased severity after twenty-four or forty-eight hours, with a return of the physical signs. The subsequent intermissions are less com- plete, but the pyrexia in such cases has always a distinctly remittent character, which may assume either the quotidian or tertian type; the cessation of the pneu- monic signs in the early stages is, how- ever, more complete in the latter than in the former variety. It is said that qui- nine, if given early, will cut the disease short; but if this is not effected, the Pneumonia tends to become double, and of a dangerous character.2 In some cases, however, of Pneumonia where there is no evidence of malarial in- fection, the type of the pneumonic py- rexia is distinctly intermittent, with apy- rexial periods whose duratian may vary from twelve to thirty-six hours. The re- missions are attended with marked sweat- ing, and also with an alleviation of the chief symptoms, though the physical signs usually remain unchanged during this period. The exacerbations are sometimes, but not always, attended by a return of the rigors which marked the primary in- vasion. This class of cases is rare, and the conditions determining their pecu- liarities are not fully explained. In some instances the exacerbations appear to be due to an irregular progress of the Pneu- monia, but in others no determining cause, either of the remissions or of the return of the fever can be discovered.1 Pathology. A. Morbid Anatomy.-The different anatomical changes which may be found in the course of acute sthenic Pneumonia have been ordinarily described under the terms of Engorgement, lied Hepatization, Gray Hepatization, Suppuration, and lieso- lution. Dr. Stokes has, however, described a stage of arterial injection antecedent to that of engorgement, and characterized by a brighter color and by dryness of the pulmonary tissue. Opportunities for ob- serving this condition are extremely rare, and its very existence has been called in question by Rokitansky and by Skoda. There is, however, reason to believe in the probability that such a state may pre- cede the subsequent changes of the in- flammatory period, and the auscultatory signs of harsh respiration, which have been described by Dr. Stokes as attending it, have been recognized by many and different authors.2 (1) The stage of Engorgement is charac- terized by intense congestion of the pul- monary vessels and by commencing oedema of the lung. The tissue is of a deep reddish-purple tint. It is heavier than natural, and has lost some of its resistance and elasticity. It pits on pressure, and is more easily torn than a healthy lung. On section a large amount of blood-stained serosity escapes from the cut surface, and in the earlier stages this is frothy from the ad- mixture of air. During this period the tissue is still crepitant, and floats in wa- ter to a degree corresponding with the extent to which the condition has ad- vanced. Under the microscope, the ca- pillaries of the pulmonary artery are found to be loaded with blood. The epi- thelial cells of the air-vesicles are seen to be enlarged and granular, and occasion- 1 Dr. Stokes (Cyc. Pract. Med. iii. art. " Gastritis") has also observed this form of Pneumonia associated with severe gastro-en- teric disturbance. An instance of this form of Pneumonia is given by Dr. Laycock, " Fe- tid Bronchitis." 2 See Morehead, Diseases of India, p. 349 et seq. Most of the other authorities on this subject will be found quoted in Grisolle's work. 1 See Wunderlich, Die Eigenwarme im Krankheiten; Thieme, Die Intermitterende Pneumonie, Diss., Jena, 1865 ; Griesinger, Virchow's Spec. Path. Therap., ii. p. 43. In none of the reported cases of this condition with which I am acquainted has the condi- tion of the spleen been mentioned. 2 The reality of its existence must, how- ever, in part depend on the question of the increased arterial supply from the bronchial vessels, since congestion of the capillaries of the pulmonary artery does not give this tint. 188 PNEUMONIA. ally they exhibit a commencing division of their nuclei: some exudation-corpus- cles may also be seen in the alveoli, min- gled with red blood-corpuscles which have escaped from the capillaries. The question of the vessels chiefly con- cerned in the pneumonic process has been largely discussed without any definite set- tlement having been arrived at. It has been maintained by some that the inflam- matory changes are mainly dependent on the bronchial artery as the nutritive ves- sel of the lungs,1 and Virchow's observa- tions have shown that the most typical pneumonic changes may ensue in parts of these organs whose supply from the pul- [ monary artery has been completely ar- rested by the occlusion of branches of this vessel.1 It is by no means, however, cer- tain that the nutrition of the lung is exclusively conducted by the bronchial artery; and it is not at all improbable that the branches of the pulmonary ar- tery, whose participation in the process of congestion so vastly exceeds that of the bronchial capillaries, may have no incon- siderable share in the exudative processes which distinguish the condition of hepati- zation. (2) Red Hepatization is the term gene- rally adopted for the appearance observed in the second stage. In it the lung has [Fig. 25. Croupous Pneumonia.-Red Hepatization.-Showing the fibrinous coagulum in one of the pulmonary alveoli, inclosing within its meshes numerous leucocytes, which are already commencing to undergo fatty metamorphosis." A few leucocytes are also seen on the alveolar walls, and. the alveolar epithelium is swollen and granular. X 200. (Green).] become solid; it sinks in water, and the section is that of a solid tissue. It is firm, as if the lung had been artificially injected with size from the bronchi; but it has lost its elasticity and resistance, it tears easily, and breaks down into a pulp under pressure. Its section is less livid than that of a simply congested lung, and is of a dull, reddish-brown tint (sometimes likened, but not very exactly, to mahoga- 1 Ges. Abliand. p. 369 et seq. Dr. Waters (Dis. of Chest, p. 30) believes that the pul- monary artery is exclusively distributed to the walls of the air-vesicles. Since, however, it has been shown that some of the products of inflammation may escape by the veins, it is possible that this may explain such cases as those described by Virchow ; though some doubt still remains as to whether the bron- chial arteries may not participate in the pro- cess more than Dr. Waters's suggestions would lead him to believe. 1 This question, according to Virchow, was first raised by Boerhaave. (See Van Swieten, Comm, in Aph. Boerhaave, ii. 712.) It has also been ably discussed by Dr. Morehead, Dis. of India, ii. 311. PATHOLOGY. 189 ny), which, however, becomes brighter after a short exposure to the atmosphere. It is also opaque, and has lost the glisten- ing transparency of ordinary pulmonary tissue.1 The color is not absolutely uni- form, but mingled with the reddened tint is a grayish appearance, as if Chinese white had been mixed with the coloring matter. Very little serosity exudes on section, but a dirty, rusty-looking, red- dish fluid with a certain degree of viscid- ity may be expressed or scraped from the surface. A characteristic appearance of the section in the Pneumonia of adults is the granular look which it presents, and which is still more distinct when the tis- sue is torn. The granulations are small and uniform; they give the torn surface the appearance seen on the exterior of a nutmeg, and they may easily be separated on scraping the tissue. This granular appearance is less distinct in children, and varies also in degree according to the amount of oedema present.2 During this stage the interlobar septa, and even the larger bronchial vessels, are still distinct, and participate but little in the inflammatory changes, but the lat- ter are sometimes filled with solid exuda- tion-matter. The vesicular character of the lung is, however, entirely destroyed, being replaced by the granular look just described. The tissue is greatly increased in weight, and, according to Gendrin, its specific gravity when compared with that of healthy lung may be as 1T5 or 1'9 to 1. The lung is expanded by the exudation present to the fullest capacity of its nor- mal dimensions. It is possible also that it may somewhat exceed this. The pos- sibility of its thus retaining the impress of the ribs has been largely discussed ; but it has been definitely settled in the affirm- ative. The pleura almost invariably partici- pates in the inflammatory changes when the part affected is superficial. It loses its normal translucency and becomes opaque, and it is generally covered with a layer of fibrinous exudation. When the stage of red hepatization has lasted some days, its color becomes paler and whiter. This is due to individual granulations becoming whiter in aspect, either singly, or in groups scattered through the surrounding reddened tis- sue ; and this change produces a mot- tled look in the inflamed part. Coinci- dently with this change of color there is a gradually increasing loss of the solidity of the affected tissue: the exudation lique- fies, and more fluid can be expressed from the cut surface, and the state may gradu- ally pass into that of gray hepatization, though it is very questionable whether perfect resolution does not often take place without the latter being fully attained. The two conditions are, however, fre- quently found intermingled, and the lung then acquires a marbled appearance, which, as Laennec remarked, may closely resemble some forms of granite. (3) Gray Hepatization.-In this condition the cut surface of the affected part is of a uniform gray tint, generally presenting, however, a somewhat greenish or olive tinge. The redness of the preceding stage has disappeared entirely, and the granu- lar character has become less distinct. The tissue has lost its firmness and has become soft and pulpy, and allows a dirty- looking, puriform, gray fluid to be abund- antly exuded, both on scraping and on pressure. Sometimes a further stage of softening is reached, though this is, com- paratively speaking, very rarely ob- served. Many minor variations of ap- pearance are presented in this state, which usually is found in persons of bad consti- tution or in cases where Pneumonia is secondary to other diseases. The differ- ence in the appearances observed, depend, however, for the most part, on the greater or less amount of oedema present, and in the comparative indistinctness of the granulations. In some instances these are entirely absent, and the tissue is uni- form, smooth, and glistening. Under these circumstances a large amount of serum may escape on pressure, containing but few solid elements, and not present- ing, therefore, the milky, puriform detri- tus usually observed. Such conditions are not uncommon in cases of Pneumonia proving fatal in the course of Bright's dis- ease, when attendant oedema of the lung complicates the inflammatory process. In some instances also this condition appears capable of remaining for some time in a chronic state, when it may form one of the stages of transition between acute and chronic Pneumonia. This is particularly the case in some forms of phthisis, but it is also seen independently of the compli- cation with tubercles. The consolidated lung still retains the gray marbled ap- pearance, and some serosity may escape on pressure, but the tissue gradually ac- quires a more resisting character, and does not break down easily into detritus.1 1 I doubt much whether cheesy changes in the exudation, as described by Niemeyer, are commonly observed in this form of Pneu- monia, independently of tubercular forma- tions in the walls of the air-vesicles. Such an event may be possible, but I believe that cheesy masses commonly found in such lungs in phthisical patients are usually, though not 1 It is to be remarked that this translucency is preserved in conditions of collapse, and that the dead opacity of appearance is one of the best characteristics of the pneumonic process. 2 See Appendix C. 190 PNEUMONIA. (4) Suppuration of the Lung.-In this state the lung presents a yellower appear- ance than that seen in the gray hepatiza- tion. The granular character is lost, and a diffluent puriform fluid exudes from the cut surface. The whole tissue of the lung is softened and pulpy, and breaks down with the greatest facility under very slight [Fig. 26. Croupous Pneumonia.-Gray Hepatization.-Showing the large accumulation of cellular elements within one of the pulmonary alveoli, which in some parts have undergone such extensive fatty degeneration that their distinctive outlines are no longer visible. X 200. ^Green.)] pressure, and it may thus give rise to the false impression that an abscess has been formed. The condition is not, however, specifically distinguished from either of those last named, in respect of the changes in the pulmonary tissue, since pus-cells are present in all stages of the pneumonic process; and the greater degree of soft- ness and the changes of color observed in the so-called gray hepatization and sup- puration of the lung are only due to the increasing anaemia caused by the pressure of the accumulated products of inflamma- tion in the interior of the air-vesicles, and by the progressive degrees of fatty de- generation in the cell-forms thus pro- duced : while the gradual softening is attributable to the liquefaction of the pre- viously solidified exudation.1 (5) During the stage of Resolution the liquefied exudation matter, and the cell- forms which have degenerated and broken down, are gradually absorbed. The ex- pectoration is often in such cases so insig- nificant as by no means to account for the elimination in this manner of these pro- ducts and the greater part must neces- sarily be removed by absorption. Oppor- tunities for the observation of lungs in this condition are rare. I once found, three weeks after the physical signs had disap- peared, a considerable amount of oedema remaining in the affected parts, together with a marked loss of elasticity of the tissue1. It is a matter of some interest that Pneumonia has been described as a disease of intra-uterine life. F. Weber2 mentions it as existing in two forms, a white hepati- zation and a red. The former, however, is now generally considered to be a syph- ilitic affection. The red hepatization of intra-uterine life occurs as a lobar Pneu- invariably, the result of a secondary tubercu- lar growth. The discussion of this question, however, belongs to that of Phthisis, and cannot be entered upon here. 1 It has been repeatedly affirmed that this condition is not a true ' ' suppuration of the lung;" as stated by Gluge, and certainly it does not specifically differ from the previous stages, since pus-cells are produced through- out the whole pneumonic process. The ques- tion is one of terms rather than of a reality, but as the contents of the air-vesicles are more purely puriform than in the earlier stages, there appears to me to be no objection to re- taining the expression. 1 An accident prevented my making a mi- croscopic examination of this lung. Similar conditions have been described by Laennec and Grisolle. Laennec's description of the process is very minute, and subdivided ac- cording to the different stages. It would ap- pear, however, doubtful whether these can be so perfectly defined as was attempted by him. 2 Path. Anat, des Neugeb. und Sauglinge, il. 41 et seq. PATHOLOGY 191 monia. It is most commonly met with during epidemics of puerperal fever, which Weber believes may produce blood-poison- ing in the mother before delivery.1 The lung is very much gorged with blood, and is softer than in the ordinary form of red hepatization, though resembling the Pneu- monia found in some conditions of blood dyscrasia. The disease usually proves fatal within a few hours after birth. The microscopical examination of a pneumonic lung1 is at once sufficient to show that the inflammatory products are almost entirely accumulated in the in- terior of the air-vesicles. This is seen in Fig. 27 (x 100 diam.); and the same ap- pearance persists throughout all the stages of the process, including that of gray hepatization, in which, as originally re- marked by Gluge,2 the elastic fibres are still distinct. The walls of the vesicles are, however, somewhat swollen, but this is almost entirely owing to the congestion of the capillaries, and there is an entire absence of any interstitial growth or exu- dative process within or external to them. In some parts, b b, in hardened prepara- tions, the contained masses of cells sepa- rate from the walls of the air-vesicles, leaving the latter intact. When examined with a higher power (Figs. 28 and 29, x 700), the alveoli are seen to be occupied by a considerable variety of cell-forms held together by a tenacious material, and mingled with a number of free red blood-corpuscles (Fig. 28, b). The amount of these latter, how- Fig. 27. Air-vesicles of Inflamed Lung. Fio-. 28. .Alveoli in Pneumonia. ever, varies greatly, but in some instances it may be so excessive as to form a large proportion of the material filling the alveoli. In the earlier stages of the pro- cess, the epithelial cells of the alveoli and smaller bronchioles are seen in different stages of transformation and proliferation. They are greatly enlarged, measuring from Yj'dTy to or of an inch in diameter. They tend to assume the 1 On this subject see also Dr. Da Costa, "Amer. Journ. Microscop. Science," 1855 ; and Rindfleisch, " Lehrb. der Path. Gewebe- lehre." 2 Anat. Microscop. 1838. 1 Forster (Handb. der Path. Anat., 2d Ed. ii. 248) says that he has met with this change under similar circumstances. 192 PNEUMONIA. round form, but some (Fig. 30, a b (7) are 1 In the early stages they are cloudy and at times irregular in shape. They are for opaque, but they clear with acetic acid, the most part very granular.1 I showing that they contain an excess of Fig. 29. Alveoli in Pneumonia. fibrinous matter ; but as tbe process ad- vances, the granular character is mainly due to the accumulation of fat drops in their interior. The nuclei in these cells are sometimes single, and show a distinct nucleolus (Fig. 28, a; Fig. 30, a cc); but Fig. 30. Altered Epithelial Cells in Pneumonia. in the majority of instances the nuclei may be seen in all stages of multiplication and division (Fig. 29, b b; Fig. 30, b cd), until several nuclei are found accumulated in the interior of the cells (Fig. 30,/). Large cells may, however, at times be found in other conditions in which the nucleus has disappeared, and the cell may only present a clear hyaline cavity in its interior, which gradually increases in size until, in some instances, only a narrow margin of the granular cell contents is seen surrounding the central space (Fig. 29, c; Fig. 30, kk). Together with these there are seen various forms of pyoid cells, some of which present one, and others two nuclei or more (Fig. 30,/). They 1 In Figs. 28 and 29, the preparations from which the drawings were made were put up in Canada balsam or Damara gum, and the antecedent modes of preparation (immersion in turpentine and chloroform) dissolved out the fat granules. PATHOLOGY. 193 are smaller than the foregoing, and ave- rage from 25'03 to 55'55 of an inch in diameter; the nuclei vary in size from to ifo'rtjOf an inch. Many round cells are also seen in which no nucleus is apparent (Fig. 30, A). Some of these cor- respond in appearance with that presented by the nuclei of the larger cells; others bear the closest resemblance to lymphoid cells or to the white corpuscles of the blood ; others again are larger than these (Fig. 30, i). The whole of these cells are finely or coarsely granular, the granules being mainly of a fatty nature. They are often stained by imbibed hematine, and in the later stages pigment granules tend to accumulate in increasing numbers in their interior. They are seen in Figs. 28, 29, to be irregularly scattered among the larger epithelial cells. As the process advances, the granule cells become more numerous, and the epithelial cells in great measure disappear. This is due to the fatty disintegration of the latter, which may be seen in?all stages of this change, large tracts being filled with coarser granule cells, and with the compound granular bodies of Gluge. They break down and their nuclei are set free, until the interiors of the alveoli are almost entirely occupied by the smaller-sized round nucleated and non-nucleated cells (Fig. 31), in which large quantities of fat granules become accumulated. These Fig. 31. Alveoli in advanced Pneumonia. appearances are most common when the stage of gray hepatization is reached ; but similar conditions are often found in parts which to the naked eye still present the aspect of red hepatization. In the earlier periods the cells are agglutinated together by a material of a cohesive nature, which is usually considered to be fibrin, but of the nature of which no very precise chemical proof has been afforded but it may sometimes present a fine network like that seen in whipped fibrin from the blood. Its cohesive nature is, however, distinctly seen in the fact that the gran- ules may be scraped or washed out entire from the cut surface, and these not in- frequently present the forms of casts of the smaller bronchi and infundibula, and consist of masses of the cells now described. If a section of the lung in this state be carefully washed over with a camel's-hair pencil, cells are seen still remaining be- tween and imbedded among the elastic fibres of the alveoli, mingled with an ad- ventitious network of a fibrinous nature (Fig. 32). These fibres have not, how- ever, the definite outline and the regular arrangement seen in the process of growth which characterizes tubercular formation, and, though in section some cells are seen irregularly scattered over the walls of the alveoli, no interstitial growth appears to take place in these during the process of 1 In the earlier stages of the pneumonic process, during the period of engorgement, the air-vesicles are loaded with a clear but very tenacious fluid, which, however, be- comes cloudy on the addition of acetic acid. During the height of the consolidation acetic acid effects a partial clearing of the effused material, while during the stage of liquefac- tion the qualities of this fluid in respect to the reaction with acetic acid revert to the first stage. (Rindfleisch, Lehrbuch der Path. Gewebelehre, 363.) VOL. II.-13 PNEUMONIA. 194 acute Pneumonia. In the later stages of the process the material holding the cells together loses much of its cohesive prop- erties, and becomes more fluid, and, to- gether with the cell-forms observed, great numbers of free oil globules and of gran- ules of protein matter become apparent. In this stage, scrapings of the tissue yield only cells and a tenacious fluid, and neither the granules nor the casts of the bronchi can be separated entire. The full discussion of the pathology of Fig. 32. Alveolus in advanced Pneumonia. these processes, involving as it does the whole question of the nature of the changes of tissues in inflammation, can necessarily be only briefly dwelt upon here. The points of greatest interest in relation to it are those regarding the nature of the ex- udation process, and the origin of the cells which are produced in such excess in the interior of the air-vesicles. Until the publication of Cohnheim's researches, the opinion generally received was that of Virchow, that the coagulable material was derived from blood-plasma, changed dur- ing its passage through the inflamed tis- sues, and that the cell-forms found were' the result of increased growth from pre- existing tissues. Cohnheim's1 statement, that the so-called pus-cells in inflammatory processes consist chiefly of the white cor- puscles of the blood which have passed through the walls of the bloodvessels, has been absolutely adopted by Professor Axel Key2 in respect to Pneumonia, though here the kind of proof obtainable in the mesentery and in the tongue of the frog is necessarily wanting. That such a passage takes place in these parts in the frog can be easily verified, but that this migration of the white corpuscles is the sole source of the vast increase of cells found in in- flamed parts appears to me inconsistent with facts. I believe that all the cells and nuclear elements (centres of nutrition) of a tissue participate in the inflammatory process, and multiply in number by di- vision. The illustrations which I have given of these processes during Pneumonia are, I think, sufficient to confirm this proposi- tion, and the same fact may be abundantly seen in the frog's mesentery, where, in parts when no escape of corpuscles from the bloodvessels is taking place, and even before this process has commenced, a great increase of the nuclei in the tissue may be observed without a single cor- puscle having migrated from elsewhere into such parts. The tendency of all irritative growth is to approximate to what may be consid- ered as the primary or lymphoid cell- forms, and hence "pus-cells," which in some cases are undistinguishable from the white corpuscles of the blood, are pro- duced wherever rapid growth of this na- ture occurs. I believe, therefore, that while a number of the cells in the pulmo- nary alveoli may be those which have es- caped from the bloodvessels of this part, another series are produced in the man- ner above described, and which in their final stages are undistinguishable from the former.1 With respect to the exudation, it may be held, when spontaneously coagulable, to consist mainly of the blood-plasma; but the condition of this product in the early stages of Pneumonia suggests at least a doubt whether it is merely a trans- udation, or not rather, as Virchow has 1 That a local production of white corpus- cles takes place either in the lymphatics or in the bloodvessels (and probably in both) of an inflamed part, is, I think, probable from the great increase of these in the blood gen- erally. If this were not the case their exit at the seat of inflammation ought largely to diminish their relative number in the sys- temic blood, whereas precisely the reverse is observed. 1 See Appendix D. 2 Hygeia, 1868, p. 530. Translated by Dr. W. Moore (Med. Times and Gazette, 1869, 452). SITE. 195 taught, that it owes some of its proper- ties to transformations which it lias un- dergone during its passage through the inflamed tissues. The terminations of acute Pneumonia in abscess and gangrene are very rare. Abscess' is probably the rarer of these. It is due directly to the breaking down of the lung-tissue, and it is most commonly found in parts which are the seat of gray hepatization. The size of such abscesses varies from that of a bean or a pea to a cavity of some inches in diameter.2 They may in rare instances give rise to pneu- mothorax, and a case is reported of an opening being effected into the pericar- dium.3 They are sometimes found sur- rounded by a thickened wall of false mem- brane, but more commonly they merely form irregular excavations in the soft- ened tissue which may hang in irregular necrotizing rags in their interior. Gangrene has been already stated to be rare in acute primary Pneumonia, but its occasional occurrence seems to be indis- putable.4 It may invade considerable tracts of tissue. The distinction between some forms of gray hepatization and true gangrene is not always very sharply de- fined. The former may be found rapidly breaking down into a pulpy detritus of a dirty and blackened appearance, but want- ing the characteristic odor of a gangrenous lung. Such states appear to occur most commonly in persons of bad constitution or under peculiar conditions of blood- poisoning.1 This state corresponds with the Ichorous (Jauchige) Pneumonia of Wunderlich, to which allusion has been already made. The condition is usually accompanied by intense typhoid prostra- tion, and the Pneumonia only appears to be part of a constitutional state which is of the extremes! gravity. When true gangrene takes place, the part affected is dark and stinking, and is commonly reduced to a pulpy debris. The gangrenous fragments are not infre- quently found floating in a pseudo-cavity amid fetid putrilage. Huss attributes its origin to thrombosis occurring in the branches of the pulmonary artery-a view originally entertained by Carswell ;2 but in some instances it may be due to the directly destructive effect of the inflam- matory process destroying the vitality of the tissue, or to an arrest of the circula- tion by the excessive accumulation of its products in the interior of the air-vesicles. The portions affected are commonly sur- rounded by tissue in a state of gray hepatization. Site.-The most frequent seat of acute primary Pneumonia is in the lower lobe of the right lung. The excess of frequency of the affection of the right lung, independently of the seat of the disease', over that of the left, is 1 Huss estimates its frequency as once in 50 or 60 cases ; Laennec only saw five in- stances, but he probably overrated their fre- quency as diagnosed by physical signs. Chomel met with it three times; Louis, An- dral, and Grisolle have each observed only one instance. Morehead (loc. cit.) in 189 cases only found five instances. Of twenty- five cases collected by Grisolle from different sources, eight occurred above setat. 70, twelve above aetat. 50, and three above aetat. 45. According to the statements of Barthez and Rilliet, and of all other authors, abscesses are very rare in the primary Pneumonia of child- hood, contrasting in this respect with the effects of Broncho-pneumonia. They appear to be proportionately more frequent in Pneu- monia of the upper than in that of the lower lobes, especially when the relative liability of these parts of the lung to the primary disease is considered. Multiple abscesses are most commonly the result of pyaemia, and have been described under this head. (See vol. i. of this work.) Rare instances may be found of abscesses in the lung caused by those formed in the different organs of the abdomi- nal cavity perforating the diaphragm. Several cases of this kind have been collected by Dr. Stokes. (See also Ulcer of Stomach, vol. ii.) Foreign bodies entering the lung are also an occasional cause. 2 A remarkable case of the cicatrization of an abscess is reported by Dr. Stokes. Laen- nec describes one involving the greater part of the middle and lower lobes. 3 Beclard, Bull. Soc. Anat. 1863, p. 356. (Grisolle.) 1 Andral, Clin. Med., obs. vol. iii. 63 and 68. Willigk (Prager Vierteljahresch. xxxviii. p. 13) found gangrene in 52 out of 583 post- mortems of Pneumonia=3'3 per cent. It oc- curred in 3-6 per cent, of the males, and 2-9 per cent, of the females. Huss, in 2166 cases of Pneumonia, met with only 12 instances: all were in males, aged from 35 to 55, and all the cases were in patients of exhausted constitutions. Dr. West (loc. cit. p. 318) says that "the lung in childhood shows a much greater tendency to pass into a state of gangrene than in adult age." This tendency, however, is not seen in the acute Pneumonia of children, and instances of such an occur- rence only occur singly in the works of differ- ent authors. (See Steffen, loc. cit.) Ziems- sen (loc. cit.) met with only one case out of 201 instances of primary Pneumonia in chil- dren. 1 See a case hy Bamberger (Deutsche Klinik, 1850, 115) of Pneumonia of this nature pass- ing into abscess. It occurred five days after parturition. A case is reported by Dr. Lay- cock (Fetid Bronchitis, p. 27) of acute gan- grenous Pneumonia destroying nearly the whole of one lung, and proving fatal within a month. Tubercles were present in this case. 3 Illust. Elem. Forms of Disease, art. "Mor- tification." 196 PNEUMONIA. variously stated by different observers1 in the proportions of 5 to 3 or 7 to 4. This predominance of the right side over the left exists from the earliest infancy, but diminishes somewhat with advancing age.2 The same relative proportions obtain equally for both sexes. The lower lobe is affected more fre- quently than the upper in both lungs col- lectively in the proportion of about 3 to 2.3 The proportion remains nearly the same for childhood4 and adult age ; but in more advanced periods of life there is a great tendency to invasion of the upper lobes. This proportion, however, accord- ing to Dr. Stokes, varies from year to year and it appears also to be sometimes influenced by epidemic causes, rendering the upper lobe more liable to suffer than the lower. In relation to the lung affected, Pneu- monia of the upper lobe is singularly more common in the right than in the left lung,5 and with a relative frequency which is greatly in excess of the proportion ob- served in the affections of the two sides, when considered independently of the locality of the inflammation. The middle lobe of the right lung is still less frequently affected. Dr. Walshe states that Pneumonia having this site is usually either the result of endocarditis, or that it depends on blood-poisoning. Double Pneumonia is comparatively much less frequent than the unilateral affection, except in the case of Broncho- pneumonia.1 The liability of old people and children to this form of the disease has, however, led to an exaggeration of the fre- quency with which both lungs may suffer. It is comparatively rare that both lungs are attacked simultaneously, and the in- vasion of one is commonly secondary in point of time to that of the other. No difference appears to exist in the relative liability of either side to be followed by the attack in the opposite lung. The Mode of progressive Extension of the disease is usually direct from the site first implicated. Exceptions to this, however, occur when the opposite side suffers sub- sequently, and also sometimes when the upper lobe is invaded after the disease has commenced in the lower lobe of the same side. It is also not very uncommon in fatal cases to find disseminated nodules of pneumonic change, varying in size from a hazel-nut to a walnut, scattered irregu- larly around, and sometimes at a consid- erable distance from the larger mass, and separated from it by apparently sound, or sometimes by unduly hypersemic tissue. The Eate of Evolution of the different stages of the process appears to be very variable. A lung may remain in a con- dition of red hepatization during eight or ten days, or even for some weeks; while in others the condition of gray hepatiza- tion may be found as early as the fourth or fifth day.2 Both Lacnnec and Huss consider the stage of engorgement to last from one to three days; whether it can persist longer than this without producing some consolidation of lung is, however, doubtful. It is not uncommon for twenty- four hours to elapse before the physical signs of consolidation become apparent; but the duration of the stage of engorge- ment may be so short that a large tract of lung may be consolidated within a few hours after the first rigor.3 The duration 1 Huss, of 2616 cases, found 53 per cent, in the right lung, 32 per cent, in the left, and double Pneumonia in 15 per cent. Grisolle, in 1430 cases, collected from various authors, found 742 cases in the right lung, 426 in the left, and double Pneumonia in 262. The latter number he regards as doubtful. 2 Hourmann and Dechambre found in old people the proportionate frequency of Pneu- monia of the right lung to that of the left, as 34 to 27. 3 This is Andral's statement. Wunderlich, in a calculation of 660 cases, from different authors, gives the following numbers : Lower lobes, 397 cases ; upper lobes, 180 cases; af- fection of a whole lung, 83 cases. Grisolle, from a calculation of 264 cases, gives the proportions as-lower lobe, 133 ; upper, 101; middle lobe, 30 cases. 4 Barthez and Rilliet (i. 516) found in 122 cases : Upper lobe, 42 ; lower lobe, 65 ; affec- tion of the whole lung, 3; double Pneumonia, 12 cases. 6 Grisolle states that Pneumonia of the up- per lobe in the right lung is two and a half times more common than in the upper lobe of the left. The observations of other authori- ties show a still more striking difference. Barth states the relative frequency of Pneu- monia of the upper lobe of the right lung to that of the left as 18 to 1; Briquet as 18 to 4; Barthez and Rilliet as 9 to 1. Ziemssen, in 234 cases, gives the following numbers: Right side collectively, 126 cases, upper lobe, 57 ; lower lobe. 55 ; middle lobe, 14. Left side collect- ively, 106 cases; upper lobe, 27; lower lobe,79. 1 The proportion of 15 per cent, given by Huss represents nearly the average frequency of its occurrence, but the smaller numbers of some observers show different ratios. Grisolle states its frequency to be 11 per cent. The Vienna returns for 1860 place it at 5 per cent. Barth, in 125 cases, at 6 per cent. Willigk, on the other hand, loc. cit., found double Pneumonia in 50 per cent. 2 I have seen this in a child under set. 1, when the disease began acutely. Laennec (Forbes' Trans, p. 206) states that the stage of purulent infiltration may be reached in thirty-six hours. 3 Dr. Stokes, loc. cit., p. 120, remarks that in some instances of typhoid pneumonia, there is no evidence of an antecedent stage of engorgement, but that of the lung may be- come solid without any crepitant rale pre- ceding this change. He further observes, however, that this rapidity of progress is not common in the sthenic forms of the disease. THE PATHOGENESIS. 197 of the stage of red hepatization was stated by Laennec to vary from one to three days, and of suppuration from two to six days. Huss reckons the former as lasting from five to seven days. The periods of resolu- tion have been already referred to. The termination in abscess or gangrene usually occur at later periods; but even the latter, as has been already stated, may be found very early in the course of the disease. The Pathogenesis of acute primary Pneumonia is involved in considerable obscurity, and has been the subject of much discussion.1 Two opposite theories have been advanced respecting its origin, both of which are supported by certain facts and are opposed by others. These theories may be briefly stated in the following terms :- (1) That Pneumonia is a " specific " fever, of which the disease in the lung is only a local effect. (2) That it is a purely local disease, of which the pyrexial and other phenomena observed are only the immediate conse- quences. The second hypothesis, as such, appears to be scarcely a tenable one, and even the first appears to require some modification. The arguments in favor of the first hy- pothesis are mainly derived from the com- parative rarity of discoverable causes for the origin of Pneumonia,2 and from the suddenness of the crisis while the inflam- mation is still at its height. The question of the mode of origin of the disease has been already considered under the head of etiology. It appears, however, deserving of remark that the theory of a "specific" cause can scarcely be maintained for Pneumonia in the same sense as that in which the term is em- ployed for the contagious pyrexial dis- eases. The causes of Pneumonia are manifold, and the disease may originate under such diverse conditions, that it seems impossible to attribute it to any single blood-poison. On the other hand, the most probable hypothesis to explain its origin is that of an altered composition of, or the existence of some morbid material in, the blood, which from its special qualities may affect a particular organ, or, as is more probable, may, under local predisposing causes, ex- cite inflammation in that part of the sys- tem which in any given individual is the most liable to suffer as a locus minoris re- sistentice. It is not improbable that some of the antecedent symptoms, the malaise, the pains in the limbs, the headache, and the slight jaundice occasionally observed, may be due to the blood alteration; but it must be remembered, that in a not inconsider- able proportion of cases, the outbreak of the pneumonic fever is sudden, without being preceded by any of these prodro- mata. The nature of the alterations in the blood capable of producing the dis- ease are, like those of all other sponta- neous inflammations, entirely unknown; and the hypothesis of an antecedent con- dition of hyperinosis advanced by Nau- mann1 seems to be disproved by some of Zimmermann's analyses. It would ap- pear indeed from these that the excess of tibrine observed in the blood of pneumonic patients is almost entirely a secondary phenomenon, and that it is, as Virchow affirms, a consequence and not a cause of the inflammatory process in the lung.2 1 Ergebnisse und. Studien aus der med. Clin, zu Bonn, 1858. Naumann has afforded no direct proof of an increase of fibrine in the blood antecedent to an attack of Pneumonia. He says, however, that symptoms resembling the prodromata of Pneumonia are sometimes associated with hyperinosis. 2 Thus, in " Prager Vierteljahresch," 1852, vol. xxxv., in a patient bled, after signs of the stage of engorgement had lasted five days, the blood contained only 1'13 per 1000 of fibrine. In a venesection practised 36 hours later, and when signs of consolidation had supervened, the fibrine amounted to 4'41 per 1000, and in a third venesection practised after 6 days it had risen to 7'16 per 1000. Zimmermann argues further, that this rapidly increasing quantity of fibrine in the blood, in the later stages of Pneumonia, is not due to venesection, for in other cases bled for the first time on the third, fourth, and eighth days respectively the fibrine amounted to 7'2, 8'0, 9-1, and 9'6per 1000. Also in "Analysedes Blutes," p. 370, he has, as the result of more extended observations, found that in eight cases of commencing Pneumonia the blood contained either a normal or a less than nor- mal amount of fibrine. In eight other cases where venesection was practised within the first 24 hours, the proportion of fibrine was between 3 and 7'5 per 1000, and in eight other cases, the blood in the second 24 hours of the disease contained fibrine varying from 3 to 7'5 per 1000. Zimmermann's method of analysis leads him to estimate the amount of fibrine in the healthy blood as lower than that given by many observers; but this only adds strength to his estimate of the propor- tion observed in inflammatory diseases. He places it at 1'689 per 1000 (loc. cit. p. 17), while Becquerel and Rodier estimate it at 2'5, and Andral and Gavarret at 3 per 1000. The increase of fibrine in the blood during the progress of Pneumonia is abundantly 1 See especially on this point a clinical lec- ture by Dr. Parkes, Medical Times and Ga- zette, 1860, i. 187. 2 It has already been stated (see Etiology) that experimental attempts at the production of a disease resembling acute primary Pneu- monia by direct irritation of the lung, have invariably failed. 198 PNEUMONIA. The theory of hyperinosis as a cause of Pneumonia has also but little support in the diseases with which it is commonly associated, for though it is a not uncom- mon complication of acute rheumatism, in which this condition of blood is present, it also occurs in other diseases when the amount of fibrine is below the normal standard,1 and in some of these, as in ty- phoid fever, the supervention of pneu- monia increases the proportion of fibrine in the blood.2 It would appear from the consideration of the various diseases with which Pneu- monia may be associated, that many, and probably different, blood-poisons may have the power of exciting inflammation of the lungs. That the lungs should be especially lia- ble to become affected by causes of this nature cannot be regarded as extraordi- nary, when we consider the importance of their functions as purifying agents of the blood. Nor does it seem improbable, from the complexity of the lymphatic structures which they contain, that other changes in the composition of the blood, in addition to its mere aeration, may be accomplished by their means, though of the nature of these changes we are as yet ignorant. The lung, from its embryological de- velopment and anatomical characters, is closely allied to the glandular organs, and it is on these that blood-poisons produce their most marked effects. It is further to be noted that other organs of this class are not unfrequently simultaneously af- fected. The frequent association of albu- minuria with Pneumonia can scarcely be regarded as a mere accidental complica- tion, and it is by no means improbable that the kidneys are, under these circum- stances, implicated by the same cause as the lung. Other glands also occasionally suffer, as the parotid: gastro-duodenal catarrh and some degree of affection of the liver are also frequent complications. In addition to these the serous mem- branes tend also to become implicated as part of the primary disease, and when these relations of Pneumonia are regarded as a whole, it appears that those organs are most likely to suffer which are ihost commonly affected by recognizable condi- tions of blood-poisoning. The fact that cases of Pneumonia presenting these com- plications are more severe and dangerous than the simple disease, would also tend to show a greater intensity of the primary cause, for their mortality is dispropor- tioned to what might be expected (par- ticularly in cases where parotitis is pres- ent) from the mere existence of these inflammations, if regarded as purely local disorders. The argument is still further strengthened by the profuse sweating which often attends Pneumonia, and also by the frequent co-existence of herpes, which is so commonly associated with dis- ordered blood-states. In some cases Pneumonia indeed is known to be caused by recognizable con- ditions of this nature, as by septicaemia, but in the case of the acute primary dis- ease it is most probable that the poison is one engendered within the system. In the cases where a discoverable cause ex- ists, such as a chill, it is probably due to retained products of secretion injuriously affecting the composition of the blood. It is also not improbable that Pneumonia secondary to uraemic poisoning may have a similar origin ; while in the cases'where no discoverable cause exists, we only stand, as has been already remarked, in the same position with respect to Pneu- monia as we do to other idiopathic local inflammations. Whether the blood-poison is eliminated by the exudation process must remain a matter of hypothesis, though the sudden cessation of the pyrexia when this stage has advanced to a certain degree would appear to lend some support to this view, and particularly when we remember the analogy, and even the various phases of transition, which exist between exudative and secretory processes. The sudden outbreak of the pyrexia occurring simultaneously with the super- vention of the inflammatory changes in the lung would, however, appear to show that the implication of the nervous sys- tem indicated by the fever is largely due to the alteration of the composition of the blood produced by the local process. We have no evidence of any distinct altera- tion antecedent to this, and much that a large proportion of the subsequent changes in the blood are due mainly to this cause. All local inflammations produce in this confirmed by other observers. Thus Andral (Ess. Hsem. Path. p. 87), in 90 cases, found in 7 cases fibrine 4-5 per 1000. 17 " 5-6 " 19 " 6-7 " 15 " 7-8 " 17 " 8-9 " 9 « 9-10 " 6 " 10 and upwards. The largest amount in Pneumonia recorded by Andral is 10-5 per 1000, and Zimmermann (loc. cit. p. 13) also found 10 per 1000. 1 I have already advanced reasons for doubting whether the Pneumonia which is secondary to many of these diseases differs essentially in anatomical characters from that of the acute primary disease. The firmness of the exudation varies in degree, but this may be influenced by the nature of the dis- ease to which it is secondary. 2 Andral, Ess. Hsem. Path. 17. PATHOLOGY. 199 respect similar results,1 and it is interest- ing to remark that the pyrexia following a purely traumatic Pneumonia may have the same typical course as is observed in that of idiopathic origin.2 That the in- tensity of these blood alterations, and particularly the increase of fibrine, should be so especially marked in Pneumonia, and may in part be referable to the pecu- liar relations of the organ (to which refer- ence has been already made), is very probable. Pyrexia per se, independently of local inflammations, has not, except in the case of acute rheumatism, any marked proclivity to the production of hyperino- sis. The large excretion of urea during the height of the pyrexia and its diminu- tion during the progress of resolution (even where effete materials from the lung must continue to be absorbed into the blood), conclusively show that this phenomenon is due to increased tissue- changes throughout the system, produced probably by perverted nervous action, and which are only secondarily referable to the process in the lung. The increased destruction of red blood-corpuscles shown by the simultaneous increase of pigment in the urine, is perhaps referable to both the general and local conditions, since it frequently persists after the excess of urea has ceased to be observed. Zimmermann has further remarked that the decrease in their number, noticed by Andral and Ga- varret, may be due not only to this cause, but to a subsequent defective formation arising from the abnormal conditions un- der which the white corpuscles are formed during the process of local inflammation and in the pyrexial period. The disorder which on a lesser scale presents the greatest analogy with acute Pneumonia is perhaps acute tonsillitis, where we have the same short initial state, a similar intensity of rigor and prostration, a similar sudden invasion of pyrexia, and a similar rapid decline of this before the local inflammation has shown any signs of abatement. In ton- sillitis also we have frequently an equal difficulty with Pneumonia in verifying a distinct cause, and a certain amount of evidence at least exists in the case of the so-called "hospital sore throat," that it may also be produced by other poisons than those originating within the system from the impeded exercise of the functions of the skin. The associated Pathology of Pneu- monia has been already almost sufficiently described under the complications of the disease. A few points only deserve fur- ther attention. In the Lungs themselves.-The mucous membrane of the bronchi is more or less injected, but the tubes seldom present much evidence of the dilatation observed in broncho-pneumonia. Plastic exuda- tions, moulded to the shape of the tubes are very common in the smaller bronchi. In some cases, however, this process may extend to the larger bronchi, which may be found thus obstructed through consid- erable areas.1 Acute Emphysema is sometimes observed in parts adjacent to the hepatized por- tion. (Edema surrounding the consolidated part is more common, and may, by its extension and by its appearance on the opposite side, prove a source of much danger to life. The Bronchial Glands are usually swol- len and medullary in appearance. They are only in the worst instances subject to suppurative changes. The Pleura is almost invariably in- flamed when the hepatized part is situ- ated at the surface of the lung. Effusion is, however, less common than the forma- tion of false membranes. In the Heart the complication of peri- carditis has been already alluded to. In some cases this is due apparently to direct extension of the inflammation, for it is most common when a part of the left lung in juxtaposition with the pericardium is the seat of the Pneumonia. It appears, however, to arise sometimes under cir- cumstances inexplicable by this cause, and it may then, according to the date of its appearance, be held to be due to the same cause as that in which the Pneumo- nia originated, or to the secondary blood- poisoning2 caused by the absorption of the inflammatory products from the lung. The right side of the heart is usually in fatal cases found distended and contain- ing large and firm clots. Bouillaud3 thought that Pneumonia predisposes to ante-mortem polypoid concretions, and this opinion is confirmed by Hasse,4 who adds that he has found secondary infarcta in the spleen from this cause. One of the most important consequences of Pneumonia on the circulation is the occasional occurrence of thrombosis in the pulmonary vessels leading to the affected part. This event, caused in all probabil- * This condition appears to have heen first described by Reynaud, M&n. oblit. des Bronches, Arch. Gen. de Med. 1835, iv. p. 157. 2 Parkes, loc. cit. s Traite Clin, des Maladies Du Cceur, ii. 716. 4 Loc. cit. 214. 1 See Andral, loc. cit. ; also Zimmermann, Arch, der Phys. Heilk. 1848. 2 See an interesting case from Mr. Hilton's practice, Medical Times and Gazette, 1867, i. p. 144, where Pneumonia supervened after a broken rib. The temperature rose abruptly to 103°, and fell by crisis on the seventh day. 200 PNEUMONIA. ity by the retarded circulation in the lung,1 is not uncommon, and may, by ex- tending to the larger branches of the pul- monary artery, be a source both of imme- diate danger from sudden death, and may also, in great probability, retard the pro- cess of resolution and the subsequent con- valescence. Catarrh of the Gastro-intestinal Mucous Membrane is by no means uncommon. The characters of the appearances found have been already described in the section devoted to diseases of the stomach. In some instances, however, this proceeds to a more serious stage by producing dysen- teric ulcerations of the colon.2 Hemor- rhage from the large intestines and stom- ach have been described by Barthez and Rilliet.3 The Liver is found congested, and the gall-bladder occasionally distended, but, even when icterus has been present, there may be no demonstrable obstruction of the ducts. The Spleen is commonly congested, soft- ened, pulpy, and opaque; characters which it presents after death in most of the acute febrile diseases. The Brain rarely shows any other change than congestion ; but in a few in- stances, when delirium has been violent, there has been found purulent infiltration of the subarachnoid space on the con- vexity of the hemispheres, and also of the base, which may also extend to the mem- branes of the cord. In many cases of delirium, however, the brain is found per- fectly healthy.4 The influence of primary Pneumonia in the production of other diseases appears to be but slight. That any permanent effect is produced on the heart appears to be disproved by Grisolle's statistics. Nor does the occur- rence of Pneumonia, in the course of a cardiac disease already existing, appear to have any specially unfavorable effect upon the cardiac state. Its effect on tuber- cular patients appears, however, to be more doubtful. It is perfectly true, as Dr. Walshe has stated, that patients with tubercles already formed in the lungs may recover rapidly and completely from intercurrent acute Pneumonia, and Gri- solle found that twenty-two patients of tubercular diathesis affected with Pneu- monia all recovered perfectly.1 In some cases, however, of tuberculosis, the con- valescence is protracted and the cure im- perfect, and in others the inflammation of the lungs tends to be followed by rapid softening and cheesy change. In fact, intercurrent Pneumonia must always be regarded as one of the greatest dangers of tubercular patients. Resolution is im- perfect-the affected parts tend to pass into gray consolidation, and in such parts fresh formations4 of tubercles rapidly form and disintegrate. Diagnosis.-The diagnosis of the ex- istence of acute Pneumonia essentially depends on the recognition of an acute febrile disease associated with the physi- cal signs of consolidation of a portion of the lungs. Without this combination its presence cannot be affirmed with certainty in the earlier stages, though it must be remembered that patients may first come under observation at later periods, pre- 1 Virchow, Ges. Abhand. 222. It appears first to have been described by Baron, Arch. Gen. 1838, ii. 17, who first had the merit of distinguishing this event from the effects of inflammation of the coats of the artery. Mal- herbe, Journ. de Nantes, 1843 (Constatt's Jahresb. 1843) first referred it to the retarded circulation. See also Mr. Paget's Memoir on this subject, Med.-Chir. Trans, xxvii.; Cars- well, Hlust. Prine. Forms of Dis., art. "Mor- tification;" Cruveilhier, Path. Anat., liv. xxxii. p. 2, who distinguishes the site of the coagulation as being in the artery, and not in the veins. 2 The result of Dr. Bristowe's observations on this subject (Path. Soo. Trans, viii. 66) have led him to regard dysentery as a very common complication of Pneumonia. Out of 16 cases of acute primary Pneumonia proving fatal, he found dysenteric ulceration of the large intestine in four. The possibility of some epidemic influence may perhaps be re- garded as not improbable in these cases, since the period over which part of Dr. Bristowe's observations extended included one of the recent epidemics of cholera. 3 Loc. cit. i. 352. 4 Grisolle. Louis, Fi^vre Typh. i. 359, ii. 37. Immermann and Heller found that out of 30 cases observed in Erlangen during the years 1866 to 1868, nine presented post-mor- tem signs of meningitis. They attribute this condition in part to the simultaneous occur- rence of epidemic cerebro-spinal meningitis ; Deutsch. Arch, fur klin. Med. v. (Virchow's Jahresb. 1868). Weber (Path. Anat, der Neugeborenen und Saiiglinge, ii. 61) has also found cerebro-arachnitis during an epidemic of Pneumonia. 1 Huss also states, p. 24, that in northern climates acute Pneumonia has very little in- fluence in the production of tubercle. He quotes, however, p. 162, from Gellersted "Bidrag till den Tuberculose Lungostens Nosographie och Pathologie," a statement that of 310 cases of phthisis, 23-5 per cent, had within a longer or shorter period suffered from one or more attacks of Pneumonia. 2 These changes belong, however, more particularly to the history of phthisis ; and their pathology, being in many points disput- ed, would involve too wide a discussion to be entered upon here, since by some authors the process of Pneumonia complicating phthisis is placed in a separate category of " catarrhal Pneumonia," or " infiltrated tuberculosis." DIAGNOSIS. 201 senting the physical signs of consolidation of the lung, but after the initial fever has subsided. It is, however, important that its early stages should be recognized be- fore the signs of consolidation are distinct. Under this head certain phenomena con- nected with the mode of invasion deserve special prominence. Among these perhaps the most import- ant and constant is the pyrexia, which, although not pathognomonic, still presents very marked and distinctive features, and is so invariable a symptom that the diag- nosis of Pneumonia during the acute stage can scarcely be made in its absence. Whether or not the invasion be preceded by rigors, the sudden rise of temperature in a subject, previously non-febrile, should always excite suspicion, and it may be re- marked that this rise of temperature may precede by hours, or even days, the ap- pearance of the distinctive physical signs in the lungs. The use of the thermometer is also often a mode of recognizing the invasion of Pneumonia when its symptoms are obscure, and appearing in the form of vomiting or convulsions in children, or of the prostration with which it often com- mences in old people. The rise of tem- perature in most of the acute febrile diseases is commonly gradual; in Pneu- monia it is sudden, and maintains a higher elevation, during the first forty- eight or seventy-two hours, than is com- monly seen either in these or in tubercular meningitis.1 The other phenomena of invasion which are most distinctive are the acceleration of respiration and the perversion of its ratio to the pulse. If to these and to the pyrexia are joined cough, rusty sputa, and pain in the side, the diagnosis of Pneu- monia becomes one of infinite probability. Of the last-named symptoms, the relative acceleration of respiration is perhaps the most valuable, if, as Dr. Walshe remarks, hysteria be excluded, since expectoration may be absent, both in adults and chil- dren, or in the former the blood-stained tint may be wanting, and on the other hand, appearances of a very similar character to those seen in the first stage of Pneumonia may sometimes be observed in the sputa accompanying cardiac disease, and also in the early stages of congestive bronchitis. It may be noted, however, that in the last-named diseases fever may be entirely absent, or if present in bron- chitis, the elevation of the temperature is rarely so considerable or so sudden as in the commencement of Pneumonia. The distinctive features presented by the physical signs have been already fully described. When, however, in the com- mencement of the disease the inflamma- tion first attacks the central parts of the lung, the signs of consolidation may be masked by healthy pulmonary tissue nearer the surface. Under these circum- stances harsh breathing or weakened respiration may be the only phenomena observed. Crepitation, when present, and when the possibility of (edema and of pulmonary apoplexy are excluded, is a valuable aid ; but it is not unfrequently absent, and con- solidation may take place so rapidly that it may not be heard in the earlier stages. As a rule it only furnishes further grounds for suspicion, until dulness on percussion, bronchial or tubular breathing, and bron- chophony are established. The chief fal- lacy attending percussion is the occasional production of a quasi-tympanitic note over portions of lung, below which deeper- seated consolidation exists.1 A compari- son of the two sides is, however, in chil- dren, often indispensable. Percussion of the chest of children should also be gently practised for reasons which I have already stated. The superaddition of the auscultatory phenomena of the breathing and voice, and the increase of vocal fremitus over the affected part, if occurring collectively, render the diagnosis absolute ; and as this combination of phenomena is the most frequent, Pneumonia may commonly be recognized with facility. In exceptional cases, however, varia- tions in these signs occur, which require some care in the diagnosis, particularly when one or more of them are wanting. This is sometimes the case in central Pneumonia, when the respiration may re- main harsh or blowing, and crepitation and bronchophony may be absent. In some of these cases the diagnosis of Pneumonia can only be of relative value, depending on the presence of the charac- teristic pyrexia accompanied by rusty sputa. The diseases of the lungs with which Pneumonia is most likely to be confounded are pleuritic effusion, oedema of the lungs, collapse, and certain forms of acute phthisis. The question of the diagnosis of Pneu- monia from pleurisy with effusion only occurs when the former affects the base of the lung or the whole organ. In typical instances of the two diseases, the distinctive physical signs may be briefly contrasted as follows: In Pneu- monia the affected side is not distinctly bulged, and the intercostal spaces are not obliterated. Neither displacement of the 1 Children are, however, liable to such sudden elevations of temperature from very slight causes, so that less reliance can be placed on this sign in them than in adults. 1 The tubular note over the larger bronchi may, however, sometimes prove deceptive to beginners. 202 PNEUMONIA. heart, nor liver, nor diaphragm are ob- served. The dulness does not encroach upon the opposite side, or only to a very moderate degree. The dulness is less absolute than in pleuritic effusion, and has often a tubular tone. It does not change its site with the position of the patient, and the percussion note over the upper non-affected parts, though some- times tympanitic, is never tubular or amphoric. The respiration over the af- fected parts is marked by a bronchial, or tubular, or metallic quality. The vocal resonance is strongly broncnophonic, and the vocal fremitus is increased. Crepita- tion may be heard in forced breathing or coughing. In pleuritic effusion the side is bulged and increased in diameter, the intercostal spaces are obliterated and may even be prominent, and fluctuation may some- times be perceived over them. Displace- ment of the heart or liver, according to the side affected, is proportioned to the extent of the effusion. When this is ex- tensive the dulness also encroaches on the opposite side. The percussion note is toneless, the sense of resistance is great. A tubular note, as observed by Dr. Walshe, is sometimes producible under the clavi- cle. In some instances the level and seat of dulness change with the position of the patient. The respiration below the level of dulness is weakened or absolutely sup- pressed. Weak, bronchial, or blowing breathing is heard near the spine and over the compressed lung. Vocal fremi- tus is diminished or abolished. Vocal resonance is also abolished below the level of dulness, and it is bronchophonic or segophonic towards its limits. Friction may or may not be present. Difficulties may, however, occasionally arise from exceptional combinations of the phenomena presented by each of these diseases. In the rare instances when, in Pneumonia, there are found, together with dulness on percussion, a simple absence both of the respiratory murmur and of bronchophony and fremitus, the most ac- complished observers have been led into the error of mistaking the condition for one of pleurisy with effusion.1 The signs which best distinguish Pneumonia under such circumstances, are the absence of the enlargement of the side of the oblite- ration of the intercostal spaces, and of the displacement of the various viscera, which characterize extensive effusion. Variation of the percussion dulness with the position of the patient, may, if observ- able, serve as a further aid if pleurisy be present, though its absence cannot always be relied upon for the exclusion of this affection. As a sign of minor value, it may be stated that the percussion note is more absolutely toneless in pleurisy, and seldom, if ever, has the higher pitch of that observed in Pneumonia. The tubu- lar or amphoric note over the upper part of the lung sometimes heard in pleurisy is not, as observed by Dr. Walshe, met with in the non-affected upper portions of the lung when Pneumonia exists at the base ; the percussion here, though hyper-reso- nant, being commonly of a lower pitch, and sometimes tympanitic in quality. The invasion of the pyrexia is commonly less acute, and the temperature less ele- vated in uncomplicated pleurisy.1 It is, however, an event of the extremest rarity that the absence of respiration and the diminution of the vocal fremitus and re- sonance are, as a matter of practice, found to coexist simultaneously over a pneumo- nic lung. In doubtful cases, the fremitus may aid in distinguishing the two diseases, being increased in most cases of Pneumo- nia and diminished in pleuritic effusion. In children, and when in adults and fe- males the voice is weak, this sign may be comparatively indistinct. In the cases of pleuritic effusion, where bronchial breathing and bronchophony persist, the diagnosis from Pneumonia may also commonly be made by the signs above enumerated. The fremitus may be a further guide,2 and, as Dr. Walshe has remarked, the true tubular respiration of Pneumonia is wanting in pleurisy, and the indistinct bronchial breathing heard is most commonly met with near the spine. (Edema of the lungs, which may be at- tended by the crepitant rale of Pneumo- nia, may commonly be distinguished from it by the absence of pyrexia, by the minor degree of dulness, by the respiration being simply weak, and by the concomitant affections in which it originates. The diagnosis of simple Pneumonia from acute phthisis when the latter is only attended by the disseminated formation of miliary tubercles, is comparatively 1 This sign is of minor value in relation to cases of Pneumonia of moderate severity, and when the temperature does not rise above 1020. it should also be remembered that the Pneumonia may come under observation for the first time after the fever has subsided. Under these circumstances the diagnosis from pleuritic effusion may depend on the physical signs alone. 2 Dr. Walshe, however, states that fremi- tus may be diminished in extensive hepatiza- tion, though not to the same extent as over an equal amount of effusion. He adds that he has often known fremitus feeble, and vo- cal resonance strong over effusion, but that he has never met with this combination in hepatization. The value of these signs in diagnosis depends on their combination, and but little reliance can be placed on either singly. 1 See Barthez and Rilliet, i. 589 ; also Win- trich, before quoted. DIAGNOSIS. 203 easy, owing to the absence of dulness in percussion in the latter affection. When, however, acute tuberculosis is attended by, or commences with, a rapid and ex- tensive pneumonic infiltration, the diag- nosis may be almost impossible during the early stages of the affection. This, however, is less common in acute phthisis than a more gradual extension of the pneu- monic process, which usually takes place irregularly and through longer periods than are observed in primary Pneumonia. The pyrexia of acute phthisis is more irregular in its course; it has more marked remissions than those of Pneumonia, and the exacerbations often occur at very varying periods of the day, the maximum temperature being attained on one day in the morning and on another in the even- ing-a phenomenon of the extremes! rar- ity in primary Pneumonia. Much de- pends on the time at which the case comes under observation. If at a later period than the first ten days, the protraction of the pyrexia may always be regarded as a suspicious circumstance. If the fever is very irregular in its course, and acute ex- acerbations with very marked remissions occur at uncertain intervals, the suspicion is still further strengthened, since in most cases, when the pyrexia of a simple Pneu- monia is retarded in its final disappear- ance, the fever maintains as a whole a low standard, and subsequent elevations of temperature to 103° or 104° are very rare. Pneumonia of the apex, running such a course, is still more open to suspicion than that affecting the base of the lung. If, in addition to these symptoms, signs of the formation of cavities become in- creasingly apparent, the grounds for an unfavorable opinion are still further strengthened, though doubts may still exist, owing to the possibility of the for- mation of abscesses in the hepatized tis- sue. Evidences of progressive disease in other parts of the lung at a late period of the case are still more serious symptoms ; and the implication of the opposite side, particularly if general rales appear here accompanied by irregular spots of con- solidation, and by signs of destruction of tissue, will, together with the conditions of pyrexia before alluded to, and in conjunc- tion with rapid emaciation and other signs of hectic, render the diagnosis of tubercle almost a certainty. Louis be- lieved that implication of the anterior and superior parts of the lung, without the invasion of the whole apex, was almost certainly an evidence of tuberculosis, but this statement, though affirmed by Barth and Boger, is disputed by Grisolle.1 The diagnosis from Collapse of the lung will be considered under the head of Broncho-pneumonia. There are certain other diseases with which acute Pneumonia is occasionally- confounded. The sudden prostration, with severe headache and high degree of pyrexia at the outset, not unfrequently simulate Typhus; so much so that from the reports of the different fever hospitals it would appear that a certain number of cases of Pneumonia are annually sent to these institutions under this error. Even in the earlier periods the mistake both from ty- phus and typhoid may be avoided, as Dr. Grimshaw has remarked,1 by the observa- tion of the temperature, which rises sud- denly in Pneumonia, but in the continued fevers rarely attains its maximum before the sixth or seventh day. At the later periods the physical signs of consolidation of the lung on the one hand, and on the other the appearance of the characteris- tic rash of the continued fevers, are suffi- cient to prevent mistakes. The existence of herpes may also serve as a clue to the nature of the affection, being very com- mon in Pneumonia, while it is scarcely ever met with in the course of the con- tinued fevers. Pneumonia commencing with cerebral symptoms in children may be easily over- looked, particularly when it affects the apex of the lung. Ziemssen has remarked that tubercular meningitis rarely gives at the outset the high temperature of acute Pneumonia. The remissions are also more marked. They are more variable in their extent, sometimes showing a range of tempera- ture of 1'8°, 2°, or even 3° Fahr., and the pyrexia is less continuously main- tained. Some differences also in the character of the nervous symptoms have been already alluded to. The diagnosis of the different forms of consolidation rests upon no absolutely reli- able signs. The stages of gray hepatization and of suppuration of the lung cannot be deter- mined absolutely by the duration of the disease. The prune-juice diffluent sputa, which were thought at one time to be charac- teristic of the former, have been shown to be by no means pathognomonic of this state, though their appearance affords strong ground for suspecting its presence. It may, however, be strongly suspected when the amount of sputa is much in- creased, and when, instead of being rusty j and tenacious, they become profuse, dif- fluent and puriform, and still more so when they are fetid and offensive. Pro- 1 Dr. Walshe also affirms that Pneumonia having this position is commonly, but not al- ways, tuberculous (loc. cit. p. 497). 1 See Dr. Grimshaw, Thermometric Obser- vations on Pneumonia; Dublin Quart. Journ., May, 1869. 204 PNEUMONIA. traction of the period of resolution, at- tended by coarse metallic rales in the chest, and by extreme prostration, pyrexia and delirium, afford, together with the signs derived from the sputa, additional evidence of this condition of the lung. The diagnosis of abscess can only be made when the expectoration of puriform matter is sudden and copious. The de- tection of elastic fibres in the sputa affords a further proof of its existence. Gangrene can only be suspected when great prostra- tion, together with extreme fetidity of the sputa, occur late in the disease; the only positive proof of its existence de- pends on the discovery of debris of the pulmonary tissue in the sputa, but in these, elastic fibres are seldom distinct. The Prognosis of Pneumonia in rela- tion to its general mortality has proved to be the same insoluble problem that An- dral1 pronounced it, when he drew atten- tion to the fact that the death rate in dif- ferent statistics varied from 33 to 2 per cent. The difficulty has, however, still further increased in later years by the varying and contradictory statistics of the result of the different methods of treat- ment adopted for the disease. The re- sults attained by Dr. Bennett,2 who in 129 cases, of which twenty-four were com- plicated, had the good fortune to see all recover except four which presented serious complications, are so singularly favorable that they might lead us to regard the dis- ease as less dangerous than it sometimes proves to be. Even in young male sub- jects of previously good health, Pneumo- nia may, as I have seen, sometimes falsify the hopes entertained from the relatively small mortality of such cases; and my own hospital experience has yielded a much greater proportion of fatal results than Dr. Bennett's, though the general methods of treatment have been very similar to his. In fifty-five cases which I have observed or collected from the case- books of University College Hospital, and the North Staffordshire Infirmary,31 have met with eight deaths, but in all these the attendant circumstances of the disease were such as fully account for the mor- tality. One was in an infant of five months, in whom the whole of one lung had passed by the fifth day into a state of gray hepat- ization. One was in a young female, where the Pneumonia was apparently developed under the influence of some intense blood- poisoning, being complicated with paro- titis occurring on the ninth day, and where there were also albuminuria, peri- carditis, and constant vomiting, dysenteric diarrhoea, and a petechial eruption under the skin, which latter in some places passed into large vesicles filled with a dirty-looking blood-stained serum, and where also disseminated spots of a gan- grenous character were found in both lungs. In two other cases there were old-stand- ing renal disease and recent pericarditis. In one, an old woman, the bronchi were calcified, and there was extensive pleuritic effusion on the opposite side and throm- bosis in the pulmonary artery. Two others also presented extensive double Pneumonia : in one, a man aged 60, there was also an adherent pericar- dium and a fatty heart. The other, a young man, had been a hard drinker, and was suffering from syphilis. In the remaining case there was also general bronchitis with emphysema, and the whole of one lung was in a state of gray hepatization. Pneumonia, when extensive, certainly carries with it conditions which may prove fatal whatever the treatment adopted. It may kill by the intensity of the cause in which it originates, or by the secondary lesions to which this may give rise, particularly in the pericardium and in the kidneys. It may prove fatal by asphyxia, especially when the affection is double, or is complicated by old-standing emphysema, by extensive general bron- chitis, by oedema of the lung, or by pleu- ritic effusion of the opposite side; and finally, and particularly in elderly people of weak constitution, death may take place in spite of the most energetic restor- ative measures, and when no previous lowering treatment has been adopted, in the prostration following the crisis, which may pass into fatal collapse. It must be remembered, also, as stated under the etiology of the disease, that the mortality varies greatly in different years under the same methods of treatment. This is seen markedly in Huss's statistics, where, under an "antiphlogistic" treat- ment, the relative numbers of 9T and 14T per cent, may be observed; and after this plan had been abandoned the mortality in different years may yet appear as 6T and 13*4 per cent. The returns from the Julius Hospital of Wurzburg1 for the tri- ennial periods of 1854-7 and 1857-60 show a similar difference ; the mortality in the former period being 11*2 per cent., and in 1 Cours, de Path. Mdd. 1836, i. 386. 2 The Restorative Treatment of Pneumonia, 1866. A very similar result is recorded by Dr. Waters, Dis. of Lungs, p. 87, who in forty-four uncomplicated cases only met with one death. 3 I do not present these as statistics of these hospitals, as I cannot feel sure that they em- brace all the cases admitted. 1 Bamberger, Wien Med. Woch. 1857, No. 5 ; Roth, Wurzb. Med. Zeit. i. Nos. 3 and 4. PROGNOSIS. 205 the latter 18'9 per cent., the conditions of treatment in both periods being very simi- lar. Brandes,1 in Copenhagen, found the mortality in two successive years vary to the degrees of 5'4 and 31-0 per cent. The same fact is borne out by the returns of the Registrar-General before alluded to. The most important etiological condi- tions which influence the mortality of Pneumonia are the age of the patients, their previous health and habits of life, their sex, the extent of the disease, and, to a less extent, its seat and the existence of complications. Age.-It was formerly thought that the Pneumonia of infancy and childhood was an excessively fatal disease,2 but these statements rested probably in the first place on the confusion between Pneu- monia and collapse of the lung, and in the second in no small measure on the severe antiphlogistic treatment then adopted. Strangely in contrast with this belief is the remark by Barthez and Ril- liet, that the opportunities for post-mortem examination in the acute lobar Pneumonia of children are excessively rare.3 The statistics of Ziemssen and Steffen bear out these assertions. The former, out of 201 cases of Pneumonia in children, only lost seven in the acute stage. In four others the recovery was imperfect, and two of these died, giving a total mortality of less than 4£ per cent. Steffen, in 94 cases, lost 13.4 It would appear from his tables that the mortality is greatest in early childhood, since nine of these were under three years of age. The period of dentition, though showing from the results of Stelfen a greater mor- tality than the later years of childhood, does not in Ziemssen's opinion unfavor- ably influence the prognosis, if all lowering treatment be withheld. This state tends, however, to be accompanied by a higher degree of pyrexia and by more severe cerebral symptoms. After the period of childhood the mor- tality remains comparatively low until the age of 30 is attained, but after this it ra- pidly advances with each succeeding dec- ade;1 so that Mark D'Espini's statement may be regarded as approximatively true, that in more than half the patients dying of Pneumonia the age exceeds 50 ;2 while Prus showed that in 129 cases whose age exceeded 60, 77-or 59 per cent.-died,3 and Hourmann and Dechambre4 give a nearly equal proportion. Sex.-Pneumonia is a more fatal dis- ease to females than to males. Huss gives the relative mortality as, males 10 per cent., females 14 per cent. The re- turns from Vienna show the mortality to be as 2 to 3 in the male and female sexes, so that although Pneumonia is a less common disease in the female sex it is proportionately considerably more dan- gerous. The disease also in the female sex appears to be more protracted, show- ing an average duration of three days in excess of that observed in the male, in the cases which recovered. Females are also, according to Huss, more liable to double Pneumonia than males. His tables also appear to show that the mortality in the female sex is less influenced by age than in the male. 1 Virchow's Archiv, xv. 213. Brandes very properly solves part of this enormous difference by the explanation that the higher mortality was due in the latter instances to the patients with delirium tremens admitted under his care. The number of cases entered in the two years were respectively 55 and 87, and out of the 27 fatal cases in the latter period, 12 were instances of delirium tremens complicated with Pneumonia; five others were cases of typhoid fever with Pneumonia, and in five more, complications with "organic cardiac disease" were present. 2 Thus Valleix (Mal. des Enf. nouveaux- n^s, pp. 45, 47, 70) says, that of 128 cases collected by Vernois and himself, nearly all died. 3 Mal. des Enfants, i. 515. Barthez and Rilliet (ib. p. 535) say that in hospital they lost one-seventh, and in town practice one- eighth of their patients, but this remark ap- pears to apply to primary and secondary Pneumonias collectively. The previous health and earlier treatment of the patients in private practice would appear to be suffi- cient to explain the difference. They dis- tinctly refer the deaths of some of their pa- tients to "poisoning" (sic) by tartar emetic. Barthez (Bull. Akad. Med. 1862, vol. xxvii. p. 676) gives a further report on this subject, stating that among 212 children aged from 2 to 15, the subjects of Pneumonia, only two deaths occurred. 4 Some of Steffen's cases were secondary to measles, scarlatina, and variola. Others were complicated with other diseases. Of his uncomplicated cases, 88 in number, he only- lost 7. 1 Among the mass of statistical evidence on this subject, the following table from Huss (p. 93) gives probably the most reliable data:- Age. No. of cases. No.of deaths. Percentage 5-10 9 1 11'11 10-20 229 14 6-11 20-30 1041 61 5-85 30-40 816 97 11-88 40-50 363 72 19-83 50-GO 127 27 21-60 60-70 29 7 24-13 70-80 4 2 50 2 Ann. d'Hygiene et Med. Leg. 1840, xxiii. p. 50. 3 Mem. Acad. M6d. 1840, viii. 13. 4 Arch. Gen. xii. 28. 206 PNEUMONIA. Certain conditions peculiar to the female sex appear to add to the dangerous char- acters of Pneumonia in them, though these are scarcely sufficient to explain the whole of the relative difference. The condition of pregnancy appears to render Pneumonia peculiarly dangerous. Eight out of 18 cases collected by Gri- solle proved fatal, and this author remarks that abortion is more liable to occur in its course than in that of any other acute dis- ease, with the exceptions of variola and cholera. Pneumonia occurring in the puerperal state has also an extreme grav- ity. Menstruation, according to Grisolle, increases the intensity of Pneumonia oc- curring during this period, though with- out necessarily adding to its mortality. The state of chlorosis, according to Huss, appears in some degree to afford a pro- tection against Pneumonia, but imparts to it when present an element of addi- tional danger.1 The extent of lung affected increases, cceteris paribus, the gravity of the affec- tion in a manner which may be readily understood, though a limited area of in- flammation may, when unfavorable com- plications exist, prove equally dangerous. Double Pneumonia must, a fortiori, be always regarded as a source of very seri- ous danger from the extreme impediment to respiration involved by it, the mortal- ity from this condition being by universal consent regarded as double that of the unilateral disease.2 Pneumonia of the apex was, especially by the authors of twenty years ago, re- garded with peculiar distrust.3 Grisolle states that the mortality in patients so affected, and under 40 years of age, is, when compared with that of the base, as 5 to 3. Louis4 regarded it as one of the elements of the increased mortality in the aged. Barthez and Rilliet speak of it in children as being especially liable to be associated with dangerous cerebral symp- toms. Ziemssen5 also, and Gerhardt, al- though recognizing the comparative fre- quency of nervous disturbance attending Pneumonia of this site in children, do not regard it as being ultimately of unfavor- able augury. Some doubt, however, still exists regarding its specially unfavorable character in adults. The occurrence of gray hepatization is of very unfavorable significance. Huss states that one-third of the patients per- ished in whom its presence could be prob- ably presumed. It usually, at least when occurring early, signifies a more rapid progress of the disease and a weaker re- sisting power of the individual. In the later stages it implies defect in the restora- tive powers which conduce to resolution. Gangrene in the course of acute Pneu- monia is of very serious augury. Of twelve cases occurring in Huss's practice only two recovered. Sestier1 and Briquet2 both thought that Pneumonia was more dangerous in cold seasons. Grisolle disputes the validity of these data, and points out that in Bri- quet's cases a large proportion of the mor- tality was due to the advanced age of the patients, and concludes that season has but little influence in any other respect. Huss's statistics, howrever, show the re- markable fact that though Pneumonia is less frequent in the last half of the year, yet that the mortality during this period is by far the greatest, in the proportion of 17'6 per cent, for the later six months to 12 per cent, in the earlier, while the excess during the last half prevails during each individual month. The contrast is still greater for some months: April, which yielded 355 cases, showing only a mortal- ity of 8*7 per cent. ; while August, with only 113 cases, had a death-rate of 25-6 per cent. The cases occurring during the hot months also presented greater severity, a condition considered by Huss to be partly due to the liability during these to gastro-enteric catarrh, and also to a larger consumption of alcoholic fluids at this season.3 Previous attacks do not per se increase the danger of the disease. The more ad- vanced ages at which later attacks may occur in adults, do, however, somewhat increase their risk. It was at one time thought that Pneu- monia was most dangerous in robust in- dividuals ; but Huss's statistics have most clearly disproved this, and show that the most dangerous forms of the af- fection, both clinically and pathologically, occur in patients of weakened constitu- tions. Of all conditions, however, which, inde- pendently of other circumstances, impart 1 Of twenty-five cases of this complication met with by Huss, five, or 20 per cent., died. 2 See Grisolle, loc. cit. Huss (loc. cit.) gives as the collective mortality - double Pneumonia, 22 per cent. ; right unilateral Pneumonia, 9 per cent. ; left ditto, 7'9 per cent. Huss's tables show further, in respect to age, that while double Pneumonia is most common from 20 to 30, the mortality from it is greatest from 40 to 70. The mortality from double Pneumonia appears to be about equal for both sexes. 3 Chomel, Diet, de M^d. xxv. 158. In 55 deaths he found 13 of the upper lobe, 11 of the lower, and 31 of an entire lung. 1 Rech, sur les Effets de la Saign^e, 42. 6 Loc. cit., 211. ' Chomel, Lee. Clin. M^d., Pneumonie, p. 455. 2 Arch. G6n. de Med. 3e S^r., 1840. 3 The returns from the General Hospital of Vienna show that in some years the mortality is greatest in the winter months. PROGNOSIS. 207 a special danger to the disease, habitual drunkenness must be regarded as one of the most serious. The mortality from Pneumonia under these conditions is nearly double that ordinarily observed, amounting to 20 or 25 per cent.1 The existence of complications forms the most serious element in the prognosis, and most largely influences the mortality of the disease. This is sufficiently appa- rent from Huss's collected results, where the mortality of the non-complicated cases was only 5*79 per cent., while that of the complicated cases amounted to 19'29 per cent. The relative danger of the various complications, as observed by him, will be best seen in the table before quoted (see p. 184). It is, therefore, only neces- sary here to remark that of the most ordi- nary of these the greatest mortality occurs in the presence of endocarditis (75 per cent.); pericarditis (54'5 per cent.); Bright's disease (50 per cent.); old valvu- lar disease of the heart (30 per cent.); tu- bercle (33'3 per cent.); emphysema of the lung (23 per cent.); chlorosis (20 per cent.); and chronic alcoholism and drunkenness (25 and 20 per cent.). The danger is pro- portionately increased if more than one complication occur in the same patient. It may further be noticed that certain complications, such as rheumatism and erysipelas of the face, do not appear un- favorably to influence the general course of the disease, while both bronchitis and pleurisy do so to a less degree than might be a priori believed. An extreme degree of pyrexia is con- sidered by many an unfavorable sign. Wunderlich regards a temperature of 104° Fahr, as the limit of mild cases. It must, however, be remembered that cases may prove fatal in which this tempera- ture is never attained.2 Wunderlich re- gards a gradual rise taking place after the fourth day as a very unfavorable symp- tom.3 The rapidity of the breathing has less influence on the prognosis than that of the pulse, but a very rapid respiration associated with a low temperature is pointed out by Wunderlich as indicative of danger. Irregular respiratory move- ments show a severe implication of the nervous system. Excessive dyspnoea amounting to orthopnoea, particularly when associated with cyanosis, are also indications of considerable gravity. A pulse above 120 always indicates weakened cardiac powers, but its unfa- vorable augury is less in young children than in adults. In the latter, a pulse above 130 or 140 is a sign of great danger, and particularly when the temperature is not markedly high.1 Grisolle says that all his cases died in whom the pulse ex- ceeded 150. Extreme dicrotism of the pulse has a very similar import. It has been already stated that in some cases the pulse may be markedly retarded be- fore a fatal issue. Irregularity and inter- mittence of the pulse except in elderly people, in whom these symptoms are not uncommon, must also be regarded as suspicious symptoms. Few signs can be drawn from the sputa. Those of liquorice or prune-juice tint are the more serious, but do not ne- cessarily indicate a fatal issue. The se- rious import of profuse haemoptysis has been before alluded to. Diffluent puri- form expectoration when profuse in the later stages of the disease, and when as- sociated with great prostration and per- sistence of the physical signs, are also symptoms of considerable gravity. Sup- pression of the expectoration from weak- ness, together with increase of tracheal rales, is of very serious augury. The total absence of expectoration throughout the disease has no influence on the prog- nosis. Marked disturbances of the nervous system are always indicative of the se- verity of the disease. A mild degree of delirium is not uncommon in children, and also in elderly people ; but in the lat- ter it is a serious symptom.2 In adults, however, severe delirium is always dan- gerous, particularly when occurring late in the disease, or when habits of drinking have preceded the attack. Convulsions, repeated after the onset of the disease, are in children a sign of much danger. Intense prostration with sunken and pallid features, and profuse sweating, are always suspicious, and have a gravity proportioned to their degree. In the more marked forms of so-called Typhoid Pneumonia, the prognosis must always be doubtful. Total suppression of the chlorides in the urine indicates a greater severity of the disease than when these are present, but does not, independently of other circum- stances, materially affect the prognosis. Severe gastric disturbance and diar- rhoea have a very similar import. Their effect is certainly unfavorable, but it can 1 Huss, loc. cit. 2 This is further confirmed by Griesinger. Of thirty fatal cases the temperature only reached or exceeded 1040 in eight. A tem- perature of 105*2, occurring in only one in- stance, was the maximum attained among these fatal cases. (Bleuler, loc. cit. p. 33.) 3 Die Eigenwarme in Krankheiten. 1 Bleuler, loc. cit. Of adults with a pulse above 120, one-third died whose age did not exceed 40 ; over aetat. 40 one-half died ; over 60 all died. 2 Bleuler (loc. cit.) observed a mortality of one-fourth of patients under aetat. 40 who ex- hibited marked delirium; over 40, three- fourths of these died. 208 PNEUMONIA. only be Judged of in relation to the gen- eral strength of the patient. Icterus does not necessarily increase the gravity of the prognosis.1 A protracted defervescence with a high pyrexia are also unfavorable. The lia- bility to relapse in the early days succeed- ing the crisis should also impose caution against a premature confidence in the cessation of danger. The terminations in a chronic state are so excessively rare that they hardly form an element in the consideration of ordinary forms of acute Pneumonia. The possi- bilities of a more protracted course are sufficiently shown in the previous account of the ordinary progress of the disease. The occurrence of herpes appears from the researches of Griesinger2 and Geisler3 to have a favorable prognostic signification. Treatment.-There is, perhaps, no subject in modern medicine which has been more earnestly discussed of late than the treatment of Pneumonia. It has been the champ de bataille between the advo- cates on the one side of "heroic" mea- sures, and the supporters of a "rational" and of "expectant" treatment on the other ; and since the first-named methods have been, to a large degree, shown to be worse than useless, the question has be- come further complicated by the assertion that a change of type has ensued, by which the nature and characters of inflammatory diseases in general have been, during re- cent years, materially modified. When, however, the natural course and the various relations of this disease are attentively considered, it is apparent that no malady can well be chosen less suited to afford logical proof, by means of statis- tics, of the relative value and the curative effects of any system of treatment applied indiscriminately, though the reverse is more easily shown by the enormous ex- cess of mortality which prevails when an "active" treatment is universally em- ployed. An acute disease with a natural ten- dency. under favorable circumstances, to terminate spontaneously by a sudden crisis occurring at periods varying from the 3d (or even the 2d) to the 7 th or 11th days, presents the most singular elements of fallacy in reasoning from the beneficial effects of active medical interference. If to these we add the manner in which its mortality is affected by age, by constitu- tion, by sex, by the presence or absence of complications, and by the other but unknown epidemic conditions which have no slight effect in the same direction, it would appear a task of the extremest difficulty to collect sufficient data in order to institute a logical comparison between patients under similar circumstances of the disease, but under different systems of treatment, so as to form any true con- clusion as to the relative value of the methods to be adopted for its cure. Looking to the evidence of statistics, and to the individual experience of care- ful observers, it must be admitted that medicinal interference and active treat- ment are, collectively speaking, of but little influence, either in shortening the duration in, or diminishing the mortality of, Pneumonia. Treatment, in its wider sense of nursing, diet, support, and reme- dies adapted to individual cases, is, how- ever, the author believes, by no means inefficacious in aiding the tendency of nature to effect a cure. The remedy which has been most ex- tensively adopted, but which has been almost completely discarded of late in this country, is venesection. Reintroduced by Sydenham1 as applied both to pleurisy and pneumonia, with the statement "Hujus morbi curatio in repe- tita vensesectione fere tota est," and sup- ported by Huxham and Cullen, the amount of blood taken by these authori- ties and their followers in the treatment of this and kindred disorders was enor- mous. Day by day, with the progress of the disease, fresh venesections were prac- tised, and Dr. Gregory, after bleeding a young man into convulsions by the ab- straction of between 4 and 5 lbs. of blood in three days, considered that he had thereby cured him of pleurisy.2 Bouilland recommends a daily bleeding to the amount of 14 or 1G oz. until the disease is cured. Andral asserts that no period of the disease contraindicates venesection, provided the other symptoms appear to require it, and that age is no barrier to this treatment, citing in its favor at ad- vanced ages the authority of Frank,3 and that it is to be applied to children equally with adults : the slightest threatening of a relapse called in his opinion for further bleeding : it is not to be omitted without the greatest danger, even if menstruation be present: profuse sweating is no contra- indication, nor is any amount of prostra- tion to prevent it, if the respiration be seriously impeded :4 it is to be equally 1 Works, Syd. Soc. Ed. p. 352. 2 Quoted by Dr. Alison. 3 Grisolle similarly quotes Morgagni (Epist. xx.), who bled a man over 80 with "suc- cess." 4 On this point he quotes Stott, who bled for the eighth time a patient covered with petechial eruption. 1 This is the almost universally adopted opinion. Bleuler, however, records a mortal- ity of 35 per cent, of cases in which icterus was observed. 2 Arch, der Heilk. 1860, vol. i. 3 Ibid. 1861, vol. ii. TREATMENT. 209 practised in the secondary pneumonias of measles, variola, and scarlatina, though with caution in typhoid fever: it is only contraindicated in the adynamic forms of the disease, and in some rare cases of special idiosyncrasy, and in the absence cf expectoration. Grisolle, even for more moderate bleedings, recommends the ab- straction of from 2 to 4 lbs. by repeated venesections, and still regards this plan as the most successful in the treatment of the disease. The treatment thus indicated continued in use with more or less freedom in this country until attention was forcibly drawn by Dr. Balfour1 to the lesser mortality of Pneumonia in Skoda's practice, and also in some of the homoeopathic hospitals where bleeding had been for some time discontinued. Even before this period Becquerel2 had shown the inutility of venesections in the pneumonia of children, and it is stated, on the authority of Le- gendre,3 that Biett and Magendie had pursued an expectant treatment in Pneu- monia with excellent results. Dr. Graves4 had also asserted that the large bleedings practised by some physicians were un- necessary, and that repeated venesections were injurious in the disease; but the statistics of Skoda's practice showed for the first time the striking contrast be- tween the " heroic" and the " expectant" methods; for while the mortality in 384 cases treated by him with small doses of extractum graminis and nitre was only 13'7 per cent., that of the Edinburgh Infirmary during a nearly corresponding period of five years was 35-9 per cent. Dietl's5 comparative statistics, which appeared almost simultaneously with Dr. Balfour's papers, seemed still more forcibly to bring into contrast these systems of treatment, and may be said to have at once exercised an important influence on medical opinion both in this country and in Germany. The arguments against bleeding have subsequently been most vigorously sup- ported by Dr. Todd and Dr. Bennett, who have at least the merit of showing that the treatment by venesection is in most cases unnecessary, and that in a very large proportion it is positively injurious, and the same conclusions have been more or less completely adopted by the majority of the physicians of the present day. The conclusion which has been practi- cally arrived at by the medical profession with respect to the influence of venesection in Pneumonia may be, with approximative truth, expressed in the following terms :*- (1) That indiscriminate bleeding im- mensely increases the mortality of the disease. (2) That it is especially fatal in old peo- ple and in young children, in patients of exhausted constitutions, and in those suf- fering from chronic diseases, and particu- larly from Bright's disease. (3) That it is absolutely unnecessary in the majority of cases of young adults and also of young children.2 (4) That in the vast majority of cases it has no influence whatever either in cut- ting short the disease,3 or in lessening its duration, or diminishing the pyrexia, but that occasionally these results appear to follow from its use when practised early. (5) That in the majority of cases it hin- ders the critical fall of temperature and delays convalescence. (6) That in the majority of cases, as shown especially by Dr. Bennett's and Dietl's data, recovery is equally, if not more rapid, when it is not practised as when it is resorted to. (7) That in a few cases a moderate ven- esection may be necessary in the early stages to avert immediate danger of death from asphyxia. Individual cases where apparent suc- cess has followed venesection are really but little capable of proving its general utility. It is a treatment to which I have never but once resorted, and have very rarely seen practised, and I can certainly affirm that those cases which may occa- sionally offer the strongest temptation to the use of the lancet recover just as well when it is withheld. The mortality among the cases which I have mentioned as com- ing under my own observation, has cer- tainly been in such as would not, with any modern knowledge, have been considered fit subjects for venesection. Even the re- lief of dyspnoea, which is thus effected, is proved by universal consent to be only temporary in its duration, for this symp- tom usually results more from attendant oedema of adjacent portions of the lung than from the actual obstruction to respi- 1 Notes in the practice of Skoda, Edinburgh Medical and Surgical Journal, 1847, p. 397. Brit, and For. Med.-Chir. Rev. 1846, vol. xxii. p. 590. 2 Sur I'lnfluence des Emissions sanguines et des V&icatories, chez les Enfants, 1838. 3 De 1'Expectation dans la Pneumonie. A posthumous memoir; Arch. Gen. 1859, xiv. 283. 4 Clinical Medicine, 1843, ii. 42. 5 Der Aderlass in der Lungen-Entziindung. VOL. II.-14 1 See Appendix F. 2 This is especially seen in Ziemssen's treatment, and also in a memoir by Barthez, who, in 212 cases of young children with lobar Pneumonia, only met with two deaths. Barely one-sixth were subject to active treat- ment. (Arch. G^n. 1859.) 3 This is most strongly affirmed by Louis and Andral, and also illustrated by the case by Zimmermann before quoted. Chomel(Dict. de Med. xxv.) held that it might sometimes effect this. 210 PNEUMONIA. ration in the part affected by the primary disease unless this be very extensive; and as the amount of fluid withdrawn by ven- esection is speedily replaced by the ab- sorption of water, the pressure on the col- lateral circulation of the lung is thereby only very temporarily diminished. It was, however, to this cause that the re- peated venesections of former times were probably due, a system whose impropriety it is scarcely needful to discuss further. Its employment in severe pyrexia is also shown by Ziemssen to be unneces- sary, for though he admits that he has occasionally resorted to its use when the temperature has appeared dangerously high, he yet states that other cases of a similar nature recover equally well with- out it. I have already stated that the fatal cases which have come under my own observation have not in any instance presented this phenomenon. When we consider, therefore, that the most urgent symptoms of the disease- the dyspnoea and the pyrexia1 are only temporarily diminished by venesection, and that they both tend in most cases to return after a few hours, the reasons for the adoption of this method of relief lose much of their validity. It may be possible that cases of such extreme urgency may occasionally arise that venesection may be absolutely neces- sary to avert immediate death by apnoea. Such cases I must believe, however, judg- ing from my own experience, to be exces- sively rare ; though, in the event of their occurrence, this remedy is probably the best that could be adopted, and should not be shrunk from if the indications are urgent, but I believe that such a condition is the only one in which it can be regarded as absolutely necessary. The mortality from Pneumonia has appeared to me to depend much more on prostration in the later periods than on asphyxia in the ear- lier stages of the disorder ; and the former result appears to be much more likely to occur when the strength of the patient is weakened by venesection. If, therefore, venesection appears to be positively re- quired at an early period of the attack, the amount of blood withdrawn should be moderate, and should not exceed six or eight ounces. With regard to the possible effect of this treatment in cutting short the disease, it may be stated that the chances in any given case are strongly against such a re- sult. Looking at the general effects of this procedure, patients will, on the whole, be probably in a worse condition for pass- ing through the later stages of disease when weakened by an artificial loss of blood than they are likely to be if their resources in this respect are husbanded : and though its dangers are the least in the case of young adults of good constitu- tion who commonly "bear" bleeding com- paratively well, this "tolerance" of the remedy by such subjects affords no proof of its general advantageous effects. [Toler- ance, however, plus immediate relief of marked symptoms, and early recovery, affords the kind of evidence which, accord- ing to all rules of clinical experience, is wanted to establish the appropriateness of a remedy in practice. While an indi- vidual case (e. </., the one in which, as above mentioned, Dr. W. Fox resorted to venesection) can prove but little, yet the aggregate of individual cases, carefully observed, furnishes a better basis than any a priori reasoning can do, for conclu- sions in inductive medicine. What is claimed by those who still advocate mode- rate venesection in a certain minority of cases of Acute Pneumonia, during the early stage, is, that having resorted to it, and seen it resorted to, in a large number of such cases, relief and early recovery fol- lowed, without any drawback of excessive weakness. Their legitimate inference is, that the unmitigated pulmonary inflam- mation would have produced greater de- bility than the timely withdrawal of a few ounces of blood. Nor does this conclusion, as a matter of fact, appear to be vitiated by the comparative effects of expectant or stimulant treatment, now so common, upon the mortality of the disease.-H.] Most of the other methods of treatment directed immediately to the cure of Pneu- monia afford nearly equal proofs of their inutility. The comparative effect of large doses of tartar emetic is shown by Dietl's statistics,1 while Rasori's2 mortality from this me- thod was 22 per cent., and Grisolle's 18 per cent.-or in those treated exclusively by this method, 13 per cent. Independ- ently also of this considerable mortality, the poisonous effects of the remedy were very frequently observed. Laennec spoke very highly of tartar emetic in more mode- rate doses, and considered that it had re- duced the mortality from Pneumonia in his practice to a minimum; but grave doubts have been thrown on the accuracy of Laennec's details3 in respect to this method. Laennec asserted and Grisolle believes that it is more useful when pre- ceded by bleeding. Louis4 also and Trous- seau5 speak favorably of its results, but the data given by the former, complicated as his treatment was by venesection, afford but little proof of its efficacy. 1 See Appendix E. 2 Ann. de Th^rap. 1847, and in Archiv. G^n. 1824. 3 See Grisolle. 4 Rech, sur la Saign^e. 5 Dictionnaire de M6decine, art. " Anti- moine. " 1 See Appendix E. TREATMENT. 211 ■Regarding the statements made, partic- ularly by Grisolle, respecting its effects in Pneumonia, it cannot be denied that tar- tar emetic produces occasionally a feeling of relief to the patient, and in some cases lowers the frequency of the pulse, and ap- parently diminishes the pyrexia.1 This effect, however, requires to be very care- fully watched. It is a depressing agent both to the nervous system and to the cir- culation, and is liable to increase the dan- gers of the later collapse. As far as my own experience goes, I believe that it is a remedy which can only very rarely prove of essential utility, and certainly, to say the least, the vast majority of patients will recover as well, if not better, without its use ; and it is absolutely inadmissible in the adynamic forms of the disease, and also in the Pneumonia occurring in old people, and in most cases in children. A very rapid pulse contra-indicates its use, and it is highly dangerous in most forms of the delirium accompanying the disease. Calomel, with or without opium in com- bination, has also fallen into disuse, prob- ably not without reason. Experience has gradually demonstrated the minor degree of power which it was at one time sup- posed to possess in aiding the absorption of exudations, and no valid proof has been afforded that the duration of Pneumonia has been shortened by its use. By most of its advocates it was only held to be effi- cacious after the previous employment of venesection and the administration of tar- tar emetic ; and a remedy requiring such antecedents is one that may with advan- tage be abandoned. Even when resolu- tion is delayed, the final termination of the disease is not, in most cases, less favor- able ; and I should not only feel extremely sceptical as to the value of mercurials in accelerating this process, but I should greatly hesitate to interfere with a remedy which often so materially impairs the gene- ral health and nutrition of the patient.2 Iodide of potassium has also appeared to me to exercise little or no influence in promoting resolution. The methods of treatment by alkaliesf or by acetate of lead,1 copper,5 and chloro- form,6 introduced in more recent periods, only serve to show that Pneumonia is a disease little influenced by remedies; that the less " active" these are, the better for the patient. Chloroform inhalations may certainly relieve the cough and allay the discomfort of the patient, as Dr. Walsh has stated, but they appear to have no influence on the progress of the disease. Digitalis, which was used by Rasori, has recently had an extensive trial, both by Thomas1 and Ziemssen.2 This remedy, from the researches of Traube3 and Wun- derlich,4 seems to have a distinct efficacy in reducing the pyrexia in typhoid fever. It would appear, however, from Thomas's observations, that at periods antecedent to the crisis (except in a few cases, when a marked lowering of the temperature and of the frequency of the pulse is observed) this effect is much less distinct in Pneu- monia, but when given in the later stages it tends to increase the post-critical fall to an abnormal degree.3 Both in adults and children it produces at times intermittence of the pulse, which, however, Ziemssen regards as not intrinsically dangerous. Duclos and Hirtz,8 who have also used it, give the alcoholic extract in divided doses, to the extent of 3, G, or 10 grains daily. Ziemssen gives gj of an infusion made with gr. v. to the ounce of water every two hours (the infusion of the British Pharmacopoeia is made with gr. iij to the ounce of water). Veratria, introduced by Aran,7 has been tested by several subsequent observers8 with varying results. A more extensive trial of this remedy by Kocher9 appears to show that in certain cases favorable results may attend its administration in diminish- ing both the pyrexia and also the frequency of the pulse. In some instances the tem- perature may be reduced by its use to the normal standard, though in many in- stances this effect is only temporary, but in Schmidt's Jahrbiicher, Ixxiii. 20. The treatment in some of these cases was mixed. 1 Arch, der Heilk. 1865. 2 Loc. cit. 3 Annalen der Charite, i. 691. 4 Arch, der Heilk. iii. 5 The effect on the pulse also appears to be uncertain, and a marked lowering of the pulse may ensue without any fall of tempera- ture, though the latter is never observed with- out the former. Occasionally the reverse effect is observed, and great acceleration of pulse may take place with or without a rise of temperature. 6 Bull. Th^rap. vols. li. and Ixii. 7 Ibid. xlv. 8 Vogt, Schweitz. Monatsch. vi., and Bull. Therap. 58; Fournier, Union M^d., 1855 : Roth, Wiirzb. Med. Zeitsch. iii. 1863 ; Uhle, Arch, der Heilk. N. F., iii. 9 Die Behandlung der Croiiposen Pneumo- nie mit Veratrum Preparaten. Wurzburg, 1866. 1 Accurate thermometrical observations on this point are wanting. 2 Wittich has published a series of twenty- three cases thus treated, and without fatal results. (Canstatt's Jahresb. 1850.) * Mascagni, quoted by Grisolle. 4 Leudet, Bull Thdrap. 1863, a mortality of 7 per cent. 5 Kissel, Canstatt's Jahresb., 1852, a mor- tality of 4 per cent. All Kissel's cases do not appear to have been thus treated. 6 Baumgartner, Wucherer, and Helbing, Canstatt's Jahresb. 1850; Varrentrapp, Henle and Pfeufer's Zeitsch. N. F., 1851, analyzed 212 PNEUMONIA. lasting in others for sixteen hours. In some, however, it appeared to accelerate the period of the crisis, and Kocher is of opinion that it also shortens the duration of the process of resolution; while in a few cases, when given early, it appeared to cut short the disease, and to prevent the occurrence of consolidation. The tem- perature is commonly affected before the pulse, but in a few cases these phenomena did not coincide ; and either the pulse or the temperature may be affected singly and without any corresponding reduction in the other. The remedy, however, appears in some cases to cause both vomiting and diar- rhoea, and to produce, when given in the later stages, a dangerous amount of de- pression. For this reason Kocher recom- mends that its effect should be most closely watched, and it appears also de- sirable that it should only be given in the earliest periods of the disease. The ver- atria, as an alkaloid, can only be safely given in doses of one-twentieth of a grain, and should be administered in pill, the resin in doses of gr. Kocher recom- mends that it should be given in frequent doses at intervals of from one to two hours, until a distinct effect has been pro- duced upon the pulse and temperature. In very severe cases he considers that its good effect is increased by venesection. Dessauer, however,2 who has also used this remedy and speaks highly of its effects, regards venesection as unneces- sary, and believes that veratria is a com- plete substitute for bleeding. He consid- ers that no prejudicial effects attend the diarrhoea which it commonly produces, and he says that delirium usually disap- pears under its influence. Aconite as a remedy does not appear to have been tested sufficiently to afford a proof of its effects in Pneumonia. In one or two cases in which I have given it I could not observe that any effect was produced by it on the temperature. The treatment which has hitherto been shown to have the most marked effect on the pyrexia consists in the external appli- cation of cold water to the body. Tepid baths had been indeed, as Grisolle shows, recommended by Hippocrates, and used by others; and Grisolle himself speaks favorably of their effects in relieving pain and also the general distress of the pa- tient. The use of cold water, though recommended by Currie in fevers, does not appear to have been employed by him in Pneumonia, but it has been largely used by the followers of Preissnitz.1 It was further introduced into modern prac- tice by Dr. F. Weber,2 of Kiel, and has been highly praised by Ziemssen, both in the lobar and lobular Pneumonia of chil- dren, and by Niemeyer3 in that of adults. Its effect during the pyrexial period only lasts during, or for a short time after, its employment, and it often requires a pro- longed application to effect any marked lowering of the temperature. The reduc- tion of the temperature also by this means appears from Ziemssen's observations to be rarely so marked as in the form of Broncho-pneumonia, and seldom appears to exceed 1£° or 2° Fahr. It appears, however, simultaneously to reduce the frequency of the pulse and of the respira- tion ; and though often unpleasant at first, it seldom fails to afford great relief to the patient, and to produce quiet sleep. The method adopted by Niemeyer is that recommended by "Weber, of applying com- presses wrung out of cold water, and changed every five minutes, to the chest, and especially to the affected side. Ziems- sen recommends the employment of Es- march's ice-bag,4 covered with linen, for the same purpose. In a few cases in children this treat- ment appears, as also in the form of Bron- cho-pneumonia, to produce a depressing effect, and it therefore requires to be care- fully watched, but it does not appear to be attended with any other risk, either of exciting bronchitis or of setting up sec- ondary complications.5 It does not ap- 1 Schedel, quoted by Grisolle. 2 Beitrage zur Path. Anat, der Neuge- borenen, ii. 63. Weber says that this method was first recommended to him in 1837 by Dr. Niessen, of Altona. Grisolle, p. 678, says that it was also recommended ly Dr. Campagnano, of Naples, who revived pa- tients in extremis by cold baths. Grisolle states that Campagnano also employed bleed- ing and antimony "avec une vigueur presque barbar e. ' ' 3 Spec. Path. Therap. i. 182. Niemeyer states that the treatment has been most ex- tensively used in Prague, with good results. He says that under this treatment cases of Pneumonia rarely last beyond the seventh day; that in an extraordinary number the disease terminates on the third day. 4 Langenbeck's Archiv fur Chirurgie, ii. 275. 5 I have employed this treatment experi- mentally in only one mild case in a child for a few hours. The continuous application of cold cloths to the chest lowered the tempera- ture half a degree Fahrenheit. It rose again with the ensuing exacerbation to the same height as on the previous evening (103°), after they were discontinued by the nurse, on account of the dislike of the patient to the treatment. 1 Kocher has found that the tincture of the veratrum viride contains very variable amounts of the alkaloid veratria. 2 Oesterreich. Zeit. Prakt. Heilk. and Schmidt's Jahresb. 1866, cxxxii. TREATMENT. 213 pear to shorten the duration of the disease, but only to act beneficially by diminishing the pyrexia. , Blisters in the earlier stages of Pneumo- nia are to be considered as both useless and as greatly increasing the distress of the patient. When resolution is progres- sing favorably, they also appear to be quite unnecessary. In a few cases when resolution is delayed, or when there is evi- dence of a small amount of pleuritic effu- sion, they may, I believe, in adults be occasionally employed with apparent ad- vantage. In children they are almost in- variably inapplicable. Warm fomenta- tions or poultices to the side often give great relief to the pain. I have by no means satisfied myself that any advantage accrues during the acuter stages from any more irritant applications, whether of mustard or turpentine, though in cases of threatening collapse, or when dyspnoea is severe, they have occasionally appeared to afford relief. It may, however, be desirable that after the foregoing analysis some account should be given of the treatment of Pneumonia which is most in accordance with the re- sult of modern observation. The author, in commencing this branch of the subject, feels it right to express his conviction that a large number of the milder cases occurring in young adults require no more medicinal interference than similar cases of other acute febrile disorders, and that neither depletory measures nor alcoholic stimulants are necessary to bring such cases to a satis- factory termination. Rest in bed ; a free supply of fresh, but not too cold, air attention to the evacu- ations, and the administration of a suf- ficient amount of liquid, nutritious, and easily digestible food-indications abund- antly fulfilled by milk and beef-tea-are often all that is requisite. [Cold and fresh air will be better for the patient than that which is warm and impure. In two very severe cases I have met with a craving for air from open windows, when the weather was very cold. One of these patients was a man about thirty-five years of age. On being called to see him in the midst of his attack, I found him lying with his two windows wide open near his bed, the thermometer indicating 17°Fahr. When I attempted to close one of the windows, he made known at once his dis- tress for want of air. Continuing, with reluctance, this aerial refrigeration of his lungs, his recovery suggested the thought, that, to the inflamed pulmonary tissue, possibly a direct "apyretic" influence may have been thus extended, similar to that of cold applications to a superficial inflammation. Almost precisely the same observation occurred to me afterwards in the case of an old lady more than eignty years of age; who manifested a craving for the admission of cold winter air through her windows. She also recovered, under that exposure, from a very severe attack of broncho-pneumonia.-IL] Pain may be assuaged if severe by a few leeches to the side, by linseed poultices, and more effect- ually by the hypodermic injection of mor- phia. Sleep also may be procured by the same means, or by moderate doses of opi- ates, or probably by the hydrate of chloral.1 When cough is distressing, and opium is not contra-indicated by cyanosis, this remedy in small doses has appeared to me to give much relief, and to have no inju- rious effects. Neutral salines also favor the action of the skin, and thus reduce the discomfort from the pyrexia, and probably aid in the elimination of effete matters by the urine. If any extensive bronchitis be present ammonia may with advantage be combined with these, and small doses of ipecacuanha have also un- der these circumstances appeared to me to be useful. When convalescence is established, solid food and a moderate use of stimulants adapted to the strength and habits of the patient, are frequently all that is necessary to promote a rapid cure. Iron and quinine or strychnia are, how- ever, to be given if there be ansemia or much weakness remaining. In severe cases of Pneumonia, threaten- ing to invade a large tract of lung, and coming under observation within the«first forty-eight or seventy-two hours of the disease, and if the dyspneea threatens as- phyxia, and the distension of the super- ficial veins indicates overfilling of the right side of the heart, a cautious bleeding may probably be practised with advantage to the extent of six or eight ounces, particu- larly if the patient be young and vigor- ous, and of previously temperate habits.2 1 "A close, narrow, stifling room is exceed- ingly incommodious to any person sick of a fever, but much more so to those ill of a peri- pneumony, as I have many times observed, especially among the lower part of tradesmen when two or three families perhaps live in a house together. Celsus's advice is never more proper, nay necessary, in any kind of fever than in a peripneumonia, in amplo conclavi tenendus ceper. If such close rooms cannot be avoided, they certainly should be frequently but prudently aired." (Huxham on Fevers, 1757, 199.) 1 I have not had a full opportunity of ex- perimenting with this remedy in Pneumonia. 2 Huss lays down the following rules :- Venesection maybe practised when the pulse is full, tense, or depressed. The large full pulse sinks at first, but venesection is to be continued until it rises again. In patients with a "tense" pulse venesection is to be continued until it becomes soft. If the pulse is depressed, venesection is to be continued until it becomes full. The indications for 214 PNEUMONIA. Under these circumstances also, if the fever be high, tartar emetic may be given in doses of gr. | to gr. j or gr. iss, com- bined with salines and small doses of pare- goric, every hour or two hours until some relief is experienced-a relief which may be further aided by the application of leeches or cupping to the side. I think it right, however, to add here, that although I have not hitherto adopted the applica- tion of cold water in such cases, I should, after the testimony adduced in its favor by the authors before quoted, feel strongly disposed to make a trial of its effects. Under all circumstances food must be given in suitable quantities, for it is im- portant to husband the resources of the patient as much as possible. Cases such as these now under consid- eration vary much in their later manifes- tations, and it is in these that judgment and decision are most required. One complication which may be re- garded as most indicative of danger is delirium, and it is to this symptom espe- cially that I now refer. By many of Dr. Todd's pupils the occur- rence of delirium in Pneumonia has been regarded as a certain indication for the administration of stimulants, and I be- lieve that in the majority of instances the practice is both well founded and success- ful. Cases do, however, occasionally oc- cur when acute delirium associated with a considerable degree of pyrexia is not benefited by this treatment, and though comparatively rare, they belong to a class which requires separate consideration. We have unfortunately but little exact knowledge of the state of the brain during delirium to serve as a pathological guide for its treatment. It is now pretty gen- erally admitted that delirium in many cases is by no means an expression of hypersemia or inflammatory irritation of the brain, and it is only clinical expe- rience which has led us to the discrimina- tion of these conditions in the various dis- eases associated with this symptom. In Pneumonia the evidences, as before stated, of meningeal or cerebral hyper- semia associated with delirium are very rarMy met with post mortem; but I be- lieve that we may with advantage dis- criminate two conditions under which de- lirium occurs in this disease. In one the state is that of weakness, for which we have no more precise pathological expres- sion ; in the other it is the expression of a blood-poisoning by the products of the pyrexial disturbance, though not, I be- lieve, as some are disposed to think, de- pending on the direct effects of over- heated blood on the nervous centres. It is probable also that in many cases both these conditions are more or less com- bined in various degrees. In conditions of pure weakness the rea- sons for giving stimulants are abundantly clear, but in delirium from blood-poison- ing this is more doubtful. It is, however, by no means easy to apply any certain clinical test to distinguish these two states. Delirium with high pyrexia should always induce aoubt as to its na- ture, and this doubt is increased when it has been preceded by severe cephalal- gia. I do not think that the special char- acters of the delirium always afford a cer- tain guide; at least its violence is no proof of the sthenic or asthenic character of the primary disease, though a low mut- tering delirium almost invariably belongs to the latter class. A correct opinion on this point must depend on the practition- er's judgment as to the state of the pa- tient's strength; and if indications of asthenia exist, it is better to depend on this as a guide, rather than on any theo- retical reasoning respecting the origin of the symptom. The state of the pulse is, I believe, the surest indication whicn we at present pos- sess. An extremely rapid pulse, i. e., one above 120 or 130, generally calls for the employment of stimulants. When the pulse presents the characters of dicrot- ism to any distinct degree, they are almost invariably necessary, and under both these conditions the use of bleedins; or tartar emetic is absolutely contra-indi- cated. Tremors and subsultus rarely co- exist with violent delirium; when they are present, they also strongly require the remedies under discussion. In doubtful cases it is safer to make a cautious trial of stimulants than to omit their use : when beneficial, their good ef- fect is usually seen early. Huss recommends the use of tartar emetic in doses of gr. j to gr. ij every hour in the delirium of drunkards, when this sets in early, accompanied by high fever and by a flushed face and tense pulse. He considers bleeding in these cases to be entirely inadmissible, and the tartar emetic is to be discontinued directly venesection to be drawn from the pulse were repeated by nearly every writer of the early part of the present century. How little these were to be relied upon, even by those in the habit of testing their practice by this means, is apparent from the following observations of Hourmann and Dechambre, who may at least be supposed to have been conversant with the fallacy of " fulness" in the pulse of old people to whom these remarks refer : " Nous avons vu des malades chez qui le pouls invitait la saignSe, cesser de rendre leurs crachats im- mediatement apres que celle-ci avait ete pratiquee et mourir en moins de douze a quinze heures." (Arch. Gen. de Med., 2e S£r. xii. 190.) Intense severity of dyspnoea appears to me to be the only positive indica- tion for this remedy. A very high amount of pyrexia in the early stages is also so, but to a less degree. TREATMENT. 215 the pulse falls in volume, or if diarrhoea or vomiting should occur. The use of all lowering remedies directed solely to the delirium is, however, only to be pursued with the greatest caution, for the diag- nosis of the pathological state present is often doubtful, and their danger, when inappropriately used, can hardly be over- rated. Opium in these forms of delirium can only be used with caution. Full doses often increase the prostration, and fail to procure sleep. Huss regards the condi- tion of the pupil as affording a valuable indication for the treatment to be pur- sued. If this be contracted, opium is contra-indicated, but belladonna, in doses of gr. | of the extract, given three or four times daily, may induce a quieter condi- tion, ending in sleep. I believe that in such cases as these the value of cold applications in lessening pyrexia will be found to be very consider- able when properly used, and may aid in solving the difficulty which has hitherto attended some of these cases. Digitalis or veratria,1 when the pulse is rapid, are remedies that appear to me to be de- serving of a further trial than I have yet had opportunities for making of their effi- cacy. The class of cases which have now been considered are fortunately comparatively rare. In the majority the discrimination is more simple, and in the severer cases of Pneumonia the administration of stim- ulants in the later stages is almost inva- riably both useful and necessary. They are, indeed, often required almost from the outset in cases marked by debility, at whatever age, but particularly in patients of bad constitution, in those who have in- dulged freely in alcohol, and in old peo- ple ; and under all these circumstances attention must be paid to the previous habits of the patient in regulating the amount given. In such cases as these I believe that all depletion and the use of tartar emetic are in the highest degree injurious, though simple salines may usually be given with- apparent advantage. In the majority of cases the amount of stimulants given during the pyrexial pe- riod may be very moderate. It is, indeed, always best to begin with a minimum dose, and to increase the quantity as re- quired ; and under all circumstances it is desirable, as far as possible, to husband resources of this nature. For infants, brandy, which is the best form of alco- holic stimulant for these purposes, may be given in doses of five to ten drops, in- creased to thirty drops, or gj every two, three, or four hours. For adults, from one to three drachms may be given at similar intervals, and in a large number of cases it is seldom necessary to give more than six or eight ounces of brandy in this man- ner in the twenty-four hours. The indi- cations for the amount and frequency of these doses are best gained from the pulse and from the general signs of asthenia. As long as these are distinct, stimulants must be persevered with; and though always to be used with caution, they must in some cases, especially in patients ad- dicted to habits of intoxication, be given both unflinchingly and unsparingly when the need arises. I have in one or two instances given 36 ounces of brandy daily for several days consecutively, in doses of six drachms every half hour, with a suc- cessful result, in cases of Pneumonia in drunkards ; every attempt to diminish the dose being immediately marked by dan- gerously increasing signs of asthenia ; and it was only when the more marked evi- dences of prostration diminished, that any symptoms of alcoholic intoxication were observable. Such cases are, however, rare, and, as before observed, much smaller amounts of alcohol are usually sufficient. The period immediately following the crisis is that in which moderate doses of alcohol appear to be most called for ; and in many cases which have not previously presented marked signs of asthenia, very considerable prostration, which in old people may prove fatal, may occur at this time. Indeed I believe that one of the chief duties of the practitioner in most cases of Pneumonia is to watch carefully for symptoms indicating the employment of stimulants, and to regulate by frequent observations the amount necessary to maintain the strength.1 1 It is due to the memory of the late Dr. Todd to point out that a great part of the reform in medical practice with respect to the administration of stimulants in acute diseases is due to him. It is possible that he may have pushed this method at times to an ex- treme, but of their general utility and of the advantage of administering them in repeated doses, as recommended by him, there can now be but little question. It is beyond the scope of this article to enter upon the rather wide discussion to which this practice has given rise respecting the mode of action of this class of remedies. The chemical side of the ques- 1 The lowering of the pulse by veratria is often very considerable. I have known it reduced in acute rheumatism from 100 to 54 in the minute within eight hours by the tincture of the veratrum viride, given in doses of n^v every two hours. The influence of this remedy on the temperature (104°) in this ease was much less perceptible. It fell half a degree, and the ensuing exacerbation did not take place. The pulse regained its former frequency within twelve hours after the rem- edy was discontinued. 216 PNEUMONIA. In cases of extreme prostration with a very rapid pulse, and attended by pro- fuse sweating, I believe from what I have seen of the effects of digitalis in the anal- ogous condition of delirium tremens, that this remedy may probably be tried with advantage.1 If in the later stages of the disease expectoration becomes profuse and co- pious, and abundant fine rales in the lung show the presence of oedema, and if reso- lution be proceeding but slowly, expecto- rants may be used with advantage. The muriate of ammonia and senega appear to be the best of these, and carbonate of ammonia may be beneficially combined with them. Counter-irritation may at this stage often prove useful. The maintenance of the general strength is, however, of paramount im- portance ; and bark, quinine, the mineral acids, or preparations of iron, will often promote recovery more rapidly than remedies devoted to the special condition of the lung. Strychnia is useful in cases where much nervous prostration is pres- ent. The use of cod-liver oil is also often beneficial at this stage. It remains to treat briefly of some of the attendant circumstances and compli- cations of the disease. Severe gastric catarrh, with a loaded and furred tongue, and whether attended or not by vomiting, is in adults often bene- fited by one or two purgative doses of calomel (gr. j to gr. iij), followed by a saline aperient, and this remedy is recom- mended by most authors for the " bilious" form of the disorder. Mustard poultices may also be applied to the epigastrium if vomiting is troublesome. In children, however, this symptom may depend on cerebral disturbance. If diarrhoea be present, a few grains of Dover's powder may be combined with the calomel, and the saline should then be omitted. Severe diarrhoea may, how- ever, require the use of astringents, though, as far as I have observed, this symptom is seldom sufficiently intense to call for their employment. Huss recom- mends cold compresses to the abdomen, or leeching to the colon, in the dysenteric diarrhoea which accompanies Pneumonia in hot seasons. If gastric catarrh continues in the later stages, simple alkaline remedies, the bi- carbonate of soda combined with bis- muth, have appeared to me the most useful. Huss and other German authori- ties recommend the muriate of ammonia for this symptom. Haemoptysis, if profuse, may be met by the internal administration of styptics. The most efficacious of these will prob- ably be found to be gallic acid, acetate of lead, and ergot. The latter is especially recommended by Huss when the pulse is quick, small, and weak. Venesection has been recommended for this symptom, but its true efficacy may be considered as doubtful. It must be remembered that large haemoptysis is most commonly a symptom of attendant tubercles, and that any reducing measures are, in such a case, specially contra-indicated. For the condition of gray hepatization, Huss and Grisolle recommend the use of camphor, musk, and turpentine. It must be remembered, however, that the full employment of stimulants does not ap- pear to have been practised by these au- thors. Their administration appears to me to be likely to be better than that of the remedies in question ; though these, of which however I have no experience, may at times be useful. Huss recommends the oil of turpentine in doses of five to ten drops every two hours, and says that it is particularly valuable in the Pneumo- nia occurring in the course of typhoid fever. He remarks that it seldom dis- agrees even when the tongue is dry and coated, but that if it causes vomiting it may be combined with hydrocyanic acid. He recommends camphor when delirium is present. This remedy, however, ap- pears occasionally to produce redness of the face and dryness of the skin, and un- der these circumstances it is to be re- placed by ammonia. For* the complication of abscess of the lung, Huss recommends acetate of lead in doses of gr. ij repeated every four or six hours, as long as the sputa continue offensive and copious. In the later stages bark or quinine with the mineral acids (Huss considers the phosphoric acid to be" the best) are the most suitable remedies. Gangrene of the lung appears to be but little open to remedial treatment. The employment of inhalations of turpentine, tion will be found discussed in the researches of Lallemand, Perrin, and Duroy, who main- tained that the alcohol so given was excreted by the kidneys ; while Strauch (De demon- stratione spiritus vini in corpore ingesti, Diss. Dorpat. 1862), Schulinus (Arch, der Heilk. 1866), Dr. Hall Smith's "Experiments on the Chromic Acid Test for Alcohol" (Brit, and For. Rev., 1861), and Dr. Anstie (Leet. Roy. Coll. Phys., Lancet, 1867, vol. ii.), have shown that this only takes place to a very limited degree. The latest researches on this subject are by Dr. Parkes and Count Wollo- wicz (Proc. Roy. Soc. xviii. 1870). 1 I have known it under these circum- stances, when combined with the administra- tion of alcohol (though the remedy had pre- viously been freely given) markedly reduce the frequency of the pulse and increase its power, while the sweating ceased within a few hours after it had been commenced. The digitalis was given in doses of jj of the tinc- ture every two hours. SECONDARY AND INTERCURRENT PNEUMONIAS. 217 recommended by Skoda, or of chloroform, has proved useless in Huss's experience. Two cases recovered in his hands ; one under the internal administration of crea- sote in doses of one drop given every two hours, and another with pyroxylic acid in doses of ten drops, combined with five drops of tinct. opii every two hours, but the same remedies proved ineffectual in other cases. More reliance must prob- ably be placed, both in this and in the last-named condition, on the maintenance of the strength of the patient by abun- dant support, and by bark and ammonia or the mineral acids. Pneumonia complicated by intermittent fever requires the use of quinine. Huss recommends that eight grains should be given during the rigor, and repeated in the sweating stage. The complication with pre-existing Bright's disease also calls in Huss's opin- ion for the use of turpentine. I have no experience of this method of treatment. It might, however, prove valuable if alco- hol appeared inadmissible in such cases. Huss does not appear to regard this remedy as productive of injurious effects on the condition of the kidneys. For the complication with pericarditis, local cupping or leeching and the internal administration of mercurials have been recommended. The utility of all these measures is, however, 1 believe, in the highest degree doubtful. ' Deaths from Pneumonia complicated with pericarditis have always appeared to me to present the most marked symptoms of asthenia. The advisability of small local bleedings must, however, be considered in relation to the general strength of the patient. For oedema of a limb remaining after the disappearance of the disease, friction, shampooing, and an elastic bandage are the most appropriate remedies. (Walshe.) SECONDARY AND INTERCUR- RENT PNEUMONIAS. Pneumonia, when appearing as sec- ondary to other diseases, presents in some cases both the anatomical and the clinical features of the acute primary form. In other instances the disease appears in spots of variable size irregularly scat- tered through the lungs, when it has re- ceived the name of Lobular Pneumonia, though it is seldom so strictly limited to individual lobules as this name would imply. The features of the disease, when of the latter class, and particularly when occur- ring in children, differ so widely from the Lobar form as to require a separate de- scription. A short account will also be given of the principal variations in the characters of Pneumonia when appearing as a com- plication of other disorders. "Catarrhal Pneumonia" is a va- riety of Pneumonia whose characters are in some respects clinically, and in others pathologically, only imperfectly defined from those of the acute primary form. Until recently it has been considered to be almost exclusively a disease of child- hood, originating either in primary bron- chitis or in the bronchitis secondary to measles, hooping-cough, and influenza, and in some cases of diphtheria. It is probable, however, that some forms of the pneumonia of old age may belong more truly to this category ; and some re- cent German authorities have been dis- posed from pathological considerations- which appear, however, to the author to rest on insufficient foundations-to regard many other cases, hitherto classed with the primary disease, as belonging to this variety. This form of Pneumonia is almost constantly characterized by being preceded by catarrh of the bronchial mu- cous membrane ; and it is a not uncom- mon complication of bronchial dilatation. The inflammation of the vesicular struc- ture of the lungs is in such cases the result either of direct extension of the inflammatory process, or it is induced through the intervention of collapse of portions of lung, owing to obstruction of the bronchi communicating with them, in a manner which requires a separate and fuller description hereafter. It does not, however, appear to me to be correct to regard all cases of Pneumonia which are preceded by bronchial catarrh as forming a separate class. In many of these the bronchitis can only be regarded as one of the prodromata of a pneumonia induced by the same cause, but preceding the true invasion by a period of from twenty-four to seventy-two hours. In others the pneu- monia is an accidental complication of pre-existing bronchitis, which possibly may have predisposed to its occurrence, but which, without the intervention of other causes, would not have led to the inflammation of the pulmonary tissue. In both these classes of cases the invasion of the pneumonia is sudden-it runs a typical course, and terminates by a crisis within the usual period.1 ' Out of fifty-three cases I found thirteen to have been preceded by catarrh. In four of these the cough preceded the rigor from twenty-four to seventy-two hours; in one, a chill had taken place a week before the rigor. In three there had been cough for a week before the sudden invasion of the Pneumonia, which commenced either with rigors or vomiting. In three others there was a history of chronic bronchitis. In all these the invasion of the Pneumonia was sudden : two of these cases 218 PNEUMONIA. In a third class, however, which may truly be termed Broncho-Pneumonia, the invasion is gradual; it is preceded by bronchitis of some standing or intensity, and the implication of the pulmonary tis- sue is only marked by an increased pyrexia, or by a slight sense of chilliness, usually without rigors, and by prostration with a quick and small pulse and a tendency to sub-delirium, sometimes attended by, but at others without, distinct changes in the characters of the cough and sputa. The latter are usually bronchitic throughout, or they may be puriform, and in a certain proportion of cases rusty sputa are ob- served. The course of the disease in these cases is protracted and indelinite, either ending fatally, or by a slow lysis and very gradual resolution. In fatal cases the lung is very commonly found in a state of gray hepatization. Ina few cases again the invasion may be insidious and grad- ual, attended by cough and by increasing weakness, but the symptoms may be of such slight comparative severity that pa- tients so affected may continue during common during epidemics of influenza, but it may occur without the direct effect of this specific poison. Huss met with it in 140 out of 2616 cases, or in a propor- tion to all forms of Pneumonia of about t'b. The mortality is, however, greater than that of the acute primary form, amounting to 14-28 per cent. It is also very common in tuberculosis, of which it forms a most dangerous complication, and markedly hastens the fatal issue. This association and the clinical phenomena attending it belong, however, more pro- perly to the subject of Phthisis, and will not therefore be considered here. BRONCHO - PNEUMONIA LOBU- LAR,2 DISSEMINATED, OR VESI- CULAR PNEUMONIA. The Broncho-Pneumonia of childhood was by earlier writers largely confounded with collapse of the lung, which was con- sidered a result of inflammation before Legendre and Bailly demonstrated its true character. The publication of their ob- servations led indeed to an almost equally strong reaction in the opposite direction, and it has been thought by many that no true infantile Pneumonia ever accompa- nies bronchial catarrh, but that all the changes in the lung attending this state are due to collapse alone. This opinion, however, is almost equally erroneous with that which it has displaced, since both pathologically and clinically, inflamma- tion affecting the pulmonary tissue has, under these circumstances, certain well- marked features which it is important to recognize. The peculiarity of this form of disease consists, as before stated, in its origin in pre-existing bronchial catarrh, either ex- tending from the upper air-passages or commencing as capillary bronchitis. It is not, however, always easy to decide the precise period at which the extension of the disease from the bronchi to the air- vesicles takes place, since this is usually gradual, and in scattered points; and hence in some cases, in children, the con- dition of Broncho-Pneumonia represents a variable combination of bronchitis and of Vesicular Pneumonia, the symptoms of which are also in part due to attendant collapse. For the proper understanding of its clinical features and physical signs it is necessary, however, to anticipate so far the description to be hereafter given of its morbid anatomy by stating that the mode of implication of the pulmonary tis- [Fig. 33. Catarrhal Pneumonia. - From a case of acute phthisis. Showing the large epithelial cells which till the alveoli. X 200. (Green.)] some weeks, although with difficulty, their usual occupations. Cases of this class, which bear a strong resemblance to the variety described as "LatentPneumonia," tend to pass into chronic forms of the dis- ease ; and, though occasionally occurring without the complication of tubercles, they have appeared to me, in most in- stances, to be more or less closely associ- ated with this diathesis. This form of Pneumonia is, however, died on the seventh and eighth days. Of these the affected lung was in one in a state of typical red hepatization; in the other, in a state of gray hepatization. In one case there was a history of previous catarrh of in- definite duration ; the invasion was sudden, but the case was protracted. In one only was the invasion gradual. It was, however, a distinct case of Acute Pneumonia. 1 The term first used by Seiffert (Die Bron- cho-Pneumonie der Neugeborenen und £aug- linge, 1837). 8 Burnet; Journ. Hebdomadaire, 1833. BRONCHO-PNEUMONIA, tOBULAR PNEUMONIA: SYMPTOMS. 219 sue ordinarily differs from that found in the Acute Primary or Lobar Pneumonia, and that the nodules of pneumonic con- solidation are usually scattered through tracts of air-containing tissue, which is often emphysematous ; that these nodules may vary in size from the dimensions of a poppy-seed to those of a walnut, and that they may coalesce until larger tracts are invaded; and further, that the in- flammatory changes often commence in portions of collapsed lung; and finally that both lungs are very frequently and simultaneously affected. Etiology.-The frequency of this form of Pneumonia in children is variously stated. Ziemssen1 observed 98 cases as contrasted with 186 of the primary form. Steffen,2 for 94 of the primary, has met with 72 of the catarrhal or lobular form. It is most common and most fatal in the earlier periods of life. Of 72 cases observed by Steflen, 52 occurred before four years of age. The age thus specially prone to it corresponds, therefore, with the period of the first dentition; but whether any increased liability to the dis- ease is induced by this process appears to be doubtful, since it is almost constantly a secondary effect of bronchitis, or of dis- eases of which bronchitis is a common complication in early life.3 The causes of bronchitis in children are therefore in some degree also causes of Broncho-Pneu- monia, and hence it is most common in cold seasons. It is also said to occur at times epidemically, but this is probably due in great measure to the prevalence of influenza or of other zymotic diseases associated with bronchial catarrh. There appears to be little doubt that a previous condition of bad nutrition mark- edly predisposes to this form of Pneumo- nia. The influence of bad air has also been strongly insisted on by Bartels as a more or less direct cause of its occurrence in cases of measles. It is probable also that ah causes which diminish the respi- ratory muscular force of children operate in the same direction particularly when it is remembered that the occurrence of partial or general collapse is frequently the immediate precursor of the inflamma- tory changes, and that a long-maintained recumbent position, by causing congestion of the posterior portions of the lungs, favors the pneumonic process. Constitu- tional predisposition to bronchitis at early ages also favors the occurrence of this dis- ease, and thus it is prone to recur in the same individual. Symptoms.- The signs of pneumonic inflammation are usually developed more acutely in the course of capillary bron- chitis and of measles,1 in which the bron- chial inflammation is more intense, than in hooping-cough, in which latter disease the invasion is more gradual, and is almost invariably preceded by pulmonary col- lapse. The period of its accession varies also in different diseases. In measles it most commonly occurs during the decline of the eruption, and it may be deferred until the second or even to the third week after the subsidence of the pyrexia and of the ex- anthem ; occasionally, however, it has been noticed to precede the eruption by a period of nearly a week.2 In diphtheria the pulmonary complications usually oc- cur within the first five or six days ; but 1 Loc. cit. 2 Klinik der Kinderkrankheiten. 3 Steiner (Prager Vierteljahresch. 1862, vol. Ixxv.) gives the following table of condi- tions coincident with Lobular Pneumonia :- Cases. Boys. Girls. Rickets 26 15 11 Rickets and tubercle com- bined 11 8 3 Atrophy 16 10 6 Tubercle of glands 15 9 6 Measles 10 7 3 Scarlatina .... 3 2 1 Smallpox .... 2 1 1 Dysentery .... 7 5 2 Noma 2 2 0 Heart-disease . . . 1 1 0 Meningitis .... 1 1 0 Burns 1 0 1 appear, however, somewhat to overrate this frequency, for in some of the cases which he cites as instances of "hepatization," the por- tions affected floated in water; and he also speaks of collapse as a stage of Pneumonia. Dr. Wilks (Guy's Hosp. Rep. 3d Ser. vi. 146) finds that burns of the skin are very frequently followed by this variety of Pneu- monia. In some instances, however, it as- sumed a more extensive and lobar form. 1 It has, however, been before stated in re- spect to measles, that some forms of Pneumo- nia occurring in this disease approximate very closely in their characters to the true primary form, both in the rapidity with which a large tract of lung is invaded, and also in their anatomical characters. 2 Steffen, loc. cit. Steffen, out of fifty-two cases, found thirty- eight arising from bronchitis, eight from hooping-cough, and six from measles. Ziemssen, in ninety-eight cases, found thir- ty-two associated with bronchitis or chronic bronchitis, twenty-three with hooping-cough, and forty-three with measles. Bartels (Virchow's Archiv, xxi. p. 75) found in an epidemic of measles that 12 per cent, of those attacked were affected with Broncho-Pneumonia. Peter (Gaz. Hebdom. 1863, p. 689) found the disease very frequent in diphtheria. He states that in 100 cases of diphtheria he found sixty-seven of confirmed Pneumonia and twelve of engorgement. Peter's data would PNEUMONIA. 220 in hooping-cough they seldom appear until the disease has been considerably pro- tracted, and both the general nutrition and the muscular power of the patient have been impaired. In acute bronchitis Pneumonia may occur early, when the affection is severe, or when other causes predisposing to pulmonary collapse are present; and among these, early infancy, rickets, or previously defective nutrition are prominent. In chronic bronchitis the supervention of Pneumonia is commonly a late phenomenon. The extension of the inflammation from the bronchial mucous membrane to the tissue of the lungs is rarely attended by the phenomena of rigors, or vomiting, or by the cerebral symptoms which mark the invasion of the primary form of the dis- ease, though the latter may occasionally be observed.1 The pulmonary complication is usually first evidenced by an increase of dyspnoea, together with the supervention of fever, if this has not been previously present, or by an aggravation of that already existing. The dyspnoea, except in very mild cases, when it may be comparatively slight in degree, is commonly both objective and subjective, and gives the patient much distress. It tends at times, and particu- larly in rickets and when collapse of lung is also present, to occur in suffocative paroxysms, and, even when these are less marked, it varies in intensity at different times of the day, and is usually most felt in the morning and evening. Great acceleration of the respiration is the rule where the disease is of any con- siderable intensity; it may then equal the extreme degrees of frequency ob- served in the primary forms of Pneumo- nia, and may sometimes attain to 107 respirations in the minute.2 Commonly the frequency of the respiration is, as in the primary disease, disproportionately greater than that of the pulse, the ratio of 1 to 1'5 being sometimes observed ; but when cerebral congestion is also present, the pulse may be rapid and the respira- tion even slower than natural (Bednar). The respiration is not unfrequently re- tarded when a fatal termination is ap- proaching. Irregularity in its rhythm is not uncommon, and this may amount to so complete a cessation of the respiratory movements during some minutes as even to simulate death3. The thoracic movements are shallow, with great elevation and little expansion. Inspiration is imperfect and short ; ex- piration is often forcible, prolonged, and noisy. The action of the accessory mus- cles is violent. The chest is raised by the elevatory muscles, but the lower por- tions are drawn in by the diaphragm. The anterior superior portions appear distended when emphysema is also pres- ent, but may yet be comparatively mo- tionless. The action of the also nasi is also greatly exaggerated. The cough varies in character. It is sometimes paroxysmal, but this character, even when previously present, as in hooping- cough, may disappear on the superven- tion of Pneumonia, and the cough may become short and dry ; and this change in its character often forms, together with the pyrexia, one of the earliest signs of the implication of the pulmonary tis- sue in this disease. The cough also often becomes painful, eliciting cries from the patient, a symptom which is also some- times a valuable indication of the pneu- monic change. I believe, however, from some cases in which I have observed this in adults, that such pain may be extra- thoracic and myalgic in its nature, and that it is partly caused by the sinking of the inferior parts of the thoracic walls due to collapse of the lung. In some cases the pain complained of may be in the epigastric and in the upper abdomi- nal regions.1 The secretion from the bronchi, if pre- viously free, as shown by the looseness of the cough, is often diminished. Expec- toration is rarely seen in young children. When brought up by vomiting, it is com- monly bronchitic and tenacious, some- times streaked with blood, but rarely if ever rusty. The same characters are ob- served in the sputa of adults attacked by Pneumonia during the prevalence of in- fluenza. The physical signs in the earlier stages are often obscure. They commonly affect both lungs simultaneously, though rarely in an equal degree. The immobility of the thorax and the sinking of the lower ribs, with deepening of the diaphragmatic depression, occur in cases of simple bron- chitis, with attendant emphysema and collapse ; but when the lung becomes ex- tensively infiltrated, the depression of the ribs may partially disappear. The percussion results may be uncer- tain : usually the upper parts of the chest are hyper-resonant, and they may be quasi-tympanitic when much attendant emphysema is present. When the spots of collapse or of pneumonic infiltration are disseminated through healthy pul- monary tissue, the sound, though less resonant than natural, is rarely dull, and ' Dr. West (Dis. of Infancy and Childhood, p. 326). Steffen has once seen spurious hy- drencephalic symptoms precede the outbreak of the Pneumonia, and cease on its appear- ance (loo. cit. 302). 2 Bednar, Lehrbuch der Kinderkrankheiten, 268. 3 Barthes and Rilliet, i. 264. i Steffen. SYMPTOMS. 221 only loses the pulmonary tone when these have coalesced into more extensive tracts. The dulness of Pneumonia does not differ markedly from that of collapse, though the latter may occasionally acquire a tympanitic tone (Ziemssen) ; but it is usually more intense. The site of col- lapse is, however, peculiar. It tends to occur at the free border of the left lung overlapping the heart, and also at both bases posteriorly, when, instead of ex- tending uniformly, it passes upwards in an elongated and quasi-pyramidal form along the lines of the intervertebral grooves, and it may, maintaining this peculiarity, extend nearly to the apices of the lungs.1 As, however, collapse often constitutes the first stage of the pneumo- nic process, this form of dulness may be maintained after the latter has set in. The respiratory sounds over collapsed portions are commonly weak or inaudible. In lobular pneumonic consolidation they usually acquire a bronchial, but never a tubular character (Walshe). This quality of respiration, though occasionally, is only very rarely met with in simple col- lapse.2 The respiration in other portions of the chest is usually exaggerated and attended by rales. Generally disseminated dry or moist bronchitic rales indicate only the bronchial catarrh. When Pneumonia supervenes, they, however, often become finer, and may thus be heard in limited spots of the pulmonary tissue, and they frequently change in site from day to day ;3 but they seldom present the typical characteristics of the crepitation heard in the Acute Lobar Pneumonia. In some cases, however, when the finer bronchi are dilated, the rales heard may be coarse, and they may acquire a quasi- metallic character if consolidation sur- rounds these dilatations. Rales are sel- dom heard directly over collapsed parts, unless they be conducted from adjacent bronchi. Vocal fremitus is commonly exag- gerated over pneumonic infiltration more than over collapsed portions of lung. The differences of degree observable in this respect are, however, very variable. Vocal resonance, as heard when a child cries, is usually much increased by pneu- monic consolidation of any extent, and frequently under these circumstances it acquires a bronchophonic tone. These characters may, however, be absent when the bronchi are extensively obstructed. The pulse is rapid. It rarely, even in the early stages, presents the fulness or strength of the primary disease. At more advanced periods it becomes exces- sively frequent, small, and feeble, so as scarcely to be felt. Irregularity of its rhythm is also occasionally observed. Fulness of the superficial veins, extend- ing even to those of the hands (Trousseau), is also observed, and oedema of the ex- tremities has sometimes been noted (Steffen). Simultaneously with these symptoms there is a great restlessness : the eyes are sunken, and the face assumes an anxious expression, which is painfully distinct in young children. Strength fails rapidly; as the disease progresses somnolence and a semi-comatose condition supervene, in which the child lies passive, but starting up from time to time into an erect or semi- erect posture, with jactitation and move- ments of distress, when attacks of cough and dyspnoea return. The skin is hotter than natural, though not commonly presenting the pungency of heat which characterizes the acute lobar form, and it is often bathed in profuse per- spiration, which occasionally alternates with a dry heat. The perspiration may be general, or in rickety patients may ap- pear chiefly about the head. The surface is generally pallid with the exception of the cheeks, which present a flushed or violet tinge, which is sometimes transi- tory and alternates with a cyanotic pal- lor. Cyanosis of the lips and finger-nails increases with the progress of the disease, and is especially distinct in the pneu- monia succeeding to hooping-cough, and when collapse forms a prominent feature. Vomiting, unless caused by the cough, is less common in this form of Pneumonia than in the acute primary disease. Diar- rhoea, on the other hand, is not unfre- quent, particularly in the Broncho-pneu- monia attending measles, and if not orig- inally present it is very easily excited by medicinal remedies, especially by tartar emetic. The tongue, at first moist, be- comes dry in the later stages, and sordes form on the teeth or on the angles of the lips, which are also dry and cracked; aphthous stomatitis may occur when the course is protracted. The appetite is completely lost, but thirst is marked ; in- fants at the breast suck it eagerly, but the power of continued sucking is lost, owing to the difficulty of breathing. A slight degree of delirium is occasionally ob- served, particularly in older children, as an exaggeration of the restlessness which tends to increase towards night. Convul- sions are, however, much less frequent than in the acute disease ; when they do occur, they form a very unfavorable fea- ture. A semi-comatose state is more common ; it passes later into deeper un- 1 Ziemssen, loc. cit. 2 Barthez and Rilliet; also Ziemssen and Gerhardt. 3 When masked by other rales it is desira- ble to follow the advice given by Barthez and Rilliet, and to repeat auscultation after the act of coughing. 222 PNEUMONIA. consciousness when the signs of mal-oxy- genation of the blood become more apparent. In some cases, however, a hydrencephalic condition with restless- ness and cries has been observed.1 The urine, owing to the early period of life in which the disease usually occurs, has not been made the subject of exact observation. Bednar says that the chlo- rides are present. In some cases the presence of a small amount of albumen has been noticed. Emaciation and loss of strength pro- gress with marked rapidity ; there is great loss of weight, the eyes are sunken, the muscles are wasted and the skin is flac- cid. These appearances may, in severe cases, become very distinct within a few days from the outset: if the disease runs a more protracted course, and particularly in the Pneumonia succeeding to hooping- cough, the wasting of the tissues may at- tain an extreme degree of marasmus- proportioned, however, in most cases to the age of the patient and to the severity of the disease. Ecthymatous pustules often form, which lead to painful sores. Excoriations of the nose and angles of the mouth are also observed, and bedsores form on the prominent parts of the ema- ciated limbs. The patient often dies completely exhausted, or sinks suddenly during a paroxysm of cough, or with the increasing cyanosis may pass into a state of final somnolence and coma. When death occurs in the early periods of the disease, it is usually due to the combined asphyxiating effects of capillary bronchitis and collapse. The course of the disease after Pneumonia has set in is usually more protracted. Many of the above symptoms, and espe- cially the increasing intensity of the dys- pnoea, may occur in severe cases of bron- chitis accompanied by extensive collapse of the lung, and uncomplicated by Pneu- monia. The most characteristic feature of the latter is constituted by the pyrexia, the presence of which is almost essential to its recognition. Acute bronchitis in children is, indeed, not unfrequcntly at- tended by fever, but when uncomplicated by Pneumonia the temperature seldom rises in it above 101° or 102°. The fever also when present is not continuous, the temperature in the morning being often nearly at the normal standard, or perhaps falling to 99° or 99*5°. The invasion of Pneumonia is marked by accession of fever rf the disease has been previously apy- rexial, or by an increased temperalure if fever has already existed, and this, in the pneumonia of measles, may speedily at- tain the degrees of 103, 104, or 105. The lower standard of 102° may, however, not be surpassed in the whole course of the case.1 Sometimes a rise of temperature may be observed to follow the accession of dulness on percussion, both at the outset and during the subsequent exacerbations, showing that collapse has preceded the inflammatory changes. This, however, is not always to be observed, and the rise of temperature may be comparatively sud- den and rapid, and may either proceed pari passu with the loss of resonance on percussion, or may precede this by some hours or days-the diminution of pulmo- nary resonance only becoming distinct when the islets of Lobular Pneumonia, by becoming confluent, affect tracts of tissue sufficiently extensive to give rise to this physical sign. In some cases again, when Pneumonia succeeds to measles, the invasion both of the physical signs and also of the pyrexia may present a great resemblance to the phenomena of the acute primary disease -the temperature rising rapidly, and maintaining a tolerably uniform elevation with comparatively slight morning remis- sions, but in its later periods, running a protracted course resembling the catar- rhal type.2 In its subsequent course, however, the pyrexia as measured by the temperature presents certain characteris- tics which aid considerably in the recog- nition of this form of Pneumonia. The chief among these are the irregular course of the fever, the extent of the remissions and exacerbations, and the absence of critical phenomena-the fever being usu- ally protracted, and ending only by a slow and gradual decline, which is often inter- rupted by renewed exacerbations. The remissions may be as great as from 1'8° to 2'5° Fahr. They occur at irregu- lar times during the day, differing in this respect from the ordinary course of the acute primary disease. It has been al- ready stated that in some cases of this form, the maximum temperature may be observed in the morning instead of at night; but this condition, which is excep- tional in Primary Pneumonia, is much more common in Broncho-pneumonia, when it may be noticed to occur irregu- larly in the course of a single case-a pe- culiarity which is probably due to the in- definite course and irregular extensions of the pulmonary inflammation. The ter- mination of the fever is also protracted. Ziemssen regards a case terminating 1 In some fatal cases the temperature may rise shortly before death to upwards of 107° (Ziemssen), but on the other hand a rapid fall of temperature, due probably to defective aeration of the blood and to extension of the collapse, may immediately precede the fatal issue. 2 Ziemssen and Krabler, Klin. Bericht ueber die Maseru und ihre Complicationen, p. 169. 1 Barthez and Rilliet (i. 467) attribute this to frontal neuralgia. PATHOLOGY AND PATHOGENESIS. 223 within seven days as a very exceptional one; and the pyrexia may last for weeks,1 in the Broncho-pneumonia both of mea- sles and hooping-cough, presenting in its irregular exacerbations and remissions a striking resemblance to the course of tu- berculosis, which, however, according to the observations of Bartels and Ziemssen, is a much less common sequela of these diseases than is usually believed. The defervescence rarely, if ever, presents the abrupt critical fall so commonly observed in the acute primary form : or if this com- mences, it is usually followed by subse- quent elevations of temperature: the decline of the fever is only gradually ef- fected, and rarely extends over a shorter period than three or four days, and it is often interrupted by irregular secondary exacerbations. In some cases the tem- perature often finally sinks during some hours or days below the normal standard. The range of temperature is commonly lower, and both the course of the disease and the duration of the pyrexia are more protracted in the Pneumonia succeeding to subacute bronchitis and to hooping- cough than in that which follows measles. In hooping-cough the degree of pyrexia may be very slight, and the morning re- missions may attain almost to the normal standard,2 but exceptional cases occur in which Pneumonia complicating this dis- ease appears in an acute form and runs a rapid course to a fatal termination. With the gradual decline of tempera- ture other signs of improvement become evident. There is rarely any appearance of critical sweating, but perspiration ap- pears from time to time, and often seems to afford relief. The dyspnoea and the cyanotic aspect diminish; the pulse and respiration fall in frequency; the cough becomes looser and less hard, and it may again acquire a paroxysmal character, if this has, as in hooping-cough, been pre- viously present; diarrhoea, if present, ceases; the appetite gradually returns, and thirst disappears or diminishes in in- tensity. Recovery is, however, almost always slow and protracted ; cough persists long; and the duration of the physical signs of consolidation, and especially of bronchitic rales, may continue during many weeks. Some acceleration of the respiration and of the pulse may also continue after the fever has subsided.3 Slight returns of the pyrexial symptoms may also be observed during this period. The restoration of the digestive powers and of the nutrition is only very gradually effected, and the patient may be for months liable to a re- newal of catarrh, attended with slight de- grees of feverishness. In some cases, after a long continuance of the pyrexia and of the physical signs, the former may subside, but the latter may change their character and present those of chronic Pneumonia or of bronchi- ectasis, or sometimes of the latter alone.1 Complications. - Independently of the diseases which exert a direct or predis- posing influence on its production, the liability of Broncho-pneumonia to other complications is comparatively slight. Some of these will be further alluded to among attendant pathological phenom- ena. One of the most important is intes- tinal catarrh, which has been attributed by M. Beau to the swallowing of un- healthy sputa. It appears, however, to be more directly due to the venous con- gestion of the intestinal canal, and to the tendency of catarrh in children to affect the whole gastro-puhnonary tract of mu- cous membranes. True dysentery was observed by Steiner in seven out of 110 cases. Pleurisy is less frequently observed than in the acute primary disease. Steffen in seventy-two cases only found six of ex- tensive pleuritic effusion. Various degrees of the affection, in the form of adhesions, are by no means uncommon. Tubercle is not uncommonly associated with the chronic form, but whether as to cause or effect it is not in all cases easy to distinguish. It is not improbable that repeated relapses may give rise to this tendency, and a statement of Steiner's, which will be alluded to hereafter, would seem to show that even collapse may suf- fice to set up tubercular formations in predisposed subjects ; and Bartels has re- marked that when present it is specially prone to occur in the condensed portions. On the other hand, the statements of Bartels appear to show that tuberculosis is a much less common sequela of the Broncho-pneumonia of measles than has been commonly believed.2 Pathology and Pathogenesis.- It has been already stated that this form of Pneumonia may be produced by the mechanism of two distinct processes. * This subject will be again referred to un- der the head of Chronic Pneumonia. 2 Bartels only found tubercle four times in twenty-one post-mortem examinations, and in two of these the affection was meningeal. Ziemssen only observed cheesy changes twice in sixty-three cases of death. Legendre and Bailly found five cases of tubercle in twenty- seven of catarrhal Pneumonia. Ziemssen and Krabler remark, however, that acute tu- berculosis is not uncommon after measles. ' Eight weeks. (Bartels.) 2 See a case by Steffen, p. 313. This case was the more remarkable, as it was one of hooping-cough complicated by tuberculosis, which had progressed to the stage of excava- tion. 3 Steffen. 224 PNEUMONIA. The pulmonary alveoli may suffer by the direct extension of the inflammatory ac- tion from the bronchi, or the inflamma- tory changes may only take place in por- tions which have already become the subjects of collapse. The pathological appearances in the inflamed lung present under these conditions several points of difference. Under both sets of circum- stances the changes in the mucous mem- brane of the bronchi are very similar, exhibiting various degrees of inflamma- tory congestion, together with swelling and softening of the mucous membrane, which are accompanied by slight super- ficial ulcerations. These changes may ap- pear throughout the whole course of the air-passages when the catarrh has com- menced in the larynx and trachea and has travelled downwards. In some cases, however, they may be limited to the smaller bronchi, and the upper air-pas- sages may present a comparative immu- nity. The walls of the finer bronchi are often so much thickened as to cause them to stand out rigidly in sections of the pul- monary tissue. Dilatations of the bronchi are very com- mon ; they are generally in the cylindrical form, but are sometimes globular, and they may be so universal throughout the lung as to give it a cribriform aspect on section, or even to present the appearance of a number of small cavities. The con- tents of the bronchial tubes are usually a creamy pus, or a denser exudation consti- tuting a form of false membrane, or some- times a clear tenacious mucus containing nucleated cells in which a large propor- tion of desquamated ciliated epithelium may be found. In other cases again little or no mucus can be found in them. The changes in the lung tissue, when the inflammation has proceeded directly from the bronchi, present the appearance of a number of small whitish-yellow spots with indistinct margins fading insensibly into the surrounding tissue. They are not very prominent,1 and do not stand out sharply defined like the gray granulations or the small softer spots of more acutely produced tubercle. They are often very thickly scattered through the pulmonary tissue, and the portions of lung intervening between them are softer, more vascular, and more (edematous than natural. They are slightly but not markedly granular, and usually, on scraping or pressure, a turbid milky fluid can be expressed from them. As they increase in age they be- come firmer and drier, but still have little ■of the granular character. That they un- dergo any cheesy metamorphosis inde- pendently of pre-existing or superadded tubercular changes is in my opinion very doubtful. In addition to these spots others are found, varying in size from a pin's point to a hemp-seed, of a brighter yel- low, consisting of dilated air-vesicles, or sometimes of groups of air-vesicles whose walls have broken down, or of the terminal extremities of dilated bronchi. In which- ever manner originating, they form little collections of puriform fluid, which escapes when they are pricked, but which also may become more inspissated, and which when evacuated leave irregular cavities. They are sometimes found under the pleura forming little sub-pleural abscesses, and in some cases may by their rupture give rise to pneumo-thorax. It is doubted by some writers whether these originate in a true inflammation of the air-vesicles of the lungs, or whether they are not merely collections of pus which nave grav- itated or have been drawn by inspiration into the extremities of the dilated bronchi and infundibula. I believe from my own experiments on animals in which, espe- cially in dogs, both these sets of appear- ances can be produced easily by injecting ammonia into the trachea,1 that they are to be regarded as truly inflammatory in their nature; though the latter mode of origin is however possible, since, as Ziems- sen (who agrees with the view previously expressed by Fauvel of their nature) re- marks, they are most commonly to be found after the prolonged paroxysms of hooping-cough. The purulent yellow spots before described are perhaps more com- monly found in the Pneumonia succeed- ing to measles than in other conditions. I have before stated that the Pneu- monia which is secondary to diphtheria may present in some cases all the ana- tomical characteristics of the acute pri- mary form. In other cases it takes place by the intervention of collapse ; but in a third class the appearances observed cor- respond with those which have just been described. When the bronchial ramifica- tions are opened it will be found, in pro- portion as these diminish in size, that the firmness of the exudation layer diminishes, and that the finer bronchi are only filled with a soft puriform fluid. In some in- stances this process does not extend be- yond bronchi of from two to four lines in diameter; but, in other cases, patches of a yellowish color and soft consistence, varying in size from that of a hemp-seed to a horse-bean, and only rarely attaining the dimensions of a hazel-nut, are found in the pulmonary tissue. These are im- pervious to air, and are only slightly granular. They fade insensibly into the surrounding tissue by an ill-defined mar- gin. They are friable, and on pressure 1 These spots are often described as ' 'promi- nent, ' ' but the author believes that as a ques- tion of degree the distinction here drawn will be found to be correct. 1 See p. 159. PATHOLOGY and pathogenesis. 225 they allow a thin yellowish fluid to exude. On microscopic examination the air-vesi- cles are found, for the most part, occupied by an amorphous exudation, in which are seen a few puriform and granular cells, together with proliferating epithelium from the air-vesicles. I agree with Sir William Jenner,1 that in most cases these spots are formed by the fluid formed in the bronchi being drawn by inspiration into the air-vesicles of the lungs. In the Pneumonia which occurs con- secutively to collapse of the lung,2 various stages may be observed in the inflamma- tory process. It requires, however, to be stated, that in many fatal cases of bron- chitis, and particularly in infants, the condition of extensive collapse, unat- tended by a trace of inflammation, may be the only morbid change present. The mechanism of the production of collapse will be more fully treated of in the section devoted to this subject. It is therefore only necessary in this place to refer to the inflammatory changes ensuing in parts which have already undergone this change. In collapse pure and simple, the parts affected are sunk below the level of the surrounding tissue. They are most usu- ally found at the bases of the lungs and at the free borders of the lower inferior lobe, and they commonly affect both lungs simultaneously, though rarely in an equal degree. They are often pyramidal in shape, with the base at the periphery of the lung corresponding to the distribution of the terminal bronchi leading to the affected parts. They, sometimes, how- ever, occur in the more central portions. They are irregularly distributed, and vary in size from that of a hemp-seed when they arise from the collapse of small groups of pulmonary lobules, to spots of one or two inches in diameter. In severe cases, both in infants and in adults, a whole lobe may be affected, though the pyramidal form is that most commonly observed.1 On section the nodules are of a bluish-purple tint, which is uniform ex- cept when traversed by bronchi, blood- vessels, or interlobular septa ; they are smooth on section, allowing only a small amount of blood-stained serosity to escape on pressure or by scraping; they are often, however, attended with scattered ecchymoses. They are resistant, and do not break down readily under pressure, and they are airless and sink in water, but can be restored to their normal condi- tion of expansion by inflation, which pro- cess, however, leaves the affected parts of a brighter red than the surrounding tis- sue. This latter is, however, more or less congested and cedematous, and not unfrequently emphysematous. When the condition has lasted longer, the ability to insufflate the lung diminishes, and may even be partly lost, and the parts thus affected may finally undergo either a sim- ple atrophy, or may become the seat of fibroid metamorphosis or of calcareous degeneration.2 These changes belong, however, rather to the pathological his- tory of bronchitis than to that of Pneu- monia, with which they have no neces- sary connection, though under the names of Carnification and Carnization3 they have often been confounded with it. The process of inflammation in the col- lapsed partsis effected through two sets of changes, which, however, differ chiefly through the degree in which they are complicated by passive congestion. In some cases this is extensive, and affects large tracts which have previously be- come collapsed, and extends also to the surrounding tissue. The cause of this con- gestion appears to be the increased impedi- 1 Oral communication. 2 Hasse (Path. Anat., Syd. Soc. Ed., p. 251) says that Pneumonia is not necessarily frequently associated with atelectasis. This may be true of primary atelectasis in the re- cently born infant, but I believe that acquired collapse frequently forms the starting-point for secondary Pneumonia. Hasse says that he has seen spots of collapse in the midst of hepatized lung, but not participating in the inflammatory changes. There is no doubt but that Pneumonia and collapse may not unfrequently be found coexisting, but I be- lieve that it is quite as common to find Pneu- monia commencing in the midst of collapsed portions, as it is to observe the condition de- scribed by Hasse. The elucidation of the origin and nature of collapse, and the recogni- tion of the distinction between this condition and Pneumonia, appear to have led many writers since the publication of the researches of Legendre and Bailly to deny too exclusively the existence of Lobular Pneumonia in chil- dren, and to attribute all the appearances of consolidation found in their lungs to the con- dition of collapse. There is no doubt as to the comparative frequency and the important pathological and clinical significance of this condition, but I believe that these have been to some degree exaggerated, and the import- ance of pneumonic changes has been in conse- quence underrated. 1 In some cases of collapse from pneumo- thorax a whole lung may thus become affected by secondary Pneumonia (Steffen, loc. cit. p. 24). 2 Hasse (Path. Anat., 250); Gairdner (Brit, and For. Rev., April 1853, p. 467; Path. Anat, of Bronchitis, p. 68). 3 It appears best to confine the significance of these terms to simple "collapse," which presents an appearance which they fully de- scribe. The application of them to other con- ditions only involves confusion. MM. Isam- bert and Robin (Gaz. M6d. 1855) have applied the title of "Gamification congestive" to a form of induration of the lung secondary to heart disease. VOL. II.-15 226 PNEUMONIA. ment to the circulation arising from defec- tive aeration of the blood, and also from the absence of the alternate expansions and contractions of the pulmonary tissue, which, under normal conditions, largely favor the passage of blood through the capillaries of the lung. To this passive congestion oedema quickly succeeds. The tissue then loses its bluish tint and be- comes of a darker purple ; much serosity exudes on section; and this, in the parts not previously collapsed, may be frothy from the admixture of air. The tissue also becomes more swollen, and the tough resistant character of simple collapse being lost, it is also rendered more friable and breaks down under pressure. To this state the term Splenization has been applied, and it is sometimes erroneously confounded with the " Pneumonic des agonises" of Piorry, though the changes now described are not, in their essential nature, of an inflammatory character. Congestion of this kind may affect large tracts of tissue surrounding collapsed por- tions, and hence it has been observed that these parts may be crepitant, or that the collapsed and congested portions may be insufflated ; and from this fact has arisen the statement that insufflation is possible in the early stages of Lobular Pneumonia. When inflammatory changes occur in such parts they appear generally in scattered nodules which are solid and granular, but very friable, and in which the interlobular septa have disappeared and the ordinary character of collapsed tissue is destroyed. These nodules are whiter in color than the dark purple tissue surrounding them, but into which they fade insensibly at their margins. They depend on the accu- mulation in the interior of the air-vesicles, of enlarged epithelial cells, mucoid cells, and pyoid cells, which fill and distend them; and hence, in addition to being solid, the parts thus affected become prominent above the level of the surrounding tissue. Collapsed portions which have become congested sink in water without pressure. Congested parts surrounding these usually float imperfectly, but sink after pressure. The pneumonic nodules sink without pres- sure. On scraping the latter a milky fluid exudes, airless, and presenting under the microscope cells of the same character as those found in the pulmonary alveoli. As the process extends, the whole of the col- lapsed and congested parts may gradually become infiltrated until the greater part is solidified, but usually the nodular form is preserved for some time with congested and. excessively oedematous tissue inter- vening between the pneumonic portions. This form of Pneumonia readily passes into the condition of gray hepatization. The congestion disappears from the infil- trated parts, and the gray appearance is produced by the rapid progressive fatty degeneration and the liquefaction of the inflammatory products, aided by the co- existence of oedema. Pneumonic changes may, however, oc- cur in collapsed portions, without being preceded by such marked evidences of congestion and oedema as those last de- scribed. Under these circumstances, the [Fig. 34. Broncho-Pneumonia.-Brom a child, aged four, with capillary bronchitis. A section of one of the patches of consolidation. Showing the stuffing of the alveoli with what appears in the main to be inhaled bronchial secretion. X 200. (Green.)] appearances presented offer a considerable resemblance to the first form of Vesicular Pneumonia, and it may be questioned whether in some cases the existence of collapse is not an accidental complication superadded to the pneumonic process, rather than an essential factor in its pro- duction. In the collapsed portions nodules ■are found of a grayish-yellow, contrasting strongly with the surrounding purplish tint of the adjacent tissue. They are also prominent about its level. They are solid, and usually granular, and yield a milky or yellowish creamy fluid on scraping or pressure. In them, however, dilated bron- chi filled with a yellowish puriform fluid are often observed, tand these may even give the appearance of small abscesses PATHOLOGY AND PATHOGENESIS. 227 scattered through the nodules; wnen evac- uated they leave small cavities. Dilated bronchi with similar characters may some- times be found in parts affected by simple collapse ;* but unless true Pneumonia be superadded, the granular character of the adjacent pulmonary tissue is absent. These appearances may occur in col- lapsed portions of lung, however origi- nating. I have found pneumonic nodules identical with those last described in the base of the lung of an adult dying of ursemic poisoning, and who had presented during life no signs of bronchitis, but in whom dulness on percussion, unattended with pyrexia, had appeared at the base during the later days of life. The whole of the lower lobe of one lung was col- lapsed, and in this part were spots of Pneumonia surrounding small dilated bronchi., which were filled with a yellow- ish pus. It has been recognized since the observations of Dr. Baly,2 that in the exhausting diseases of adults collapse may easily occur, probably from muscular weakness, though this change is compara- tively less frequent in them than in chil- dren, owing to the more yielding charac- ter of the chest-walls and the smaller calibre of the bronchial tubes in the lat- ter. Collapse is thus in many cases the first stage in the production of hypostatic Pneumonia, so frequently found in post- mortem observations. Hourmann and Dechambre had previously described ap- pearances identical with these in the lungs of the aged, as consisting of scat- tered yellow or whitish spots, from which a yellow fluid escaped, leaving behind small vesicles situated in the midst of con- gested tissue,3 and passing at times into larger nodules of a granular appearance ; and Durand-Fardel4 has confirmed these observations. It is not uncommon to find the pro- cesses of collapse, congestion, and Lobu- lar Pneumonia intermingled in the same lung, and every stage may be occasion- ally observed between them. The char- acters of the pneumonic change also vary, and in some parts nodules may be found resembling in all their essential features spots of red hepatization, as observed in the acute primary form, while in others the pneumonic portions may be white or gray, or almost diffluent, as if softening into abscesses. In all the forms now described, and in fact in nearly all cases where nodules of Pneumonia reach the surface of the lung, the pleura participates in the inflamma- tory changes, and a layer of lymph is found on the surface, which is congested and roughened. These characters may sometimes aid in the distinction between Pneumonia and simple collapse, for in the latter, though sub-pleural ecchymoses are sometimes observed, a true inflamma- tion of the pleura is rarely found. Ex- tensive pleural effusion is, however, very unfrequent in Lobular Pneumonia. Scattered nodules of red hepatization, occurring apparently without the inter- vention of collapse, and also without any appearance of direct extension from the bronchi, are found in other blood diseases. I have seen them in smallpox1 and diph- theria, and they also occasionally occur in scarlatina and typhoid fever. It is probable also that some forms of the Pneu- monia occurring in the course of typhus originate in a similar manner. These cases certainly militate against the view expressed by some recent writers, that the acute primary or croupous Pneumonia is a specific disease with special anatomi- cal characters. All these disseminated varieties of Pneu- monia, including the true vesicular or broncho-pneumonia of measles, may occa- sionally coalesce and occupy large tracts of the lung,2 and under these circum- stances also the anatomical distinctions from the acute primary disease become very uncertain, though the consolidated tissue is generally paler and whiter, and presents a greater number of puriform spots arising from the accumulation of pus in previously dilated bronchi, than are commonly observed in the acute pri- mary form. In the rarer cases, when a Lobar Pneumonia appears to be produced in adults by a gradual extension from the bronchi, there are few, if any, exact ana- tomical observations respecting the con- dition in the earlier stages. Most of these, except in old people, occur in tubercular subjects. A few pass into the condition of Chronic Pneumonia, hereafter to be described. The leading characteristic of such cases, when non-tubercular, appears to be a tendency to pass early into a state of gray hepatization. There is also in the typical forms of ca- tarrhal Pneumonia a greater amount of' proliferation of epithelial cells, and a smaller number of pus corpuscles, at least in the earlier stages, than is ob- served in the primary disease. A spon- taneously coagulable fibrinous exudation is rarely present, and the material in which the cells are imbedded is semi-fluid 1 Dr. Graily Hewitt, " Pathology of Hoop- ing Cough." 2 Communicated to and cited by Dr. West (Dis. of Infancy and Childhood, p. 291). 3 Arch. Gen., xii. 2e Ser. 274. 4 Maladies des Vieillards, 475. 1 Steffen says that yellow spots correspond- ing to puriform collections in dilated bronchi may occasionally be found in the secondary Pneumonia of variola (loc. cit. p. 294). 1 The " Pneumonie Lobulaire Generalises" of Barthez and Rillie,t. 228 PNEUMONIA. and allied to mucus, approaching in this respect the characters of the gelatinous- looking exudation which fills the air-cells in the pneumonia attending many cases of tuberculosis; I believe, however, that all gradations can be observed between these products.1 In some cases also of the most distinct hypostatic Pneumonia I have found the air-vesicles filled almost entirely with pyoid cells, resembling those seen in the later stages of the acute pri- mary disease. (See Fig. 31, p. 193.) In the further progress of Broncho- pneumonia there is little doubt but that in many cases a perfect restitutio ad integ- rum may occur, and that the lung may Fig. 35. Alveoli in Broncho-pneumonia, regain its normal condition. In other in- stances, however, dilated bronchi may persist long with some condensation of the pulmonary tissue surrounding them, but may gradually return to the normal state, as far as may be judged of from the physical signs. Abscesses also may occa- sionally form, though usually they are small in size, and gangrene is also some- times observed in the affected portions.2 In rarer instances, general consolidation of the lung may remain in a chronic form, the characters of which will be described under the head of Chronic Pneumonia. In some instances the pneumonic nodules, particularly in scrofulous and rickety children, may pass into cheesy changes with destruction of tissue, and may run the subsequent course of tubercle. Ziems- sen describes these as a true tuberculiza- tion. Barthez and Rilliet3 also describe them as surrounded by a zone of gray in- duration, precisely resembling in this re- spect the changes found around tubercles in the adult. Bartels, as already stated, has found tubercle to be a less common complication of the pneumonia of measles than is commonly believed ; but I am con- vinced, from my own microscopic observa- tions, that tubercle may occur in these spots of pneumonic change, although it may be masked, and may be undiscover- able by mere ocular inspection.1 The pneumonic changes are always limited to an accumulation of cells in the interior of the air-vesicles and terminal bronchi, and, except in very chronic forms, when interstitial thickening occurs, the walls of the alveoli themselves are not the seat of nuclear growth. The associated pathology of Broncho- pneumonia presents but few special feat- ures independently of those of the diseases of which it constitutes a complication. The dilatation of the right side of the heart, resulting from obstruction to the pulmonary circulation, may lead to per- manence of the openings of the foramen ovale and ductus arteriosus.2 Throm- 1 Legendre and Bailly only found five cases of tubercle in twenty-seven of catarrhal Pneu- monia (loc. cit. 215). Steiner (loc. cit.) de- scribes accumulations of nuclei as occurring in the interstitial tissue of parts affected by collapse, proceeding to such an extent as to fill the cavity of the alveoli. Other observers describe in the chronic forms of collapse a thickening of the interstitial tissue. I can- not but believe that such accumulations of nuclear growth as Steiner describes are of a tubercular nature. Steiner speaks of miliary granulations of tubercle in the pleura as not uncommon. I am disposed to believe, in spite of the recent statements of some high authorities, and particularly of Niemeyer, that cheesy changes in the lung are a very rare event when not caused by or associated with tubercle. 2 The patency of the foramen ovale with attendant cyanosis was observed, as early as by Jorg, to be a frequent complication of col- lapse (Diss, de Pulmonum vitio Organico, p. 1 See Appendix D. 2 This is, however, rare. Steiner only ob- served two cases. Steffen also reports two such. It is rather more common in the indu- rations surrounding chronic bronchial dilata- tions. 3 Loc. cit. i. p. 436. DIAGNOSIS. 229 bosis of the pulmonary artery is occasion- ally observed. Pericarditis is also an occasional complication. The bronchial glands are swollen and medullary-looking. Sometimes they are distinctly hypersemic, but when the swelling is extreme they may be pale. In a few cases they are unaffectea. Sometimes cheesy spots or calcified nodules are found in them, but these usually accompany tubercles in the lung. Suppuration of the post-tracheal glands leading to an ulcerative opening into the trachea was once observed by Steiner. The appearances observed in other or- gans are for the most part the result of venous congestion. (Edema and conges- tion of the brain is common in fatal cases. Meningitis of the base is a rare complica- tion. The liver is congested, and hyper- semia and catarrh of the stomach and intestines are also common. In the large intestines the catarrhal congestion may even give rise to dysenteric changes. The kidneys are also congested, and concre- tions of urates are often found in the straight tubules of the pyramids. Gen- eral dropsy is an occasional complication. Amyloid changes in the liver, spleen, and kidneys, which are sometimes present, must be regarded as pre-existing and accidental conditions rather than as re- sults of the pulmonary disease. Diagnosis.-The diagnosis of Broncho- pneumonia may be occasionally difficult, as may be inferred from the preceding description of its symptoms and physical signs. The chief points requiring to be alluded to here are the actual existence of Pneumonia in some cases of bron- chitis, and its distinction from collapse in others. Under all circumstances, the indications afforded by the thermometer are most valuable, and often aid in the interpreta- tion of the physical signs. The latter are often obscure ; but when sufficient lung-tissue is consolidated to alter the qualities of the percussion-reso- nance and of the respiratory murmurs, the following characteristics may aid in the diagnosis of Pneumonia from collapse, though, in the intermediate stages by which the latter passes into the former, many of them are but little available. The loss of resonance is more absolute in Pneumonia, and the note, though sometimes tubular, seldom possesses any of the tympanitic quality occasionally ob- served in collapse. The side is more retracted, and the sinking in of the ribs and elevation of the diaphragm are more distinct in collapse than in Pneumonia. Indeed, when the latter is extensive, falling in of the lower ribs is not observed. In collapse the respiratory murmur is weak or nil. In Pneumonia it is bron- chial or blowing, but seldom tubular, in the form of Broncho-pneumonia. Excep- tions, however, occur on this point, and pure collapse may give a metallic tone to the respiration.1 Rales are not heard as a rule in collapsed lung (though the possi- bility of their presence when dilated bronchi traverse the collapsed portion can hardly be disputed). In Broncho-pneu- monia, rales more or less approaching the crepitant or sub-crepitant type are toler- ably constant, though not invariably pre- sent. Vocal resonance and vocal fremitus are increased in Pneumonia, and the former may acquire a bronchophonic tone. They are both, as a rule, dimin- ished over collapsed portions, without alteration of the quality of the vocal resonance. Many of these points may, however, fail, and the distinction by the physical signs alone is not always easy. Under such circumstances, observations on the temperature materially assist the diag- nosis. Whether the condition of the patient be pyrexial or not, collapse alone will neither give nor increase fever ; and the presence of consolidation, together with the super- vention or increase of fever, is at least an indication that some portions of this are due to true pneumonic changes. Among other indications, the following, taken in conjunction with the pyrexia, are also of value in the recognition of the pulmonary disease : The change in the characters of the cough from a paroxysmal and painless to a short, dry, and painful one; the acceleration of the respiration and of the pulse, and the increased dis- tress and restlessness of the patient, may also serve to point attention to the true nature of the disease. When Pneumonia occurs in the lobular form in the course of bronchitis or measles, without the intervention of collapse, the diagnosis may be much more difficult. In both diseases the increase of the pyrexia, which rarely attains in the simple bron- chitis of children a temperature exceeding 100° Fahr.,2 or its continuance in measles beyond the period of the specific fever, should, even in the absence of distinct pneumonic dulness, afford grounds for a strong suspicion of pulmonary mischief, and particularly when moist bronchitic rales are also present. The distinction of Broncho-pneumonia 1 Ziemssen, loc. cit. 335. 2 I have recently seen two cases in adults where a temperature of 105° was attained in the course of apparently uncomplicated bron- chitis. 16), and also by Weber (Path, der Neuge- borenen, ii. 39). 230 PNEUMONIA. from the lobar form of the acute primary disease may in measles be occasionally difficult when the patient is seen for the first time after a large tract of lung has been invaded. If the affection be purely unilateral, the difficulty is further in- creased. In most forms of Broncho-pneu- monia the affection exists in both lungs simultaneously, though seldom to an equal degree.1 In some cases, however, when collapse has preceded the Pneumonia, the peculiar pyramidal form of the dulness may aid the diagnosis. Moist rales in the opposite lung, or in other portions of that affected, are a further clue. The characters of the pyrexia in the two affec- tions are in most cases a valuable guide, but it must be borne in mind that in the fever of the acute primary form a crisis may occasionally be wanting, and that its subsequent course also may be sometimes protracted. The diagnosis from pleurisy, under these circumstances, rests on the same grounds as that of the acute primary disease. The diagnosis of Lobular Pneumonia from acute tuberculization, or the recog- nition of tuberculosis as a complication of the Pneumonia, may at times be very difficult. This is especially the case when the disease originates in simple bronchitis ; and when the general dissemination of moist rales, accompanied by pyrexia, may often closely resemble the phenomena ob- served in disseminated miliary tubercle. In measles and hooping-cough, a febrile state associated with pulmonary symp- toms developed in the course of these affections would raise a presumption of its acutely pneumonic character. The rapid development of signs of con- solidation, with or without antecedent collapse, will, under all circumstances, favor the diagnosis of Pneumonia, but especially so in the two latter affections. As points of minor value may also be noted the fixity of the rales in cases of tuberculosis, while the dyspnoea is often more distinctly disproportioned to the physical signs than it is in Pneumonia. Usually also the strength is less markedly or suddenly prostrated in tuberculosis than in Pneumonia. Even in the later stages the difficulties may increase rather than diminish, since the progressive dilatation of the bronchi may closely simulate the formation of cavities from softening tubercle. The emaciation also and loss of strength in protracted cases of Broncho-pneumonia may bear a great resemblance to the phenomena observed in the later stages of tuberculization. Under such circumstances the observer must often remain in doubt, though his opinion may be influenced by the previous health of the patients, by their constitu- tional or hereditary predisposition, and by the evidence or not of the existence of tubercle in the lymphatic glands* The Prognosis of Broncho-pneu- monia is of much greater gravity than that of the acute primary disease. Ziems- sen records thirty-six deaths in ninety- eight cases in children, and in nine more various sequelae remained. The mor- tality of Steffen's cases, also in children, amounted to forty-one out of seventy-two cases ; in six of these, however, the lung affection was complicated by heart dis- ease, noma of the external genitals, tu- bercle, pleurisy, and meningitis. Steiner records a mortality of one in three cases. The results of different authors vary as to the relative mortality of the disorder in the different diseases of which it is a complication but, as a rule, the acute forms appear to be less dangerous than those running a more protracted and chronic course. The age of the patients affected has, however, a marked influence on the mor- tality. Bartels says that Broncho-pneu- monia after measles was fatal in all the children who had not completed their first year. From jetat. one to five the mortality was 39 per cent., and after the age of five years it was 37 per cent. The collective mortality of all the cases enu- merated by Ziemssen under one year old was as 1 : 1, occurring in equal propor- tions in measles, bronchitis, and hooping- cough :2 of the whole number of Steffen's cases the mortality before two years of age amounted to 54 per cent. The condition that most unfavorably influences the prognosis is the weakness of the patient, not only as affecting the direct possibility of recovery, but also as predisposing to further collapse. This statement explains the mortality at very 1 Ziemssen's data give the following per- centage of mortality :-Measles, 25 per cent.; bronchitis and chronic bronchitis, 43 per cent. ; and hooping-cough, 51 per cent. Steffen found the mortality from measles the greatest, amounting to five-sixths, but his cases of this disease were few in number, and affected children of very early ages. His mortality from the pneumonia of hooping- cough was as 8 : 10, and in bronchitis and chronic bronchitis, as 14 : 41 cases. Bartels' mortality in pneumonia from measles was 42 per cent., and he states that 80 per cent, of all the deaths in 573 cases of measles were due to the lungs. 2 There appears to be some omission in Ziemssen's subsequent tables (p. 329), as the totals of those affected at different ages do not correspond to the whole numbers of his cases. 1 Ziemssen and Krabler remark, however, that a double pneumonia may occasionally occur in measles so acutely as to be undistin- guishable from the primary " croupous" form (loc. cit. 169). TREATMENT. 231 early ages, and is specially applicable to hooping-cough, where collapse, which is itself due in great measure to exhaustion of the muscular powers, is frequently the direct agent in the production of pneu- monic changes ; and hence the forms of Pneumonia occurring at late periods of the disease are not only indicative of loss of strength, but also predispose, by still further increasing the already existing weakness, to induce an extension of the pul- monary changes in which they originate. For the same reasons a higher degree of fever, when of short duration, may be regarded as less unfavorable than a lower range of pyrexia, but protracted over a longer period. A temperature exceeding 105° Fahr, must, however, be considered as being of very serious augury. Among other symptoms which are to be regarded as unfavorable must be enumerated a great extension of the bronchitis over both lungs, signs of extensive collapse, increasing cyanosis, and diminished power of cough and expectoration, as shown by rales in the trachea and larger bronchi. To these must be added extreme fre- quency and particularly great feebleness of the pulse.1 Somnolence and coma, indicative of mal-oxygenation of the blood, are also serious symptoms, not only in their direct indications, but also through the injurious influence produced on the respiratory muscles and on the heart by the impaired conditions of in- nervation of which they are the evidence. Convulsions in the later stages of the disease are a most unfavorable sign. Treatment. - In the treatment of Broncho-pneumonia it must be constantly borne in mind that in the vast majority of cases this is a secondary disorder, and one whose very existence and mode of origin are very commonly indicative of weakness. This statement, which is ap- plicable to all the forms of the disease originating in collapse of the lung, is hardly less true of the cases when, as in measles and diphtheria, the pneumonia originates by direct extension of the in- flammatory process from the bronchial mucous membrane. When this fact is remembered it is scarcely necessary to mention all meas- ures of treatment calculated to depress the powers of the patients, such as ab- straction of blood by bleeding, by leeches or by cupping, tartar emetic, calomel, and mercurials in general, except to state that their employment in such cases is only to be regarded with the strongest reproba- tion, since there is no doubt but that they tend to increase the mortality of the dis- ease. Even when there is the temptation to abstract blood in order to relieve ur- gent dyspnoea, it must be remembered that the subsequent duration of the dis- ease is long, that its tendency is to pro- duce death by exhaustion, that all deple- tory measures diminish the muscular powers, and that by increasing the difficulty of expectoration they favor an increase of the collapse of the lung, which under such circumstances may speedily prove fatal. In the earlier periods of the Broncho- pneumonia of measles, unless the fever is severe, an expectant treatment, with the administration of nutritious food and the employment of salines, is all that is abso- lutely necessary. When, however, expec- toration is difficult, and when the rales in the chest are abundant, and dyspnoea is marked, the occasional employment of emetics is productive of considerable re- lief. Of these, ipecacuanha in emetic doses is the most serviceable, since its ad- ministration tends, simultaneously with the evacuation of the contents of the bron- chi, to favor a freer and looser secretion, and thus to ward off the tendency to col- lapse. The beneficial effects of emetics are seen in the relief of dyspnoea and in the diminution of cyanosis, and the tem- porary depression which they sometimes occasion is speedily recovered from in con- sequence of the relief which they afford to the breathing. If the cough is very trou- blesome and frequent, opiates may be cau- tiously used, particularly as the continued expiratory efforts, when prolonged and forcible, are among the chief agencies by which collapse is produced. This state- ment, though applicable to all forms of the disease, is especially true of those originating in hooping-cough ; and in this disease other agents capable of diminish- ing the violence of the spasmodic cough, such as opium, belladonna, alum, zinc, or the bromide of ammonium, may be also employed with advantage. In the admin- istration of opiates, however, narcotism is to be carefully avoided; and it must be remembered that this effect is easily pro- duced in all diseases in which the aeration of the blood is impeded. Such.an effect is also doubly dangerous through the dimin- ished muscular powerwhich.it entails, and the doses given must therefore be in the minimum amount sufficient to allay the cough. In cases where the expectoration con- tinues difficult and the pulse is weak, sed- atives may with advantage be combined with the carbonate and! muriate of am- monia,1 together with small doses of the 1 The preparations of ammonia are best ad- ministered. to infants in milk. Mr. Squire has recently, at my request, made a number of experiments in order to discover the best method of disguising the unpalatable flavor of the muriate of ammonia, and has done so ' Barthez and Rilliet record a case where the pulse could not be felt during many days. 232 PNEUMONIA. vinum ipecacuanlue (TTLiij to Blv), and with preparations of benzoic acid and of senega. When prostration is more marked, wine or brandy should be given in doses pro- portioned to the age of the patient. For infants it is best to commence with brandy in doses of from 5 to 10 drops every two or three hours, gradually increasing both the quantity and the frequency of the dose, until a decided effect is produced on the pulse and on the respiratory move- ments. It may occasionally be necessary to give as much as 5ss or even 3j every hour, to infants of a few months old, though it is very rarely that such an amount is required during long periods. Under its influence, however, both the pulse and the respiratory movements be- come slower, and the latter deeper and fuller; the convulsive movements are ar- rested ; the prostration and semi-coma sometimes observed are diminished or dis- appear, and the pallor mingled with cya- nosis gives place to a more natural color. It is most important that the employment of these agents should not be too long de- layed; and when dyspnoea and prostration are extreme, the action of emetics may often be assisted by their administration. When from the intensity of dyspnoea deglutition has become difficult, it is oc- casionally advisable to administer stimu- lants combined with beef-tea, or with Liebig's extract of meat, or with egg or milk, by the rectum, until the patient has rallied, and the state of depression is alleviated. Under these circumstances also, quinine and the preparations of bark may often with advantage be combined with the expectorant remedies. If diar- rhoea exists, it must be carefully combated by astringents, and by bismuth combined with these and with small doses of opium. Stimulating liniments or the application of mustard poultices to the chest are ad- visable in all these conditions, but the employment of blisters is highly undesira- ble, since they weaken the patient, and in children are liable to cause a dangerous sloughing of the subcutaneous cellular tissue. The method of treatment by cold com- presses applied to the chest has received the strongest encomiums both from Bar- tels and Ziemssen, and from their state- ments and observations it appears to be one of the most valuable of our remedial agents, particularly when the fever is high ; nor does any danger appear to arise during its employment from any exten- sion of the pulmonary disease. It appears to operate favorably in two directions, both by increasing the strength and depth and by lessening the frequency of the res- pirations, and also by the reduction which it effects in the temperature-a result which appears unattainable by any other agent, at least in an equal degree.1 Bartels particularly insists on the bene- fit derived from the first deep inspirations excited by the application of the cold compress to the thorax, in promoting the expansion of the lung, and warding off the threatened danger of increasing collapse. The reduction of temperature which follows their application is also very re- markable. In eight hours Bartels wit- nessed a fall from 105'25 to 90'8° Fahr., or of more than 8° Fahr. ;2 and Ziemssen, within seven and a half hours, observed in the rectum a fall of 5'8° Fahr. This effect is not, however, permanent, for after a few hours' intermission of the treatment the temperature again rises, and the application of cold requires there- fore in some instances to be continued during some days before the temperature is permanently reduced to the normal standard. This treatment needs to be carefully watched, since when it is prolonged with- out intermission, a dangerous degree of depression may ensue. It is, however, rarely observed until after several hours' application of cold ; but in a case recorded by Ziemssen it was noticed within half an hour after the treatment had commenced. The face under such circumstances be- comes pallid, the eyes sunken, the skin cold, and the pulse small and almost im- perceptible. This alarming state is said by Ziemssen speedily to disappear on the temporary intermission of the cold appli- cations, and neither in five cases of this nature observed by him, nor in a similar one occurring in an infant aged only thir- teen months, recorded by Bartels, did any further injurious or fatal consequences ensue, and the treatment was repeated with favorable results after the depression thus excited had passed off. Although the first application of the cold compresses is often disagreeable to the patients, a remarkable improvement usually appears speedily in their general state. Both the pulse and the respirations fall in frequency, and the former becomes fuller and the latter deeper. The pulse may fall from 170 to 130, and the respira- tions from 80 to 34 in the minute. The appearances of cyanosis simultaneously diminish, and the patient, previously rest- less, often sinks into a sound sleep while 1 Digitalis has little or no effect on the temperature of Broncho-pneumonia, and only very rarely has it any influence in lessening the frequency of the pulse. 2 This result was obtained in the axilla, and is therefore less trustworthy than Ziems- sen's as regards the general effect on the temperature of the body. very successfully by combining it with the tinct. limonis and sp. chloroformyl. OTHER FORMS OF SECONDARY PNEUMONIA. 233 still enveloped in the cold wet cloth. With the intermission of the applications the pulse and respiration again increase in frequency, simultaneously with the rise of temperature which is then observed.1 It is probable, as Bartels has remarked, that these favorable effects are not attributable solely to the artificial abstraction of heat, but that they are also due in part to a diminished destruction of tissue through- out the body, and that thus the produc- tion of an excess of carbonic acid, for the elimination of which the diseased lungs are incompetent, is also favorably held in check. The favorable effects of this system are strikingly shown by Bartels' results ; for whereas under other methods of treat- ment he lost, in the pneumonia following measles, seventeen out of twenty-six cases, or 65 per cent., the mortality after its adoption, and when no other remedies were employed, amounted to only thirteen out of forty-two cases, or little more than 30 per cent. In some cases, even when it was employed, the duration of the pneu- monic consolidation was, however, very protracted, extending in one instance to eight weeks. Under all the circumstances of the dis- ease, the hygienic treatment of the patient requires to be carefully attended to. Fresh warm air, and the avoidance of draughts, are most important points to be insisted upon, and flannel should be worn next to the skin. During convalescence the same precau- tions are to be observed, and the liability to relapse must be constantly remem- bered. It may be necessary during some months to enforce the extremest precau- tions against causes of catarrh, and during the winter months a confinement within the house, but in well-ventilated rooms, which should have a southern aspect, may be absolutely necessary in the case of children of delicate constitutions, or in those whose strength has been much re- duced by the disease. Careful attention to diet, and the maintenance of the nutri- tion of the patient, are also most import- ant. The administration of cod-liver oil and of preparations of iron, and small quantities of wine sometimes given two or three times daily, are often necessary to complete restoration; while in many in- stances a change of air, particularly in children brought up in large towns, is the most effective remedy that can be em- ployed. When the consolidation becomes more chronic, and is attended with profuse se- cretion from the bronchial mucous mem- branes, and particularly when dilatation of the bronchi exists, as shown by coarse rales in the chest, the same method of treatment must be sedulously followed. The administration of stimulants must, however, be pursued with caution when any tendency to pyrexia persists; and under these circumstances, when the weakness of the patient appears to require their employment (a condition frequently observed), it is well to administer them during apyrexial periods of the day, which must be carefully ascertained and subse- quently watched by the aid of the ther- mometer. The use of inhalations, and particularly of turpentine, has under these circum- stances been tried by Ziemssen, and with some favorable results. Other Forms of Secondary Pneumonia. Pneumonia occurring in the course of DrighVs Disease may in some cases pre- sent no special variations from the char- acters observed in ordinary acute Pneu- monia. In others it may begin, as before stated, in collapsed portions, resembling more or less in its course and characters the Lobular Pneumonia of children. Even when this is not the case, the characters of the primary disease are modified by this complication. The pyrexia is usu- ally moderate, but the sputa tend to be thin and watery, and there is a consider- able liability to oedema of the lungs and to consecutive gray hepatization. The tend- ency to pericarditis is also, I believe from my own experience, increased by this complication. Rosenstein1 has observed that when Pneumonia supervenes in Bright's dis- ease, the total quantity of the urine is diminished, but that, in contradistinction to what is observed in other conditions, the amount of urea and the specific gravity 1 Path. Therap. Nieren. Krank. The fol- lowing are the results of Rosenstein's analy- ses :- Day of pneum. Amount cc. Density Naoi, gram. Urea gram. Album, gram. 1st 600 1013 2-4 3-6 1-8 2d 650 1013 2-47 4-37 3-25 3d 600 1012 2-10 4-5 2-4 4th 700 1012 2-24 5-85 2-8 5th 700 1012 2-8 .... 2-1 6th 580 1012 2-32 4-98 1-7 7th 190 1013 0-76 1-04 0-95 1 Even in the most advanced and seemingly hopeless cases, and when the eyes appeared insensible to the stimulus of light, Bartels observed a gradual return of power, and a finally favorable result, after the adoption of this method. Death on the seventh day from suppuration and oedema of the lung. 234 PNEUMONIA. still remain below the normal standard. M. Jaccoud has drawn attention to the fact that a low specific gravity with dimin- ished water and a minor amount of urea may'aid in the diagnosis between chronic Bright's disease complicated by Pneu- monia, and the cases where albuminuria occurs as a complication of the primary disease, but in which, nevertheless, an ex- cess of urea is commonly present and the urine retains a high specific gravity. The dangers of this complication have been already alluded to. Rayer1 remarks that Pneumonia occur- ring as a complication of diseases of the urinary organs, associated with alkaline urine, has the tendency to render this secretion acid, and his statement is con- firmed by Grisolle. The Pneumonia occurring in the course of the Acute Febrile Diseases has its features materially modified by the special symp- toms of these, and presents in conse- quence so many variations that no gen- eral description will embrace the whole of the phenomena observed. In typhoid fever it usually commences during the later stages. Its invasion is rarely marked by rigors, but commonly by a rise of temperature above the stand- ard previously maintained. Fuller data are wanting on the subject of its further course. In cases which I have observed, the phenomena of crisis were absent, and when improvement has taken place it has been by a gradual fall of temperature, which may only occur after the pyrexia of the primary disease has subsided ; the resolution of the infiltration also is often slow and protracted. Greatly increased prostration and asthenia attend this com- plication. The pulse and respiration are accelerated and their ratio is perverted, and the increase in the rapidity of breath- ing, together with that of the pyrexia, may be the first indication of the changes in the lung. Cough may be almost en- tirely wanting, and the rusty sputa are, as observed by Louis, comparatively rare. The insidious mode of invasion of Pneu- monia in these cases renders a frequent examination of the chest necessary in all cases of continued fever. The Pneumo- nia commonly assumes the anatomical characters of red hepatization, but the tissue is softer and more gorged with blood than in acute primary form. Various stages of transition to gray hepatization are also found. The Pneumonia arising from diseased heart presents also in many cases the fea- tures which are most characteristic of catarrhal or broncho-Pneumonia. This is especially evident in cases of marked disease of the mitral valve. The conges- tion thus produced in the bases of the lungs may be so extreme as to give rise to dulness on percussion, but the respiratory murmur at this stage is blowing rather than tubular. There is almost always chronic cough, with frequent exacerba- tions, until finally a more acute attack supervenes, attended by oedema of the lungs, and accompanied by coarse rales. The sputa are bronchitic, clear, watery, or frothy, sometimes blood-stained, but rarely distinctly rusty or tenacious. The dulness gradually progresses, and the breathing becomes more bronchial in char- acter ; and these physical signs, accom- panied by increased vocal fremitus and by intensified though rarely by broncho- phonic vocal resonance, often appear in scattered patches, which may vary in site from day to day. Rigors are hardly ever observed as the pneumonic changes pro- gress : the invasion is gradual, and the temperature is often scarcely elevated even when the pneumonic consolidation is considerably advanced. Portions of lung thus affected are found intensely oedematous, but airless ; the sec- tion is smooth or indistinctly granular, and the pneumonic consolidation usually begins in patches of variable size, in which all gradations of the inflammatory changes may be observed. They finally, however, tend to coalesce and to pass into the condition of gray hepatization, yielding, from the oedema present, an ex- cessive amount of turbid fluid on pres- sure. The frequency with which Pneumonia occurs in the course of other chronic and exhausting diseases has been already re- ferred to. It is usually of the hypostatic form, and tends to appear in scattered nodules in the midst of congested tissue ; and, as before stated, it is not improbable that in many cases it is produced through the intermediate mechanism of collapse. The nodules are very soft and friable, often whitish, and distinct, and break down easily into a pulpy debris. Its invasion is rarely preceded by rigors; cough and sputa may be alike absent, and the only evidence of the disease until de- tected by the physical signs, are the su- pervention of pyrexia-commonly mod- erate in amount-and some acceleration of respiration. Pneumonia is under these circumstances, very frequently the direct agency by which a fatal termination is induced. The Pneumonia from pycemic condi- tions, or Metastatic Pneumonia, has been already described in this work under the head of Pyaemia. (See Vol. I.) The treatment of these forms of Sec- ondary Pneumonia rests upon the same principles as have been described as ap- plicable to all the adynamic forms of the acute primary disease. Briefly, it may be described as consisting almost exclu- 1 Maladies des Reins, i. 573. APPENDICES TO ARTICLE ON ACUTE PNEUMONIA. 235 sively in the administration of sufficient quantities of stimulants and support. In the Pneumonia of the continued fevers, these indications are especially called for, and considerable amounts of alcoholic fluids must sometimes be given in order to sustain the patient's strength. In Pneumonia complicating heart dis- ease, digitalis may often be given with advantage in moderate doses, wrhen the pulse is rapid and small; but the admin- istration of stimulants is by no means to be omitted. The carbonate and muriate of ammonia may also be used with benefit under these circumstances. APPENDICES TO ARTICLE ON ACUTE PNEUMONIA. Appendix A. ON THE PULSE IN ACUTE PNEUMONIA. The accompanying wood-cuts represent the chief forms assumed by the pulse in various stages and in different degrees of severity of the disease. The first three were taken from a man, aged thirty, with consolidation of the lower two-thirds of the right lung, and they depict the gradual improvement fol- lowing the crisis and during the adminis- tration of stimulants. No. 1 was taken on the eighth day, when the temperature was 104'8, and when great prostration was present. The frequency of the pulse was 110. It was distinctly jerking and excessively com- pressible. The number of the respira- tions was forty. The tracing shows a slight tendency to dicrotism. The recoil is rapid, and the curve with the convexity downwards, corresponding to the normal condition of arterial tension, is almost entirely absent. On the evening of that day the first marked remission took place by a fall to 102'8, and by the ensuing evening the temperature had fallen to 98'4, above which no further rise ensued. No. 2 represents the pulse on the ninth day of the disease and after the tempera- ture had fallen to normal, and the patient 236 PNEUMONIA. had taken during twenty-four hours rather more than three ounces of brandy, in doses of 5ij every two hours, with carbonate of ammonia gr. iij every four hours. The arterial tension and also the cardiac power are shown to be greatly increased, by the prolongation of the recoil, and by the even, gradual, downward curve of the descending line. The tendency to dicro- tism has also almost disappeared. On the eleventh day, as seen in No. 3, the pulse had nearly regained the normal standard. The same treatment had been persisted in throughout this period, though the brandy was given at the longer inter- vals of from three to four hours. During this period the pulse had fallen to 72 and the respirations to 30 in the minute, and on the following morning the normal pro- portion of 84 to 20 was regained in their ratios. No. 4 is a tracing taken on the fifteenth day of the disease, from a man of dissi- pated habits, who was accustomed almost daily to drink excessive quantities both of beer and of spirits. The Pneumonia in- volved the lower two-thirds of the right lung. The disease in this case ran a pro- tracted course. An imperfect crisis took place on the ninth day, but the fever re- turned, and only subsided on the twenty- second day, with occasional slight subse- quent exacerbations occurring until the thirtieth ; on the fifteenth day, when this tracing was taken, the temperature was 100°, the pulse 92, and the respirations 32. Puriform sputa, indicative of gray hepa- tization, appeared early; and constant delirium with intense prostration, and profuse perspirations, were prominent symptoms throughout the case. Large quantities of brandy were necessary from the outset, and from the eleventh to the twentieth days (including therefore the time when this tracing was taken) brandy was administered in doses of an ounce and a half every hour continuously. The pulse was very weak throughout, and was fre- quently intermittent. The tracings show great deficiency in cardiac power and arterial tension, but dicrotism is not ob- served here. Tracings 5 and 6 are those taken on the sixth and seventh days in a case ending fatally on the tenth day. The Pneumonia was double, affecting nearly the whole of both lungs. Pericarditis was also present. The pulse tracings show an extreme de- gree of dicrotism, and in No. 6 "hyper- dicrotism" (Anstie) is seen in the line of the recoil falling below the level of the rest of the tracing. The temperature on these days was respectively 104° and 104-8°. The pulse was 120, and the res- pirations 60 in the minute. Brandy was given freely in this case, but not in the same amount as in the last instance. Appendix B. ON THE RETENTION OF CHLORIDE OF SODIUM IN THE SYSTEM, AND ITS PRESENCE IN THE SPUTA IN PNEU- MONIA. A diminution of the quantity of chlo- ride of sodium in the urine is common to a great number of febrile diseases. It is not, however, constant in them, nor is total suppression invariably observed in cases of Pneumonia. It would appear, therefore, that it is governed by some of the general laws of pyrexia; and although in Pneumonia the sputa and also the in- flamed pulmonary tissue are found to present a considerable amount of chloride of sodium, as pointed out by Dr. Beale, yet this is hardly sufficient to account for "the deficiency below the normal average (177 grains, Parkes). Dr. Beale found in one case that while the urine was abso- lutely deficient in chloride of sodium, the amount contained in the sputa was 10 per cent, of the solid matters. Dr. Beale thought that the chlorides were attracted to the inflamed lung as a consequence of the rapid cell-formation taking place there. When the chlorides were reap- pearing in excess in the urine, a similar excess was found in the serum of a blis- ter, amounting to 8'93 of the solids, which Dr. Beale attributes to re-absorption from the lung during the period of reso- lution. (It must be remembered, how- ever, that the serum of a blister is also an inflammatory product.) In a case ending fatally, the following proportions of chlo- ride of sodium were found by Dr. Beale in different parts:- Chloride of Sodium. Per cent, of solids. Urine 0 Blood from heart 0'68 Hepatized lung 2'59 Healthy lung 1'43 It would appear desirable that some anal- yses of the blood should be made during the period of absence of the chlorides from the urine. I subjoin analyses of the urine and sputa in a young adult man, the subject of double Pneumonia, in whom, however, the temperature did not rise to any marked height. The analyses of the urine were conducted for me by my friend and then clinical assistant, Dr. Poore; those of the sputa were conducted by Dr. Meusel, assistant to Prof. Williamson, in the Birkbeck Laboratory in University College. The case is so far complicated that until the tenth day the patient took daily 40 grains of hydrochlorate of ammo- nia, which would probably increase the amount of chlorides both in the urine and sputa. It will be seen, however, that in APPENDICES TO ARTICLE ON ACUTE PNEUMONIA. 237 the early days the amount excreted in the sputa by no means complemented the de- ficient excretion by the urine. No cause could be assigned for the diminution of the urea on the eleventh day. A similar decline will also be noticed in the urinary chlorides from the eleventh to the four- teenth days. The patient perspired freely during this period, and possibly a consid- erable amount of chlorides may have been thus eliminated by the skin, though the amount of the water of the urine was less affected than the chlorides during this period. Day of disease. Temp, max. Urine, amount in co. Sp. gr. Urea. Grains. Chlorides. Grains. Sputa Chlorides. Grains. Total. Total excreted chlorides in urine and sputa. Grains. 3d day 102-8 | 17-6 4th " 103 5 th " 101-2 970 1020 598-68 11-19 I 1 ^•'7 19-7 (est.) 6 th " 101-4 870 1020 535-72 16-786 24-586 " 7 th " 101-5 1450 1019 792-71 50-204 5-37 55-574 8th " 100 1210 1020 670-82 64-142 6-0 70-742 9 th " 99 1560 1020 792-79 95-896 6-34 102-236 10th " 100 1830 1016 605-86 119-658 3-803 123-461 11th " 99-8 1510 1015 488-33 36-806 2-78 39-586 12th " 99 1370 1015 506-35 71-610 14th " 98 1860 1015 657'20 48-756 ...... 15th " 97 (?) 1380 1013 382-33 147-955 16th " 98 2135 1012 509-58 50-880 17th " 98-5 1800 1011 388-20 157-850 18th " 98-5 2050 1010 473-5 115-808 The amount of urea subsequently va- ried between 385 and 462 grains during the succeeding five days. On admission the right base alone was affected, the left became implicated on the fourth day. Free perspiration commenced on the sev- enth day and continued on subsequent days. The sputa, which at first were copious, on the ninth day had lost their rusty tint, and had become bronchitic in character; on the tenth day they were much diminished in amount, but on the eleventh some rusty tint remained. The physical signs had only completely disap- peared on the thirtieth day. Appendix C. The cause of the granular appearance of a pneumonic lung has been a subject of much dispute. The question will be found discussed at length in the works of most writers on the subject of Pneumonia, particularly by Laennec, and also by An- dral, "Clin. Medicale;" Chomel, "Lee. Clin. Med., PneumonicDr. Williams, art. "Pneumonia," Cycl. Pract. Med.; Addison, "Works," Syd. Soc. Ed.; Hodgkin, "Morb. Anat, of the Mucous and Serous Membranes," vol. ii. It was by these writers, in varying degrees, at- tributed to swelling of the walls of the air-vesicles, to interstitial exudation in the walls, and to the filling of the air- vesicles themselves with exudation ma- terials. The merit of having first dis- tinctly asserted in this country that the exudation took place into the interior of the air-vesicles, is claimed for Dr. Addi- son, and Dr. Hodgkin admitted that his views on the question had been changed by Dr. Addison. Dr. Addison's state- ments on this subject are, however, some- what contradictory, as it would appear from his writings that he regarded the solidification of the lung during the stage of red hepatization as due to the swelling of the walls of the air-vesicles (loc. cit. pp. 8, 21), and that even gray hepatiza- tion was attended with a similar change (loc. cit. p. 22), and that at a later stage the softening of the walls admitted "of an albuminous material being poured into their cavities." In another passage, however, he states (loc. cit. p. 18) that "Pneumonia has its original and essen- tial seat in the air-cells of the lungs, and that the ordinary pneumonic products are poured into these cells." Dr. Addison's editors and former pupils asserted that he distinguished red hepatization from gray hepatization by the fact that the former consists in the swelling and gum- ming together of the walls of the air-cells without effusion into them, and that the latter consists of an albuminous effusion into the cells. (Editor's preface, loc. cit. p. 25.) This distinction cannot now be regarded as tenable; for in the first stages of Pneumonia the inflammatory products accumulate in the interior of the vesicles, and the walls are unaffected except by vascular hypereemia. In the recognition of the intra-alveolar exudation, Addison was, however, according to Virchow (Ges. Abhand. p. 725), preceded by Lobstein (Arch. Med. de Strasbourg, 1835, No. 1). 238 PNEUMONIA. Virchow (loc. cit.) states that the inten- sity of the granular appearance depends on the solidity of the exudation, and that it is less marked in the lungs of children, of old people, and also in dogs, because the exudation in them is commonly more fluid in its consistence. The granular appearance may, however, be distinct in the lungs of children, though on a finer scale than in adults. It may be still a question whether this appearance may not be in part due to the post-mortem co- agulation of fibrinous and other materials, which during life are semi-fluid; and whether the exudation matter in the lungs may not undergo changes similar to those which ensue after death in other organs, such as the liver, the spleen, and the mus- cles (as shown by Kuhne's researches), through which they acquire increased firmness after life has ceased. Toul- mouche (Gaz. Med. x. 489) found in pneumonic lungs examined very shortly after death, that a quantity of fluid blood escaped from the cut surface. Appendix D. THE ORIGIN OF EXUDATION AND OF CELL-PRODUCTS IN INFLAMMATION. The account of Cohnheim's researches may be found in Virchow's Archiv, vol. xl. 1867. It is due to earlier observers to state that although Cohnheim has by means of woorara found an admirable me- thod of observing the escape of the white corpuscles through the walls of the blood- vessels, and has reduced it to a true dem- onstration, he was, however, anticipated in his observation by Dr. Addison of Brighton (Exp. and Pract. Researches on Inflammation, 1843; Healthy and Dis- eased Structure, 1849), by Dr. Waller in 1846 (Philosoph. Mag. vol. xxix. pp. 271- 398), (I am indebted to Prof. Sharpey for this fact), by Zimmermann (Prager Vier- teljahresch. 1852, vol. xxxv. p. 145), and still more recently by Dr. Lionel Beale (Microscop. Journ. xii. 1864). Dr. Beale describes the so-called white cells of the blood as multiplying in loco from the germinal matter of the nuclei of the capil- laries, and he states that portions of this germinal matter pass through the capil- lary walls, and grow externally into cell- forms in the exudation. If I rightly interpret Dr. Beale's view expressed in other places on this point, he regards the solidified parts of the exudation as the " formed material" produced by "germi- nal matter"-an opinion corresponding in some respects with Virchow's that fibrin- ous exudations are the product of tissues in an excessive state of nutritive activity. Virchow, indeed, believes that in most instances the connective tissue, from the close relation which it bears to the lymph- atic structures, is the origin of fibrinous exudation (Gesch. Abhand. p. 137). Buhl, however (§itzungsbericht der Akad. der Wissensch. zu Munchen, 1863, vol. ii. p. 59), has argued that, when this exudation occurs on mucous stirfaces, the material so produced may be the result of trans- formations effected in the blood-plasma by the agency of epithelial structures. Vir- chow (loc. cit., and also in Archiv, vol. iv. p. 310, and in Spec. Path. Therap. vol. i. art. " Entziindung") has pointed out that the exudative processes of inflamma- tion have a close analogy to secretions, and that the fibrinous exudations are at times more or less interchangeable with those in which a material resembling mucin is formed; and further, that all de- grees of transition, in respect to the quali- ties of the exudation, may be observed between catarrhal and "croupous" inflam- mations. These statements have a great interest and an important bearing in the processes observed in Pneumonia, where these transitions in the nature of the exu- dation may be observed in its different stages. They serve also to show that the boundary-line between the so-called croup- ous and catarrhal forms, on which some recent authors have especially insisted, is by no means so sharply defined as is now sometimes believed; while in the latter, as noticed by MM. Ilerard and Cornil (Phthisie Pulmonaire, p. 135), a true fibrinous exudation may be occasionally observed. Appendix E. ON THE TREATMENT OF PNEUMONIA BY VENESECTION. As it is still at least theoretically main- tained by some that the statistics of cases of Pneumonia treated by venesection show a superiority for this procedure over other methods, it appears desirable to give a short sketch of the principal data which are accessible on the subject. All statis- tics on this subject are more or less beset with fallacies, but the final conclusions to be drawn from them appear to me to be those which I have stated. The arguments in favor of venesection rest chiefly on the data given by Louis' and Grisolle,2 with whom also may be ranked Wunderlich,3 who has recently supported the same view. The weight of Louis's and Grisolle's argument goes to show that cases bled early, within the first four days, have a more speedy recovery than those bled at 1 Rech, sur la SaignSe. ! Loc. cit. 3 Arch. Phys. Heilk. 1856, xv. APPENDICES TO ARTICLE ON ACUTE PNEUMONIA. 239 iater periods. Louis stated that cases bled within the first period had an average duration of seventeen days, those within the second, an average duration of twenty days ; and in a second series he contrasted the duration under the same circum- stances, as being in the first instance be- tween twelve and fourteen days, and in the second between fifteen and eighteen days. Grisolle states that in patients bled in the "first stage," convalescence began on the tenth day and was completed within three weeks ; while in those bled in the second stage, convalescence began on an average on the twelfth day, and they were discharged on an average on the twenty-second day. Both Louis and Grisolle date convalescence from a day or two after the cessation of the fever. If, however, these data are compared with the periods at which it is shown that the fever naturally tends to decline without active interference, it would appear not unjustifiable to infer that, regarded from the "positive" side, this evidence has no bearing on the absolute value of early bleeding, though demonstrating the rela- tively injurious effect of late bleeding in the disease. Looking at the general results of these test cases, we find, however, that the mortality under Louis 1 amounted to 32 out of 107 cases, or 30'8 per cent., while that of Grisolle in 233 cases was 15'8 per cent., or 10 per cent, for the earlier bleed- ings, and 17'5 per cent, for the later ; a mortality which in Louis's cases is vastly in excess of the average results of an ex- pectant treatment, and in Grisolle's is only so to a less degree. Por an absolute comparison of the re- sults of the bleeding and non-bleeding plan by the same individual, the most authentic data are those of Grisolle, Wun- derlich, Huss, Dietl, and Dr. Todd. The two former have attempted to show that a number of cases treated by venesection have on the whole a shorter duration and a more favorable course than those in which no abstraction of blood is practised. Grisolle's data only rest on a comparison of eleven mild cases left to absolute expec- tancy (including a rigorous French diete), and thirteen of the same type treated by bleeding. In the former, he states that the convalescence only began on the tenth day, and the disappearance of the physi- cal signs was protracted to the twenty- seconder thirtieth, while in the latter the fever disappeared on the average on the seventh, and the physical signs on the twelfth days. These data have a certain incontestable value, but the number of cases is too small to weigh largely in the balance of evidence derived from the natural history of the disease. Wunderlich's evidence is also in favor of bleeding. Ue gives a total of 190 cases, with an average mortality of 11'57 per cent.; 76 were treated without bleeding, with a mortality of 17'10 percent., and 47 with bleeding, with a mortality of 6'38 per cent. The data as to sex, age, and complications are, however, here also very imperfect.1 In contradistinction, how- ever, to the almost universal evidence of other authorities, he considers that in eighteen cases of those bled on the first or second day, there was an almost immedi- ate cessation of the pneumonic process in ten (i. e. crisis on the second,2 third, and fourth days), and in five more a diminu- tion of the pyrexia. Traube (Ueber Krisen und kritische Tagcn) had before asserted that as the natural tendency of Pneumonia is to a crisis in the uneven days, active therapeu- tic interference by emetics or bleeding was likely to induce the crisis at these periods. Thomas,3 however, as the result of his researches, made eight years later than Wunderlich's, but in the same hospital, asserts that bleeding has little or no influ- ence in the reduction of temperature, and that the course of Pneumonia is identi- cally the same, both under " active" and indifferent treatment; and the same re- sult had been before arrived at by von Baerensprung,4 one of the earliest obser- vers on this subject. Thomas further points out that the effect of bleeding short- ly before the crisis is in some cases to pro- 1 Wunderlich, gives collectively 114 cases in whom local bleeding (58) (?), general bleeding (47,) and spontaneous hemorrhage (9) occurred. The evidence deduced from the latter is, however, almost valueless; in seven of these epistaxis occurred simulta- neously with the crisis ; in two females men- struation took place at an early period of the disease, and in one of these the crisis followed its cessation. Wunderlich gives no collective data, but only selects typical numbers ; e. g. he only analyzes thirty-two of the seventy-six cases where no bleeding was practised. 2 This result is certainly remarkable when compared with the average frequency of the crisis on the third day. The amount of blood drawn was from seven to sixteen ounces. 8 Arch. Phys. Heilk. 1864. It may be worth remarking that Thomas's data respect- ing critical days, before quoted, do not include these cases of Wunderlich's, though made in the same hospital. Thomas states that his observations date from 1860. Wunderlich's paper was published in 1856. 4 Muller's Archiv, 1851, p. 174. 1 Louis's own data afford one of the best evidences of the fallacies inherent in this class of statistics, for the percentage of mor- tality in his first series is greater in those bled during the first four days than in those bled later, in the proportions of 42'8 to 25 per cent.; a fallacy which Louis himself pointed out and rightly attributed to the comparatively advanced ages of the patients who constituted the former class. 240 PNEUMONIA duce an unnaturally low temperature after this has occurred. As such extreme de- pressions of temperature are almost always associated with marked prostration, this result of venesection can by no means be considered a desirable one. Dietl's observations have been before alluded to, but they afford very strong arguments against the utility of venesec- tion. Uis first observations1 on 380 cases gave the following results :- Huss asserts that there was no differ- ence in the character of the pneumonias admitted during these periods, and he concludes that the difference is to be at- tributed solely to the influence of treat- ment.1 Huss further adds that, in his that the corresponding numbers of the two sexes during these periods were as follows:- 1840 to 1847. Males . 773 cases. Females 147 " 1848 to 1855. Males . 1195 cases. Females 220 " Venesection. Tartar emetic, large doses. Expectant. No. of Cases 68 106 189 Mortality per cent. 20 20'7 7-4 1 I have analyzed Huss's tables, to see if any difference in age of the patients treated could have had any influence on these re- sults, but the subjoined table, constructed from his, would appear to negative the possi- bility :- Dietl's statistics, in exact opposition to Grisolle's, show that cases left to a purely expectant treatment have a shorter dura- tion of the pyrexial period, and a more rapid convalescence than those treated either by bleeding or tartar emetic, while the age of the patients and the complica- tions present appear to have been nearly equivalent under all the systems tried. In a later publication2 he gives the statis- tics of 750 cases (412 males and 338 fe- males), all treated without venesection in the four years 1847-50, with a mortality of 9'2 per cent. Many of these were com- plicated (389 cases), including all the fatal cases; a large proportion (515 cases) suf- fered from "severe" dyspnoea. In the majority of those who recovered, the py- rexia lasted only from five to eight days, and the convalescence in most, from seven to fourteen days. Huss's observations, extending over a period of sixteen years, brought him to the conclusion that during the time in which bleeding was indiscriminately prac- tised in the hospitals of Stockholm, the mortality was greater than after it had been discontinued. During the former period of eight years, from 1840 to 1847, when venesection was generally employed, the mortality was 11'54 per cent., and during the succeeding eight years, from 1848 to 1855, when it was rarely resorted to, it was 10'21 per cent.; or the mortal- ity of the former period exceeded that of the latter by 1 '33 per cent. The average duration of the disease in those who re- covered during the latter period was also shorter, being 20'9 days in the former, and 18'12 days in the latter. The contrast of the effects of the two systems of treatment on the duration of the disease was markedly greater in the females than in the males ; the average duration in the former being 7'6 days shorter in those not bled, while in the latter the difference was only 1'83 days.3 Age .... 5-10. 10-20. No. of cases. Per cent, of deaths. No. of cases. Per cent. of deaths. 1840 to 1847 Bleeding 3 333 104 7-6 1848 to 1855 Non-bleeding 6 0 125 4-8 Age .... 20-30. 30-40. No. of cases. Per cent, of deaths. No. of cases. Per cent, of deaths. 1840 to 1847 Bleeding 1848 to 1855 Non-bleeding 430 611 6 5-2 321 495 10-5 10-8 Age .... 40-50. 50-60. No. of cases. Per cent, of deaths. No. of cases. Per cent. of deaths. 1840 to 1847 > Bleeding 1848 to 1855 ) Non-bleeding 5 125 238 22-4 16-7 49 76 18-3 23-7 - Age .... 60-70. 70-80. No. of cases. Per cent, of deaths. No. of cases. Per cent. of deaths. 1840 to 1847 Bleeding Non-bleeding 1848 to 1855 7 22 14 2 27-2 1 3 0 66.6 The totals of those above and below aet. 40 may be represented thus.- Under 40 Years. Over 40 Years. No. of cases. Per cent, of deaths. No. of cases. Per cent, of deaths. 1840 to 1847 1848 to 1855 858 1201 9-5 7-4 182 341 20-8 19-3 1 Der Aderlass in der Lungen Entziindung. * Wien. Med. Woch. 1852. Schmidt's Jahresb. 1852, Ixxvi. p. 30. 3 An analysis of Huss's statistics shows It will thus be seen that a minor degree of mortality exists both for cases below and APPENDICES TO ARTICLE ON ACUTE PNEUMONIA. 241 opinion, treatment by bleeding disturbs ' the natural tendency of the disease to crisis, a result before pointed out by Baglivi and adopted by Grisolle. If we look at the effect of large bleed- ings indiscriminately practised, we see an enormous excess of mortality attending the treatment. Many of the data of these are very contradictory, but some are all but conclusive.1 Andral's mortality amounted to more ! than half his cases, or thirty-six out of sixty-five. Of the uncomplicated cases, nine were bled in the first stage of con- gestion, and two died ; of thirteen bled in the second stage, five died ; of seven bled in the third stage, all died ; and of thirty- six complicated cases, twenty-two died.2 The mortality of Bouillaud, according to his own report, was only 11 per cent., ac- cording to Pellatan's 12 per cent. Louis's mortality we have already seen. That of Chomel, according to Louis's report, was 32 per cent. Rasori's-a treatment com- plicated with enormous doses of tartar emetic-gave a mortality of 22 per cent. The mortality of Broussais is given at 68 per cent. Many will contrast with these the re- sults of Dr. Bennett before alluded to, which even if considered exceptionally favorable, demonstrate that during a period extending over sixteen years a very large number of cases of Pneumo- nia, taken indiscriminately, may recover perfectly without venesection,1 in the ab- sence of serous complications, although presenting in some instances the most marked forms of dyspnoea and lividity of face, associated with double Pneumonia, or an extensive affection of one side in- volving in fifteen cases the whole of one lung. They further show that the period of convalescence and the duration of the disease do not exceed, and in many cases fall very short of, those observed when venesection is practised. Nor can we re- fuse to admit the conclusive evidence of his facts adduced from the same field of observation, that while the mortality from Pneumonia in the Royal Infirmary of Edinburgh, prior to 1848, and when large bleedings were practised, was 36 per cent., this diminished during eight years when bleeding was less employed to 21 percent., and in the following nine years to 11 per cent., while in Dr. Bennett's own practice it has only amounted to 3 per cent. Dr. Todd2 also pointed out that while the mortality from Pneumonia treated by bleeding combined with the use of tartar emetic amounted to one in six cases, this under a treatment by salines, nourish- ment, and support was only one in nine. The argument that Pneumonia has changed its type and has acquired of late years a more asthenic character than it formerly possessed, is one on which exact data are necessarily wanting.3 above 40 in the second half of this period of sixteen years, though the number of cases in both instances is larger than in the preceding period, but that in the later decennial epochs of life, after aetat. 50, the mortality, as shown by the first table (in the second period of non-bleeding), absolutely appears to be great- er. This is, however, probably fallacious, owing to the smaller number of cases on which they are calculated, since, in the face of the positive evidence to the contrary, it would be absurd to believe that venesection is relatively less dangerous at advanced ages. The data in Huss's tables give no means of forming further accurate comparisons on the influence of sex as compared with age, or of the complications present. The former, as far as I can gather from his tables, appears to be immaterial-the latter remains unan- swered ; but in dealing with such large num- bers the probable influence of this cause of fallacy in the comparison is reduced to a minimum. The fluctuations in the mortality in different years appear, as already pointed out, to have been almost as great in the lat- ter as in the former period. 1 How uncertain such data may be appears from a communication made by Skoda to Dr. Balfour, that in 1840 he treated sixty-four females by large bleedings and tartar emetic, with only one death, but that in the same year the deaths among the males brought this average mortality to 12-5 per cent. (Brit, and For. Med. Chir. Rev. 1846, xxii. p. 590.) 2 Analysis by Dr. Markham. 1 Nine of Dr. Bennett's cases were bled be- fore he saw them, and to an extent varying from twelve to thirty ounces; sixteen more were subjected to limited bleeding by leeches or cupping: the amount so lost is calculated by him as varying from one and a half to eight ounces. These cases had not a more favorable course than those not so treated. 2 Clinical Lectures, p. 310. 3 It is impossible to give more than a very superficial sketch of the able and elaborate arguments which have been advanced in this controversy. They will be found for the most part contained in the Edinburgh Medi- cal Journal for the years 1856-59, in papers by Drs. Alison and Christison, Sir Thomas Watson, Dr. Bennett, Dr. Gairdner, Dr. Bal- four, and Dr. Mitchell. An admirable sum- mary of them is contained in an article at- tributed by Dr. Bennett to Dr. Sibson, " The Blood-letting Controversy," in Brit, and For. Med. Chir. Rev. 1858. The question of the theory of the "change of type" in acute in- flammation is fully considered and negatived by Dr. Markham in the Gulstonian Lectures for 1864, "Bleeding and Change of Type in Diseases," and also by Dr. Balfour, " Haema- tophobia, an historical sketch," Edin. Med. Journ. 1858. To the latter the author is in- debted for much of the earlier history of the schools of opinion on this subject. To Dr. VOL. II.-16 242 PNEUMONIA. Cullen's description of high fever and of a full bounding pulse applies to pleu- risy as well as to Pneumonia, and in- stances of this class of symptoms in both diseases in young adults are not now, I believe, so very rare as they are sometimes stated to be. Such cases of Pneumonia, however, are those most likely to recover under any circumstances, and the state- ment that they " bear" bleeding better than the more adynamic forms of the dis- ease is no proof of the utility of the treat- ment, but only of the minor degree of danger attending it under these circum- stances, while there is abundant evidence that in the majority of such cases it is, to say the least, superfluous. Further, the soft and yielding pulse, which is the most common in Pneumonia, has been shown by Dr. Balfour, from Dr. Gregory's own records, to have been prevalent in his time, as now, but that it certainly formed no obstacle to his course of venesection. The argument of Drs. Balfour and Mark- ham, that this asserted change of type was not recognized by some of the most acute observers then practising for nearly twenty years1 after it was said to have begun with the epidemics of cholera and influenza in 1830 and 1832, and that bleeding was only discontinued after the experiment of an expectant treatment had proved its inu- tility, appears also a very forcible one. Bleeding was instituted and practised on the theoretical ground of humoralism, or on the mechanical (or " hydraulic, " Bal- four) ground of relieving the congested lung. It was held to be the almost univer- sal remedy for fever and inflammation, irrespective of age or sex, and that at a pe- riod antecedent to the more perfect recog- nition of Pneumonia by means of physical diagnosis, which has been supposed to have extended the practice ; but the final proof of experiment necessary to an in- ductive science was not applied by its advocates, and when thus applied the inutility of the treatment was immedi- ately demonstrated. The analogy also of a change of type in fevers is a most doubtful one, since there is the strongest reason to believe that those referred to by Sydenham and others were not differ- ent manifestations of one disease, but were in reality the different forms of ty- phus, typhoid, and relapsing fever, whose specifically diverse nature was not recog- nized until the writings of Sir W. Jenner. Dr. Balfour's historical researches have proved that this question is by no means a new one, but that it has descended to us from the followers of Pythagoras as opposed to those of Galen, and that even in the last century the same argument was advanced when the opponents of ven- esection had demonstrated its inutility in acute disease; Dr. Markham has also shown that it was supported by no less an authority than John Hunter. The opinion that such a change of type has taken place within more recent periods is further controverted by contemporary though indirect evidence. Laennec stated that the success of Dumangier in the treatment of Pneumonia without bleed- ing was equal to that of Corvisart, who bled freely; and Dr. Balfour observes that at the very time Dr. Gregory was practising his enormous bleedings, Laen- nec asserted that the treatment of Pneu- monia by tartar emetic alone had reduced its mortality to 3 per cent. The argu- ment also involves this remarkable para- dox, that a disease in its asthenic form is, in the abstract, vastly less dangerous than when presenting a sthenic type; a paradox utterly confuted by our daily ex- perience, not only of this, but of all other inflammatory diseases. This paradox ap- pears in some of the ablest arguments advanced in support of the theory of a change of type in acute disease, since one of its most eminent advocates hails with satisfaction some signs of a return of the sthenic character. The history of the origin of the change of treatment from venesection to a milder system also militates strongly against this view. Skoda and Dietl commenced their investigations on the results of expectant treatment on purely experimental grounds, and the former to the present day denies1 any recognizable change of type in the forms of Pneumonia observed by him.2 As a final conclusion of the argument, it must, the author believes, be admitted on the evidence brought forward, that at no period since A. D. 1700 has blood-letting in Pneumonia been shown to be a general necessity in the disease; and that although on more than one occasion since this date a change in the vital characteristics of the disease has been asserted, in order to ex- plain the recovery of patients suffering from it, on whom no venesection was practised, yet that no valid proof has been afforded that such a change has really at 1 Allg. Wien. Med. Zeit. viii. 1863. Schmidt's Jahrb. cxx. 34. 2 A denial also maintained by Bouilland, who is stated by Dr. Bennett to pursue his system of venesection coup sur coup with una- bated energy, and with the fullest belief in its success; while Grisolle, on the other hand, though still holding venesection to be the best treatment, asserts his belief that "la constitution medicate est moins inflammatoire qu'il y a vingt ans." Bennett's work on Pneumonia, and to Dr. Sibson's article, the author is indebted for many valuable statistical contributions. 1 Dr. Balfour cites Dr. Alison as writing in 1844 ("Pathology"), that bleeding was the most important remedy for Pneumonia. INTERLOBULAR PNEUMONIA. 243 any time taken place. [To indicate that I am not alone in maintaining that the use of venesection is not obsolete (but rather has of late partially revived) in American practice, I may quote some re- marks made recently, in a discussion in the Philadelphia County Medical Society,1 by Prof. Wm. Pepper : "If a patient is seen early, before hepatization has oc- curred, and while, although the central part of the affected area is probably so seriously damaged that fully developed inflammation will there occur, there is a zone surrounding this where the vessels are merely extremely congested, and where, if a prompt relief of this engorge- ment can be effected, proliferation and diapedesis (i.e., inflammatory exudation) may be prevented. Now, at this stage I feel sure that prompt venesection will favor such a good result, and thus may possibly abort or, at all events, limit the extent of the inflammatory process. This same effect may be secured in a less de- gree, but with more safety, in cases where any doubt exists as to the propriety of general venesection, by leeching or wet cupping; but later, when the local dis- ease is fully developed, venesection seems to me of doubtful propriety. The only advantage to be hoped for would be the relief of a laboring and over-loaded right heart, and this relief would necessarily be transient, since the mechanical cause would remain. It seems, therefore, that in most cases, after full development of hep- atization, failure of the right heart from over-loading may be treated more success- fully by other means than venesection."] INTERLOBULAR PNEUMONIA. - INFLAMMATION OF THE IN- TERLOBULAR TISSUE OF THE LUNG. Tins is the acute form, and in the human subject is a disease of the ex- tremest rarity. Dr. Hodgkin2 alludes to it, and it has been figured by Sir R. Cars- well.3 Dr. Stokes4 also describes a case where "the substance of the lower lobe was completely dissected from its pleura by the suppurative inflammation of the subserous mucous membrane. This pro- cess also was found to have invaded ex- tensively the interlobular and intervesicu- lar cellular tissue, so as to cause this part of the lung to resemble nearly the struc- ture of a bunch of grapes. All these nearly isolated lobules were surrounded by puriform matter, in which they hung from their bronchial pedicles." The ex- act condition of the vesicular texture is not described by Dr. Stokes, but his de- scription would lead to the inference that it was in a state of hepatization. Roki- tansky1 has also described the disease in a form very similar to that met by Dr. Stokes. In Dr. Stokes's case death took place on the twelfth day from the first symp- toms of the disease. Large rales were heard over the site of the change, and the characters of the respiration led Dr. Stokes to suspect the existence of a cav- ity. Renewed rigors and copious sweat- ing occurred on the seventh day, and were repeated up to the time of the pa- tient's death. I have seen one instance of this change in the interlobular tissue, caused by the direct extension of a post-pharyngeal ab- scess along the posterior mediastinum to the roots of the bronchi. There was effu- sion with recent lymph in both pleurse. The interlobular septa of the lower lobe of one lung were greatly thickened and of a yellowish color, and were found to be the seat of a purulent infiltration. The lung tissue intervening between them, was con- densed, but was otherwise healthy, with the exception of several pysemic abscesses scattered through its tissue. Thrombi were, however, found in several branches of the pulmonary artery. In this case also there were considerable pyrexia and fre- quent rigors followed by sweating. Dul- ness on percussion existed at the base for nearly a fortnight, and was attended by weak bronchial breathing and by fine crepitation, mingled with fremitus in these situations. The physical signs present, however, cannot be referred in this case exclusively to the condition of the inter- lobular septa, since other complications were present. It may be noticed as worthy of remark, that this implication of the interlobular septa, though so rare in man, is the ordi- nary appearance of the pleuro-pneumonia of the bovine species. A full description of its characteristics has been given by Professor F. Weber of Kiel.2 There is no evidence at present existing that such a condition precedes those thick- enings of the interlobular septa which are occasionally observed to follow inflamma- tion of the pleura, but it is by no means improbable that the occurrence of this process in a modified form may be the origin of such appearances to which further allusion will be made. [* Feb. 19, 1879 ; reported in Phila. Medi- cal Times, April 26, 1879.] 2 Mucous and Serous Membranes, ii. 149. 3 Museum Univ. Coll. c.b. 573. In his manuscript account of this drawing, Sir R. Carswell states that the patient was a man aged 60, who died of disease of the bladder Without pulmonary symptoms. 4 Diseases of Chest, 144. 1 Anat. Path. 1861, iii. 72. 2 Virchow's Archiv, vi. 244 CHRONIC PNEUMONIA. CHRONIC PNEUMONIA. By Wilson Fox, M.D., F.B.C.P. Synonyms. - Cirrhosis (?)'; Intersti- tial Pneumonia ;2 Lungen - Induration (Heschl), German; Sclerosis of Lung (Jaccoud); Fibroid Phthisis; Phthisic avec Melanose (Bayle); Scirrhus of Lung (Avenbrugger and older writers). Definition.-A chronic induration of the pulmonary tissue, depending on a thickening of the walls of the alveoli by a fibrous growth, which causes a gradual obliteration of the cavity of the air-vesi- cles. This condition leads finally to con- traction of the lung. It is commonly uni- lateral ; it is frequently associated with dilatation of the bronchi; and it tends, either through ulcerations proceeding from these, or from secondary inflamma- tion of the indurated tissue, to give rise to cavities in, or gangrene of, the lung. It is associated with dyspnoea, with cough, occasionally with fetid expectora- tion, and with haemoptysis. The course of the disease is protracted, but it tends to a fatal issue after considerable periods, through impairment of sanguification, dropsy, diarrhoea, and gradual marasmus, or through acute intercurrent diseases af- fecting the opposite lung. History.-The condition of the lung included under this title is one whose na- ture and pathological relations are as yet only imperfectly defined. The views expressed by some recent pathologists respecting the inflammatory nature of the changes in the lung in many instances of phthisis would, if correct, necessarily involve the inclusion under this title of a very large proportion of cases hitherto regarded as tubercular, and indeed the estimate of the frequency of Chronic Pneumonia formed by different authors has varied largely with their opinions respecting the nature of tuber- cular changes. This division of opinion dates at least from the period of modern pathological research. By some authori- ties, and in particular by Broussais,1 Cru- veilhier,2 Reinhardt,3 and more recently 1 Dr. Walshe, for whose opinion I entertain the most profound respect, and to whom as a former teacher I cannot sufficiently express my obligations, regards Chronic Pneumonia and Cirrhosis as independent diseases. The habits of inquiry which he taught his pupils will, I trust, serve as an excuse for one of them expressing an opinion on this point which differs in some respects from his own. The illustrations of the final effects of a pneu- monia which has lapsed into a chronic state, appear to me to show that the result of the changes thus induced differs in no essential particulars from those which are met with in " cirrhosis" of the lung, in regard both to the induration of the pulmonary tissue and the dilatations of the bronchi, which so commonly are found in this state. M. Charcot is indeed disposed to make the existence of such dilata- tions a ground of distinction between the two diseases, but there is evidence enough to show that such dilatations are found in cases where induration has succeeded to an attack of Acute Pneumonia. They are not indeed so evident in the early as in the later stages of such cases, and induration found in the latter is only a progressive change ; but it appears to be an inevitable consequence of the disease if sufficiently protracted. The question is in one sense a purely pathological one, but as far as clinical diagnosis rests on a pathologi- cal basis it is not without its significance. There is abundant proof that thickening of the walls of the air-vesicles, resulting in the complete obliteration of their cavities, is a final result of Chronic Pneumonia, and it is this condition which is described in all (the few) authentic cases of "cirrhosis." I have discussed at some length the possibility of its origin in idiopathic changes independently of such inflammatory action. In the light in which I regard this state, and with this ex- planation, I have ventured to use Dr. Walshe's recorded case of this disease, which is the most perfect extant, and also his no less admirable commentary, as an illustration of chronic pulmonary induration. 2 The term Interstitial Pneumonia also ap- pears to me etymologically to express only very imperfectly the real character of this affection. The most important secondary effect of chronic inflammatory action on the tissue of the lungs is the thickening of the walls of the alveoli, and not of the interstitial tissue. It is indeed a question how far the latter is implicated, at least primarily, in this process. 1 See especially Examen, vol. i. Aph. 161 to 171 ; Hist, des Phleg. i. Proleg. p. liv. v. vi. ib. p. 3 ; Examen, iv. 245, 402 ; Hist, des Phleg. ii. 385. Broussais recognized a pul- monary non-tubercular phthisis, but he re- garded tubercles as the result of inflammation or irritation of the lymphatic tissues. 2 Anat. Path. G6n. vol. iv. 1862. 3 Annalen der Charite, vol. i. HISTORY. 245 by Lebert,1 all tubercular changes have been regarded as essentially inflammatory in their nature. Others, with Andral,2 who recognized only the softer and more opaque granula- tions as tubercular, have regarded the gray granulation of Bayle, which many now consider the type of " true tubercle, " as the result of a Chronic Vesicular or Lobular Pneumonia. A third series of observers-among whom may be named Gendrin,3 the late Dr. Addison,4 and, more recently, Niemeyer5 and Colberg6- maintain an opinion precisely the reverse of Andral's, and assert that the greater part of the softer " tubercles," and nearly all caseous changes found in the lung, are due to a Pneumonia which some of these authors have termed "cheesy" or "scrofulous." This view has also been in part supported by Virchow,7 but it has been generalized by some recent writers to a wider degree than has been done by him. It is undesirable in this place to enter further into the discussion of these widely diverse views. They have however largely influenced, and particularly of late, the opinions ex- pressed respecting some forms of indura- tion of the lung classed under the head of Chronic Pneumonia, and even the de- scriptions given of this condition, and they appear to have caused, not a little discrepancy of statement respecting its relative frequency. Thus authors who, like Hasse, Grisolle, and Chomel, maintain the doctrines of Laennec respecting tubercle, assert that Simple Chronic Pneumonia is a disease of extreme rarity, and that it is hardly ever met with except when complicated with tubercles.1 Grisolle2 states that he has only met with six cases in twenty-five years, and only four where the acute dis- ease passed into a chronic state; and Chomel3 writes that in sixteen years, dur- ing which he performed nearly three thousand post-mortem examinations, he only met with two examples. Andral,4 however, regarding the subject from a dif- ferent pathological point, stated that he had met with the disease much more fre- quently than Chomel. Dr. Stokes5 says that in his experience Chronic Pneumonia is a very rare affection, but that it is " dif- ficult to define the meaning of the words Chronic Pneumonia, or to draw the line of distinction between it and that low irritation of the lung which is followed by tubercular infiltration." In the suc- ceeding pages the author proposes to treat only of such forms of chronic induration of the lung as may be reasonably pre- sumed to have been caused by processes in which tubercular changes have had no share. In this sense the disease is of great rarity, and examples of it can only be found in isolated cases scattered in dif- ferent journals and in monographs on dis- eases of the lungs. The author's own experience would almost confirm the statement of Hasse, that it seldom occurs except in the presence of tubercles; for out of five apparent examples of the dis- ease which have come under his own observation, in one only were the lungs found on microscopic observation to be free from tubercles. In the analysis of 1 Gaz. Med. de Par. 1867. Sur la Pneu- monic disseminee chronique. 2 Prec. Anat. Path. ii. 518 et seq. ; Empis, De la Granulie. ^ee also Reynaud, Mal. des Bronches, Diet, de Med., vol. vi. 3 Hist. Anat, des lull. ii. 334. 4 Works, Syd. Soc. Ed. Dr. Addison's statements on this subject are somewhat con- flicting, and some passages in his writings would almost lead to the conviction that he held tubercle to be an inflammatory product; e. g. loc. cit. p. 33: " Unless the simple trans- parent tubercle already alluded to can be considered as a separate and distinct body, there is not one of the varied morbid condi- tions coming under the denomination of tuber- cle which has not appeared to result from changes in or on the natural tissue. . . . These morbid changes have appeared to me perfectly identical with those of inflamma- tion." " The immediate morbid changes pro- duced by ordinary pneumonia and by phthisi- cal disease are the same, with the exception of the albumen, .... being much more susceptible of organization, and consequently more likely to become permanent in the for- mer than in the latter" (ib. p. 34). " If called upon to give an expressive name to tu- bercular phthisis, I should venture to desig- nate the disease Scrofulous Pneumonia." In other places (e. g. p. 30), however, he treats of the gray granulation as occurring indepen- dently of inflammatory change ; and at p. 49 Restates, "However analogous and closely allied the abnormal condition which produces tubercle may be to that which constitutes in- flammation, we cannot in the present state of our knowledge admit their identity." In an- other passage, however, he distinguishes two kinds of tubercle, a firm transparent, and a soft opaque form (loc. cit. pp. 49, 50). 5 Lehrb. Spec. Path. Therap. Ed. 1868, ii. 233-5. Klinische Vortrage fiber die Lungen Schwindsucht, passim. 6 Deutsch. Arch. Klin. Med. ii. 7 Wien. Med. Woch. 1856. Die Krankhaf- ten Geschwfilste, vol. ii. pp. 600 et seq. 1 Hasse, Path. Anat., Syd. Soe. Ed., p. 225. This is admitted to a great extent by Prof. Niemeyer, but he explains the concur- rence of cheesy products with tubercle by the theory that the tubercles are secondary to Pneumonia. 2 Loc. cit. pp. 82, 338. 3 Diet, de Med. xvii. 223, 4 Clin. Med. iii. 491. 6 Loc. cit. 353. 246 CHRONIC PNEUMONIA. cases by other authors those cases will be spoken of as tubercular which present granulations-gray, or soft, or cheesy- in the lungs or other organs.1 Chronic Pneumonia, in the restricted sense in which it appears to the author desirable to employ this term, is found principally in the forms described by An- dral,1 of red, gray, yellow, and black in- duration.2 The two former are almost invariably a direct consequence of a pro- longation of the acute disease. The last- named is often found under circumstances which leave considerable doubt respecting its mode of origin, though in not a few instances it can also be referred to past inflammatory conditions. To these, per- haps, may be added the induration of lung occurring in connection with heart dis- ease, and designated by Virchow3 as the brown or pigmentary induration of the lung, syphilitic disease of the lung, and also certain rare conditions associated with non-tubercular ulceration. 1 The author feels considerable diffidence in thus somewhat dogmatically criticising cases by other observers, and he is aware that ex- ception may be taken to the view here ex- pressed, which differs from the opinions enter- tained by many advanced pathologists of the present day, but which has only been arrived at by him after a prolonged and careful inves- tigation of this subject. The question of the nature of tubercle underlies the whole of this question, and he can only shortly state here the opinion which he entertains, that tuber- cle as a growth is not only liable to ' ' cheesy' ' degeneration, but that it is also capable of be- coming a more or less permanent tissue by fibrous transformation ; and the last-named change forms, in his opinion, a much more important element in the history of tubercle than is generally recognized. Also, that it consists of a multiplication of nuclei and cells in dense masses, the interstices of which are occupied by a delicate fibre network or by a solid intercellular substance; that this growth may be peri-bronchial and peri-vascular, but that it also appears in the walls of the air- vesicles ; that when found in the latter situa- tion, it is often, but not always, accompanied by a proliferation of epithelial cells of an in- flammatory character in the interior of the air-vesicles ; and that in a large proportion of the so-called "catarrhal," " gelatinous," and " scrofulous" pneumonias the cheesy changes found in the lung are accompanied by this "tubercular" infiltration of the walls of the alveoli; that these "cheesy" changes may occasionally be due to fatty metamorphosis of the epithelium, attended by destruction of the pulmonary tissue, but that in a far larger proportion of cases they are due to a true tu- bercular change, and that even when they are not the direct cause of such changes in isolated spots, tubercles are almost invariably found in other parts of the same lung, and also in other parts of the system. Patients whose lungs present this peculiarity of " cheesy" or " scrofulous" change, are therefore almost in- variably those who are at the same time the subject of tubercle ; and the author believes that he is correct in stating that in the vast majority of cases such "cheesy" changes oc- cur under the influence of the tubercular dia- thesis, and are mostly associated with if not caused by the presence of tubercle. On the other hand, he is fully prepared to admit with Dr. Addison and Cruveilhier that a large proportion of the alterations in the lungs of such patients are due to attendant Pneu- monia. This Pneumonia is commonly chronic, and when not destructive, it leads to a thick- ening of the walls of the air-vesicles by the growth of fibrous tissue. This thickening takes place by means of a fibro-plastic growth with elongated and fusiform cells, indepen- dently of the tubercular masses before de- scribed. Tubercular masses may, however, be mixed with these, and the two sets of changes may goon pari passu, while the tuber- cular growths may either soften and break down, or may themselves at later periods un- dergo the same fibrous transformation. Fi- broid transformation of the lung tissue is therefore an exceedingly common event in tubercular phthisis, and forms in fact, in one Sense, a mode of cure of tubercle, as has been long recognized. The mode of evolution of most forms of tubercular growth in the lungs is indeed closely allied to an inflammatory change, but it presents in addition other phe- nomena which are not ordinarily met with in inflammatory processes ; and until the purely inflammatory nature of tubercle is more dis- tinctly proved than has yet been done, it ap- pears desirable, at least in a clinical sense, to maintain the separation of these processes. A discussion of this question is, however, im- possible here. As regards the coexistence of " cheesy" changes in other organs being taken as an evidence of the tubercular nature of changes in the lungs, the author is fully aware that this subject is yet subjudice, but he believes that the discussions respecting it rather tend to show diversity of opinion re- specting the nature of tubercular changes in general than that they affect the questions of the identity of these " deposits" with tuber- cular changes in other parts. Some recent writers, indeed, appear altogether to ignore the termination of tubercle in a "cheesy" metamorphosis ; and forgetting that this is its most common change, and also that tubercle is the most common source of this pathologi- cal product, they appear anxious under all circumstances toprove its origin in some other process. The author hopes shortly to be able to lay before the profession in a more complete manner the grounds on which these opinions are based. i Clin. M^d. iii. 489. 2 Bayle (Rech. Phthisie Pulm. p. 12) de- scribed " engorgement" of the lung as a form of Chronic Pneumonia, but the nature of this must be regarded as doubtful. 3 Archiv fur Path. Anat. i. 463. This state is also alluded to by Andral (Prec. Path. Anat. ii. 517); Hasse (loc. cit. p. 227). ETIOLOGY. 247 Etiology.-I have already stated, in the section devoted to the clinical history of the acute disease, that I have only known one case of Pneumonia where the patient left the hospital without a perfect resolution of the physical signs in the lung ; but I have also given instances where this process was protracted.1 I do not think that cases of the latter class, in which a somewhat tardy but progressive improvement takes place, can properly be called instances of Chronic Pneumonia. Huss, however, dates the tendency to pass into the chronic state from the fourteenth to the twenty-first day of the acute dis- ease. He says that this protracted course is somewhat more common in Pneumonia of the upper lobes, and that the Pneumo- nia of drunkards has a similar tendency. Grisolle states that Libermann has as- serted it to be common amongst opium- smokers in China, and Dr. Stokes con- siders that Chronic Pneumonia ending in induration of the lung is more common after the typhoid forms of the disease. Chomel attributed to excessive bleeding an injurious influence in protracting reso- lution. The pneumonia of the aged has also a similar tendency, particularly after the stage of gray hepatization has been attained. Circumstances interfering with convalescence, and fresh exposure leading to relapses, may also protract the course of the disease and give it a chronic charac- ter. Thus Broussais2 gives three cases of induration of the lung from military hos- pitals, ending fatally on the twentieth, fifty-first, and ninety-first days after an attack of Pneumonia. In two of these, a condition of induration alone is men- tioned, but in the second, the state de- scribed approaches closely to Andral's description of the red induration. Gri- solle also states that the appearance of the lung, in cases of Pneumonia ending fatally within five or six weeks, presents but little difference from the characters of the acute stage,3 though exhibiting a more marked degree of induration ; the surface on section being somewhat smooth, but in other cases still presenting the granular character of the primary disease. The only case which I have met with of this nature was in a man, aged forty-six, the subject of chronic albuminuria: cough, with haemoptysis, began two months be- fore admission, but he was only compelled to leave off work a fortnight before admis- sion into hospital. Dropsy in the legs had been present for six months. The sputa were thick, puriform, and uniformly blood-stained. The patient died suddenly three days after admission. The bronchi of both lungs were dilated. Both apices presented a gray infiltration, which was most marked in the left upper lobe, which was also considerably indurated ; the kid- neys were granular. The condition of lung, however, most commonly described as Chronic Pneumo- nia, is that in which the pulmonary tis- sue has undergone a fibrous induration, more or less deeply pigmented, usually attended with complete obliteration of its vesicular structure, and commonly, but not constantly, traversed by dilated bron- chi. It is this state which received from Sir D. Corrigan the name of "Cirrhosis,"1 and which some modern English patholo- gists have regarded as the result of an idiopathic change, which has also been termed "Fibroid Degeneration of the Lung,"2 or "Fibroid Phthisis."3 The condition, has, indeed been long knowm. It was described by Morgagni,4 and later by Avenbrugger,5 under the title of " Scir- rhus" of the Lung, and by Bayle as "Phthisie avec Melanose," and the last- named author recognized its occurrence independently of or complicated by tuber- cular disease :6 the same condition was hepatization to firmer degrees of induration were found. 1 Dublin Journ. 1837. Dub. Hosp. Gaz. 1857. 2 Dr. Sutton, Med.-Chir. Trans, xlvii. 3 Dr. Andrew Clark, Trans. Clin. Soo. i. p. 174. 4 Epist. section 23, xviii. section 30. 6 " Inventum novum ex percussione thora- cis humani ut signo abstrusos interni pectoris morbos detegendi," 1761. Trans, by Sir J. Forbes, 1824. He describes this state as hav- ing the consistence of cartilage. Scirrhus was the term universally applied by older writers to pulmonary indurations, however originating, as by De la Boe, Sylvius, and Bonetus.. (See Waldenburg, " Die Tubercu- lose," pp. 30, 31, 42.) Avenbrugger does not seem to have described tubercles, though they were recognized before his time. Aven- brugger's commentator (Corvisart) has left almost as complete a description of the symp- toms as any subsequently furnished. 6 Phthisie Pulmonaire, p. 209 et seq. The first two cases are typical illustrations of this 1 Also Andral (Clin. M^d. iii. 550). A case where the signs of consolidation only disappeared at the end of four months. 2 Hist, des Phlegm, i. p. 13 et seq. 3 Cf. a case by Bayle (Phthisie Pulmonaire, obs. 46, p. 373)-Pneumonia of three months' standing-red, firm hepatization ; also a case by Durand-Fardel (Mal. des Vieillards, p. 589), where death took place after two months, and red hepatization was found passing in spots into gray; also (lb. p. 594) a case of three months' standing, where gray indura- tion existed at the bases, together with recent gray infiltration of one apex. Hourmann and Dechambre (loc. cit.) also speak of this protracted course as common. See also a case by Rayer (Gaz. Med. 1846, p. 983), du- ration not stated ; also a case by Grisolle (loc. cit. p. 72), of a patient dying on the sixtieth day, when transitions from red and gray 248 CHRONIC PNEUMONIA. also described by Laennec1 as occasionally complicating dilatation of the bronchi, and as existing around tubercular excava- tions. The pigmented form was, how- ever, included by him under the term melanosis, which he regarded as an inde- pendent disease, but which Andral first showed to result from a chronic inflamma- tory action. The difficulty in arriving at a conclu- sion respecting the mode of origin of this state is, however, very considerable, owing to the length of time during which pulmonary symptoms may exist before death, and also in many cases from the incompleteness of the reports furnished. I have, however, analyzed thirty-nine cases2 returned as " Chronic Pneumonia, " "Cirrhosis," "Interstitial Pneumonia," or " Induration of the Lung," which are all that I can find in modern medical litera- ture capable of throwing any light on the general bearings of this question. Many of these are more or less imperfect in re- gard to history or to pathological details, so that the facts thus gained are only of comparative value. As far, however, as they are available, I shall give the results in a numerical form. Sex and Aye.-Of these cases twenty- two were males and sixteen were females. In one case the sex is not mentioned. The ages at which death took place in thirty-eight cases are given in the sub- joined table; but the smallness of the numbers involved and the uncertain dura- tion of the pulmonary affection in many cases, greatly diminishes the value of these results. They show, however, that the disease materially shortens life, since nearly two-thirds of the patients died be- fore attaining the as;e of forty. (See Prognosis. ) 1 to 10. 10 to 20. 20 to 30. 30 to 40. 40 to 50. 50 to 60. 60 to 70. 70 to SO. 1 5 10 6 4 9 1 2 AGES AT DEATH. state, and were evidently, from Bayle's de- scription, associated with dilatation of the bronchi. Bayle considered melanosis to result from a diathetic disease (loc. cit. 84). 1 Forbes' Trans. 2d Ed. 1827, p. 112. Laennec's description of melanosis of the lung, under which title he also included melanotic tumors, contains one case of chronic black induration, associated with tubercle (lb. p. 390). 2 The cases included in this analysis will be enumerated in the Appendix at the end of this article. Both in the Appendix and in reference to special points I have marked such cases by *; cases not so included I have marked in my references by J. I have not included thirty-four cases tabulated by Dr. Sutton as instances of ' ' fibroid degeneration of the lungs" (Med.-Chir. Trans, xlvii.), nor thirty-five cases of bronchial dilatation de- scribed by Biermer, many of which presented similar alterations (Zur Theorie und Anato- mie der Bronchien-Erweiterung, Virch. Arch, xix.) Both these and Dr. Sutton's cases will be alluded to separately. In addition to these I have only been able to find fifty fur- ther cases where any allusion is made to this affection. Many of these are wanting in ne- cessary details of history, or in descriptions of the other lung, or of other organs. Some which relate to cases of recovery, or which illustrate special points, will be again alluded to. I have not, however, included cases de- scribed as tubercular, but only such published as cases of "cirrhosis," "induration of lung," " interstitial pneumonia," or " chronic pneu- monia," and Dr. A. Clark's published case of "fibroid phthisis." I have thought it best to retain in this category some of the The great difficulty in the recognition of the true pathenogenesis of pulmonary indurations arise from the occasional im- possibility of determining the origin of masses of cicatricial tissue in the lung, when all signs of the affection in which it originated have passed away. A cicatrix is not a disease, but represents the cure of a past disease, and it is only by a know- ledge of the diseases which commonly produce such changes in this organ and of their attendant circumstances, that we can form any conclusion as to the proba- bilities respecting the antecedent condi- tions in which it may have originated. There can, however, I think, be little doubt that in the majority of cases of in- duration of the lung found post mortem, whether occurring in isolated patches or extending over very considerable areas, the cause lies in the presence of tubercle and of tubercular pneumonia-using these terms in their wider sense to include all cases which appear to me to have been tu- bercular in their nature, although not de- scribed as such, in order to express more clearly the fallacies inherent to this branch of the subject. It must, however, be noticed as remarkable from these numbers how very rare this affection is when uncomplicated with tubercle; and even some of the cases included in this analysis appear to have had a tubercular origin, or to have been thus complicated. Chomel based his description of the disease on eight cases, including two of his own, which were all that were accessi- ble to him. ETIOLOGY. 249 forms of granulation ordinarily described as tubercular, and also most of the cheesy changes found in the lungs.1 This condi- tion has been long recognized, and the fibrous or indurating termination of tuber- cular processes has been fully described in most works on Pathological Anatomy.2 So commonly is tubercle found as a com- plication of this state, that out of four cases quoted by Steffen3 as examples of "Interstitial Pneumonia," three are most probably tubercular, and the fourth is not free from a similar suspicion. Out of the thirty-four cases of "Fibroid Degenera- tion" given by Dr. Sutton (loc. cit.), I should regard fifteen at least as present- ing similar evidences of indurating tuber- culosis, and eleven more as probably hav- ing been produced by the same condition, inasmuch as they presented this state as a double affection of both apices associated with cavities,4 making a total of twenty- six. If indeed the indurated gray granu- lations, whether occurring singly or in masses, are, as Andral thought, the result of Chronic Pneumonia,1 this hypothesis vastly extends the range of this affection ; but this theory of their inflammatory ori- gin is, I believe, just as applicable to the nature of tubercle in general as it is to this special form in which it is sometimes found post mortem. Even out of the thirty-nine cases which I have analyzed, I regard eleven to have been thus associated. In four cases tuber- cles were found in both lungs; in four others, where the whole of one lung was indurated, they were found in the oppo- site lung, and in three they were found only in the affected side. Of three cases published by Sir D. Corrigan as instances of "cirrhosis," one was regarded by him as coming under this category, inasmuch as there were cavities in the affected side, and tubercular ulceration of the intes- tines.2 Dr. Walshe also alludes to the possibility of "cirrhosis" complicating tubercular disease of the lungs.3 The question, respecting the other pa- thological relations of this condition is, however, a complex one, and may be con- veniently discussed under the following heads :- (a) The evidence in favor of its origin either in Acute Primary or Broncho-Pneumonia. (&) The evidence of its origin in inflam- mation of the pleura. (c) The evidence of a simple chronic inflammatory action of the inter- stitial tissue of the lung, not pre- ceded by either of the above- named acute conditions, and therefore akin to cirrhosis of the liver, or to the granular condition of the kidney. (d) The evidence of an idiopathic "fibroid change" in the walls of the alveoli occurring independ- ently of inflammatory action. (a) The possibility of the origin of fibrous induration of the lung from an at- tack of Acute Primary Pneumonia is con- clusively shown by a case of Andral's,4 where the acute attack had occurred eigh- teen months previously, and where alter death the lung of the affected side was 1 The cheesy concretions formed by inspis- sation of puriform matter in the bronchi are, in my experience, much less frequent than is sometimes supposed. 2 See especially Rokitansky's work. Sir D. Corrigan speaks of "cirrhosis" represent- ing a species of cure for tubercle. See also Cruveilhier, "Tubercles de Cicatrization" (Anat. Path. liv. xxx. pl. iii. p. 6). He also gives a case where the whole of one lung was indurated by chronic tuberculosis (Anat. Path. Gen. iv. 631). In some cases, how- ever, a microscopic examination will reveal, in cases of fibroid induration, evidences of tubercular growth which are undiscoverable by the naked eye. I have recently observed this in a case which clinically, as well as in the post-mortem appearances, presented a most typical apparent example of "cirrhosis," in the retraction and induration of nearly the whole of one lung with only a small nodule of induration in the other. 3 Klinik der Kinderkrankheiten. J 4 It is undoubtedly true that bronchial dilatations may lead to secondary ulcerations in indurated tissues, but the proportional number of these when independent of tuber- cle is strangely small when compared with those given by Dr. Sutton. See especially Biermer's paper on " Bronchial Dilatation." Out of thirty-five cases, only twelve were as- sociated with ulcerations of the bronchial mucous membrane, and of these seven were tubercular ; while of the five remaining, two were examples of gangrene, and another was a case of abscess of the lung communicating with the bronchi. Barth also considered ulcerations of the bronchi as being very rare, having only met with three instances out of sixty-two cases. The possibility which may be argued that cavities may arise from ob- structions of the bronchi only rests upon what must, when actually tested by observa- tion, be regarded as an exceedingly small number of cases. 1 It is under this title that Dr. Sutton de- scribes most of these granulations, and he attributes the same opinion to Dr. Addison. Dr. Sutton has, however, carefully distin- guished these cases, and has thereby avoided the confusion which might otherwise be caused in pathological descriptions when such a reservation is not adopted. It must be remembered that Andral regarded cheesy matter as the type of tubercle, which he be- lieved to result from an inspissated secretion. 2 Dubl. Hosp. Gaz. 1857 * 3 Dis. of Lungs, p. 407. 4 Clin. Med. iii. obs. 64, p. 474.* 250 CHRONIC PNEUMONIA. found universally indurated and traversed by dilated bronchi, in the walls of which a gangrenous action was taking place. The opposite lung was in a condition of recent hepatization; the other viscera were healthy. In addition to this in- stance, five other cases among those anal- yzed present a similar history, making a total of six, and seven others afford a strong suspicion of a similar origin. Thus, of the only three cases published by Sir D. Corrigan with post-mortem results, one began with an attack of influenza, and in another (the tubercular case before alluded to) the disease appears to have originated with a catarrh, attended with severe pains in the side. Similar evidence is also afforded by three cases reported by Weber1 of children whom he had himself treated previously for Pneumonia; and he states that he was acquainted with two others still living, who, after attacks of Pneumonia, retained for years the phy- sical signs of induration of the lung, with dilatation of the bronchi ; and a similar origin is shown in cases reported by Ziemssen,2 Reinhardt,3 Dr. Addison,4 and Biermer.5 The conditions of Catarrhal or of the Secondary Broncho-pneumonias, which are more liable than the acute disease to lapse into a chronic state, appear, how- ever, to be more favorable for the produc- tion of this change, and it is not improba- ble that some cases of induration of the lung with dilated bronchi may owe their origin to this form of the disease. Bron- chial dilatation is a common event in the Broncho-pneumonia of children, and this condition may persist in cases •where the pulmonary consolidation, instead of re- solving, passes into a condition of indura- tion. This is shown conclusively by a very instructive case by Bartels,6 and by two others reported by Dr. Bennett.7 Another is afforded by Dr. Addison,8 where the induration of the lung, asso- ciated with dilated bronchi, commenced with hooping-cough. Two others with less details are given by Steiner and Neu- retter1 as secondary to bronchitis, and Barth's2 fourth case is probably an ex- ample of the same kind. If we consider the course of acute bronchitis in children, and recollect how constantly dilatation of the bronchi occurs in this condition, both in the idiopathic form of the disease and also in the course of measles and hooping- cough, it can only be a subject of surprise that permanent lesions of this nature are not more commonly met with as the re- sults of these diseases. It has been al- ready stated that the Pneumonia which attends them has a more prolonged course and undergoes a more protracted resolu- tion than is observed in the typical forms of the primary disease ; and it is probably owing in no small degree to the higher reparative powers of childhood that such indurations do not more commonly occur as the sequelie of these affections. Two cases by Legendre3 might indeed give rise to the question whether collapse of the lung, together with bronchial dilatation, may not subsequently lead to induration of the pulmonary tissue independently of pneumonic changes, particularly when we recall the statement of Rokitansky,4 that fibro-nuclear growth in the alveolar walls tends to occur in cases of collapse of long standing. The mere existence of bronchial dilata- tion, however acquired, appears to afford a predisposition to pneumonic changes, and to thickening around the bronchi, which may well explain a large proportion of the instances where these conditions co-exist, and when no definite history of their joint origin in a single attack of an acute affection can be obtained. The progress of interstitial thickening does not, however, appear to affect in this manner large tracts of lung when uncom- plicated by other changes, though in some instances it extends inwards, through the interlobular septa from the pleura.5 There can be no question that bronchiectasis and induration of the pulmonary tissue may 1 Path. Anat, der Neugeb. ii. 58. J 2 Pleuritis und Pneumonie in Kindesalter, p. 257.* 8 Ann. der Charite, Lf 4 Collected writings, p. 45. f The second of Dr. Addison's cases. 5 See cases i.f and xviii.f 6 Virch. Arch. xxi. p. 144. J This case, where Pneumonia of the apex succeeded to measles, showed in the course of nine months some improvement in the physical signs, but persistent dulness remained at the apex, with signs of dilated bronchi. 7 Rep. City of Lond. Hosp, for Dis. of Chest. J I have not been able to gain access to the originals of these cases. They are quoted at length in the Journal fur Kinderkrank. 1858, p. 305. In both, persistent signs of con- solidation of the lung succeeded to measles, and in one case lasted nearly four years. 8 Loc. cit. p. 44$. The first of Dr. Addi- son's three cases of induration of the lung. 1 Padiatrische Mittheilungen, Prager Vier- teljahresch. 1864, Ixxxii. p. 22.$ 2 Loe. cit. p. 501.* 3 Rech. Mal. de 1'Enfance, 223-283.$ It appears, however, most probable from Legen- dre's descriptions, that these changes had been the result of a partially diffused Bron- cho-pneumonia. He applies to them the term " carnization," which, from its unde- fined meaning, has been a frequent source of confusion. Two cases of a very similar na- ture are cited in Legendre and Bailly's origi- nal papers on " Collapse" (loc. cit.). It is possible that they are identical with these. 4 Path. Anat. 1861, iii. 50. 6 Biermer, loc. cit. ETIOLOGY. 251 reciprocally act as cause and effect to one another, and also that the process leading to induration may simultaneously give rise to dilatation of the bronchi. This explanation, however, fails to explain in- stances of chronic bronchitis when the clinical evidence of induration of the lung would show that this change is of more recent origin than the cough and expect- oration, which in some cases date from an earlier period ; and for these I think that the theory of a pneumonia secondary in point of time to the bronchial dilatation affords the best elucidation. The fre- quency with which such secondary pneu- monias occur is variously estimated. Biermer's cases show that they were found in twelve out of fifty-four cases ; Rapp (quoted by Biermer) found them in twenty-one out of twenty-four cases ; and Barth in twelve out of forty cases. The pneumonia attending bronchial dilatations is also commonly of the dis- seminated catarrhal type. It tends espe- cially to occur around the dilatations, when it is frequently set up by the irrita- tion arising from the retained and decom- posing products of secretion, or by the direct extension of ulceration or inflam- matory action through the bronchial wall. Such forms of Pneumonia are very liable to pass into gangrene, but where this is not the case, the persistence of their cause tends to diminish the possibility of a speedy resolution, and to produce fibrous thickening. Of this tendency several re- corded cases afford very good illustrations, which may be regarded as almost conclu- sive of the nature of this process.1 Pneu- monia having this origin is insidious in its invasion, and does not produce the marked symptoms ordinarily presented by the acute form ; and this probably ex- plains some of the reported cases where the commencement of the induration can- not be referred to any single acute attack. It will readily be understood that when this process has once been established, and when Pneumonia ending in indura- tion has attacked a lung the subject of bronchiectasis, it tends to recur and to re- peat itself in other parts of the same organ. The dilated bronchi surrounded by indurated tissue, being a locus minoris resistentice, are continually liable to be- come the seat of fresh catarrhal inflam- mation, from which the process extends to other divisions of the bronchi in the same lung. These in their turn excite disseminated pneumonic changes, which are again prone to the same indurating process. The disease thus tends to pro- gress saltatim until the greater part of the lung is invaded. Bronchial dilatation may indeed exist, and apparently long, without giving rise to other changes than those caused by the compression which is produced by the enlarged tubes encroach- ing on the surrounding tissue, but the proportion of cases in which this state is found to exist alone and without attend* ant induration is comparatively small, amounting to only eleven out of the thirty- five cases reported by Biermer. The unilateral character of these pul- monary indurations, which forms a re- markable feature in the history of the disease, and to which allusion will again be made, may also be compared with the frequency with which bronchial dilata- tions are found limited to one lung.1 The frequent coincidence of the two affections is also very remarkable, for dilatations of the bronchi are stated to have existed in thirty-one out of the thirty-nine cases of pulmonary induration which I have ana- lyzed ;2 while, conversely, on analyzing Biermer's cases I find that induration was present in twenty-four out of the thirty-five cases of bronchial dilatation reported by him ; and Dr. Grainger Stew- art3 also regards it as a very common though not a necessary complication of this condition. Lastly in this category belongs a very large proportion of those cases w'here in- duration of the lung is found in patients exposed by their occupation to the inhala- tion of irritating particles of solid matter, such as the Sheffield grinders, stonema- sons, miners, potters, and cotton-workers. In some cases even of this class I am dis- posed to believe that tubercular changes may play some part in the production of the indurations discovered ; but in others, and as far as is at present known, no evi- dence of tubercle has been shown to exist. It appears most probable that the passage of these particles into the air-vesicles, and their lodgment in their walls, set up a slow pneumonic process attended by a fibrous growth in the alveolar walls and septa, by which the indurations observed are pro- duced. These diseases form a class which requires a separate consideration, but their relation to the origin of chronic pul- 1 Barth, says that out of forty-three cases of bronchiectasis the affection was unilateral in twenty-seven. Biermer says that it occurs wite about equal frequency as a double or as a one-sided affection (Virchow's Handbuch, v., section i. 245). This is probably in part explicable from the number of cases in which it originates in pneumonia, pleurisy, or col- lapse. See Laennec's first case (loc. cit. p. IIOJ), where unilateral bronchiectasis re- mained as the result of hooping-cough. 2 In two others there is no sufficient ac- count. In six only is this condition stated to have been absent. 3 On Dilatation of the Bronchi, 1867. 1 See Case iv. of Dilatation of Bronchi, by LaennecJ (loc. cit. 113); also Biermer'st. Obs, i. ii. xiv. xviii. xxi. xxiii. xxiv. xxix.; also Dr. Stokes, Dis. of Chest, p. 159.* 252 CHRONIC PNEUMONIA. monary induration is of no small import- ance in their features of pathological affinity.1 (6) Pleurisy again seems to be in some cases the exciting cause of this condition. One such case2 occurs among those which I have analyzed, and Biermer3 gives two others. The manner in which this effect is produced is somewhat doubtful. It is possible that in such instances Pneumo- nia may have complicated the pleurisy. Biermer attributes to pleuritic adhesions an important part in the production of bronchiectasis, but it may still be ques- tioned if they are not rather the effect than the cause, though in some instances, however, there appears to be pretty clear evidence that they have been the first cause leading to the subsequent dilatation of the tubes. Some thickening may at times extend from the visceral pleura through the interlobular septa, but I do not think that any evidence at present exists that, except at the surface of the lung, such a process can extensively in- vade the alveolar walls of the pulmonary air-vesicles unaccompanied by an attend- ant Pneumonia. (c, d) If now we turn to inquire whe- ther any other conditions may exist tend- ing to produce pulmonary indurations, we find that the number of cases in which such an explanation is required is remark- ably limited. The cases in which either a history of phthisis, of acute affections, of the lung, or pleurisy, may be inferred to have been the antecedents of this state, amount in those which I have analyzed to twenty-six out of the whole number. The great duration of some of the other cases would afford a probable ground of belief, that to many of these, where no history is obtainable, a similar explana- tion by the theory which I have raised of progressive attacks of Broncho-pneumo- nia is also applicable; and the probability of this will become more apparent when the pathology of the disease has been con- sidered. Morbid Anatomy and Pathology. -(1) The forms of lied and Gray Indura- tion of Chronic Pneumonia have been al- ready described as presenting but little difference from the appearances presented in the acute stage. Instead, however, of presenting the usual friability of a recent- ly hepatized lung, they are firm and re- sistant, and are drier, and sometimes rather paler. The finely granular aspect persists during some time, but tends to disappear with the progress of the case. It may, however, be apparent on tearing the tissue, even when the section appears smooth. In some cases the tissue assumes a yellow tint, but without (from the de- scriptions given by Hope1 and Lebert)2 passing into a cheesy change; and this would appear to result from a gradual fading of the brighter tint of the red hep- atization.3 The induration in this state depends on a gradual thickening of the walls of the air-vesicles - a thickening which is commonly found in large tracts of the forms of Pneumonia associated with tubercle, as well as in the simpler forms. I have met with this chronic red induration of the base in one case only, and in this there were also masses of tu- bercular induration in the apex of the same lung, the other lung being free. The patient was an old woman with syphi- litic cicatrices in various parts of the body, and a history of earlier syphilis. She had had haemoptysis seven years be- fore, and no distinct history could be ob- tained of the date of the invasion of the Pneumonia, but she was under observa- tion for three and a half months with the physical signs of consolidation of the base. Pericarditis with effusion formed the im- mediate cause of death. The bronchi were dilated in spots of cicatricial con- traction of the apex, where indurated tu- bercles were present, and also in the tract of red induration at the base. This tract (Fig. 3G) showed on microscopic exami- nation a dense fibre tissue consisting of a network interlacing in all directions, thickening the walls of the pulmonary alveoli, and spreading in all directions through them (a, a). The contents of the alveoli (&, ft) were round nucleated cells mostly resembling the pyoid forms seen in the third stage of Pneumonia, but mingled with occasional epithelial cells, and with granular corpuscles and free fat granules. In places (c, d) the air-vesicles are seen to be almost obliterated by this growth, and in some tracts scarcely any traces of them were discoverable. There was compara- 1 For an almost complete series of references to the literature of this subject, see Zenker, Die Staubinhalations Krankheiten der Lun- gen, Deutsche Arch. Clin. Med. vol. ii. Also ib. Seltmann, Anthracosis der Lungen. See also Peacock, Brit. For. Med.-Chir. Rev. xxv. 1860 ; Dr. Greenhow, Path. Soc. Trans, xviii. xx.; Dr. Hall, Brit. Med. Journ. March and April, 1857; Calvert Holland, Edinb. Journ. 1843. 2 Dr. Peacock, Edinb. Journ. 1855, p. 281.* 3 Cases v.t and xxvi.f Biermer's cases are for the most part merely pathological studies without any clinical history. 1 Morbid Anatomy; " Yellow Induration." 2 Physiol. Pathologique, i. 137: "Yellow Hepatization." 8 I have never seen this state. Hope and Lebert each only speak of one instance. Le- bert's case was in a child, and the disease was of two months' duration. Another is quoted by Charcot from Monneret (case ii. loc cit. p. 30). The disease was here only of three months' duration. MORBID ANATOMY AND PATHOLOGY. 253 tively little nucleated growth discoverable in the walls in this case. The process in this condition appears to be only slowly evolved ; the growth and thickening of the fibres is gradual, and a rapid develop- ment of nucleated cells is not discover- able. In the earlier stages, however, this is sometimes seen as figured in Figs. 37 and 38. The fibro-nucleated growth is com- monly, as is seen in these figures, in the form of elongated fusiform cells, they are Fig. 36. Chronie Red Induration in a tuberculous case -a, a. Fibrous network in walls of alveoli. &, S. Round nucleated cells within alveoli, c, d. Air-vesicles, almost obliterated. not densely massed, as in the tubercular growths. Heschl has convinced himself that the nuclei of the capillaries partici- pate in the change, and my own observa- tion would confirm his, inasmuch as all ceeding side by side, and occasionally it may even be doubtful what the destina- tion of the nucleated tissue thus originat- Fig. 38. Fig. 37. Case of Chronic Gray Induration associated with Tuberculosis, but without tubercle in this part. The contents of the vesicles are an amorphous exudation with few cell-forms. the nuclei of the alveolar wall appear to multiply, and to yield fibrous elements. In tubercular indurations, the process may take place in a manner similar to those above described, and without any growths differing from the ordinary fusi- form cells of the fibro-plastic type, or on the other hand they may be associated with a dense growth of nuclei character- istic of tubercle. In some cases, indeed (see Fig. 39), the two may be found pro- From Heschl (Lungen Induration, Prager Viertel- jahresch. 1856, vol. xli.). This is given by Heschl as the mode of growth of the dense fibrous induration, but his case also presented some reddish-gray and rusty granulations, though the tissue was indurated to the consistence of fibro-cartilage. ing may be, and whether it shall ulti- mately form a fibre tissue, or a tubercular mass. The latter, indeed, may finally shrivel by a species of fibrous transforma- tion, or it may be the seat of cheesy trans- 254 CHRONIC PNEUMONIA. formation or softening leading to the naked-eye appearance of scattered yellow cheesy masses in the midst of indurated tissue. I have only alluded to this mixed growth as an illustration of the frequency with which this combination occurs. With the exception of cases where tuber- cle is mixed with the indurating growth, Fig. 39. Mixed tuberculous and fibro-plastic growth, a, a, a, Alveoli filled-with enlarged epithelial products. 5. Recent tuberculous growth of round nuclei, imbedded in a fine alveolar network, mingled with masses of pig- ment. e. The same growing into the interior of an alveolus. <1. Fibro-plastic growth of fusiform and nucle- ated fibre cells, e. The same mixed with round nuclei like the tubercular mass. (700.) I believe that little and probably no histo- logical distinction exists between the forms of indurating Pneumonia unasso- ciated with tubercle, and those where the pneumonic process occurs in a lung in which tubercle is also present, but with- out the necessary formation of this growth in the inflamed portions. Other authors have described the indu- ration of the lung as depending on an in- filtration of an amorphous substance be- tween the interstices of the alveoli. This is, I believe, the condition described by Dr. Addison as the " iron-gray indura- tion," or the "uniform albuminous indu- ration," and also by MM. Bouchut and Robin.1 My own observations have failed to show this condition. Dr. Addison's descriptions were anterior to the use of the microscope, and I believe that when this appearance is found in large tracts of indurated tissue, it arises from the thick- ening and fusion of large tracts of fibrous growth into a uniform semi-cartilaginous material, closely analogous to the tissue produced during earlier stages of ossifica- tion, and by a process which in the two cases presents very striking forms of re- semblance. 1 The material occupying the interior of the alveoli is often mainly amorphous, particularly in the forms of la Granulie." This confusion meets us at every turn in relation to this subject. Bou- chut, however (loc. cit. p. 386), says that he has twice seen acute Pneumonia pass into the chronic stage. See also Lorain and. Robin, Comptes Rend. Soc. Biol. 1854, 2d ser. i. 62. 1 This formation of tissue with dense fibrous bands is an exceedingly common complication of the fibrous forms of tubercle. It is beyond the limits of this article to enter into a minute histological description, or to give further il- lustrations of'the processes by which this re- sult is obtained. I hope shortly to be able to give in another place a fuller description of these changes. 1 Mal. des Nouveanx-n€s, Ed. 1852, 371. Their description is quoted by Grisolle and Charcot as the type of the process. Bouchut and Robin describe this state as being very frequently associated with gray granulations. In the sense in which I have used these terms I regard such cases as instances of tubercular Pneumonia. It must be remembered that Robin, whose descriptions Bouchut gives, does not regard the gray granulation as a form of tubercle, but as a product sui generis •-a view further developed by Empis, "De MORBID ANATOMY AND PATHOLOGY. 255 the "gelatinous infiltration" of Laennec, as seen in Fig. 37, which is equally liable, with the other forms of Pneumonia, to undergo the same thickening of the walls of the alveoli; but cell-products mingled with a variable amount of exudation may also be seen in them. (2) The Gray, Black, or Fibroid Indu- ration of the lung presents a further stage than those last described. In the former cases the lung may re- tain apparently its natural volume, but when the change now in question has been undergone, it is almost always shrunk and diminished in size, to a degree pro- portioned to the extent of the process. The period in which this change and the loss of the ordinary characteristics of pneumonic consolidation may follow an acute attack, varies in different instances. Grisolle reports a case where the transi- tion between the two forms was apparent within sixty days, and the first case of Sir D. Corrigan's,1 of three months' duration, still showed by its color traces of its origin. A case of Charcot's,2 however, showed marked gray induration, with black mot- tling, in less than three months from the acute attack. In characteristic cases of this nature the cut surface of the lung is smooth and glistening; it is hard, and creaks like cartilage, or resembles the tissue of the uterus. It tears with the greatest diffi- culty, and no longer presents the granular appearance of ordinary Pneumonia.3 No fluid can usually be expressed from this tissue. The surface is homogeneous, ex- cept where traversed by dilated bronchi or by dense white lines, which may rep- [Fig. 40. Chronic Pneumonia.-Vascularization and fibroid development of intra-alveolar exudation products. Bloodvessels are seen in the exudation products, which bloodvessels communicate with those in the alveolar Walls. The alveolar walls are also thickened by a fibro-nucleated growth. X 100, and reduced (Green.)] resent either these tubes when obliterated, or thickened and obliterated bloodvessels, or which may arise from thickening of the interlobular septa. In some instances, when the disease is less advanced, and particularly when the induration appears to have been secondary to bronchial dila- tation, these bands tend to pass as thick- enings around the larger bronchi, and thence to extend into the surrounding tissue. The tissue is variously pigmented, and the irregular dissemination of black coloring matter among the white fibrous growth gives it a marbled gray appear- ance, which is very characteristic. The alveolar texture of the lung is entirely destroyed, though portions may still be found which show traces of pulmonary tissue, and representing earlier stages of the process. In general, however, the indurated parts, except when occurring around dilated bronchi, are pretty sharply circumscribed ; and the change is usually lobar, or it affects the greater part of a lobe or the whole of one lung. The state of the bronchi in the affected lung is somewhat variable. In the major- ity of cases they are dilated, this condition being mentioned in thirty-one out of thirty-nine cases. In eight only is a negative stated. Charcot says that neither in his, nor in Monneret's, nor in Hardy and Behier's cases was this dilata- tion present, but these must to some de- gree be regarded as exceptional, and Charcot's own cases refer to earlier stages of the disease. In some instances, when the bronchi have been found dilated in both lungs, induration has been discov- ered in one only,4 but usually in such cases the dilatation is greatest on the in- durated side. In other instances the dila- tation has been general throughout a sin- gle lung, a portion of which only has been found occupied by the indurated tissue ; while in a third and most common form, the dilatation of the bronchi has been limited to the indurated part. ' Dub. Journ. 1838 * 2 Log. cit. p. 19 (Charcot's third case).* s Laennec (loc. cit. 233) described indu- rated portions around gangrenous excavations as presenting an appearance of granulations resembling the eggs of insects. I should re- gard these as indurating tubercles. 4 See Ziemssen's case, before quoted. 256 CHRONIC PNEUMONIA. The origin of this dilatation of the bronchi has been a subject of much dis- cussion. In some it is, as before ex- plained, extremely probable that it has existed prior to the induration; and in others, as in the form of Broncho-pneu- monia of childhood, the two may not un- frequently originate simultaneously. In acute primary Pneumonia, however, dila- tation of the bronchi is a rare event, and its absence is probably due to the consoli- dation of the pulmonary tissue preventing their enlargement within the period at which death usually occurs in this disease. "When the Pneumonia passes into the chronic form, which is attended with re- traction of tissue, various explanations have been offered of the mechanism of the process.1 This subject, however, belongs rather to the history of the dilatation of the bronchi than to that of Chronic Pneu- monia. Sir D. Corrigan attributed it to a compensatory dilatation of the tubes, in order to fill the space within the thorax left by the contracting lung. It appears, however, to me to be most probable that the mechanism of this condition is similar to that in -which bronchial dilatation takes place under other circumstances, and that it is mainly due to the expiratory force of cough acting on tissues which in the earlier stages of the disorder are soft- ened, and have lost their elasticity through the inflammatory processes going on in them. It must be remembered that though in the later stages the fibrous tis- sues formed in this process have a ten- dency to shrink and contract, they are still deficient in natural elasticity. ' This defect persists even after they have con- solidated into a denser material, and the subsequent contraction would rather have a tendency to diminish the calibre of the bronchi than the reverse. It is less easy to explain the occasional absence of such dilatations, but much would depend on the degree in which the bronchial walls participate in the inflammatory softening, and possibly also on diversities in the rapidity of induration with -which we are not yet familiar.2 In Chronic Tubercular Pneumonia, dilatation of the bronchi is a very common phenomenon, but it is not always easy to decide whether it has been prior or subsequent to the pneumonic changes. The extent to which this bronchial di- latation may proceed is sometimes very remarkable, and the enlarged tubes may constitute a considerable part of the bulk of the retracted and shrunken lung.1 The form of the dilatation is not uncommonly globular, and tiie dilated ends may then form large cavities. It may, however, be simply fusiform. The mucous membrane of the tubes is sometimes smooth; more commonly it is intensely congested, thick- ened, and villous: in some cases it is ul- cerated, but this is rare, unless the dila- tations are of large size, or except in the presence of tubercle or of sloughing action in the surrounding tissue. Their contents are either the usual muco-purulent secre- tion, or they may be highly offensive even without the presence of discoverable gan- grene in the rest of the lung. Secondary inflammation in the indu- rated parts is not uncommon; probably in some instances it extends from the bronchi. It leads to the formation of ex- cavations, and is prone, in some instances, to take on a gangrenous action. Traube, indeed, regards this process as one of the most common causes of gangrene of the lung.2 In the cases which I have ana- lyzed, I find gangrene mentioned twice on the same side as the induration, once on the side opposite.3 Biermer found gangrene in five out of fifty-four cases,4 and Barth in three out of forty-three cases of bronchiectasis.5 1 See a case by Dr. Wilks, Path. Soc. Trans, viii. 39*; also Sir D. Corrigan's cases. This condition is common in the extreme degrees of the affection. The resemblance noticed by Sir D. Corrigan to the bronchi of the tortoise aptly expresses this appearance in many cases. 2 Deutsche Klinik, 1853-1859. From Prof. Traube's manner of speaking of chronic Pneu- monia, he would appear to regard the disease as more common than many other observers do. 3 Case by Dr. Walshe, Med. Times and Gaz. 1856, i. 156.* 4 In the thirty-five cases reported by Bier- mer, gangrene is mentioned in three. In two of these there was induration of the lung. I do not regard bronchiectasis as synonymous with chronic induration, but introduce these numbers for the sake of comparison. Gan- grenous Pneumonia may take place in this condition as an acute affection. 5 In Cruveilhier's Path. Anat. liv. xxxii. is an illustration of this process in a case of chronic tubercular Pneumonia, when a large portion of tissue was separated and lying in a cavity. Cruveilhier does not, however, re- gard this as a case of gangrene. Dittrich (Lungen-Brand im Folge der Bronchien-Er- weiterung) regarded these inflammatory ef- fects as septic, and as arising from retained secretions, and when occurring in the oppo- site lung, as resulting either from the gravi- tation of the fluids into the bronchi of the 1 Charcot considers that the dilatation of the bronchi in " Cirrhosis" distinguishes it from Chronic Pneumonia, where he believes it to be absent; but indubitable evidence is afforded that it attends induration of the lung secondary to Pneumonia. See cases by Andral, Weber, and Biermer, before quoted.' 2 The same difference exists with respect to the inflammatory softenings of the aorta which in some cases are the origin of aneuris- mal dilatations, while in others they indurate without having yielded to the pressure of the blood current. PATHOLOGY 257 The Pneumonia in other cases, of which four are reported, has led to ulceration of the tissue, and the formation of cavities. The total number of cases in which Pneu- monia is reported on the same side as the induration is four. In seven others it oc- curred on the opposite side. In one of these it was gangrenous, and in two others it had led to the formation of abscess. The pleura is almost invariably thick- ened, and adhesions to the costal wall are also nearly constant when the disease has made any extensive progress, or has reached the surface. The thickening is sometimes extreme, and occasionally it extends through the interlobular septa into the tissue of the lung. There is one remarkable feature about this condition to which allusion has been already made, and that is the preponder- ant number of instances in which one side only has been indurated, amounting to thirty-one out of thirty-nine cases. In five there was Chronic Pneumonia of the opposite side. The whole of the right lung was effected in ten cases, the whole of the left in fourteen, the base alone in eight, and one apex alone in three cases. A double affection of th® apex existed in three, but in two of these there is evidence that the affection was tubercular. Chomel's data are, that out of eight cases, in five the base was affected, in one the whole of one lung, in one the apex, and in one the middle two-thirds of the posterior part of the lung. He states also that in these the bronchi were generally dilated. Durand-Fardel1 says that in his observations the upper lobe was affected five times, the lower lobe three times, and the middle lobe twice. The non-affected parts of the lung some- times present emphysematous changes. This change, usually of the hypertrophous type, is often exceedingly well marked in the sound lung, when only one is exten- sively affected by retraction and indura- tion. The bronchial lymphatic glands have sometimes been found to be much en- larged. In other instances they have been simply indurated. When tubercle has existed in the lungs, cheesy spots have in some cases been found in the glands. Pathology.-There appears to be but little to add in explanation of cases where the ordinary appearances of pneumonic consolidation in the forms of red, gray, or yellow induration can be traced in direct continuity from a recent but acute attack of primary Pneumonia. Some points, however, require to be noticed with re- spect to the state of fibrous induration and its relation to other diseases. Addison denied that this state ought to be called a chronic Pneumonia, and so far as Pneumonia is a process this criticism is probably correct as applied to the final condition of complete induration, for, as I have before stated, a cicatrized tissue can hardly be termed an inflammatory disease. The question is, however, a dif- ferent one when we consider the process by which such indurations are produced ; and I believe that the evidence which I have analyzed will suffice to show that they are very frequently the result of a pneumonia which has passed into a chronic stage. It remains to be asked whether these indurations result from a process which, as Sir D. Corrigan supposed, has any analogy to cirrhosis of the liver, and from such a condition I believe that sufficient points of difference may be found, to cause serious hesitation in placing the two dis- eases in the same nosological category. In the first place, there is this marked diversity between these indurations of the lung and cirrhosis of the liver, that in the lung the fibrous induration of the walls of the pulmonary alveoli is almost invariably, if not constantly, associated with the ac- cumulation of the products of inflamma- tion in the interior of the air-sacs. In a very large number of cases this is demon- strably the result of acute inflammation, and in many more it proceeds, though in a more chronic form, as an accompani- ment of the inflammatory process attend- ant on the presence of tubercle, or deter- mined by the tubercular diathesis. Fur- ther, the change in the liver takes place in a great measure through an increase of the fibrous tissue between the acini; while in the lung, though some thickening is found in the interlobular septa, the most important pathological alterations are those which occur in the walls of the pulmonary alveoli, which certainly have not yet been shown to be the anatomical analogues of the interstitial tissue of a glandular organ, but rather to correspond to the walls of the terminal extremities of the ducts of a gland. Or, to state the difference more briefly, in cirrhosis of the liver the change is external to the lobules and perilobular, while in induration of the lung the fibrous thickening is intralobular. In the liver it is still a question whether the condition known as cirrhosis can be called an inflammation, but in it, at least, there is scarcely any evidence that the cells of the acini of this gland have under- gone any changes analogous to those seen in the interior of the pulmonary alveoli. previously sound side, or from constitutional septicaemia. See also Briquet, Mem. sur un Mode de Gangrene du Poummon dependant de la Mortification des ExtrSmites dilatees des Bron dies (Arch. Gen. de Med. 1841). 1 Mal. des Vieillards, 601.f Durand-Far- del's cases do not all refer to instances of induration. VOL. IT.-17 258 CHRONIC PNEUMONIA. The granular contracted condition of the kidney, which may be regarded as the most marked analogue of the cirrhotic liver, offers in another respect a striking contrast to these indurations of the lung. In the kidney-a double organ-the affec- tion is almost invariably bilateral, and it is a very rare event to find a single kidney alone affected.1 In the lung, the double affection is the exception, and generally explicable by a tubercular origin, and the single affection is the almost invariable rule when tubercle is not present. On these grounds, therefore, I am strongly disposed to doubt whether, in the vast majority of cases, these thicken- ings originate in the alveolar walls as a primary affection, but rather to believe that they are an almost constant sequence of an alveolar Pneumonia which has passed into the chronic stage. That thickenings of the interlobular septa may at times extend inwards into the lung as a consequence of chronic pleurisy is an undoubted fact; but more proof is at present required than has, I think, been afforded, that these can im- plicate the walls of the pulmonary alveoli to such an extent as to produce a general induration of the lung with obliteration of the air-vesicles, independently of a superadded pneumonic process, or of the co-existence of tuberculosis. I am only acquainted with two recorded cases which would appear to bear out such an opinion. One is in a note of a post-mortem by Dr. Wilks, reported by Dr. Sutton, where it is stated that "sections of the lungs showed that they were uniformly invaded by a tough fibre tissue, which had de- stroyed the natural structure and ren- dered them partially airless and very hard. There were no circumscribed masses of hard tissue, as is sometimes seen, but the pulmonary texture appeared invaded in all parts ; thus the natural as- pect was lost, being striated or interwoven with fibrous filaments."2 Parts of the lung were emphysematous ; the other or- gans were healthy. The other case is reported by Drs. Barlow and Sutton,3 where one lung only was affected. Islets of normal pulmonary tissue appeared among the indurated portions, and thick- enings could be seen around the bronchi. It would require, however, a larger body of proof than these two cases appear to me to afford, in order to establish the existence of an independent pulmonary disease, whose essential characters con- sist in the thickening of the aveolar wall, as a primary affection occurring independ- ently of inflammatory processes or of tubercular or syphilitic changes, and it is necessary that this proof should be fully established before such a class can be ad- mitted into our nosological categories. I must confess that, though during many years I have paid much attention to this subject, I have never seen any patholo- gical specimens supporting such a view, and nearly all the cases of pulmonary in- duration which have fallen under my own observation have been connected with previous Chronic Pneumonia associated with the presence of tubercles. For this reason I think that the term "fibroid degeneration," when applied to this state, fails to express its true nature. The new tissue is a growth produced under conditions of irritation, and though pre- existing tissues may disappear in its pro- gress, and so far it may be appropriately termed, as by my friend and colleague Dr. Bastian,' an instance of " fibroid sub- stitution," it appears to me most import- ant that the inflammatory conditions of its origin should be borne in mind.2 The associated pathology of chronic in- duration of the lung presents some fea- 1 Cirrhosis of the Lung (Trans. Path. Soc. xx.). 2 The term ' ' Fibroid Phthisis, ' ' proposed by my friend Dr. A. Clark, has been very largely debated of late. If it is used to in- clude all diseases tending to produce indura- tion of the lung, it must necessarily compre- hend many and widely different pathological processes which conduce to the same result. It is undoubtedly true that the symptoms of "phthisis" may arise from some non-tuber- cular diseases, and so far the exclusive limi- tation of the word to tubercular affections may be in a certain sense illogical; but as in the" lung, at least, these form an enormous proportion of the whole, we shall have no option but to retain the term in the present sense, or to fall back upon the heterogeneous classification of Sauvages and Morton ; and the former plan appears likely to be product- ive of the least amount of confusion in our nomenclature. It is important, doubtless, to recognize the origin of the induration of the lung, and to distinguish the purely pneumo- nic forms and those which are the result of bronchial dilatation or pleuritic thickenings, from those complicated by tubercle. In the same manner, while recognizing the "phthisi- cal" tendency of ulcerative Pneumonia, or of some cases of chronic bronchitis, it would ap- pear more desirable to classify these diseases in their pathological relations rather than in their occasional clinical aspects. 1 Curiously, a Unilateral affection of one kidney has been noticed by Dr. Hilton Fagge, in a case of induration of the lung (Path. Soc. Trans, xx.*). The kidney was partially atro- phied in its cortical substance. A calculus, however, existed in one of the calyces. 2 Med.-Chir. Trans, xlvii. 309.J 3 Path. Soc. Trans, xvi. p. 39.* The liver and spleen were enlarged. The heart was enlarged, and tricuspid regurgitation had ex- isted during life. The other organs presented nothing special. CHRONIC ULCERATIVE PNEUMONIA. 259 tures of interest. The heart is very com- monly displaced when retraction of the lung is considerable. It also tends to hypertrophy, but not constantly, as I only find this condition described in eight cases. In four the heart is described as having been healthy. In thirteen its state is not mentioned. In two cases there was con- traction of the mitral orifice, and in one tricuspid regurgitation, attended by a char- acteristic murmur.1 In one it is described as fatty. In some cases thrombi were found in the pulmonary artery, which un- der these circumstances has been con- tracted :2 Dr. Walshe, however, found it dilated. It may be a subject for further inquiry whether the coagulation of the blood in the branches of this vessel may not in some cases be a cause of protracted resolution of acute Pneumonia, or even of the secondary changes which have now been described. The fact that their mere obstruction may, as shown by Virchow,3 give rise to inflammatory changes in the pulmonary parenchyma, which are usu- ally persistent, would at least be ap argu- ment in favor of this hypothesis. Thick- enings have been found in the coats of the pulmonary artery, both by Dr. Schmidt and by Dr. A. Clark. The liver is re- ported as healthy in eleven cases ; granu- lar and cirrhotic in six ; enlaged and con- gested in two ; fatty in one ; in nineteen cases there is no mention of its condition. The kidneys were healthy in eight cases; granular in twelve; congested in one; their state is not mentioned in eighteen. The spleen is not mentioned with suf- ficient frequency to make any analysis useful. The intestines are commonly reported as healthy: tubercle existed in them in some of the tubercular cases: diarrhoea without tubercle is reported in a few others. Chronic catarrh and congestion of the stomach are reported in a few cases ; but the data of a large proportion are imperfect as regards the condition of the gastro-intestinal canal. When ulceration or gangrenous action has ensued in the indurated parts, metas- tatic abscesses may be found in other organs. Three instances of this nature are reported where the brain was affected,1 and another where abscesses of the same kind were found in the liver, spleen, and kidneys.2 It does not appear to me, on looking at the general results of this analysis, that the state of the other viscera affords any special ground for the assumption of a "fibroid diathesis" which has been re- cently maintained to exist as a primary cause of the pulmonary induration. The alterations of the liver and kidneys do not appear to be more common in chronic pulmonary induration than they are in many other chronic diseases, and particu- larly in those affecting the main con- duits of the circulation, whether directly through the heart, or indirectly through the lungs. Both cardiac and pulmonary diseases, which give rise to systemic ven- ous congestion, are liable to cause indu- ration both of the liver and of the kid- neys, associated with an increased growth of their interstitial tissue; and these changes appear to me to be equally com- mon in cases of simple chronic bronchitis and of chronic tubercular phthisis, as in the special affection now under considera- tion. There are some other conditions which appear most properly to take their place under the category of Chronic Pneumo- nia, but which are also of rare occurrence. The chief of these are Chronic Ulcerative Pneumonia and Syphilitic Disease of the Lungs. Chronic Ulcerative Pneumonia. -The recorded cases of this state occur- ring independently of tubercular disease are comparatively few. Broussais,3 in- deed, speaks of having met with several, but none are recorded by him except a case of ulceration secondary to the lodg- ment of a bullet in the lung. Dr. Stokes also speaks of being acquainted with cases of chronic pulmonary abscess arising from Pneumonia, and gives one case where cicatrization had ensued.4 Bayle,5 under 1 Drs. Barlow and Sutton's case, before quoted.* 2 Dr. Dickinson, Path. Soc. Trans. xvi.J Schmidt, Zwei Faile von Chronischen Pneu- monic. Schmidt's Jahresb. 1866.* 3 Gesammelte Abhandlungen, 368. One case of Virchow's (loc. cit. p. 274), where old thrombi were found in the pulmonary artery, associated with indurated Chronic Pneumo- nia, would appear to give a further support to this view. Lebert's and Wyss's experi- ments (Virchow's Archiv, xl.) on the intro- duction of solid particles into the circulation have shown that this may give rise to thick- ening around the obstructed branches of the pulmonary artery, and that such thickenings may extend into the tissue of the lung. 1 Biermer (loc. cit. p. 244) ; Lancereaux (Gaz. Med., Par. 1863) ; Herard and Cornil (loc. cit.) A very similar case is also reported by Virchow (Archiv fur Path. Anat. v. 276). 2 Lancereaux, loc. cit. 3 Examen, iv. 156, 336 ; Hist, des Phleg- masies, ii. 6, note. Broussais here says that during a long period he never met with an instance of this disease uncomplicated by tu- bercles except when caused by a foreign body in the lungs. 4 Loc. cit. 316. 6 Phthisie Pulmonaire, obs. 25 and 26. All the other cases reported by Bayle are more or less complicated by tubercles, but in obs. 28 the only evidence of this consisted in laryngeal ulcerations. 260 CHRONIC PNEUMONIA the title of "Phthisie Ulcereuse," gives three cases of this nature. The first, of about two months' duration, showed one lung only affected with several ulcerated cavities, the contents of which appear to have been gangrenous. In the second, which was of three years' standing, and where a portion of bone entering the larynx was supposed to be the exciting cause, both lungs were indurated and con- tained numerous cavities. Bayle says that he has seen several other cases in which, commonly, there was only one ulcerated cavity. The size of these cav- ities was sometimes very considerable. Two are reported by him where a la^ge cavity existed in one lung without disease of the other. One of these (Obs. 27) ap- pears to have been a case of secondary ulceration, such as I have before described as occurring in a lung which has already undergone fibrous induration, and the same condition is present in some cases reported by other authors, so that it is difficult to come to a conclusion whether the induration or the cavity formed the primary lesion.1 A case is recorded by Dr. Risdon Bennett,2 where the history of the symptoms, which dated from an attack of scarlatina eighteen months previously, would appear to support the latter view, since a large cavity existed at the root of one lung surrounded by a gray infiltra- tion. The twenty-ninth case recorded by Biermer3 bears a very close analogy with that last quoted, but here the disease in the lung appeared as secondary to typhus (typhoid ?), and was only of a month's standing. Numerous spots of Broncho- pneumonia passing into abscesses or form- ing cavities were found in both lungs. Dilatation of the bronchi was also present, and it may be questioned whether this was not of recent origin, since Buhl has shown that this condition tends to occur under identical circumstances, after continued fever associated with acute destructive Broncho-pneumonia.4 There are two fallacies to be guarded against in estimating the pathological significance of ulcerative processes in the lungs, which are (1) their origin in tuber- cle, and (2) their origin in pysemic pro- cesses. The latter need only to be mentioned as a frequent cause of pulmonary abscess, the origin of which may at times be diffi- cult to discover. It is not unimportant also to remember that hemorrhagic in- farcta may be the cause of indurated spots of cicatricial character, which, after long periods, may show but few traces of their origin. Ulcerations may also take place from nodules of tubercle situated in the midst of gray or gelatinous hepatization, either recent or of a more chronic and indurated type, and the tubercle, having perished by softening, may leave only a cavity sur- rounded by gray infiltration, or by moye or less induration.1 Symptoms and Physical Signs.-A considerable variety has been noticed in these, depending on the stage of the in- flammatory action, but still more on the co-existence of bronchial dilatation, or of secondary ulceration or gangrene of the pulmonary tissue, and also on the pres- ence or absence of secondary Pneumonia in the opposite lung. (a) In the cases where the state of consoli- dation has been traced in continuous sequence from an attack of acute primary Pneu- monia, the symptoms present have been chiefly those indicating a prolongation of the pyrexial state, together with a per- sistence of the physical signs of consolida- tion of the lung. The fever does not, however, maintain the acuteness or the typical course ob- served in the primary disease. In some instances it is scarcely apparent, though the patient remains weak and continues to lose flesh. monia, following typhoid fever and associated with collapse. Buhl considers that such conditions lead to subsequent shrinking and induration of the pulmonary tissue. The distinction which Buhl establishes for this form of Pneumonia appears to be that it is associated with collapse, and that it passes into acute desquamation and fatty degenera- tion of the epithelium of the air-vesicles ; a process which he regards as being allied to acute atrophy of the liver. 1 A case reported by Charcot as Chronic Ulcerative Pneumonia (loc. cit. Appendix, p. 66) appears to me to be of this character. Tubercle existed in the opposite lung. A case recorded by Louis (Case iii. Phthisis, Syd. Soc. Ed., trans, by Dr. Walshe, p. 19) was considered by him to belong to this class, inasmuch as tubercle was found in a lym- phatic gland in the neck. There were, how- ever, no tubercles in other parts of the body. 1 See a case by Dr. Green (Path. Soo. Trans, xx.*) ; also the eleventh case by Barth (loc. cit.J). 2 Path. Soc. Trans, xii.J The sudden ex- pectoration of a large amount of puriform matter in this case led to the suspicion during life of the evacuation of a loculated empyema through the lung, but no distinct evidence of this was afforded by the post-mortem exami- nation. The symptoms and the subsequent expectoration would be quite explicable by an abscess communicating with the bronchi. There was some evidence of a tubercular dia- thesis. 3 Loc. cit. p. 274. 4 Virchow's Archiv, xi. 275, "Ueber Acute Lungen Atrophie." The name does not ap- pear well chosen, since the cases alluded to were those of disseminated gangrenous Pneu- SYMPTOMS AND PHYSICAL SIGNS. 261 In other instances, however, it assumes more of the character of hectic, with irregular exacerbations and remissions, and usually a marked febrile movement takes place towards night. Exact ther- mometric observations on this subject are wanting, owing to the rarity of the disease in this form. I have already described the characters of the pyrexia in the only case of the kind which has come under my own cognizance. Night sweats some- times, but not constantly, follow the evening exacerbations; and emaciation may be very rapid. There is usually dyspnoea, but this is not always present in a subjective form. The rapidity of respiration also remains greater than natural; but as the pulse is usually accelerated, the degree of perver- sion of their ratio to one another, wit- nessed in the acute stage, is not com- monly maintained. Cough may in some cases be slight, in others it is persistent and troublesome, and may cause a return of the pain in the side. The sputa may in some cases retain a rusty tinge-more commonly they are mucoid or puriform, and with the latter character they may sometimes be expec- torated in considerable quantities. Hae- moptysis has not been observed at this period of the disease, though it is com- mon when dilatation of the bronchi and ulcerations have occurred. The physical examination of the chest reveals at this period phenomena differing in little from those observed in the acute stage. Retraction of the side to any notable degree does not take place until further induration and contraction of the pulmo- nary tissues have occurred ; but the tend- ency is shown even at earlier stages by the case already quoted, of recovery after a protracted convalescence. Respiratory movements are diminished on the affected side. Percussion gives a toneless want of res- onance which increases in intensity with the progress of the case. Bronchial or tubular breathing, bronchophony or pec- toriloquy, with increased vocal fremitus, are the typical phenomena accompanying this state ; but in some instances these have been noticed either to be entirely ab- sent1 or to have only been intermittingly present, alternating at times with an en- tire absence of breath-sound.2 Rales are generally heard during this period. They are commonly subcrepi- tant, and the fine crepitation of the acute stage does not appear to persist in the chronic form ; large bubbling rales are more common, and they may be suffi- ciently metallic as to stimulate the char- acters of an abscess or an excavation even when none exists. The respiration in the opposite lung is commonly exaggerated. If the progress of the case is unfavor- able, the digestive system suffers, con- gestion and catarrh of the stomach su- pervene, and vomiting is occasionally observed. Thirst is a common, symptom. Diarrhoea may also be present, without tubercle or ulceration of the intestines. Anasarca and ascites occasionally occur in the latter stages,1 without any appreci- able cause, other than that afforded by the disturbed circulation through the lung. (6) When the condition has passed into the more advanced stage of induration, the symptoms present depend, in great meas- ure, on the coexistent conditions. In some cases the cicatricial tissue formed is perfectly quiescent, and life may be long protracted, without much manifest impair- ment of the general health, and with only a minor degree of dyspnoea on exertion, although the physical signs of pulmonary induration persist. The presence, how- ever, of dilatation of the bronchi, or the existence of ulcerations of these extend- ing into the pulmonary tissue, or the oc- currence of secondary Pneumonia, im- parts to the disorder a gradually pro- gressive character, which may strongly simulate the features of tubercular phthi- sis. These correspond closely to the de- scription of the disease furnished by Avenbrugger and Corvisart. Avenbrug- ger pointed out that want of respiratory movements and of resonance on percus- sion were the leading physical signs, while the symptoms present chiefly con- sisted in dyspnoea on exertion and disten- sion of the jugular and external veins; cough being unfrequent, expectoration scanty, and the decubitus of the patient remaining unaffected. Corvisart, in his Commentary, adds to these symptoms a progressive emaciation, and also a febrile diathesis, occasional partial perspirations, loss of appetite and of sleep, paroxysms of dyspnoea, and, in rare instances, oedema, which occasionally is limited to the limbs of the affected side. When the complication of bronchiectasis is absent, the contraction of the indurated pulmonary tissue produces a gradual re- traction of the chest-wall on the affected 1 Requin, quoted by Grisolle, p. 340. Cho- mel, loc. cit. 277. 2 Charcot, loc. cit. p. 39. Charcot only mentions the disappearance of the breath- sound, and not of the other phenomena. Neither he nor Requin have described the state of vocal fremitus. Charcot regrets that the relation of these phenomena to the expec- toration was not noticed. It may be remem- bered. that the same condition is sometimes observed in the acute stage. It has also been noticed by Bamberger over bronchial dilata- tions : Oest. Zeitsch. 1859 (Charcot). 1 Durand-Fardel, loc. cit. 608. 262 CHRONIC PNEUMONIA. side, which is general when the whole of the lung has been affected, or partial in the upper or lower parts of the chest, ac- cording to the site of the induration. If the affection is extensive, displacement of the heart occurs either upwards when the consolidation is seated at the apex of the lung, or if the affection be general, or im- plicates a large part of the base, the heart is drawn towards the affected side. The contraction of the side has been stated by Dr. Stokes to be as great as that following pleurisy, with the same approximation of the ribs, and procidentia of the shoulder. Dr. Walshe, however, denies that this form of retraction is produced by simple " cirrhosis." The respiration in some cases, when there is no dilatation1 of the tubes, has been observed to be bronchial; but there are very few, if any, authentic records of the physical signs in this state. Weak or suppressed breathing must be admitted as being a priori possible. We have, I be- lieve, no data respecting the condition of the vocal fremitus and resonance in this condition. (c) When dilatation of the bronchi coexists with chronic pulmonary induration, many variations occur both in the symptoms and in the physical signs. As a whole, as before stated, they closely simulate those of tubercular phthisis; but the prog- ress of the disease is usually slow, and the deterioration of health and strength pro- ceeds rather through a series of exacerba- tions than by any marked continuously progressive disease. Dyspnoea is almost constant, though not an absolutely inva- riable symptom. The decumbency (when mentioned) is commonly on the affected side. The pulse perspiration ratio does not appear to be necessarily or notably per- verted.2 Cough is usually persistent, and is liable at times to marked exacerbations. It may be dry, as originally noticed by Avenbrugger and Chomel, but more com- monly it is attended by expectoration. The sputa, when present, are variable in their characters: sometimes they are simply mucoid ; more commonly they are puriform. Under the influence of inter- current Pneumonia they may become at times rusty in tint. When ulceration is proceeding they acquire a brick-dust ap- pearance, and under these circumstances they are often profuse. They often pre- sent a dirty greenish-gray appearance, which may approach a bottle-green or inky tint,' and they are either confluent, or consist of floating masses of irregular outline, marked by black specks and spots of the size of a millet or hemp seed, and they may contain a large amount of pig- ment and fragments of the elastic tissue of the lung.2 The color of the sputa de- scribed by Traube has also been noticed by other observers. That these charac- ters are common to dilatation of the bron- chi is apparent from Barth's description3 of their appearance under these circum- stances. In one of his cases, where there was a "black softening" of the pulmo- nary tissue, they were of a chocolate tinge. Fetidity of the sputa and also of the breath is a very frequent accompaniment of this condition. I find it mentioned in eleven out of the thirty-nine cases which I have analyzed. In four of these it ac- companied gangrene of the lungs, but in five others there was no evidence of this state. In two cases, however, the data are imperfect. This offensive character of the sputa may indeed coexist with sim- ple bronchitis or with bronchial dilatation without pulmonary induration; but the latter is the most common condition in which it occurs, particularly when ulcera- tion and the formation of cavities4 have taken place. Haemoptysis is comparatively a com- 1 Traube (Deutsche Klinik, 1859, 477) con- siders these characters, and particularly the dark specks, as sufficient to distinguish the sputa of Chronic Pneumonia from those of tubercular phthisis, which he says are masses of yellow or whitish color, float in water, and keep their round shape, and do not present these black specks. The sputa of phthisis are, however, more varied in their appearance than those here stated, and masses of pig- ment are not, I believe, uncommon in them. 2 Dr. Walshe. 3 Loc. cit. 524. 4 See Dr. Laycock on "Fetid Bronchitis," Case iv. p. 27. Fetidity of the sputa and of the breath, in connection with chronic pul- monary induration, was recognized as early as by Willis. Dr. Laycock, (p. 9) quotes a case by this author, of a dignitary of the Church who was long troubled with this symptom, and in whom some years later the whole of one lung had undergone the change in question. Dr. Laycock distinguishes this odor as fecal, in contrast to the special odor of pulmonary gangrene. In a chemical in- vestigation undertaken of one case by Dr. Gamgee, the reaction of the sputa was alka- line. I have found the reaction alike in sev- eral cases of fetid sputa; in one also, now under my care, presenting the physical signs of the state at present under consideration. Dr. Walshe (loc. cit.) notes that the sputa are particularly fetid without being gan- grenous, though in his case there was gan- grene of the opposite lung, but probably of more recent date. 1 E. g., in Dr. Andrew Clark's case. Res- piration was bronchial under the clavicle of the affected side, where there was only a " thickened sub-pleural nodule," and where the lung tissue otherwise appeared healthy. There were, however, cavities in the central parts of the lung. 8 Dr. Walshe's case. SYMPTOMS AND PHYSICAL SIGNS. 263 mon symptom. I find it mentioned in sixteen out of thirty-nine cases ; in seven- teen the data are imperfect; in six others its absence may be reasonably inferred. In six cases it was the first symptom that attracted attention, though cough had ex- isted in some antecedently ; in two, how- ever, of these there is evidence of tuber- culosis, and tubercles were also present in three other cases in which it appeared in the course of the disease. In nine others there were either ulcerations or cavities present, and in two only (in both of which it was slight) are neither of the above conditions recorded. In some cases where it appeared early, it is possible that the ulceration of previously dilated bronchi may have been the cause of its appear- ance, and that the Broncho-pneumonia thus excited may have led to the subse- quent induration of the lung, since in most of these many years intervened be- tween its appearance and the final fatal issue. The amount of blood expectorated varies considerably. In the majority of cases it has been moderate, but it is occasionally repeated and it may prove the cause of death.1 In a case by AV. Schmidt,2 where there was no evidence of tubercle, the pa- tient had had seventy attacks of pulmo- nary hemorrhage in the course of twenty- three years. The physical signs depend on the exist- ence of dilated bronchi and of cavities in an indurated and retracted lung. The re- traction of the side and the displacement of the heart reaches its extreme degree in this condition; and when the right lung is affected, the right ventricle of the heart may be found beyond the nipple3 on that side. There is an absolute deficiency of expansion, though some elevation move- ments may persist over the affected lung. Percussion gives a high-pitched wooden resonance, which may even be amphoric or tubular, when large dilatations occur near the surface, and particularly in the infra-clavicular regions. The respiration presents in varying degrees the characters of bronchial or blowing. Bronchophony and pectoriloquy, the latter also occurring in the whispering variety, are most com- monly met with over the affected parts. The vocal fremitus is usually exaggerated, but its absence has been noticed when both bronchial breathing and broncho- phony have been present.1 Rales of vari- able size are usually heard over the di- lated tubes. They are commonly large and bubbling, and are not unfrequently metallic or cavernous in character. AV hen one lung only is implicated, or unless re- cent secondary Pneumonia has supervened on the opposite side, the unaffected side is generally hyper-resonant, and the in- creased clearness on percussion may ex- tend across the middle line, so that under the clavicle on the affected side, as was pointed out by Sir II. Marsh,2 the dulness is greater towards the acromial angle than towards the sternal articulation of the clavicle. The respiration in the sound side is exaggerated-puerile ; rales are only heard here when bronchitis or Pneu- monia is present as a complication. Liv- idity of the face, amounting to a minor degree of cyanosis, is observed, and dis- tension of the jugular veins appears to be comparatively not unfrequent. Peculiar white spots on the face have been noticed by Drs. Barlow and Sutton, and by Dr. Andrew Clark.3 Gangrene of the ex- tremities has been noticed as a complica- tion in elderly people.4 Clubbing of the fingers was noticed in a case by Ziemssen. Pyrexia, though commonly existing only to a slight degree, is more or less present during the progress of these cases. There are periods when fever is not present, and its occurrence appears to be due either to intercurrent Pneumonia or to ulcerations and inflammatory action in the indurated tissue surrounding the dilated bronchi. In some cases of long continuance it is noticed as having occurred at variable in- tervals, alternating with apyrexial periods of considerable duration during the course of many years.5 A large proportion of the recorded cases show a certain inter- mitting degree of febrile action, which in some instances has been severe and of a hectic type towards the close of life. In other instances, even under these circum- stances, the febrile action has been slight, or almost imperceptible. Exact ther- mometric observations appear, however, to be entirely wanting in all the recorded cases of this disease. Dropsy is a very common symptom. It is mentioned in thirteen out of thirty-nine cases. Its absence is only distinctly re- corded or presumably inferable in eight. It is seldom extensive, and most com- monly affects only the lower extremities. 1 As in Dr. Sutton's second case,i and in one by Dr. Foot, Dub. Journ. 1866, xli.* The latter case was probably tubercular, and the former is not free from the same suspi- cion. 2 Zwei Faile von Chronischen Pneumonie; Erlangen, 1863. Schmidt's Jahrb. 1866, p. 132.* 3 Dr. Walshe's case. 1 As in a case by Dr. Green, Dub. Quart. Journ. 1846, p. 510.* 2 Note by Sir D. Corrigan, Dub. Med. Gaz. 1857, p. 284. 3 Dr. A. Clark considers these to be indica- tions of fibroid degeneration of the skin. 1 Durand-Fardel, loc. cit. 604. 5 Schmidt's second case, loc. cit. 264 CHRONIC PNEUMONIA. It is sometimes associated with albumin- uria and casts of tubes, but in other cases the absence of these has been noted.1 Ascites, as noticed by Durand-Fardel, is extremely rare.2 Diarrhoea is not uncom- mon even without ulceration of the in- testines. The latter cause, and probably of a tubercular character, existed however in some cases.3 Vomiting is also occa- sionally observed. In some cases where it has been severe, albuminuria has been simultaneously present. In other in- stances it is excited by spasmodic cough, by difficulty of expectoration, or occa- sionally by the offensive character of the sputa. In a few instances no explanation of its occurrence has been recorded. Emaciation and loss of flesh proceed in some cases to an extreme degree; in others, though cough had lasted long, there does not appear to have been much wasting of the tissues, but there arc very few cases which do not present this to some extent. Diagnosis.-The diagnosis of Chronic Pneumonia rests on the recognition of the consolidation of the lung, with or without the presence of cavities. As a general rule, the affection being unilateral, we have to deal only with causes which may affect one lung singly ; and the diseases with which this state may be confounded are-pleurisy with effusion, or pleurisy with retraction, col- lapse of the lung, tubercle, and cancer. The possibility of Pleuritic Effusion can only be admitted in the more recent cases when retraction of the side has not already occurred. Under ordinary circumstances in chronic induration, the absence of en- largement of the side, the distinctness of the intercostal spaces, and the presence of bronchial breathing, bronchophony, and increased vocal fremitus, are usually suffi- cient to exclude the idea of fluid in the pleura. In the rare cases where the res- piratory sbunds together with the vocal resonance have been inaudible, the mis- take has actually occurred,4 but attention to the state of the intercostal spaces would probably prevent this fallacy. A further guide in such cases is the position of the heart, particularly when the affection is on the left side. In effusion it is pushed from the dull side. In Chronic Pneumonia without retraction it is not displaced. Depression of the diaphragm would also aid in the reeognition of pleurisy. In the majority of cases, however, these difficul- ties are unlikely to occur. Pleurisy with retraction of the side may offer greater difficulties, particularly if the indurated lung does not contain dilated bronchi. In Chronic Pneumonia, however, the retraction is more general than in pleurisy, and is not, according to the most recent evidence, attended with the same degree of twisting of the ribs on their axes, or with the procidentia of the shoulder and tilting outwards of the angle of the scapula, which attends the retraction following pleurisy.1 Bronchial breathing and bron- chophony are common to both affections ; and in pleurisy, even signs of excavation may occasionally be simulated by marked pectoriloquy. But such cases, which are the exception in chronic pleurisy, are the rule in pulmonary indurations associated with dilatation of the bronchi; and there- fore the existence of signs of cavities, par- ticularly when general, and w'hen asso- ciated with large and metallic rales heard over the affected lung, will be strong evi- dence in favor of the latter condition. The diagnosis will also be aided by the other features of the case. The charac- ters of the expectoration are often peculiar in Chronic Pneumonia. In pleurisy, if bronchitis be present, they are simply bronchitic, and their source may be dis- covered by the rales in the opposite lung. Hemoptysis can only take place in simple pleurisy under some conditions affecting the opposite lung. If these be undiscover- able, the presumption would be in favor of Chronic Pneumonia. Pyrexia and emaciation are rarely found in simple chronic pleuritic retraction ; and diarrhoea is also uncommon except in the later stages of cases complicated with albumin- uria. Regarded 'as a whole, although no single diagnostic sign exists for the dis- crimination of the two affections, the group of symptoms characterizing Chronic Pneumonia are sufficiently distinct to pre- vent, in the majority of cases, the possi- bility of this error in diagnosis. Simple Collapse of the Lung, sufficiently extensive to simulate retraction with in- duration, can only occur in the adult as a consequence of obstruction of one of the main bronchial tubes. Except from the introduction of a foreign body, this can only occur from external pressure-as from an aneurism or a tumor originating in the bronchial glands-and would then be attended with other pressure symptoms, 1 In Ziemssen's case floc, cit.) albumen was absent from the urine when anasarca was first noticed, and only appeared later together with casts of tubes. The-data re- specting the urine are, as a general rule, im- perfect in most of the recorded cases. 2 Loc. cit. 612. 8 As in one by Sir D. Corrigan, Dub. Hosp. Gaz. 1857. 1 Grisolle, p. 342. 1 Dr. Walshe, Med. Times and Gaz. 1856, i. 1858. The author is indebted to Dr. Walshe's masterly analyses for most of the data on the subject of diagnosis. PROGNOSIS. 265 or by the physical signs indicative of the nature of the disease. Collapse of the lung is further attended with weakened or suppressed respiratory murmurs. Bron- chophony, also, is rarely heard over such parts, and would be practically impossible when the collapse originated from obstruc- tion of the bronchi. Signs of dilated bronchi are also entirely wanting except in the acute form of Broncho-pneumonia. Pyrexia, and other symptoms enumerated, are also absent in uncomplicated cases of collapse. Cancer of the Lung produces retraction of the side, and may lead to signs of ex- cavation. In it, however, the displace- ment of the heart is much less considera- ble. The dulness commonly extends across the middle line, while in retraction from Pneumonia the sound lung usually encroaches on the affected side. In can- cer, also, pressure signs may be present: the excavations are more extensive, and haemoptysis is commonly more profuse and repeated. The peculiar currant-jelly- like expectoration of cancer has not'been met with in any of the recorded cases of pulmonary induration. Pain in the chest is also much more common in cancer than in Chronic Pneumonia ; in the latter dis- ease it appears scarcely ever to be a prominent feature. Local limitation to one side, and the absence of secondary cancerous affections, are less certain guides, but they are pro tanto in favor of simple induration. The existence of the cancerous cachexia has not been distinct in the cases which I have seen of primary cancerjof the lung. Emaciation and py- rexia are common to both classes of dis- ease. The duration of the case, where it has exceeded more than two years, is, ac- cording to Dr. Walshe, almost sufficient to exclude cancer; and this, together with the features first enumerated, are adequate for the diagnosis of the two dis- eases. The diagnosis from tubercle presents considerable difficulties in some aspects of the question. It is, I think, by no means improbable that a tubercular Pneumonia may, under favorable circumstances, pro- duce a local induration of a part or even of the whole of one lung without neces- sarily entailing a secondary affection of the opposite lung or of other organs. The indurations attending chronic tubercular phthisis are almost," if not absolutely, identical in their nature with those re- sulting from a non-tubercular inflamma- tion ; and the final result in both cases, of cicatricial tissue traversed by dilated bronchi, produces a condition in which the physical signs and symptoms of the two affections are precisely similar. Such cases are, however, exceptional. In tu- bercle the disease is commonly progres- sive, and it is only in very rare cases that the opposite lung is not implicated. The difficulty of diagnosis, however, refers rather to affections of the apex than to those of the base of the lung. A double apex affection, attended with the signs of cavities, is immensely in favor of the tu- bercular origin of the disease. When, as in some instances, the consolidation af- fects the base of one lung and the apex of the other, this presumption has also the greatest amount of probability in its favor. A unilateral induration of the whole or the greater part of one lung, when the opposite lung is hypertrophous and healthy, affords on the other hand strong evidence against the tuberculous nature of the affection. Neither the presence nor absence of haemoptysis, of pyrexia, or diarrhoea, afford any material additional aid, since they may all occur in chronic induration, and may be absent in cases of chronic phthisis, at least during long pe- riods. Fetidity of the sputa is rare in phthisis, very common in Chronic Pneu- monia with dilated tubes ; but it may ex- ist in the former and may be absent in the latter. Under all the circumstances to which I have now alluded, the history of the patient may afford some aid. The history of a previous acute attack occur- ring on the affected side is largely in favor of the diagnosis of simple induration. The existence of an antecedent but long- continued bronchitis, coupled with occa- sional attacks of pyrexia, and gradually increasing dyspnoea, would lead to the same conclusion ; and practically-though some cases have been recorded as errors in diagnosis-the data for the recognition of the disease are usually sufficiently clear to avoid most of the fallacies which may lead to an erroneous conclusion. Prognosis. -This may be best studied by considering the duration of the record- ed cases. Of these the duration in eight was unknown. In four, death appears to have taken place within twelve months from the first serious symptoms, though whether this represents the whole dura- tion of the disease may be considered as doubtful. The shortest recorded period is three months, mentioned in two of Charcot's and in one of Sir D. Corrigan's cases, and both the former appear to have been simply cases of the acute disease running a protracted and fatal course and ending in ulcerative excavation of the lung. In the case before quoted from Andral, where also the pulmonary indu- ration succeeded to an acute attack of Pneumonia, death took place within eighteen months; but in a similar case recorded by Ziemssen in a child, nine years of progressive illness elapsed be- tween the first attack and the fatal ter- mination. In the remainder analyzed, 266 CHRONIC PNEUMONIA. the disease was of unknown duration in six cases. Dating from the first symp- toms, death took place in four cases with- in 2 years, in two within 3 years, in four within 4 years, in four within 5 years, in two within 6 years, in two within 8 years, in three within 11 years, and in six cases life was protracted to 14, 20, 23, 27, 34, and 44 years. Excluding the cases of un- known duration-in many of which, how- ever, pulmonary symptoms had existed during some years-and excluding also those where death took place in less than 12 months, we find that fourteen died within 5 years, and twelve, or nearly an equal number, lived for variable, and sometimes for considerable, periods be- yond this date. The general conclusion which may safely be drawn from these figures is, therefore, that under favorable circum- stances life may be considerably protract- ed after distinct signs of consolidation have become apparent, and even when there has been an occasional recurrence of threatening symptoms.1 The possi- bility, indeed, of a nearly perfect restora- tion to health, though a considerable ex- tent, sometimes amounting to nearly the whole of one lung, is rendered impervious to air, may be seen in some of the cases before quoted, especially in children, where the affection has succeeded to an acute attack of Pneumonia or of Broncho- pneumonia. In none of these cases, how- ever, is there any evidence that the af- fected part ever regained its respiratory function ; and it may be regarded as more than doubtful whether organized cica- tricial tissue of the lung is ever removed by any process, so as to restore the natu- ral condition. In some cases, 'where only a part of the lung has been thus indu- rated, its gradual contraction is compen- sated for by an hypertrophous emphysema of the remainder; and thus the area over which the physical signs of induration exist may gradually diminish, and may become replaced by those of healthy pul- monary tissue.2 If the whole of one lung has been indurated, the process of respi- ration is necesarily confined to the other, and this increases the danger arising from any subsequent disease, by which the sound organ may be incapacitated from performing its functions.1 The other elements in the prognosis de- pend on the progress of the disease in the affected parts, and on the general consti- tutional state of the patient. Evidences of chronic inflammatory ac- tion in the bronchi, as shown by catarrh, with pyrexia and profuse expectoration, have, in addition to the exhausting effects which these directly produce, the fur- ther unfavorable significance, that they threaten an extension of the inflammatory action to the surrounding pulmonary tis- sue, and are thus a source of danger from ulceration and the formation of cavities. The more quiescent these symptoms ap- pear, the more favorable therefore is the ultimate prognosis. The existence of ulceration as shown by haemoptysis, or by the expectoration of grumous fragments of lung tissue, are un- favorable signs ;2 and though haemoptysis may, as before stated, be in some cases frequently repeated during many years, yet, in the majority of instances, cases presenting this symptom to a marked de- gree have a more unfavorable course than those in which it is slighter in amount or altogether absent; and it must further be remembered, that such haemoptysis may occasionally prove immediately fatal. Cases commencing with haemoptysis are always open to the suspicion of being of tubercular origin, but the very existence of an indurating tendency in tuberculous disease imparts to such cases a compara- tively favorable prognosis; and some of these, as recorded, appear to have quite as favorable a chance of prolongation of life as those cases where the primary in- duration appeared to be of simple inflam- matory origin. An offensive character of the sputa al- most invariably gives a more serious char- acter to the case; but life may in some instances be long protracted even after this has appeared. Fetidity of the expec- toration may coexist with simple dilata- tion of the bronchi, but the character of the secretion in such cases imparts to them a septic tendency, and increases the liabil- ity to septic or gangrenous Pneumonia, either in the affected or in the opposite lung. In many cases, indeed, such fetid- ity is immediately associated with ulcera- tive processes, and the recognition of 1 This is particularly seen in two cases re- corded by Schmidt before quoted, where the patients with signs of pulmonary consolida- tion with cavities were under observation during periods of fifteen and twenty-three years, and where it is stated that the second of these outlived three physicians who at- tended him. A boy under the care of Dr. Mayne, whose case is not free from the suspi- cion of tubercle, lived six years of a laborious life involving great exposure, after distinct disease had been observed in one lung, and died only of acute bronchitis affecting the other. (Dubl. Hosp. Gaz. 1860, vii.*) 2 As in Bartel's case, before quoted. 1 As in Dr. Mayne's case (Dubl. Hosp. Gaz. 1860, vol. vii.), where death was caused by acute bronchitis affecting the previously sound lung. 2 The discovery of elastic lung fibres in these fragments is the only positive evidence of pulmonary destruction ; but when ulcera- tion affects an old induration, the elastic fibres may be undiscoverable. TREATMENT 267 these may probably be aided in great measure by the coexistence of pyrexia with this state. The presence of fever under such cir- cumstances usually depends on the exist- ence of secondary Pneumonia ; and when it is undiscoverable on the sound side, it is a matter of great probability that it is extending in that already affected. Py- rexia, when of long continuance, has been indeed one of the final phenomena in nearly all the recorded cases, and its existence is always to be regarded with the gravest suspicion, both in its diagnostic signifi- cance and also through its exhausting ef- fects on the nutrition and strength of the patient. Emaciation is naturally an unfavorable sign, but in some cases death may ensue without any extreme degree of marasmus being attained. Dropsy is always an unfavorable symp- tom. Very few cases attained to any con- siderable prolongation of life after it had appeared. Even when albuminuria is ab- sent, it is indicative both of serious dis- turbance of the circulation and probably also of an hydsemic condition of the blood; and the coexistence of albuminuria and the presence of casts of tubes in the urine adds an additional gravity to the progno- sis, by their significance as expressions of a general impairment of nutrition. Diarrhoea and vomiting are also signs of the gravest import. They rapidly ex- haust the patient, and in some cases lead directly to the fatal issue. Finally, when ulcerative action is proceeding, the possi- bility of secondary metastatic affections must also be recollected. In one case, by Andral, sudden death is reported to have occurred without any adequate explana- tion being afforded of the cause of such a termination.1 Treatment. - The treatment of Chronic Pneumonia may be considered under two categories. The first includes the cases where the disease has recently lapsed from the acute stage. The second comprehends those where thickening and fibrous growth have taken place in the walls of the air-vesicles. (a) Cases of the first type are often serious in their character, and the con- tinuous pyrexia and progressive emacia- tion tend to a fatal issue. The great principle to be followed in such cases is steadily to maintain the strength of the patient, and to meet indi- vidual symptoms as they arise. Sufficient evidence exists to show that under these conditions progressive im- provement may be observed, and that the lung may be restored to its healthy state. I have the strongest doubts whether medi- cinal agents have any direct effect in ac- celerating the absorption of the exudation matter from the interior of the air-cells of the lung, and I believe that the adminis- tration of mercurials, or even of the pre- parations of iodine with this purpose, is likely to defeat the main object which should be pursued of maintaining and improving nutrition. As long as pyrexia persists the patient should be kept in bed, in order to econo- mize, as far as possible, the expenditure of strength and the waste of tissue. The diet should be liberal, but proportioned in quantity and quality to the digestive powers ; and milk may, when it agrees, be freely taken with advantage. Alcoholic stimulants, in moderation, are required in most cases ; the form selected is best de- termined by their effects on the individual case. It is important to watch their effects on the pyrexia, which should be made the object of careful and repeated thermometric observations. It has ap- peared to me that they are best given as far as possible during the periods of remis- sion, and that they should be withheld or given in diminished quantities before and during the febrile exacerbations. When night perspirations are present, a mode- rate dose of stimulant will often have the effect of checking these, and also of ob- viating some of the exhaustion which is felt on the succeeding morning. Cough may be allayed by small doses of opiates combined with three or four drops of the vin. ipecacuanha;, and with from five to ten grains of the muriate of ammo- nia. Iron, quinine, bark, and the mine- ral acids may all be employed according to the special indications of anaemia, failure of appetite, sweating, or profuse expectoration. If the latter be present, ipecacuanha should be withheld, and ammonia with infusion of senega or ser- pentaria may be given. The existence of gastric catarrh often forms an unfavorable complication of these cases. Its presence appears to me to contraindicate most of the remedies last enumerated, and it is usually aggravated by the whole class of "tonics." If it co-exists with much cough and expectoration, these may be met with opiates and the muriate of am- monia, while the gastric disorder is best treated by bismuth, alkalies, and occa- sionally by small doses of hydrocyanic acid. Under this management a gradual improvement will often take place, and it has appeared to me that this may be aided by small blisters repeatedly applied over the affected side-a method which I think better than the use of extensive vesica- tion, which may disturb sleep and exhaust the patient. (&) In the treatment of chronic indura- tion, it is, I believe, best to recognize the 1 The suspicion here may arise of throm- bosis of the pulmonary artery. 268 CHRONIC PNEUMONIA. fact that fibrous tissue once formed is in- capable of being removed by medicinal treatment. The management of such cases is therefore mainly hygienic, and should be directed to maintain the health and to prevent extension of the disease in the affected side or secondary affections of the opposite lung. The dilatation of the bronchi which commonly attends this condition, renders the patient liable to catarrh; and since it is from repeated attacks of bronchial inflammation that the most dangerous effects of the disease are likely to arise, the avoidance of all causes of this nature is therefore of primary importance. Flan- nel worn next the skin, the avoidance of exposure, and the resources of a climate suited to the individual case, and which may be in part determined by experience and in part by the conditions of irrita- bility or of more or less tendency to bron- chial secretion, are among the most im- portant elements to be considered among the prophylactic agencies. Every fresh catarrh should be at once and promptly met, at least in its acute stage, by confinement to a regulated atmosphere, by counter-irritation to the chest, and by opiates, ipecacuanha, or muriate of ammonia. The maintenance of the general health and of the nutrition are also of essential importance. A liberal diet, of which milk may form a large share, and a judi- cious use of alcoholic stimulants whenever pyrexia is absent, are almost always re- quired. Cod-liver oil may also be taken with advantage during long periods when the digestion will tolerate its use. Iron and bark should be given, if the indica- tions for their administration arise. If any of the severer complications are present, they should be appropriately treated-haemoptysis by gallic acid or the acetate of lead or ergot: diarrhoea by astringents; vomiting by small doses of opiates or by hydrocyanic acid ; and gas- tric catarrh by bismuth and alkalies. Profuse expectoration may be met by inhalations of oleum picis, creosote, or carbolic acid, either in the form of vapor or by means of a weak solution in an atomizer; and the muriate of ammonia may sometimes be used with advantage in the same manner. The inhalation of the vapor of the oil of turpentine has been tried in some cases where the sputa have been fetid, but unfortunately without much success. The vapor of iodine has appeared to me to give more relief in some cases when gangrene has imparted this character to the sputa. Port wine in full doses often has a most beneficial effect in cases characterized by profuse expectoration, and preparations of bark and the mineral acids have also a favor- able influence. Opiates not only check secretion, but diminish the violence of the cough, and relieve the bronchi from the continual tendency thus excited to produce further dilatation. The treatment of albuminuria, dropsy, or ulceration of the pulmonary tissue, when this has occurred, is unfortunately almost beyond the reach of remedial agents : and though much may be effected before these complications have occurred, the later stages of this condition can only be met by such indications as may pro- mote the comfort of the patient, rather than with any hopes of restoration. APPENDIX TO ARTICLE ON CHRONIC PNEUMONIA. The rarity of this disease and the difficulty attending some points of its pathology induce me to believe that references to the most im- portant published cases illustrating it may possibly be useful to others. I shall continue to mark the cases which I have tabulated by an asterisk (*). Bayle (Phthisie Pulmonaire), two cases of "phthisie avec mManose."* Laennec (Forbes's translation, 2d Edition, p. 112), a case of dilatation of the bronchi with pulmo- nary induration.* Andral (Clinique Medi- cale, iii. obs. Ixiv.), a case where induration of the lung succeeded an attack of acute pneumonia.* Dr. Stokes (Diseases of Chest, p. 150), a case of chronic pulmonary indura- tion with dilatation of the bronchi.* Jaccoud Clinique Medicale, p. 82), sclerosis of the lung with dilatation of the bronchi-tubercu- lar?* Herard and Cornil (Phthisie Pulmo- naire, 167), induration of lung with bronchial dilatation.* Ziemssen (Pleuritis und Pneu- monie im Kindesalter), a case of nine years' standing in a child, probably resulting from an attack of acute pneumonia; dilatation of bronchi in both lungs; induration of one.* Barth (Rech, sur la Dilatation des Bronches ; Mem. Soc. Med. Obs. 1856), six cases ;* some probably tubercular. Heschl (Prager Viertelj ahr- esch. 1856, ii.), two cases : only pathological details.)* W. Schmidt (Zwei Faile von chron- ischen Pneumonie, Diss. Erlangen, 1863).* Charcot (De la Pneumonie chronique), three cases,* two acute. Dr. Green (Path. Soc. Trans., vol. xx.), ulcerative pneumonia.* Dr. Peacock (Edinb. Journ. 1855).* Raim- bert (Journ. Med. et Pharm. de Bruxelles: analysis in Gazette Hebdom. 1856), one case incomplete ;* others referred to are described as " carnification." Dr. Andrew Clark, a case of fibroid phthisis* (Trans. Clin. Soc. L), probably tubercular. The following are described as cases of " cirrhosis- Sir D. Corrigan (Dublin Journal, 1838, and Dublin Hospital Gazette, 1857), three cases with post-mortem results.* Dr. Walshe (Med. Times and Gazette, 1856), the most fully-re- corded case extant with commentary.* Dr. Mayne (Dub. Hosp. Gaz., 1857 and 1860), APPENDIX TO ARTICLE ON CHRONIC PNEUMONIA. 269 two cases,* the last doubtfully tubercular. Dr. Green (Dublin Quarterly Journal, 1846).* Dr. Law (ib. 1848),* probably tubercular. Dr. Jennings (ib. 1866).* Dr. Foot (ib. 1866), doubtfully tubercular.* Dr. Wilks (Path. Soc. Trans., viii.), probably tubercular, mentions ' ' spots of strumous deposit' ' in the opposite lung. Drs. Barlow and Sutton (Path. Soc. Trans, xvi.).* Dr. Fagge (ib. vol. xx.).* Dr. Bar- low (Guy's Hosp. Rev. 1847, 2d Ser. v.).* The following cases not included in the analysis as being either of doubtful nature or imperfect in general details, may also be re- ferred to:- Dr. Dickinson (Path. Soc. Trans, xiii.). Dr. Risdon Bennett (Path. Soc. Trans, xii.), a case of ulcerative pneumonia of doubtful origin. Biermer (Zur Theorie und Anatomie der Bronchien - Erweiterung, Virch. Arch, xix.), many instances of induration of lung. Macdowell (Dublin Quarterly Journal, 1856), entitled as "Cirrhosis," but lung described as "carnifled;" no dilatation of bronchi; thickened pleura and fluid in pleural cavity. Weber (Path. Anat, der Neugeborenen und Sauglinge, ii.), three cases referred to where induration of lung commenced with acute pneumonia, with post-mortem results, and two more of recovery. Bartels (Virch. Arch, xxi.), a similar case commencing with bron- cho-pneumonia. Steffen (Klinik der Kinder- krankheiten), four cases of interstitial pneu- monia ; three at least tubercular. Legendre (Rech. Anat. Path. Maladies de 1'Enfance), two cases of induration of lung in children ; secondary to catarrhal pneumonia. Dr. Ben- nett (Rep. City of London Hosp, for Dis. of Chest), two cases of induration with signs of dilated bronchi in children; recovery. Traube (Deutsche Klinik, 1859, § iv.), two cases, chronic ulcerative pneumonia; general re- marks. Dr. Addison's Works (Syd. Soc. Ed.), three cases. Steiner and Neuretter, Padiatrische Mittheilungen (Prager Viertel- jahresch. 1866, Ixxxii.), two cases of indura- tion after broncho-pneumonia. Macquet (Bull. Soc. Anat. xxii.). Gabalda (ib.). Charnal (ib. vol. xxx.), induration of lung in conse- quence of acute pneumonia; other data im- perfect. Barth (ib. vol. xxix.), induration of base with dilated bronchi. Barset (Bull. Soc. Anat, xxx.), microscopic examination by Robin after maceration. Lancereaux,two cases of gangrenous pneumonia, surrounded by induration, and associated with secondary abscesses in other organs (Gaz. Med. Paris, 1863). Powell (Trans. Clin. Soc. ii.), cases of phthisis with contracted lung; excellent description of appearances, all of tubercular nature. Sutton, fibroid degeneration of lungs (Med.-Chir. Trans. 1865, xlviii.). Bastian, Cirrhosis of Lungs (Path. Soc. Trans, xx.), tabulated series of thirty-four cases of indura- tion. Durand-Fardel (Mal. des Vieillards), various forms of chronic pneumonia. Cotton on a prevailing form of Chronic Pneumonia (Med. Times and Gaz. 1855. i.) ; general de- scription, pathological appearances of two cases. Hardy and Behier (Path. Interne); gen- eral description, ref. to four cases. Grisolle (Traite de la Pneumonie), ref. to various cases. Lebert (Physiologie Pathologique), ref. to pa- thological appearances in two cases. Chomel (Diet de Med. xvii.), general description. Avenbruegger (Inventum Novum, &c., 1761), "Scirrhus of Lung," with commentary by Corvisart (Eng. Trans, by Sir J. Forbes). Sir J. Forbes (Appendix to Trans. Laennec, Ed. 1824), two cases, one probably tubercu- lar, the other doubtful, tissue of lung floated. Broussais (Hist, der Phlegm, vol. ii.), three cases. Hasse (Path Anat., Syd. Soc. Ed.). Hope (Morbid Anatomy). Rokitansky (Path. Anat.). Cruveilhier (Anat. Path., liv. xxxii.). In addition to these, the following works, to which I have not been able to obtain access, are referred to by Grisolle, Durand-Fardel, and Charcot, but the data of many appear from the statements of these authors to be unreliable or imperfect: Letenneur (Diss. Pneumonie chronique, These de Paris, 1811). Baziere (Diss, sur 1'Emploi du Seton dans la Pneumonie chronique, 1819). Rat, Theses de Paris, 1845. Raymond, Sur la Pneumonie chronique simple, Diss. 1842. The author is indebted to Dr. Bastian's tables and to M. Charcot's thesis for several references to cases, some of which are included in the foregoing analysis. (Since this article was printed I have met with, two other illustrations: Dr. E. Long Fox (Med. Times and Gaz. 1870), a case of chronic ulcera- tive pneumonia-thermometric observations; Im- mermann (Deutsch. Arch. Klin. Med. V. p. 235 et seq.), a case of chronic pulmonary induration (tubercular If attended with stenosis of the pulmo- nary artery.') 270 SYPHILITIC AFFECTIONS OF THE LUNG. SYPHILITIC AFFECTIONS OF THE LUNG.1 By Wilson Fox, M.D., F.R.C.P. The manner in which the tissue of the lung may be affected by the syphilitic poison, although it has been made the subject of much recent research, still re- quires a more accurate definition than has yet been attained. The opinion that certain forms of phthisis may arise from changes in the pulmonary tissue due to the syphilitic poison, is no new one. Morgagni noticed the frequent connection of tubercle with this dyscrasia, and Portal and Morton de- scribed a syphilitic phthisis, but failed to show that any special pathological changes were connected with this condition. Dr. Graves and Dr. Stokes2 have both enter- tained a similar opinion, based upon the success of the mercurial treatment of bronchitis in patients who had formerly been the subjects of venereal sores. Bayle, Laennec, and Louis failed to find any evi- dence of a special form of phthisis which could be distinguished as syphilitic, and it is only within recent periods that any changes have been identified in the lungs, which can probably be attributed to this cause. The difficulty of the inquiry lies in es- tablishing any certain criteria by which such alterations can be distinguished from the changes produced either by simple in- flammatory, or by the tubercular pro- cesses. Each of these may affect syphi- litic patients, and may run a course ap- parently unmodified either clinically or pathologically by the specific dyscrasia; and looking at the general history of sy- philitic affections, it is at least probable that the lungs are less prone to suffer from secondary or tertiary affections of a syphilitic character than the mucous membranes of the upper air-passages, or than the skin, the eye, or the bones. What their comparative liability may be in respect to the liver, the spleen, the tes- ticle, or the brain, is a point which must yet be determined by further research. In the lungs of syphilitic patients which I have examined, I have seen no appear- ances differing from those of ordinary pneumonia, of ordinary tubercle, or of tubercular or cheesy infiltrations; and one marked case of this kind has come under my observation, where there was the most distinct syphilitic ulceration of the larynx, but where the lungs only pre- sented a gray infiltration, together with tubercles and indurations referable to a previous attack affecting the apices, the cure of which I had myself witnessed at an earlier date. Other instances of an analogous kind have come under my ob- servation, where the most careful micro- scopic examination failed to reveal any peculiarities which I could ascribe to a syphilitic process. The inquiry into the nature of changes attributable to syphilis is therefore for the present almost a purely pathological one, though the importance of the question in its clinical aspect can scarcely be over- rated. A large amount of the evidence on this subject is derived from premature or stillborn children, the offspring of sy- philitic parents; but some cases are re- corded where syphilitic gummata have been found in the lungs of~idults. There are two sets of changes in the lungs, regarding the syphilitic nature of which there is a considerable unanimity of opinion. In another large class there is more doubt as to their true connection with this poison. The former are at least rare, and only isolated instances are re- corded by observers having large oppor- tunities for pathological research. The 1 I have not met with any indubitable in- stances of these affections in my pathological studies on the disease of the lungs, and the information contained under this head has been drawn from the following authors, in addition to those alluded to subsequently: Virchow, Archiv, xv., Krankhaften Gesch- wiilste, vol. ii.; historical data and complete references. E. Wagner, Arch, der Heilkunde, 1863, vol. iv. Foerster, Wiirzb. Med. Zeitsch. 1863, vol. iv.; Berkeley Hill, Syphilis and Local Contagious Disorders, many references. Von Baerensprung, Die Ilereditare Syphilis ; many cases ; microscopic figures of gummata in the lungs. Lancereaux, Traits Hist, et Pract. de la Syphilis; extensive bibliography, numerous cases. Lebert, Traits d' Anat. Path. Pl. xciii., figures of gummata in the lungs. Wilks, Guy's Hosp. Rep., 1863, and Path. Soc. Trans, ix., figures of gummata in the lungs; also A Lecture on Syphilis. Pihan Dufeillay, Des D^ggnerescences Syphilitiques des Visceres, Union M&L, 1861, and in Bull. Soc. Anat. 1861; comments in a case of Cor- nil's ; numerous references and critical obser- vations. 2 Graves. Clin. Med. ii. 27. Stokes, Dis. of Chest, 94-432. SYPHILITIC AFFECTIONS OF THE LUNG. 271 latter class requires a most careful and critical examination before their specific nature can be admitted. The most authentic changes in the lungs which can be ascribed to syphilis are gum- mata, or masses of low fibrous growth, evincing a great tendency to necrobiotic changes of the dry cheesy type, and which are very closely analogous to similar masses found in the liver and in other in- ternal organs. They are found in the lungs of adults, and in newly-born syphi- litic children. In the former, however, they are so extremely rare, that Lancer- eaux has only been able to collect ten cases by different authors. They are ir- regularly distributed through the lungs, having no special seat of predilection, but according to Wagner they are more com- mon in the deeper than in the peripheric parts. They may be single or multiple, and their dimensions may vary from the size of a pea to that of a walnut, or even of a goose's egg.1 They are generally rounded, rarely irregular in outline, and are sharply defined, but are not always encapsuled.2 In their earlier stages they are gray or brownish red, completely homogeneous to the naked eye, and are firm and dryish :-later they become of a comparatively uniform yellowish tint, but still maintaining their dry firm character. In some instances, however, they soften and form actual, or, more commonly, po- tential cavities.3 On microscopic exami- nation they are found to consist of imper- fectly formed fibres, which are often gran- ular and are intermixed with abortive nuclei and a few fibre cells. Both the nuclei and the cells are commonly found in various stages of fatty degeneration. The lung tissue is entirely destroyed by this growth, by which the walls of the alveoli become progressively thickened, until the cavity of the vesicles is obliter- ated, while the epithelium lining them appears to participate but little in the change. In some cases the bronchi show an infiltration of the submucous cellular tissue with a fibro-nucleated growth, which may form small prominences on the surface. Similar masses are some- times found in their deeper structures, but these as a general rule are unaltered. In these changes the preponderant and distinctive character consists in the growth of an indurating fibrous tissue, mingled with abortive nuclei, into distinct masses, and presenting a strong tendency to an early necrotic change. Another form, termed by Wagner the "diffused," is the appearance described by Virchow1 and Weber2 as the "white hepatization of the lungs" of newly-born children : it has also been named "Epi- thelioma of the lungs," by Lorain and Robin :3 and its syphilitic character has been shown by the last-named authors, who traced a relation between it and sy- philitic pemphigus, and also by Hecker,4 Ilowitz,5 and Wagner,6 and this has also been admitted by Virchow. Lungs in this state are distended so as to com- pletely till the cavity of the thorax, and to bear the impress of the ribs. The pleura covering them is usually found un- affected. They are white, dense, firm, and hard. They occasionally admit of partial insufflation, but this is not con- stant. Their weight when the affection is general is four or five times greater than natural. Their color is whitish with a shade of yellow, and it is uniform with- out any shading. Their section is smooth and opaque. They are resistant in some cases in others, as described by Weber, the finger can be pressed into them as into a fatty liver. They are quite exsanguine, and not a trace of blood or of the smaller bloodvessels can be discovered in them. The lobular texture is apparent-the in- terlobular tissue sometimes presents a slightly reddish tinge. The bronchi con- tain a tough mucus. The bronchial glands are enlarged, grayish, homogene- ous, or in parts presenting a dry cheesy aspect. The extent of infiltration varies -sometimes the whole of both lungs are affected7, sometimes only parts. When 1 E. Wagner. 2 lb. (loc. cit.) Von Barensprung describes smaller masses in the lungs of newly-born children as sharply defined by a layer of well- developed fibrous tissue. The nodules in Dr. Wilks's case do not appear to have been thus encapsuled. 3 Dr. Wilks (loc. cit.) Ricord (Clin. Icono- graph. Pl. 28) gives a case where numerous softened masses were found in the lungs, but he questions whether they were not the result of pyaemic infection. Depaul, one of the ear- liest authors who has published authentic observations on this subject (Bull. Soc. Anat. 1837; Gaz. Med. 1851; Mem. Acad. Imp. de Med. 1853), has also found the centre of these masses softening into a puriform fluid, and sometimes presenting real abscesses, whose walls were formed by a yellowish gray and indurated tissue. 1 Archiv, i. 146. 2 Path. Anat, der Neugeborenen, ii. 47. 3 Gaz. Med., Par. 1855. 4 Verhand, der Berlin. Geburtshiilf Gesell. 1854, viii. 130. 5 Behrend's Syphiologie, 1862, iii. 611. 6 Loc. cit. 7 Wagner in six cases found the whole of both lungs affected four times; once the half, and once the sixth part of the lung. Kostlin (Arch. Phys. Heilk. xvii.) met with it in four cases, generally limited to the lower lobe, or in isolated masses, varying in size from a pea to a pigeon's egg. In one child, who lived a fortnight after birth, the signs of the disease in the lungs appeared coincidently with ecthymatous pustules, with a measly rash, and with excoriations of the skin. 272 SYPHILITIC AFFECTIONS OF THE LUNG. the affection is partial, there may be found in addition to the general infiltration iso- lated spots of the same kind, but resem- bling more or less the gummata before described, which sometimes merge at their margins into the neighboring infiltration. There is some discrepancy between the statement of different observers regarding the histological characters of this consoli- dation. Virchow described the air-vesi- cles as filled with epithelial cells, and Robin and Lorain make the same state- ment, and add that this process extends into the ultimate bronchial ramifications -but that at the same time the walls of the alveoli are thickened and rigid. Weber described the contents of the alveoli as cellular; while Wagner, from his recent researches, says that the characteristic by which this change may be distinguished from gray hepatization is, that nothing can be brushed or washed out from the interior of the vesicles, and that the dis- ease essentially consists in a thickening of the alveolar walls, by which the cavity of the vesicles is gradually obliterated, and that in this process the epithelial lining is but little affected. This thickening takes place by the growth of an imperfect and scantily fibrillated tissue mingled with nuclei, and of a few fibre cells which are found in various stages of fatty and molec- ular disintegration ; granular and fatty debris are also found in large proportions throughout the tissue. The interlobular texture is normal or contains a small amount of nuclear and cell growth. The vessels and capillaries are almost com- pletely destroyed in the affected parts. The submucous tissue of the bronchi is affected in the same manner as has been described as occurring in connection with the gummata, by a growth of nuclei limited to the superficial structures. The bronchial glands are enlarged, and show concentric masses of cells bounded by a tough fibre tissue. It will be observed that in both of these forms of disease the essential character- istic of the change described consists in a thickening of the walls of the air-vesicles by a growth of imperfect fibre tissue mingled with nuclei which tends to pass into an early molecular detritus, and that this change thus produces a structure apparently identical with the syphilitic gummata found in the liver. Even in this form it would be very diffi- cult to state any precise definition which might absolutely distinguish the process from the similar changes which occur in tubercular growths, and in the thickenings which affect the walls of the air-vesicles in tubercular pneumonia.1 This difficulty is further increased in relation to some of the other changes which are frequently found in the lungs of syphilitic children, and also in some cases of adults. These, if separately distinguished, may be enu- merated as follows:- (a) Foerster has shown that lobular, vesicular, and broncho-pneumonia, either in a disseminated or in a confluent form, is very common in the lungs of children affected with hereditary syphilis and dying shortly after birth. In the majority of cases such pneumonias are identical in character with the ordinary forms of the disease, and consist only of an excessive development of epithelial cells and of their derivatives filling the vesicles. (b) Suppurative changes occur at times in these spots and give rise to abscesses, the specific nature of which, however, may still be considered doubtful, since similar processes also occur in the non- syphilitic forms of catarrhal pneumonia. (c) Foerster, however, has in some of these cases met with a gradual thickening of the walls of the alveoli, by the growth of a fibre tissue mingled with ovoid nuclei surrounding the spots of lobular pneu- monia. These then become hard, smooth, pale and glistening, and in a later stage they show a yellow change which gradu- ally extends throughout the nodule. This process has the greatest analogy with the growth of tubercular granulations, and if due to the syphilitic poison it w'ould es- tablish a close anatomical affinity between its effects and the changes which are most distinctive of tubercles. Similar appear- ances have been described, though on rather a larger scale, by Von Baeren- sprung and others, when the nodules so formed may attain the size of a walnut. Virchow has also remarked that these may coexist with peri bronchitic thicken- ings, and that they may pass in spots into ulceration ; and he further observes, that when met with in stillborn children of syphilitic parentage, their specific nature is rendered the more probable from the fact that tubercle proper is never met with as a disease of the fcetus. (d) Virchow is also disposed to regard as being in some cases of syphilitic origin, indurated masses of fibrous structure more or less pigmented, and presenting a rasp- berry-like appearance, which are found scattered through the lungs. They are either seated immediately under the pleura, where they cause puckering and contraction, and also around the bronchi, where they form a cicatricial tissue, and they are often attended by pleural ad- hesions ; cheesy spots are not uncom- relied upon. My own observations on tuber- cular formations have convinced me that such granular cells are by no means uncommon in these. 1 Lancereaux (426) says that large granule cells are not found in tubercular growths ; but this distinction is not, I believe, to be SYPHILITIC AFFECTIONS OF THE LUNG. 273 monly found scattered through them. The nature of these is however still more doubtful, since such masses are very com- mon in the indurating form of tuberculosis when there is no suspicion of syphilis.1 Virchow states that the more fibrous structures present no distinctive features of difference from the indurating forms of chronic pneumonia which occur in the " grinder's asthma," and probably also in the whole class of diseases produced by the inhalation of irritating solid particles into the lungs. (e) Virchow is further disposed to con- sider that fibrous induration of the pleura, and also certain forms of peribronchitic thickening which extend into the pulmo- nary tissue, may be due to the syphilitic dyscrasia, and that they may hold a place analogous to the cirrhotic indurations of the liver, and to indurations which are met with in the testicle under the same influence. Dr. Wilks has also raised the question whether some forms of "cirrho- sis" of the lung may not have a similar origin, but this point still remains to be settled by further observation2. (f) Virchow has also met with a change in the lungs closely analogous to the brown induration to be hereafter described, but occurring independently of heart diseases, and which from its associations he thinks may also be placed in this category. (g) Dr. Hermann Weber,3 in a case where there was evidence of constitutional syphilis, and where nodules which he was disposed to regard as early forms of gum- mata existed in the liver, found in the lungs a general enlargement of the super- ficial lymphatics, which were filled with a thickened cheesy lymph which could be expressed from their interior. These en- larged lymphatics presented on section the appearance of white spots scattered over the lungs : their contents presented granular corpuscles with multiple nuclei. The bronchial glands were also enlarged, softened, and crowded with cells exhibit- ing considerable activity of growth. Dr. Weber regarded it as doubtful whether the pathological condition of the pulmon- ary lymphatics or of the bronchial glands constituted the primary affection. The appearances described, as Dr. Weber him- self considered, differed in many respects from those which have hitherto been re- garded as syphilitic. Syphilitic growths in the lungs certainly bear a closer resemblance to tuberculous formations than is presented by almost any other morbid change in this organ. It is useless at present to revive the for- mer speculations which have been held with respect to the influence of syphilis on the production of tubercle. The question, however, may be looked at in another as- pect, and it would appear to be a subject for inquiry, how far a pre-existing " tuber- culous" or "scrofulous" constitution may aid in the development of these special local manifestations. Syphilis has long been known to exhibit its most virulent characters in patients of this diathesis, and it appears to be not impossible that such a predisposition may render the lungs specially liable to suffer from the syphilitic affection, the characters of which may be partially modified by the tubercu- lous tendency. Tubercular changes are in many points of view so closely allied to the processes of inflammation that it has become increasingly difficult with further research to assign to them any specific character; but in the lungs at least, whether occurring in the form of granula- tions or of an infiltration, they are almost constantly attended by a fibro-nucleated growth of the alveolar wall, in which sometimes the fibrous and sometimes the nuclear element predominates. It would appear also by no means improbable, in the light of recent researches on the pro- duction of tuberculosis in the lower ani- mals,1 that various poisons, as well as simple irritants, may serve as the starting- points for tubercular changes in predis- posed individuals. I -would not, without much further personal experience than I possess on this subject, venture to affirm that syphilitic changes in the lung are identical with tubercle ; but it is impossi- ble to study the observations of those who 1 Addison regarded these as pneumonia, and Virchow also speaks of them as the re- sults of chronic pneumonia. For the reasons before given, I venture still to express an opinion respecting their tubercular nature. An appearance of this kind is described by Cornil as syphilitic (Bull. Soc. Anat. 1861). 2 Wagner relates a case of the same kind. Vidal (Traits des Mal. Ven.) describes in a syphilitic patient a condition of fibrous indu- ration surrounding the bronchi, and extend- ing into the pulmonary tissue. It was chiefly limited to the lower lobes. The condition of the bronchi is not mentioned. Vidal notices the resemblance of the tissue to that produced by a chronic periostitis. Proof of the syphi- litic nature of these is, however, wanting. Lancereaux (loc. cit. p. 424) considers that cicatricial contractions of the lung may also be due to this cause, but this must be re- garded at present as being simply hypotheti- cal. s Path. Soc. Trans, xvii. (Two plates of the appearances in the lungs and liver. VOL. II. -18 1 It is certainly a remarkable fact that in my experiments guinea-pigs inoculated with syphilitic virus were the only class that com- pletely escaped secondary tuberculization; but this, when the difference of species is considered, would be no argument against the possible effects of this virus in the human subject. See lecture by the author "On the Artificial Production of Tubercle." 274 BROWN INDURATION OF THE LUNG. have investigated both processes, and particularly the researches of Virchow, without being convinced of the close analogy between them ; and it would ap- pear to me that the conclusion that some of the changes thus described as syphilitic have a quasi-tubercular nature, is at least quite as likely to be correct as the con- verse, viz., that a large number of pro- cesses hitherto considered tubercular should be ascribed, when found in syphi- litic patients to the exclusively specific effect of this dyscrasia. The clinical history of these changes is as yet an almost untrodden ground. The majority of the reputed syphilitic affec- tions of the lungs have been observed in stillborn children, or when found in adults have only been accidentally discovered on post-mortem examination. Lancereaux cites a few instances where pulmonary symptoms had been present before death. In one of these, quoted from Vidal, and where the chief change was peribronchitic induration, there were the physical signs of consolidation at the bases, associated with slight haemoptysis, little cough, and no fever, but with a dyspnoea gradually increasing in intensity, and apparently proving, at last, one of the causes of death. The duration of the disease in this case, after pulmonary symptoms were first ob- served, extended over two years. In another case under Lancereaux's own observation, and where the presumed gummata had formed cavities surrounded by much induration, the affection was limited to one lung, and the physical signs were those of induration with exca- vation ; haemoptysis, however, occurred also in this instance, and the sputa, at first scanty, became subsequently copious and fetid ; oedema of the legs, and slight pyrexia were present, and the patient died cachectic. Lancereaux remarks that a unilateral affection of the lung, with signs of chronic induration or excavation, and in the pres- ence of a syphilitic history, may lead to the diagnosis of its specific origin, but it must be remembered that the syphilitic affection is not invariably confined to a single lung. In respect to treatment, Lancereaux cites several cases where a mercurial course has been followed by the cessation of phthisical symptoms, and by the im- provement in some instances of the phys- ical signs of the disease. I have more than once subjected phthisical patients with a history of syphilis, to treatment both by mercury and by iodide of potas- sium, but the results which I have hitherto obtained have been by no means favor- able. The treatment by iodide of potas- sium would appear to be the least dan- gerous, and the most deserving of a more extensive trial. BROWN INDURATION OF THE LUNG. By Wilson Fox, M.D., F.R.C.P. Synonyms.-Pigment Induration (Vir- chow) ; Brown Condensation (Zenker) ; Carnification Congestive (Isambert and Robin). History.-This state of the pulmonary tissue occupies a doubtful ground between the indurations which succeed to long- continued congestion and the process de- fined as chronic inflammation. Some of the difficulty of determining its exact nosological position depends on discrep- ancies in the statements made by differ- ent observers with respect to the exact changes which lungs to which this term has been applied have presented. It was described originally by Andral' under the title of Hypertrophy of the Lung, and as existing in cases of chronic catarrh. lie states that the change con- sists in an enlargement of the vesicles, together with thickening of their walls, and Rokitansky1 appears to have observed a very similar condition. It has also been noticed by Hope2 and Hasse3. Morbid Anatomy and Pathology. -The state to which the term Brown In- duration is applied is the result of long- continued congestion, most commonly 1 Path. Anat. 1861, iii. 46. A drawing ac- companies this description. 2 Morbid Anatomy. 3 Loc. cit. Hasse appears to have proposed the title of "Brown Induration," which seems, from its simplicity, to be the most eligible for this affection. 1 Prec. Path. Anat. ii. 516. MORBID ANATOMY AND PATHOLOGY. 275 arising either from marked incompetency or constriction of the mitral valve. Vir- chow,1 wrho first after Andral gave a min- utely detailed account of its appearances, also describes the lungs as enlarged, prominent, and not collapsing when the thorax is opened. They feel more com- pact than the normal lung, and they are also heavier and inelastic ; they crepitate but little, and have a peculiar tint of yel- low, shading into a brown or a reddish- brown. On section the tissue is dense and is speckled with red spots of variable size, shading into blacker tints, and be- tween these also the tissue has a more or less rusty appearance. A brownish fluid (brown cedema, Virchow) exudes on pres- sure. Virchow described the essential characteristic of this condition as depend- ing on the accumulation of hsematoidine in the epithelial cells of the air-vesicles, which are either natural or more or less enlarged, and also in granule cells, which probably result from the transformation of the former. The pigment is for the most part in the form of granules, insolu- ble in acetic acid, but which are destroyed by caustic alkalies and by sulphuric acid. Various transformations of the yellow pig- ment into black granules can be seen within the cells themselves, and later it is found free in the walls of the alveoli and in the interstitial tissue. Further ac- counts of this state have been given by Friedreich2 and by Buhl.3 The latter de- scribes and figures a series of varicose dilatations of the capillaries coexisting with the pigment in the walls of the alveoli. Friedreich's description of the filling of the aveoli with enlarged epithe- lial cells, and with the products of their proliferation, agrees very closely with Vir- chow's. The point on which most difference of opinion exists is that which refers to the thickening of the alveolar walls. Virchow does not describe this change, and Zenker4 says that he has not met with it. Roki- tansky, however, figures it, and Isambert and Robin,5 who, under the title of " Car- nification Congestive," have described a very similar condition, state that the walls of the alveoli and the interstitial tissue, in addition to containing a large quantity of pigment, are infiltrated with an amor- phous exudation matter. In the speci- mens which I have examined I have found such thickenings in considerable tracts, together with a distinct increase of fibrous tissue in the walls of the alveoli; but this change is not uniformly present, and in other places the alveoli are found filled with catarrhal cells, while their walls present no other change than that arising from the distension of the capillaries. I have also observed a considerable thicken- ing of the coats of the branches, both of the pulmonary artery and of the pulmo- nary vein; an appearance, however, which has not been described by some writers. The change in the lung has appeared to me to be referable to two stages. In the first there is intense congestion, some- times general, but more commonly found in limited parts, and in these congested parts a considerable amount of pigment may be seen in the pulmonary epithelium. Such parts float in water, and are more or less oedematous, yet crepitant, but com- paratively inelastic. Their tint is of a uniform reddish brown. In the later stages the pulmonary alveoli gradually become filled more or less completely with epithelial products resembling those of catarrhal pneumonia, and the tissue, to a great extent, loses its crepitant char- acter. In this stage also it is not so prominent, and closely resembles a con- gested and collapsed lung, except that the surface is finely granular, and is mottled with spots of yellowish pigment on the brown and indurated tissue. It has none of the friability of ordinary pneumonia, but is comparatively tough and inelastic. This latter change corresponds with the " carnification congestive" of Isambert and Robin, and the parts so affected sink in water, but not in all portions. The alveoli are loaded with epithelial cells and with granule cells containing an ex- cessive amount of hsematoidine. Isam- bert and Robin describe the pigment as sometimes existing in the crystalline form, and this, in the condition of melanine, can be seen in the walls of the alveoli and in the fibrous tissue surrounding the arte- ries and veins. The extent of lung thus implicated varies considerably. The change may exist only in patches, or it may extend to considerable tracts of tissue. I have seen it throughout the greater part of the lower lobe. Isambert and Robin have seen it affecting the whole of one and the greater part of the opposite lung. The appearances thus presented are quite different from those of hemorrhagic infarcta, though these are not unfrequently present in other parts of the lung. The parts affected want both the density and also the prominence of portions of lung into which hemorrhage has occurred, and the escape of the coloring matter of the 1 Archiv, i. 1847, p. 461 et seq. 2 Virchow, Arch. x. 201. Friedreich de- scribes corpora amylacea as existing in such lungs. I have also seen these under similar circumstances. 3 lb. xvi. 559. Drawings accompany this description. 4 Beitrage zur Normalen und Path. Anat, der Lungen. 5 M6m. Soc. Biol. 1855, 2e Ser. ii. p. 3 et seq. 276 BROWN INDURATION OF THE LUNG. blood appears to be due to mere capillary rupture, and not to any extensive extrav- asation. The nature of the change seems to depend on long-continued congestion gradually giving rise to a catarrhal pneu- monia of a chronic type, and the thicken- ing of the alveolar walls may probably occur in the later stages of the process- [Fig. 41. Pigmentation of the Lungs.-From a woman, set. sixty-flve, with slight emphysema. Showing the situa- tion of the pigment in the alveolar walls, and around the bloodvessel v. X 75. (Green.)] thus creating an analogy with some of the other forms previously described.1 Zenker states that this pneumonia may pass into true hepatization, though fibrinous exu- dations are commonly wanting. The pneumonia, however, may at times be mingled with so much extravasation as to give it a hemorrhagic character. The enlargements of the lung described by Virchow has not appeared to me to be essential to the process-at least such en- largement has not existed in two of the best marked instances of the disease which have come under my own observation. It would appear not improbable that, when such enlargement has existed, the lungs had been affected by emphysema during or prior to the other changes. Zenker states that an extreme degree of atrophous emphysema existed in some specimens which he examined. This change, according to Zenker, ap- pears to be more common before than after the age of forty. Symptoms.-Bamberger2 describes the earlier conditions of this state as associ- ated with diminished resonance on per- cussion, together with weakened respira- tory murmur; but these physical signs are common to many cases of pulmonary congestion from cardiac disease when the induration now described does not exist. Dyspnoea is commonly present, and cyanosis is observed in extreme cases; but neither these nor the rusty sputa often seen are necessary signs of the condition in question. Isambert and Robin describe dulness on percussion, together with bronchial breathing over the affected parts, and this also has existed in one case which I have observed. The temperature in both the best marked cases which have come under my observation has been elevated, but not exceeding 102° Fahr. In one case a fluctuating pyrexia, sometimes reaching 102°, and on other days not exceeding 99|° or 100°, continued during nearly a month-death finally taking place from gradually increasing asthenia and cyano- sis : the heart was much hypertrophied, adherent to the pericardium, and pre- sented extensive disease of the mitral valve. Another case was complicated by erysipelas of the leg passing into gangrene. It must therefore be regarded as doubtful whether the pyrexia depended on the pul- monary condition. Rusty and blood- stained sputa are common, but neither these nor any of the physical signs as yet observed afford any positive grounds for the diagnosis of this affection, though there might be strong reason to suspect its existence from the persistence of signs of consolidation during a long period, and associated with cyanosis and dyspnoea depending on marked disease of the mitral valve. 1 Grisolle, p. 71, describes two cases of chronic pneumonia associated with heart af- fection, but the appearances observed do not show positively that they belonged to this class. In one the condition was simply that of gray induration; in the other the tissue was of a reddish tint and finely granular, but in other parts it presented more the appear- ance of being of recent origin. 2 Lehrb. Krank. des Herzens, 204. The Treatment must be mainly di- rected to the cardiac conditions present. CIRRHOSIS OF THE LUNG : NATURE AND HISTORY. 277 The indications for the relief of pulmo- nary congestion, such as the application of revulsives and counter-irritants, and the internal administration of stimulants, are those which would appear to be the most suited to this state. (See Secondary Pneumonias, p. 235.) CIRRHOSIS OF THE LUNG.1 By H. Charlton Bastian, M.A., M.D., F.R.S. Nature and History.-This is a rare disease, mostly of a chronic type, in which the individual has suffered, perhaps for many years, from cough and muco- purulent expectoration, with or without usemoptysis ; in which the wasting is not very marked, whilst the constitutional symptoms of the ordinary form of phthisis are almost absent. There is usually marked dulness, accompanied by immo- bility and retraction, of one side of the chest, with or without cavernous sounds on auscultation ; whilst there is generally increased resonance, accompanied by pu- erile respiration on the opposite side. The heart is more or less displaced to- wards the affected side ; whilst there may be signs of dilatation and hypertrophy of its right cavities, associated with anasarca and ascites. After death the lung on the retracted side is found to have become shrivelled to one-half or even one-fourth cf its natural size-owing to its conversion into a tough fibrous material, with obliteration of its air-cells and usually more or less dilatation of its bronchi; whilst that on the opposite side is much enlarged, and presents no evidence of the existence of tubercle or chronic disease. This pathological condition was in- cidentally alluded to by Laennec2 as a variety of dilatation of the bronchial tubes, and was afterwards referred to by Dr. C. J. B. Williams, only a few weeks before the appearance in 1838 of a most interest- ing memoir on the subject by Sir Dominic Corrigan.3 In this memoir the disease was first really described, so far as the state of knowledge at the time allowed, and an entirely hew interpretation was given of its pathology. The above name was proposed, on account of the close re- semblance between the pathology of this affection and that of cirrhosis of the liver. And so far as it serves to indicate the pathological relationship between the two diseases it is a good one; though, if its derivation be considered, the word "Cir- rhosis" (from yellowish or tawny) is as inapplicable as it can well be to the lung affection about to be described.1 Whilst Laennec, in his admirable ac- count of dilatation of the bronchi-a mor- bid state which had never been previously described-looked upon the condensation of tissue around the dilated tubes as being invariably secondary to and .he effect of the dilatation, Corrigan, on the other hand, maintained that in a certain num- ber of cases, which he proposed to range under the name " Cirrhosis of the Lung," the fibroid metamorphosis and induration was the primary and essential anatomical lesion, and that the dilatation of the bronchi was only a secondary effect. Omitting for the present the consideration of the question as to whether Corrigan was correct in the explanation he offered of the mode of origin of the bronchiecta- sis, I may state that his main position appears to have been a correct one. It seems to be undoubtedly true that, in a certain number of cases in which dilated bronchi have been met with after death, an original fibroid conversion and shrink- ing of the lung-tissue has entailed this as a consequence: the bronchiectasis has been secondary, and not primary. Notwithstanding the enunciation of Corrigan's views, however, the French 1 The name " Cirrhosis" was, in fact, origi- nally given by Laennec to the now well-known liver disease, under the influence of a mis- conception as to its nature. He thought that it was due to the deposition within the organ of a peculiar morbid substance of a tawny or rust-brown color. These patches and islets, however, are now known to be only the natural acini of the liver, bile-stained and isolated by what is the real anatomical ele- ment of the disease-the new growth of fibre- tissue. 1 This article also includes some account of the pathology of Bronchiectasis (p. 826 et seq.). 2 Diseases of the Chest, translated by Forbes, 4th Ed. 1834, p. 107. 8 Dublin Medical Journal, 1838. 278 CIRRHOSIS OF THE LUNG. pathologists, with the exception of M. Jaccoud, adhere to Laennec's interpreta- tion of the sequence of these phenomena ; and Cirrhosis of the Lung is, moreover, scarcely considered to be entitled to rank as a distinct disease by many English and German pathologists. From facts subsequently to be men- tioned, it will be seen that Corrigan placed too much stress upon the dilatation of the bronchial tubes. This is not an essential element in the disease, but is, rather, a very frequent accompaniment. It will be observed that in several re- corded cases bronchiectasis was either ab- sent altogether or only very slightly marked. In these cases the fibroid infil- tration and shrinking of the lung, w hich are the essential characters of Cirrhosis, existed alone. Those who still doubt the propriety of regarding this as a disease with clinical characters of its own, distin- fjuishable from bronchiectasis, may per- laps be influenced by an attentive con- sideration of the following facts. From the analysis of 43 cases by M. Barth,1 and by Lebert2 of 24 cases of bronchiectasis, it appears that this affec- tion most notably increases in frequency with advancing age, and that by far the larger proportion of cases are met with in persons who are more than 60 years old. Thus in Lebert's 24 cases, it was met with four times before the 10th year, ten times from the 10th to the 55th year, and ten times from the 55th to the 85th year ; wdiilst, according to Barth it was met with as follows:- in the 30 instances of Cirrhosis the follow- ing ages were attained No. of Cases. 2 . . . . Age. Ito 15 th year 3 . . . . 15-20 t • 7 . . . . 20-30 u 9 . . . . 30-40 ll 2 . . . . 40-50 ll 3 . . . . 50-60 ll 4 . . . . 60-70 ll From these figures it appears that 19, or almost two-thirds of the total number of cases of Cirrhosis, occurred between the ages of 15 and 40; whilst of Barth's 43 cases of bronchiectasis, only 7, or less than one-sixth of the total number, were met with at the same ages. On the other hand, more than one-half the cases of bronchiectasis (26 : 43) were in individuals over 60 years of age; whilst rather less than one-seventh (4 : 30) of the cases of Cirrhosis were encountered after the same year. Even these facts alone tend strongly against the view that well-marked fibroid infiltration with shrinking of the lung is to be considered as a sort of sequence of dilated bronchi. Whilst, on the other hand, seeing that bronchiectasis is met with in such a large proportion of the cases of Cirrhosis of the Lung occur- ring at the ages above mentioned-when dilatation of the bronchial tubes is other- wise very rare-there are strong grounds for the opinion that such a condition of the lung is especially favorable to the pro- duction of more or less dilatation of the bronchi. Other striking differences, how- ever, exist between the two affections. Thus, well-marked Cirrhosis is almost invariably confined to one lung: not so with bronchiectasis. More or less haemop- tysis was present in more than one-half (17 : 30) of the cases of Cirrhosis, in only four of which was anything which could be called "tubercle" said to be present in one or other of the lungswhilst the same symptom was met with in less than one-sixth of Barth's cases of dilated bron- chi (7 : 43)-and of these no less than four were also suffering from phthisis. There are differences, moreover, as regards sex. According to Lebert,2 dilatation of the bronchi is as common in females as in males; whilst only one-fifth of the total number of cases of Cirrhosis have been observed in females. Though believing that in the majority of cases" condensation of the lung-tissue from fibroid metamorphosis precedes the dilatation of the bronchi with which it is so often associated, still it would appear quite obvious that in some other cases the order is just the reverse. What No. of Cases. Age. 2 . . . . . 1 to 20th year 3 . . . . . 20-30 " 3 . . . . . 30-40 " 4 . . . . . 40-50 " 5 . . . . . 50-60 " 7 . . . . . 60-70 " 19 . . . beyond the 70th year. But an analysis of 30 cases of Cirrhosis of the Lung, which I have collected, ap- pears to show a most striking difference as regards the prevailing age at which this lung affection is met with in the post- mortem room,3 and that at which dilata- tion of the bronchi is encountered. Thus, 1 Rech, sur la Dilatat. des Bronches, Mem. de la Soc. Med. d'Observat. de Paris, tome iii. (1856), p. 469. 2 Anat. Patholog. tome i. p. 620. 8 Although it is perfectly true that Barth's cases (with one exception) were collected at the general hospitals for adults, and also at the Salpetribre, and therefore may not at all fairly represent the frequency of the disease in childhood; still, that his figures do show the determining influence of age may be also seen from the fact that in the course of six years 25 examples were met with at the Sal- pStri^re, whilst only 18 were met with during 25 years at the general hospitals of Paris- 1 In only one of these four cases did the "tubercle" exist in the cirrhosed lung. 2 Barth does not give the proportion of males to females in his observations. NATURE AND HISTORY. 279 Laennec maintained to be the rule, does really obtain in some cases : the cirrhotic change is then secondary to the bronchi- ectasis. The two morbid conditions have undoubtedly most intimate relations with one another, and occasionally it may be difficult to pronounce which was the pri- mary lesion. There is no reason, of course, why the cirrhotic change should not invade a lung whose bronchi are di- lated, just as it invades one in which the bronchi are healthy. But in the cases where this has been the order of events, the amount of condensation and indura- tion of lung-tissue is far greater than what is often entailed by the mere dilata- tion of the bronchi. So that, although there may have been some amount of pre-existing bronchiectasis, Cirrhosis af- terwards becomes the predominant affec- tion. But there is another condition of the lung, known for the most part by the name "chronic pneumonia," under which are recorded cases that may better be re- garded as instances of Cirrhosis of the Lung. Much uncertainty and confusion have resulted from the use of the former term, on account of the shifting significa- tion which has been given to it by differ- ent writers. But the perusal of Charcot's memoir, "De la PneumonieChronique."1 and of the account given by Grisolle in the last edition of his work "De la Pneu- monie," cannot fail to convince the reader that, instead of referring to any condition of lung especially characterized by the impaction of the air-vesicles with a more or less solid accumulation of cells or cel- lular debris, these writers understand this name to imply a fibroid infiltration of more or less of the organ, and the grad- ual substitution of a tissue of this kind in the place of the proper substance of the lung. Pathological states of the lung very similar to, or even identical with, this, wrere originally described by Laennec2 as forms of infiltrated "tubercle," under the names of gray tubercular infiltration and jelly-like infiltration. The tubercular na- ture of these morbid states was after- wards denied by Chomel,3 who looked upon them as evidences of a non-specific chronic pneumonia-a view which has been more or less adopted since his time by succeeding pathologists. . Andral4 de- scribed a red, a yellow, a gray, and a me- lanic induration of the lung, which seems to represent only different stages and va- rieties of a fibroid infiltration of the organ, and correspond with what Hasse,1 Roki- tansky,2 Forster,3 and other German pa- thologists mean by interstitial pneumonia and lungen-induration. Lebert4 also de- scribed a hepatization induree, and a hep- atization jaune; whilst Cruveilhier,5 refer- ring to the later stages of the same pathological transformation, spoke of a phlegmasie induree and an induration mela- nique ardoisee, understanding that the es- sence of these conditions was a "meta- morphose fibreuse" of the proper lung- tissue. Addison6 also described two of the sequences of acute pneumonia under the names albuminoid induration and iron- gray induration. With regard to the sec- ond of these pathological states, this un- doubtedly corresponds with the fibroid induration of other writers, and a careful examination of Addison's plates, together with a comparison of the descriptions given of the two conditions, almost suf- fices to show that the first is but a rarer modification of the second pathological state-into which it often seems to pass by insensible gradations. Dr. Wilks7 also describes chronic pneumonia as a fibroid induration of the lung substance, due to an actual new growth of fibre-tissue which slowly increases in amount. Thus there seems to be a pretty general agreement between the writers I have named (some of the principal of those who have written upon the subject), con- cerning the essential nature of the con- dition which often goes by the name "chronic pneumonia." When affecting any considerable extent of the lung it has been generally recognized as a condition of great rarity. Charcot imagined that at the time he wrote there were only about ten or twelve cases on record, which could be indubitably regarded as exam- ples of this disease. Grisolle, also, had only met with six cases during his long experience. Both these writers believe that this state of the lung may be the al- most immediate sequence of an ordinary acute pneumonia, although they think that at other times it is chronic from the first, and commences in the most obscure and insidious manner. Both these writers also, as well as most of the others I have mentioned, are fully satisfied that the 1 Patholog. Anatomy (Syd. Soc. Transla- tion), 1846. 2 Man. of Path. Anat. vol. iv. (Syd. Soc. Translation), p. 60. 3 Lehrb. der Patholog. Anatom, p. 296. Jena, 1862. 4 Anat. Patholog. tome i. p. 648. 5 Ibid., livraison xxxii. p. 8; and Anat. Patholog. Gen^r. tome iii. p. 608. 6 Guy's Hosp. Reports, 1843, p. 365. 7 Leet, on Path. Anat. 1859, p. 236. 1 Paris : These, 1860. Containing copious references. 2 Diseases of Chest, translated by Forbes, 4th Edit. 1834, p. 256. 3 Art. " Pneumonie Chronique," Diet, in 25 vols., 1842. 4 Precis d'Anat. Patholog. tome iii. p. 517, and Clinique Medicale. 280 CIRRHOSIS OF THE LUNG. minute anatomical characters of this so- called chronic pneumonia are essentially similar to that of the ordinary indurated tissue surrounding vomicse or foreign bodies in the lungs. I need only add that the tissue-changes in these cases are es- sentially similar to those which Dr. Sutton has described as "fibroid degeneration of the lung," and that such a change, prevail- ing to a wide extent, is the anatomical characteristic of Cirrhosis of the Lung. It seems to me expedient to do away altogether with the name " chronic pneu- monia," as an appellation for the patho- logical changes in question. This seems desirable for the following reasons:-1. Any pathological state to which the term " chronic pneumonia" is applied ought to be characterized by anatomical characters similar in kind to those which are met with in the acute condition-conditions which are fulfilled by the " chronic lobu- lar pneumonias" of phthisical patients. 2. Admitting that the fibroid overgrowth and substitution, which has been hitherto styled "chronic pneumonia," is some- times the direct sequence of an acute pneumonia, still this secondary condition is not a modified persistence of the old state, but is due to the supervention of an entirely new and different process : in these cases, in fact, we have to do with a sequence to, rather than with a chronic persistence of, the original malady. 3. Although such a pathological state is oc- casionally the direct sequence of an acute inflammatory condition, still in the large majority of cases it seems to be due to an essentially chronic process-to one which is deficient in some of the most important characters of an inflammatory change, and which more closely resembles a mere infiltrating new growth. The term "interstitial pneumonia" seems to be almost as unsuitable as that of "chronic pneumonia," as an appella- tion for the fibroid indurations in ques- tion. Whether such changes are met with in the lung, in the liver, or in any other organ, their mode of initiation, progress, and minute anatomical charac- ters, seem to be essentially similar. They advance insidiously, in the great majority of cases, without affording the least clin- ical evidence that the patient is suffering from an inflammatory disease and when the organs in which such changes had been advancing are submitted to micro- scopical examination, there is a similar absence of the signs of an inflammatory process. A new growth is met with, sup- planting the proper anatomical elements of the part, and it seems to me to be no more suitable to speak of such a process as an inflammation than it would be to apply the same term to a slowly increas- ing but infiltrating cancerous growth. The more partial and local changes might simply be styled " fibroid indura- tions," reserving the term "Cirrhosis" for the more extensive and advanced change, when it affects either an entire lung or at least one lobe of the organ. From what has been said it will be seen how intimately related Cirrhosis of the Lung is, not only to bronchiectasis, but also to what has been hitherto called "chronic pneumonia." It will not be so much a matter of surprise, therefore, that some of the cases of which I have given an abstract in this paper, have been originally recorded under one or other of these names. No sharp lines of demarca- tion can exist between fibroid indurations of the lung ("chronic pneumonia" of other writers) and Cirrhosis, because they are merely different degrees of one and the same pathological condition. There- fore, one or two of the cases that I have included amongst the thirty instances of the disease on which this paper is based, may seem doubtfully entitled to the latter name; but I have placed them in this series precisely because they serve to in- dicate this relationship, and to show what are the early stages of the disease which we are now describing. Since diseases have no distinct and inde- pendent existence, but are merely groups of symptoms, or of pathological changes, which tend to repeat themselves with varying degrees of frequency, it is only to be expected that intermediate conditions should at times present themselves. Our nomenclature and classification of these sets of symptoms, or pathological changes, must inevitably be more definite and sharply defined than actual facts or occur- rences would warrant. We can but seize upon certain combinations of symptoms or changes which are apt to recur, and ticket them in their typical condition as so many " diseasesthough in doing this we should ever recollect that the symptoms or changes are not distinct and independent, but are variously related to, and miscible with other possible combina- tions. With the distinct understanding that the diseases enumerated in our nos- ologies vary immensely, not only in respect to the frequency, but also in respect to the definiteness of character, with which they tend to recur ; still, one must regard all such described diseases as little better 1 Dr. Wilks says (loc. cit. p. 237) : "For my own part I believe such a process is es- sentially chronic, and at no time, if an oppor- tunity had been given for examining such a lung, would it have presented any different appearances, except in amount; growing, in- deed, like a tumor, and, like it, having, no doubt, some elementary forms preceding the fibrous structure, but the mode of production and development so slow and continuous that no distinct stages or changes in the structure ean even be distinguished." PATHOLOGICAL anatomy. 281 than rallying points, round which special groups of symptoms or changes may be conveniently ranged. The disease which we are now consider- ing is comparatively rare, and it can only be arbitrarily marked off from the fibroid indurations of smaller extent, out of which it is developed. Still a certain set of symptoms do tend to recur in association with a certain set of advanced anatomical changes, and these have been ticketed as a disease which is distinguished by char- acters of its own, as much clinical as ana- tomical. On these grounds Cirrhosis of the Lung has the same right to be con- sidered as a distinct disease that many others possess whose claim to a place in our nosologies is unquestioned. This paper is essentially based upon an analysis of thirty recorded cases of the disease. One of these cases was originally re- ported by Sir Dominic Corrigan ; one has been taken from Dr. Sutton's paper; and two others are from M. Charcot's memoir, "De la Pneumonie Chronique." On the other hand, seven cases have been in- cluded which had been described under the head of Bronchiectasis.1 One of these was recorded by Laennec (though quoted by Corrigan as an instance of Cirrhosis); one wras observed by Dr. Stokes; one by Dr. Bright and Dr. Hughes ;2 two are from M. Barth's memoir ; whilst the last of the cases, previously recorded under the head of Bronchiectasis, has been taken from MM. Herard and Cornil's re- cent treatise.3 The remaining nineteen cases of which I have given abstracts were recognized as cases of Cirrhosis of the Lung, and sixteen have been pub- lished as such-fifteen in one or other of the periodical publications of Great Britain and Ireland, and one in Paris during the present year (1867)4 by M. Jac- coud. The other three cases have not been hitherto published : one occurred in the practice of Dr. Gull at Guy's Hos- pital, and one in that of Dr. Pollock at the Brompton Hospital, and to each of these gentlemen I have to express my best thanks for their kindness in placing reports at my disposal. To Dr. Wilks I am also much indebted for granting me access to, with permission to publish, the records of a case which formerly occurred in the practice of Dr. Addison at Guy's Hospital. In order to show the kind and range of variation met with in different cases, I have deemed it most advisable to give a tabular abstract of these eases, which it is hoped will be of use for future refer- ence. 1 Pathological Anatomy. - Adhe- sions of the pleural surfaces, serving to unite the affected lung to the parietes of the chest and to the diaphragm, have been met with in almost every case. They were reported as present in twenty-six out of the thirty cases ; only in one case were they stated not to exist, whilst in the remaining three the presence or ab- sence of adhesions was not noted. Of the twenty-six cases in which the adhesions are described as existing, they were some- what loose in five, but firm, tough, and often even cartilaginous in consistence in the twenty-two other cases. In nine of these the adhesions were more or less par- tial, whilst in thirteen, or nearly one-half of the total number, they were general, and the lung was at the same time usu- ally much reduced in size. Adhesions between the diseased lung and the peri- cardium were not uncommon, and in one case the posterior surface of the greatly enlarged opposite lung was also united to the diseased organ. Where the adhesions were well developed and general, it was frequently necessary to cut the tongue out of the corresponding side of the thorax ; and more or less extensive plates of firm fibro-cartilaginous looking material were found covering a certain portion of the surface of the organ, and gradually shad- ing away peripherally into an ordinary tough fibrous coating. This layer over certain parts of the lung, having a fibro- cartilaginous appearance, may be more than an inch in thickness-and then its inner strata evidently correspond in situ- ation to what had previously been proper lung-tissue. In only one case was any fluid found, and in this the pleura is stated to have been nearly one inch in thick- ness ; whilst in a cavity between the ad- hesions, which were only partial, there was contained nearly a quart of clear serum. The lung was, moreover, only as large as a man's fist; its tissue was remarkably hard, and its bronchi were not dilated. The size of the lung, in the more recent cases, has undergone no appreciable alter- ation ; in all the more chronic cases, how- 1 These are here recorded, because they not only serve to show the intimate and natural relationship existing between the two "diseases," but also because, owing to the extent and character of the morbid changes met with, they have almost an equal title to be ranked under either head. 2 See Guy's Hospital Museum, with descrip- tion in catalogue. 3 De la Phthisie Pulmonaire, Paris, 1867. 4 It seems only right to state that this pa- per has been written nearly three years and a half-ever since October, 1867. A few other cases have been recorded since this date. [' These tables, except those of the first five cases, have been omitted from this edi- tion ; their substance being fully conveyed in Dr. Bastian's article.-H.] 282 CIRRHOSIS OF THE LUNG. ever, it has exhibited a variable amount of shrinking. This is often very consid- erable : in one remarkable case it was scarcely the size of a man's hand, and there was no pleural effusion of any kind (to help to bring about the contraction), similar to what existed in the other case, in which the size of the lung was reduced to such an extreme degree. All interme- diate grades are to be met with between this amount of contraction and the nor- mal dimensions of the organ. On section, it is often seen that the lobes of the lung are firmly connected together by a dense flbro-cartilaginous material, similar to what more frequently occurs in connec- tion with the pleura on the surface of the lung. The tissue of the organ varies much in appearance in different cases, owing to the different degrees of progress which the disease may nave made; and also to the varying amount of black pig- ment present, and to the number and mode of distribution of dilated bronchi or ulcerated caverns throughout its sub- stance. Occasionally, islets of healthy lung-tissue are left here and there, in the midst of the fibroid induration. The dis- ease may affect only one lobe, the two lobes unequally, or the whole organ pretty uniformly. When existing in its early stages either generally or partially, the nature of the pathological change is even then most obvious to the naked eye. The texture of the lung being firm, tough, dense, and incapable of being broken down by the finger, one sees a smooth or only very slightly granular surface of a black- ish or iron-gray color, intersected in all directions by white bands of ligamentous- looking tissue, often forming a sort of tra- becular network, and dotted with white circles of varying sizes, produced by the cut walls of the thickened smaller bron- chial tubes. Very often, in its early stages, this invasion of fibre tissue is most distinctly seen to extend inwards from a greatly thickened pleura ; for continuous with it may be seen portions of lung tis- sue which have been completely converted into a fibro-cartilaginous looking mate- rial ; while this may pass, internally, into a simple ligamentous-looking tex- ture. Still further internally there is a trabecular structure, such as I have just described, the white bands of which be- come narrower and narrower, and may gradually fade away into almost unaltered lung-tissue. In other cases where the consolidation spreads from different cen- tres within, rather than from the surface of the organ, the fibroid thickening and white bands seem to radiate principally from the thickened walls of the bronchi. In its more advanced form, almost the whole organ, or large parts of it, grate under the knife when a section is made, cutting more like a tendon or mass of fibro-cartilage than anything approaching to normal lung-tissue, and whole tracts of it may in this later stage present the smooth yellowish-white appearance of cut tension, and be almost free from pigment. As the fibroid induration advances, air- cells and vessels become more and more obliterated; the lung-tissue gradually yields less and less fluid when squeezed, and becomes at the same time more in- compressible. In the great majority of instances, changes such as I have mentioned are those which are apparent from the very commencement of cases of Cirrhosis of the Lun". But on those rarer occasions when the cirrhotic process is the direct sequence of an acute pneumonia, the first process is one which has been termed induration rouge by Andral and other writers. We have an instance of this change in the case recorded by Dr. Sutton,1 when, on section, the upper lobe of the right lung was of a dark red color and the interlobu- lar- tissue appeared to have undergone an increase. Only a very small quantity of fluid appeared on the divided surface, and the tissue did not easily break down under the finger. The whole of the lower half of this lung was solid, firm, and somewhat tough. It had a reddish-gray color and offered some amount of resistance to the knife ; whilst it sank in water, and exuded scarcely any fluid on pressure. Here the lower lobe was evidently in a more ad- vanced stage of the disease than the up- per, and it seems to have been in much the same condition as the upper lobe of the left lung in the case of M. Legendre. A more advanced stage is recorded in the case of the child reported by Sir D. Cor- rigan, where the right lung was solid, non-crepitant, grayish-red, tough, and traversed in all directions by thickened white bands of fibro-cellular tissue- though there still seemed to have been no contraction of the affected organ. But in the case of the man observed by M. Charcot, who had suffered from an attack of acute pneumonia about four months be- fore his death, the disease seems to have made rapid strides, and presents us with a still more advanced phase. The whole right lung was pretty equally affected, 1 It seems to me most probable that this state of the lung was the sequence of an acute pneumonia. This must either have been the case, or else it must have been due to the supervention of an acute fibroid change without the existence of a previous pneumo- nia. Even if the latter alternative were true, the results would seem to be much the same in either case, since the condition of this lung appears to agree in all respects with Andral's description. PATHOLOGICAL ANATOMY. 283 and had undergone an evident diminution in volume.1 Its tissue was so dense that the finger could not penetrate it, and, on section, it resisted the scalpel like fibro- cartilage. The three lobes were seen to be firmly united, and the surface of the section was smooth, non-granular, grayish- blue marbled with black, whilst pale liga- mentous partitions of fibrous tissue sub- divided the lung in all directions, and formed a minute network. These are the stages by which the Cir- rhosis that supervenes as the sequence of an acute pneumonia appears gradually to approximate to the condition of the lung which is characteristic of the earlier stages of the more chronic process. In only one out of the thirty cases which I have tabulated is there any certain evi- dence of the existence of even a small quantity of " tubercle" in the cirrhosed lung. This was in the case of M. Jaccoud, ■when a very small quantity of crude and slightly softened2 ''tubercle" was found in the posterior part of the apex of the lung affected. In three other cases, how- ever, a small amount of "tubercle" was said to have been found in the non-cir- rhosed lung. But, although the existence of "tuber- cle" in cases of Cirrhosis seems to be a perfectly accidental occurrence, the same cannot be said with regard to the pres- ence of zdcerated caverns in the indurated lung-substance, since these have been met with in about one-fourth of the total num- ber of cases. Sometimes these caverns appeared to have been formed slowly, owing to the molecular disintegration of portions of the new tissue which had un- dergone a fatty metamorphosis, whilst at other times they have originated by a gangrenous process, as occurred in one of M. Charcot's cases. Here, one of the excavations had irregular walls, and seemed to have arisen by a gangrenous process about two months previous to the patient's death ; whilst another appeared to have been on the eve of forming, and was represented by a softened patch of yellowish tissue, with a disagreeable, though not gangrenous odor. In a case reported by Dr. Mayne, the patient died from the supervention of gangrene in the diseased lung, though there were no cav- erns. Towards the lower part of the con- solidated organ the tissue had the olive or purple tint of gangrene with a correspond- ing odor. In all the recorded cases, how- ever, in which caverns existed in the-lung, save tlie one previously mentioned, they seem to have been formed by the slower process of ulceration or molecular disinte- gration, since there was no preceding his- tory of gangrene. In two cases a recent coagulum of blood was found in the ulcer- ated cavity; in one the cavity was old and very large, being 4" in length by 2f" in breadth ; in two the cavities were single and small; in one there was ulceration of portions of the walls of two bronchial dilatations ; whilst in another case there was a small excavation of the size of a hazelnut, whose nature was doubtful. In only one of these cases were there several excavations existing in the same lung. In addition to these ulcerated cavities- having more or less ragged walls, and bounded by lung-tissue rather than by an altered mucous-membrane-there are usu- ally found other cavities- and enlarged canals resulting from dilatations of "the bronchi. These are not commonly met with in the early stages of the disease, such as have been hitherto spoken of un- der the name of "chronic pneumonia," and they are by no means always present, even when the disease is fully established and when great contraction of the lung has taken place. There was no dilatation of the bronchi at all in one-fifth of the thirty cases which I have collected, and. in four other cases it was present only to a very slight extent. In one-third of the cases, therefore, it has been either altogether absent, or else an insignificant feature of the disease. In the remaining two-thirds of the cases it existed to a variable extent. In one of the cases-that of a child-where the amount of dilatation was extreme, and in which, moreover, the fibroid change seems to have advanced upon, a lung whose bronchi were already dilated, it was a most typical instance of what has been called uniform dilatation. The bronchi wrere found to be healthy as far as their first division, but beyond this point, in- stead of diminishing at the successive bi- furcations, they preserved the same cali- bre as far as their termination-and in some places the diameter of a distal branch was even greater than that from which it proceeded. At their extremities there was a simple cul-de-sac, and no tend- ency towards the formation of an am- pulla. The mucous membrane was gray- ish-black,1 slightly villous, and evidently thickened. In two other cases recorded by Barth and occurring in adults, in which the amount of dilatation was extreme, it was of the mixed kind-consisting partly of cylindrical and partly of spheroidal di- latations. But in these two cases also it seems most probable, from a consideration 1 It was one-third smaller than the right lung, which was noted as being very large. The actual amount of contraction of the cir- rhosed lung, therefore, had not been very great. 2 Even this was, therefore, in all proba- bility, merely a cheesy patch of chronic lobu- lar pneumonia. 1 Most probably a post-mortem coloration. 284 CIRRHOSIS OF THE LUNG. of the histories of the patients, that dilata- tion of the bronchi had existed for many years before the fibroid change made any notable advance in the diseased organs.1 The mucous membrane lining the vari- ously dilated bronchi was in both cases smooth, dark red, and thickened. In only one other case was the amount of bronchial dilatation extreme. Here the lower lobe of the affected lung contained an extensive series of bronchial cavities between the size of a fowl's egg and that of a sparrow, some of which were partly filled by a semi- solid mucous secretion. In one case one of the cavities was as large as an apple, and in one two large cavities-each as large as an egg-were the only ones exist- ing. In other instances the dilatations were much smaller; thus in one case a vast number of little cavities existed, vary- ing in size between that of a pea and a marble, and all full of a muco-purulent secretion. In other cases caverns, vary- ing in number, and of all sizes between these extremes, were encountered. The more or less spheroidal cavities were al- most invariably associated, also, with cylindrical dilatations of the tubes ; and in some cases the rounded enlargements were decidedly more common towards the periphery of the organ. The condition of the membrane lining the dilated bronchi has only been specified in twelve cases : in seven of these it was dark red, con- gested and thickened (and in two of them even velvety or slightly villous), whilst in the five others it was rather a smooth, dull, or glistening membrane. In none of the cases is there any mention made of the slightly prominent transverse strife which are so often met with in dilated bronchi according to Barth, and which I have myself seen extremely well devel- oped in one instance, where the mucous membrane covering an enormous extent of dilated bronchi had quite a reticulated aspect, owing to the thickening of trans- verse and longitudinal fibres external to the mucous coat.2 The bronchial dilata- tions are occasionally empty, though they are generally found to contain a consider- able quantity of pus or muco-pus,-this being often thin, but at other times thick, tenacious, or even semi-solid in consist- ence, owing to partial inspissation. This fluid may be blood-stained, and it has often a peculiarly stale, disagreeable odor, amounting in some instances even to fetidity. In two cases there were emphysematous bullae observed on some parts of the sur- face of the diseased lung; in one they were situated on the upper lobe, and in the other, dilatations the size of a nut skirted the anterior border of the lower lobe. Modifications in the state of the pul- monary artery of the diseased lung have been noted in five cases. In one its branches were said to be simply dilated, whilst in another case, observed by Dr. Wilks, he thus describes its condition: " The pulmonary artery was very much diseased. It was, in the first place, con- siderably dilated, the branches through- out the tissue being much larger than natural. The coats of the vessel were also very much thickened, and the whole under surface was covered with athero- matous deposit. The vessel, in fact, very much resembled a diseased aorta. Some of the smaller branches were entirely ob- structed by ante-mortem coagula, as were also some of the pulmonary veins. In the main pulmonary vessel there was a layer of fibrine closely adherent to the wall, and with difficulty separable." Of the remaining three cases, in one the pulmonary artery was contracted to about the size of the coronary artery, whilst within it was a mass of fibrine which occupied the entire course of the artery even to its smaller branches, and at the same time was continuous with an ad- herent fibrinous mass in the right ven- tricle ; in another the pulmonary artery " seemed to be quite contracted and in the last the vessel is not stated to have undergone contraction, but to have been completely filled with firm laminated colorless fibrine which adhered to its walls. In four cases the bronchial glands were enlarged and had become more or less in- durated from a fibroid infiltration of their texture. In only four out of the thirty cases I have tabulated was there any fibroid in- duration of the opposite lung, and, except in one of these cases, it was very small in amount, forming only two or three patches. In almost every case the lung of the opposite side was enlarged, and sometimes to a very considerable extent, it being mostly soft and crepitant through- out, and occasionally emphysematous. In many cases it extended as far as and be- yond the opposite border of the sternum, 1 These cases, in fact, seem to me to belong just as much to the subject of " Bronchiecta- sis" under which they were described by Barth) as to that of "Cirrhosis." I have in- cluded them here simply because they serve to show the intimate and natural relationship that occasionally exists between the two dis- eases. 2 After describing the lining membrane as smooth or granular, generally of a dark-red color, and as almost invariably thickened, Barth adds: "Mais ce qui les distingue par- ticulierement, ce sont des especes de stries irrgguli&rement circulaires qui apparaissent plus ou moins distinctement sous la mem- brane interne, laquelle se continue manifeste- ment avec la membrane muqueuse des con- duits aeriens."-Loc. cit. p. 511. PATHOLOGY. 285 and in one case where its development was most extreme, it was just double its natural size, and seemed to fill almost the whole thoracic cavity.1 In three cases only, as previously stated, was any "tubercle" found in the non-cirrhosed lung, and in these it was small in quantity. In one there was a "tubercular" cavity in the apex, about the size of a walnut, filled with a coagulum of blood, death having been produced by a severe haemop- tysis ; in another " a few tubercles ex- isted," and in the third a few "gray granulations" were said to have been scattered throughout the lung. As a rule, the only morbid characters belonging to the enlarged lung were those character- istic of the acute bronchitis, complicated with more or less of recent pneumonia- conditions which had been the immediate cause of the patient's death. In nearly all the cases where the con- traction of the lung had been great there was a proportionate traction of the heart out of its normal position. Where the right lung was involved, the heart was frequently found behind the right mam- mary region, and its displacement seemed generally to be greater where this lung was affected than when the left organ was the seat of the disease. Cirrhosis of the left lung tends to raise the heart, and in one remarkable case reported by Dr. Law, it was found immediately under the left clavicle. In no less than ten out of the thirty cases there was more or less hyper- trophy with dilatation of the right cav- ities of the heart, and in seven of these more or less dropsy also existed; whilst in two cases only was the heart reported to be rather small. In one case it was fatty, and in two of those in which the right ventricle was hypertrophied the left was said to be small and weak. Pathology.-Various views have been entertained as to the pathology of this affection, to which we must allude before entering more fully into the relative im- portance of those having the most de- cided claim to recognition. (a) Laennec first attracted attention to the disease, and considered it to be one of the modes in which dilatation of the bronchi occurred. He believed that chronic catarrh, giving rise to an in- creased secretion from the bronchial tubes, caused an accumulation of mucus within them, which led to their dilatation. The dilated bronchi, by pressure upon the surrounding lung-tissue, then led to its collapse and condensation. (6) Dr. C. J. B. Williams' held that it was the sequence of a pleuro-pneumonia. His words were: "In pleuro-pneumonia the lung is inflamed, and at the same time compressed by an effusion in the sac of the pleura. If it remains long in this state, the smaller air-tubes and cells be- come obliterated by the adhesion of their sides, so that when the liquid is removed from the pleura they will not expand again with the enlargement of the chest; but the large and middle-sized bronchi are not obliterated ; they bear the whole force of the inspired air, and become con- sequently dilated by it. This kind of di- latation is usually conjoined with con- traction of the affected side. These cases, although not very uncommon, were first noted by the writer." And in a note to a subsequent work he said : " Dr. Corri- gan has since described cases which ap- pear to be similar, although he has given the disease the name Cirrhosis of the Lung." (c) Sir D. Corrigan maintained that the obliteration of the air-cells and con- densation of tissue were primary, and were owing to the growth throughout the organ of a fibre-tissue similar to that ex- isting in cirrhosis of the liver. The dila- tation of the bronchi was a secondary effect, due partly to the greater stress of the inspiratory force, and partly to the traction, in different directions, exercised upon the tubes by the contracting fibre- tissue. (d) By M. Grisolle, M. Charcot, and others, what may be considered the early stages of this disease have been supposed to be the results of a " chronic pneumo- nia," or inflammation of the lung-tissue. (e) Dr. Hughes Bennett seems to ignore Cirrhosis of the Lung as a substantive disease, and to maintain that all cases of so-called Cirrhosis are, in reality, in- stances of tubercular disease advancing towards a cure. Laennec's theory seems to be quite in- adequate to account for the production of such a disease as Cirrhosis. And with regard to the second theory-that of Dr. C. J. B. Williams-it cannot be con- sidered to apply to the class of cases to which Sir D. Corrigan gave the name Cirrhosis of the Lung. The mode of origin of these latter, as subsequent ex- amination has fully shown, is entirely dif- ferent ; the contraction of the lung being produced quite independently of the com- pressing effects of an effusion into the pleura. Although Dr. Hushes Bennett is quite right in the view that there are certain cases in which a cirrhotic process is asso- ciated with "tubercle" (chronic lobular pneumonia) in the same lung, and in the opinion that this combination may, very rarely, terminate in a result differing but slightly from what may be produced by 1 The Pathology and Diagnosis of Diseases of the Chest, 1840, p. 99: his first allusion to the affection being in "Lectures" published in the Med. Gaz. for 1838. 286 CIRRHOSIS OF THE LUNG. the pure cirrhosing process, still, what has been already said fully shows that in many cases Cirrhosis of the Lung is an independent affection, having no relation whatever to the presence of "tubercle" in the organ. The relations of Cirrhosis to the com- mon forms of Phthisis will be immedi- ately considered ; and also the anatomical affinities between the tissue-changes in this disease and those which characterize Tubercle. The real relationship existing between dilated bronchi and Cirrhosis, will also be carefully considered. These questions will be discussed under the fol- lowing heads : 1. The Relations existing between the Cirrhosing Process and Chronic Lobular Pneumonia. 2. The Anatomical Affinities between the Early Stages of Fibroid Indurations and Tuber- cle. 3. The Mode of Production of Dila- tation of the Bronchi, and their Relations to surrounding Induration of Tissue. 1. The Relations existing between the Cir- rhosing Process and Chronic Lobular Pneu- monia.-The evidence I have brought for- ward in the last section seems to show very conclusively that the cirrhosing pro- cess as it invades the lungs has no nece.s- sary connection with the development of "tubercle" in the same organ, whilst other considerations seem to show just as conclusively that its occurrence is not de- pendent upon the presence of a " tubercu- lar diathesis." In four only, out of the thirty cases of Cirrhosis, did any morbid product, which the observer was able to call " tubercle" exist in one or other of the lungs, in company with this fibroid conver- sion ; and even in these cases the amount of the product (which most pathologists now consider as the anatomical mark of "Chronic Lobular Pneumonias"1) was so slight as not to interfere with our belief that its presence was an accidental rather than a necessary element of the disease. There is nothing antagonistic between these two pathological changes,-far from it. There cannot be a doubt, however, that each may, and does, exist by itself2 as an independent affection, although they are so frequently combined in ordi- nary cases of phthisis-which differ from one another principally in respect to the relative proportion, and different modes of distribution, of these two tissue- changes. In proportion to the number of times in which the two processes are met with in combination, however, it may fairly enough be considered somewhat ex- ceptional for either of them to exist, to a fatal extent, alone. The facts at present known seem fully to establish the independent nature of the fibroid change met with in Cirrhosis. The word Phthisis is now generally ad- mitted to be merely a generic term, under which are included different morbid con- ditions of the lung, which may either ex- ist alone or in various degrees of combi- nation. Thus amongst other forms, there may be an almost pure pneumonic phthi- sis, due to the infarction of the air-cells and minute bronchi with epithelial pro- ducts, the whole mass of which rapidly degenerates, and may break down into ulcerous cavitiesor a pure tubercular phthisis,2 understanding by this a lung filled with products after the type of the gray granulation ; or a pure fibroid phthi- sis, such as exists in Cirrhosis of the Lung.3 On the other hand, any two of these changes, or even all three of them, may co-exist in various proportions in one or both lungs of the same individual, and thus give rise to the more common forms of phthisis.4 1 In these cases the amount of new fibre- tissue is reduced to a minimum. Some slight amount, however, always exists, even in sit- uations where there is no perceptible indura- tion. The very early stages of the fibre over- growth, when it is principally in a nuclear condition, do not produce indurations of the organs in which it occurs. 2 If indeed such an affection is entitled to be considered as a form of phthisis, since those suffering from it usually die before de- struction of lung ensues. 3 Here, again, I do not mean that abso- lutely no trace of chronic lobular pneumonia exists, but rather that, in the typical cases, this is reduced to a minimum. A microscopi- cal examination may often show a minute amount of such tissue-changes even where none is visible to the naked eye. It is almost impossible that any one portion of lung-tissue should overgrow to a considerable extent without entailing some amount of increase in contiguous tissue elements. In some cases, however, one kind of change almost wholly predominates. 1 Since this paper was written, Dr. Andrew Clark has proposed to range a certain num- ber of cases of lung disease under the term "Fibroid Phthisis" (see Trans, of Clinical Soc., vol. i. p. 174), with the understanding that they differ from what he terms "common cirrhosis." After a careful study of his very able report, I entirely fail to see any good reason for separating the case which he re- cords from those which are here ranged under 1 In only one of the cases is there any men- tion made of the existence of "gray granula- tions," and in this case their nature is more than doubtful, since no similar granulations were found in any other organ. 2 Occasionally, in some cases of "galloping phthisis," both lungs may at the autopsy be found thickly studded from base to apex with soft patches of " lobular pneumonia." These patches, of the size of a inustard-seed and upwards, are whitish or yellowish, breaking down here and there into minute cavities, whilst there may be a singular absence of all indurating tissue. PATHOLOGY. 287 When an extensive process of fibroid overgrowth is set up in a lung, around or intermixed with patches of lobular pneu- monia, this tissue-change may invade not only previously healthy portions of lung, but also those which are filled with the old pneumonic accumulations, so that, at a later stage, portions of tissue previously widely dissimilar, may become almost in- distinguishable from one another.1 And in this sense, so far as the two processes are associated in the same lung, we may agree with Sir D. Corrigan,2 and with Dr. Hughes Bennett, when they maintain that the process of Cirrhosis has a cura- tive agency in many cases of phthisis. 2. The Anatomical Affinities between the Early Stages of Fibroid Indurations and Tubercle.-The process of fibroid substitu- tion characterizing Cirrhosis of the Lung advances by two or more successive histo- logical stages. This seems to hold good of fibroid substitution, in whatever organ it may occur-whether arising in the brain or spinal cord, in the kidney, in the liver, or in the lung. In all these situa- tions it appears to commence by an exces- sive growth and the multiplication of nuclei in the part affected. These nuclei3 are not necessarily fusiform, but are far more frequently round or oval, about in diameter, containing no distinct nucleolus, but only a few granules. They are interspersed with a few fine fibres so as to form a fibro-nuclear stroma. These are the anatomical characters of the first stage of fibroid substitution, and though, even at this early stage, the nuclear tissue may have supplanted the proper elements of the organ in some parts, this as a whole is not found to have undergone any con- traction or diminution in bulk.4 But gradually the nuclei disappear, and where the change is older, actual fibre tissue be- comes more and more apparent. As this is developed contraction in bulk com- mences, and induration of the organ be- comes more and more distinct. In the lungs this nuclear overgrowth seems to commence either in the connective tissue which enters into the formation of the walls of the bronchi and of the bloodves- sels, in that lying between the larger and smaller lobules of the lung, or in that on the inner surface of the pleura. Or, on the other hand, it seems quite possible that the new growth may originate in a hyperplasia of certain masses of adenoid or lymphatic tissue in these situations, which, from the researches of Dr. Sander- son1 would seem to be widely distributed throughout the healthy organ. From any, or all of these situations, the nuclear and fibrous growth spreads in various directions -gradually obliterating the air- cells, the bloodvessels, and the proper tis- sue of the organ, and substituting itself in their place. This is what occurs when fibroid indurations alone advance in a chronic manner, and, as I have already stated, the tissue changes are identically the same when induration is gradually set up round a cavern existing in a phthi- sical lung. Now, as I have also pre- viously stated, this induration was origin- ally described by Laennec as due to what he called " gray tubercular infiltration," though Chomel and succeeding patholo- 1 See "Eleventh. Report of the Medical Offi- cer of the Privy Council," 1868. The too extensive use of the terms "adenoid" or "lymphatic" tissue, seems tome undesirable. Even if it be true that in all or some cases the morbid tissues of which, we are speaking take their origin as hyperplasias of real though microscopic nodules of lymphatic tis- sue, still, in a very large number of cases, the new tissue soon loses these characters al- together, and becomes an unmistakable fibroid growth. What was "adenoid" or "lym- phatic" tissue, thus gives place in a short time to a simple fibroid tissue, to which the former names are no longer applicable. There is, however, another inconvenience of even graver import. New views are being ad- vanced concerning tubercle, of such a kind that, after a time, those who consistently adopt them will be compelled to look upon all chronic indurations as "tubercular." Cir- rhosis of the liver will, in fact, become a tu- bercular affection. This result can only be avoided by the recognition of the non-specific nature of the new growths which may be artificially induced in the rodent animals. If we cease to call this new growth Tubercle, science will have lost nothing; if we persist, another almost hopeless confusion will be in- troduced into pathology. (See a paper by Dr. Sanderson, entitled, "Recent Researches on Tuberculosis," in Edin. Med. Journ. 1869, p. 387.) the head of Cirrhosis of the Lung. It seems to have been an instance of Cirrhosis in which cheesy patches of lobular pneumonia existed in rather larger quantity than in any of those which I have brought together. What more likely, however, to occur in some cases than such a combination ? Its association with a distinct constitutional tendency I cannot help considering to be more than doubtful. (See p. 294.) 1 This subject will be again alluded to in the section on Etiology. • Dub. Hosp. Gaz., Dec. 15, 1857. 3 In later stages, when some of them undergo a fatty change,the nuclei become enlarged, and assume the form of cells resembling "granu- lation corpuscles." 4 I have examined a kidney which pre- sented an excellent example of this first stage of Cirrhosis. The organ was of its natural size, only pale, with an extremely adherent capsule, and a very tough, leathery consist- ence. When examined microscopically, it was found to be more or less pervaded throughout with a nuclear overgrowth, such as I have described, though in some parts this was replaced by a more decided fibre-issue. 288 CIRRHOSIS OF THE LUNG. gists denied its tubercular nature, and considered it to be a non-specific result of chronic inflammation. From a histological point of view', how- ever, there is now much more to be said in support of this nomenclature than was admitted by many of Laennec's succes- sors ; though their inability to perceive the relationship is not to be wondered at, seeing that though this has only come out strongly since the date of the renunciation of many of Laennec's views as to the con- stitution and nature of "tubercle," and since pathologists have begun to recognize the fact that, if the word "tubercle" is to be preserved 1 at all, the gray granulations of Acute Tuberculosis must be considered as its type. This alone of all the morbid products which have been so named has a definite constitution in whatever organ of the body it may be encountered ; whilst the so-called "crude tubercle," and cheesy products generally, may have had the most diverse origin in different cases, and are always nothing but the dead and im- pacted remains of various secretions and tissues. An examination of very thin transverse sections of gray granulations in the lungs, brain, liver, kidneys, and other organs, suffices to convince one that its structure-closely allied to that of lym- phatic tissue-is always that of a small fibro-nuclear tumor infiltrating and sup- planting the normal tissues of the part in which it is found. But, further, it seems to me that the structure of tubercle is almost indistinguishable from that of the tissue existing in the first stage of that state which I have just been describing- hitherto known by the various names of " gray tubercular infiltration," "chronic pneumonia," or "fibroid degeneration." There are in each case the same round and oval nuclei or embryo-cells, imbedded in a fine and somewhat scanty fibrous stroma. This resemblance only exists, however, between one temporary stage of the process of fibroid substitution, and the gray granulation.2 Tubercle seems to be the mark or index of a general consti- tutional disease, and how long the gray granulation may remain as such, or what may be the degree of frequency with which it undergoes changes, are questions to which we are unable to give very satis- factory answers. Although fibroid in- duration may, on the other hand, owe its origin partly to a constitutional cause, it seems much more dependent upon special local conditions operating in the organ or part in which it is set up ; then again, it exists not only in minute patches, but spreads over considerable areas, and ad- vances through stages of development which are well known and pretty con- stant.1 Where the process of fibroid substitu- tion is advancing in a lung, there appears to be not only an increased growth of the connective tissue and lymphatic elements, but also a rapid formation of epithelial products, as evinced by the number of cast-off and fattily degenerated cells of this kind which are seen within the air- vesicles. These are always to be seen in places where the fibro-nuclear growth has not completely invaded the tissue, though after a time they appear to be stifled, and stamped out as it were, by the superior energy in growth of the advancing fibre- tissue. This, in fact, appears to be the rule in pathological conditions of the lung, that a morbid change is rarely or sont ni un tissu accidentel sui generis, comme il le pensait, ni le premier d^gre du tubercle comme Font admis MM. Laennec et Louis, mais qn'elles consistent dans 1'induration de quelques v^sicules Or, ce qui arrive & un lobe dans sa totality peut aussi arriver a quelques v£sicules ; la lesion est seulement moins 6tendue; mais du reste, sa nature est la meme." * It seems the so-called "artificial tuber- cle" in the rodent animals whose anatomical characters have now been fully revealed by the admirable researches of Dr. Sanderson, Dr. Wilson Fox, and others, is less allied to tubercle (as occurring in acute tuberculosis) than to some more local manifestation, such as that which characterizes "tubercular peri- tonitis." All these morbid products are, however, as I think, more akin to those of acute cirrhosis. In acute tuberculosis, as it occurs in the human subject, the gray granu- lations appear to develop almost if not quite simultaneously in meninges, lungs, liver, &c. In acute cirrhosis in the human subject there is often a slight tendency to extension of the process to other organs, and this tendency becomes more marked and constant in the rodent animals, though the spread to other organs is distinctly successive, and seems to take place by actual local contaminations. The frequency of cheesy degenerations in the infiltrating patches of "artificial tubercle" is probably referable in the main to their rapid growth, and the instability of tissue elements which this usually entails. 1 For my own part, I think that pathologi- cal science would gain much if this word, and all the erroneous associations, as to specificity, which its use seems inevitably to entail, could be entirely forgotten, save as errors of the past. Old things might receive new names, and thus, at last, old theories might possibly be shelved. 2 It is interesting to find that, nearly forty years ago, Andral seems to have anticipated, in a measure, the results of recent microsco- pical research, since he fully recognized that the gray granulation was quite distinct from other kinds of what was then called " tuber- cle," and was closely allied rather to the forms of pulmonary induration which we now know to be of fibroid origin. His words were (Precis d'Anat. Patholog. 1829, t. ii. p. 518): ' ' Les granulations pulmonaires de Bayle ne PATHOLOGY. 289 never absolutely restricted to one tissue. The change originates and is predomi- nant in one, whilst it extends to and may be only more or less slightly developed in the other. The nutrition of the organ, or of parts of it, may be generally deranged, but the stress of the disorder falls in one case principally upon the vascular prov- ince of the pulmonary artery, and in an- other upon that of the bronchial arteries: thus a bronchial or a catarrhal pneumonia may be associated with a certain amount of fibroid induration, and an advancing fibroid change is often mixed up with an increased growth and shedding of epithe- lial elements from the mucous membrane. Such being the anatomical nature and mutual relations of these various tissue changes, in what light should we regard the one with which we are now concerned -that which has been spoken of succes- sively under the names of gray tubercu- lar infiltration, chronic pneumonia, and fibroid induration or degeneration ? That it is tubercular, or in any way an essen- tial appanage of the tubercular diathesis, may, I think, at once be dismissed from consideration, as there is no evidence to support this view.1 Is it then an inflam- matory change, or one partaking rather of the nature of a degeneration ? To Dr. Handheld Jones the merit is due of hav- ing first fully pointed out1 the essential similarity of these indurating processes in various organs of the body (all of which had been previously spoken of as effects of "chronic inflammation"), of having shown that in all alike the essential na- ture of the change is an hyperplasia or overgrowth of the connective tissue of the part, and for ably insisting that the process by which this was brought about was one totally distinct from what is ordi- narily understood by the word inflamma- tion. He held that they were effected, in fact, by a process substantially different -by one which was slow and chronic from the first, and which partook rather of the nature of the process by which an infil- trating new growth spreads.2 It seems to me, also, that the word inflammation is quite inapplicable tc the changes by which these effects are brought about. In inflammation we almost invariably find an accelerated formative process resulting in the production of elements of an unsta- ble composition; such as quickly degene- rate and decay-a process of necrobiosis or destruction in fact goes on simultane- ously with one of formative increase- whilst in the process which results in the production of fibroid indurations, there is principally an increased formative stimu- lus by which an overgrowth of connective tissue or lymphatic elements takes place. The necrobiotic process, however, is al- most entirely wanting, since the new- formed elements persist as a developing fibroid growth. Thus, whilst the change differs materially from inflammation, so also does it differ from a degeneration. The proper tissues of the part are not merely degenerated and structurally spoiled, they are actually killed, and disappear before a new fibro-nucicar tissue which supplants them. So that we have the increased formative energy of an inflammatory process without its un- stable products; and we have the func- tional degradation characteristic of a de- generation-though this results not from mere spoiling of texture, but rather from the complete substitution of a tissue of a lower grade in the place of that which is proper to the part. Surely in this fibroid hyperplasia, or fibroid substitution^ as I think we should term it, we have a pro- cess strictly intermediate in kind between inflammation on the one hand, and de- 1 When the above passage was written, I could speak thus confidently ; now, however, since the experimental researches of Dr. Wil- son Fox, Dr. Sanderson, and others, upon the "Artificial Production of Tubercle," patho- logical doctrines show signs of undergoing some modification. In the article before re- ferred to, in the Edin. Med. Journ. 1869, Dr. Sanderson's view is most clearly stated. It comes out in this form : "Tubercles are ade- noid bodies enlarged: . . . the disease progresses, not by continuous growth, but by .the distribution or dispersion of infective ma- terial from one point." For the development of "consumption" in man, three things are necessary: 1. A constitutional tendency; 2. A local irritation ; and 3. A process of infec- tion. Referring to the latter, Dr. Sanderson says: "The word designates the fact that wherever a chronic induration, due to over- crowded corpusculation, exists in any organ, it is apt to give rise to similar processes else- where." Dr. Sanderson would apply these views even to the mode of extension of " the so-called infiltrated forms of induration" met with in ordinary cases of phthisis; and he would, of course, be compelled to apply it to in- filtrating indurations (of cirrhosis processes) generally, because they are almost always characterized by an "overcrowded corpuscu- lation" in the part. Thus the present ten- dency, with some pathologists, is to consider that all infiltrating fibroid indurations may increase by a process of infection, and the logical outcome of their doctrines is the belief that such indurations are tubercular in na- ture. The chronic inflammations of many writers would thus be transmuted into "tu- bercular" affections, and the simple nuclear hyperplasia which characterize them in their early stages would be even more likely to be considered as a new "specific product," if it is to receive the name of " adenoid" tissue. 1 Brit, and For. Rev. 1854. This, as we have seen, is also the opinion which was sub- sequently expressed by Dr. Wilks. 2 Loc. cit. p. 345. VOL. IL-19 290 CIRRHOSIS OF THE LUNG. generation on the other-it is a sort of neutral ground from which the other two processes may be considered as diver- gences in opposite directions.1 3. The Mode of Production of Dilatation of the Bronchi, and their Delations to sur- rounding Indurations if Tissue.-The opin- ions expressed as to the mechanism of dilatation of the bronchi have been most various since the subject was first intro- duced by Laennec. His theory was, that bronchial dilatation was one of the effects of chronic bronchial catarrh-that it was brought about by the accumulation and stagnation of mucus in the inflamed tubes, and that the dilatations, by the pressure they exercised, led to the col- lapse and consolidation of the surround- ing lung tissue. Andral's views2 were also somewhat unsatisfactory. He recog- nized three forms of dilatation : one spe- cies, with thin walls, he believed was pro- duced after the manner stated by Lacnnec, whilst two others he attributes to hyper- trophy of the bronchial walls, though he does not explain how the modification in texture is to bring about the alteration in calibre of the tubes. Dr. Stokes3 believed bronchitis to be in all cases the primary cause of the dilatations, inasmuch as this leads to loss of elasticity in the longitudi- nal contractile fibres of the bronchi, and also to paralysis of the circular muscular fibres. He thought also that the epithe- lial ciliary action ceased, and thus per- mitted the accumulation of mucus, which (in conjunction with the other causes mentioned) tended to bring about a dila- tation of the tubes, under the straining influence of forced inspirations, during repeated attacks of coughing. Dr. C. J. B. Williams4 also laid great stress upon the influence of inflammation in bringing about alterations in the texture of the tubes, by which their elasticity and power of resistance was impaired-so that they more easily yielded to pressure during the act of coughing. This was his theory as to the mode of production of the ordinary forms of bronchial dilatation-those which exist without great induration of the sur- rounding lung texture. Where extreme induration was also present, however, he gave the explanation which has been quoted at the commencement of this sec- tion. (See p. 285.) Very shortly afterwards Sir D. Corri- gan1 published his explanation of the pro- duction of bronchial dilatation, as met with in the class of cases to which he gave the name of Cirrhosis of the Lung. This must be given in his own words, lie says: "The dilatation of the bron- chial tubes is partly owing to the con- tractile process going on in the tissue of the lung-partly to the expansive action of the parictes of the chest in the act of inspiration. ... If there were but one bronchial tube with contracting fibro- cellular tissue placed around it, then the contracting tissue would, as in the in- stance of stricture of the oesophagus or rectum, cause narrowing of the tube ; but when there is, as in the lung, a number of bronchial tubes, and the contracting tissue not placed around the tubes, but occupy- ing the intervals between the tubes, then the slow contraction of this tissue will tend to draw the parietcs of one tube to- wards the parictes of another, and neces- sarily will dilate them." He also says: " In proportion as the contraction of the fibro-cellular tissue obliterates the small air-vesicles, and as these contracting fibres, like so many strings, extending from the root in all directions, tend to contract or draw in the tissue of the lung, obliterating its small air-tubes and its bloodvessels, the larger bronchial tubes dilate to supply the place thus left, until, when the disease has reached its last stage, the tissue of the lung, diminished to a very small size, presents no longer any permeable air-vesicles, but a dense fibro-cellular or fibro-cartilaginous tissue with its fibres radiating in every direction, through the second and third sized bron- chial tubes dilated into cells, or ending in culs de sac, of every variety of size." Rokitansky2 adopted Dr. Stokes's view as to the mode of production of the un- complicated form of bronchial dilatation : he believes it to be a result of obstructive bronchitis in the ramifications of the bronchi beyond those which become di- lated. "It is produced," he says, "by the hindrance which is presented to the free ingress of the inspired air, and is pro- portional to the difficulty of breathing and the prolonged length of each indi- vidual inspiration, and is especially de- veloped in and about the perfectly im- permeable bronchial tubes. The paren- chyma surrounding this portion of the bronchial system collapses, and this pro- duces a space which becomes filled by the dilating bronchus. The dilatation thus lies entirely, or for the most part, in a collapsed, and apparently compressed, portion of the parenchyma; hence the latter appears to be the primary anomaly, 1 The phrase "fibroid substitution" will not be applicable to all instances of the kind of change alluded to, since, where it occurs in some of the fibrous membranes, such as the arachnoid, there is no substitution, but only an increase or hyperplasia of the part. 2 Precis d'Anat. Patholog. tome ii. p. 496. 8 Diagnosis and Treatment of Diseases of Chest. Dublin, 1837. 4 Pathol, and Diagn. of Diseases of the Chest, 1840, p. 96. 1 Loc. cit. p. 270. 8 Pathol. Anat. (Syd. Soc. Trans.). PATHOLOGY. 291 and the bronchial dilatation merely a resulting and consecutive morbid change." The opinions expressed by Dr. Gairdner1 were very different, and are as follows : "The conclusion to which I have been led by this survey is, that almost all the so-called bronchial dilatations, and all those presenting the abrupt sacculated character here referred to are in fact the result of ulcerative excavations of the lung communicating with the bronchi." He then adds: " The usual origin of bronchial dilatations is in cavities formed in atrophied lungs, in consequence of bronchitis or tubercle, and afterwards ex- panded beyond their original dimensions by the inspiratory force." Dr. Peacock2 thinks Sir D.* Corrigan's views unsatisfac- tory, but he says, in reference to the views of Dr. Williams and Dr. Gairdner: "I believe both to be correct in some cases, and that by one or other of the modes mentioned by these writers all the various forms of so-called dilatation of the bron- chial tubes which are observed may be explained." M. Barth3 believes to a cer- tain extent in the views advanced by Stokes, and also partly in those of Corri- gan-to the effect that condensation of tissues usually precedes the bronchiectasis. He also attributes an influence to firm pleuritic adhesions when combined with a shrinking of lung-tissue, and to the pres- sure exercised by retained and heated air which has been forcibly drawn, through accumulated mucus, into certain bronchi. Lebert4 agrees, in the main, with Stokes, though he thinks the weakness of the bronchial walls is ultimately dependent rather upon a disturbance in their in- nervation than upon an inflammatory state. Quite recently Dr. Grainger Stew- art5 has objected to the theory of Stokes, urging that if bronchiectasis depended simply on bronchitis, it would necessarily be much more frequent than it is. He thinks that Lebert's doctrine is the only one which is not opposed to known facts, and draws the following conclusions from his own observations: "1. That the essential element of bronchiectasis is atrophy of the bronchial wall, that the cause of such atrophy is not yet ascer- tained, but may perhaps be connected with constitutional peculiarities. 2. That the walls being so thinned and weakened, readily yield to the pressure of air, it may be in deep and sudden inspirations or during violent muscular exertions, cer- tainly in the sudden expiratory effort made while the glottis is closed in the act of coughing. 3. The enfeebled and dilated condition of the bronchi favors the accu- mulation of the mucus secreted by the bronchial membrane. 4. That the mucus accumulating and undergoing decomposi- tion in the dilatations, irritates the mucous membrane, leads to inflammation, and the formation of villous processes from it, to the formation of increased connective tissue in the walls, to irritation of the cartilages, and frequently to consolidation of the surrounding lung-tissue and pleu- ritic adhesions, sometimes also to abscess or to limited gangrene." With regard to the primary atrophic change which takes place in the walls of the bronchi, Dr. Stewart says that this is obvious even in the slighter dilatations, in which the mucous membrane is as yet unaffected, and that the atrophy shows itself in the muscular and elastic fibres, which appear granular and indistinct. Such are the various opinions that have been expressed concerning the mechanism of bronchiectasis, and the relations of this pathological condition to surrounding in- duration of lung-tissue ; and one cannot help being struck with the very opposite views which certain of the writers take as to the interdependence of these two states. This very diversity of opinion, however, seems to indicate that condensa- tion or induration of lung-tissue cannot in all cases be considered as a necessary prelude of bronchiectasis. Those who have formed this opinion must have arrived at their conclusion from an ex- amination of a limited class of cases, since it is a well-known and admitted fact to those who have studied the subject more widely, that in certain cases dilata- tion of the bronchi exists with scarcely any appreciable alteration of the sur- rounding lung-tissue. But whilst in some cases it seems certain that adjacent indu- ration either does not exist, or is present to such a limited extent as to be alto- gether unimportant in an etiological point of view (even if, in these cases, it has not been mechanically produced by the very dilatation with which it coexists), it seems also just as evident that, in a certain class of cases, the bronchial dilatation is to be looked upon as a secondary consequence of induration and contraction of lung- tissue. What the precise means are by which the dilatation is brought about in these cases, we shall consider presently ; but that the existence of a disease of the lung-tissue, which entails contraction, is favorable to the occurrence of bronchial dilatation, may be seen, I think, from the facts before mentioned, - to the effect that nineteen or nearly two-thirds of the thirty cases of Cirrhosis I have analyzed, occurred in individuals between the ages of fifteen and forty years, and that, out of these nineteen cases, eleven presented 1 Monthly Journal of Medicine, vol. xiii. 1851, pp. 248 , 249. 2 Ibid., April, 1855, p. 285. 3 Loc. cit. p. 517. 4 Anat. Patholog. tome i. p. 620. • Edinburgh Monthly Journal, 1866. 292 CIRRHOSIS OF THE LUNG. well-marked dilatation of the bronchi; whilst in forty-three cases of dilatation of the bronchi collected by Barth, only seven --or less than one-sixth of the total num- ber-were met with between these ages, though more than one-half (26:43) were in individuals over sixty years of age. The occurrence of Cirrhosis of the Lung, therefore, seems to be favorable to the production of bronchiectasis at such ages when dilatation of the bronchi alone, or as a primary phenomenon, is not prone to occur. With reference to the occurrence of bronchiectasis in lungs which are not contracted, and have no consolidation of tissue in them, it seems to me that if a primary atrophy of the bronchial walls exists like that which Dr. Grainger Stew- art has observed, the order or succession of the phenomena would probably be such as he describes. This mode of origin, also, seems to ke the only one capable of accounting for such cases of bronchiec- tasis as have been met with unexpectedly, in individuals who have not had any long-continued cough or bronchitis: it may, moreover, obtain in the first in- stance, and be the determining cause of the dilatation in a certain number of those persons who have previously suffered from bronchitis. By reference to such a mode of origin only, docs it seem possible to explain some of the anatomical characters of dilated bronchi, such as the occurrence of bridge-like portions of prominent and unatrophied tissue, and the occasional communication between the dilated por- tions of contiguous tubes. But it seems equally plain that it is not necessary for us, in all cases, to assume the existence of such an atrophy, when we recollect in what a large proportion of cases the indi- viduals in whom bronchiectasis has been met with have suffered from chronic bron- chitis and long-continued cough. To ex- plain the occurrence of dilated bronchi in many of these cases, we have only to refer to the view's of Dr. Williams and Dr. Stokes, before alluded to; and I would also add, that one important kind of al- teration in the walls of the bronchi, in- duced by chronic inflammation, is the production of a certain amount of fibroid substitution. Then, as in most of the cases of dilatation of portions of the vas- cular system, more or less of the muscu- lar and clastic tissue of the tubes is re- placed by ordinary distensible, though comparatively unclastic, fibrous tissue.1 A tube thus altered, having once yielded under a powerful inspiratory effort,-or more especially under the powerful ex- piratory effort, with closed glottis, pre- ceding the act of coughing, - does not regain its normal calibre, and each incre- ment of dilatation successively brought about remains as a persistent abnormal- ity. In those instances of what may be called acute dilatation of the bronchi, met with after attacks of hooping-cough, the inflammatory changes in the walls of the tubes, combined with the powerful in- spiratory and expiratory efforts, seem to be the conditions which are most instru- mental in bringing about this effect. Then again, the modes of origin suggested by Dr. Gairdner must not be forgotten. There seems every reason to believe that many of the abruptly sacculated cavities which have been described as bronchial dilatations, have really had an ulcerative origin, though their walls may have be- come perfectly smooth. Cavities thus formed may subsequently be increased in volume by the same means as those which usually suffice to augment the size of the more simple bronchial sacculi. Although in a certain number of cases little or no alteration of the lung-tissue around the dilatations exists, in many others more or less condensation is met with. This is oftentimes merely a col- lapse of the adjacent textures, brought about by the pressure of the dilating bron- chus ; whilst, in other instances, there is an actual induration of tissue, which mu: t be regarded as a consequence of the pri- marily existing bronchial dilatation. Dr. Grainger Stewart has suggested what may be considered to be a real and feasi- ble explanation of this secondary indura- tion in his fourth conclusion, where he says that influences which suffice to irri- tate the bronchial wall must, if continu- ously or intensely applied, affect the structures lying beyond them. In one case, around the dilated bronchi, he found the lung-tissue indurated and pneumonic; and in another case, around cavities which were livid with reddened ami inflamed mucous membrane, the lung-substance was consolidated. On microscopical ex- amination of this consolidated lung-tissue, " little trace of air-cells could be made out, and it was mostly composed of fibrous tis- sue." In other rare cases, the irritation manifests itself in the formation of an ab- scess, in the centre of which the dilated bronchus is seen; or even-as first pointed out by M. Briquet,1-in the establishment 1 Dr. Stewart says that many of the dilated bronchial tubes present an appearance simu- lating hypertrophy of their walls, but which is really dependent upon changes in the mu- cous membrane, by which it becomes granu- lar or villous, and upon the presence of ill- formed connective tissue among the denser elements of the bronchial walls. He adds, "The irritation which causes the inflamma- tory thickening of the mucous coat may well also account for the spurious hypertrophy of the other." 1 Archives Generates de Medecine. 1841. PATHOLOGY. 293 of a limited gangrenous inflammation, in- volving the walls of the dilated bronchus and the surrounding lung-tissue. In other instances, where the bronchi- ectasis is primary, instead of the inter- vening lung-tissue remaining unaltered, being simply compressed, or undergoing either of the secondary changes just men- tioned, it gradually disappears-seem- ingly as a result of atrophy and slow ab- sorption-so that, in extreme cases, abso- lutely no intervening tissue may be left between the dilated tubes of the greater part of one lobe of a lung.1 We must now come to a consideration of the mode in which dilatation of the bronchi is brought about in Cirrhosis- that is to say, in those cases where indu- ration and contraction of the lung-tissue is the primary occurrence, and where di- latation of the bronchi is an altogether secondary phenomenon, which may occur or may not, according to the presence or absence of other occasional accompani- ments of the disease. An analysis of the thirty cases I have tabulated seems to show that dilatation of the bronchi in this disease is of a compensative charac- ter, owing to the fact of its being gen- erally most marked in those contracted lungs where the space which would have been left by contraction is not otherwise filled up-either by inshrinking of the thoracic parietes, by elevation of the cor- responding half of the diaphragm with proportionate displacement of abdominal organs, or by hypertrophy of the opposite lung and its extension into the diseased side of the thorax. If the space which would have been left by the shrinking lung is not otherwise filled up, then the increased pressure of the inspired air, act- ing upon bronchi in whose walls more or less fibroid substitution has most likely occurred, tends to dilate some of those which are most favorably situated for undergoing this expansion. It is obvious that something must go towards filling up the space left by the shrinking lung ; and if the thoracic parietes are so firm as not to yield easily, or if displacement of the viscera does not take place, then the bron- chi must yield and dilate in some of their weakest parts under the continually in- creasing pressure of the inspired air. It is, however, in great part a mechanical question. In a case where the proper texture of the tubes has become weakened by inflammation or fibroid changes, and where other conditions are favorable, a dilatation may be brought about ; whilst in another case, where the lung is equally affected, dilatation of the bronchi may not occur, because, in this particular in- stance, it may be easier for displacement of viscera or inshrinking of the thoracic parietes to occur in its stead. Of course, this dilatation need not necessarily be situated-and in fact would be less prone to occur-in parts of the lung which had already undergone an extreme amount of induration. So long as the dilatation ex- isted in some part of the organ, the par- ticular region in which it occurred would be altogether immaterial. The weakest part, other things being equal, would most readily undergo dilatation. How far the contractile influence of the fibre- tissue itself may, as suggested by Sir D. Corrigan, directly tend to bring about the dilatation of the bronchi, or be a real cause of their enlargement after a certain amount of dilatation has once been estab- lished, seems doubtful. I certainly do not think, however, that this is one of the principal causes of the production of bron- chiectasis. If it were really the method by which dilatations of the bronchi had been produced, it might reasonably be ex- pected that they should be most marked precisely in those parts of the lung which had undergone the most notable contrac- tion and condensation. Such a distribu- tion is, however, by no means invariable, and often the arrangement met with is quite the reverse. Taking the view of the case I have proposed, it will be seen that in those instances where dilatation of the bronchi did not exist, or was only very slightly marked, this was explicable from a consideration of other coexisting conditions observed post mortem. Thus, in two of the cases in which there was no bronchiectasis, the lung affection was comparatively acute and recent, and no shrinking of the organ had as yet taken place; in the next the amount of lung shrinking was probably not great, as no note was made of its existence : in another the lung was described as "small and solid" on the right side, but then the liver was very large, and the right side of the chest was also flattened ; in another the disease was restricted to the lower lobe of one lung on the right side, but then this was universally adherent to the dia- phragm, and the upper lobe of the same lung was notably emphysematous ; whilst in the last, although the right lung was as small as a closed hand, there was flat- tening beneath the clavicle, and the right side of the thorax contained a large and displaced heart, in addition to nearly one quart of pleuritic fluid.1 Of those cases in which the dilatation of bronchi was only slightly marked, in one the diseased lung was universally adherent, and its 1 This was the only one of thirty cases, however, in which any pleural fluid was found, or in which there had been any reason to suspect its previous existence. 1 There is a good example of this in Guy's Hosp. Museum, 171851. See also Path. Trans, vol. xii. p. 78. 294 CIRRHOSIS OF THE LUNG. amount of shrinking was probably not ex- treme, since it was not specified, whilst there was a most remarkable dilatation of the pulmonary artery throughout the or- gan ; in another, the disease being on the right side, there seemed to have been a falling in of the lower part of the thoracic parietes, whilst the heart was situated entirely in the right side of the thorax, and the enlarged left lung extended under the sternum and partly into the right side ; in another, although the amount of contraction of the lung was extreme (the disease being of six years' duration, and having commenced when the boy was only fourteen years old), still the left side was described as being " contracted to an extraordinary degree," both vertically and horizontally ; in the last the reason why there was only slight dilatation of the bronchial tubes is not quite so evident, though some of the points which might have explained it have not been distinctly alluded to. Concurrent evidence of this kind strongly tends to support the view now advanced concerning the method of production of the bronchiectasis which may occur in the course of Cirrhosis. From these considerations as to the mode of production of bronchiectasis gene- rally, and its relation to different states of the surrounding lung tissue, we may venture to draw the following conclu- sions :- 1. That dilatation of the bronchi may be present, and take place quite inde- pendently of alterations in density of the surrounding lung-texture ; although such dilatation may be favored by a primary atrophy of the walls of the bronchial tubes, or by the effects of inflammation in weakening them and diminishing their natural elasticity, or by a combination of the two. The actual mode of production, even when these favoring conditions exist, being always the expanding force of powerful inspirations, and more especially the tension occasioned by the expiratory effort, with closed glottis, which imme- diately precedes the expiratory part of the act of coughing. 2. That in these cases of primary bron- chiectasis the intervening lung-tissue may be found almost natural, or compressed and airless, though it may subsequently become so far irritated as to be found in a condition of inflammation, of fibroid in- duration, of purulent softening, or even of gangrene. 3. That in certain other cases the bron- chiectasis is compensative, and seems to be secondary to a certain amount of col- lapse of lung-tissue, though its actual production is still aided by the effects of cough and inflammation; or, as in so many of the instances of Cirrhosis of the Lung, the bronchiectasis is secondary to an actual shrinking with fibroid consoli- dation of the lung-texture-when dilata- tion of some of the bronchi results, as a physical necessity, if displacement of viscera or inshrinking of thoracic parietes cannot be so easily brought about. Etiology.-Are we to look upon Cir- rhosis of the Lung as a constitutional affection or as one of a strictly local nature ? If constitutional, we should have to regard it as one of the local mani- festations of a general diathetic condition upon which fibroid degeneration of organs and tissue seems in some cases to depend.1 The question of the existence or not of such a diathetic condition has been ably discussed by Dr. Handfield Jones,2 who has shown that not unfrequently we meet with wide-spread degenerations of this kind existing in various organs of the body, which it seems only possible to ex- plain by the assumption of the existence of some particular condition of the blood or diathetic state, favorable to the occur- rence of such anomalies of nutrition in many parts of the same organism. Thus, coinciding with a cirrhosis of the liver, we may find a similar condition more or less developed in the kidney, together with opaque thickenings of the capsule of the spleen, fibroid thickenings of the cardiac valves, fibroid degeneration of the parts of the arterial system, opaque thickenings of the arachnoid, &c. Do we in these cases meet with similar changes in the lungs, and is Cirrhosis of this organ to be looked upon as a sequence of the diathetic condition in question ? To the first inquiry our answer must certainly be in the affirmative. Fibroid thickening and induration of parts of the lungs is frequently met with in association with similar changes in other parts of the body, as the tables of Dr. Sutton3 fully prove. An answer to the second question is, how- ever, not quite so easy. Although in a certain number of cases, and more especially in elderly persons, disseminated fibroid indurations are to be met with, still, in other cases, a notable amount of fibroid substitution may have taken place in one or other organ alone. This latter state of things, so far as I have seen, is more apt to occur in in- dividuals who have not yet passed the 1 In the paper before alluded to, Dr. An- drew Clark has, since this was written, strongly urged that his cases of "Fibroid Phthisis" are local manifestations of a dia- thetic condition, characterized by the dis- semination of waxy degenerations and fibroid indurations in different organs of the body. 2 " Fibroid and Allied Degeneration," Brit, and For. Med.-Chir. Rev. 1854. 8 Med.-Chir. Trans, vol. xlviii. ETIOLOGY 295 meridian of life. But fully two-thirds, or perhaps more, of the cases of Cirrhosis of the Lung, are met with in individuals under forty years of age. Moreover, an examination of the post-mortem records of the thirty cases which I have tabulated, lends little or no support to the idea that the induration and shrinking of the lung has been only one manifestation of a general diathetic condition entailing simi- lar changes in other organs. Again, it may be seen from a consideration of the pathology of that form of bronchitis which is set up by the continued inhalation of foreign particles, that a similar fibroid change may be initiated in the lungs, without the agency of any diathetic con- dition. By the powerful action of a local irritation only, such changes are set up and may be seen in association with the chronic bronchitis of miners and artisans. In these cases the determining cause acts upon both lungs, and the effects are seen in both. Not so, however, with the ordinary cases of Cirrhosis of the Lung : here the fibroid induration, when existing to the marked extent which constitutes Cirrhosis, is almost invariably unilateral (which of itself tends strongly to negative the idea of its being entirely of diathetic origin), and in only three or four out of the total number of cases does there seem to have been any well-marked coexisting fibroid substitution or hyperplasia in other organs. But we do find in more than two-thirds of the cases, old adhesions of a firm and almost cartilaginous consistence uniting the two pleural surfaces on the side affected. Chronic bronchitis, in fact, when it oc- casions a dry pleurisy on one side with the gradual formation of adhesions, seems to be the most frequent determining cause of that local overgrowth of fibroid tissue which constitutes the essential feature of the disease. The new growth gradually encroaches upon and replaces the proper lung texture, till at last the whole nutri- tion of the organ seems to become leav- ened by this change, and many indepen- dent centres of transformation are estab- lished. In almost all cases, however, in which thickening of the pleura is pro- duced, the new growth seems to spread inwards from this with greater rapidity than it does from other centres. In a few cases chronic bronchitis alone seems to have been the determining cause, since no notable adhesions of the"pleural surfaces have existed, and the invading new tissue has seemed to start, through- out the organ affected, as direct prolonga- tions from the walls of greatly thickened bronchi.1 Why in these latter cases the change should be limited to one lung is rather difficult to understand:l we can only suppose that this may be due to the unequal incidence of the irritating cause acting alone or else in combination with some obscure, though positive tendency to perpetuate a tissue-change of this kind when it has been once initiated. But there seems to be still another way in which well-marked Cirrhosis of the Lung may occur, and that too by a pro- cess which is usually much more rapid in its progress than when the change origin- ates in the manner I have hitherto de- scribed. I refer to those cases in which fibroid induration immediately follows an acute inflammation of the lung-the pro- cess which Grisolle, Charcot, and other writers describe as "chronic pneumonia." This is a subject surrounded with doubt and difficulty. I have already said that the name "chronic pneumonia" appears to me to be altogether unsuitable and contradictory as applied to this affection. But, apart altogether from the question of names, there are other difficulties, since -partly owing to the rarity of the occur- rence-many physicians are not prepared to admit that such a pathological state is ever the immediate sequence of an acute pneumonia. Several physicians and path- ologists, however,-such as Bayle, Sir John Forbes, Addison, Lebert, Grisolle, Charcot, Hughes Bennett, and others- believe in this sequence, and have re- corded cases which tend most strongly to support their opinion. Bayle's2 case of "Chronic Peripneumony, which resem- bled Phthisis," seems to be one of this kind. Grisolle says that, during his very long experience, he has only seen four ex- amples of the passage of acute into chronic pneumonia. He believes that this sequence is a consequence of neglect, though it may, perhaps, depend even more upon peculiarity and debility of con- stitution. Huss says it is liable to occur in habitual drunkards, but Grisolle states that such does not seem to be the case in France : neither does he place any more credence in the opinion of Heschel, who, because he found that this complication was rare at Vienna but somewhat more in rare cases that it attains an extreme degree in one lung, and so produces the condition of the organ with which we are now concerned. 1 A somewhat similar difficulty, however, presents itself in the case of simple dilated bronchi, owing to the frequency with which this condition, in association with chronic bronchitis, is met with only in one lung. Here, we must resort principally to the sup- position that there is some difference in the texture of the bronchial tubes on the two sides. 2 Researches on Pulmonary Phthisis, trans- lated by Barrow, 1815, p. 415. 1 In very many cases this induration may never reach an extreme degree, and it may affect both lungs pretty equally. It is only 296 CIRRHOSIS OF THE LUNG. common at Cracow, attributed it to the influence of malaria. In one of Grisolle's patients, who died at the end of the tenth week from the commencement of an acute pneumonia, which he considered to have passed over into the chronic form, the lung affected was found in the following condition : It was almost entirely hepa- tized ; the lower lobe being hard, com- pact, reddish-gray, and the cut surface being smooth -though granulations ap- peared when portions were torn. This differed from a state of acute inflamma- tion by the greater hardness and gray color of the part. The whole of the upper lobe was indurated, with the exception of a portion extending rather more than one inch from the summit. The anterior bor- der, which presented the most recent traces of inflammation, was in a state of well-marked gray hepatization, the rest of the lobe being in a condition of red in- duration, and showing granulations on both its cut and torn surface. This granu- lar appearance may be met with, accord- ing to Grisolle, when the malady has only been of two or three months' duration, though after this it gradually disappears. Then with regard to the case (II.) re- corded by Dr. Sutton, although a previous history of inflammation of the lung was by no means distinctly made out, Dr. Sutton seems to have been quite convinced that the state of the organs was just such as has been described under the name "red induration," and it does appear quite certain that the change was one of an acute character. So that either the old interpretation must be the correct one (that this "red induration" is the imme- diate sequence of an acute pneumonia) or else we must accept Dr. Sutton's supposi- tion, that it is possible for an acute fibroid change, of the kind he describes, to occur in a lung not previously diseased. But, in the lace of other evidence, the first sup- position seems the most probable one, and I look upon the case (III.) recorded by M. Charcot, as affording the strongest sup- port to this view. Whilst believing, there- fore, that this sequence may occur in cer- tain cases, it must be clearly borne in mind that it is an occurrence of extreme rarity, supervening only under the in- fluence of exceptional conditions, which as yet may be said to be almost entirely undiscovered. In fine, then, exposure to cold and wet, leading to the advent of bronchitis, pleu- risy, or pneumonia, in certain individuals seems to be the principal determining cause of this disease. It is apparently much more prone to occur in males than in females, though this difference may perhaps be due more to the much greater frequency of exposure of individuals of the male sex than to any inherent ine- quality in liability to the disease quet sex. And, although met with occasionally in children and in old people, this disease seems much more prone to occur in indi- viduals between the ages of fifteen and forty. But what has just been said with regard to the apparent determining influence of sex, and its subordination to relative amount of exposure to wet and cold, may also hold good with regard to age, since, ceeteris paribus, individuals be- tween the ages I have mentioned, are more likely to be exposed in this way than persons who are either older or younger. With regard to the supposed connection between this disease and the rheumatic diathesis, or the predisposing influence of long-continued habits of intemperance, nothing positive can be said ; only the extreme rarity with which either of these circumstances has been mentioned would seem to show that neither of them can be considered as essential antecedents of the disease. No casual relationship, either, can be established between syphilis and Cirrhosis of the Lung. Neither does there seem to be any evidence to lead us to imagine that this malady is ever propa- gated by hereditary transmission : and of course if it be true, as I suppose, that the disease is a local one, set up for the most part in the individual by accidental con- ditions, this absence of any tendency to hereditary transmission is quite in ac- cordance with what might have been ex- pected. Cases of Cirrhosis of the Lung. I. M., set. 7. Dr. Corrigan, Dublin Journ. of Med., 1838, p. 226. General History. Influenza three months before, followed by cough and expectoration, with loss of flesh, and oc- casional haemoptysis.-Symptoms. Febrile symptoms for sixteen days, with severe cough, dyspnoea, and hurried respiration. -Inspection, Percussion, Auscultation, etc. Right side perceptibly flattened. Bron- chial respiration, and distinct broncho- phony over flattened portion of chest.- Autopsy: Hight side, slight pleuritis; lung solid, non-crepitant, grayish-red, tough, and traversed in all directions by thick- ened white bands of fibro-cellular tissue. Bronchi dilated towards pleura, terminat- ing in spherical sacculi; lining membrane dark red. Left lung, healthy. II. M., set. 26. Dr. Barlow (recorded by Dr. Sutton), Med.-Chir. Trans., 1865, p. 299. General History. A well - developed muscular man, of middle height. Always had good health, except for an occasional winter cold. Four months ago appetite began to fail and cough commenced. Pur- sued his work for one month, and then CASES OF CIRRHOSIS OF THE LUNG. 297 gave up, owing to increasing weakness. Afterwards became weaker and weaker, the cough continuing. Three weeks be- fore admission spat phlegm streaked with blood.-Symptoms. Oct. 12. Admitted into hospital. During the first ten days cough became easier, and he seemed to gain strength. Appetite variable. Oct. 21. Immediately under right clavicle scarcely any respiration heard, but dis- tant crepitation. Posteriorly over right apex tubular breathing, with moist sounds and whispering bronchophony. Tubular breathing also at right base, with crepita- tion all down the left side. Oct. 25. Res- pirations labored, 35; pulse 140, very small and feeble. Profuse perspirations ; friction sounds over right base. Died same day.-Inspection, Percussion, Auscul- tation, etc. Heart sounds clear and sharp; pulse small and compressible. Skin not particularly hot. Over right side, poste- riorly, respiration feebler than over left; though, on left side, the percussion reso- nance was also diminished over the base. Vocal resonance markedly increased over right base.-Autopsy: Right lung. Signs of recent pleurisy, but no firm adhesions. On section, upper lobe of dark red color, and interlobular tissue appearing in- creased. Very small quantity of fluid from surface of section, and tissue not breaking down under finger. The whole of lower half of right lung solid, firm, and somewhat tough ; of reddish-gray color, and offering some amount of resistance to the knife. Sank in water, and exuded scarcely any fluid when pressed. Left lung in a similar condition, except that the consolidation was arranged more in patches. Bronchial tubes much congested, but not dilated. Bronchial glands much enlarged. Heart healthy, except for con- traction and puckering of one of columnte earner. Liver, normal. Spleen, very large and firm. Kidneys, large, very firm, and tough. Intestines, healthy. III. M., set. 61. M. Charcot, De la Pneumonie Chronique, These de Paris, 1860, p. 37. General History. A hosier; delicate- looking ; generally enjoyed good health, but has had a cough for some months, and has grown rather thin.-Symptoms and Physical Signs. March 30, 1850. Ad- mitted. Five days ago, rigors, pain in side, and rusty sputa appeared. Had all the signs of pneumonia of whole of right lung, with, at first, simple febrile, and af- terwards typhoid, symptoms. April 4. General condition improved ; muco-puru- lent, instead of rusty, sputa. April 12-18. Some improvement in general condition : bronchial breathing and dulness continu- ing in upper part of lung; whilst over the lower lobe, with intense bronchophony and dulness, there was respiratory silence, not even bronchial breathing. No sego- phony. April 18-29. Local signs con- tinued without change; but return of appetite; feverishness at night, and weakness. April 29. Rigors, frequent respiration, fever, crepitant rale, mixed with bronchial breathing on right side. Epistaxis. Large blister applied. May 8. Better; but still occasional shiverings; eyes injected at night, and cheeks red ; but little appetite. Signs of pulmonary induration continuing. May 9. Lower an- gle of right scapula raised by a large and deep abscess, from which, on incision, is- sued about 15 oz. of pus. Up to June 1st the abscess continued to discharge, though fluid gradually more serous in nature. During this time there were hectic fever and rapid wasting, but no diarrhoea. All the signs of pulmonary induration still continued. Slight cough ; expectoration scanty and muco - purulent; no night sweats. During the month of June no alteration. Still losing flesh, but no cough, diarrhoea, or night sweats. July 1-9. Gradually became worse ; the hectic persisting, but still none of the last-named symptoms or oedema of legs. On the 9th, the expectoration (being before scanty) became very abundant and somewhat nummulated. On this day the following Physical Signs were recorded. On left side, resonance good, with puerile respi- rations. On right side, below clavicle, marked dulness; respiratory murmur faint and indistinct. Posteriorly, dulness throughout; over superior lobe, respira- tory murmur very indistinct. Vocal reso- nance over lower lobe, with marked bron- chial breathing mixed with large metallic rales, simulating gargouillement. Bron- chophony, but not pectoriloquy. But not always the same result: sometimes com- plete silence over whole of upper and lower lobes, and sometimes tubular breathing mixed with large metallic rales. No note made as to variations in expectoration at these times. Died on July 19th, much emaciated.-Autopsy: Right lung, univer- sally adherent by old and tough adhe- sions ; pleura constituting a fibrous en- velope in thickness. Whole organ j smaller than left lung. Tissue heavy, dense ; finger cannot penetrate it; on sec- tion, resisted scalpel like fibro-cartilage. The three lobes were seen to be firmly united, and the tissue change was the same throughout the whole lung. The surface of section was smooth, non-granu- Dr, grayish-blue marbled with black. Bronchial tubes not at all dilated. Pale ligamentous partitions of fibrous tissue subdividing lung in all directions, forming a minute network. No trace of tubercle. Left lung, large and perfectly healthy throughout. Heart, slightly large, flac- cid ; otherwise healthy. Other viscera carefully examined, and found to be healthy. A fistulous opening existed 298 CIRRHOSIS OF THE LUNG. near the lower angle of right scapula, leading into the cavity of an old abscess over the third, fourth, fifth, and sixth ribs, whose external surface was in a ca- rious and necrosed condition, whilst the intercostal muscles were partly destroyed. The internal surface of these ribs was quite healthy, and no communication ex- isted between the cavity of the abscess and that of the chest. IV. M., set. 30, Dr. J. E. Pollock. General History. A soldier in India for 54 years, and afterwards a warehouse porter. Tall, well-made, and pretty well nourished, though he had lost flesh. Gen- eral health good.-Symptoms. Suffering from cough for the last nine months, and streaky haemoptysis for six months. Ex- pectoration profuse, frothy, and muco- purulent. Bowels constipated. Occa- sional pain in back between the shoul- ders. Death from rupture of aortic aneu- rism into left bronchus.-Inspection, Per- cussion,. Auscultation, etc. Heart's impulse visible from apex region to second left cartilage. General contraction of whole left side, with flattening in front, and slight depression of shoulder. Dulness not absolute over left side ; respiration very deficient in sub-clavicular region, with increased vocal resonance over apex posteriorly. On right side, increased res- onance up to and beyond left of sternum. Respiration normal.-Autopsy: Left lung, adherent throughout, contracted ; could only be removed together with costal pleura. On section, bronchi greatly di- lated, with intervening tissue fibroid and airless. Right lung enlarged, covering pericardium. Heart healthy; aortic valves thickened, but not incompetent. Aneurism of descending part of aortic arch, ruptured. V. M., jet. 74. (M. Legendre.) Barth, in Mem. de la Soc. Med. d'Observat. de Paris, 1856, t. iii. General History. Parents healthy, was brought up by hand, took violent cold a few days after birth. Three weeks after began to vomit food, which continued for a long time. Cut teeth and walked at usual time. When 34 or 4 years old, be- gan to expectorate large quantities of pu- rulent matter. Two or three times a day at most, after feeling of anxiety and face becoming red, there were paroxysms of cough, with copious ejections of pus. Felt relieved immediately after this. In intervals neither coughed nor spat. Ha- bitual dyspnoea; skin hot at night, and copious sweats, but no diarrhoea ; and ap- petite always good. From this time to 7th year continued much the same, but grew and was by no means thin. Of moderate size and fatness; skin pale; ends of fingers thick; intelligence good. No in jection of face.-Symptoms. Oct. 11, 1841. In morning, skin cool, pale; pulse 80 ; but about 5 o'clock face becomes red, skin hot, pulse 116-120, respiration fre- quent, and in night abundant sweats. Two or three hours after meal, at 11 A. M., feeling of malaise with anxiety, and in fifteen or twenty minutes the cough comes with floods of expectoration, and often vomiting of food. Fluid thin, puru- lent, with stale odor; from 6 to 8 oz., though less when night attack also, as often. Dec. 13. Has lost flesh lately; evening attack constant, night sweats co- pious. Dec. 31. Thinner; bad diarrhoea for two days. Jan. 12. Feebler and thin- ner, much wasted, slight bed-sores. Breath fetid; ulceration of gums and inner side of right cheek. Appetite less ; still diarrhoea. Jan. 14. Gangrene of gums inside of right cheek progressing, and breath very fetid. Jan. 16. Died.- Inspection Percussion, Auscultation, etc. Tongue moist, belly big, with tenderness over region of enlarged spleen. Right side resonant all over. On left under clavicle, as good as right side, but behind com- pletely dull from top to bottom. On right side, and under left clavicle, respi- ratory murmur normal; but over whole of left back, respiration cavernous, with rales, and also great vocal resonance. Dec. 31. Not having been auscultated for several days in addition to previous signs, there was detected under left clavicle a slight dulness, with bronchial breathing and large mucous rales.-Autopsy: Pleu- ral adhesions very slight, principally on left side. Left lung not diminished in size. Lower lobe heavy, hard; no ap- pearance of air-vesicles on section, but seen to be converted into a dense, red- dish, homogeneous tissue, containing cav- ities from size of pea to almond filled with expectoration matter. This part-in co- lor, consistence, and density-was like tissue of an enlarged uterus. Bronchi normal, as far as first division ; but after- wards uniformly dilated throughout. Up- per lobe nearly as heavy as lower, but not nearly so dense; and consistent, though airless. Tissue reddish-gray, granular on surface of section, but breaks down less easily than recent hepatization. Bronchi only slightly dilated. Not the least trace of tubercle or gray granulation. Right lung, healthy and crepitant, except for a few "gray granulations" scattered through its substance. Bronchial glands on left side enlarged, reddish-gray. Kid- neys and liver healthy. Spleen large and very consistent. Mucous membrane of intestine healthy. Symptoms.-The symptoms of this af- fection present a considerable range of variation in different cases, according to the different modes in which the disease originates, and the amount of change which has been induced, not only in the SYMPTOMS. 299 diseased lung, but also in the position and size of the heart. Thus one class of cases - and this includes a considerable propor- tion of the whole-are chronic from the first, appearing to commence obscurely, and being afterwards characterized by the symptoms of chronic bronchitis, with a limitation of the local signs to one lung. The cough, in these cases, dates some- times back for a period of twenty years or more. In another class, the affection dates definitely from some acute chest disease- either a bronchitis, a pneumonia, or a pleurisy without notable effusion - and then goes on, from this starting point, in much the same chronic way as when th'e mode of origin is indistinct. The cases in these two classes may or may not be associated with deviation in the position of the heart, signs of enlargement of its right cavities and dropsy. In a third class, the cases are more acute in their progress, and the morbid change seems to be the immediate sequence of an attack of acute pneumonia. The sufferers included under this last head usually succumb pretty early, and before the disease has attained to its later stages of develop- ment. It frequently proves fatal before the end of the first year from the date of the acute pneumonia. The particular combinations of symp- toms in individual cases may be best seen in detail, as they are given in the analyti- cal table. I shall here confine myself to a more general consideration of the differ- ent symptoms and signs met with in the disease, and to an estimation of their rela- tive importance. Although the patient may have many of the physical signs of phthisis, its con- stitutional symptoms are almost entirely absent. There are no feverish symptoms, no signs of hectic, no copious night-sweats, no disorders of digestion, and the disease for the most part seems altogether of a more stationary and chronic character. No laryngeal symptoms have been noted in any case. Diarrhoea, although an oc- casional symptom, is less frequent than in ordinary cases of phthisis, and when if exists it may be an accompaniment of blood-poisoning from coexisting gangrene. Once diarrhoea was occasioned by an ul- ceration of the caecum, which was rather obscure as to its nature and origin. Cough is one of the most constant symp- toms ; it is sometimes present through- out, and undergoes but little variation, though it is often aggravated during the winter months. Where the disease is advanced and there is much dilatation of the bronchi, the cough is often paroxys- mal, coming on in violent fits after long intervals of comparative quiet. Such in- dividuals may have violent paroxysms of coughing in the morning, at the end of which the secretion that had accumulated in the dilated bronchi, during the inter- val between the present and the last fit of coughing, is voided in copious gulps. Vomiting of food may also take place at this time, and one, two, or even three such fits of coughing may, in some cases, occur during the twenty-four hours. The attacks are preceded by a feeling of dis- comfort and malaise, although compara- tive relief is experienced as soon as the irritation and pent-up secretions have been got rid of. Where there is little or no dilatation of the bronchi, the expectoration is not very abundant, but rather tenacious, and occa- sionally somewhat nummulated in char- acter. But where the disease includes dilatation of the bronchi, the expectora- tion is generally copious, muco-purulent, yellowish, or ash-green in color; having a tendency to run together into an almost homogeneous mass, which is often frothy on the surface. Owing to the thin sero- purulent nature of the secretion in some cases, the fluid separates, after standing, into three more or less distinct layers- the lowest yellowish, containing most of the solid matter which has settled ; a middle stratum of greenish fluid ; and an upper frothy stratum, or one composed of mucous and fat granules. In these cases, the amount of fluid excreted daily may reach as much as ten or fifteen ounces. It has often a very stale and nauseous odor, and is sometimes even fetid,1 though 1 Upon the presence of what particular substance the fetor depends, different opin- ions have been held, as may be seen by the following quotation from Dr. Grainger Stew- art's paper: "Professor Laycock concludes (Edin. Med. Journ., May, 1865) from experi- ments and observations made by the late Professor Gregory, Dr. Arthur Gamgee, and himself, that the odor must be due to butyric acid. He also states that Dr. Gregory detected the odor of methylamine in some of the pro- ducts of the sputa. Professor Bamberger (Wurzburg. Mediz. Leitz. 1864) concludes that the characteristic smell of the sputa in bronchiectasis appears to.depend upon a va- riety of odorous matters, among which are the members of the series of acids of the type to which butyric and formic acids belong, ammonia and sulphuretted hydrogen, all of which may proceed from the decomposition of organic substances. He further states that purulent sputa-e. g., that of tubercular pa- tients-sometimes undergoes the same decom- position out of the body, and if long kept, have the same smell as the sputa in question. Dr. Arthur Gamgee (Edin. Med. Journ., March, 1865), from a considerable number of analyses of sputa, concludes that the occur- rence of butyric acid cannot at present be proved to have any semeiological value, and that its presence is in no way characteristic of fetid bronchitis, under which term he in- cludes bronchiectasis." 300 CIRRHOSIS OF THE LUNG. the smell is quite distinct from that of gangrene. On agitating the recent spu- tum with water, opaque, grayish fila- ments, of varying diameter, may soon separate and sink to the bottom. These are cases of minute bronchi, which, as first pointed out by Dr. Arthur Gamgee, assume a purplish tint on the application of iodine. They are met with more par- ticularly in the fetid sputa, and, accord- ing to Niemeyer, the fine acicular crys- tals of margaric acid may also be detected by the aid of the microscope in the fetid sputa from dilated bronchi-though they are said not to be encountered in the bronchial secretion in any other lung af- fection, save that of gangrene. Dr. Grain- ger Stewart has found these crystals in the dilated cavities after death, but has failed to detect them in the sputa during life. In more than one-half (17 :30) of the recorded cases, there has been hcemoptysis -sometimes small in quantity, streaking the expectoration, and in others pretty abundant from time to time. Out of the thirty cases there are only four in which there is any mention made of the exist- ence of " tubercle," either in the sound or in the cirrhosed lung. In one of these cases (V.) there was no haemoptysis at all, in another the hemorrhage seems undoubt- edly to have proceeded from the non-cir- rhosed but "tubercular" lung; in the third it must, almost certainly, have pro- ceeded from the cirrhosed lung ; whilst in the fourth the hemorrhage (which was fatal in this case) seems to have mainly proceeded from the enlarged lung, al- though there was also a small cavity con- taining blood in the retracted lung. Thus there were fifteen, or one-half of the total number of cases of cirrhosis, in which haemoptysis was one of the symptoms, and in which the hemorrhage undoubtedly proceeded from the cirrhosed lung, and in only one of these did "tubercle"1-and that in the smallest quantity-coexist with the fibroid change. This is an important fact in connection with the disease, and is in opposition to the view inclined to by Dr. Walshe and Dr. Law, who have both expressed their opinion as to the proba- bility of the hemorrhage, in most cases, proceeding from the non-cirrhosed lung, in connection with the formation of "tu- bercle." In a small number of cases the patients have complained of pain in the affected side, either localized or indefinite in site. Dyspnoea, though a constant symptom, is often moderate in degree, even in ad- vanced stages of the disease-so long as the patient remains quiet, and the oppo- site lung continues to be healthy. It is occasionally more marked as an objective than as a subjective symptom, and is gen- erally much increased after the slightest exertion. With reference to the pulse-res- piration ratio, no definite details are given, except as to its condition in the case re- corded by Dr. Walshe. Here he says, "It never fell lower than 3:1, and was sometimes found at the par of health, 4:1; even above this on one occasion-4'7 :1." The dyspnoea is most marked in cases where there is dilatation of the right side of tiie heart and dropsy ; orthopnoea is then a constant symptom, attended with more or less lividity of lips, face, and even sur- face of the body generally, whilst there may also be pulsation in both jugular veins. Purpuric spots of hemorrhagic effusion appear on the body occasionally. When an acute attack of bronchitis or pneumonia supervenes, the dyspnoea be- comes asphyxial in its intensity, owing to interference with the breathing power of the previously sound lung, and death often speedily ensues. The patient almost habitually lies on the retracted side ; and any attempts to lie on the other cause great increase of dyspnoea and cough, so as to make it im- possible to continue in this position. The pulse is often regular and full, not- withstanding the frequent deviation in position of the heart. The appetite is usually pretty good ; and in spite of the chronic nature of the cough, and the al- most habitual copious expectoration, the patient does not lose much flesh. To- wards the end slight emaciation is com- mon, but extreme emaciation is rare in this disease ; when it is uncomplicated by cancerous or other wasting affections.1 The mode in which the third class of cases originates has been well described by MM. Grisolle and Charcot. The in- dividuals do not recover from the attack of acute pneumonia as they do in ordinary cases. On this subject the former observer says: "One sees at first the disease de- cline-in appearance at least; the pain in the chest disappears ; the sputa lose their viscosity as well as their hemorrhagic color; Ihe appetite reappears ; but not- withstanding this improvement some symptoms obstinately persist; the patient, far from gaining flesh and strength, grows worse and worse in these respects, and one finds, on examination of the chest, that a more or less considerable portion 1 Since this was written I have seen and made the autopsy of a man who suffered from an extreme degree of cirrhosis of the left lung, and in whom there also existed an enormous liver, studded throughout with the most typi- cal cancerous nodules. No cancer was found in any other organ except in the bronchial glands, which were completely infiltrated-- not even a trace of it could be discovered in either lung. 1 Really, in all probability, a patch of chronic lobular pneumonia. PHYSICAL SIGNS. 301 of the lung still remains impermeable to air-that is to say, percussion reveals dul- ness for a certain extent, whilst over the same part, on auscultation, bronchial res- piration and bronchophony, with sub- crepitant and mucous rales, are heard." But it must be clearly understood that it is not the mere persistence of the local symptoms alone which have any signifi- cance, since M. Grisolle has shown that a slow return of the lung to its normal con- dition is a common, if not an habitual, sequence in a pneumonia whose result is favorable. Feebleness of the vesicular murmur, and a coarse breath-sound, mixed with sub-crepitant rales, are often the only signs of the unfinished resolution ; though much more rarely, as M. Charcot says, " tubular breathing, bronchophony, and a more or less marked dulness, have been capable of persisting for two or three months after the complete cure of a pneu- monia, and, notwithstanding this, there has not been the least tendency to a re- lapse, or the least return of febrile symp- toms." Cases of this kind, however, which are not those to which we are more especially alluding, may be interpreted, as M. Charcot believes, by supposing that the new consolidating "materials have not been re-absorbed, and have remained for a time in the tissue of the lung, with- out the coexistence of any inflammatory action." But, in the cases where an in- flammation of the lung is about to termi- nate in what MM. Grisolle and Charcot term "chronic pneumonia" (or, as we prefer to say, in a fibroid induration lead- ing to cirrhosis), although the general symptoms occasionally subside for a brief period, they soon reappear. The symp- toms, then, have more or less of a hectic character from the first; or there may be a preliminary and short reappearance of the symptoms of the acute condition-in other words, a relapse, of short duration. Gradually tlie hectic symptoms become more marked ; every evening the skin be- comes hot and the face flushed; some- times night-sweats are profuse, and at others they are absent altogether ; nutri- tion soon becomes impaired and the pa- tients lose flesh, whilst cough and dys- pneea continue. (Edema of the lower ex- tremities may supervene, and the patient, already wasting, may be still further lowered by the setting in of an obstinate diarrhoea. The resemblance of the gene- ral symptoms to those of phthisis is often most striking.1 When the individual does not perish In the course of a few months from gradual exhaustion or from uncon- trollable diarrhoea, the symptoms gradu- ally diminish and the disease lapses into the chronic state. Physical Signs.-Retraction or shrink- ing of the thorax, to a greater or less ex- tent, on the side of the affected lung, is very frequent after the disease has existed for a certain time. It is, however, not commonly met with till after the lapse of about eighteen months. In two only out of seven cases, which proved fatal at or before this period, was there any flatten- ing of the chest. One of these (I.) was that of a child only seven years old, at which age of course the flexible parietes would readily follow the shrinking lung; whilst in the other case (IV.), that of an adult, although the disease only presented symptoms for nine months, it seems to have made rapid progress, and there was obvious shrinking of the chest on the af- fected side, and even slight lowering of the shoulder. In the great majority of the individuals who live longer than eigh- teen months after the commencement of the disease, some amount of retraction of the chest is observed, either general or sub-clavicular ; and in almost all, there is a proportionate amount of immobility on the retracted side. Moreover, in those cases where contraction cannot be de- tected, comparative immobility may be easily established. The flattening and retraction is an almost purely physical process dependent upon the shrinking of the lung within ; and its amount depends principally upon the degree of rigidity of the thoracic parietes at the onset of the malady, and upon the rapidity of its course. If the lung-shrinking goes on pretty rapidly and the patient is young, the amount of contraction may be enor- mous-as actually occurred in Dr. Mayne's case, where the disease had existed for six years, and had commenced when the patient was only fourteen years old. The more the neighboring viscera are pulled into the space gradually vacated by the shrinking lung-the more the opposite lung enlarges - and the more the actual amount of lung-shrinking is diminished by the formation of dilated bronchial cavities-the less will be the amount of contraction or flattening of the thoracic parietes; all these conditions must be considered together, as they have a sort of complemental relationship to one an- other. On percussion over the affected side- where the disease is well marked-we do not get a merely dull sound, but rather a more or less marked, high-pitched, tubu- lar note, with firm, wood-like resistance under the finger. Over portions of the surface corresponding with large dilated bronchi, the note may present a well- 1 The symptoms even of "galloping phthi- sis" may be imitated, where the disease is more rapid in its progress, and when it be- comes associated with acute pleurisy, as in the case of M. Monneret, recorded by Charcot. (Loc. cit. p. 27.) 302 CIRRHOSIS OF THE LUNG. marked amphoric or tympanitic sound. The dulness is sometimes as distinct an- teriorly as it is posteriorly ; but occasion- ally the anterior area of dulness is dimin- ished owing to the overlapping of the sound but hypertrophied lung, which ex- tends into the diseased side of the thorax. In some extreme cases the percussion note may be good over almost the whole of the affected side in front, whilst it is abso- lutely dull with characters of resistance posteriorly.1 On the opposite side of the chest the percussion note is almost always clearer than usual, and more like that which is met with when the subjacent lung is emphysematous. On auscultation the normal respiratory murmur is either altogether absent or heard only over limited areas; whilst at other parts the respiration is high-pitched and bronchial, with cavernous and am- phoric characters here and there. These sounds may be of the dry character ; but, more frequently, there are moist rhonchi of various kinds-sometimes smallish, but mostly of the large bubbling kind and of a metallic character-such as constitute what is frequently described as gargouille- ment. The loud bubbling rales may be so abundant as to drown almost every other sound. Vocal resonance may be either diffused and bronchophonic, or various degrees of pectoriloquy may exist. Vocal middle of the lung, at the base-or, per- haps, in all of these situations at the same time. It can scarcely be said, positively, that they are more frequent in one situa- tion than in the other. Sometimes such signs, however, may be absent altogether. The breath-sounds over the opposite en- larged lung mostly deviate from the con- dition of health, only by being louder and more puerile than natural. When an intercurrent attack of bronchitis or pneu- monia sets in, the character of the respira- tion on this side will, of course, undergo a corresponding modification. The position of the heart often deviates much from that which is normal. The amount of displacement, of course, de- pends in great part upon the amount of lung-shrinking; but it is generally more considerable when the disease is in the right lung than when it is in the left. When the right lung is affected, the whole heart seems to be drawn over bodily into the right side of the thorax, so that its impulse may be felt only to the right of the sternum, whilst its apex impinges under the nipple. An amount of displace- ment so considerable as this has been encountered several times. In one case, in which the disease was on the left side, the heart's impulse was perceived close under the left clavicle ; but in other in- stances the organ seems only to have been slightly drawn up, and the area ofimpulse, therefore, only slightly raised. Though its position is altered, the heart mostly beats with regularity, and no bruits seem to be produced by the dis- placement. 1 More or less dilatation and hypertrophy of the right side of the heart has occurred in one- third of the cases. The deviation in position of the heart would often make it difficult to establish this by percussion and ausculta- tion, but in three of the cases there were the signs of a loud tricuspid regurgitant murmur, associated with pulsation in the jugular veins and more or less dropsy. And in almost all the cases where the right side of the heart was found to be enlarged after death, there had been drop- sy during life-either anasarca alone, or anasarca and ascites combined in a few of the cases. Dropsy existed in more than one-third (12 : 30) of the cases; so that it was present (mostly in the form of anasarca of the lower ex- tremities) in a few cases where there was no dilatation of the right heart, and in [Fig. 42. Unilateral retraction of chest; consequent upon cirrhosis of left lung in a girl of fourteen years. The figures indicate antero- posterior and transverse diameters, and semi-circumferences of right and left half of chest (Dr. Gee).] fremitus is generally much increased over the dull parts, and this, together with the great sense of resistance on percussion, has, when it exists to a marked extent, considerable diagnostic value. The signs indicative of cavities may exist most plainly under the clavicle, towards the 1 This was most notably so in two cases recorded by M. Barth. 1 Dr. Andrew Clark, however, states that "a low-pitched systolic bruit is commonly heard over the pulmonary artery." DIAGNOSIS. 303 which it depended upon disease of the kidneys or other coexisting conditions. In the acute form of the disease, answer- ing to what has been called "chronic pneumonia" (which may affect the whole of one lung, or only one lobe1), the physi- cal signs are almost identical with those of the early stage of the chronic form, be- fore much contraction of the lung has taken place. Thus, there is absolute dul- ness over the diseased part, with a con- siderable sense of resistance to the finger, whilst the vocal fremitus is much intensi- fied. On auscultation over the dull part, bronchial or tubular breathing is heard ; the latter being sometimes so loud as to be of a cavernous character even where no cavities exist. Rales are generally heard also - often loud, large, and metallic, though they are sometimes smaller or even absent. The vocal resonance is mostly bronchophonic. Occasionally, however, there may be a complete absence of all breath-sounds, either healthy or morbid, and of vocal resonance, whilst the percus- sion sound is quite dull-a combination which occurred in a case observed by M. Requin and quoted by Grisolle, and which led to its being mistaken for one of pleuritic effusion. In another ease (III.) which has been recorded by M. Charcot, remarkable alterations were observed on different days. At one time, over the whole ex- tent of a lung which was diseased through- out, there, was a complete silence-no sound or rale of any kind ; whilst at other times, on the contrary, there was loud and universal tubular breathing mixed with metallic rales. Unfortunately no observations were made as to the state of the expectoration at these times-either as to its quantity or quality.2 Contraction of the chest-walls is of course not met with until the diseased lung has under- gone a certain amount of shrinking, and by that time, if the patient survives so long, the intensity of the general symp- toms has diminished, and the condition comes to resemble that of a person who is suffering from the more chronic form of the disease. Diagnosis.-The diagnosis of this affec- tion in certain well-marked cases can be made almost with complete certainty, though in other instances only with great difficulty. The diseases with which it is most likely to be confounded are chronic pleurisy with retraction of the side, cam cerous infiltration of one lung, certain forms of " tubercular" phthisis, simple general collapse of one lung, and simple or primary bronchiectasis. In chronic pleurisy with retraction of the side, according to Dr. Walshe, the ribs are twisted downwards and inwards, the spine is curved, and the shoulder is drawn down ; which effects are not pro- duced by Cirrhosis alone. The lowering of the shoulder was, however, distinctly produced in one case of Cirrhosis occur- ring in a youth, with whom the amount of chest contraction was extreme ; and it also existed to a slight extent in another case. Cirrhosis being so frequently com- plicated with dilatation of bronchi, is more frequently associated with physical signs of the hollow class; though the bronchial symptoms are not always most severe in cases where there is the greatest amount of contraction of the chest-walls. The heart is generally much more dis- placed by Cirrhosis than by chronic pleu- risy. Then the frequency of haemoptysis in Cirrhosis, with its non-occurrence in chronic pleurisy, must be borne in mind ; and also, the greater frequency of enlarge- ment of the right side of the heart with dropsy in the former affection. As Dr. Peacock has suggested, it will be well also to bear in mind the possibility of confound- ing Cirrhosis of the Lung with contraction of the organ succeeding an empyema which is evacuating itself through the bronchi, by means of a fistulous commu- nication between them and the pleura. Cancerous infiltration of one lung also causes retraction of the side, though, according to Dr. Walshe, the retracted ribs are not altered in axis, and the tend- ency seems to be to draw in an upward direction rather than latterly, so that when the disease occurs in the right side, the liver may be much elevated, though the displacement of the heart is much less than is met with in Cirrhosis. Occasion- ally, however, as we have seen, the same upward traction occurs in Cirrhosis. In both there is frequently cough, expectora- tion, failure of nutrition, and often haemop- tysis. The existence of well-marked signs of cavities of a stationary character, such as are due to dilated bronchi in Cirrhosis, would be absent almost universally in cancer. The condition of cachexia is generally more marked, however, in can- cer, as well as the amount of intrathora- cic pain; and the disease is often more rapid in its progress, its duration being sometimes much less, and never exceed- ing two and a half years. As Dr. Walshe points out, also, cancer of the lung is 1 In this latter case the lower lobe of the right lung is said to be the most frequent seat of the disease. 2 Charcot says: "Cela eut et6 cependant fort interessant; car dans la pneumonie aigue, oil l'absence de tout bruit respiratoire, nor- mal ou anormal, s'observe quelquefois, c^ phenomene parait en general dependre de I'obstruction des tuyaux bronchiques des parties hepatisees par une grande quantity de liquide visqueux ou par un bouchon d'ex- udation concrete." A similar temporary si- lence has been occasionally observed in cases of bronchiectasis. 304 CIRRHOSIS OF THE LUNG. generally associated with a mediastinal tumor of the same nature, so that not only may the morbid percussion note extend across the middle line, but there is apt to be greater dyspnoea, with lividity of face, and other pressure signs-such as dilata- tion of the superficial veins, and oedema of the thoracic parietes. In cases of cancer of the lung, moreover, cancerous tumors may exist in other parts of the body, and towards the last the cancerous cachexia often becomes extreme. This affection could, therefore, as a rule, only be confounded with the more acute forms of Cirrhosis. " Tubercular" disease of the lung, pre- senting such characters as would render it liable to be confounded with Cirrhosis, is only encountered with extreme rarity. The characters of the latter disease which are most opposed to those of the more ordinary forms of phthisis are the signs indicative of an almost absolute freedom from morbid deposit in one lung, com- bined with the gravest amount of implica- tion of the other-producing, perhaps, not only retraction of the side, but also cavi- ties, and more or less complete imperme- ability of the lung-tissue between them. Then with local signs of so pronounced a character on one side (whilst the other lung appears to remain intact), we not only have no laryngeal disease, but there is a comparative absence of the constitu- tional symptoms peculiar to phthisis : so that there is an utter disproportion be- tween the gravity of the local and the constitutional signs, and at the same time the disease presents a comparatively stationary character. Cirrhosis also fre- quently exists in previously strong indi- viduals with well-formed chests; and, in one-third of the cases, there have been signs of hypertrophy and dilatation of the right heart, associated with dropsy. Only the contraction of an enormous tubercular cavern could produce such an amount of displacement of the heart as we frequently meet with in Cirrhosis ; and that such an amount of disease and disorganization of one lung as this implies, should have ex- isted without the least implication of the other, is contradictory to all experience as to the nature of ordinary phthisical affec- tions. Any great contraction occurring in a "tubercular" lung is almost certain to be due to a considerable admixture of fibroid substitution with the other morbid product, so that the points of diagnosis just considered may be said to be those distin- guishing the. pure fibroid from the mixed fibroid and "tubercular"-or rather fibroid and pneumonic-forms of phthisis.1 Simple general collapse of one lung is a condition of extraordinary rarity, which, as Dr. Walshe says, could only result from the pressure of an aneurism or a ru- mor upon the main bronchus. In such a case, in addition to the signs of the tumor wdiich might exist, there would in all probability, be a dull, toneless sound on percussion, instead of resonance of a wooden or even tubular character, whilst the respiration would be simply weak in- stead of bronchial, with more or less signs of cavities. Simple primary bronchiectasis of one lung may exist, and then be followed by more or less fibroid induration of tissue.1 Many of the signs and symptoms of this disease would be similar to those of Cir- rhosis ; only, in the early stages, the signs of cavities would be marked, whilst those indicating consolidation of the inter- vening lung-tissue would be comparatively slight. The signs of retraction of the chest and displacement of heart are al- most or completely wanting. Prognosis.- In almost all cases, the individuals suffering from this disease are ultimately carried off by an acute affection of the hitherto sound lung. An attack of bronchitis or a pneumonia supervenes, or a mixture of these two conditions, and the breathing power becomes so seriously interfered with, that the patient rapidly dies in an asphyxiated condition. Death may take place, also, from gangrene in the cirrhosed lung ; or a copious effusion of blood proceeding from an ulcerating cavern in the lung may prove fatal-al- though usually the amount of blood lost in this way is not extreme. In those cases hitherto styled " chronic pneumonia," and in which an extreme amount of fibroid induration follows an attack of acute pneumonia, the patient is apt to die in a state of marasmus, or from uncontrollable diarrhoea, before the local disease has attained its maximum-that is to say, before much contraction of the lung has occurred, or many bronchial caverns have been formed. Death may also take place, however, when the disease is fully established, without the advent of acute inflammation experience. Dr. Clark says (Trans, of Clinic Soc. vol. i. p. 188): "Experience has peremp- torily taught the writer, that the occurrence of ulceration of the bowels in the course of chronic disease of the lungs is not conclusive as to its tubercular nature. Deposits in and ulcerations of the intestinal glands may occur in almost any form of chronic disease to which the lung is liable." 1 In rare instances, as before stated, owing to the amount of secondary induration and contraction, some of these may actually de- velop into cases where the cirrhosis becomes the most prominent feature. * With reference to the presence or absence of diarrhoea, it will be well to bear in mind the following remarks by Dr. Andrew Clark, which are in perfect accordance with my own TREATMENT. 305 in the opposite lung, but gradually, owing to the mere exhausting influence of the disease-when it is associated with marked bronchiectasis, and when the amount of purulent fluid daily expectorated is ex- treme. The occurrence of dilatation of the right side of the heart to such an ex- tent as to produce tricuspid regurgitation, is, of course, a most grave complication. In other cases, the patient is cut off by some acute or chronic coexisting malady, such as disease of the brain, cancer of the stomach, or uncontrollable diarrhoea from ulceration of the caecum-diseases which actually proved fatal in a few of the cases included in my list. Although the ultimate prognosis in this disease is most grave, still, if the sound lung can be maintained in its condition of health, the fatal termination may be warded off for some time, and the indi- vidual may live for years after the disease has been fully established. Treatment.-The indications in this disease are to pay prompt attention to the very earliest signs of bronchitis, or pneu- monia in the non-cirrhosed lung, so as, if possible, at once to arrest its progress. The patient's life should, moreover, be so regulated that, whilst exposed to wet and cold as little as possible, he may be brought under the influence of habits which are best calculated to promote the general health. The development of the non- cirrhosed lung should be favored by such carefully regulated exercise as can be in- dulged in without distressing the heart's action or causing much dyspnoea. Plenty of time should be spent in the open air; the diet should be good, simple, and nour- ishing ; and the functions of the skin should be stimulated by the daily use of baths and dry friction. Whilst these general measures are being adopted, their action may be supplemented, when neces- sary, by various medicines. The dilute mineral acids or salts of iron, combined with bitter infusions, or iron and quinine, may be had recourse to ; whilst in some cases, cod-liver oil, either alone or com- bined with iron, will be of much use. In cases where diarrhoea sets in, every effort must be made to arrest this by the careful administration of dilute sulphuric acid, or by opiates and the various vege- table astringents ; and, in like manner, where dilatation of the bronchi is well marked, and the daily flux from these is excessive, we must endeavor to check the copious flow by the administration of as- tringents combined with balsamic reme- dies (such as tolu, copaiba, or turpentine), and an application of counter-irritants externally. Where necessary, also, we must endeavor to bring about a regular and periodical evacuation of the dilated bronchi; so as to prevent decomposition of the retained secretion within the tubes, which is liable to produce general distress, and may also entail local gangrene. For this purpose Niemeyer strongly recom- mends the inhalation of turpentine two or three times a day. About half a drachm of the spirits of turpentine is to be placed in a bottle of hot water, and by means of some suitable addition to the neck of the bottle its vapor is to be inhaled. In this way the amount of secretion not only is diminished, but violent fits of coughing are induced in from ten to fifteen minutes, which are accompanied by an evacuation of the contents of tlie dilated bronchi. Niemeyer says he has seen great ameliora- tion thus induced in the symptoms of pa- tients whose condition had been previously most distressing. With regard to the possibility of bring- ing about an actual disappearance of the new fibre-tissue, and a reappearance of the lung-tissue which it has supplanted, this seems a result beyond our most san- guine expectations, and one to which we are scarcely likely to attain. But, whilst the disease is still advancing, we may hope and ought to endeavor to prevent the spread of the morbid change to pre- viously healthy portions of lung-tissue. This desirable result will be best brought about, not only by the means before al- luded to, which are destined to bring the patient's general health up to the highest possible standard ; but will, perhaps, be also encouraged by the use of iodide of potassium internally, in conjunction with counter-irritation to the affected side, and the free inunction of iodine locally. As Dr. Walshe suggests, a trial might also be made of some of the natural iodurated water, such as those of Kreuznach or Woodhall. The amount of influence which the iodides have in checking the over-growth of fibre-tissue seems in some cases to be most marked, and in a disease of so grave a character as this we are bound to try the influence of remedies which may have a favorable action, so long as they exercise no deleterious effect. vol. ii.-20 306 APNEUMATOSIS. APNEUMATOSIS. By Graily Hewitt, M.D., F.R.C.P. Definition-.-Apneumatosis is that condition of the lung-tissue characterized by the return of certain air-cells to a quasi-fetal state ; the portions of lung so affected have once been physiologically active and efficient in promoting the res- piratory change in the blood circulating through them, and have ceased to be so. History.-The older observers of the diseases of children record the great fre- quency with which they found after death certain parts of the lungs solidified. The death was in such cases attributed to this alteration of the lungs ; and as it resem- bled, in many of the outward appearances observed, the solidification found in the lungs of adults, and which had received the name of " pneumonia," they naturally enough gave the two conditions the same name. Only within a comparatively re- cent period has it been established that the two conditions are essentially different. One circumstance, however, was ob- served as peculiar. The consolidation was always in the cases of young children seen to be abruptly separated from the adjoining sound lung, to be mapped out as it were by the lobular divisions of the lungs. Hence it was called "lobular pneumonia." It was said that in the case of infants and young children the pneumonia was lobular. The mortality from the disease so-called was found al- ways to be very considerable, and hence children were considered to be par excel- lence predisposed to pneumonia. Valleix1 has given an admirable account of this lesion. Unable, however, to re- concile the facts observed with the theory that the lesion in question was true pneu- monia, he thus expresses himself: "La forme particuliere de cette hepatisation ma parait done inexplicable dans 1'etat actuel de la science." Before Valleix, Gerhard and Rufz and De la Berge had described in a very suggestive manner the peculiarities attending this alteration of the lungs in young children, both in respect to its essential characters, and to the circumstances under which it was found to be present. Earlier still, Leger pointed it out as peculiar pneumonia un- der the term "latent." Seifert1 recognized the nature of the so- called lobular pneumonia so far as its mode of production was concerned, giving it the name of "bronchio-pneumonie," and he pointed out the counterpart of the lesion in that kind of pneumonia seen in adults which Laennec termed "peripneu- monie des agonisants," and Piorry "pneu- monic hypostatique. " There is reason to believe, however, that some of the cases alluded to by him were really cases in which the lung had never been expanded at all at the affected parts, but remained from the day of birth in the state described and truly explained by Jorg as atelectasis. Barthez and Rilliet2 first, in 1838, dis- tinguished between "lobular" and "lo- bar" pneumonia, laying down the princi- ple that lobular pneumonia was always a secondary affection connected with bron- chitis. MM. Legendre and Bailly,3 however, have the merit of first pointing out the essential nature of the condition known as lobular pneumonia. They used the very simple expedient of artificially in- flating the lungs after death, and observed the effect of the inflation on the portions consolidated and in a state of lobular pneumonia. The result was, that the apparently hepatized parts swelled out, became filled with air, and were, as it seemed, suddenly converted into healthy- looking lung-tissue. The lung so inflated was found to possess all the physical char- acters of lung in a normal condition, and it was evident to these observers that the essential difference between the pseudo- hepatized and the sound lung only con- sisted in this,-that in the former case the air was withdrawn from the air-cells, the tissue of the lung itself not being necessarily altered. They were led to this result by observing how closely the lobules so collapsed resembled in external characters those of the lungs of the foetus which has never respired ; hence they re- placed by the term "etat foetal" the old designation "lobular pneumonia." The results of this discovery have been most important in enabling us by a simple and easily applied test to ascertain whether 1 Die Bronchio-Pneumonie der Neugebore- nen; Berlin, 1837. 2 Traite des Maladies des Enfants. 3 Archives de M^decine, 1844, p. 157. 1 Clinique des Maladies des Enfants nou- veau-nes, p. 197 ; Paris, 1838. PATHOLOGICAL ANATOMY. 307 the condition of the lung present in a par- ticular case is one only of collapse, or whether it is due to a change of another character altogether. MM. Legendre and Bailly showed that in the cases in which their "etat foetal" was present, there was no true inflamma- tion of the lungs present such as would entitle them to be considered as cases of true pneumonia; pneumonia, as it is gen- erally understood, being constituted by a breaking-dowm or softening of the lung substance, whereas in cases of lobular pneumonia the lung-tissue is quite firm, and, with certain exceptions, not easily broken down under the finger. The pe- culiar limitation of the morbid change to certain lobules, the change beginning and ending abruptly, and not shading off gradually, also evidently gave to it a character altogether distinctive, and such as is not found in true pneumonia. Ref- erence more in detail will, however, be made to these several points further on. The subsequent history of " lobular pneumonia" will include an account of the more or less complete adoption by re- cent writers of the views of MM. Legen- dre and Bailly. By West, Gairdner, and Jenner, the terms "bronchial" or "pul- monary collapse" are used instead of "etat fcetal." The term "Apneumato- sis" was first employed by Fuchs1 in an excellent treatise on the subject, and its adoption was recommended by myself in a paper read before the Royal Medical and Chirurgical Society of London.2 The old term "lobular pneumonia" being cal- culated to give very erroneous ideas of the condition to which it is applied, a new term was necessary. "Pulmonary col- lapse" was not sufficiently distinctive, the word "collapse" being already in use, and very properly, in another sense, to indicate the spontaneous collapse of the lungs, which always occurs to a greater or less degree on opening the thorax after death. In the absence of a better, the word Apneumatosis (a, privative, and a condition of being filled with air) was considered the most appropriate, expressing, as it does, precisely the condi- tion which is present,without involving any theory as to its cause or mode of origin. Apneumatosis is not simply an anatomi- cal alteration; it must be regarded as a diseased condition of the lung manifesting itself by a variety of symptoms and signs, producing certain important effects on the system at large, and very frequently prov- ing fatal. Its importance fully justifies its being considered separately from bron- chitis, with which it is always, or almost always, associated. The bronchitis of early childhood is, when fatal, almost in- variably attended with Apneumatosis. Pathological Anatomy.-A descrip- tion of the physical characters of those portions of the lungs affected with Apneu- matosis will in reality include more or less completely a description of those le- sions variously designated by authorities up to the present time as Disseminated Lobular Pneumonia, Cornification, Pulmo- nary Collapse, etat foetal," Marginal Pneumonia, Catarrhal Pneumonia (Roki- tansky), Dronchio-Pneumonie (Seifert), to- gether with some of those described as Atelectasis, all these terms applying to one condition which is somewhat modified in certain cases. The account given by Legendre and Bailly of the physical characters presented by the lung so affected is remarkably true to nature, and our own observations, as well as those of others, confirm the accu- racy of the facts stated by the authors in question. There is no material difference between Apneumatosis and Atelectasis, anatomi- cally speaking, and it would be exceed- ingly difficult, judging from the mere physical characters present, to distinguish between them. In the first place, the lobules affected are remarkably distinct; abruptly sepa- rated from adjoining healthy lobules, gen- erally depressed below the surface of the healthy lobules ; for the most part they are found at the margins of the lobes,- those portions of the lobes most distant from the root of the bronchial tree. The distribution of the afiected lobules is evi- dently connected with their relation to the divisions of the bronchial tubes, and is such as to preclude the idea of the affection having spread by simple con- tiguity. The lobules supplied by one par- ticular bronchial tube all present the physical characters of the lesion, whilst the lobules supplied by the closely con- tiguous bronchial tube may be perfectly healthy. The number of lobes affected is of course subject to great variety : it oc- casionally happens that the whole of one particular lobe is affected, but this is not very frequently observed, and it most commonly happens that nearly all the lobes present a greater or less number of apneumatic patches, although it is some- what rare to find apneumatic portions present in all the lobes.1 Certain parts of the lungs present this lesion with re- markable frequency. These are, first, the lower margins of the lower lobes of both lungs, the tongue-like prolongation of the upper left lobe, and the middle lobe of the right lung. Next in order come the pos- terior surfaces of the lower and of the 1 Die Bronchitis der Kinder; Leipzig, 1849. 2 See Proceedings of Roy. Med. and Chir. Soe. No. I. 1 See Valleix, op. cit. p. 62 et seq. 308 APNEUMATOSIS. upper lobes. The order of occurrence here laid down is rarely departed from, a very interesting circumstance, and one which will again be alluded to in consid- ering the essential nature and mode of production of the lesion in question. The lobules situated at the periphery of the lung are thus the first affected, and in slight cases the alteration is confined to them. In many cases the apneumatic patches are symmetrically placed on the corre- sponding parts of each lung. This is especially the case with the posterior sur- faces of the lower lobes, where we have frequently observed a line concave supe- riorly passing across this aspect of the lobe on each side, and forming the upper boundary of an apneumatic portion of the lung almost identical in form and equal in superficies on the two sides. It generally happens, when Apneuma- tosis of the kind to which the description given above would apply is present, that the healthier parts of the lungs are pitted and depressed at certain parts, and these depressed portions have a rather darker color than usual. The little pits are caused by the partial collapse of the air- cells there situate, and, although slight in degree in particular lobules, the aggregate number of air-cells thus rendered useless may be very considerable. Apneumatosis thus slight in degree disappears com- pletely on inflation, and between this and the more complete form involving the ■whole of several adjacent lobules, many gradations may be witnessed. To the naked eye the apneumatic patches appear like islets of a darkish- red colon abruptly separated from the lighter and more healthy lobules, and having a sharp determinate outline. On a more minute inspection fine whitish streaks are evident on the surface, divid- ing the affected portions into compart- ments. These indicate the boundaries of the small lobules affected, and it is thus evident that no inflammatory destruction of the lung substance has taken place. With reference to the color of the afiected patches, nothing is more variable. The lung of the young child is naturally of a light-pink color, and the various shades of darkish-red presented by the apneumatic lobules contrast in a striking manner with the lighter and more healthy portions which lie close to them. The typical color is a darkish-red. with a shade of violet. The intensity of the color present often depends on the degree to which the lobules are congested. Sometimes the color is a lightish-red, like that of a piece of anse- mic muscle, but at other times it is a deep purple ; and between these two extremes many varieties of color are observed. The depth to which the lung tissue is affected is in an almost direct ratio to the degree in which the lung is seen to he ap- neumatic superficially. Section of the part shows the same definite limitation of the Apneumatosis which is evident externally: the shape of the portion of lung involved in the change is determined by the out- line of the lobules to which certain bron- chi are distributed, and each apneumatic portion has thus a more or less pyramidal form, the base of the pyramid being to- wards the periphery. The apneumatic lobules are generally depressed below the level of the adjacent part of the lobe. This is not always the case however. When these lobules are less in bulk than usual, they have a somewhat lighter color than in the other condition of things. Thus the apneumatic portions which are of a deep violet color have usually the normal bulk, and may even exceed it. This circumstance is connected with the greater or less quantity of blood contained in the vessels of the part. The consistence of the apneumatic lobules is open to some variation. This is in like manner connected with the quantity of blood within the vessels of the part, and also with the length of time the lesion has existed. The paler, less bulky lobules have a loose texture exactly resembling that of a piece of flesh : the anterior tongue of the left upper lobe often pre- sents this peculiarity. The more con- gested and darker parts have, on the contrary, a very firm consistence, much resembling that of a piece of liver, and resist pressure much more effectually than the looser portions. In all cases the ap- neumatic lobules are found to sink in water. The section is very smooth and even, and when the part is much con- gested it resembles that of a firm clot of blood. The bronchi cut through often contain mucous fluid in considerable quantity. Where the lobe is thin, as in the anterior tongue of the upper lobe, the lobules are in many cases felt quite dis- tinctly between the fingers. This is due to the fact that the air-canals within the individual lobules are filled and distended with mucous secretion, which everywhere extends into the air-cells. This peculiar feel is lost on cutting through the lobules in question, for the fluid then escapes out of the cut vessels. This extremely distended state of the air-channels is chiefly found in those parts in which less congestion is evident. Inflatability.-The most important cir- cumstance, however, in reference to the apneumatic lobules is the absence of air. No air-cells are visible on the pleural sur- face, none on the surface of the section. The difference presented between two parts of the same lobe, one of which is apneumatic and the other healthy, is in this respect most remarkable. All around the affected lobule the air-cells are most PATHOLOGICAL ANATOMY. 309 distinct and evident: none are visible where the Apneumatosis exists. These lobules are, in fact, as a rule completely destitute of air ; the opposite walls of the air-cells are in apposition; the finer air- tubes are either tilled with fluid or in the same condition as the air-cells themselves -i. e. collapsed. As a consequence of this non-aerated state of the lobules, they are found to be absolutely non-crepitant on pressure. If a blow-pipe be intro- duced into the bronchus leading to the collapsed portion, and air be then forcibly injected, an instantaneous change takes place in the color, appearance, and phys- ical characters of the apneumatic lobules : they swell out, become of a light rose-red, air-cells are at once visible on the surface, and the affected lobules come to so far re- semble the adjoining healthy ones, that they are not to be distinguished from them. As has been already stated, this effect of insufflation was first pointed out by MM. Legendre and Bailly. Now the effect of this insufflation is not always the same. It is not always entirely successful, some portions of the affected lobules resisting this forcible refilling of the air-cells. As a rule, the operation is performed easily and with the use of very little force, and it always partially succeeds. The por- tions which resist the attempt to intro- duce air are those which are the most congested, and in these small portions re- main uninflated, whatever may be the force used by the lungs of the operator. This point it is important to remark upon, for there is reason to believe that a want of success in the operation of inflation in cases of the kind alluded to, has induced some observers to doubt the correctness of the general statement with reference to the nature of the lesion now under dis- cussion. The fact is, however, that where the Apneumatosis and considerable con- gestion coexist, the pressure of the contents of the bloodvessels effectually prevents the re-distension of the air-tubes, and air cannot be made to pass into the ultimate air-cells. A difficulty of the same kind occurs when the air-tubes are much dis- tended with fluid secretion, but here it is hardly ever practically productive of much opposition to the operation of inflation. After inflation has been performed the dilated air-cells have a tendency to col- lapse again in a short time if the bronchus leading to them be not tied. The operation of inflation is to a cer- tain point a test of the presence of Apneu- matosis as distinguished from pneumonia. In Apneumatosis, as has been already explained, it generally succeeds. In pneumonia, however, the lung-tissue can- not be restored to its natural appearance by inflation. It is not often that an op- portunity presents itself of verifying this statement so far as the pneumonia of children is concerned, it being very rare to meet with true hepatization at this period of life, but in two or three cases which have come under our notice this verification has been completely effected. Lastly, the pleura is almost invariably found to be healthy in cases of Apneuma- tosis, uncomplicated with diathetic dis- ease ; in pneumonia it is just as rare to find it free from disease. The physical characters of Atelectasis as distinguished from those of Apneumatosis.- The two conditions are almost identical, anatomically speaking, and in some in- stances, indeed, the history and other particulars of the case must be examined in order to decide the matter at issue. Some go so far as to say that Apneuma- tosis and atelectasis are one and the same thing, that the lobules presenting the characters described above as those of Apneumatosis have never been expanded at all, and have been in the condition in which they are found.1 The grounds on which this statement is made are very insufficient, and will not bear examina- tion. The following fact is quite suffi- cient to settle the contested point: a child, previously healthy, is seized with a catarrhal affection of the air-tubes; up to that time there has been evidence that the act of respiration has been habitually performed in a regular manner; after a few days the child dies, and a large por- tion of all the lobes is found collapsed ; the physical signs and symptoms, during the last few days, having indicated, step by step, the progressive and increasing disease of the lungs. A few instances, perfect in every particular, it is not a dif- ficult matter to collect. With such an amount of lung implicated in the lesion it is difficult to conceive that symptoms could have been previously absent. A weakly child affected with atelectasis is easily the prey to bronchitis, and this lat- ter affection is so fatal because in such a case it is so often followed by Apneuma- tosis. This seems to be the proper way of stating the relation of the two lesions, atelectasis and Apneumatosis, one to the other. When the lung has undergone mechan- ical compression, and thus become hard- ened, reduced in bulk, as in cases of pleu- ritic effusion, &c., its physical characters to a certain degree resemble those of Apneumatosis. It seems desirable to re- strict to this condition the term ramifica- tion. Carnified lung is firmer and denser than is the case in Apneumatosis, and differs from it in the essential particular that it is not susceptible of inflation; added to this, the peculiar circumstances 1 Such appears to be the opinion of Friedle- ben. " Ueber die Pneumonie der Kinder," in Archiv, fur physiologische Heilkunde, 1847. 310 APNEUMATOSIS. under which it is found are sufficient to establish its true identity. In order to prevent unnecessary confusion we have hitherto described only Apneumatosis of a typical character, or rather Apneuma- tosis in which the condition of the air- cells present is one of simple collapse. The air-cells are destitute of air, their walls are in apposition. In certain cases, however, on the surface of the apneumatic portions are seen little elevated oval or rounded spots of a yellowish-white color, resembling at first sight tubercular masses. These little cavities are situated imme- diately under the pleura, communicating freely with the bronchial tubes. They are the "granulations purulentes" of Fauvel. They are for the most part, ac- cording to our own experience, found in portions of lung affected with Apneuma- tosis, but they may be found in other situations, and are not therefore perhaps so entirely a part of this affection as to justify their being considered fully in this place. It will suffice here to say that in chronic cases in which Apneumatosis is present the little cavities in question are rarely absent. They are often described as "bronchial abscesses," "vesicular bronchitis," &c. Etiology. - Apneumatosis is a me- chanical effect of the presence of certain morbid conditions of the air-tubes, these morbid conditions appearing to be par- ticularly efficacious in the production of Apneumatosis during infancy and early childhood. Catarrhal inflammation of the bronchi, either existing per se, or forming a part of other diseases, is a very common affection in early childhood, and Apneumatosis is one of its effects, the presence of a mucous secretion in the finer air-tubes preventing the due aeration of the lobules to which they lead. The connection between the two circumstances, excessive secretion and collapse of the air-cells, is one which is supported by considerations the result of experimental and pathological inquiry. It appears that any obstruction of the bronchial tubes is sufficient to produce after a time the appearances of Apneu- matosis in the distal lobules. The experi- ments of Mendelssohn and Traube, de- scribed by Fuchs,1 are especially interest- ing as demonstrating this fact. In one of these experiments tracheotomy was performed on a dog, and a shot intro- duced which was afterwards found in the left bronchus. In two days death took place, and the appearances found were as follows:-The right lung was emphyse- matous, enlarged ; the left lung was col- lapsed, its lower lobe was in great part congested, devoid of air, and also the upper lobe in certain parts, near winch lay emphysematous patches. Inflation distended the whole lung. In other ex- periments, a like effect was produced by the introduction of a ball of paper, certain portions of the lungs becoming hard, con- densed, and no air-cells being visible on the surface. The resemblance between these cases and those of children affected with Apneu- matosis due to the obstruction produced by the bronchial secretion is, as Fuchs remarks, at once apparent. The relation of bronchial obstruction to pulmonary co- hesion, also indicated by Legendre and Bailly, has been more completely devel- oped by Dr. Gairdner,1 so far as the me- chanism of the process is concerned, with whose acute and original remarks our own almost completely agree. Dr. Gaird- ner has demonstated the nature of certain lesions of the lungs, met with in adults, and identified them with Apneumatosis. " Bronchitic" collapse, as he describes it, is therefore not peculiar to children, al- though very much more common in them than in adults. Dr. West gives to the theory of the connection between bron- chial obstruction, produced by secretion, and "pulmonary collapse," his entire support, in common with Bailly and Le- gendre, laying also some stress on the imperfect inspiratory power of weakly in- fants as an additional predisposing ele- ment in the production of the lesion in question. Gairdner's satisfactory and lucid explanation of the rationale of the process by which Apneumatosis, or col- lapse of the lung, is produced, is as fol- lows :- Commenting on the experiments of Mendelssohn and Traube, before alluded to, he says, "It is clear, therefore, from experiment, as well as from pathological observation, that the most usual and most direct effect of obstruction, or of diming ished calibre of the bronchi, however caused, is not accumulation" (as Laennec had contended), " but diminution in quan- tity of the air beyond the obstructed point." The author then shows that an- other mechanical condition which comes into play in producing collapse from ob- struction is to be found in the form of the tubes; these diminishing in size as we approach the periphery of the lung ; con- sequently, if the calibre of a tube be nearly filled at one point by a plug of mucus, the effect of inspiration, propelling it towards the air-cells, will be to completely close the tube, when it arrives at a part the calibre of which is less than that which it originally occupied. The plug of mucus will thus act as a ball-valve, and at every 1 Loc. cit. p. 61 et seq. 1 On the Pathological State of the Lung connected with Bronchitis and Bronchial Ob- struction: Edin. Monthly Journal, 1850-51. ETIOLOGY. 311 expiration a portion of air will be expelled, which, in inspiration, is not replaced. In the end, the lobule to which the bronchus in question leads, contains no air at all, and the condition to which it is reduced is one of Apneumatosis. Fuchs, in the work referred to, and also quoted by Gairdner, accounts for the disappearance of the air from the lobules, by supposing it to be absorbed by the bloodvessels, having been first shut in and confined by the presence of mucus in the tubes, these latter ha ving, moreover, their calibre diminished by the thickening of the mucous membrane al- ways present. Dr. Gairdner's explana- tion is rather too much dependent on the supposition that the bronchi contain a tenacious, viscid material; this may be the case in adults, but in the case of chil- dren an examination of a considerable number of cases has convinced us that the bronchial tubes are rarely found to con- tain mucus having the characters of te- nacity and viscidity : in almost all cases indeed, the mucus readily flowed out of the vessels when cut across, and had the consistence of thin pus. Here of course Dr. Gairdner's explanation also holds good, but it is only necessary to add that tenacity and viscidity of the contained mucus is not an indispensable element in the explanation in question. With reference to the opinion of Fuchs as to the cause of the disappearance of the air, it is probable that it is in part true; the fact of the disappearance is suffi- ciently accounted for by a combination of the theories of both of the authors. If such absorption take place, it is natural to suppose that the oxygen will disappear first, and be replaced by carbonic acid; this latter product being'readily dissolved in fluid will also finally be carried away, together with the nitrogen. The dark coloring of the apneumatic portions Fuchs attributes to the excessive quantity of carbonic acid present. The inability to cough and expectorate is another circumstance to which Dr. Gairdner alludes as a cause of bronchitic collapse. It appears to us, however, that this is rather to be looked upon as a con- sequence than as a cause of the collapse, at least at the commencement. The effi- ciency of the cough in expelling mucus from the tubes is dependent on the pres- ence of air in that part of the tubes be- yond the obstruction. Each lobule is a miniature lung, and the sudden expulsion of the air from the lobules drives the ob- structing agent before it. As long, there- fore, as the air-cells contain air, so long will the cough aid in the expulsion of mu- cus from that part of the lung. When the Apneumatosis has been produced in cer- tain lobules, those lobules are in great part unaffected by the cough, and there is no expulsion of mucus from the air-tubes with which they are supplied. The Ap- neumatosis is thus perpetuated by the in- ability to cough and expectorate, but it is not produced by it except in a secondary manner. The fatal result of cases in which Apneumatosis occurs is probably con- nected with the absence of expectoration, and the imperfect character of the cough.1 It is evident that the condition here supposed to be effective in the production of Apneumatosis is only the last step of the process. Why, it will be inquired, is Apneumatosis so especially common in young children, while it is so rarely ob- served in adults ? In the first place, it must be answered that Apneumatosis is not so rare in adults as has been imagined, which fact is shown by a perusal of Dr. Gairdner's papers just alluded to; his statement being in great part, indeed, founded on observations made in adults. But, on the other hand, it cannot be de- nied that Apneumatosis is comparatively much more common in early life, and there must accordingly be certain power- ful predisposing circumstances leading to this result, favoring circumstances or conditions, without which Apneumatosis would not more readily occur in the one than in the other. These predisposing circumstances it may be well to consider a little more closely. Whatever tends to lessen the intensity of the inspiratory effort, and thus to impair its efficiency, will certainly favor the oc- currence of Apneumatosis. The intro- duction of air into the air-cells is the re- sult of a mechanical process, the walls of the chest are separated, and the diameters of the chest increased by the action of certain muscles: the lungs follow the walls of the chest, and increase in bulk, and air is driven in to fill up the vacuum which would otherwise exist within the chest. The principle, indeed, precisely resembles that of the pump. Now, in order that a pump may act efficiently, a rigid state of the walls of the tube which the piston traverses is necessary; the at- mospheric pressure would otherwise pro- duce collapse of these walls. In like manner it is necessary that the parietes of the chest be sufficiently rigid to prevent their being driven inwards by the pressure of the atmosphere from without during the process of inspiration. The walls of the chest in the child are very far from presenting that firmness and resistance which is observed in the adult; the result of this is that at certain situations the ribs fall inwards during the act of inspira- tion, and at the corresponding part of the lungs little expansion of the pulmonary tissue occurs.2 This collapse of the tho- racic walls may sometimes be observed in infants who are breathing vigorously when 1 Dr. Stokes. 2 Rees. 312 APNEUMATOSIS. the air-tubes are everywhere quite patent. The diaphragm, which is the chief inspi- ratory muscle in early life, also tends to draw in the chest-walls at the points of the ribs to which it is attached, if those walls do not present a sufficient degree of rigidity. The point at which the chest- walls most readily give way is at the junc- tion of the cartilages with the ribs, and the ribs which more especially exhibit this want of power to resist the atmospheric pressure are those just above and below the nipple, the fourth to the seventh in- clusive. Not unfrequently a groove may be observed passing downwards at the junction of the cartilages with the ribs on each side, marking the degree to which these parts have given way. Rickets is a frequent source of this, rendering the bones more pliant than they should be. Sir William Jenner has particularly dem- onstrated the great influence of rickets in producing this result. Another circum- stance which acts in a somewhat different way, is congenital or induced general weakness. In this case, the muscles which elevate and draw asunder the ribs are not powerful enough to withstand the opposing force of the diaphragm; the ribs here may be rigid enough, but the muscles are in- capable of retaining them separated and elevated, while the diaphragm acts. A combination of the conditions here men- tioned-viz., deficient rigidity of the bones or framework of the thorax, and deficient power of the muscles-will obviously have a very considerable influence in diminish- ing the efficiency of the inspiratory act. But under ordinary circumstances na- ture provides a remedy for these defects. If the chest-walls give way at one point, and the diameter of the thorax be thus diminished in that situation, it is increas- ed in a corresponding degree at another situation. It is only when to the me- chanical defects here pointed out others are added that serious diminution of the oxygenation process results. We have hitherto supposed the channels by which the air is admitted to the air-cells to be free. If any obstruction arise in the bron- chial tubes, the mechanical defects first described enhance in a very considerable degree the difficulty which the child expe- riences in performing an efficient inspira- tory act. The already defective apparatus is impeded in its action, and the quantity of air inspired is proportionately small. Catarrhal inflammation of the air-tubes is generally the origin of the obstruction in question. It produces, in the first place, a swelling of the mucous membrane, and secondly, a secretion of fluid; the one diminishing the calibre of the air-tube, the other obstructing it. Unless the child possess sufficient strength to over- come this obstruction (a strength often wanting) by exercising a greater effort than usual, Apneumatosis of certain parts of the lung will be produced in the man- ner previously described. The fact that, on the one hand, the small air-tubes are proportionately less in the child than in the adult (Fuchs), and on the other, that bronchial inflammation is so exceedingly common in childhood, will present condi- tions highly favorable for the production of the lesion, coupled, as they often are, with the partly inherent defective mech- ism of the inspiratory act at this period of life. The researches of Hutchinson and others have shown that the act of inspira- tion is one-third less powerful than that of expiration. Under the morbid condi- tions just pointed out the disadvantage under which the inspiration labors is in- creased, while the efficiency of the ex- piratory effort is but little impaired. All the conditions mentioned are such as render the inspiration more difficult, and tend to prevent the passage of air into the air-cells. Inspiration being entirely de- pendent on muscular effort, is directly in- fluenced by the degree in which that effort can be exercised, subject to certain modi- fications already pointed out; whilst the expiratory act being in part the result of the reaction of the elastic tissue of the lung, is much less liable to alteration of this kind. This, then, is another circum- stance facilitating the removal of air from the air-cells when the tubes contain an undue quantity of fluid, the obstruc- tion interfering with the inspiratory, but not to a corresponding degree with the expiratory, effort. A condition which somewhat interferes with the inspiratory act is undue disten- sion of the abdominal cavity, from what- ever cause.1 The diaphragm cannot de- scend to the full extent necessary, and less air than usual enters the chest. In common with most of the other conditions named this distension of the abdomen will not be effective in the production of Apneumatosis, unless coexisting with obstruction in the air-tubes themselves. The practice which often prevails of bind- ing up the abdomen of the infant tightly must act in precisely the same way, and if the child be attacked with bronchial catarrh it is not difficult to conceive that the mechanism of the inspiratory act may be so impaired, under this combination of evils, as to favor the occurrence of Apneu- matosis. Certain affections of the air-tubes more readily than others produce obstruction and consequent Apneumatosis. Infants having portions of their lungs in a state of atelectasis are more liable to suffer from Apneumatosis than those in whom > This point has not escaped the notice of Dr. Gairdner (loc. cit.). ETIOLOGY. 313 the lungs have been fully aerated at birth: atelectasis is therefore a predisposing cir- cumstance. Apneumatosis is not by any means fre- quently observed, in such a degree at least as to prove fatal, after the age of five or six years; it is very common, however, before this period, and in general terms its frequency may be said to be inversely as the age. " The first few months of the infant's life are those in which the lung most readily returns to the quasi-foetal state, loses its gaseous contents, and be- comes apneumatic. As the muscular power becomes greater, and the frame- work of the thorax becomes firmer and more consolidated, Apneumatosis less commonly occurs. The mortality from affections described in the Registrar-Gen- eral's Reports as pneumonia, hooping- cough, bronchitis, and influenza, in the first year of life, is a rough index of the comparative frequency with which Apneu- matosis occurs at this period of life. The result of examination of a large number of cases of children dying from bronchitic and allied affections during the first year of life, was, that with hardly an excep- tion Apneumatosis was present in all, other complications being in many cases also noticed. I am inclined to speak less positively of the state of the lungs present in children dying of such affections after the age of about five years, opportunities being much more rarely afforded of study- ing the post-mortem changes after this period. In round numbers the deaths during the first five years of life, and set down in the Registrar-General's Reports under the heads Hooping-cough, Influenza, Bronchitis, and Pneumonia, amount to 25 per cent, of the total mortality at those ages; between the ages of five and ten years, they amount to 10 per cent, of the total mortality ; between the ages of ten and fifteen, to 5 per cent. After the sec- ond year the mortality from these dis- eases gradually diminishes : the inference to be drawn is, that the frequency with which Apneumatosis occurs is subject to a corresponding diminution. The effects produced on the system gen- erally by the presence of Apneumatosis.- Children in whom the lungs are exten- sively affected with Apneumatosis die of a slow asphyxia, and the manner in which this effect is produced is sufficiently obvious. No respiration, in the mechan- ical or physiological sense of the word, can take place in the lobules which are collapsed; these portions have become absolutely useless so far as the oxygena- tion of the blood is concerned ; the effect is the same as if the size of the lung had been reduced in a corresponding ratio by complete removal of these portions. It has been shown that the degree to which lobes may be affected is often very con- siderable in the aggregate; as much as half of the entire lungs has been found to be involved in some cases. The fact that the surface still available for respiration is thus diminished explains the symptoms observed in such cases - the quickened movements of the chest, the distress, and dyspnoea. It is a curious circumstance, and one which of all others should have pre- vented the older observers from deciding as to the purely inflammatory nature of the lesion in question, that in cases of Apneumatosis a stage soon sets in char- acterized by great pallidity of the surface, bloodlessness of the integument, and ex- cessive debility. The Surface becomes cold and the decarbonization of the blood is thus shown to be reduced to a mini- mum. The condition of a child in an advanced state of Apneumatosis in fact bears a great resemblance to that of one of the cold-blooded animals. The as- phyxia comes on very slowly and grad- ually, the system apparently accommo- dating itself to the lowered respiratory function, less blood circulates through the lung, and less in the system generally. All organs suffer; the energy of the mus- cles is impaired ; they no longer contract with force and vigor. Further portions of the lungs become apneumatic from this very circumstance, and when this has reached its extreme limit the patient dies. In the outset there is no congestion in the skin, face, &c., but the asphyxia after- wards observed is of a more chronic, and apparently less congestive form. The circulation is necessarily greatly affected. The blood ceases to circulate in the lobules deprived of air. The cessation does not take place immediately, but after the lapse of a certain time. The first effect of collapse of the air-cells on the circulation in the lobules affected is to re- tard the flow of blood-to produce con- gestion. The blood which at first flows through the part more slowly than usual soon ceases to flow at all. What then becomes of it ? Dr. Richardson's experi- ments have shown that blood will remain for some little time fluid, if preserved from contact with air at rest within the body, but after a time it coagulates. Thus then a second effect, and one occurring later, is coagulation of the blood in the apneu- matic lobules. The presence of these clots within the bloodvessels of the lobules, and their various conditions as regards consistence, density, color, &c., explain the difference observed in individual cases, in the appearance of the section of apneu- matic lobules. Fuchs' describes after Still- ing, the changes which the clot ("der thrombus") found within the vessel un- dergoes as follows: At first it lies free 1 Loc. cit. p. 75. 314 APNEUMATOSIS. within the vessel, but after a time varying in the smaller vessels from two to three days ; in the larger, from five to six days, it becomes adherent to the walls of the vessels. Later still it becomes whiter and more dense and contracted, resembling the walls of the vessel in appearance ; finally the vessel becomes obliterated, this termination taking place in the small ves- sels in 20-22 days, in the larger in 30- 40 days. The difficulty occasionally ex- perienced in inflating apneumatic lobules is attributed by Fuchs to the contraction which the lung-tissue has undergone as a consequence of the process thus described. The changes which take place in the bloodvessels must after a certain time be an insuperable obstacle to the restoration of the function of the parts involved. An effect of the retardation of the current will be distension of the bloodvessels, and the bulk of the lobules reduced by collapse of the air-cells is still preserved by this dis- tension. Various dynamical effects may thus result. The forcible inspiratory ef- forts may even produce such distension of the bloodvessels as to render the lobule in question larger than usual. This accounts for the increased size of the apneumatic lobules which, as before stated, is some- times observed. A further remarkable dynamic effect is the unnatural distension of air-cells in other adjacent portions of the lung ; emphysema' is in fact almost invariably present in cases of Apneu- matosis. Large patches of lung present air-vesicles greatly increased in size. Symptoms.-The symptoms observable in cases of Apneumatosis are quite pecu- liar, and more reliance can be placed upon them as indicating the presence of the lesion in question than on the physi- cal signs, unless large portions of certain lobules are affected. When the lungs are extensively affected, the state in which the child is found is generally as follows : There is great prostration and debility, restlessness, and inability to sleep. The temperature of the skin and extremities rapidly falls, and the skin is either very pale or of a dusky hue, the lips have a bluish cast, the eyes are sunken, the skin hangs in folds on the attenuated and wasted limbs, and the child appears pre- maturely aged, having lost the infantine expression peculiar to a healthy child. The pulse is very quick and often hardly to be felt. There is a constant cry, this being of a whining character, and often very feeble. The respiratory function undergoes important changes, manifest in the altered characters observed. The dis- tinctive feature of the respiration is its shallowness, it being very evident that very little air enters and escapes from the chest at each successive movement of the walls. The respiratory movements are much quickened ; in a child a year old, the number of respirations in a minute may be as high as seventy or even eighty, and if younger than this higher still. The rhythm of the movement is altogether changed, being what is called "expira- tory," the interval occurring between in- spiration and expiration instead of be- tween expiration and inspiration. This is not pathognomonic of the presence of Apneumatosis, for it may be observed in other cases, but it always coexists with the lesion in question. The dyspnoea in fact is extreme, though not accompanied with that degree of lividity of the face and evident distress usually a concomitant of intense dyspnoea. It is evident also that the dyspnoea is not dependent upon pain in the chest as is the case in pleurisy ; the child gives no sign of that kind of suffer- ing which is observed when inflammation of the pleura is present; the suffering is of another character altogether. The cough is very distinctive. In bad cases it can hardly be called a cough at all; the little patient is perpetually making feeble expiratory efforts which produce no effect in evacuating the contents of the tubes, and if the thorax be uncovered, it will be seen that little or no diminution of its bulk takes place during these ineffectual attempts to free the bronchi from the ob- structing mucus. These attempts are moreover generally followed by a cry, an expression of impatience at the inadequate result obtained. Nothing can be more significant than the character of the cough, the inefficient nature of which is explained by the fact that there is a de- ficiency of air in certain parts of the lungs ; for as already pointed out each lobule is a miniature lung, and the presence of air is necessary for the production of that jerk- ing expulsive effect constituting a cough. The dyspnoea present in these cases is usually attributed to the presence of mucus in the tubes, but this is not the whole truth ; that mucus would be ex- pelled if there were sufficient air behind it, and the patient had, so to speak, the usual control over that air, and could thus drive it out. The dyspnoea observed in bronchitis alone is of a different character, more suffocative, and more productive of congestion ; there is more heat of skin and fever present also; but these febrile symptoms disappear in great part when the lungs become extensively apneumatic. The physical examination of the chest affords information of a very valuable character. The yielding nature of the thoracic walls in infancy has been spoken of as predisposing to the occurrence of Apneumatosis. That the chest-walls do actually give way during life we have practical proof on watching the move- ments of the chest during respiration in a child whose lungs are extensively apneu- SYMPTOMS. 315 matic. The younger the child the more readily does this tak& place. During in- spiration the lower part of the chest is strongly retracted, and the diameter of the chest diminished at this situation, the converse of what is observed in health. Not only do the firmer parietes of the chest thus fall in, following the tractile influence of the diaphragm, but the inter- costal spaces become much more manifest, sinking in during the act of inspiration. Conversely, during expiration the same parts may be seen to move outwards to a slight extent. The retraction of the chest-walls during inspiration may be ob- served when Apneumatosis is not present in consequence of unnatural mobility of the parts, a circumstance previously al- luded to, but it is, nevertheless, a sign of considerable importance. The change in the shape and contour of the chest pro- duced by Apneumatosis has been already described. The results of percussion and ausculta- tion in the young child are in all cases less to be depended on than in the case of the adult. Where the Apneumatosis is extensive, the percussion sound is dull and attended with some degree of resist- ance ; but as it generally happens that the lobules affected are more or less inter- mixed with others which are healthy, or which even contain a greater amount of air than usual, this dulness on percussion often escapes detection in cases where the aggregate amount of Apneumatosis is considerable. Emphysema, as before stated, is constantly combined with Apneumatosis. The presence of these emphysematous patches will interfere with the results of percussion practised immediately over them in a manner suffi- ciently obvious. When the whole of one lobe is affected, or when, as it frequently occurred in cases coming under our own observation, the greater part of the lower lobe on either side has lost its gaseous contents, the dulness on percussion has been very marked, and the width of the surface presenting this dulness has in- creased from day to day under observa- tion. Generally speaking, then, the presence of dulness on percussion is a positive sign, but its absence is, for the reasons just stated, not a negative one. It is to be looked for at the basis of the chest posteriorly, and next in order of frequency at the same position anteriorly. The respiratory murmur disappears over those parts of lung affected with Apneumatosis, if the disease be widely spread. On the whole, however, it is rare to meet with entire absence of respi- ratory sound on auscultation, some sounds being still transmitted from deeper parts. We have observed its complete absence more especially in the case of very young infants. The more usual circumstance is that the breath-sound is, when not masked by rhonchi, somewhat bronchial in charac- ter, the solidified lung transmitting the sound from the larger air-tubes. It is somewhat rare, however, to meet with cases in which rhonchi, due to the pass- age of air through mucus, are not audible. With reference to these rhonchi, the most striking character they possess is a degree of coarseness and roughness, not often noticed in the case of the adult. Khon- chal fremitus is only present in the early stage. The true crepitant rhonchus, which is in the adult the chief distinctive sign of the presence of pneumonia, is not heard. Authors have generally accounted for the absence of this pneumonic crepitus in young children, supposed by them to be the subject of "pneumonia," by con- cluding that the peculiarities of the struc- ture of the child's lung prevented its de- velopment ; but the fact is, there being no pneumonia, there is, therefore, no crepitus. It is unnecessary further to describe the various kinds of rhonchi which are found to be present in these cases. They de- pend on the bronchitis present. An im- portant circumstance is the rapidity with which these changes from the normal con- dition may take place. A large surface of the lung may become solid, causing dulness on percussion and loss of respira- tory murmur in twenty-four hours ; thes limits within which the alterations are observed may also change in as short a time as this. Valleix observes that a dulness of all the posterior part of the right and of the lower third of the poste- rior surface of the chest may supervene in the space of twenty-nine hours, no sign of this dulness having been present the day before.1 This is, perhaps, more espe- cially the case in very young infants, for in older children the lung requires to be longer subjected to the necessary process in order that large portions may become apneumatic. The changeableness of the character of the sounds conveyed to the car by the stethoscope, is of course pro- duced by and follows the alterations in the lung-tissue here alluded to. The peculiarity of the child's voice interferes with any observations on the intensity of the resonance as felt by the hand, the vocal fremitus. iv; Such are the symptoms and signs ob- served in cases where the Apneumatosis is tolerably extensive and well marked. In cases where it is inconsiderable in amount, and scattered over different parts of the lobes, the physical signs may be wholly inadequate to determine its pres- ence, and the general symptoms then afford more information. Cases, indeed, not unfrequently occur in which death having taken place, the Apneumatosis is 1 Loc. cit. p. 128. 316 APNEUMATOSIS. found to be considerable, but having the characters here alluded to, no dulness on percussion, no positive sign of solidifica- tion having been detected during life. The course, duration, and mode of termi- nation of the disease must necessarily vary in different cases. The disease is gen- erally fatal, when involving the lungs to a considerable degree. A child, badly fed, living in a close, confined apartment, breathing constantly a vitiated air, may, if attacked by bronchitis, die in conse- quence of the Apneumatosis resulting therefrom, in a short space of time, but the time will vary in different cases. If the child be affected with atelectasis to begin with, the disease is more quickly fatal, but if previously strong and toler- ably healthy, its duration is proportion- ately prolonged. Hooping-cough is ex- ceedingly fatal to very young children, because the bronchitis which accompanies it so readily gives rise to Apneumatosis but it is well known that it is amongst the children of the poorer classes only that the disease occasions so great a mor- tality, where, in fact, the predisposing causes before alluded to are allowed to come into operation. The hygienic con- ditions being favorable, Apneumatosis both less readily occurs, and, when pro- duced, is less likely to prove fatal, than when this is not the case. Unless inter- fered with, the natural course of the mal- ady is from bad to worse: from the nature of things, the disease tends to in- tensify itself, and from day to day the affection increases by involving more of the lung substance. As the disease ex- tends, the patient becomes very feeble, unable to cough, or expel the mucus from the tubes, and the quantity of blood in the system seems to undergo a diminu- tion. This is proved by the result of post- mortem examination in chronic cases, and is made evident during life by the pallid, bleached appearance of the patient. After suffering under the symptoms for, it may be, two or three weeks, the death takes place by what is, in reality, a slow asphyxia. The course of the disease may be more rapid, as is sometimes the case in infants who have previously enjoyed a better state of health. These are seized with a severe attack of bronchitis, per- vading the smaller as well as the larger tubes, and large portions of the lungs suddenly, or comparatively so at least, become apneumatic and deeply congested; death then rapidly supervenes, the as- phyxia being more suffocative and acute in character than in the former case. In both cases, recovery may of course be the result, although the lungs are a long time before their functional activity is com- pletely restored ; the seeds of future mis- chief are some of them left behind, and may subsequently induce a return of the disease: chronic emphysema is a very frequent result of Apneumatosis. That large portions of lung substance may, within a very short space of time, return to the healthy state, which a short time before had been obviously apneuma- tic, has been with us matter of observa- tion, and the same circumstance has been noticed by others. The effect of judicious treatment, in restoring clearness of per- cussion sound and respiratory murmur, is occasionally indeed very marked, and is of itself a sufficient evidence that the dulness which before existed was not due to true pneumonic consolidation of the lung. The cure is often impeded, may often be prevented by the emphysema which coexists; for although the child may have the power of inspiring forcibly restored, the thorax being already fdled by the emphysematous distension of cer- tain of the air-cells, no expansion of the apneumatic lobules occurs. The Prognosis, in a particular case, is favorable if the affection be recent, oc- curring in a tolerably healthy child, and when the muscular power is not greatly reduced : the hygienic and other condi- tions in which the patient may be placed, are very important features in the case, as regards the prognosis. In infants, Ap- neumatosis occurring in connection with hooping-cough is especially fatal; few re- cover from it when placed, as are the children of the low'er orders in large towns, under unfavorable hygienic con- ditions. Diagnosis.-Dulness on percussion and bronchial respiration are of most value, where they are present; under other cir- cumstances the altered character of the respiratory movements, the retraction of the chest-walls, combined with the gen- eral condition of the patient, and the his- tory of the case, are data on which a diagnosis may be arrived at with tolerable facility. The diagnostic signs of atelectasis can- not be entered on here. In reference to the other conditions with which Apneu- matosis may be confounded, and which it is necessary therefore to distinguish, a few remarks will suffice. True pneumonia is very rare in early infancy ; the presump- tion in a particular case will be, there- fore, that this condition is not present. The absence of the continued and persist- ent heat of skin, the absence of the pneu- monic crepitus, afford negative evidence tending to the same conclusion. It will 1 See the author's essay "On Pathology of Hooping-cough" (Churchill, 1855), contain- ing the results of the examination of the lungs after death in nineteen fatal cases of this disease. TREATMENT. 317 be more difficult, however, to distinguish between a case of true pneumonia, in which the inflammatory acute stage has passed away, leaving consolidation of the lung, and one in which Apneumatosis is present. Another condition-extensive de- posit of miliary tubercle in the substance of the lungs-might present symptoms and physical signs somewhat resembling those observed in the case of Apneumatosis. The history of the case would, however, show that symptoms, as cough, wasting, &c., had been observed for some time pre- viously ; and the general condition of the patient, together with this circumstance, could hardly fail to lead to a correct con- clusion as to the nature of the case. It may be remarked, however, by the way, that Apneumatosis, as a complication, is often discovered after death in tubercular disease of the lungs. In cases of pleurisy, with effusion, there would be dulness on percussion over the lower part of the base of the thorax, together with absence of breath-sound on auscultation, both of which physical signs are present in cases of Apneumatosis; it is to be distinguished from the latter condition, by the greater intensity and width of the dulness on per- cussion, by the more complete absence of respiratory murmur, observed in the former case. Moreover, in cases of Ap- neumatosis, it is generally found that the dulness is not limited to one side, as is more frequently the case in pleurisy. Treatment.-Patients affected with Apneumatosis have lost for all functional purposes large portions of the lungs ; it is our business to endeavor to restore these portions to their functional activity, and to prevent others from falling into a simi- lar condition. Clear indications for treat- ment will be found on examining the class T>f causes, effective in the production of Apneumatosis. As every circumstance which tends to lower the muscular and vital power of the patient favors the pro- fl notion of Apneumatosis, it is very ob- vious that we are not likely to improve matters by the exhibition of medicines having a lowering character, or by the ab- straction of blood, in a case where the child is already too feeble. Setting aside for a moment the consideration of the bronchitis itself, which is or has been present in a particular case, there seems to be no good reason for the employment of depletive or depressing remedies in the treatment of Apneumatosis. There are many reasons against this procedure. The older observers carried their principles into practice: they considered that they had to treat pneumonia, and they treated it accordingly. It is no less incumbent on us to adopt a treatment precisely the reverse. We are decidedly of opinion that, as a general rule, when an infant is the subject of Apneumatosis, depletion, local or other- wise, is not admissible. The same must be said of the internal administration of tartar-emetic in repeated doses. One of the chief difficulties to be en- countered is the impediment offered to the entry of air, by the presence of mucus, which the child is unable to expel. A primary object is then to assist the respi- ratory efforts of the patient, at the same time that we endeavor to diminish the ex- cessive secretion of mucus in the air-tubes. Counter-irritation is a valuable means to this end, the degree of which must be adapted to the strength of the patient and the duration of the disease. Mustard poultices are very useful; they can be frequently repeated, and do not produce prostration. Blisters are objectionable from their weakening tendency. We have found frictions of the chest to be followed by markedly good effects, when performed in the following manner :-The hand, lu- bricated with sweet oil, is to be rubbed tolerably briskly over the whole surface of the chest for ten minutes or a quarter of an hour together, two or three times a day. The result obtained is twofold, a counter-irritant effect is produced, the blood being drawn to the surface and the internal congestion thus diminished, and the movements of the chest are very much facilitated. The movements of the walls of the chest, which the pressure of the hand produced, also aids in the expulsion of the matters blocking up the air-tubes. The warm bath, producing increased ac- tion of the skin, is occasionally of service, but is less suited to cases of Apneumatosis than at the outset of an attack of bron- chitis ; its operation, if continued, or too often repeated, is too weakening. Nothing is more effective in removing the contents of the air-tubes than an emetic, for which purpose ipecacuanha seems to be the best; eight to ten grains of the powder is a proper dose for an infant a year old. Effective, however, as is the emetic in question, it is not to be administered rashly, or under certain circumstances. If the patient be very weak and the dis- ease of some days' duration, the emetic may be unsafe. When not contra- indicated, it may be given once, but is not to be repeated. If it acts efficiently, the object in view is attained, and most patients will not bear its repetition unless after the lapse of a certain time. A little ipecacuanha wine (about ten drops), given in a little syrup, every four or six hours, has the effect of promoting expectoration. The state of the bowels must not be neg- lected, but mild aperients only are ad- missible. The food must be extremely simple, but at the same time nourishing. The breast milk for an infant, milk and water for an older child, are quite suffi- 318 BRONCHITIS. cient in ordinary cases. The case is, how- ever, different when the lungs are exten- sively affected. Then all our efforts must be directed to the maintenance of the vital powers. Emetics are not safe, even mild expectorants may be improper. Small doses of aromatic spirit of ammonia, or steel wine, or at a later period, the syrup of the phosphate of iron, must be given, and together with the milk diet a little port-wine and water, or brandy-and- water, and weak beef-tea. In dieting young children it is too often forgotten that concentrated food is not well digested, and rich cream and strong beef-tea in many cases act as irritant poisons if taken into the stomach of an infant; great care must be taken to dilute the food given, so that it may be easily digested, or it will do considerably more harm than good. BRONCHITIS. Frederick T. Roberts, M.D. Bond. Definition.-An affection of the mu- cous membrane lining the bronchial tubes, varying from mere hypersemia of limited extent, to an intense and widely-distrib- uted inflammation, which may involve the deeper structures. It usually gives rise to an increased and altered secretion, containing abundant cells, but in some cases a plastic exudation is thrown out into the tubes. Hence there are two chief forms of Bronchitis, named the Ca- tarrhal and Plastic or Croupous, each oc- curring as an acute and chronic affection. Synonyms.-Bronchial Catarrh; Ca- tarrhus Pituitosus; Catarrhus Suffoca- tivus ; Angina Bronchialis ; Erysipelas Pulmonis; Peri-pneumonia Not ha ; Bron- chite (French); Bronchialentziindung (German). Acute Catarrhal Bronchitis. Acute Bronchial Catarrii. Natural History. - Causes. - I. Predisposing.-These are due partly to the individual, partly to surrounding ex- ternal conditions. The following include the most important:- 1. Age.-There is no age at which Bron- chitis does not occur, but it is far more commonly met with at the extremes of life. It is a very frequent complaint among children, especially during the first two years of life, while dentition is going on, and persons of advanced years are also exceedingly subject to it. The occurrence in children of various affec- tions which tend to have Bronchitis as a complication, and in old persons, of chronic pulmonary, cardiac, and other diseases, will to some extent account for this ; while, in addition, they possess less vital power to resist the ordinary exciting causes. The table below shows the rate of mortality at the various ages, during the year 1868, as contained in the Registrar- General's Reports, but it only gives an ap- proximate idea of the relative frequency, as Bronchitis is so much more fatal among the old and young. MALES. Under one year . . 3849 One year . . . .1585 Two years.... 562 Three years . . . 289 Four years . . . 139 Five years . . . 207 Ten years .... 40 Fifteen years... 52 Twenty years . . 85 Twenty-five years . 331 Thirty-five years . 728 Forty-five years . . 1369 Fifty-five years . . 2430 Sixty-five years . . 3002 Seventy-five years . 1956 Eighty-five years . 300 Above ..... 10 FEMALES. Under one year . . 2969 One year .... 1585 Two years.... 594 Three years . . . 243 Four years . . . 161 Five years . . . 211 Ten years ... 47 Fifteen years... 61 Twenty years . . 93 Twenty-five years . 327 Thirty-five years . 615 Forty-five years . .1267 Fifty-five years . . 2316 Sixty-five years . . 3218 Seventy-five years . 2158 Eighty-five years . 440 Above 20 NATURAL HISTORY. 319 2. Sex does not seem to influence the number of cases materially. In the year 1868, 16,934 deaths were recorded among males, as compared with 16,324 among fe- males ; and it will be seen from the tables that the first year of life gives the greatest difference. Probably men have bronchitic attacks more frequently than women dur- ing the adult years, being more exposed to cold, &c. 3. Habits.-Unquestionably those who indulge in luxurious and enervating hab- its, and who wrap themselves immoder- ately, or live in rooms of a high tempera- ture, produce a relaxing and depressing effect upon the system, and render them- selves more obnoxious to slight external influences. The excessive care which many children receive in these respects is certainly injurious ; while, on the other hand, their resisting power may be in- creased by a judicious process of inuring them to various atmospheric changes. 4. Temperament.-It is said that those of a sanguineous and lymphatic tempera- ment are more liable to be attacked, but I am not aware of any positive facts bear- ing out this statement. 5. State of General Health.-.A constitu- tionally weak state of the system, or de- bility resulting from any cause, such as deficient and improper food, or severe ill- ness, predisposes to Bronchitis; while the existence of any positive constitutional disease, such as tuberculosis, rickets, Bright's disease, gout, diabetes, cancer, &c., is still more favorable for its occur- rence. 6. Condition of the Lungs and Bronchi. -The presence of any deposit in connec- tion with the lungs, as tubercle or cancer, as well as the existence of certain chronic affections, especially emphysema and di- lated bronchi, necessarily favors the set- ting up of Bronchitis. If the mucous membrane has been once attacked, it is rendered more susceptible, and this sus- ceptibility is increased with each attack ; hence it is not at all uncommon for a per- son to suffer every year when the cold weather sets in. 7. State of the Heart and Circulation.- Any heart disease that interferes with the return of the blood through the bron- chial veins, or anything that causes extra pressure upon the circulation in the bron- chial arteries, has a considerable predis- posing influence as regards catarrh, and may even excite it. tn the manner last mentioned, abundant ascites is said to act by exerting pressure upon the aorta below the origin of the bronchial arteries, and thus throwing an extra strain upon them. 8. Occupation.-The occupations which seem to be specially favorable to Bronchi- tis, are those which involve much exposure to cold and wet, or sudden and marked changes of temperature, and those which lead to the inhalation of irritating parti- cles floating in the atmosphere, such as cotton, steel, charcoal, &c. 9. Social Position.-Those among the poorer ranks of society are, for several reasons, very liable to Bronchitis. A large number of cases occur among hospi- tal and dispensary patients. 10. Climate.-Bronchitis is very much more common in climates characterized by considerable moisture of the atmo- sphere, combined with low temperature ; and especially where there are sudden and marked variations in temperature. The same observation applies to individual districts ; those that are bleak and damp being rarely free from bronchitic cases. It is an exceedingly prevalent disease in this country, and stands very high as a cause of death. In 1867, 40,373 deaths occurred from Bronchitis, being in the proportion of 1902 to every million per- sons living, and of 86,554 in every million deaths, tn 1868, the number of deaths was 33,258, giving a proportion of 69,765 per million deaths. The mean rate of mortality for 15 years, from 1850 to 1864, was 1344'4 in every million living. It oc- curs in different districts with very vari- able frequency. The following statistical summing up gives, approximately, the proportion of deaths from Bronchitis to the number of inhabitants in the different districts during the year 1868 :- London, 1 in 442'3; South Eastern Counties, 1 in 805'01 ; South Midland Counties, 1 in 834'7 ; Eastern Counties, 1 in 987'5; South Western Counties, 1 in 844'8; West Midland Counties, 1 in 665'03 ; North Midland Counties, 1 in 876'2 ; Northwestern Counties (Cheshire and Lancashire), 1 in 379'5 ; Yorkshire, 1 in 541'5 ; Northern Counties, 1 in 774'8; Monmouthshire and Wales, 1 in 955'4. 11. The foregoing statistics prove that Bronchitis is much more prevalent in large towns and cities than in country places, and the reasons for this will be obvious. The same remark applies to the fact that the poorer districts of cities and towns furnish by far the greater number of cases. Places where extensive manu- factures are carried on, loading the atmo- sphere with various irritating materials, have also always a considerable propor- tion of cases. 12. Season.-By far the largest number of cases is met with during the colder months of the year, extending usually from the end of autumn, through the winter, into early spring. Much, how- ever, will depend on the kind of weather that is experienced. The number of cases was considerably less in the year 1868 than in 1867, on account of the com- parative mildness of the weather ; a sud- den change in the weather is very likely to bring with it numerous bronchitic at- 320 BRONCHITIS. tacks, and the prevalence of north-easterly or easterly winds has a similar influence. II. Exciting.-1. In the great majority of instances, cold, in some form or other, acts as the immediate exciting cause of Acute Bronchitis. It may produce its effects in various ways: thus, an attack may arise from the breathing of cold air, especially if at the same time loaded with moisture, and particularly if there has been a sudden change from a warm and dry atmosphere ; emerging from a warm room into a cold atmosphere, particularly when in a state of perspiration, and sitting in a cold draught, contribute numerous cases. Wearing an insufficient amount of clothing in cold weather, and exposing the upper part of the body; neglecting to change damp clothes, or having wet feet; sleeping in damp beds, &c., are all fre- quent causes. Infants who drivel con- stantly and profusely, so that the gar- ments covering the chest are always moist, are said to be very subject to Bronchitis. In most of the instances where the cause cannot be traced, it is probable that the patient has " taken cold" in some way or other. The modes in which cold produces its injurious effects appear to be, first, by causing local irrita- tion of the bronchial mucous membrane, and disturbing its circulation and nutri- tion ; secondly, by acting upon the system at large in some way or other not under- stood, the Bronchitis being only a part of a general disturbance. 2. On the other hand, sudden great heat after cold, e. g. passing from the night air into a very hot room, is said sometimes to cause Bronchitis, but this is difficult to substantiate. 3. Another important exciting cause is the direct action of various irritants upon the mucous membrane lining the air- passages. This may arise from certain conditions of the atmosphere inhaled, such as a very high or low temperature, or from its containing any irritant gas or vapor, e. g. sulphurous anhydride, chlo- rine, ammonia, &c. ; or having certain minute particles floating in it, such as dust, steel-filings, charcoal, cotton, flour, &c., and in the same category may be in- cluded those cases of Bronchitis that re- sult from inhaling certain vegetable sub- stances, viz., the powder of ipecacuanha and the emanations from hay. "London fogs" undoubtedly act in this way, and, it is said, also miasmatic productions. The blood remaining in the tubes after hemorrhage, and unhealthy secretions from cavities in the lungs, &c., coming into contact with the mucous membrane, may excite inflammations. 4. Certain morbid conditions of the blood are very prone to give rise to Bron- chitis. To this is attributable that form which complicates certain febrile affec- tions, especially typhoid fever and mea- sles, and, less commonly, scarlatina, smallpox, hooping-cough, diphtheria, typhus fever, &c. it is particularly liable to occur in the eruptive fevers, if the eruption comes out imperfectly, or sud- denly recedes. Neglect of proper precau- tions during convalescence from these affections, is very apt to lead to dangerous Bronchitis. The poison of syphilis, as well as that of gout and rheumatism, also produces this affection, and it is particu- larly prone to occur in the last two dis- eases if sudden metastasis takes place. The state of the blood must also account for those cases that are said to result from the rapid disappearance of the eruption of erysipelas, the suppression of long-contin- ued discharges, whether natural or mor- bid, and the too rapid cure of an old-stand- ing skin disease. Iodine taken internally sometimes causes bronchial catarrh, evi- dently due to its presence in the blood. 5. Various deposits in the lung may not only predispose to, but actually excite inflammation of the mucous membrane. It is constantly met with more or less when tubercle or cancer is present, and is then prone to be localized. 6. In connection with influenza, Bron- chitis occurs epidemically, without our being able to trace it to any special cause. At certain times of the year a large num- ber of persons are often simultaneously attacked, so that the complaint may al- most be said to be epidemic, but this is due to obvious atmospheric conditions already alluded to. Symptomatology.-The clinical his- tory of Acute Bronchitis varies consider- ably under different circumstances, and an attack may range from a slight " cold in the chest," to one inducing suffocation and gravely affecting the system at large. The chief reasons for these variations are to be found in the age, general condition, and health of the patient, the previous state of the lungs, the extent of mucous membrane involved, and the immediate cause of the disease. In practice, the following forms are met with :- I. Acute Primary or Idiopathic Bron- chitis, the result of "cold," there being no previous evident lung affection :- 1. Involving the larger and middle- sized tubes only, and not extend- ing into the smaller tubes. 2. Implicating the smaller tubes - " Capillary Bronchitis. ' II. Secondary Bronchitis :- 1. In connection with the exanthe- mata. 2. In certain blood-diseases. 3. After chronic lung and heart affec- tions. symptomatology: acute idiopathic bronchitis. 321 III. Mechanical:- 1. Hay-asthma, &c. 2. That resulting from mineral and other irritant particles. IV. Epidemic. The primary forms it will be necessary to describe at some length, but the others will call for only a few remarks, pointing out in what respects they differ: whereas Epidemic Bronchitis it will not be requi- site to allude to again, as it belongs to Influenza. 1. Acute Idiopathic Bronchitis, not extending beyond the middle-sized tubes. Invasion.-This is almost always char- acterized by the occurrence of symptoms of so-called "catarrh," in consequence of the mucous membrane lining the nasal cavities and their communicating sinuses being affected, and, frequently, the con- junctivse. There is an irritating watery flow from the nose and eyes, and a feeling of fulness, heat, and soreness in these parts, with frequent sneezing fits. Fron- tal headache exists, due to the state of the frontal sinuses. The upper and back part of the throat often feels sore and rough, and frequent attempts are made to clear it from mucus. There is gener- ally uneasiness over the larynx, and the voice is more or less hoarse and husky, indicating that the mucous membrane here is also implicated. Not uncommonly the catarrh seems to spread regularly downwards along the respiratory tract, beginning in the nose. In some instances the larynx is alone involved at first, while in others the bronchial mucous membrane seems to suffer from the outset, the upper part of the tract escaping ; but this rarely happens in the form now under consider- ation. Along with these local symptoms there are others of a general character, almost always present more or less. The patient feels chilly, or there may be even rigors in a sensitive person, but they are never of marked intensity, and several occur at irregular intervals, not a single prolonged fit of shivering. Their severity is usually in proportion to the extent of the inflammation. In the intervals be- tween them the patient feels hot, but the temperature is not raised, as evidenced by the thermometer, or only slightly. The pulse is often somewhat increased in frequency. The limbs and joints, or even the body generally, are affected with pains of an aching, contused character, and there is a general sense of fatigue, languor, and want of energy, the patient experiencing a disinclination for any oc- cupation, mental or physical. He is heavy and drowsy, but sleep is often rest- less and uneasy. There is frequently a furred tongue, anorexia, and constipation. evidencing that the alimentary canal also suiters. In nervous, irritable persons, and in the older children, slight delirium is said to be present sometimes ; while in younger children, especially during the period of dentition, and in those who are weakly, a tit of convulsions may usher in the attack. After the initiatory symptoms have lasted a brief but variable time, those characteristic of the bronchial inflamma- tion set in. They may be very slight, or tolerably severe, and are "local" and " general." Local.-Various unpleasant or painful sensations are experienced behind the sternum, especially towards its upper part, and in the supra-sternal notch. These are, more or less heat, sometimes reach- ing to actual burning, and a sense of sore- ness or rawness, which may amount to considerable pain-as a rule, however, it is not severe, when the patient is quiet. A deep inspiration aggravates these feel- ings in a variable degree, while the act of coughing gives rise to much positive pain, of a raw, aching, burning, or tearing character. This is not only complained of behind the sternum, but also radiates towards the sides, as if in the course of the primary bronchial divisions. If the cough is severe and frequent, a feeling of soreness or aching is soon felt all over the chest, but especially towards its sides, and the base where the abdominal muscles are attached. A very unpleasant irrita- tion or tickling is also experienced above and behind the sternum, which excites the cough. Tenderness over the sternum is often present, the skin feeling sore on percussion. These sensations vary much in intensity, and may merely amount to a diffused feeling of slight heat and uneasi- ness over the front of the chest, but most marked behind the sternum. Dyspnoea is not a prominent symptom, but the frequency of the respirations is often somewhat increased, and the pulse- respiration ratio may be more or less altered. The act of breathing is labored in many cases, and there is always a sense of oppression, weight, and tightness about the chest, especially towards its upper part. Cough is one of the earliest and most striking symptoms. It is loud, and usually a little'hoarse at first, owing to the larynx being affected; otherwise it is free from hoarseness. It comes on in paroxysms, either spontaneously, or from any slight irritation, as inhaling cold air. These last a variable time, and cannot be sup- pressed. They increase in frequency as the disease advances, and often become very violent, especially after a sleep, and on first lying down at night. There is no expectoration at the outset, the cough being hard and dry, but afterwards each VOL. II.-21 322 BRONCHITIS. fit ends with expectoration. It is evi- dently due at first to the abnormally irri- table condition of the mucous membrane, and subsequently to the presence of ex- cessive and altered secretion in contact with it, which is itself probably of an irri- tating nature at first. The expectoration varies in its characters at different periods of the case. At the beginning it is small in quantity, thin and watery in appear- ance, almost transparent, but frothy, and has a saltish taste. The changes it under- goes are : increase in quantity to a varia- ble degree; diminution in transparency, becoming at last almost or quite opaque ; increase in consistence and viscidity; diminution in frothiness; loss of taste; and change in colors. Thus, it generally passes through stages of viscid, semi- transparent, slightly yellowish or grayish, frothy mucus, to a muco-purulent or puru- lent-looking substance, nearly opaque, of a grayish-yellow,yellowish, or a greenish- yellow color, and but slightly aerated. It usually runs together into one mass, but a distinct, nummulated form of sputum is sometimes met with, which is thoroughly opaque. Its tenacity and adhesiveness may be so great as to make it stick close- ly to the vessel containing it, and to ad- mit of its being drawn out into threads. Sometimes it is quite ropy and gelatinous. A few streaks of blood may be seen, espe- cially at the early period. Should an ex- tension of the inflammation take place, this is indicated by the expectoration once more assuming its early characters in part. As the sputa become altered they are more easily expelled, especially from the larger tubes, and hence the cough abates and is much less painful. Microscopical characters. - In the early stage, pavement, columnar, and ciliated epithelial cells are seen, with a few imper- fectly formed cells. Later there are abun- dant young cells, discharged from the surface of the mucous membrane, many resembling the so-called exudation cor- puscles, and at last pus cells. Molecular and granular matter is seen in quantity; a few blood disks may be present, and occasionally amorphous, fibrinous coagula. Crystals of oxalates, &c., are sometimes visible. General.-In the slighter cases there are no notable signs of "general indisposi- tion, but if the attack is at all severe, the system gives indications of being affected. More or less febrile reaction occurs, the pulse becoming frequent, but rarely above 100 ; at the same time in a healthy person being strong and full. The skin feels hot, but not acridly ; and it may soon be moist. The actual temperature is never very high, but it follows the ordinary rule of increasing in the evening. If the fever precedes the bronchitic symptoms, it is said to be notably more severe. Slight rigors may continue throughout the at- tack. The tongue is generally more or less furred, but moist; and there is some thirst, with loss of appetite. The bowels are mostly confined. Vomiting may oc- cur, especially after a severe fit of cough- ing. The urine presents the ordinary febrile characters in a varying degree : the urea and pigments are increased, but the chloride of sodium may be notably diminished. There may be heat during micturition, probably from slight catarrh of the urethral mucous membrane. A sense of languor and weakness continues throughout the case, and there may be considerable depression, quite independ- ent of, or out of proportion to, the febrile state. A favorable case of this description may run its course in three or five days, or may last two or three weeks, according to the number and size of tubes involved, the depth of the inflammation, and the state of the patient. The fever, if any existed, soon abates, and the local symp- toms gradually subside, the cough, how- ever, often holding on for some time, especially in the mornings, on account of the secretions having accumulated. These cases do not always end in recovery. In very old patients, and in those weakened by disease or want, fever of an adynamic type is apt to be present from the first, or to follow sthenic fever, especially if tins has been severe. Then there is great de- bility, a quick, feeble pulse, a dry, brown tongue, and low delirium. Or it may happen that the patient is unable to expel the secretion formed in the tubes, which therefore collects and tends to pass into the smaller tubes, thus possibly causing inflammation in them, or blocking them up, and leading to slow suffocation. In young infants, even a very little bronchial catarrh may lead to serious results, espe- cially if they are feeble and ill-nourished, or are the subjects of rickets. They are unable to expectorate, and thus the fluids accumulate, and a large tube, or a num- ber of tubes, become blocked up, collapse of portions of the lung resulting from this. Under any of these circumstances a fatal result may ensue. In a comparatively few instances this form of Bronchitis re- mains as a chronic affection, particularly if it implicates the deeper structures of the tubes. 2. Acute Bronchitis, involving the minute tubes. Capillary Bronchitis.- This is a very dangerous condition, even in a healthy and robust adult; but it is peculiarly grave when children, old people, or very debilitated persons are the sub- jects of it, among whom it occurs with considerable frequency, in the order in which they are mentioned. This results partly from the great interference with the SYMPTOMATOLOGY: CAPILLARY BRONCHITIS. 323 blood-aeration that it involves, partly from the accompanying fever, which has a strong tendency to become adynamic. In the majority of cases it is preceded by symptoms of inflammation in the larger tubes, or the whole tract may be more or less involved simultaneously or very rapidly. In some instances the smaller tubes seem to be alone affected from the first. The early symptoms may be those already described, or well-marked rigors, severe headache, and sickness may usher in the disease. There may be only slight or very considerable pain behind the ster- num, but it is absent if the capillary tubes are alone implicated. Children and aged persons often do not appear to suffer any particular pain. There is always, how- ever, much aching and soreness about the base of the chest and epigastrium, owing to the severe spasmodic contractions of the expiratory muscles during the fits of coughing. This is aggravated during each paroxysm, and patients frequently sit up or bend forwards while they cough, in order to release their abdominal muscles, at the same time pressing their sides, so as to give them support. Dyspnoea always attracts attention, but its degree varies materially. It may be limited to accele- rated and somewhat laborious breathing, with a feeling of constriction and oppres- sion across the chest; or the respirations may be extremely frequent and hurried, attended with violent efforts during inspi- ration, and an urgent craving for air. There may be constant or paroxysmal orthopnoea, the latter supposed to be due either to spasm of the bronchial tubes, or to the sudden blocking-up of a large tube with secretion. The absolute frequency of the respirations may rise to 50 or more, and being increased out of proportion to the pulse, the normal ratio is disturbed, being sometimes 2-5 to 1. Wheezing and whistling sounds are often present, audi- ble at a distance, and attending both in- spiration and expiration. Cough occurs almost continuously, but it also comes on in extremely violent, prolonged, and dis- tressing paroxysms, during which the face becomes turgidly red or purple, the veins swell, and the arteries throb. Expectora- tion is effected with much difficulty, owing to the secretion being exceedingly tena- cious and sticky, and having to be expelled from the smaller tubes, while the muscu- lar fibres of the bronchi, which normally assist expectoration, are probably para- lyzed in many cases. The sputa are scanty at first, but soon increase greatly in quantity, becoming chiefly muco-puru- lent, yellowish-green, or bright green and opaque; or extremely viscid, glutinous, and ropy: they may partly retain the form of the smaller tubes, and minute cylindrical casts, consisting of fibrinous exudation, may be present, or irregular particles of the same substance. Some frothy, lighter mucus from the larger tubes is mixed, more or less, with the above. Children do not expectorate, or rather they swallow what they bring up, but some of it may be obtained for exami- nation by wiping the base of the tongue with a handkerchief after a fit of cough- ing. The constitutional symptoms are always severe. At first there is ordinarily con- siderable fever, which, in the case of healthy adults and plethoric children, is of the sthenic type, but in the aged and feeble is prone to be asthenic from the outset, or speedily to assume this charac- ter. The pulse is frequent, quick, and generally full. The skin is hot, but may be dry or moist. The temperature may reach 103'5° Fahr, in the evening, when it is often 2° in excess of the morning. Flushing of the face, and headache, in- creased by the cough, are commonly pre sent. Pains are complained of in th<. trunk and limbs, and there is a feeling of great weakness and exhaustion. Wast- ing occurs in proportion to the fever and to the interference with sleep, which is gene- rally great. Loaded tongue, anorexia, constipation, are usually marked symp- toms, and there may be much sickness. The urine, in addition to being febrile, is sometimes slightly albuminous tempo- rarily, and it is said a trace of sugar is occasionally present. Chloride of sodium may be almost totally deficient. The symptoms, both local and general, may, after reaching a certain point, sub- side, and gradual recovery take place; but in the majority of cases this favorable result does not occur. Indications of more or less imperfect aeration of the blood are observed in almost every instance, owing to the impaired respiratory process; but in many, especially children, this consti- tutes the main source of danger, and leads to a fatal issue. Gradual suffocation is brought about, and the blood becomes charged with carbonic anhydride, while its oxygen is proportionately deficient; and hence the various organs essential to life are supplied with blood which cannot maintain their functions. When this hap- pens the face assumes at first a turgid, bloated, and more or less red, dusky, or livid appearance, but it soon becomes generally pale, while the lips, tip of the nose, malar prominences, and external ears deepen in their lividity, which con- trasts strongly with the surrounding pallor. The veins of the head and neck swell. The surface generally is also cya- notic in a variable degree, particularly the fingers and toes, this appearance being very marked under the nails. The feet and hands may swell from oedema, which may extend even to the trunk. The tem- perature rapidly falls, especially that of 324 BRONCIIITIS • the extremities. Cold, clammy sweats break out about the face and upper part of the body, and then spread universally. Rapid exhaustion of the vital powers fol- lows, and the patient allows his head to sink on the pillow or droop in any direc- tion. The pulse becomes greatly accele- rated, weak, small, and compressible, and at last often irregular. Intense thirst is complained of. Cerebral symptoms set in early ; the mind wanders, and in many cases a persistent desire to get out of bed is manifested. I have seen this well marked in some adult cases. There is at first perpetual restlessness, with a deeply anxious expression of countenance, and great dread ; but these conditions soon change, and the patient becomes more and more indifferent, with dull and heavy eyes, then falling into a drowsy state, out of which for a while he starts suddenly, but which gradually deepens into perma- nent stupor, and finally complete coma, which precedes death. Convulsions may occur before the final coma. The cough ceases after a time, the power as well as the desire of expectorating being lost. Breathing becomes much quieter, but very hurried and shallow. As a con- sequence, the secretions gradually fill up the air-tubes, and thus are produced rhon- chal sounds, audible at some distance, which change into gurgling as the fluids rise into the larger tubes. " The expired air is cool. The urine is greatly diminished in quan- tity, and may be totally suppressed. Death sometimes occurs suddenly, be- fore the brain is much involved, owing to the blocking up of a large bronchus with secretion ; which is most liable to happen in young children. Instead of the symptoms just described, those characteristic of adynamia may arise, especially in the aged or feeble, and where the fever has been excessive. The tissues are rapidly consumed, and the blood loaded with the resulting impuri- ties. The tongue becomes dry and brown- ish, with a red tip and margins, or a thick dark fur may form upon It behind. The pulse is very frequent and small, often irregular and uncountable.. Low, wandering delirium sets in, succeeded by coma. Profuse, clammy sweats break out, the extremities becoming cold. There are no marked cyanotic symptoms at first, but owing to the condition of the sensorium the need of expectoration is not felt, and thus the secretions accumulate in the tubes, this being aided by paralysis of the muscular fibres in the walls of the bronchi, which finally leads to slow suffo- cation. In many fatal cases, two classes of symptoms above described appear to be combined more or less. Certain compli- cations may occur greatly increasing the danger, the chief being lobular or more extensive pulmonary collapse, acute em- physema, lobular or lobar pneumonia, congestion ending in oedema, and pleu- risy. The term " Peripneumonia Notha" is applied rather vaguely to some cases of Bronchitis. With some it is synonymous with Capillary Bronchitis; but it seems more appropriately to refer to the disease occurring in an old or enfeebled subject, after some chronic malady, with febrile symptoms at first, but signs of adynamia, and deficient aeration of the blood setting in early 3. Bronchitis occurring in con- nection with the Exanthemata.- Some of these are never free from a cer- tain amount of bronchial catarrh, more especially typhoid fever and measles, and it may constitute the chief source of dan- ger. It is very apt to come on insid- iously without pain or difficulty of breath- ing, and scarcely any notable cough or expectoration. In short, physical signs may alone indicate the existence of the catarrh. On the other hand, the attack may be exceedingly severe, and mask for a time the nature of the fever. In mea- sles constantly, and in scarlatina usually, coryza exists at the outset, but in the other fevers it is commonly absent. The Bronchitis may come on early or late in the case. Should it be extensive, or the patient be much weakened, it is a serious complication, and may rapidly lead to a fatal result. It is important to bear in mind the non-occurrence of subjective symptoms, and that it is necessary to em- ploy physical examination of the chest at frequent intervals. 4. Bronchitis in connection with Blood Diseases.-In some instances it may be considered as truly secondary, de- pending immediately upon the poisoned state of the blood ; but in others this only acts as a strong predisposing cause. Here again the disease is prone to come on in- sidiously, without any marked symptoms, and also to last a long time, often becom- ing chronic. The expectorated matters are said to contain some of the poisonous materials which accumulate in the blood, such as sugar in diabetes, urea in Bright's disease, uric acid in gout, &c. 5. Bronchitis in connection with Chronic Lung and Heart Diseases. •-When occurring as the result of de- posits in the lungs, especially tubercle, Bronchitis is very commonly localized to their immediate neighborhood, and hence is often confined to the apex. It is not preceded by coryza, and there are usually no marked symptoms. Should there have been previous chronic Bronchitis, espe- symptomatology: MECHANICAL bronchitis. 325 cially with emphysema, upon which an acute attack has supervened, dyspnoea is ahvays considerable, and is liable to be- come extremely urgent, with early and grave cyanotic signs, particularly if the heart is also affected. (Edema of the ex- tremities, or even of the trunk, readily occurs. Pain is frequently absent, but the cough is distressing and severe. In cases of emphysema, the expectoration is at first very frothy, as wrell as abundant. Even a slight amount of acute Bronchitis, superadded to extensive chronic catarrh with emphysema, brings with it much danger. 6. Mechanical Bronchitis. - The various irritating substances, such as charcoal, &c., when inspired, at first give rise to slight but repeated attacks of acute catarrh, without coryza, not attended with pain or fever, but having an exceed- ingly irritable and frequent cough, with- out much expectoration, which contains some of the particles inhaled. The con- dition soon becomes chronic, and will call for a few further remarks when Chronic Bronchitis is treated of. Under this head it will be necessary to notice briefly those cases in which bron- chitic symptoms are brought on by the inhalation of certain vegetable matters, the most important being " hay-asthma," or "hay-fever." The symptoms of bron- chial irritation are prominent. There are frequent and severe paroxysms of cough- ing, but there is generally no expectora- tion, or at most, a small quantity of clear, thin, watery mucus. Breathing is much oppressed, and there is often considerable soreness behind the sternum. Marked coryza occurs, and other indications that the whole tract of the respiratory mucous membrane is involved ; much general lan- guor and want of energy is experienced, but fever is absent. Only a few, possess- ing a special idiosyncrasy, are liable to this complaint, and they are attacked on the slightest exposure to the exciting cause, and sometimes apparently even without this; hence they usually suffer every hay season. The symptoms come on suddenly, and are severe almost from the outset; they may last from two to six weeks or more. Ipecacuanha produces very similar ef- fects, and I am acquainted with a case which recently occurred, in which a severe attack resulted from smelling for a mo- ment a bottle containing ipecacuanha powder, as an experiment, the patient having previously suffered in a similar way. Physical Signs:-1. Inspection, (a) Form and size of chest rarely altered, but if the lungs are greatly distended, the chest may be somewhat enlarged, but equally so throughout. (6) Movements more frequent and more rapid than in health, in propor- tion to the amount of dyspnoea. Expira- tion is evidently difficult and ineffectual, and hence protracted. In most cases the abdominal movements are in excess of the thoracic, but if there is extensive ac- cumulation in the tubes, the upper costal movements become considerably the more marked, and elevation is often in excess of expansion. Much, however, will de- pend on age, sex, the extent of the tubes involved, Ac. In children, particularly if they are subjects of rickets, signs of more or less imperfect inspiration are com- monly observed. The epigastrium, ensi- form cartilage, and contiguous rib car- tilages sink in during each inspiratory act, the lower ribs are drawn in laterally, and the supra-clavicular regions become deeply hollow. Niemeyer mentions an- other sign of the same condition, viz. " prominence of the supra- and infra-clav- icular regions, with feeble respiratory movements. " 2. Palpation.-In addition to the signs mentioned under "Inspection," palpa- tion reveals usually "rhonchal fremitus," of variable quality and extent. It may be felt over a large area, without a large number of tubes being necessarily in- volved ; but should it continue thus for some days, it indicates widely-spread Bronchitis. The presence of this fremi- tus shows that some of the more super- ficial tubes are affected. It generally accompanies both inspiration and expira- tion, but it is often more marked during one or other act. A cough may cause it to disappear, or alter its position. Stokes states that it is more marked in females, and over the lower and middle part of the chest. It may be felt only in front, and over the upper part of the chest. This sign is of great importance in the physical examination of very young in- fants. Vocal fremitus varies widely, and cannot be relied on. Tussive fremitus is often well marked. 3. Percussion.-In most cases the area and amount of pulmonary resonance are not obviously altered. It not unfrequently happens, however, especially in children, that owing to the air-vesicles and small tubes being permanently distended in con- sequence of obstruction, the resonance is in excess, both in extent and degree, and is not diminished after expiration in the normal proportion. Rarely, a certain amount of deficiency in tone may be no- ticed over the base of the lungs poste- riorly, owing to great accumulation of secretion, congestion with oedema, or lobu- lar collapse; and the same may be ob- served in other parts of the chest, if col- lapse has resulted from obstruction of a large tube, or even extensively should the main bronchus be pressed upon by en- larged glands, which is said to happen 326 BRONCHITIS. sometimes. In infants, a sound resem- bling the " bruit de potfele" may often be produced by sharp percussion, especially during expiration, variable in its site. 4. Auscultation, (a) Respiratory Sounds. - These vary considerably in different parts of the chest. Where the tubes are free the sounds are loud and exaggerated, and this is usually the case towards the upper part of the thorax. Over the affected regions they are weak, and may become totally suppressed, owing to the narrowing or complete closure of the tubes by thickened membrane and secretion ; or temporarily, from spasm of the muscular fibres. Their quality is always harsh and coarse, and expiration is prolonged. In the early stage the sounds seem dry, but later on certain rhonchi are mingled with them, by which they may be completely masked. (b) Adventitious Sounds. - These in- clude the various "rhonchi" produced by the air passing through tubes containing fluid, or diminished in calibre by thick- ened mucous membrane or spasm. They vary with the nature and quantity of the fluids, the size of the tubes in which they are originated, &c., and are divided into "dry" and "moist." The former com- prise the " sonorous," which are very low- pitched and grave in tone, resembling the sound of snoring generally, but sometimes of rubbing or other quality, often heard extensively, and giving an impression of superficialness in their origin; and the "sibilant," which are high-pitched, and may be musical, hissing, or whistling. If the sibilant rhonchi are extensively heard, it indicates that the smaller tubes are affected. Occasionally " clicking" sounds of dry character are observed. The "moist" rhonchi are all more or less bubbling, being caused by the passage of air through fluid. They vary much in size, quality, and pitch, according to the quantity and consistence of the fluid and the dimensions of the tubes in which they are produced, and the varieties are named "mucous," "submucous," "sub- crepitant," &c. Occasionally they have a "rattling" character. It will be readily understood that these rhonchi are variously combined, and are heard in different parts of the chest, ac- cording to the seat, extent, and stage of the Bronchitis. Generally they exist on both sides, though not to the same degree, but may be localized to a part of one lung. At first the "dry" may alone be present, but the "moist" are soon added, and frequently both forms are perceptible from the first. The "moist" are usually most marked behind and towards the base of the lungs. All kinds are liable to change their sites, as well as to disappear for a time, sometimes suddenly, either from the secretions having been driven out of the tubes, or because these have become thor- oughly blocked up. A strong cough will often disperse many of them. These re- marks are especially true with regard to the sonorous and sibilant rhonchi. When Capillary Bronchitis is present, abundant and very minute bubbling rhon- ich are heard towards the lower part of both lungs, accompanying inspiration and expiration, and completely hiding the breath-sounds ; while higher up they are larger, and the respiratory sounds are perceived, altered in quality. This may be partly the result of gravitation, but very extensive and minute rhonchi indi- cate that the smaller tubes are themselves implicated. (c) The action of the heart sometimes causes rhonchal sounds. Vocal resonance is not materially al- tered in either direction. The cough is generally very loud, and gives rise to a number of rhonchal sounds. 5. Position of Organs.-As a rule this is normal, but if the lungs are greatly dis- tended the diaphragm is depressed, and with it the liver and spleen somewhat. The heart is said to be pushed downwards and to the right. In some cases which have recently fallen under my notice in the post-mortem room, the heart was so placed that its right border lay almost horizontally on the diaphragm,' and its apex was outside the left nipple-line, oc- cupying a similar position to that de- scribed by Niemeyer as occurring in em- physema. Duration and Termination. - In the milder forms the duration varies from four or five days to three weeks or more, but a case is usually convalescent under nine to twelve days. In fatal cases of Capillary Bronchitis death generally oc- curs in a few days, but it is difficult to lay down any certain average. Walshe gives from the sixth to the eighth day for chil- dren, from the tenth to the twelfth for adults. Convalescence is not thoroughly established for some time in cases that recover, but generally begins under three weeks. The clinical terminations are: (a) complete recovery, (b) death, (c) transi- tion into the chronic state. Relapse may occur, or an extension of the Bronchitis ; but this is not common. As already men- tioned, it is an affection very liable to re- cur. It should be mentioned that it may leave behind it permanent emphysema, or may be the foundation of certain forms of phthisis. Niemeyer believes that ex- tensive acute bronchial catarrh is the most common cause of " galloping con- sumption." Diagnosis.-The characteristic symp- toms of ordinary Bronchitis are the vari- ous sensations behind the sternum, a PROGNOSIS AND MORTALITY. 327 greater or less sense of oppression, often amounting to dyspnoea, with wheezing, cough, and expectoration, having the characters already described. The pre- vious catarrh, as well as the general symp- toms, with slight but repeated rigors, and absence, or comparatively small degree, of fever, are also important. The more significant physical signs include absence of dulness, or any material alteration in the vocal fremitus or resonance; the char- acters of the breath-sounds, but especially the presence of the various rhonchi, as indicated by palpation and auscultation. In the majority of cases there is no diffi- culty in arriving at a proper diagnosis, but doubt may arise in some instances. It will be necessary to notice briefly the special diagnosis of Bronchitis from cer- tain other affections. It cannot be decided in the earlier stage of hooping-cough, whether the case is not one of Bronchitis. Subsequently the paroxysmal nature of the attacks-with the peculiar cough and expectoration, often followed by vomiting-is sufficiently characteristic of hooping-cough. How- ever, it may be complicated with Bron- chitis, which is then revealed by its phy- sical signs. In some children the breathing of Bron- chitis may at first somewhat resemble that of croup, the cough being at the same time hard and ringing or husky, and the voice affected. The evidences of Bron- chitis in such a case are, the presence of catarrh ; breathing less affected, and not truly stridulous, but wheezing ; fever ab- sent or slight; the cough is soon moist, and expectoration may be obtained by wiping the base of the tongue, which does not contain any shreds of membrane. Physical examination also shows the ex- istence of rhonchi, &c. Laryngitis in the adult is distinguished by its own special symptoms, which are localized in this part, and by the absence of the chest-symptoms and physical signs of Bronchitis. Pneumonia occurring in the adult is usually easily diagnosed from Capillary Bronchitis by attention to the following points. There is a single, prolonged, and severe introductory rigor, followed by in- tense fever, with a burningly hot and dry skin. A sharp pain is experienced in the side, and the cough is less marked, being usually attended with rusty expectoration. The pulse-respiration ratio is more dis- turbed, but the sense of dyspnoea is less, and there are no cyanotic appearances. Physical examination discloses dulness, increased vocal fremitus and resonance, crepitant rhonchus, and bronchial or tu- bular breathing, in pneumonia, usually limited to one base. When an acute at- tack supervenes upon Chronic Bronchitis, it may give rise to dulness at one base, and respiration may become high-pitched, bronchial, or even diffused blowing, but it is never actually tubular, and vocal resonance is not of a metallic and sniffling character. In such a case attention must also be paid to the symptoms. From lobular pneumonia occurring in children the diagnosis is often difficult. In this affection frequently no dulness can be ob- served, or it may be present in Bronchitis from collapse. In the latter the moist rhonchi are much more diffused, and of larger size ; at first they are generally limited to, and throughout are most marked at the bases, whereas in lobular pneumonia they are scattered irregularly. Tubular breathing is not heard in Bron- chitis. There is less fever, and the skin is not acridly hot, being often moist. The respirations are more frequent in lobular pneumonia, but the sense of dyspnoea is much less as well as the asphyxial appear- ances and general anxiety. The symptoms and physical signs of pleurisy are so totally different from those of Bronchitis, that it does not appear necessary to say anything as to their diagnosis. When a child is attacked with bronchial symptoms, it is sometimes difficult to de- termine at first whether they constitute the entire ailment, or are associated with one of the exanthemata. The amount of fever as evidenced by the thermometer, and the special symptoms premonitory of the various fevers, must be the guides until the eruption appears. The same applies to typhoid fever, at any age, which may be at the early period masked by the bronchial catarrh if its ordinary symp- toms are not prominent. The thermome- ter will prove of great value in any such cases. From the various forms of acute phthisis, Capillary Bronchitis may be distinguished by the following characters. The fever is much less, and consequently the temperature is considerably lower; the pulse-respiration ratio is less pervert- ed ; signs of asphyxia set in ; there is free expectoration of a muco-purulent charac- ter. There are abundant dry and moist rhonchi, the latter being most marked be- low. In one form of acute phthisis there are signs of consolidation, followed by those of cavities. In the true tubercular miliary form there are hardly any physi- cal signs except scattered rhonchi, which are most abundant towards the upper part of the lung. The dyspnoea is very great, and there is violent fever. Prognosis and Mortality.-As will be seen from the tables given when con- sidering the causes ofBronchitis, this is a disease attended with much danger, espe- cially if it be extensive. Its prognosis must be guided by the following circum- 328 BRONCHITIS. stances: 1. Age. The mortality is far greater among children, especially young infants, and the aged, than in adults. 2. State of Health. The danger will be increased in proportion as this is below par, and particularly if there is any posi- tive disease present, either acute or chronic. 3. Extent of inflammation. If both lungs are widely affected with Capil- lary Bronchitis, the prognosis is grave, even in healthy adults. 4. Previous state of the lungs and heart. Any chronic dis- ease of these organs will seriously aggra- vate the danger, but especially extensive emphysema, with dilatation of the right cavities of the heart. 5. Special symp- toms. Those of evil import are-exces- sive expectoration, of thick and viscid character, and brought up with difficulty ; suppression of cough, with accumulation of secretion in the tubes; very frequent and rapid breathing, with signs of as- phyxia ; quiet and shallow breathing in an otherwise bad case ; evidences of im- perfect inspiration in children ; very fre- quent and feeble pulse ; adynamic symp- toms ; the head being kept on a low level from the first in a grave case. 6. Presence of complications. Those that add gener- ally to the gravity of the case are-col- lapse ; pneumonia, lobar or lobular; con- gestion with oedema ; acute emphysema : pleurisy; gastric or intestinal catarrh. 7. Epidemic character. 8. Time and method of treatment. The sooner appropriate care and treatment are adopted, the more likely is a case to be brought to a favor- able issue. Pathology. - Bronchitis is in most cases a catarrhal inflammation of the mu- cous membrane lining the bronchial tubes, and is often associated with a similar con- dition in the trachea. The membrane becomes hypersemic, and, as a result of this, excessive fluid is soon poured out into the tubes, as well as into the sub- stance of the tissues. Nutrition is per- verted. and an excessive formation of cells takes place on the surface of the membrane; these are thrown off* in a more or less imperfect state, and, min- gling with the fluid, give rise to the va- rious corpuscles seen in the expectoration, to which this principally owes its increas- ing opacity. In many cases it is a purely local complaint, the result of direct irrita- tion ; in others it is but a part of some general condition of the system, produced under the influence of " cold" and other agencies, in which the mucous membranes are very liable to suffer more or less ex- tensively. Again, in some instances it appears to be an attempt on the part of the membrane to assist in throwing off some morbid material contained in the blood, which is attended with congestion. With regard to what is termed "Capil- lary Bronchitis," in many instances un- doubtedly this term is properly applied. There is an actual inflammatory state of the smaller tubes, which may either ex- tend from the larger tubes, or originate there in the first instance, or, I believe, may in some cases be caused by the irri- tation of secretions formed in the larger tubes, running back into the smaller. But in other instances there are no evi- dences of any inflammation in the capil- lary tubes, and it seems probable that there is merely a collection of fluid in these tubes, which has flowed down from those of larger calibre, in consequence of a want of power to expectorate. This would be aided by gravitation, as well as by the destruction of the ciliated epithe- lium, and, after a while, by paralysis of the muscular fibres in the walls of the bronchi. The fluids thus accumulating, added to that normally forming in the tubes, which might be somewhat increased from congestion, would account for the serious symptoms in these cases. The fever which may accompany Bronchitis is not usually due to the inflammation, but is a part of the general state. None is present if the affection is local and limited. The asphyxial symptoms are easily explained by the obstruction in the air-tubes, and consequent interference with the due aeration of the blood. In proportion as the vital powers are below par will be the tendency of the combined fever and imperfect respiratory process to lead to a fatal result. Morbid Anatomy.-On opening the thorax of a person who has died from ex- tensive Bronchitis, the lungs do not col- lapse, but remain distended, or may even bulge out: this is caused by the air being unable to escape through the obstructed tubes, and even pressure cannot mate- rially diminish their bulk. The degree of this distension will, of course, vary with the number and size of the tubes affected. The mucous membrane pre- sents various forms of redness, and gene- rally all are seen more or less in the same case. Thus, it may be arborescent, ca- piliform, mottled, streaked, in points, or diffused, but it is not uniformly spread over a large surface as a rule. In tint it may vary from a bright, vivid pink-red, to a somewhat dark, venous hue, the lat- ter being observed in the later stages. It is sometimes scarlet, and has a velvety appearance. The redness does not ordi- narily extend beyond the fourth or fifth divisions, often not beyond the second or third, but it is said that even the finest ramifications may exhibit it. It is gener- ally more marked towards the upper part of the lung. Possibly the action of the elastic and muscular fibres in the walls of the bronchi may diminish it after death. TREATMENT. 329 Where the tubes bifurcate, it is often well marked. Thickening and opacity of the membrane are also observed, to a greater or less degree, from distension of the vessels and infiltration into its sub- stance ; from this cause, as well as fre- quently from the presence of exudation in the submucous tissue, the tubes are re- duced in calibre, but unequally, and the surface of the membrane appears uneven. The more minute tubes may be completely closed up; and this is especially apt to happen in young children. The tissue of the membrane is relaxed and softened ; often it cannot be stripped off for any length. Patchy abrasions of the epithe- lium are frequent, giving sometimes an appearance of slight ulceration, but this is never observed in children (Vogel). In the very early stage abnormal dryness is observed, or a very small quantity of transparent tenacious substance covers the surface. Soon excessive secretion is formed, and various materials are found in the tubes, corresponding to the differ- ent stages of the expectoration. They may be so abundant as to extend from the finest ramifications up even to the trachea, completely filling all the canals. In appearance the contents of the tubes resemble frothy mucus, or a muco-puru- lent, or even purulent-looking fluid; the degree of viscidity and adhesion to the surface of the membrane varies, but is usually marked. More or less blood may be present. Sometimes a fibrinous-look- ing material is seen attached to the sur- face, lying loose in flakes or masses, or even forming complete casts of the smaller tubes, which may be hollow or solid. The microscope reveals epithelium scales, per- fect and ciliated in the early stage, but afterwards imperfect, small and some- what oval in shape ; so-called mucus and exudation corpuscles; large pus-corpus- cles, containing numerous granules; some- times blood disks; granular material in abundance. More cells are observed in proportion to the opacity of the fluid. It is in the lower and more dependent parts of the lungs that the secretions are found in largest quantity. In some cases, es- pecially in children, small yellow spots are visible near the surface, due to accumu- lation in the air-cells and minute tubes. Along with the Bronchitis, and as the result of it, lobular collapse is very com- monly observed, as was first pointed out by Dr. Gairdner. This condition is par- ticularly frequent in young children. If a large tube is blocked up, more extensive collapse is present. In some cases the bronchial tubes are slightly but uniformly dilated, and acute emphysema is said to occur, but it is a question whether in these cases the air-vesicles are usually ac- tually distended beyond their normal size in deep inspiration, and therefore whether the term emphysema can be properly ap- plied to this condition. Lobular pneu- monia is occasionally present, and may be preceded by collapse. Ordinary lobar pneumonia is rare. There may be more or less congestion of the lungs with oede- ma, or these organs may be natural in hue, or even paler than normal. The bronchial glands are often large, red, and softened. The blood is dark, and the venous sys- tem, with the right side of the heart, over- loaded. Of course the morbid appearances char- acteristic of Bronchitis will vary accord- ing to its extent. Both lungs are usually involved, but seldom to the same degree ; nor is one lung affected uniformly through- out. Different conditions are seen in dif- ferent parts of the same lung. The mem- brane lining the smaller tubes suffers less than that of the larger, but more secretion is sustained in the former. In cases of death from other causes, more or less Bronchitis is often present. Treatment.-No case of Bronchitis, however slight, should be neglected, be- cause a little care and appropriate treat- ment at the outset may soon put an end to an attack which otherwise might become very serious or even lead to a fatal result. It must be remembered also that a ca- tarrh, if overlooked at first, may lay the foundation for certain favorable chronic affections. The treatment will necessa- rily vary much according to a variety of circumstances, and therefore no uniform method can be laid down. I shall first consider the mode of dealing with an or- dinary case resulting from cold, and after- wards notice any modifying conditions which may appear to call for remark. It is always well, if possible, to make the patient keep to the house, or even to one room, maintained at a uniform tem- perature of 04° to 66° Fahr., if the weather is at all unfavorable; but under any circum- stances damp night air must be avoided. Lying up thus for two or three days, will often cure a catarrh. It is customary as well as, I believe, useful in these cases, to endeavor to bring about a free action of the skin. For this purpose a copious warm drink may be given before going to bed, such as hot milk, mulled claret, warm elder wine, or even some strong alcoholic stimulant, such as hot spirit and water. A warm foot-bath should be used, and some mustard and salt may be added to the water. A large quantity of bedclothes should be put on the bed, and the patient should sleep between blankets. Finally a full dose of Dover's powder may be ad- ministered, or a diaphoretic and saline draught. -Some recommend a hot-air or vapor bath, and a Turkish bath has cer- tainly often the effect of curing a cold. 330 BRONCHITIS. Wrapping the body in wet sheets is em- ployed by some in order to procure free perspiration, and does not seem to be at- tended with danger. It is generally ad- visable to apply a large mustard poultice over the front of the chest, and to allow steam to be inhaled for a few minutes. If the case is a severe one from the first, and attended with fever, or if it is not checked by the above treatment, more active measures will be required. Venesection has been practised exten- sively in this disease. In most cases it certainly is not required, while in those of a more serious type it is extremely rare to meet with the combination of condi- tions which warrant the taking of blood from the arm. These conditions are said to be where the inflammation is marked and extensive, occurring in a robust and healthy young or middle-aged adult, and accompanied with severe sthenic fever. It can be safely affirmed that venesection is scarcely ever called for, at all events in town districts. Local bleeding by leeches or cupping may certainly be employed with advantage in some cases, but great discrimination is necessary even in the use of these modes of removing blood, and in the great majority of instances they can well be dispensed with. If leeches are used, they should be applied over the front of the chest, or sometimes at the base posteriorly. Their number must vary according to circum- stances, but certainly more than from five to ten are seldom advisable. In plethoric children, the blood removed by two or three leeches sometimes relieves great dyspnoea very effectually. Cupping may be performed either in front or behind, if thought necessary, to the extent of from three to six ounces. It is certainly improper to adopt, as the ordinary practice, any mode of removing blood in cases of Bronchitis; it is far safer to act on another principle. In any doubtful case the patient will stand a better chance of recovery if no blood is taken away. Free dry cupping over the chest, both front and back, is often of much service, relieving the oppression and dyspnoea, and it is quite devoid of danger. An Emetic, in the form of tartar emetic, or ipecacuanha, is made use of by some at the outset, especially in children. Though extremely valuable in certain conditions, it appears to me that it may well be dis- pensed with at this time. The bowels may be freely opened by some aperient, varying according to the age and condi- tion of the patient, and throughout the case mild purgatives must be used as re- quired. [There is a strong and reasonable ob- jection in the minds of many practitioners, to the use of tartarized antimony as an emetic with young children. With infants under two years of age, 1 believe it ought never to be so employed ; and rarely, with them, even as a sedative in minute doses. Very small quantities of it will sometimes, in children, produce alarming depres- sion.-H.] Among medicinal substances, tartar emetic ranks as one of the most important during the early stage of Bronchitis. The dose must be regulated by circumstances, but from a third to half a grain every four hours is usually sufficient for an adult. It may be given in a saline draught, con- taining liquor ammonise acetatis, and its effects should be carefully watched. Tincture of digitalis is also employed by some at this period of the case, and often with marked benefit. Calomel with opium is recommended if either of the above can- not be taken from any cause, but it seems to me of very doubtful efficacy, and might be often injurious. As the case progresses, and secretions form in the bronchial tubes, the main indications which medicines have to fulfil are the following: 1. To assist expectoration. 2. To alleviate cough, due regard being had to the proper discharge of the secretions. 3. To diminish the quantity of the expectora- tion. 4. To allay spasm of the tubes, if present. These are carried out by the administration of various expectorants, sedatives, narcotics, and antispasmodics, in different combinations, along with dia- phoretics or demulcents. The chief ex- pectorants are ipecacuanha wine, tincture or oxymel of squills, compound tincture of camphor, and, later on, sesquicarbonate of ammonia or chloride of ammonium, senega, serpentary, galbanum, ammonia- cum, tincture of benzoin and balsam co- paiba. The sedatives and narcotics prin- cipally used are hyoscyamus, conium, opium, or morphia, and hydrocyanic acid. The most important antispasmodics in- clude sulphuric ether, ethereal tincture of lobelia, and spirits of chloroform. These various medicines must be em- ployed as they are required, and no rules can be laid down as to their precise use ; but it may be stated that the less stimu- lating expectorants should be given at first, and narcotics, especially opium, must be used with very great caution if expectoration is difficult, and the secre- tions tend to accumulate. Local Applications.-Sinapisms are bene- ficial even from the first, and may be re- peated over different parts of the chest. Hot applications are also of much value in the early period, especially hot moist flannels, which may be sprinkled with turpentine, or linseed-meal poultices, which should be large, applied very hot, changed frequently, and continued for some time. The latter are particularly valuable in children. Blisters are called TREATMENT. 331 tbr after expectoration sets in and the acute symptoms have subsided. One of good size may be placed over the front of the chest, or some recommend the inter- scapular region behind as the best place for a blister, because more fluid will be drawn there, but the discomfort caused is a great objection. In children the blister maybe left on only for two or three hours, and afterwards a linseed-meal poultice applied. If the affection is tending to become chronic, other forms of counter-irritation may be employed, as the application of croton oil liniment, or acetic acid. Inhalations.-In the early stage inhala- tions of simple steam are decidedly useful in many cases, especially if the larynx is in an irritable condition, and giving rise to constant cough. Later on medicated inhalations are of service under certain circumstances, such as those of conium, sulphuric ether, or chloroform, if there is much spasm; those of tar, or creosote, if the expectoration continues very abundant. Diet and Regimen.-It is quite unne- cessary to keep patients on too low a diet, and they may have a fair quantity of beef-tea and milk from the first. With regard to stimulants, it is impossible to lay down any positive rules. Ordinarily they are not required, and might be in- jurious ; but if there are any indications for their administration, such as a tend- ency to adynamia or asphyxia, they should be given without delay, and their effects watched. Any case that is at all severe should be absolutely confined to the bedroom, kept at a temperature of 66° to 68° Fahr., the air being moistened by steam from a kettle kept constantly boiling ; at the same time the room should be occasionally well ventilated, the pa- tient being protected from draughts. Warm clothing must be worn, including flannel, with a sufficient amount of bed- clothes. The head should be kept high, and cough should be encouraged, if there appear to be any indication that the secretions are not properly discharged; on the other hand an irritable cough may sometimes be subdued by an effort of the will. In treating children, emetics are useful at the outset, if the attack is severe. For ordinary cases, ipecacuanha wine consti- tutes a valuable medicine. They should be encouraged to cough, if old enough, and means should be used to make them breathe freely and expectorate; sleep must not be too prolonged or deep. The throat should be cleared occasionally from mucus by means of the finger; and if the physical signs show that fluids are accu- mulating in the tubes, an emetic ought to be given, the best being sulphate of zinc. Narcotics must be used very cautiously in children. They should drink freely. Attention must be paid to their constitu- tional state, such as rickets, tuberculosis ; and if either of these exist, all depressing treatment must be carefully avoided. The quality and quantity of the milk should be looked to. In aged persons and those who are de- bilitated or are suffering from any acute or chronic disease, depletion in any form is inadmissible. Antimony can only be given very cautiously, and, in most cases, stimulants and stimulant - expectorants are required from the first. Wine or brandy, with plenty of strong beef-tea and other nourishment, must be adminis- tered, in quantities according to the re- quirements of the case. Sesquicarbonate or muriate of ammonia, cinchona, cam- phor, sulphuric ether, spirits of chloro- form, senega, squill, galbanum, ammoni- acum, are the medicines called for. In most cases of Capillary Bronchitis the stimulant treatment is decidedly that which yields most favorable results. If the Bronchitis originates from any con- stitutional condition, such as gout or tu- berculosis, the treatment appropriate for these affections must be employed. When an acute attack supervenes upon Chronic Bronchitis, free dry cupping, with flying blisters over the chest, are very serviceable. If asphyxial symptoms set in, the stimulant treatment must be per- severed in. Chlorate of potash may be given frequently as a drink ; artificial res- piration and galvanism along the course of the vagus nerve are recommended in extreme cases, and the former may be carried out in children persistently when- ever there are signs of danger. A warm bath, with cold affusion while in it, is also advocated by some as an effectual mode of combating asphyxia. If there is a great amount of fever, and there seems to be danger from this cause, quinine is advisable, in doses of from two to three grains every three or four hours. During convalescence, tonics, such as quinine, mineral acids, iron, may be added to the other medicines. The cloth- ing should be warm, and a pitch-plaster may be worn on the chest. Cold and damp must be avoided for some time, and the patient should not neglect proper precautions until perfectly convalescent. In those who are subject to Bronchitis, prophylactic measures are called for. All causes likely to bring it on must be avoid- ed ; if possible, a change to a warm cli- mate during the cold season should be enjoined. Cold sponging is useful, espe- cially for children, who should be properly clothed, but not immoderately. Consti- tutional treatment may be called for. With regard to the treatment of hay- asthma, during the attack small doses of dilute hydrocyanic acid, with tincture of lobelia and other antispasmodics, fre- 332 BRONCHITIS. qucntly repeated, seem to act best. In- halations of creosote are also recommend- ed, or of an atmosphere containing a small proportion of chlorine. In the in- tervals general tonic measures are useful, such as quinine and iron, with cold bath- ing. Arsenic and nux-vomica are also employed. Dr. Reynolds has found much benefit from the systematic inhalation of chloroform, from a handkerchief, four or six times a day.1 In the spring any one subject to this affection should go to the sea-side or take a voyage. Chronic Bronchitis. Chronic Bronchial Catarrh. Causes.-Much that has been said on this head with regard to Acute Bronchitis applies to the chronic form also. In fact, it usually is the result of the acute affec- tion, remaining sometimes even after a single attack, especially if the deeper structures of the tubes have become in- volved, but in the great majority of cases being due to several repeated attacks. The complaint may be chronic from the first, coming on slowly; and this is par- ticularly the case in old people. It is commonly associated with any chronic lung disease which may exist, but espe- cially emphysema or dilated bronchi and the various forms of phthisis. In the lat- ter affection much of the expectoration arises from a chronic catarrh of the mu- cous membrane. The presence of certain heart diseases, interfering with the circu- lation, frequently leads to Chronic Bron- chitis, especially some forms of it. Va- rious blood affections, notably gout, pre- dispose to it greatly. The inhalation of the different irritating particles, already alluded to, soon causes the affection to be- come permanent and chronic. Old peo- ple suffer in a much larger proportion than those who are younger, but the com- plaint may be present even in children, particularly after measles and hooping- cough, or where tuberculosis exists. It frequently exists in connection with chronic alcoholism. Symptomatology.-The local symp- toms of Chronic Bronchitis are in kind similar to those attending the acute form, viz. cough, usually accompanied with ex- pectoration, more or less oppression in the chest or dyspnoea, and frequently un- easiness behind the sternum, which, how- ever, is never considerable, and may be absent. These differ materially as to their degree in different cases, and they are variously combined, while certain con- ditions of the lungs and heart modify them, so that it becomes necessary to classify them into certain groups. The constitution may not be aflected in the least, or, on the other hand, may suffer severely. It will be necessary to describe three chief forms, which are mainly distin- guished by the quantity and characters of the expectoration attending each variety, and the qualities of the cough. 1. The first group about to be consid- ered includes the ordinary cases of Chronic Bronchitis, which present innumerable grades of severity, both in the intensity of the symptoms and in their degree of persistence, and the same case will often exhibit these grades during its progress. At first the patient is only attacked during the winter, having what is termed " winter cough," and being perfectly well during the warmer months. Afterwards the attacks become more frequent, until finally the complaint becomes permanent, but is always aggravated whenever cold weather sets in. The cough may not be severe, only occurring in comparatively slight paroxysms, at considerable inter- vals ; or it is more or less constant, but also increased in paroxysms, which are often very violent and distressing. They are worse at night usually, on first going to bed, but they are especially severe in the mornings, on account of the secretions having accumulated. In bad cases, sleep is much disturbed by fits of coughing during the night. The expectoration may be brought up without much difficulty in the less ad- vanced cases, but later on it is discharged only with great trouble, as well on ac- count of its own characters as the state of the bronchial tubes, in the smaller of which it is chiefly formed. It varies in quantity greatly, being sometimes incon- siderable, at other times exceedingly abundant. In the slighter cases, it con- sists of yellowish-white or grayish masses of muco-purulent matter chiefly, contain- ing a number of young, imperfect cells. In others it may be partly in the form of viscid, tenacious, grayish mucus, but the greater portion of it is muco-purulent or purulent in appearance, usually of a yeh lowish-white color, but often greenish-yel- low, and sometimes bright or dark-green. As a rule, it is not much aerated, and often not at all; hence it may sink in water, either partly or entirely, but often floats. The different masses may remain distinct, but usually run more or less together. True " nummulated" masses of large size are occasionally seen. All the forms of expectoration tend towards opacity, and it is not uncommonly thor- oughly opaque ; an exceedingly disagree- able odor is often present in bad cases, which may amount to extreme fetor. This is supposed to be due to some chem- 1 See Lancet, " On the Value of Chloroform Inhalation in certain Classes of Spasm." CHRONIC BRONCHITIS: SYMPTOMATOLOGY. 333 teal change, and butyric and other acids have been detected, as in a case of Dr. Laycock's. Minute microscopic sloughs of the mucous membrane have also been considered as its cause. Streaks of blood may be observed, especially if the cough is very violent and expectoration diffi- cult, and still more if heart-disease exists. With the aid of the microscope, abundant imperfect epithelium-cells are seen with pus-cells and granular matter. Blood- corpuscles are frequently visible also. There may be not the least uneasiness or pain behind the sternum, or it may be present at first, and afterwards cease. Generally a certain amount exists, and particularly a sense of soreness after severe cough. In severe cases, breathing is somewhat short on exertion, and during the fits of coughing the respirations are increased in number, but evident dys- pnoea does not exist, unless there is em- physema. The constitution does not suffer in the milder attacks, and the general condition is unimpaired ; but in permanent and ex- tensive Chronic Bronchitis the system is gravely affected, on account of the inter- ference with sleep, abundant expectora- tion, and other circumstances. The flesh wastes, and emaciation may become mark- ed, but it does not go beyond a certain point, and then remains stationary. The strength is reduced in proportion to the wasting. A slight degree of fever often sets in towards the evening, followed by copious sweats at early morning, and there may be marked hectic fever. This in- creases the loss of flesh materially. The digestive organs usually suffer to a greater or less extent, as evidenced by a furred tongue, deficient appetite, and constipa- tion. If the system is much implicated, the patient is quite unable to follow any employment. 2. A very characteristic class of cases is that which is described under the terms "dry catarrh" ("catarrh sec" of Laen- nec), or "dry bronchial irritation." In this form of Bronchitis very little secre- tion is produced, and that principally in the smaller tubes. The mucous mem- brane is in an exceedingly irritable state, and hence violent, prolonged, and very distressing fits of coughing come on. dur- ing which the face becomes turgid and red, and the veins swell out, the smaller vessels at last remaining permanently dis- tended. There is, as a rule, no expectora- tion at the close of the paroxysm, but sometimes a small mass of tough, viscid, semi-transparent grayish mucus is dis- charged, compared to boiled starch or pearl, or a little thin watery fluid. Much soreness is frequently experienced in the chest after a spell of coughing. There is persistent shortness of breath, which may amount to extreme dyspnoea at times, should a large bronchus be blocked up, or acute catarrh set in. In some instances spasm of the bronchial tubes evidently exists. A feeling of constriction about the chest is always present. Vomiting may occur during a paroxysm of cough. Febrile symptoms are usually entirely ab- sent, but there may be an occasional slight rise of temperature ; as a rule the general condition is unaffected. This form of Bronchitis is liable to lead to emphysema, and is commonly associated with this con- dition in variable degree. It is frequently met with in gouty people, and is said to be prevalent at seaside places, and to come on after the cure of chronic cutane- ous diseases, and in those weakened by excesses. 3. The third variety is named "bron- chorrhoea," which, as its name indicates, is distinguished chiefly by the abundance of the expectoration, but also partly by its characters. It often occurs in old, feeble persons, after several attacks of acute Bronchitis, particularly when there is some heart affection present obstructing the circulation. The cough comes on in paroxysms, which are often spasmodic and severe, but may be slight compared with the quantity of expectoration. A fit may set in every day, or even several times a day, and it ends with, and is re- lieved by, profuse expectoration, which is almost clear, transparent, thin, and watery; or thick, ropy, and glutinous, compared to unboiled white of egg mixed with water. It is a little frothy on the surface, but the general mass contains no air. The quantity discharged may be very great, sometimes amounting to four or five pints in the twenty-four hours, and frequently a quarter or half a pint is ex- pelled within an hour ; and the amount of fluid poured out into the tubes may be so excessive as to cause fatal exhaustion or asphyxia, especially in aged individuals who are unable to expectorate. During the paroxysms there is considerable dys- pnoea, but at other times this is not much observed. The strength fails and the flesh wastes in severe cases, but the con- stitution may not suffer for years if the expectoration is limited, and it may even relieve the local symptoms produced by certain forms of cardiac disease, which lead to congestion and inflammation of the lungs. With regard to the form of disease pro- duced by irritant particles, all that it seems necessary to add here is, that after a while the symptoms of bronchitic irrita- tion become chronic, with a constant dryish cough, and subsequently consolida- tion takes place, which leads to destruc- tion of the pulmonary tissue, and thus cavities are ultimately produced. At first there are no general symptoms, but after- wards emaciation and exhaustion set in. BRONCHITIS. 334 Usually the course of these cases is very chronic, but it may be tolerably rapid. It must be borne in mind that very rarely does Chronic Bronchitis exist in an uncomplicated form, and its symptoms will be materially modified by co-existing states of the lungs and heart, and also by the constitutional condition of the patient. Physical Signs.-It is difficult precisely to define what physical signs are associated with Chronic Bronchitis as its direct re- sults, because there are so many other morbid conditions generally added to it. 1. Inspection.-In ordinary cases there is nothing abnormal in the form and size of the chest, but it may be equally and generally enlarged, especially in dry catarrh, in which it is drawn up and made more convex; but here, probably, more or less emphysema exists. The movements are deficient in bad cases, es- pecially that of expansion, and expiration is seen to be prolonged and labored. 2. Palpation reveals rhonchal fremitus over various parts of the chest, subject to changes in amount and site. The vocal fremitus is not obviously altered. 3. Percussion. - In most instances of confirmed Chronic Bronchitis, it will be found that the resonance is increased in extent and degree on account of co-exist- ing emphysema. Similar conditions to those mentioned under the acute form may cause temporary and localized dulness. 4. Auscultation. - The breath-sounds are much weakened usually, but vary in different parts of the chest. After a free expectoration they may be heard exten- sively. Their quality is always harsh and coarse, and sometimes markedly so. In unaffected parts they are exaggerated. Expiration-sound is much prolonged in long-established cases. Rhonchi of vari- ous kinds are heard, but the "dry" are most abundant. The " bubbling" rhonchi are of large, coarse character, and are often temporarily absent. They are al- tered by cough and deep inspiration, as in the acute affection. It will be readily understood that these rhonchi will vary in the different kinds of Chronic Bron- chitis, according to the quantity and con- sistence of the fluids contained in the tubes. In bronchorrhoea the bubbles give the idea of being produced in a thinner fluid than that of the ordinary form, while in dry catarrh they are necessarily absent. Vocal resonance is very variable. It may be bronchophonic, normal, deficient, or absent. 5. Displacement of Organs.-Owing to the emphysema accompanying Bronchitis, there is usually more or less displacement, particularly of the heart. Diagnosis.-There is scarcely ever any difficulty in diagnosing the presence of Chronic Bronchitis, but this is frequently experienced in determining with what conditions it is associated. Where there is much emaciation, with abundant puru- lent expectoration, it may simulate cer- tain forms of phthisis, but the compara- tive degree and rapidity of wasting, absence of or only slight fever as a rule, want of haemoptysis, and other symptoms present in phthisis, as well as the physical signs, will distinguish them. It is only when there are dilated bronchi, that usu- ally much difficulty is felt in arriving at a correct diagnosis, and these cases are con- sidered elsewhere. Prognosis.-No case of Chronic Bron- chitis ought to be looked upon as unim- portant or treated lightly. Though it does not of itself often cause death yet in proportion to its extent does it become dangerous, as an acute attack may set in at any moment; and however slight this may be, the danger in such a case be- comes considerable, on account of the difficulty in expelling the secretions from the tubes. At the same time it is a se- rious affection, because it tends to become more diffused, and also to give rise to certain important and incurable sequelae. These are chiefly emphysema, dilated bronchi, and collapse. Many pathologists believe, also, that by extending into the air-vesicles it may be the immediate cause of a form of phthisis; in fact, what they consider the ordinary form of pulmonary consumption. Others are of opinion that by causing irritation it leads to a deposit of true tubercle. Much will depend upon the variety of the disease which is present, the amount of expectoration, its effect upon the constitution, the age of the pa- tient, the state of the lungs and heart, and other circumstances. It is said that complete and permanent recovery may take place in the young, if they are taken to a proper climate and treated carefully. In almost all cases it is incurable, when once it is well established. Pathology and Morbid Anatomy. -Many cases of Chronic Bronchitis are simply due to congestion, usually passive, sometimes more or less active, of the bronchial mucous membrane; others pre- sent a so-called inflammatory condition of the membrane, also involving the deeper structures after a while. Hence there is permanent hypersemia, with perverted nutrition and excessive cell-formation. The morbid appearances met with are usually as follows: The mucous mem- brane is discolored, being of a more or less dull red, often of a deeply venous hue; a dirty grayish or brownish color may mingle with the redness. It is usually in patches, but may be diffused extensively. The minute vessels are di- lated, and frequently varicose. Swelling CHRONIC BRONCHITIS: TREATMENT. 335 and increased consistence of the mem- brane are usually marked characters; hence reduction in the calibre of the tubes, and an uneven surface. The sub- mucous tissue in time becomes infiltrated, contracted, and indurated, thus in some parts completely closing up the smaller tubes, while the larger tubes tend to dilate diffusely, or even saccularly; a fibroid material is produced, which may increase, and at last fibroid phthisis be established. The elastic and muscular coats of the tubes become hypertrophied, but their elasticity is lost. The cartilages are prone to be the seat of calcareous deposit. Owing to the thickening and induration of their walls, the tubes gape when cut across, and many appear enlarged. Epithelial abrasions are common and diffuse, or fol- licular ulceration is said to be observed occasionally, especially in tubercular phthisis. The contents of the tubes cor- respond to the matters expectorated. There is often a large quantity of yel- lowish purulent-looking fluid, which may completely fill the smaller bronchi. Usual- ly frothy mucus exists in the larger ones. In dry catarrh the membrane is much swollen, and has upon it a small amount of tenacious, glairy, semi-transparent mu- cus. Emphysema is constantly present to a greater or less extent. Treatment.-Much harm unquestion- ably results from the indiscriminate treat- ment of cases of Chronic Bronchitis by expectorants and narcotics, which is often practised. There is no disease in which a careful study of each individual case is more required than this, in order to take proper measures for its relief. Of course the primary object that should be kept in view is the cure of the complaint; but, failing this, it is very important to pre- vent it from extending, and hence early and persistent treatment is called for, not merely with the aid of medicinal agents, but also with regard to general manage- ment and hygienic measures. In ad- vanced cases, all that can be done is to relieve certain symptoms, and to ward off various dangerous complications. In dealing with any particular instance of the disease, the following points should be taken into consideration : 1. Whether there is any obvious cause, either external to the individual or depending upon some internal condition, which keeps up a state of congestion of the bronchial mucous membrane, and consequent catarrh. 2. The constitutional state of the patient, and the degree to which the system has become affected. 3. As regards the im- mediate symptoms, the treatment must depend upon (a) the quantity of secretion formed, and the degree of difficulty which is experienced in its discharge ; (b) the condition of the mucous membrane ; and (c) whether there is any spasmodic ele- ment present in connection with the mus- cular fibres of the bronchial tubes. With regard to the immediate cause of the affection, if it is kno vn to result from any irritant inhalation, removal from ex- posure to this is the first thing called for. The same applies to the atmosphere of any particular district which may appear to disagree; a change to some other at- mosphere is necessary, as will be pointed out when the subject of climate is con- sidered. Certain cardiac affections seem to keep up bronchitic symptoms, by in- ducing congestion of the mucous mem- brane ; when any such is present, treat- ment directed against it may afford much relief, especially the administration of tincture of digitalis in moderate doses, which may be combined with such other remedies as the case requires. This drug is especially recommended in the variety named " bronchorrhoea. " Various constitutional conditions are associated with Chronic Bronchitis, and these demand careful attention. If pie- thora exists, this must be reduced by appropriate diet and general management, and the use of watery purgatives. On the other hand, an anaemic state of the blood must be rectified by the different preparations of iron, which are frequently of much value. In many instances a gouty diathesis is present, especially when "dry catarrh" is the form of the affection assumed ; if such be the case, colchicum with alkalies often proves of much service. Alkalies are also useful if there is a rheu- matic tendency, as well as sulphur, cer- tain mineral waters, and other remedies employed in rheumatism. Iodide of po- tassium is said to afford much relief in certain cases, and probably those accom- panied with rheumatism would be most benefited. When the complaint occurs in children, in connection with rickets or tuberculosis, the treatment requisite for these diatheses must be thoroughly and perseveringly carried out. In the great majority of cases of Chronic Bronchitis, it will be found that a general tonic plan of treatment is attended with most success. A course of quinine, or mineral acids with decoction of cinchona or some bitter infu- sion, often proves of great service. The quinine may be combined with sulphate of iron, or some other cha lybeate prepara- tion. Mineral nervine tonics, such as sulphate or oxide of zinc, are also of use in some cases. It is especially in those instances where there is excessive expec- toration, and consequent loss of flesh and strength, that tonics are valuable; and here also cod-liver oil is of essential ser- vice, given in small doses at first, which may be gradually increased. Bronchor- rhoea is also much benefited by tonics, especially the different preparations of 336 BRONCHITIS. iron. A course of mercury is said to have a very favorable influence over some cases of Chronic Bronchitis. The Symptomatic treatment is often at- tended with much difficulty, and remedies have to be variously combined, and fre- quently changed, in order to afford relief. It will be necessary to consider briefly the main indications. The secretions may be formed in excessive quantity, and then the indication is to limit their formation. For this purpose various inhalations are of much importance. Among these, tar and creosote, or naphtha with steam, rank high. The vapor of iodine, chlorine gas, muriate of ammonia, the different balsams, and resins, are also used with success as dry inhalations. They should be employed freely diluted, and their effects carefully watched ; but when pro- perly administered they certainly often prove efficacious. [In some cases, pre- senting great irritability of the bronchial tubes, with frequent, worrying cough, I have known inhalation of the fumes of tobacco (from a cigar or pipe) to have a very soothing and relieving effect. A pa- tient unaccustomed to smoking, for ex- ample, may puff away to the extent of a quarter or half a cigar at a time, leaving it off as soon as the slightest nausea is produced.-H.] General tonic measures are called for here, and iron, especially its astringent preparations, as the tincture of the sesqui- chloride, is of much value. Other astrin- gents must be given also, such as tannic or gallic acid, acetate of lead, and the mineral acids; also the various resins and balsams, especially galbanum, myrrh, ammoniacum, and balsam copaibee ; the last - mentioned is often very useful. Muriate of ammonia has been recom- mended. This treatment applies gener- ally to cases of bronchorrhoea. The fluids may not only be produced in excess, but there is also a deficient power of expectoration, owing to the state of the tubes, the adhesive character of the secre- tion, or other causes. Under these cir- cumstances stimulant expectorants are required, and may be combined with the former class of remedies. The chief of these are sesquicarbonate of ammonia, muriate of ammonia, squill, senega, ser- pentary, camphor, and tincture of ben- zoin, in addition to the resins. Alkalies, such as the carbonate of potash or soda, or liquor potassse with balsam copaibse, may be tried along with ammonia, if the expectoration is very adhesive and viscid. If there is any tendency to great accumu- lation, an emetic of sulphate of zinc occa- sionally will do no harm and may give much relief. Narcotics and sedatives, but particularly opium, must be either avoided or used only with great caution in these cases, particularly in old persons; and the patient should be encouraged to cough frequently, in order to prevent accumulation. In other instances, the mucous mem- brane is in an extremely irritable state, but scarcely any secretion is produced ; hence there is constant cough, with scanty or no expectoration. Should there be any sign of irritative fever under these circum- stances, small doses of tartar emetic or ipecacuanha wine may be given. The most important drugs in these cases, how- ever, are the narcotics and sedatives, which should be administered in full doses. Opium is of essential value here, and may be combined with ipecacuanha, in the form of Dover's powder, or it may be given as the tincture, Battley's solu- tion, or compound tincture of camphor. Solution of morphia is also extremely use- ful. Hydrocyanic acid, tincture of lobe- lia, hyoscyamus, conium, stramonium, belladonna, are other beneficial agents, and may be variously combined with other medicines. Gout is frequently pre- sent, and hence alkalies and colchicum may prove efficacious. Inhalations are to be recommended here also, but of the sedative class, viz., conium, hyoscyamus, stramonium or ether, with steam. " When there is evidently much spasm, as shown by the breathing and cough, the narcotics and sedatives are likewise employed with advantage, associated with different ethers, especially sulphuric ethers. Tincture of cannabis Indica ap- pears to act well in some cases. Ipecacu- anha and tartar emetic, in doses sufficient to nauseate, but not to cause vomiting, are also recommended. A few drops of chloroform may be inhaled occasionally if the tendency to spasm is great, and the sedative inhalations previously mentioned may be employed. In these cases there is always more or less emphysema. The symptomatic indications just considered are generally associated to a greater or less degree in practice, and hence the remedies have to be given in various combinations. Local Treatment. - Free dry-cupping over the chest is often very serviceable, especially in case of irritable mucous mem- brane. Different forms of counter-irrita- tion should be employed according to circumstances, viz., sinapisms, blisters over different parts, croton oil liniment, turpentine, acetic acid, or tartar emetic ointment. The croton oil liniment is certainly very often beneficial. Some recommend an issue or seton. When these are not being used, a large warm plaster, such as a pitch-plaster covered by a thick layer of cotton-wool, should be worn over the chest in front. Under no circumstances does it appear necessary or desirable to remove blood, either generally or locally, in cases of PLASTIC OR CROUPOUS BRONCHITIS. 337 Chronic Bronchitis ; and if an acute attack supervened, the less this mode of treat- ment were followed, the better would be the patient's chance of recovery. Stimu- lants, such as sesquicarbonate of ammo- nia, with chloric ether and squills, as well as wine or brandy, should decidedly be employed in preference when this hap- pens. General Management. -This requires careful attention. It is necessary that the patient should breathe an atmosphere of good, uniform temperature, without ex- cessive moisture, and should avoid sud- den changes. Most patients cannot leave this country during the winter season, and then they should remain indoors when the weather is at all severe, their room being maintained night and day at a regular temperature of 62° to 65° Fahr., and Should always wear a respirator when out. Especially must night air and cold winds be avoided. If possible, they should re- side in a part of the country possessing suitable atmospheric conditions, which vary in different cases. An entire change of climate to some more temperate region is of the greatest importance, if it can be obtained, or a long voyage may be taken. Different forms of Bronchitis require dif- ferent climates ; but they all require toler- ably warm temperature, without sudden changes, a moderately high altitude, and protection from cold winds. For "dry catarrh" a soft and relaxing atmosphere with moderately high temperature, is rec- ommended. One more or less stimulat- ing, dry and hot, is advised where there is much expectoration. In this country the principal places which receive this class of invalids are, Torquay, Penzance, Bournemouth, Grange, Clifton, and Tun- bridge Wells. Among foreign parts the chief are Mentone, San Remo, Pisa, Rome, Cannes, Algiers, and Corfu. [To these, for the winter season at least, upper Egypt may be added ; and, in America, Florida, and Southern California.-II. j Some go to Harrogate and other places, on account of the mineral waters, which are useful in certain cases. Sufficient warm clothing should always be worn, with flannel next the skin. The functionsof the skin must be maintained in an active state, and a warm or hot-air bath, or even a Turkish bath, may be employed from time to time. When the weather permits, moderate exercise is advisable. The diet should be at all times nutritious, and especiaily if there is much emaciation. As to stimulants, no definite statement can be made; but in most cases a moderate amount of some alcoholic stimulant will be of service. The digestive organs must be attended to, and aperients administered if required. When a severe attack of bronchorrhcea comes on, stimulants and sedatives are called for, with a hot-air or vapor bath, and sinapisms over the chest and to the extremities, or free dry-cupping. Emetics may be also employed if the fluids appear to accumulate, and cannot be expelled. Plastic or Croupous Bronchitis. This is a very rare form of disease, and will only require a brief notice. Patho- logically it differs from ordinary Bronchi- tis, in that a plastic material is thrown out into the tubes of which it forms casts. These are either solid or hollow, this de- pending much upon the size of the tubes in which they are formed, and they usu- ally present a series of concentric layers ; but this appearance is sometimes wanting. Their size necessarily varies according to the size of the containing tube. Usually they are confined to a limited number of the bronchial divisions, but may extend from the smallest even to the largest, though they never pass into the trachea ; whereas the exudation of croup or diph- theria may even reach to the most minute bronchi. Their color is whitish, like de- colorized fibrine, but spots of blood may be attached to them. Some have regarded them as the remnants of blood poured out into the tubes, which has coagulated and lost its color. Possibly such casts may be met with occasionally, but those now under consideration are usually, and with greater reason, regarded as the residt of a true exudation on the surface of the membrane. Microscopically they consist of an amorphous or fibrillar material, in which there are exudation-corpuscles and fusiform or ovoid cells, most of which are non-nucleated, but some contain nuclei, abundant granular matter, and some oil- globules are also present. The causes of this affection are very ob- scure. It is supposed to be due to some diathetic state, and is said to be sometimes associated with tuberculosis. It is most frequent in young adults, but may be met with at any age. Females suffer rather more frequently than males, and those of feeble and delicate constitution are more subject to this form of Bronchitis than those who are strong and healthy. Symptoms.-In the great majority of instances Plastic Bronchitis is a markedly chronic affection, but it has been known to occur in an acute form, particularly in infants. Though chronic in its general course, there are, however, acute exacer- bations on the occasion of the discharge of the casts. The severity of the symptoms will depend upon the size of these and the degree of facility with which they are ex- pectorated. In most cases an irrepressible hacking cough sets in, painful and spas- modic, either dry or attended with slight vol. ii.-22 338 BRONCHITIS. expectoration of ordinary characters. This is followed by dyspnuea, which may gradually increase, or come on rather sud- denly. It often becomes very intense, with a sense of great tightness and oppres- sion across the chest ; and there may be an appearance of threatened asphyxia if some of the larger tubes are obstructed. Walshe has found the pulse-respiration ratio to vary from 2'2 :1 to 3*5 :1. The cough becomes more and more severe, and the distress greater, until particles of fibrinous material are expectorated, mixed more or less with ordinary mucus ; and finally one or more masses varying in size will be expelled, which, on being disen- tangled under water, will be found to pre- sent complete casts of the tubes, in the form of tree-like branchings, and having the characters already described. The cough and dyspnoea are then either entirely or partially relieved. Streaks or spots of blood are frequently seen on the outside of the casts, and occasionally on their inner surface; and there may be streaks or drops of bright blood in the mucus which is expectorated for a short time after the casts have been discharged. Copious haemoptysis may occur before the attack comes on, but Walshe believes that the concretions are then merely altered coagula. The length of a paroxysm varies within wide limits, and it may be followed by complete or temporary recovery, or the attacks may recur at longer or shorter intervals for weeks or months. There may be an entire absence of fever, but in many cases febrile reaction sets in, preceded or not by a rigor, and it may be considerable in degree. Frequently abundant muco- purulent expectoration takes place, and extensive Acute Bronchitis or pneumonia is sometimes set up, giving rise to the usual symptoms of each affection. The general health does not suffer much as a rule between the acute paroxysms, and there may be no chest symptoms. Often, however, there is a certain amount of habitual dyspnoea, and signs of imperfect respiration. Physical Signs.-Sometimes pulmonary resonance is in excess over a part of the chest, owing to partial closure of a tube, and the portion of lung to which it leads being over-distended with air. More com- monly localized dulness is met with, owing to complete obstruction and consequent collapse. The respiratory sounds are either weak or totally absent, according to the amount of obstruction. When this is removed, the above signs disappear. Dry rhonchi, especially sibilant and a few of the moist kind, are heard in different parts. Should pneumonia or Acute Bron- chitis be produced, the physical signs characteristic of either complication will be present. Diagnosis.-This form of disease may be mistaken for ordinary Acute Bronchi- tis, pneumonia, or pleurisy. The history of the case, the characters of the parox- ysms, expectoration of membranous frag- ments or casts, and physical signs serve to distinguish them. The degree of fever will also be important, and the absence of the symptoms usually met with in the above diseases. Prognosis.-It is not attended with much danger in itself as regards life, but it may lead to pneumonia, phthisis, &c., and thus cause death. Complete recovery sometimes occurs, but usually this is only temporary, the disease being one which has a great tendency to recur. Treatment.-Various remedies have been recommended, but apparently their use has not been attended with much suc- cess. During the paroxysms venesection has been practised, sinapisms and blisters applied to the chest, and various drugs administered, viz., the different sedatives, tartar emetic, ipecacuanha, calomel and opium, alkalies, and salines. Inhalations might be of use, and the patient should be kept in a warm room, having the air well saturated with moisture. In the in- tervals, Fuller has occasionally seen ben- efit result from the use of tartar emetic, in moderate doses, for several weeks. Iodide of potassium and inhalations of iodine have been employed with success. The alkalies and their carbonates have also been recommended. The health must be maintained, and tonics given if necessary, more especially if there is any sign of tuberculosis. Quinine, iron, and cod-liver oil are often called for. A change to a warm climate, or a long sea- voyage, might be tried ; while every pre- caution should be taken against cold and wet. If an attack threatens, inhalation of steam should at once be had recourse to, and persevered in. PLEURODYNIA. 339 PLEURODYNIA. By Francis E. Anstie, M.D., F.R.C.P. Definition.-Sharp unilateral pain, greatly aggravated by respiration and other movements, in the extra-thoracic or in the intercostal muscles; unattended, except accidentally, with fever. History.-The attack is sudden, and is usually brought on by either exposure to wet and cold, or by some rather ener- getic movement of the trunk or of the arm; often it is the sequel of a prolonged effort involving continuous contraction of the muscles of one side of the chest. Very commonly the patient will remember that for some days past movement of the affected part has always been irksome, and followed by aching pain. The affec- tion tends to subside spontaneously under the influence of rest, in a few days. Often the patient has been previously subject to muscular pains in other parts. Symptoms.-The patient, after experi- encing more or less preliminary soreness or aching of the part, is suddenly attacked with stitch-like pains, most commonly in the infra-axillary or infra-mammary region, and more usually in the left side than in the right. The natural play of respiration is interfered with by the severe pain which the movement causes, the ex- pansion is therefore jerking and irregular, and the respiratory sound corresponds with this in character. No percussion- dulness, friction-sound, or other of the physical signs of pleurisy, can be detected ; there is no fever, unless by accident the patient is suffering from some coincident febrile affection. Superficial tenderness is not a characteristic of Pleurodynia, but there may be dysphagia, and pain on movement of the arms. Etiology and Pathology.-It has been customary to class Pleurodynia as a variety of rheumatism, affecting the tho- racic muscles and their tendinous inser- tions ; but I can discover no satisfactory grounds for this proceeding. It appears to me that Pleurodynia is merely an in- tense variety of the myalgia which, in less striking forms, is very much too common, and besets far too large and miscellaneous a class of patients, to allow us for a moment to assume that the rheumatic taint is a necessary factor, or indeed a factor at all. I have several times seen very severe Pleurodynia in patients whose history showed no trace of rheumatic ten- dencies ; and on the whole there seems to be far better evidence for the connection of this malady with the neurotic than with the rheumatic constitution. In the absence of any sufficiently accurate and extensive statistics, I must provisionally believe that the exciting cause of Pleuro- dynia, like that of myalgia generally, is over-long or over-severe exertion of a muscle in proportion to the state of its nutrition, and that the predisposing cause is the neurotic constitution. As regards the intimate pathology of Pleurodynia we know little. There is nothing to point out any special anatomi- cal condition of the affected muscles as a constant attendant of the malady except this, that Pleurodynia occurs, for the most part if not always, in persons with slight and thin muscles, suggesting under- nutrition of those structures. I can see no shadow of reason to suppose that a local inflammation has anything to do with Pleurodynia; and the results of treatment are* directly opposed to such an idea. Diagnosis.-This is the really import- ant aspect of Pleurodynia. It is ex- tremely likely to be mistaken for pleurisy, thus causing alarm, and, in the hands of some practitioners, a disastrously heroic treatment. The total absence of altera- tion in the pulse-respiration ratio, and of the physical signs of pleurisy, must soon undeceive any one who is even moderately careful; but during the first few hours the ablest practitioner may be at fault. This is especially the case in two situations : first, when the malady accidentally coin- cides with a catarrh, or some other affec- tion causing feverishness ; secondly, where the patient is a highly nervous person, whose circulation is habitually much ac- celerated by pain or any other cause of distress. Such being the fact, it is the more fortunate that the modern treatment of pleurisy no longer includes those heroic measures by which it was once the fashion to attempt to cut short the disease at the outset. Prognosis is scarcely worth mention- ing. The affection is trivial, and certain to yield in a few days at most. 340 PLEURISY. Treatment.-Two remedies only are necessary. The side should be covered with a sheet of spongio-piline or with fla nnel and oilskin ; or a simpler and readier method is to surround the side with a piece of thin mackintosh, which may be put on over the flannel shirt, jersey, or spun-silk vest. One quarter of a grain of morphia should be subcu- taneously injected, and repeated if neces- sary, in two hours' time. This plan never fails to give complete relief, but the patient should be sedulously warned against all movements not absolutely necessary, for a lew days after the pain has ceased. PLEURISY. Francis E. Anstie, M.D., F.R.C.P. Definition.-Inflammation, partial or general, of one or both pleurae, attended with the effusion of lymph, lymph and serum, or pus. History.-The circumstances under which Pleurisy may arise are very vari- ous ; but a practical line of distinction separates two main varieties of the dis- ease. Pleurisies may be divided into Primary and Secondary. By Primary Pleurisies we mean those in which the cause of the affection oper- ates directly or mainly upon the pleura itself; and the inflammatory affection of that serous membrane arises, so to speak, in a time of health, and only secondarily implicates the rest of the body, by means of the constitutional fever which it excites, or by some other results, mechanical or physiological, of the local disease. By Secondary Pleurisies we mean those cases in which the pleural inflammation is a complication, or a secondary produc- tion, of some other visceral disease, or of some constitutional malady which has gained a hold upon the organism. Even this classification may require to be re- modelled at a future day ; we may possi- bly find it to be too absolute : but it ap- pears to correspond well with the facts as we know them, and it marks out in a con- venient manner some broad features by which two kinds of Pleurisy are distin- guished in the important matters of vital significance and appropriate treatment. Far less practical is the attempt to divide pleurisies into acute and chronic: at least it is only in discussing the strictly clinical aspect of the disease that we can say anything useful under this heading. Two facts which are the eminently char- acteristic results of modern investigation have mainly tended to supersede the divi- sion into acute and chronic ; first, the in- creasing certainty that primary acute pleurisy is but rarely fatal; and secondly, the discovery that those chronic cases which are merely the prolongation of the acute primary variety, both may and ought to be treated with a boldness and energy which tend greatly to abridge the course they would formerly have been allowed to run. With modern means and maxims of treatment, it is not too much to say that primary chronic pleurisy has lost its most important features and its peculiar terrors : and the only reason for regarding Pleurisy of chronic type in any special way is the fear that under- neath the apparently merely local affec- tion there may lurk the taint of, or the tendency to, a constitutional disease like tuberculosis. Of the acute primary disease, in robust subjects, the history is essentially this. It attacks suddenly, lasts from ten clays to three weeks, and then, in the majority of cases, departs, leaving behind it no other than trifling local changes, which are of no injury to the patient's subsequent health and activity. In a smaller number of cases, however, it produces an amount of effusion which is with difficulty got rid of, and unless evacuated by surgical means may remain, and protract the state of ill health, for many weeks longer. In such cases, also, the amount of permanent mechanical danger to the organs may en- tail disastrous after-consequences ; or it may even happen that constitutional dis- ease of a fatal kind (especially tubercu- losis) may be secondarily set up. Of Pleurisies that are "chronic" throughout-i. e., that commence in an insidious manner,-by far the greater number are not primary, but secondary to some constitutional malady or some dis- ease of another viscus. Nevertheless, it unquestionably happens, in a few cases, that apparently healthy persons are at- tacked with pleuritic mischief of so insidi- ETIOLOGY. 341 ous a kind, that almost before the patient knows that he is ill (although he may have been slightly ailing for some days or weeks), it is discovered that one pleura is half or three-quarters full of fluid. Such cases are commonly very tedious in their course, and, if they do not compel the performance of paracentesis at first, take the form of an empyema or collection of pus. When we turn to the consideration of secondary pleurisies, we find a far greater variety of type, and a much more serious prognosis, attaching to these maladies. To speak first of the Pleurisies which come in as a secondary complication of acute fevers. The whole type, and the vital significance of this class, depends on two factors-the virulence of the original disease, and the power of resistance which the organism has so far presented to it. That a patient with typhoid fever, or acute rheumatism, for instance, is sud- denly attacked with Pleurisy, may be of the greater or less consequence, according to the amount of vital power of resistance which the tissues generally, and the or- gans of vegetative life (especially the heart and kidneys) retain. The main points, however, which the history of the pleurisies secondary to acute fever pre- sents, are the protracted course, the tend- ency to purulent character of the effusion, and the frequent termination, either in death or in disastrous results in the way of constitutional disease, especially tuber- culosis. The pleurisies produced by pyemic in- fection are mere incidents of an almost necessarily fatal blood-poisoning. Far different is the history of the pleu- risies which are secondary to the common form of pulmonary phthisis. The great majority of these take the shape of acute and strictly limited fibrinogenic inflamma- tion, and, unlessvery injudiciously treated, tend to rapid termination with no worse result than a local adhesion of the pleural surfaces. More must be said on this point hereafter; at present it will be enough to state that until the later stages of pulmonary phthisis, it is decidedly un- common, in my experience, to see pleuri- tic attacks causing considerable serous or sero-purulent effusions, unless they are " actively" treated, in the sense of a free use of depressing remedies. But when once a patient, with an already consider- able development of chronic destructive lung disease, has acquired, in addition, a large serous or sero-purulent effusion in his pleura, the chances are heavily in favor of a disastrous termination of the disease, and it may even happen that a swift development of true tuberculosis may carry the patient off in a very few weeks, though the pleuritic effusion were, in itself, quite incompetent to endanger life. The pleurisies which are consequent on acute or subacute diseases of other vis- cera are of various types. Pneumonia, for instance, is in numberless, perhaps almost in all cases, attended with a cer- tain amount of fibrinogenic pleurisy ; but fortunately this is, in the majority of cases, limited to the production of a cir- cumscribed effusion of lymph, which leads to no serious results. It is far otherwise with the more infrequent cases of pneu- monia, which become complicated with effusion of a considerable quantity of pleuritic fluid: this form of secondary pleurisy usually presents acute and highly dangerous symptoms at first, and if not rapidly fatal (as it often is) is usually in- tractable in its after-course. The form of Pleurisy which is second- ary to Bright's disease, is always a grave and intractable affection ; but its history differs greatly according to circumstances. Where it is the immediate consequence of the acute albuminuria of scarlet fever, the tendency is towards a rapid change of the effused fluid into pus ; and the mild- est result probable is a chronic empyema, with too often fatal secondary results. A different type of Pleurisy may be seen occurring as a complication, often a late one, of the cirrhotic or contracting form, or (much more rarely) of the amyloid form, of renal disease. In neither of the two latter forms is there the same tend- ency towards the rapid production of pus, but rather a tendency towards the effusion of a large quantity of fibro-serous (chiefly serous) effusion. As for the pleurisies said to be second- ary to acute cardiac disorders, it may well be doubted whether these are not always to be considered as results of some blood- poisoning, or constitutional vice, to which the heart affection is also due. Their course depends upon the degree of vital power which the organism has retained in its struggle with the constitutional malady. They can only be considered as incidents in a more formidable disease. It is, however, an open question whether pericarditis may not excite Pleurisy by direct extension of the inflammatory pro- cess. Etiology.-Upon the etiology of Pri- mary Pleurisy we possess no sure informa- tion at all. There is, indeed, a limited class of cases in which the inflammation is the direct result of a blow or some other injury; but we know of no other causes, properly so called. Among ex- citing causes, cold has often been con- fidently stated to be a frequent one ; but some of the best authorities of late years entirely deny this ; and Ziemssen, out of 54 cases of Pleurisy of which he minutely examined the history, could not trace the disease to exposure to cold even in a sin- 342 PLEURISY. gle instance. I have myself had some reason to think that extreme muscular over-exertion and exertion in continuous public speaking produces Pleurisy, some- times, in otherwise healthy persons. Of predisposing causes, age has been reckoned an important one. It was sup- posed by some that it never occurred in very young children ; e. g., Barrier for- mally denied its occurrence at all in chil- dren under six years of age. It is difficult to ascertain the exact degree of frequency of Pleurisy in young children, because in them the disease is particularly likely to occur without being detected. But all the best authorities now agree that Pleu- risy is quite common among children-at any rate, after the first year of life ; and Guinier, of Montpellier, actually tapped an empyema in a child twelve months old. Steiner and Neuretuer,1 in a note- worthy series of papers, express the opin- ion that in young children Pleurisy with liquid effusion is the rarer, Pleurisy with proliferation of connective tissue the more common. Ziemssen2 tabulates the ages of 54 children whom he treated for Pri- mary Pleurisy : First year of life, 3 ; sec- ond, 1; third, 7 ; fourth, 4 ; fifth, 2 ; sixth, 4 ; seventh, 4 ; eighth, 5 ; ninth, 9 ; tenth, 7 ; eleventh, 2 ; twelfth, 1, thirteenth, 1; fourteenth, 2 ; fifteenth, 1; sixteenth, 1. This very interesting record sufficiently disposes of the idea that there is any im- munity in infancy. A similar investigation of Ziemssen seems to show that there is no well- marked influence of seasons of the year as a predisposing cause. Of Secondary Pleurisies, the exciting causes are numerous. Among the fevers, scarlatina and typhoid are especially no- table in respect of frequency of occur- rence, variola in regard of danger ; acute rheumatism is a frequent cause ; alcohol- ism and pysemic poisoning often pro- duce Pleurisy, inter alia. Of tuberculosis proper and catarrhal pneumonic phthisis, it may be said that they frequently act as predisposing, and frequently as exciting causes of Pleurisy. Of diseases of other viscera pneumonia is the most common cause of Pleurisy ; after this comes kid- ney disease, which is, at any rate, a very powerfully predisposing cause; finally, any organic disease which necessitates mechanical pressure on, or irritation of the pleura: and it is possible that inflam- mation now and then passes over to the pleura, by mere contiguity, from neighbor- ing parts, e. g. the pericardium. Clinical History. -The symptoms of Primary Pleurisy of acute type are as follows : The patient, after suffering for a variable number of hours, or hardly suf- fering at all, from general malaise and loss of appetite, is attacked almost simul- taneously with sharp stitch-like pain in some portion of the thoracic wall (by far the most frequently in the anterior or the lateral portion, a little below the level of the nipple), and with more or less shiver- ing. The face is generally pale and con- tracted with the lines of pain; the patient bends over towards the affected side, and draws his breath with visible difficulty, in a hurried, uneven, and shallow manner (respiration entre-coupee). After this has lasted a short time flushing of the face ap- pears,1 the pulse rises in frequency, and the general phenomena of pyrexia are evident; in some eases the pain now greatly diminishes, in others it maintains its intensity. The frequency of the pulse in the early stages of Pleurisy varies considerably. There are plenty of slight cases of local- ized fibrinous inflammation in which hardly anything like pyrexial rapidity of pulse is present; the frequency may not be more than 86 or 90, and I have even seen a case in which it never rose above 80. In cases of primary fibrino-serous Pleurisy the pulse-frequency may be said to vary between 90 and 120 in the stage of febrile reaction after the initial rigor ; on examining the notes of twelve such cases, I find the average rate at this period was 99. It must be said that all these patients were adults, and that a considerably higher pulse-rate may be found in young children, though this is by no means always the case. The quality of the pulse is a point which I have particularly investigated in a con- siderable number of cases, and it seems to me quite certain that this follows a uni- form course on the whole, regard being had to the general vital status of the pa- tient. In the first stage of acute pain, with more or less tendency to shivering, the pulse, as tested with the sphygmo- graph, presents the "algide" form, i. e. the pulse-waves are very small and nearly devoid of secondary markings. As soon, however, as flushing of the face occurs, and a general sense of burning heat of the skin, the pulse passes to the true pyrexial type; the waves become large and dicrotic. Oue reads constantly, in standard works, of pleuritic patients with (sensibly) hot skin, flushed face, and a hard bounding pulse : but the sphygmograph, in my be- lief, destroys this clinical picture, for it uniformly shows that the large and some- 1 Prag. Vierteljahresch. 1864-65; Schmidt's Jahrbuch, 129, p. 189. The papers are part of a series of " Clinical Records of Children's Diseases." 2 Ziemssen, Pneumonie und Pleuritis im Kindesalter. 1 The flushing is never so fixed and deep a color, and especially never so markedly one- sided, in pure Pleurisy as in pneumonia. CLINICAL HISTORY. 343 what bounding pulse is always decidedly less resistant than that of health. The temperature follows no regular course in Pleurisy; in the primary disease we rarely derive any useful indications from it. On this point I agree, in the main, with the conclusions of Wunder- lich, 1 and I shall say more about it when treating of Prognosis. It is enough here to say that temperature-changes keep no sort of parallel with the pulse or the res- pirations. The respirations in acute Pleurisy are both absolutely rapid, and especially so in comparison with the pulse ; the rapidity being mainly due to the impossibility (from pain and soreness) of taking deep breath. Cough is a very usual, though not uni- versal, accompaniment of the acute stages of Pleurisy. It is short and hacking; and is either perfectly dry or attended with only a moderate amount of thin mucous expectoration; except, indeed, when the Pleurisy is complicated with pneumonia. The decubitus has been made a strong clinical feature by some writers on Pleu- risy ; but there are contradictory state- ments, and from my own observation I should say that there is no attitude char- acteristic of the disease except that which very generally prevails in the first acute agony, viz., half lying, half crouching, on the affected side. The decubitus is fre- quently changed two or three times in the course of the illness, and, except as attracting our attention to the physical examination of the chest, is seldom of any moment. Along with these phenomena there is a variable amount of nausea, white-coating of the tongue, thirst, and anorexia; the last usually complete. It must be observed, however, that the above is only the picture of the early stages of a typical acute case in an adult. Even in adults there may be, in cases that run a pretty severe course, scarcely one noticeable symptom to arrest attention in the early days of the malady.2 And in children the febrile symptoms, particu- larly the initial rigor, are often inconsider- able, and the cough scarcely attracts notice, especially in slight cases.3 Physical Signs.-It is to these that we specially direct attention when suspicion of Pleurisy exists, and the information they afford is more valuable than any other. Inspection.-When the chest is laid bare, it will be seen, in the very early stages, that the pleuritic side of the chest is some- what retracted, and its intercostal mus- cles nearly or quite motionless, while in- creased play and movement of the sound side is observed. At a later period of effusion a positive dilatation of the pleu- ritic side and a bulging of the intercostal spaces may often be noted, but it is pos- sible, even in cases of very extensive ePusion, for the chest wall to remain apparently unaffected, the force of dis- placement being spent mainly on the neighboring organs. But in all cases where there is the least suspicion of Pleu- risy, accurate repeated measurements of both sides must be adoptedit will not do to trust the eye, for enlargement of the side may be obscured by the general con- figuration of the thorax, or it may happen that the expansion of the sound side (in its compensatory efforts of breathing) may assist in concealing the fact. One of the most striking pieces of evidence offered to the eye is the visible displace- ment of the heart which usually presents itself when the effusion is large: in the case of left pleurisy, the apex will be seen beating under or to the right of the sternum, or in the epigastrium ; in right pleurisy it may be found beating to the left of the left mammary line, and, in ex- treme instances, even in the left axilla. Mensuration.-In the early stages there is commonly no enlargement of the af- fected side ; the sound side, indeed, ap- pears, and is, the most expanded. But as effusion comes on the balance is re- stored, and when the fluid becomes co- pious the intercostal spaces yield, the ribs become more separated, and in pro- portion to the yieldingness of the thoracic wall a real increase in the size of the af- fected side is observed. It is only in the slight-made chests of young children that this is early perceptible; in adults, the displacement is rather on the side of the viscera until the effusion becomes very large. Strict daily comparative mensura- tion of the two sides ought nevertheless to be practised from an early stage. Percussion yields no information in the first stage, nor can it be well tolerated. Supposing the case to be one of merely fibrinous exudation, we may get, from first to last, scarcely any abnormality in the sound elicited; but the chest wall gives a strange sense of deadness and in- elasticity to the percussing finger. Very solid and thick fibrinous deposits may cause a really dull percussion sound. When serum is poured out in any quan- tity, however, the evidence from percus- sion becomes striking: over the whole 1 Das Verhalten der Eigenwarme in Krank- heiten. 2te Auflage. Leipzig, 1870, pp. 374-6. * See, among other authors, Trousseau (Clin. Medicale, tome i.) for some striking examples. • Ziemssen, Pleuritis u. Pneumonie im Kind alter. 1 Cf. Verliac (Epanchements pleuritiques, Paris, 1865), particularly case at pp. 19, 20. j 344 PLEURISY. space occupied by the fluid there is found a dulness, more pronounced in some cases than in others, but always with a charac- ter of its own, which must be heard to be recognized, but is much more marked than that produced by lung-consolidation. In ordinary cases, where the fluid is not bound and localized by adhesion, the dul- ness reaches upwards from the base of the chest to a variable height, according to the amount of the effbsion : its charac- ter is very perceptible in comparison with the sound side, but the line of its termi- nation above is by no means always an evenly horizontal one. As the case pro- ceeds, and an increasing quantity of serum is effused, the dulness may extend quite up to the clavicle in front and to the supra-spinal fossa behind ; after this, any further extension of the effusion necessi- tates expansion of the pleural cavity in some fresh direction. So far, space for the fluid has been obtained chiefly by the compression of the lung into the spinal fossa, but already, in most cases, there has been also displacement of the sur- rounding organs. This displacement may affect chiefly the ribs. But the diaphragm even more certainly yields, and its dis- placement downwards pushes the liver down (in right pleurisy), and percussion can recognize the depression of this organ; similarly, the stomach and colon may be recognized, by their tympanitic percus- sion-sound, at an unusually low level, and the spleen • dulness may sometimes be traced at a point below the margin of the right false ribs (in left pleurisy). The most striking phenomena of displacement are, however, connected with the heart. In left pleurisy a large effusion often pushes the heart so much to the right that the cardiac percussion-dulness is found to occupy a space beneath the lower end of the sternum, and even extending considerably beyond its right border. The displacing effect of right pleuritic effusion is less immediately obvious to percussion; though readily identified by inspection and palpation, or at any rate by the stethoscope. Palpation, often gives us very important information. In early stages, and in those cases where the effusion remains merely fibrinous, the grating of the lymph-covered pleural surfaces may com- municate a thrill to the chest-wall which is appreciable by the hand; these phe- nomena, however, are not very frequently observable. More constantly useful is the absence of vocal fremitus when liquid has been poured out in any quantity; this is usually striking when we compare the pleuritic with the sound side. The fre- mitus of lymph-covered pleural surfaces may sometimes be felt in the later stages after the fluid effusion has become ab- sorbed. Auscultation rarely reveals much in our earlier examinations. Fluid has not yet been poured out. We may happen to catch the moment when the pleura is rubbing its two fibrine-covered surfaces together at some point or points, in which case the "friction sound" is heard ac- companying inspiration and expiration. There is no use in attempting to describe this sound minutely; it does, in fact, con- siderably vary in pitch and in character; the student must himself repeatedly hear it, and compare it with other sounds (es- pecially various clicking bronchial sounds) before he can identify it with confidence. The rarity with which, as I have said, it is heard in the early stages, holds good in the ordinary type of Pleurisy that goes on to liquid effusion; and in the wards of hospitals this is the prevailing type of the disease that is seen ; but I have been for some years past surprised at the fre- quency with which I have detected slight and limited Pleurisy, by means of the friction-sound, in the out-patient room. Most of these cases were tuberculous ; but a considerable number afforded no room for any suspicion of the kind. The fric- tion-sound is far more commonly heard in the stage of resolution, where liquid is getting absorbed, and the roughened pleural surfaces come together again. In the stage previous to fluid effusion, the ear detects only the fact that the lung of the healthy side is expanding more vigorously and noisily than the other. When fluid becomes effused, however, the tendency is at first often towards a bronchial character of the breath-sound, accompanied by bronchophony on the af- fected side, while the effusion is small. In adults, however, the progress of the effusion rapidly replaces this by weaken- ing, and finally absence, both of breath and voice sounds; meantime the breath- ing on the healthy side is more and more noisy and puerile. On the pleuritic side, the lung getting pushed back into the spinal fossa there are bronchial breathing and bronchophony to be heard in the up- per and inner scapular region and be- tween the scapula and spine, and com- parative or complete silence elsewhere. Of cmgophony, the curious bleating sound of the voice which is sometimes heard at the upper level of the fluid, I feel inclined to say very little. It is in truth one of the fancy signs of Pleurisy-interesting rather than useful; it is so inconstant, and there are so many fallacies attending its recognition, that I believe it to be, for ordinary auscultators, rather a snare than a help. In a similar way one must speak of the succession sound, the splashing noise supposed to be heard on shaking the pa- tient ; this also is very inconstant. And we may here notice that the changes, both of voice and breath-sounds, and also CLINICAL HISTORY. 345 of percussion sounds, which are commonly supposed to be induced by changing the patient's posture, are very uncertain and unreliable in true Pleurisy. Auscultation is of great value in indi- cating the altered position of the heart, which occurs in cases of large effusion. Physical Signs in Pleurisy of Children. -There are several most important vari- ations from the above general picture of the physical signs of Pleurisy, to be ob- served in the pleurisies of infancy and childhood. These variations are due to two circumstances : the small size of the chest, and the greater yieldingness of the chest-walls.' As regards the auscultation, it is all-important to note that bronchial breathing and voice persist, in nearly every case, even when the effusion occu- pies the whole chest, and when vocal fre- mitus is entirely absent. Rilliet and Bar- thez were the first to notice the remark- able fact that even a pneumonic broncho- phony and bronchial breathing, so far from being diminished, are usually much intensified by a supervening pleuritic effusion. Yet there are many text-books that take no notice of this peculiarity of children, and ignorance of it has certainly been the cause of many disastrous mis- takes in practice, the practitioner believ- ing firmly that he had merely to do with a consolidated lung, till surprised by the appearance of fluctuation and evident signs of pointing in one or more of the intercostal spaces. Another very import- ant distinction of Pleurisy in young life is the comparative absence of signs of dis- placement of viscera. The fact is that the chest-wall yields more easily, and the force of pressure is not expended, to any- thing like the same extent as in adults, in dislocating the heart and in driving downwards the diaphragm and the ab- dominal viscera. This, also, is a peculi- arity too little noted in text-books written by those whose experience of Pleurisy is not large; and, joined with the persist- ence of bronchial breathing and voice, has doubtless caused numbers of mistakes. Fig. 43. A. Line of original lipper level of fluid ; B. Line of fluid on twentieth day: C. Conjectural upper level ol liver ; o. Termination of dulness below (tympanitis begins). D. Maximum heart-impulse at time of greatest effusion; b. Ditto on twentieth day ; F. Ditto in natural state. Such errors probably cost the lives of many patients who might have been saved by prompt tapping. It is, however, a mistake to say, as some have done, that displacement of viscera never takes place in children. Ziemssen1 quotes a conclu- sive series of cases, observed by himself and others, to the contrary effect. We must now complete the clinical his- tory of Pleurisy by describing what may be called its critical symptoms. If the case takes the turn towards recovery by simple absorption, which is the natural destiny of primary Pleurisy, then, after 1 Op. cit. pp. 67, 68. 346 PLEURISY. the subsidence of pyrexia, there occurs, usually, a pause of a day or two, after which the work of absorption begins to show itself by physical signs, and by a small but increasing degree of relief to respiration. Among the signs most care- fully to be looked for as indicating the commencement of this process is the re- turn of the percussion dulness of the liver, or the tympanic sound of the sto- mach, to a higher level. The return of the heart to its proper position, even when absorption has made considerable progress, is not always rapid or at first very evident. In the accompanying sketch is represented, with rough but sufficient accuracy, the state of things in the chest of a young but intemperate man, C. J., who, between the sixteenth and twentieth days of right Pleurisy, ex- perienced an amount of absorption of the effused fluid indicated by the distance between the lines A and B. The liver was believed to be somewhat enlarged and fatty in this man. Instead of a speedy commencement of absorption, the fluid may remain in a passive condition, and the patient may continue in a state marked by no discom- fort except some mechanical embarrass- ment of respiration and heart movements, impeding him in any but the gentlest movements. It is fortunate, but com- paratively rare, when a protracted period of this kind is terminated by the occur- rence of absorption. More commonly a slight but steady increase of ill-health is experienced, till at last there arises de- cided febrile disturbance, settling more and more into a hectic type, with copious sweat, morning remissions and evening exacerbations, and, in short, a more or less complete series of indications of ex- tensive suppuration. It is here, at last, that the thermometer, so little to be de- pended on in other stages of Pleurisy, often gives us precious information of the changed aspect of affairs. There is no need to carry the clinical description any further, since under the heads of Prognosis and of Treatment suf- ficient information will be found concern- ing the favorable and unfavorable termi- nation of suppurative Pleurisy. Complications and Sequelae.-Of primary Pleurisy the most frequent complication is pneumonia, and this may either exist from the first or supervene at any tolera- bly early stage. It does not appear to occur with any frequency after the lung has been compressed into a small space by fluid exudation. Laennec believed that the compression by the fluid always tended to prevent the occurrence of severe pneumonia in connection with Pleurisy; but it will be seen, under "Prognosis," that he was at least wrong in this, so far as relates to children. But when the lung is compressed to carnification, it is doubt- less very incapable of inflammation. The most formidable way in which pneumonia may complicate Pleurisy is where, a con- siderable effusion existing in one pleura, inflammation attacks the opposite lung. It may be doubted, however, whether this ever occurs in truly primary Pleurisy: personally I have never seen a case where inquiry did not show the existence of kid- ney disease, fever, pyaemia, or some of the many causes of secondary Pleurisy. This is the place to speak of double Pleurisy, which may fairly be looked on as a complication; and in regard to it I can only repeat the same observation. Primary Pleurisy, as we call it, does seem, at any rate, peculiar in this-that it is an essentially unilateral disease : and I have never been able to see a double case in which there were not ample rea- sons for thinking the Pleurisy a secondary affection to some condition of general blood-poisoning. It is in the same point of view that we must regard the super- vention of other serous inflammations, e.g., peritonitis; but there is a possi- bility, perhaps, that pericarditis may sometimes arise by simple extension of the inflammatory process from the con- tiguous pleura. In cases of empyema of some standing a not very uncommon complication is dis- charge of the pus through a pulmonary fistula into the bronchi; this is associated with phthisical lung disease in a large majority of cases, but a considerable num- ber are recorded in which the accident has occurred in primary Pleurisy without tubercular disease.1 The cases are rare in which the channel of evacuation has proved sufficient: usually the bronchial discharge is only a preliminary to subse- quent perforation outwards, and as re- gards treatment this is the view that should be taken. The accident of pul- monary perforation must be looked on as the probable commencement of a period of fetid suppuration and pyo-pneumo- thorax. Of the sequelae of Pleurisy one out- weighs all others in interest, viz., tubercu- losis. It is now well established, not merely that Pleurisy often occurs in phthisical hmg-disease, but that Pleurisy itself is capable of setting up true tuber- cle, even in previously healthy persons. This is specially apt to occur where a purulent effusion has been allowed to re- main too long in the pleura, or where paracentesis has been performed repeat- edly for empyema, the wound being closed in the interval. But the latter practice 1 For a good discussion of the subject of bronchial fistula, see Aristide Attimont, "Re- sultats de la Paracentese dans la Pleurisie purulente," Paris, 1869. PATHOLOGICAL ANATOMY. 347 is one which, it may be hoped, will no longer be followed. The other sequelse of Pleurisy, though they may be very troublesome, are less important. Retraction of the chest-wall and consequent deformity of the spine and shoulder is the ordinary result of the ab- sorption of a large effusion, where the lung has been too much bound by adhe- sions to re-expand at once, or perhaps at all. The same thing occurs where a col- lection of pus has been allowed to burst externally; here the lung is firmly bound down, and the orifice of the rupture being valvular no air enters the chest, and so the ribs sink in under atmospheric pres- sure. It may be at once said, however, that these deformities are merely tempo- rary, and that with proper attention they will always be found to right themselves, in the course of a year or two, almost en- tirely; this is especially the case in chil- dren. As regards the fistulous opening left after the natural bursting of an em- pyema, the course of events depends on the amount of local mischief which was done during the passage of the pus to the surface ; when this has been very tedious, more or less extensive destruction of peri- osteum and necrosis of ribs may occur, and may give much trouble. A single fistulous opening is merely to be looked at as an unpleasant fact which will dis- appear in a certain number of months or years. Pathological Anatomy.- The first stage of change in every case of Pleurisy appears to consist of ordinary injection of the vessels beneath the pleural mem- brane ; in primary cases by far the most frequently this change begins in the costal pleura. Slight ecchymoses are more or less plentifully scattered over the hyper- vascular and bright-red part. The clear serous membrane also begins to be cloud- ed and swollen, and if the inflammatory process goes on for a very few hours, there occurs a visible deposit of fibrinous lymph, of a reddish-yellowish tinge, and at first very tender and soft, and small in quan- tity. If the inflammation goes on to be an affair of more than a day or two, not only does the amount of fibrinous deposit increase by successive layers, but a varia- ble proportion of serosity is mixed with the lymph; and often serum is poured out in large quantity from an early pe- riod, so as to fill a large portion of the pleural cavity within a few days, more rarely within a few hours. There is great variability in the relative amount of the serous and fibrinous elements of effusion, but in general the contents of the in- flamed pleura may be described as con- sisting of yellowish serum in which float a quantity of concrete masses of the same fibrinous matter which lines the inflamed portion of the membrane; and, as the case advances, bands of fibrinous matter, at first tender and yielding, afterwards firm and tough, form adhesions between the costal and the opposite portions of the pulmonary pleura. In some instances it happens that the fibrinous adhesions are so many and so dense over a limited area, that they inclose and limit the serous exu- dation, confining it to a comparatively small portion of the pleural cavity. In ordinary cases the pleural cavity becomes progressively and more or less evenly filled to a higher and higher level, the lung receding before the fluid, and being pushed upwards, backwards, and in- wards, till it is compressed into the me- diastinal or spinal fossa. On the other hand, it may happen that a compara- tively small amount of fluid spreads itself rapidly over a large portion of the lung, and, though reaching a high level in the chest, does not greatly compress or alter the position of the lung, at any rate at first. In those pleurisies where the inflamma- tion is limited to a small area, the effusion often consists almost entirely of plastic fibrinous matter, and then the regular course of the affection is short, ending in an adhesion of a limited portion of the opposed pleural surfaces. Undoubtedly the most frequent examples of this kind are found to occur in the course of chronic pneumonia and of phthisis ; but it is cer- tain that they also occur, sufficiently often, in individuals who are otherwise appa- rently healthy. [Fig. 44. Inflammation of the Diaphragmatic Pleui'a.-Show- ing the adherent fibrinous layer. a. Muscular coat of diaphragm, i. Subserous tissue, c. Serous mem- brane. e. Fibrinous layer. X 400. (Rindfleisch.)] Another outcome of inflammation is the effusion of pus, which may either exist from an early period or may slowly de- velop in the course of an ordinary fibro- serous pleuritic effusion, the pus-cells more and more invading the serosity, un- til at last the whole mass of fluid assumes a truly purulent character. Pus in the pleura is known under the name of em- pyema. Acute empyema is rare as a 348 PLEURISY. primary disease in adults (more common in children), and is usually the direct re- sult of injury, but is common enough as a complication or sequela of certain acute fevers, especially scarlatina, and also py- semic poisoning; it occurs also in a cer- tain small number of cases of pulmonary phthisis; and one special variety-pyo- pncumo-thorax form of perforation of the pulmonary pleura-is in such a large pro- portion of instances due to chronic lung- phthisis, that it may for practical pur- poses be almost entirely left for considera- tion along with that malady. The fibrinous element is, I believe, never really absent from a genuinely pleu- ritic effusion: many times as I have looked for such a thing in the post-mortem room, I have never seen a purely serous nor a purely purulent Pleurisy. [The cases of miscalled purely serous Pleurisy are always merely hydrothorax, occurring either as a mechanical result of embar- rassed circulation, or else as a consequence of poisoned or depraved blood.] The ex- tent to which the fibrinous element exists varies from a slight coating of soft lymph upon limited portions of the pleura (both costal and pulmonary), with some light floating flakes in pretty clear serous fluid, to a dense cortex enveloping the whole of the lung and coating the whole of the pleura, and from one to several lines in thickness; the latter condition is only produced in old-standing cases, and the lymph is deposited in concentric layers of which the external are yellow and rather soft, the deeper ones dense and tough, reddish in color, and exhibiting traces of vessels. The longer the pleural cavity remains distended with fluid, the more firmly the lung is bound down to the neighborhood of the vertebral column ; and if the conditions of mechanical pres- sure last long enough, the fibrous adhe- sions grow too dense ever to be removed so as to allow the lung to expand again. The final result, in cases of recovery, is the conversion of the layer of fibrinous lymph into a rudely organized cellular tissue, bands of which also stretch be- tween the lung and the chest-wall, and either bind them firmly together, or (ac- cording to their length) allow more or less free play. In exceptional cases the whole surface of the lung is left firmly adherent to the chest-wall by a layer of fibrinous matter, which may vary in tex- ture from that of loose cellular tissue to a tough semi-cartilaginous material. The latter condition has been occasionally seen in cases where, apparently, there has been little or no serous effusion, and where the lung, though thus universally coated, has been found (after death from some other disease) fairly expanded and permeable to air. If we now inquire into the minute anatomy of these changes, we find that the earliest stage, beyond that of mere congestion of the subpleural vessels-that, namely, of cloudy swelling of the mem- brane- is microscopically distinguished by the appearances of proliferation of the epithelial cells, which tend more and more to multiply and also to be shed from the surface.1 very soon there appear, also, masses of fibrinous materials which have nothing to do with epithelial changes, but apparently exude directly from the bloodvessels, and belong to the same pro- cess by which the serous effusion is poured out. The proliferated epithelial cells, together with exuded blood-cells, form the cellular element of the fluid; and upon their numbersand the stamp of their vitality depends the question whether that fluid shall turn to pus or not; they are present, along with fibrinous matter, in the flocculi which float in the fluid.2 As to the retrograde changes which take place in the solid matters when ab- sorption takes place, the most important matter is this. If the cellular elements are in large quantity, the retrograde pro- cess is slow, and passes through a stage of cheesy formation, which may be very lingering : and there is much probability that this state, though not so frequently as the long-continued persistence of a purulent effusion, may give rise to tuber- cle. Where a very abundant and thick fibrinous deposit, with scattered cells, is the only thing left after the liquid has disappeared, there is still some danger : part of the material must pass through the stage of caseous formation: and it will be well if the patient escapes with a thick, almost cartilaginous, coating of his lung, scattered with calcareous deposits. The most favorable result is when the only trace of the effused matters is a few adhesions, composed of cellular tissue, be- tween the lung and the chest-wall. Such appearances are, as is well known, among the commonest things found after death in the pleura even of persons who may never have been conscious of the pleuritic attacks at the time of their occurrence. The condition to which the lung is re- duced by the pressure of the effusion and the strangulation induced by the com- pressing fibrous adhesions, is of the high- est importance. In simple Pleurisy, without pneumonic complication, the lung, pressed back by the side of the spine, is reduced to a state of so-called carnification: the tissue is hard and un- yielding, and does not crepitate under pressure. This is the effect of extreme compression ; when the effusion has been 1 Rindfleisch, Handbuch der pathologischen Gewebelehre: Leipzig, 1869. 2 See the striking engraving in Rindfleisch, op. cit. p. 211. DIAGNOSIS. 349 small, the lung-tissue may still be par- tially crepitant. Even the extreme degree of carnification does not seem to exclude the possibility of re-expansion, if once the pressure were fairly taken off. The dan- ger is rather-especially when the fluid has been purulent-that cheesy masses, and even true miliary tubercle, may de- velop within the compressed lung. It is in these conditions that the re-expansion of the lung becomes almost beyond hope. On the other hand, when there has been antecedent pneumonic inflammation, the lung may never become greatly com- pressed from first to last; it will be found heavy and solid, much less resisting to the finger than true carnified tissue, perhaps still crepitant, but presenting the charac- ters of hepatization. Diagnosis.-The most frequent source of fallacy is confusion between Pleurisy and pneumonia. In both diseases there are fever, dys- pnoea, and cough. But in primary Pleu- risy the temperature rarely attains a high grade, especially in early stages ; while in pneumonia it is not unusual for the thermometer to reach 103° or 104° within the first twenty-four hours. The skin is much more dry and burning to the touch in pneumonia than in Pleurisy : the flush on the face more fixed, and often remark- ably unilateral. The feeling of dyspnoea is often much more remarkable in Pleurisy than in pneumonia, but the relative fre- quency of respiration and pulse is more altered in the latter. The cough in Pleu- risy is short and hacking, but attended with no expectoration or with only the discharge of a little thin mucus ; whereas in pneumonia expectoration is present in an immense majority of cases, and soon becomes "rusty" in color, and very tena- cious. Sharp stitch-like pain in the side is a very frequent characteristic of Pleu- risy, whereas in pneumonia there is com- monly no pain, or else a much duller and more diffused pain. As regards physical signs, the dulness on percussion is more absolute in Pleurisy than in Pneumonia, and as the case proceeds the breath-sounds and voice become weakened and finally abolished'in the former, while they be- come more and more " bronchial" in the latter. [This is true of adults, but in children bronchial breath and voice per- sist in Pleurisy.] The vocal fremitus be- comes weakened and finally abolished in Pleurisy; it increases in pneumonia as the consolidation proceeds. Displacement of the neighboring viscera is never seen in i pneumonia ; it is common in Pleurisy, es- ' pecially in adults. Increase in the volume of the affected side, with widening and bulging of the intercostal spaces, and in ex- treme cases fluctuation there, are charac- teristic of Pleurisy, but not of pneumonia. Several of the above remarks are chiefly applicable to primary Pleurisy, which, as already stated, is nearly, if not quite, al- ways a unilateral disease ; whereas pneu- monia is more frequently than not bi- lateral. More absolutely distinctive of Pleurisy, however, is the absence of that fine hair crepitation which in pneumonia precedes consolidation and establishment of bronchial breathing and voice. Where the chest affection is only secondary, Pleurisy is frequently double, and much of the value of comparison of the two sides is lost. Here the percussion and auscultation sounds require to be more finely appreciated ; and the presence or absence of special sounds, like the fine pneumonic crepitation, is of the greatest importance. The possibility of the coex- istence of pneumonia and Pleurisy must always be kept in mind ; and when to fine crepitation, mixed increasingly with patches of bronchial respiration, there succeeds a weakening and then absence of breath and voice sounds, we have good primd facie reason for thinking that the latter disease has supervened upon the former. Undoubtedly the most generally ser- viceable physical characteristics of Pleu- risy are the combination of very pro- nounced percussion dulness, absence of vocal fremitus, loud bronchial breathing limited to the superior internal and intra- scapular space, and (where the pleura is not yet full) tympanic percussion and al- most cavernous respiration just below the clavicle, with more or less complete ab- sence of breathing elsewhere. The diagnosis of Pleurisy from simple hydrothorax-passive exudation resulting from mechanical obstruction of circula- tion, or in chronic blood-poisoning-rests chiefly on two facts : the absence of fresh febrile disturbance, and the more gener- ally double effusion in the latter affection. Often there is corroboration of these indi- cations, in hydrothorax, from the simul- taneous occurrence of dropsical effusions in other parts. Pleurisy is to be distinguished frompi^- monary phthisis by the history of the attack, the absence of characteristic expectoration and emaciation, the physical signs of fluid effusion, the family history, &c. But as regards limited attacks of merely fibrinous pleurisy, it may be very difficult to say whether or not there is phthisis also, the form of pleuritic attack being a very common complication of phthisis at all stages. , The" presence of a solid tumor, occupy- ing a considerable portion of the pleura, or bulging into it from the mediastinum, may closely simulate most of the physical signs of Pleurisy. We must here depend mainly upon a very accurate inquiry into the history and the " rational" symptoms : 350 PLEURISY. the absence of all febrile disturbance at the commencement will assist our judg- ment. But although I might draw out to a much greater length this catalogue of the possible snares which lie in wait for us in the diagnosis of Pleurisy from affections more or less resembling it, I think this unnecessary, because the means of dis- crimination are now augmented by a most potent test, the modern practice of explo- ratory puncture. We may fairly say that, with the assistance of the small trocar, fitted with the glass vacuum syringe, it is possible for us to make a puncture into a chest without the least apprehension of damage, whether the trocar shall enter a pleuritic effusion, a hepatized lung, a can- cer, or even an aneurism ; and with the great advantage of discovering whether there is fluid at all, and if so, what the fluid is. It is unnecessary to say, that except under the stress of urgent symp- toms, this should not be done while high febrile excitement is present, unless there is strong probability that fluid effusion is the sole cause of the maintenance of the fever. Prognosis.-The prognosis of primary Pleurisy is very favorable, though there is by no means that complete immunity from fatal consequences which was as- serted by Laennec and Louis. The dan- ger of sudden death from orthopnoea was shown by Trousseau to be a serious one in a small percentage of cases-more espe- cially the latent type, with insidious com- mencement-when the effusion completely fills one pleural cavity ; and at the present day it is generally acknowledged that this is a real peril. For prognostic purposes it is now pretty well understood that it is not the mere quantity of the effusion that should most alarm us: the rule is that, large effusion being present, the occur- rence of one or more attacks of severe dys- pnoea-orthopnoea-indicates a dangerous want of tolerance by the organism, and calls for direct interference. The other danger which must be reck- oned with is where a primary pleuritic effusion has remained stationary in the chest without any tendency towards ab- sorption for a considerable period, and signs of its conversion to pus, with attend- ant severe hectic fever, increasing ema- ciation, and general prostration of vital power, show themselves. Here the least of dangers is that involved in protracted suppuration: far more formidable is the risk, now well established, of an infective absorption leading to tuberculosis. It must be said, however, that both the chance of suffocation from mechanical pressure, and the risk of secondary tuber- cular processes, are indefinitely diminished by the modern practice of prompt para- centesis. It may be questioned whether the experience of the next twenty years will not enable us to ensure an absolute immunity from fatal results of either of these complications. Very different is the prognosis in secondary pleurisies : though even here we may reckon on a considerable percent- age of recoveries. Most fatal of all is the Pleurisy which occurs in the course of pygemic (e. g., puerperal) infection ; here, death is the rule, recovery a rare excep- tion. A considerably smaller mortality, but still a very high one, attends the cases which supervene on scarlatinal albumi- nuria ; and a somewhat similar ratio of deaths, though scarcely so high, attends all pleurisies secondary to the acute gene- ral fevers. But the fact is that every case of Pleurisy supervening on a consti- tutional fever has its individual progno- sis depending on the time of its occurrence, the amount of vital resistance which the original disease has spared, &c. ; and we are driven here to a minute observation of particular symptoms. It is here that thermometry plays an invaluable part. The following conclusions of Wunderlich, respecting temperature in serous inflam- mations generally, apply, according to my experience, with admirable correctness to pleurisies secondary to fevers:1 "Subnor- mal temperatures are always highly sus- picious ; death occurs either shortly after their first appearance, or when they have persisted for some time, or have alter- nated with normal and excessive tempe- ratures. Temperatures of considerable, especially of increasing height, though not necessarily in themselves of bad omen, yet add something to the dangerous momenta. If the temperature falls again, the danger is not past, yet it is less threatening than if the heat had been maintained. Be- sides the height of the febrile temperature, its constancy, and the absence of remis- sions, especially heighten the peril; more particularly the long continuance of a high temperature, even if it alternate with con- siderable morning remissions. In the first case the disease is dangerous, in the latter complete recovery is at least doubt- ful Very considerable and irregular fluctuations between tfie highest and the lowest temperatures (resembling those of pygemia) occur, especially in en- docarditis ; occasionally also in pericardi- tis, pleurisy, and peritonitis; they are always extremely dangerous, and a fatal result is very probable." To this element of prognosis let me add examination of the pulse with the sphyg- mograph, of the value of which I can hardly speak too strongly. The subject would occupy too much space in discuss- ing here ; but I would refer the reader to * Wunderlich, op. cit. p. 375. TREATMENT. 351 what I have written elsewhere1 respecting the favorable and unfavorable pyrexial pulse-forms, and shall merely say that subsequent experience has strengthened my convictions already expressed. I be- lieve that in the dangerous secondary pleurisies the combined use of thermome- ter and sphygmograph is more valuable for prognostic purposes than all other modes of observation put together. As regards the prognosis of Pleurisy secondary to pneumonia, it may be said, in general terms, that the amount of dan- ger depends entirely on the moment at which the Pleurisy supervenes. If the system has been severely tried, the chances are bad: thus, Riliiet and Bar- thez reckoned eight deaths out of ten such cases. Of Pleurisy secondary to phthisical lung-disease, as already said, the prog- nosis is usually very favorable, for the moment at any rate ; but there is always the danger that any fresh pleuritic process may be the starting-point for a true tu- bercular infection. And, on the other hand, the subjects of tubercle who (not a very common case) develop extensive Pleurisy with liquid effusion, nearly al- ways die. Be it said, however, that the increasing tendency to paracentesis, even in second- ary pleurisies, will not improbably result in a greatly decreased mortality, even from the most formidable varieties of the disease. It is almost impossible to rate too highly the significance of such a case as that of Kussmaul, hereafter to be cited (vide Treatment). There is one variety of secondary Pleu- risy of which I must say a few words here, because it is scarcely discussed in the text-books, viz., Alcoholic Pleurisy. Except in the advanced stages of chronic alcoholism, supervening Pleurisy is rarely of bad prognosis: nearly always it leads only to a certain amount of fibrinous exu- dation and proliferation of connective tis- sue. It is only in the last stage of drink- degeneration that a fatal form of empy- ema is apt to develop itself: I have seen only one such case purely traceable to the results of drink alone, but there are a con- siderable number of cases in which the fatal result is, perhaps, equally due to this influence and to blood-poisoning from renal disease. Treatment.-The treatment of Pleu- risy is naturally divided into that of the primary and that of the secondary forms. Primary Pleurisy, of a well-marked type, is perhaps as little the fit subject of treatment by drugs or other artificial means, in its acute stages, as any disease that could be named, or rather, the drugs needed are very few, and all of the stimu- lant-narcotic class. For the vast majority of patients, indeed, the only drug which is of considerable value is opium in one or other form, until the febrile period has passed over, when preparations of iron sometimes become very useful. I do not make this statement without having care- fully watched and considered the effects of a number of internal remedies which are still used as a matter of course, and indeed considered essential, by various physicians of good repute. To take, first, the case of primary sim- ple fibrinogenic pleurisy, one may at once decide against all heroic remedies, since evidence abounds on all sides to show that the disease is a perfectly harmless one, unless the patient has strong tenden- cies to constitutional disease, and that it tends always to recovery. In fact, one has no need to adopt any treatment what- ever beyond keeping the patient in one room, free from draughts, and in the pos- ture which he finds easiest to him ; feed- ing him steadily with nutritious food of the kind best adapted to the degree of fever and digestive derangement that may happen to be present: forbidding unne- cessarymovementsand talking; applying hot poultices to the side, and administer- ing an occasional hypodermic injection of j or | grain morphia to keep the pain in check. Acetate of ammonia, in doses just short of those which produce decided sweating will sometimes greatly relieve the pain and distress even without the aid of opium, and is at all times a harm- less, even if an unnecessary medicament. Recently, the acetate of methylamine (a base which exists in roasted coffee, owing to the transformation by heat of a part of the coffeine) has been proposed, and ap- parently used with good effect, by Profes- sor Behier of Paris.1 There is usually no necessity for alcohol, and it had better be avoided. After from six to seven days in bed, the patient will probably be well able to sit up, and the only thing neces- sary to forbid to him is movement. He should sit perfectly still. If any ansemia remains, the tincture of muriate of iron, in twenty-minim doses thrice daily, is advisable as a tonic; and, on the whole, a very few days ought to see the patient completely fit to resume his ordinary work. In Pleurisy evidently of considerable extent, and with a notable amount of se- rous effusion, the ideal of treatment should be still, as much as may be, that given above. It is now very decidedly proved ' See a paper in the Practitioner, October, 1868, "On Tonic Medication and on Acetate of Methylamine: a new tonic remedy." By MM. Behier and Personne. 1 Lectures on Acute Diseases, delivered be- fore the Royal College of Physicians. (Lan- cet, 1867, vol. ii.) 352 PLEURISY. that the old heroic methods of attacking severe Pleurisy ought to be abandoned. In the first place, as to general blood-let- ting, I have witnessed enough of this treatment to be sure of two things: first, that the older physicians were perfectly right in the statement that it usually re- lieves pain with great promptitude ; and secondly, that the relief thus given is not in the least degree superior to that afford- ed by hypodermic injection of morphia, except that it operates more quickly, per- haps by some five minutes, than the latter. As to bleeding checking the tendency to effusion, that is to me quite incredible. No such effect has been wit- nessed in either of the five cases of phle- botomy for acute Pleurisy that I have watched at various times ; and I observe that Dr. Aitken,1 while still adhering to the use of this remedy, recommends us not to be discouraged by the fact that the effusion may go on increasing after the bleeding, and the patient also may feel very depressed. It is true, he says, that after a certain time absorption will set in, and that it will then go on more rapidly and well than if the patient had not been bled. I cannot at all imagine on what evidence this last opinion is based; cer- tainly it utterly conflicts with the fact of my own experience; and though I have personally seen little of the actual treat- ment of Pleurisy by bleeding, I have ex- amined a pretty large number of persons whose past history included one or more pleuritic attacks which had been so treat- ed. The accounts given by such persons show a melancholy uniformity: long weeks and months of suffering from the presence of effusion in the chest, occasion- ally leading (through empyema) directly into active and rapidly fatal tuberculosis, nearly always slow and imperfect recov- ery, with diminished vital energy, and especially weakness in the chest, and only in the rarest cases a tolerably prompt and complete recovery. The homoeopath- ists have made their fortunes in no small degree by their "treatment" of Pleurisy, which has had the one sole merit of being purely negative, and avoiding all destruc- tive agencies. [In view of Dr. Anstie's statement (above) that he had seen little of the treatment of Pleurisy by venesec- tion, it may be pardonable to refer to his expression on a later page, in regard to the opposition to paracentesis: not "by men who have fairly tried the practice, but only by theorists who are afraid of its imaginary results." It is hardly too much to say, that those who decry bleed- ing now maintain their position almost entirely upon theoretical grounds.2 It is true, however, of Pleurisy as it is of pneumonia, that not nearly all cases re- quire, or will properly bear, venesection ; and that almost never will it be appro- priate later than the third or fourth day of an acute attack.-II.] A much better case, no doubt, might be made out on behalf of local blood-letting. Cupping ought never to be mentioned, being actually barbarous in the suffering it inflicts on a pleuritic patient. But leeches unquestionably do relieve pain very often in a speedy and effectual man- ner, and I only know of one objection to their use, viz., that morphia will relieve the pain with even greater certainty. During five years of dispensary practice I determinedly abstained from the use of leeches in Pleurisy and found morphia, even given by the mouth, a perfectly satis- factory substitute. But since the use of the hypodermic syringe has become more common, the advantages of morphia are far more manifest; and I have no doubt, personally, that leeches are now unneces- sary. The first act of the physician in treating a pleuritic patient in the agony of the early acute stage, should be to inject | or 5 grain of acetate of morphia (for an adult) under the skin,1 and to envelop the painful side in a hot poultice. For a child under 2 years, fa or fa grain is enough. Such doses as these may be repeated every four hours, if necessary ; but in fact it is seldom that more than twro or three doses are needed in the first twenty-four hours, and afterwards one dose in each twenty- four hours is generally enough. I would insist strongly on the advan- tages, indirect as well as direct, of subcu- taneous over gastric administration of opiates; in a direct way, the former is superior as acting much more rapidly ; in an indirect way, because it so much less disturbs the functions of the alimentary canal. Of the treatment by mercury, I can ex- press only the most unqualified disap- proval. I have watched many cases of Pleurisy in which, according to the rule formerly acknowledged, mercury was given, either to complete or partial saliva- tion, as soon as the signs of effusion be- came unequivocal, and I can truly say that these cases, even when they were not further complicated by the depressing influence of blood-letting, contrasted very unfavorably with the results of a treat- ment which entirely abjures mercury for of Penna., used to say to his class, that, in a long experience in practice, he had never had occasion to regret having employed the lan- cet ; while he had often seen reason, too late, to regret that he had not used it.-H.] * I believe, with Mr. Hunter, that there is no need to inject locally : the arm does quite well for the purpose. 1 Science and. Art of Medicine, 3d edition, vol. ii., article "Pleuritis." [2 Professor N. Chapman, of the University TREATMENT. 353 any purpose except that of an occasional purgative. I am glad to cite, on this point, the late Dr. Hillier, who says (in his Monograph on Children's Diseases) that from experience he had been led to abandon mercurial treatment for Pleu- risy ;* and I believe that, whatever some of the class-books may still say, mercury is practically given up by the best physi- cians in this country, not only in children's pleurisy, but in that of adults. It seems the general opinion among those with whom I have conversed, that the absorp- tive action with which mercury used to be universally credited is more than doubtful in the case of pleuritic effusions, whether fibrinous or serous. And certainly, if it fails to do good, mercury may do very sensible harm. I have seen cases in which it apparently produced the most decided ansemia-at least there was scarcely any other possible cause for the latter condition-which set in rapidly after the first occurrence of ptyalism.2 The treatment by so-called "counter- irritants," as pursued by many physi- cians, is no less repugnant to me than is that by mercury or bleeding. Let me make two admissions. In the first place, the mere application of a mild mustard plaster, or, still better, of a hot poultice, or epithem, undoubtedly may give some ease ; perhaps even arrest incipient in- flammation ; and the use of small flying blisters, in the limited attacks of Pleurisy which are so common in phthisis, un- doubtedly appears to give relief in many cases. But the use of large blisters, espe- cially if kept open, appears to me both useless and often prejudicial. I shall not repeat here what I have said at length elsewhere suffice it to say that I adhere to my opinion already stated, which is the same as that previously announced by many of the greatest masters of practical medicine in the present century. The practice of painting the chest-wall with iodine, though not open to the same positive objections as apply to blistering, has never, in my experience, yielded any very positive results. It is, I believe, very inferior in utility to the application of the simple adhesive or the Burgundy pitch- plaster, to afford mechanical support; this really does sometimes appear to favor ab- sorption of the fluid, and it usually gives much comfort. The employment of diuretics to promote absorption is another point on which I find myself at issue with the opinions of many. The only drug which has ap- peared to me, in some cases, directly to promote absorption by means of increased diuresis, is iodide of potassium, in quanti- ties amounting to from 6 to 18 grains daily, according to the age of the patient. I think it is worth trial for two or three days (along with the external use of iodine) when effusion comes to a standstill. [Dr. Da Costa, in a case of chronic pleuri- tic effusion, recently reported, gave a drachm of jaborandi, four times daily ; with the effect of profuse diaphoresis, fol- lowed by disappearance of the fluid, and recovery.-II.] The medicine, however, which stands quite alone in its power to promote the process of absorption is iron-best given in the form of the muriated tincture; and in all cases where there is marked ansemia it should be exclusively employed from the moment when the necessity for ad- ministering opium ceases. As regards purgative medicines, the utmost that I can recommend is that, if necessary, such mild medicines may be used as may suffice to prevent actual loading of the bowels, which, especially in the case of children,2 might seriously increase the mechanical distress in the chest. Actual purgation is always mis- chievous in Pleurisy, although it is some- times very useful in hydrothorax. The use of alcohol is a matter requiring much care and judgment. In primary acute pleurisy it is usually best dispensed with, unless the patient is unable to take other nourishment; in this respect Pleu- risy differs much from pneumonia. But in secondary pleurisies stimulants will often be needed, and here the amount of the dose must be ruled, not by any rou- 1 See also Meigs and Pepper on the Diseases of Children. 2 I cannot help making a digression here on the subject of the supposed absorptive ac- tion of mercury on inflammatory lymph. So repeatedly have I seen attempts made, with- out one particle of success, to induce the ab- sorption of pleuritic, peritonitic, and pericar- ditic lymph by means of this drug, that I have seriously reflected on what could possi- bly have given rise to the old unreasoning confidence in its power to act in this way. After the best inquiry possible to me, it seems pretty certain that the only groundwork was the assumption of a necessary analogy be- tween lymph effused in the iris and that effused elsewhere. Now, to say nothing of the spe- cial relations (unintelligible, no doubt) of mercury to syphilitic products, it is certain that mercury possesses a strong physiological predilection for the whole territory innervated by the trigeminal nerve; and I believe that there is something quite peculiar in its action on the nutrition of the eye, the mouth, the nose, and the face, and on the pathological products of inflammation in these parts. 1 "On the Popular Idea of Counter-irrita- tion," Lancet, Feb. 26, 1869; "The Theory of Counter-irritation," Practitioner, April, 1870. 2 Ziemssen (op. cit.) particularly points this out. vol. ii.-23 354 PLEURISY tine, but according to those indications of the pulse, the temperature, and the urine, which I have fully described in my lec- tures on Acute Diseases, at the Royal College of Physicians,1 and elsewhere. 2 As regards all other matters in the treatment of secondary pleurisies, it is absolutely necessary that I should leave them to be dealt with by the authors who describe in this "System of Medicine" the various diseases of which Pleurisy is apt to be a complication. One word must be said about a mode of treatment for Pleurisy which I confess that I have never attempted : I mean the employment, so common on the Continent, of cold to the chest, and the use of cool baths. I desire to pronounce no judgment whatever on the matter; but those who wish to know more of the system should study the remarkable statements of Nie- meyer,3 a very trustworthy witness, as to the effects of ice-cold applications to the chest. Paracentesis Thoracis.-A new era has been inaugurated in the treatment of Pleurisy by the development which the operation of tapping the chest has received within the last few years. There is prac- tically no use in going back further into the history of the operation than about thirty years ; previously to this there was no real certainty or agreement as to its use except as a last resort. It was Trous- seau who first had the acuteness and courage to lay down the proposition that in extensive effusions, whether of serum or pus, we ought not to wait till death is imminent, but operate with the view of warding off the dangerous attacks of orthopnoea which, as he proves by a series of remarkable cases, may unexpectedly seize the patient, and carry him off with great rapidity. Trousseau, however, en- countered great opposition, both in his own country and elsewhere, and although some of his brilliant results undoubtedly startled the medical world, it may be doubted whether the operation would not have been relegated, after his death, to its former limited sphere, had it not been for the interposition of a very able and clear-sighted American physician, Dr. Bowditch.4 This gentleman had long felt the futility and the culpable ineffi- ciency of treatment which allowed pa- tients to suffer the misery and danger in- volved in the retention for months to- gether of fluid in the pleura, but it was not until the invention by Dr. Morii! Wyman of his excellent suction instru- ment, that Dr. Bowditch saw his way to the safe and effective performance of paracentesis on the large scale. From that date (1850) till the present time Dr. Bowditch has performed the operation 250 times, in 154 persons, without once seeing any evil, or even any very distressing symp- toms resulting from it; while, on the other hand, it has saved a large number of lives that must otherwise have been sacrificed. "Surely," as the author remarks, "this amount of experience by any one deserves the attention of the profession." To this I warmly assent, and must add that there appears to me to be no opposition to Dr. Bowditch's views by men who have fairly tried his practice, but only by theorists who are afraid of its imaginary results. Formerly paracentesis was supposed to have two functions only in Pleurisy : that of averting suffocation which was actually impending, and that of letting out collec- tions which were pretty certainly conjec- tured to consist of pus. But against these advantages were to be set, it was thought, the fact that the fluid would inevitably re- form, and re-form ad infinitum, and after very few tappings would become purulent (even if air could be excluded from the pleura, which was held almost impossible), thus surely undermining the patient's constitution. But the great and dreadful danger was that of admitting air into the pleural cavity ; that, it was said, inevita- bly led, not merely to a continuance or aggravation of the purulent formation, but also to the putrescence of the pus, and the rapid depression of the vital powers under the combined influences of profuse suppuration, the absorption of noxious gases, and often the absorption of matter capable of inducing pyaemia. Tapping was therefore held to be inappli- cable to the treatment of a merely serous effusion which did not immediately threaten life from mechanical pressure. This feeling prevailed the more strongly because some of the greatest masters of medicine of the present century had de- clared that primary Pleurisy, with proper medicinal treatment, should never be fatal; while in secondary pleurisies it was felt that an element Of uncertainty underlies the whole prognosis, which dis- inclines the physician for doubtful, and possibly dangerous, modes of treatment. It can hardly be doubted that the whole feeling about the dangerousness of para- centesis rested upon the use of clumsy and imperfect means of operation, and on exaggerated ideas of the evil effects of ad- mitting a small quantity of air into the pleural sac. With regard to the first 1 Lancet, vol. ii., 1867. 2 Practitioner, "Wines in Acute Diseases," August, 1870. 3 Handbuch der Speciellen Pathologic u. Therapie, vol. i. 4 Dr. Bowditch's original papers are in American Journ. of Med. Science, April, 1852; American Med. Monthly, January, 1853; Boston Med. and Surg. Journ., May, 1857. See also his final paper before New York Academy, 1870. TREATMENT. 355 point, we are entitled to say that it is quite possible so to operate as to ensure that no damage will be done to viscera, and that no more than a trifling quantity of air will be admitted to the pleura. And upon the second point we may certainly now assure ourselves that there is no reason to fear serious mischief from the admission of a limited quantity of air if the opening made in the operation be afterwards properly closed. It is even unnecessary, as Dr. Bowditch's large ex- perience has shown, to make the opening valvular. But the most important ad- vance that has been made is the invention of apparatus which allows of the opera- tion being made either simply exploratory, or carried on at once to evacuation of the fluid. With the instrument either of Bowditch or of Dieulafoy1 we intro- duce a very small trocar and canula guarded with a tap, and by attaching a suction syringe and opening the tap, we withdraw a small amount of fluid, the exact nature of which we can identify : if we elect to continue the evacuation, we can do so with the aid of the syringe ; if, on the other hand, no fluid can be ob- tained, the guard-tap has prevented the entrance of air, and we can withdraw the canula and close the wound without hav- ing done the least mischief. By the use of the small canula we are able to operate without risk, because, in the case of an [Fig. 45. The aspirator, a. The perforated needle or sharp-pointed canula, which is introduced into the collection Of fluid. It communicates with the hottie, d, by means of an india-rubber tube, which is interrupted at & by la portion of glass tubing, so that the nature of the fluid evacuated can be judged of at once, and the canula Either plunged deeper or withdrawn. When the handle, c, is in the position shown, the communication oteween the canula and the bottle is closed. The bottle is then exhausted of air by means of the pump,/. IWhen c is moved to c', the canula-tube is opened, e is the waste-tube of the bottle, and is closed by a button at e. In using this aspirator the vacuum is formed, and the handle, c, is kept in the position shown till the canula has been introduced into the fluid, then it is turned to c', and the fluid fills the bottle. If there be still more fluid, the handle is turned back to c, the waste-pipe opened, and the fluid emptied out of the bottle, which is then again exhausted, and the handle turned back to c'. This is one of the simplest of the many forms of the aspirator. (Holmes.)] entirely mistaken diagnosis, we should have done no damage, even though we had perforated a consolidated lung, a solid tumor, or an intercostal artery. The suction power of the vacuum-syringe will enable even thick fluid, such as some- what concentrated pus, to be withdrawn through the smaller-sized Canute ; but the puncture is such a trifle that, in case of our desiderating a larger tube, the smaller one can be withdrawn, the finger being pressed on the spot as it emerges, and the more capacious canula introduced at the same place. The site of puncture should be selected in ordinary cases according to Bowditch's rules : Find the inferior limit of the sound lung behind, and tap two inches higher than this on the pleuritic side ; at a point in a line let fall perpendicularly from the angle of the scapula. Push in the inter- costal space here with the point of the finger, and plunge the trocar quickly in at the depressed part; be sure to puncture rapidly and to a sufficient depth, or you may be balked by the false membranes occluding the canula. It will sometimes happen that with the greatest care and trouble we are unable to get a flow of fluid at the point where we first puncture ; it is then our duty to try elsewhere, for our failure may be owing to unusual thickness of the false membranes in the lowest inch or two of the pleural cavity. We thereupon repeat the puncture a little higher up, and further 1 It is right to say that Dr. Protheroe Smith claims, with apparent reason, to have been the actual inventor of the instrument now made by a French instrument maker, and employed by Dr. Dieulafoy. 356 PLEURISY. towards the axillary line;1 and here we perhaps find fluid : at any rate, no harm has been done by the two punctures. The circumstances under which para- centesis ought to be performed for Pleurisy are the following:- 1. In all cases of Pleurisy, at whatever date, where the fluid is so copious as to fill one pleura, and begins to compress the lung of the other side ; for in all such cases there is the possibility of sudden and fatal orthopnoea. 2. In all cases of double Pleurisy, when the total fluid may be said to occupy a space equal to half the united dimensions of the two pleural cavities. 3. In all cases where, the effusion being large, there have been one or more fits of orthopnoea. 4. In all cases where the contained fluid can be suspected to be pus, an exploratory puncture must be made ; if purulent, the fluid must be let out. 5. In all cases where a pleuritic effusion occupying as much as half of one pleural cavity has existed as long as one month, and shows no sign of progressive absorp- tion. The limits of the operation form an im- portant question. Formerly one great error seems to have been, that operators were often too anxious to extract the whole of the fluid ; in this way they often protracted the operation to a mischievous extent, and gave abundant opportunity for that very entrance of air to the pleura which was theoretically so much to be dreaded. Among the latest writers, Bow- ditch and Murchison2 have most authori- tatively shown that it is neither necessary nor useful to extract the whole of the fluid, and that the removal of just so much as may be necessary to relieve sub- stantially the mechanical distress will in most cases give the necessary spur to the natural process of absorption, by means of which the rest of the fluid will be taken up. One rule seems absolute: the with- drawal of fluid must be arrested the moment that the patient begins to com- plain of constricting pain in the chest or epigastrium. Even in the case of purulent effusion there can be little doubt that absorption often takes place, though un- questionably there is here a danger that concrete cheesy matter may be left un ab- sorbed, and under unfavorable circum- stances may become the starting-point of tubercular infection. The case of Pleurisy in children, as re- gards paracentesis, requires special con- sideration. There can be no doubt that in young subjects there are physical and vital reasons which might lead one to hope more strongly for complete recovery by natural means than we could do in the case of adults. The softness of the lymph exuded is proportionably greater than in later life, and it is comparatively rare to find adhesions so strong as to bind the lung down with a firmness which renders subsequent expansion impossible; and, unquestionably, the vital activity of the processes of absorption is greatest in early life. But, on the other hand, there is a much greater tendency of effused serum to take on a purulent character in chil- dren than in adults ; and the dangers of a long-retained purulent effusion are now seen to be much more formidable in presence of recent investigations as to the artificial generation of tuberculosis than they formerly appeared. This latter view of the case has been painfully impressed on my mind by a succession of cases, three in number, in all of which empyema has preceded and apparently caused tu- berculosis in children who were, indi- vidually, remarkably well formed and robust. Two of the patients belonged to families in which there was a taint of phthisis, the other to a family perfectly free, for at least two generations, from any such disease. And seeing that there is in children a greater possibility of rapid re-expansion of the lung (both on account of the vigor of their respiratory efforts and the relative 'weakness of the fibrinous ad- hesions), we may the more reasonably hope that the removal of the whole or a portion of the liquid will be followed by a favorable turn in the progress of the disease. I regard as a typical instance of judicious and successful treatment the case recorded by Dr. Murchison (Lancet, loc. cit.), in which a boy of seven years was tapped on the twelfth day from the initial shivering and attack of pain, and twenty-four ounces of clear serum were withdrawn. Only two days were spent in therapeutic experiments after his admis- sion into the hospital; and as these were without effect, and the effusion was large, displacing the heart and causing some (though not great) dyspnoea and weakness of pulse, the operation was done. Only part of the fluid was with- drawn, and, notwithstanding precautions, some air entered ; but the case did per- fectly well, and in one month more re- covery was substantially complete. The only thing lacking in this case, according to my thinking, is, that the vacuum in- strument of Bowditch or of Dieulafoy (Protheroe Smith) should have been em- ployed ; the discharge-pipe terminating in an india-rubber tube which dipped under water (ex abundante cauteld}. The following statistics of the operation on children, as gathered from the hospital service of M. Barthez, are reported by Verliac.' Thoracentesis was performed on nineteen patients:-1. Simple acute 1 Bowditch, last pamphlet, 1870. * Lancet, 1870, vol. i. p. 221. 1 Op. cit. p. 107. TREATMENT. 357 Pleurisy, two cases ; simple puncture, cure of both without reproduction of the liquid. 2. Serous tubercular Pleurisy, two cases ; simple puncture, one cure without repro- duction of the liquid, one death from con- vulsions six days after the operation. (It is not likely that the latter caused the fatal attack.) 3. Pleurisy symptomatic of heart-disease and vascular compression, one case; cure of Pleurisy after six punc- tures. 4. Pleurisy with purulent effusion, twelve cases ; five cures, seven deaths. Let me add to this the statistics col- lected by M. Guinier1 of Montpellier, of 31 cases of children tapped by himself and others. The patients were of all ages up to 14; as many as 16 were in their seventh, eighth, or ninth year. In one case the operation cured a large sero-purulent effusion in a sucking child twelve months old. There were six times as many suc- cesses as failures, and the mortality was not in the ratio of the age. The opera- tion itself never seemed to do any harm ; in every case much immediate relief was obtained, and in the few fatal cases the operation never seemed to accelerate, but rather to retard, the advent of death. I must cite, also, the valuable authority of Hillier for operation in Pleurisy in chil- dren ; if done early, he says, it is not dangerous.2 Among other highly respected names, may be quoted Dr. Gairdner, of Glasgow,3 Dr. J. W. Begbie,4 and Dr. Fraser,5 who have had the courage to follow out the more extended application of thoracente- sis which Dr. Bowditch has inaugurated. Personally I have been so unfortunate that I have scarcely had any opportunities for employing the improved vacuum instru- ments since I became acquainted with them : although I have witnessed their results in the hands of others. But I was a believer in the need for more extended use of the operation long before I chanced to hear of Bowditch's discovery : and in two cases, as far back as 1862 and 1863, I tapped with the distinct intention of with- drawing a part, only, of a serous effusion (of four and six weeks' date respectively) and employed no other precaution than that of making the opening valvular. I did not conduct the liquid under water, but merely guarded the orifice of the canula with the thumb the moment the stream showed signs of interruption, took much pains in withdrawing the canula without unnecessary admission of air, and immediately well closed the external wound. No doubt some air entered, but no harm was done ; both patients steadily recovered without reproduction of the fluid. One was a girl aged 17, otherwise healthy ; the other a lad of 12, singularly bright and precocious, but with a dan- gerously suggestive family history. I have thought it pardonable, and even necessary, to devote a somewhat large pro- portion of this article to the question of paracentesis, because I believe it is the duty of the writer on Pleurisy, in a " Sys tern of Medicine" published at the present day, to speak with no uncertain sound on this question; and in ordei* to command the confidence of readers, it has been neces- sary to show the manifest tendency of a large number of the best practical men of the day. Fortified by the evidence above cited, and by the remembrance of a great deal more that could be produced, I ven- ture to say, decidedly, that practitioners must throw aside the timid and vacillat- ing rules of conduct which the majority of the text-books still prescribe. Tapping is not to be looked at as a dangerous last resort, appropriate only to a few cases. It must become an every-day remedy for cases where an effusion, purulent or not lingers for more than a very limited period: for the operation may be so conducted as to be perfectly harmless, while no one who knows the facts of recent pathology dare say that even a serous effusion will remain harmless, still less a purulent one. It remains to say a few words on the treatment of those least fortunate cases where from one cause or another, a puru- lent fluid forms and re-forms with great rapidity after each tapping, and perhaps becomes putrid and stinking. Where it is only a question of excessive purulent se- cretion, simple washing out of the pleura with warm water after tapping may pos- sibly change the action of the membrane, but in most cases it will be necessary to keep the canula in, cork it up, and daily allow the exit of pus, and then wash out the cavity. But in my opinion, if it comes to this, the better plan by far is the drain- age tube. A needle-eyed probe, being introduced through the original opening, is carried through to the opposite chest- walls, and is there made to protrude the muscle and skin of an intercostal space, the finger outside carefully feeling for it. The probe is cut down upon, forced out through the chest-wall, and threaded with a strong thread; this is then drawn back through the chest till it comes out at the original opening. The thread is fastened to an india-rubber drainage tube (pierced with openings in the manner devised by Chassaignac), and the latter is then drawn through the chest till it issues through both orifices. Noth- ing more then remains but to tie the ends of the tubes lightly together. The use of iodine injections need not, I ' Bull, de l'Acad. de Medecine, tome xxx. p. 645. 2 Brit. Med. Journal, Aug. 3, 1867. * Clinical Medicine, 1862. 4 Edin. Med. Journal, 1866. 8 London Hospital Reports, June, 1865. 358 HYDROTHORAX. think, be recommended, save in cases of fetid purulent secretion ; in this I agree with the opinions of Guinier, Fraser, and other high authorities. The solution should be one part tincture of iodine to four of tepid water. There is abundant evidence that even a long course of such injections does no harm, and it often ap- pears to do good. Possibly the iodine injections may alternately be altogether superseded by the use of weak carbolic acid solutions. The combined use of dis- infectant injections and the drainage tube has proved successful in a good many cases apparently of the worst augury; even, for example, in putrid empyema, secondary to puerperal fever.1 I shall sum up the treatment of Pleu- risy in a few words. The pain must be met by opium or morphia (preferably in- jected), by hot poultices, and abstinence from movement (at a later stage the side may be supported by stout adhesive plas- ter for the same purpose). Acetate of ammonia or acetate of methylamine may be given-not in doses to produce sweat- ing- but in moderate stimulant doses. The diet should be highly nourishing, but carefully adapted to the state of digestion. The bowels should be kept from actual loading, but no purgation should be at- tempted. The only diuretic worth trying in the stage of fixed effusion is iodide of potassium in small doses ; and if this fails, it is best at once to have recourse to mu- riate of iron. But if at the end of four- teen to twenty days for a child, or three weeks to a month for an adult, from the initial symptoms, the fluid does not show real signs of diminution, paracentesis should be performed : and this rule is ab- solute, both for primary and secondary pleurisies, except where the case is hope- less on other grounds. HYDROTHORAX. Francis E. Anstie, M.D., F.R.C.P. Definition. - Passive non-inflamma- tory effusion of serum, due either to me- chanical obstruction of ciiculation, or to blood-poisoning. History.-The history of Hydrothorax really constitutes a part of the history of the various organic and constitutional diseases of which it is a mere episode. It was once the custom to speak of this malady as if it were a variety of pleurisy; in reality there is a broad distinction be- tween the two affections. We shall dis- cuss the points in which they approximate under the heading of Pathology; mean- time, we may say that their history is essentially different. Hydrothorax, prop- erly so-called, lacks several of the most important "notes" of inflammation. It arises, without febrile disturbance, in the later stages of disorders which either mechanically embarrass the circulation through the chest, or alter the specific gravity and the chemical relations of the blood-serum, or do both these things so as to promote a purely physical exosmosis. It is thus often due to diseases of the heart, particularly those of the right side, and it is not a very infrequent result of renal disease ; but in perhaps the majority of cases a combination of renal and car- diac mischief is the cause. The course of Hydrothorax is eminently chronic, and the disease is often entirely intractable ; in fact, Hydrothorax occurs in many cases only as a part of the closing scene of chronic organic disease. Symptoms.-The invasion of Hydro- thorax is usually stealthy and unnoticed, there is no febrile movement, and the only noticeable matter is the steady in- crease of dyspnoea. At last, and some- times after a day or two only, the patient is in a state of gasping orthopnoea, with livid lips and the greatest appearance of distress ; he is quite unable to lie down. Then, on examination, we find the phy- sical signs of fluid in both pleurse; it may be also in the pericardium. The effusion being bilateral, we find no displacement of the heart; but the diaphragm is nearly always pushed downwards, sometimes very greatly. When the effusion is large, the embarrassment of the heart is shown by the small and feeble pulse. 1 See Kussmaul (Deutsches Archiv fiir Klin. Med. iv. 1868) for some interesting recoveries after paracentesis and disinfection of stinking fluids. Pathology.-The nature of the effu- sion in Hydrothorax may vary within DIAGNOSIS-PROGNOSIS - TREATMENT. 359 rather wide limits ; but it usually contains far less albuminous and fibrinous material, and far fewer cells (whether of epithelium, or white blood-corpuscles) than are found in pleuritic effusions. It may even be doubted whether the fluid of a passive effusion contains any blood-corpuscles at all; but from the readiness with which a clear Hydrothorax serum sometimes con- verts itself, if air be admitted to the chest, into pus, the presence of blood-corpuscles would appear probable.1 When death has taken place without any puncture having been made, the pleura is found free from all lamellar fibrinous deposit, and the lung is simply compressed, not bound down by adhesions. Diagnosis.-The distinction of this affection from real pleurisy is not always easy ; but in most cases the history points strongly to the true nature of the effusion. The simultaneous occurrence of other dropsies, together with the absence of in- itial fever, enable us, usually, to say that Hydrothorax and not pleurisy is present; but on the one hand there may be no dis- tinct dropsy anywhere but in the chest; and, on the other hand, true pleurisy may sometimes (e. g. after scarlatina) coincide with anasarca. Acute rheumatism super- vening on old cardiac, or cardiac and renal disease, sometimes presents signs of a double pleural effusion, the nature of which it is difficult to decide ; especially as the greatest pallor and depression in such cases may coincide equally with a pleurisy or a Hydrothorax. Notwith- standing these occasional difficulties, how- ever, it is usually possible to give a toler- ably decided diagnosis from a comparison of the history and the clinical features of the disease. Prognosis.-How bad this is will be evident from the circumstances of great bodily depression in which Hydrothorax always arises, and from the necessarily more or less constant operation of the cause of dropsy, tending to a continual reproduction of the fluid even if we have been fortunate enough to witness its re- duction or removal. Nevertheless there is great room for bold and intelligent treatment in a certain percentage of cases of Hydrothorax; and recoveries some- times take place in a surprising manner. Many patients have had weeks, months, or even a few years, added to their lives in this way. Treatment.-The tendency of the best modern practice in regard to Hydro- thorax may be said to be nearly the re- verse of that with regard to pleurisy. The operation of paracentesis is rarely applicable : it should be reserved almost exclusively for the prevention of threat- ened asphyxia when both pleurae fill rap- idly to a great height. On the other hand, the effect of diuretics, and still more of hydragogue purgatives, is often most striking. Of the former, infusion of digitalis in half-ounce doses, with thirty grains of bitartrate of potash twice or three times daily, has yielded me better results than any other. Of purgatives I only recommend one, viz. elaterium, which is incomparably superior, in my opinion, to all others. Great care ought to be taken to select a first-rate specimen of the drug, and then (diuretics having been fairly tried first) we need not scruple to use the elaterium boldly. One-fourth of a grain may be given (combined with a little hyoscyamus), and repeated in four hours ; very usually two, or at most three doses will suffice to produce a very copious watery catharsis. It might be thought that this would kill such feeble creatures as Hydrothorax patients generally are, but if care be taken to give a little stimu- lant at the time that the bowels act, the effect is very far from exhaustive; the rapidity with which the fluid diminishes in the chest, and the consequent relief to all the patient's sensations, in favorable cases, must be seen to be believed. The moment that a decided impression has been produced, either by diuretics or by purgation, we must begin the use of mu- riate of iron, in twenty-drop doses of the tincture four or five times in the twenty- four hours: in this way we secure the best chance open to us of preventing the re-accumulation of the fluid. Do what we will, however, it is of course inevitable that a majority of our patients will succumb: and those whom we for the moment cure of Hydrothorax are only temporarily relieved from danger. 1 I tried to convince myself on this point, some time since, by microscopic examination of a typical hydrothorax fluid ; but could not make up my mind upon the matter. Dr. Walshe speaks of "pus-cells" as being pres- ent. 360 PNEUMOTHORAX. PNEUMOTHORAX. By Francis E. Anstie, M.D., F.R.C.P. Definition.-Accumulation of atmos- pheric air, or other gas, in the pleura. Varieties.-I. Non-perforative. Col- lection of gas (ct) from decomposition in gangrene of the pleura ; (6) from decom- position of an ordinary pleuritic fluid ; (c) air replacing sero-purulent fluid, suddenly absorbed ; (d) secretion of air by pleura. II. Perforative. (a) Surgical, from penetrating wounds of thorax, or frac- tured ribs lacerating the lung, or violent contusion tearing the lung. (6) Perfora- tion of lung and pulmonary pleura, from disease in the lung: (1) Tubercular, (2) gangrenous, (3) diffuse pulmonary apo- plexy, (4) hydatids, (5) cancer, (6) em- physema, (7) abscess, (8) rupture in hoop- ing-cough. (c) Perforation of lung from without: (1) by disease of bronchial glands, opening into pleura and bronchi, (2) by emphysema, (3) by parietal ab- scess. (d) Rupture of oesophagus opening into pleura. This formidable-looking list of possible varieties of Pneumothorax simplifies it- self greatly when looked at from the prac- tical physician's point of view. We may usefully abstain from special considera- tion of the non-perforative kinds alto- gether, from their great rarity. Of the perforative kinds, we put aside the sur- gical varieties, as not coming within the scope of this work. Of the remaining varieties of perforative Pneumothorax, all, save one, are individually so rare as to deserve little more than the bare record of their occasional occurrence. More than 90 per cent, of perforative cases from dis- ease of the lung itself are, according to Walshe, "tuberculous" (i. e. produced by some form of phthisical lung-disease), and, in fact, the subject of Pneumothorax, from the physician's standpoint, falls almost en- tirely under the domain of phthisis. Clinical History.-The typical ac- cess of Pneumothorax is distinguished by the sudden occurrence of sharp pain in the side, and intense dyspnoea of the most distressing kind ; occasionally, besides these, there is the distinct sensation, at the moment, of tearing inside the chest followed by a feeling as if fluid trickled or poured down the side. Collapse, with coldness of surface and cold sweat, is pres- ent in the majority of cases. But the symptoms by no means always take this striking form ; there are cases .in which neither pain nor dyspnoea is present at first in at all a high degree ; and there are many more in which, after the first moments of severe suffering, the patient enjoys comparative repose until the secondary symptoms, viz. those of pleural inflammation, set in; and this sometimes represents a considerable peri- od of comparative pause. But the inflam- matory process invariably, and for the most part very speedily and severely, sets in : and often there is again very rapid breathing before the recurrence of great conscious distress. In fact, rapidity of breathing is almost a physical necessity from the moment of the rupture, and it is great, not merely absolutely, but relatively to the pulse frequency, though the latter is also very much augmented. In the worst cases there is never one minute's cessation, from the moment of the catas- trophe till death, of the most acute pain and the most distressing orthopncea ; this was exemplified in a little boy who was under my care at the Belgrave Hospital for children about four years ago. The physical signs of Pneumothorax give a very decided answer to our suspi- cions as to the nature of the case. The chest is very much, the affected side al- most altogether (especially at the lower part), debarred from movement, the breathing is carried on mainly by the abdominal muscles; if the affected side moves at all evidently, the intercostal spaces are seen to be greatly depressed. Percussion gives out at first a merely much louder sound, with a graver pitch than in health ; as the distension increases it becomes quite drum-like, and, if dis- tension reaches the very highest grade, it becomes dull and muffled again-a well- known phenomenon of extreme air-ten- sion. Occasionally percussion gives out an amphoric note. Palpation discovers weakening or abolition of vocal fremitus. Auscultation detects either great enfeeble- ment or complete suppression of the breath-cough, and voice-sounds, accord- ing to the amount of air in the pleura ; the heart-sounds are either greatly weak- ened, or, occasionally, they are trans- mitted with a metallic ring. As the distension proceeds the case be- comes the more unmistakable ; the medi- DIAGNOSIS - PROGNOSIS. 361 astinum, heart, and diaphragm are nota- bly displaced, and the tympanitic percus- sion-sound is heard to extend continuously even beyond the further sternal border. When fluid becomes effused to a notable extent there are of course the signs de- scribed under pleurisy, of a liquid effusion in the lower part of the chest, together with the signs above mentioned, of air in the chest. There is also, when the fluid reaches any considerable amount, easily detectable fluctuation when the patient is shaken ; and more occasionally and vari- ably we can thus produce the true splash, with metallic ring. Moreover, with rare exceptions, the fluid demonstrably changes [Fig. 46. Displacement of mediastinum, heart, and liver from pneumothorax of the right side. (Weil.)] its position with changes of the patient's posture: in this respect Pneumothorax assimilates to hydrothorax rather than to pleurisy. At the boundary line between fluid and air there may be amphoric per- cussion note, and a vibratile sensation communicated to the fingers. The dis- placement of viscera reaches, in bad cases of hydropneumothorax, the extreme de- gree which is ever observed. Diagnosis.-The only affection with which Pneumothorax can possibly be con- founded is extreme emphysema; but there cannot be more than a momentary difficulty even here. Emphysema must be most unusually pronounced before the percussion note reaches anything like the tone of that heard in Pneumothorax ; but then such emphysema is always symmet- rical, while Pneumothorax affects only one side. But, indeed, the whole aspect of the two affections is quite different. Prognosis.-The prognosis of Pneumo- thorax is, on the whole, very bad, espe- cially during the first day or two ; if the patient survives for two or three days, his chances have materially improved. The great majority of fatal cases die within a week, and of these the largest part within the first two days. By com- mon consent of authorities, however, there is a great uncertainty in the matter, cases which appear comparatively slight at first sometimes terminating fatally in a few days, while others, which at the out- set seemed desperate, go on steadily im- proving, and regain comparative health ; usually, however, they retain the signs of air and fluid in the pleura. In a few cases an absolute cure takes place ; these 362 PNEUMOTHORAX. •are mostly instances either of traumatic I Pneumothorax, or else of empyema dis- charging itself through the bronchi. A few cases, however, even of phthisical Pneumothorax do recover; the opening becoming closed by lymph, and the air and fluid getting partly or wholly reab- sorbed. A variety of Pneumothorax from which striking recoveries have taken place is that in which the rupture has been more the consequence of great mus- cular exertion than of any severely dis- eased condition of the lung. Such are some of the cases where the rupture has taken place during the paroxysms of hooping-cough; and a remarkable in- stance of an analogous kind has been reported by A. Vogel.1 An unmarried woman, aged twenty-nine, who had borne ten children, had acted as a wet-nurse for a long time after each confinement, and had been perfectly well except that recently she had suffered from catarrh and an obstinate cough, in the midst of a sudden muscular exertion felt a sharp pain in the right side, and was seized with the most intense dyspnoea. When seen some hours later there were all the signs of the most complete Pneumo- thorax of the right side, with great dis- placement of the heart, lung, liver, &c., and severe collapse. Opium gave tem- porary ease, but on the next morning the anguish returned with waking, together with vomiting and choking sensations ; yet no sign of pleuritic exudation could be detected. Morphia again gave relief to the pain and dyspnoea, and from this time all the symptoms speedily declined. In four days from the attack the patient had entirely recovered, and when seen a year later not a single trace of any mis- chief could be detected. Of late years, indeed, a great deal of evidence has been collected to show that the mere influence of air upon a healthy pleura is extremely slight, and scarcely predisposes to inflammation at all: this comes out remarkably in the experiments and observations of Demarquay.2 The same observation has also shown that a gradually decomposing collection of gas in the pleura is likewise harmless, except where sulphuretted hydrogen or sulphide of ammonium is developed. On the whole, it can scarcely be doubted that the larger part of the influences which determine the fate of patients with Pneumothorax de- pends upon unknown vital differences Which there is little probability of our ever being able to estimate beforehand. Treatment.-The treatment of Pneu- mothorax is, necessarily, entirely pallia- tive, and directed to the object of enabling the patient to survive the intensely de- pressing influence of the first shock, and that of the subsequent inflammation. The first step to be taken is the hypodermic injection of a full dose (half-grain) of mor- phia ; and this medication may be admin- istered twice, or in exceptional cases three times a day during the first two or three days, the hope being that it may possibly avert the threatened pleuritic inflamma- tion. Dry cupping to the chest, fre- quently repeated, has been said to give very great relief in many cases. I cannot approve either of blood-letting, in any form, or of mercury; for the phthisical cases they are directly injurious, and in any case hypodermic morphia is likely to effect all the good which either of these remedies could be supposed capable of producing. Hot poultices to the chest undoubtedly give ease; they should be continually renewed. The great depres- sion which is felt can, I think, generally be more suitably met by the internal administration of ^ss doses of ether, every three or four hours, than by alcoholic stimulants, though the latter are some- times absolutely necessary.1 If the pa- tient survives the first few days, it will be proper to administer mineral acid and bark, cod-liver oil, or muriate of iron. And throughout the illness the greatest pains must constantly be taken to main- tain the strength by easily digestible nu- triment ; and if the stomach be too irri- table to bear this well, nutritive enemata must be unhesitatingly resorted to. The question of paracentesis may be suggested by the extreme distress of res- piration. In the phthisical cases, which form the large majority of those which the physician has to treat, this step could only be regarded as a very temporary pallia- tive, and accordingly should only be em- ployed as a last resort to procure a tem- porary respite when some very important object is to be secured by keeping the patient alive a little longer. It might be far more justifiable in cases where we had strong reason to suppose that the rupture was mainly accidental, and that the lung was free from serious internal disease. But I am not aware that any consider- able statistics exist which might guide us to a conclusion on such a very doubtful point. 1 I have seen cases in which alcoholic stimulants apparently much increased the acute pain. On the other hand, they occa- sionally do striking good. 1 Deutsch. Arch. f. klin. Med. ii. p. 244,1866. 3 Gaz. Medicale, 32, 1865. diseases of the organs of circulation. A. The Heart. Weight and Size of the Heart. Position and form of the Heart AND GREAT VESSELS. Malpositions of the Heart. Lateral or Partial Aneurism of the Heart. Adventitious Products in the Heart. Pneumo-Pericardium. Pericarditis. Adherent Pericardium. Endocarditis. Carditis. Hydropericardium. Angina Pectoris and Allied States ; INCLUDING CERTAIN KINDS OF SUD- DEN Death. Diseases of the Valves of the Heart. Atrophy of the Heart. Hypertrophy of the Heart. Dilatation of the Heart. Fatty Diseases of the Heart. Fibroid Disease of the Heart. WEIGHT AND SIZE OF THE HEART. Thomas B. Peacock, M.D., F.R.C.P. 1. Of the Healthy Heart. - From an early period pathologists have felt the necessity of some standard by which the size of the heart might be estimated, and its healthy and diseased conditions com- pared. Corvisart was unable to suggest any such, and Laennec compared the size of the healthy heart to the fist of the subject--a comparison too indefinite to afford any satisfactory estimate. Meckel and Kerkring, as quoted by Senac, were apparently the earliest writers who gave any estimate of the normal weight of the heart; and Lobstein and Bouillaud were the first to suggest the employment of the balance as a means of comparison be- tween the healthy and diseased organs. The latter writer, in the first edition of his work, published in 1835, gave some observations of the weight both of healthy and diseased hearts, but they were too few in number to form the basis of satis- factory conclusions. Bizot conceived that the dimensions of the organ would fur- nish a better standard ; and in 1837, in the Memoires of the "Societe Medicale d'Observation," published a large series of very careful measurements. Dr. Glendinning, in 1838, contributed nume- rous observations of the weight of the heart in a paper in the " Medico-Chirurgi- cal Transactions and Dr. Ranking, in 1849, published in the Medical Gazette a series of measurements, both of healthy and diseased organs. In 1843 the late Professor Reid appended to his paper on the weights of the different organs of the human body, tables of the weight and dimensions of the heart; and in 1854 I published a considerable number of ob- servations of the weight and size of the organ, under different circumstances of health and disease ; together with various tables compiled from them. Both these sets of observations were published in the Edinburgh Monthly Journal, More re- cently, Dr. Boyd has recorded in the ''■Philosophical Transactions" a larger and more complete series of observations than had been published by any previous writer. It is useless to refer to the estimates of the weight of the healthy heart given by any of the earlier writers, for we have no means of knowing the number of observa- tions upon which they are based ; the age and sex of the subjects; the condition of the organs weighed, or the precise weight employed. Of the more recent observers, M. Bouillaud estimated the weight of the 363 364 WEIGHT AND SIZE OF THE HEART. healthy heart in adults, not distinguish- ing the two sexes, as ranging from 8 oz. 10 drachms to 9 oz. 11 drachms imperial. Dr. Glendinning inferred that the mean weight of the healthy organ was in adult males 8f oz., and in females 7f oz. ;*and Dr. Reid deduced the average in males as 11 oz. 12 drachms, and in females as 9 oz. These estimates are sufficient to show how wide the differences maybe according to the mode in which the calculations are made. It is evident that the weight of the heart must vary considerably accord- ing to the cause producing death; the organ being heavier when the patient dies suddenly or after only a short attack of illness, and lighter when death has taken place from lingering diseases, pro- vided the diseases are not such as to in- terfere with the functions of the organ, and so give rise to over-nutrition. Thus, while Dr. Reid, as just stated, estimated the average weight of the male heart at about 11 oz., he found that in twelve men who were killed the weight attained an average of 12 oz. ; and, on the other hand, I have examined the hearts of per- sons who have died from cirrhosis of the liver and cancer of the pylorus, &c., which were only 5 or 6 oz. in weight. To form, therefore, an accurate estimate, not only must the age and sex be taken into con- sideration, but the weight of the organ must be given in acute and chronic dis- eases separately ; and the cases in which the nutrition of the heart may have been materially modified by the disease causing death must be excluded from the calcula- tion. The size of the heart will also be similarly influenced, and especially the dimensions must vary with the degree of distension of the cavities at the time of death. To form a thoroughly satisfactory estimate, the weight and dimensions of the heart must therefore both be given, and the previous circumstances must be taken into consideration. In the following tables I have endeav- ored to carry out these views. In the first table the weight of the heart in the adult is given separately, for males and females, and for acute and chronic dis- eases. In the second, the dimensions of the organ, also in the adult and in males and females, are stated, in Paris lines, millimetres, and parts of English inches. The third table gives the average weight of the heart in males and females at dif- ferent ages. From the first table it will be seen that Average Weight of Healthy Heart in Males and Females and in Acute and Chronic Diseases from Twenty to Fifty-jive Years of Age. Males- Mean weight 9 oz. 8 drs. Ordinary range in acute eases 9 oz. to 11 oz. " " in chronie cases . . . . . 8 oz. to 10 oz. Females- Mean weight 8 oz. 13 drs. Ordinary range in acute cases 8 oz. to 10 oz. " " in chronic cases 7 oz. to 9 oz. TABLE I. in adult males who have died from acute diseases, or from the effects of accident, the ordinary weight of the heart is from 9 to 11 oz. ; and in those who have died from chronic diseases, 8 to 10 oz. In fe- males, the ordinary weight of the heart in acute cases may be estimated at from 8 to 10 oz., and in chronic diseases from 7 to 9 oz. Occasionally, however, in persons of small and delicate frame, who have died from emaciating diseases, such as cancer of the stomach, bowels, or mesentery, or chronic affections of the liver, the heart will be found to weigh only 5 or 6 oz. ; and in large and powerful men who have been killed or have died after short illnesses, the organ may weigh 12 oz. or even more, without exceeding the limit of health. Some writers have given calculations of the relation of the weight of the heart to that of the whole body, but the bulk of the body, and also, as before stated, the size of the heart, vary so greatly from the duration of illness and the mode in which death occurs, that such calculations do not possess much value. The height of the subject and the weight and size of the heart probably bear a more just relation. From the second table it will be seen that the girth of the right ventricle, measured externally, exceeds that of the left, in males by about one-sixth, and in females by one-fifth. The length of the cavity of the right ventricle is greater than that of the left, in males by one-seventh, and in females by one^sixth. In both WEIGHT AND SIZE OF THE HEART. 365 TABLE II. Dimensions1 of the Healthy Heart (in French Lines, Millimetres, and English inches') in Males and Females. Male§. Females. Lines. Milli- metres. Inches. Lines. Milli- metres. Inches. Circumference of heart ..... 103-7 233-32 9-209 104 234 9-236 Girth of right ventricle ..... 55-4 123-85 4-919 58-4 131-4 5-184 " left " 48-3 108-67 4-289 45-6 102-6 4-049 Length of cavity of right ventricle 43-3 96-42 3-821 44-3 99-67 3-925 11 " left " ... 37-6 84-6 3-333 37-1 83-47 3-197 Thickness of walls of right ventricle, base " " " " " midpoint 1-85 4-16 ■164 1-85 4-16 •164 1-98 4-35 •176 2-0 4-5 ■177 " " " " " apex 1-42 3-19 •125 1-3 2-92 •118 " " " left " base 5-15 11-58 •425 4-9 11-02 •432 " " " " " midpoint 6 13-5 •532 5-6 12-6 •497 " " " " " apex 2-4 5-4 •214 2-5 5-62 •222 Thickness of septum. ..... 5-73 12-89 •51 4-7 10-57 •421 Circumference of right auriculo-ventricular ) 53-4 120-15 4-74 51-4 115-65 4-562 aperture ...... J Circumference of left auriculo - ventricular ) 45-2 101-7 4 45 101-25 3-996 aperture ...... J Circumference of pulmonic aperture. 40 90 3-552 39-3 88-42 3-493 " of aortic " 35-6 80-1 3-146 34 76-5 3-019 sexes the thickness of the walls of the right ventricle is about one-third that of those of the left. The thickness of the septum is intermediate between that of the external walls of the right and left ventricles. In males the pulmonic orifice is about cne-eighth more in circumference than the aortic. The left auriculo-ven- tricular aperture is one-fourth more than that of the aorta, and the right auriculo- ventricular aperture one-half larger. In females the differences between the aortic and other orifices are somewhat greater. It has been generally supposed that the heart increases in weight with the progress of life ; and this opinion is supported by the facts recorded relating to males, in the third table. It may, however, be doubted whether the result thus indicated is ap- plicable to the heart in its strictly healthy state. It is well known that in advanced age there is a decided dimi- nution in the weight of the brain, and there seems no reason wrhy a similar de- crease of weight should not occur in the heart, provided that organ be not the seat of disease interfering with its normal nutrition. As we well know, but few elderly persons, especially men, are en- tirely free from any form of disease which, by occasioning obstruction, might lead to over action, and so to some degree of hy- TABLE III. Weight2 of the Healthy Heart at Different Ages in Males and Females. Males. Females. Ages 10 to 14 inclusive-Mean weight. . 6 oz. 1-5 drs. 5 oz. 0 drs " 15 " 20 " " " . 8 " 2-66 " 8 " 1-66 " From 20 "30 " " " . 8 " 0-14 " 8 " 10-42 " " 30 " 40 " " " . 9 " 7-95 " 8 " 13-94 " " 40 " 50 " " " . 9 " 11-11 " 9 " 3 " " 50 " 60 " " " . 9 " 12 " 9 " 7-33 " " 60 " 70 " " 11 . 10 " 13-33 " 7 " 0 " Mean weight between 20 and 55 years of age-in 76 males 9 oz. 8*74 drs. " " " " " " " in 49 females 8 " 13T6 " Difference ........ 11*58 " pertrophy. And even if the heart be not itself diseased, there are few old persons who do not display some affection of the lungs, kidneys, or other parts of the sys- tem, which might more or less interfere with the functions of the heart, and so lead to its enlargement. That this is the more correct view is supported by the diminution in the weight of the organ in elderly females, as also shown in the table. 2. The alterations in the weight of the 1 The dimensions of the orifices are taken by balls, the first of which is 12 lines in cir- cumference, which increase in circumference three Paris lines, and are numbered from 1 to 20. 1 The weight employed is Avoirdupois or Imperial. 366 WEIGHT AND SIZE OF TIIE HEART. heart in disease are illustrated by Tables IV. and V. It was supposed by Dr. Glendinning, that the heart in cases of phthisis, contrary to what would d priori have been expected, acquires an increase of weight, while the rest of the body becomes emaciated. This idea appears to have arisen from a misapprehension of the facts which he col- lected. The effect of the pulmonary affec- tion upon the nutrition of the heart ap- pears to vary with the form of the disease. In cases of uncomplicated constitutional or tubercular phthisis, the progress of which is generally rapid and which is usually attended with great emaciation, the heart is found to weigh considerably below the healthy average, and the organ, on examination, often displays the appear- ance of atrophy. In cases of chronic phthisis, whether tubercular or inflamma- tory, on the other hand, and especially when one or both lungs are considerably contracted, or when there have been marked bronchitic symptoms, so that the blood has for a long time been transmitted with difficulty through the lungs, the heart is generally found to be enlarged, or, at least not to have undergone any marked diminution in size ; its weight equalling or exceeding the healthy stand- ard. So also when, in cases of phthisis, there is any great impediment to the transmission of the blood from the heart from valvular or aortic disease, notwith- standing the general tendency to emacia- tion, the organ may exceed even very greatly the natural size. TABLE IV. Mean. Extremes. oz. drs. oz. drs. oz. drs. Phthisis. Males . 9 3-4 6 4-5 to 11 0 " Females........ . 8 6-06 5 9 " 11 0 Chronic Bronchitis. Males ...... . 14 8 11 8 " 21 0 " " Females...... . 12 2-0 9 0 " 12 8 Morbus Renum.-Males ....... . 9 12 7 4 " 14 8 " " Females . . . ' . . 10 5-4 7 4 " 15 8 Simple Hypertrophy.-Males ...... 12 0 " 40 12 Aortic Disease.-Males ....... 10 0 " 24 0 " " Females 8 8 " 20 0 Aortic valvular obstruction.-Males .... 14 0 " 21 0 " " " Females .... ... 13 0 " 18 8 Aortic valvular regurgitation.-Males .... 14 0 " 34 0 " " " Females .... ... 16 0 " 23 0 Mitral valvular obstruction or regurgitation, or both-Males ... 14 0 " 17 0 " " " " " " Females ... 13 0 " 18 8 Combined aortic and mitral valvular disease.-Males . ... 14 8 " 21 0 " " " " " Females • 7 8 " 23 0 Range of Weight of Heart, in Different Forms of Disease and when Diseased. Chronic Bronchitis. - When there is long-continued obstruction to the pulmo- nary circulation from chronic bronchitis, with or without deformity of the spine, the right side of the heart becomes hyper- trophied; but, even a great increase in the thickness of the walls of the right ventricle does not very much augment the weight of the heart, and it is only after the left side has become implicated that TABLE V. Lines. Milli- metres. Inches. Circumference.-Males " Females 182 409-5 16-16 In simple hypertrophy. 127 285-75 11-27 Mitral disease. Thickness of walls of right ventricle.-Males . " 11 " " Females 5-75 12-93 •51 Mitral disease. 7 15-73 •62 Congenital obstruction at pulmonic orifice. " " left " Males . 14 31-5 1-24 Aortic valvular disease. " " " " Females 11 24-75 •97 Combined aortic and mitral disease. Circumf. right auriculo-vcntricular apert.-Males . " " -' " " Females 63 141-76 5-59 Simple hvpertrophy. 60 135 5-32 Aortic valvular obstruction. " left " " " Males . 60 135 5-32 Simple hypertrophy. " " " Females 45 101-25 3-99 Aortic valvular obstruction. " pulmonic aperture.-Males .... " " " Females 54 121-5 4 79 Simple hypertrophy. 39 87-78 3-46 Mitral valvular disease, chronic bronchitis, and deformed spine. " aortic " Males .... 45 101-25 3-99 Aortic valvular disease. " " Females . . . 35 78-85 31 Aortic valvular disease and combined aortic and mitral disease. Extreme Dimensions of the Heart with the Different Forms of Disease in which they occur. WEIGHT AND DIMENSIONS OF THE DISEASED HEART. 367 the weight is found much to exceed the healthy standard. In some such cases, however, the organ may attain a weight considerably greater than the natural, amounting, in hearts I have weighed, to 15 or 16 oz. Morbus Renum. - Dr. Bright noticed that the heart in cases of chronic disease of the kidneys was frequently found in- creased in size without there being any valvular disease to explain the enlarge- ment ; and the occurrence of simple hy- pertrophy in such cases has been noticed by other pathologists. Of eighteen cases in which the organ was weighed by my- self, in seven the weight was below the average of chronic diseases, while in eleven it exceeded it, attaining in some cases in males the weight of upwards of 14 or 15 oz. In these cases the hyper- trophy is doubtless due to the over-action of the heart from its efforts to overcome the obstruction to the transmission of the blood through the capillaries. 3.-Weight and Dimensions of the Diseased Heart. Simple Hypertrophy. - The most re- markable case of increase in the weight and size of the heart which I have myself met with was in a case of hypertrophy, without any material valvular disease or any obvious source of obstruction in the aorta, to explain the condition. In this instance, which, however, is a very ex- treme one, the organ weighed 40 oz. 12 dr.; but in various other cases I have found the weight considerably to exceed the average or extreme limit of health. In a heart which I examined with Mr. Hutchinson, the weight attained was 26 oz.; and Dr. Bristowe exhibited one at the Pathological Society which weighed 27 oz. The ages of these patients were sixty-five, thirty-five, and forty-one re- spectively. It is difficult to explain the great enlargement which exists in some cases of this description. It may depend on some disease of the smaller arteries which may have escaped observation, or on obstruction in the capillaries; but in other instances, it is probably due to ha- bitual over-action from athletic pursuits, and possibly in some cases to palpitation, at first originating in emotional causes. Enlargement unconnected with valvular disease is, however, rarely seen except in men, and in no instance have I found the heart much hypertrophied in females without there being some obvious source of obstruction to which the change was referable. Aortic Obstruction and Aortic Valvular Disease.-The occurrence of obstruction in the aorta, and especially in the upper portion of that vessel, is generally at- tended by considerable increase of weight in the heart. In various cases of this de- scription I have found the heart to range from near the natural standard to 24 oz. in males, 17 oz. in females. In the Trans- actions of the Medico-Chirurgical Society, a case is recorded by Dr. Risdon Bennett, in which the heart weighed 224 oz. in a man fifty-three years of age, who died from rupture of the aorta, giving rise to dis- secting aneurism and hemiplegia. The increase of size in the heart was appa- rently due to atheromatous disease of the aortic coats. In aortic valvular disease still greater increase of weight is often met with. In cases of obstructive disease, I have weighed hearts ranging from 14 oz. to 21 oz. in males, and from 13 oz. to 18 oz. 8 drs. in females. In cases of aortic valvular in- competency, I have found the heart to weigh from 14 to 34 oz. in males, and from 10 oz. to 23 oz. in females. Dr. Vanderbyl, in a paper in the "Patho- logical Transactions," relates instances in which the heart weighed 36 oz. in a case of aortic valvular incompetency, in a man of twenty-eight; 30 oz. in a case of aortic disease with aneurism in the aorta, in a man of thirty-three; and 30 oz. in a case of aortic and mitral disease, in a man of sixty-two. In the cases of incompetency of the aortic valves, it is often impossible to say how much of the great enlargement of the heart is due to the obstruction, and how much to the incompetency of the valves ; for the latter condition is generally only the final stage of the former. In cases of rupture of the aortic valves during violent effort, we have, however, the opportunity of seeing the remarkable changes which may occur in the heart even during short periods of time, when, in organs previously healthy, the valves are rendered incom- petent and the left ventricle rapidly be- comes hypertrophied and dilated. Thus, in a case of this description which oc- curred to myself, the patient, a man of thirty-three years, survived the accident only twenty-seven months, yet the heart was found to weigh 17 J oz. In a case re- lated by Dr. Quain, the patient lived two years, and the heart weighed 22j oz.; and in another case which I had the op- portunity of examining after death, though the patient, a man thirtyrsix years of age, only survived three and a half months, the weight was 23 oz. If, in this instance, the heart was sound at the time of the occur- rence of the injury, the process of enlarge- ment must have been most rapid ; but it may be doubted whether the organ was not more or less hypertrophied before the accident, though the patient stated that he was previously quite well. In some cases of disease, also, the en- largement must take place very rapidly. 368 WEIGHT AND SIZE OF THE HEART. In a boy of eighteen, who died of aortic valvular disease originating in malforma- tion, the duration of active illness was only three and a half years, yet the heart weighed 28 oz. In a case of aortic valvu- lar' incompetency, with probably regurgi- tation through the left auriculo-ventricular aperture from maladjustment of the valves, described by Dr. Bristowe in the " Patho- logical Transactions," the heart weighed 46| oz. avoirdupois, though the subject of the disease was only twenty-two years of age. In an instance of very great obstruc- tion at the aortic valves, doubtless from malformation, which I have recently ex- hibited at the Pathological Society, the heart weighed 24 oz., the patient being only twenty-three years of age. These examples show that the heart may attain a very great increase of size even in com- paratively young subjects ; but, usually, those in whom the heart is very large are advanced in age. Probably, also, in most cases, the disease must be of long dura- tion for the organ to become very greatly hypertrophied, and this great prolonga- tion of life is only compatible with com- paratively slight disease, or with disease which has been very slowly progressive, though at the time of death it may have become extreme. In mitral valvular disease, whether con- sisting in obstruction and regurgitation, from contraction of the orifice and rigidity of the valves, or in free regurgitation from expansion of the aperture or maladjust- ment of the valves, the heart does not or- dinarily attain by any means so great an increase of weight as in cases of aortic dis- ease. In the former class of cases, the hypertrophy is chiefly limited to the right ventricle, and only affects the left ventri- cle secondarily, though in the latter the left ventricle also partakes of the change from the first. In cases of mitral disease, the weights have ranged from 14 oz. 8 drachms to 17 oz. 8 drachms in males, and from 12 oz. to 18 oz. in females. As might be expected, in combined aortic and mitral valvular disease, the weight of the heart is intermediate between that which obtains in the two separate forms of disease, the organ being lighter than in aortic, heavier than in mitral disease. In males, in cases of this kind the heart was found to weigh 14 oz. 8 dr. to 21 oz. 8 dr., and in females fjom 17 oz. to 23 oz. In cases of obstruction at the right side, consisting in congenital contraction of the pulmonic orifice, the effect produced on the nutrition of the heart is very similar to that which results from chronic bronchi- tis. In the first instance the right ven- tricle is chiefly hypertrophied, but subse- quently the left also becomes involved; and similar changes ensue in the cases in which the aorta communicates wfith both ventricles, provided the life of the patient be sufficiently prolonged. In a male of twenty, in whom the pulmonary orifice was contracted from adhesion of the valves, the heart weighed 12 oz. ; and in a female of nineteen, in whom there was similar disease of the pulmonic valves, and the aorta arose from both ventricles and the ductus arteriosus was open, the organ weighed 174 oz. The effect produced by adhesions of the pericardium on the functions and nutrition of the heart has been the subject of much discussion. On the one hand, adhesions have been supposed to interfere with the free movement of the heart, and so to give rise to hypertrophy ; on the other, it has been thought that by the compression exercised upon the organ they might cause atrophy. The question is one which it is very difficult to decide, for there are few cases in which the pericar- dium is entirely adherent, in which the valves are not also more or less involved, and in which therefore the effects produced by the one condition may not be modified by the other. I find, however, that in three men in whom the pericardium was entirely adherent, while the valves were free from disease, the hearts weighed 16 oz., 17 oz. 4 dr., and 18 oz. ; but I have examined other organs under similar cir- cumstances in which the weight did not exceed the healthy standard. The gene- ral rule is, however, that in cases of adhe- sion the heart becomes hypertrophied. General Remarks on the Weight of the Heart.-M. Bouillaud has collected some cases in which the heart otherwise healthy weighed considerably less than natural; and others in which in various states of disease it exceeded that point. The former are all cases in which the organ was reduced in weight with the progres- sive emaciation of cancer, consumption, &c. The lightest heart, that of a female of forty-five, weighed 4 oz. 5 dr. in a case of cancer; the heaviest organ weighed 24 oz. 4 dr. in a case of obstructive and prob- ably also regurgitant disease of the aortic valves, in a female of fifty-three. From these observations, and his estimate of the average weight of the healthy organ as ranging from 8 oz. 10 dr. to 9 oz. 11 dr., he infers that the heart may attain when diseased three times the weight of the average healthy organ, and five times that of the most atrophied organ. These estimates are, however, considerably less than the variations of weight which actu- ally obtain. I have found the heart to weigh only 5 oz. in a man fifty-three years of age who died of cirrhosis of the liver, and 6 oz. in a man of thirty-nine who had cancer of the pylorus. The average weights I have estimated in males at 9 oz. 8 dr., and the heaviest heart weighed was 40 oz. 12 dr. It follows therefore that in men the heart may attain a weight WEIGHT AND DIMENSIONS OF THE DISEASED HEART. 369 which is four times that of the healthy and eight times that of the atrophied organ. In females, the variations in the weight of the heart are sufficiently re- markable, though considerably less than in men. The average weight has been shown to be 8 oz. 13 dr. : the lightest hearts weighed 5 oz. 8 dr. in cases of phthisis in twenty-five and thirty years of age ; the heaviest organ was 23 oz. The most enlarged heart was therefore three times the weight of the average, and four times that of the atrophied organ. It has also been mentioned that Dr. Bristowe has placed on record a case in which the heart of a man twenty-two years of age weighed 46| oz.; and Dr. Church has re- cently exhibited at the Pathological So- ciety the heart of a female forty-seven years of age, who died of cancer of the pylorus, which weighed only 3 oz. 1 dr. The heart described by Dr. Bristowe is, as far as I know, the heaviest on record. Dr. Hope says that he examined at St. George's a heart which weighed 2| lbs., which, if the weight employed were avoirdupois, would nearly equal the size of the largest heart which I have myself weighed-40 oz. 12 dr. M. Lobstein re- fers to a heart which weighed 34 oz., and Dr. Vanderbyl to one of 36 oz, The dimensions of the heart in different forms of disease bear a general relation to the weights of the organ in similar condi- tions. Of the observations which I have myself made, the greatest weight was at- tained in cases of simple hypertrophy, ob- struction in the course of the aorta, and obstructive, or obstructive and regurgitant disease of the aortic valves. It is equally in these forms of disease that the dimen- sions of the organ are most considerably enlarged, the cavities and orifices, espe- cially those of the left side, being the most expanded, and the walls the most remark- ably increased in thickness. There are, however, differences in the condition of the organ in these several forms of dis- ease. In cases of obstruction, on what- ever cause dependent, the heart is not generally so large as in cases of incompe- tency, and the form of the organ is also somewhat different. In the former class of cases the heart is peculiarly long and pointed at the apex, and the walls attain the greatest width near the base. In the latter the ventricle is usually of larger size and rounded at the apex, and the thickening is more equally diffused over the walls. In both forms of disease, the enlargement, though most marked on the left side of the heart, affects the right also very considerably. In cases of mitral valvular disease, the size of the organ is considerably less than in the former class of cases, and the shape is very different, but the precise condition of the organ varies with the form of dis- ease. In cases of great contraction of the left auriculo-ventricular aperture, the stress falls chiefly on the left auricle and the right cavities, and they are all found expanded and the walls increased in thick- ness, and much firmer than natural; the orifices also being dilated ; while the left ventricle is not much if at all enlarged, and its walls are not materially hyper- trophied. It has, indeed, been supposed that the left ventricle becomes atrophied. In cases, on the other hand in which the defect consists chiefly or to a marked de- gree in incompetency of the valves, on whatever cause dependent, the left ven- tricle is found to be considerably dilated and hypertrophied, and the changes on the right side are less marked. In both these forms of disease, however, the alter- ation in the shape of the heart is very marked, the organ being wide and blunted at the apex-in the one case chiefly in consequence of the expansion of the right side, in the other of the dilatation of the left ventricle, and especially the widening of its apex. In cases of combined aortic and mitral valvular disease, the enlarge- ment is intermediate, both in shape and extent, between the other two forms. In cases of chronic bronchitis, chronic phthisis, deformity of the chest, and pul- monic valvular obstruction, the hyper- trophy and dilatation are at first limited to the right side, but subsequently, if life be much prolonged, involve the left also. Table V. shows some of the extreme di- mensions which I have recorded in differ- ent forms of disease. It will be observed that not only do the size of the cavities and the width of the walls vary greatly in different forms of disease, but the capacity of the orifices also undergoes remarkable change; and this not only in cases of old disease, but even during comparatively short periods of illness. Thus it will generally be found in cases of acute bronchitis and very acute phthisis, that the pulmonic aperture, which ordinarily exceeds the aortic some- what in capacity, is disproportionately larger than the aortic, and the right au- riculo-ventricular aperture equally out of proportion with the left. I have also rea- son to believe that the apertures may not only expand in a short time, but may have their dimensions reduced without being otherwise diseased, and thus it is possible that in some forms of valvular defect the size of the orifice may be re- duced and the incompetency diminished. VOL. U.- 24 370 POSITION AND FORM OF THE HEART. POSITION AND FORM OF THE HEART AND GREAT VESSELS. By Francis Sibson, M.D., F.R.S. FRONT VIEW; AFTER DEATH. The following observations on the po- sition and anatomical relations of the healthy heart and great vessels after death are founded on the examination of a, number of diagrams showing the posi- tion of the internal organs after death. This examination was restricted to those instances in which the heart was healthy and was not enlarged. The diagrams were made by drawing the outlines of the organs on a piece of lace or net, stretched upon a frame and placed over the body. The heart and great vessels present great variety in form and position both after death and during life. During the illness or injury that ends in death, at the time of death and after death, the heart and great vessels undergo a series of changes in position and form. According to the nature and direction of these changes, the heart after death may, in different instances, be (I.) higher or lower in position; or (II.) it may deviate more to the right or more to the left. (I.) The Higher or Lower Position of the Heart and Great Vessels. Three main conditions may influence the higher or lower position of the heart after death: (1) The contraction or ex- pansion of the lungs ; (2) The distension or flaccidity of the abdomen ; and (3) The state of the heart itself. (1) When death is associated with bron- chitis, or pneumonia, or affections of a like nature, in which the lungs are large, and are expanded after death, the chest is broad and deep, the diaphragm is low, and the heart, which is charged with blood, especially in its right cavities, is large, and occupies a low position. As a rule, however, the lungs, when they are not thus affected, lessen in size and con- tract during the final expirations. The cage of the chest then becomes more flat and narrow ; it lengthens downwards, and the sternum and costal cartilages and ribs in front are all lowered in position. The diaphragm at the same time is elevated. While the front of the chest is thus lowered, the heart, resting on the dia- phragm, is raised, and the whole organ, and the great vessels occupy a higher position. We thus have a double and contrary movement in the descent of the bony framework of the front of the chest, and the ascent of the heart immediately behind that framework. As the heart within, and the sternum and cartilages without are both thus elevated by the dis- tension of the abdomen, the actual eleva- tion of the heart and great vessels is much greater than their apparent elevation, estimated as that usually is by the rela- tion of those parts to the walls of the chest immediately in front of them. (2) When the abdomen is distended, whether by fluid or air in the cavity itself, by an accumulation of gas in the stomach and intestines, or by other causes, the whole diaphragm is forcibly elevated, and the heart, resting as it does on the central tendon of the diaphragm, is lifted up- wards. The sternum and costal car- tilages in front of the heart are, at the same time, also raised in position, and the lower ribs on either side are pressed out- wards. Although the actual elevation of the heart is, in these cases, often very great, its apparent elevation, which is measured by the relation of the heart to the walls of the chest in front of it, may be slight, owing to the simultaneous ele- vation of the heart and the sternum and cartilages in front of the heart caused by the distension of the abdomen. When the abdomen is flaccid, owing to the stomach and intestines being empty, the reverse effects take place. The dia- phragm descends, the heart drops down- wards, the sternum and costal cartilages are lowered in position, and the inferior ribs fall inwards. (3) During the final illness or injury that precedes death the heart may lessen or enlarge. Fatal hemorrhage or wasting disease reduces the size of the heart and great vessels. On the other hand, the heart is swollen, especially on the right side, under the influence of suffocation or bronchitis ; while its left ventricle may be thickened and enlarged in cases of Bright's disease with contracted kidney. Thus the right or the left side of the heart may be enlarged when the obstacle to the flow THE HIGHER OR LOWER POSITION OF THE HEART. 371 of blood is respectively in the lungs or the body. At the time of death, the left ventricle usually closes firmly upon itself; while then or soon afterwards the right cavities of the heart become permanently swollen with blood. After death the heart shrinks upwards to a greater or less extent. This is owing partly to the diminution of the organ, but mainly, I believe, to the contraction of the aroh of the aorta, for the shortening of that vessel draws the heart upwards, just as its lengthening pushes the organ downwards. The exact extent to which the heart is thus raised, is measured by the space that is left between the lower boundary of the heart, and the lower boundary of the front of the pericardium. During life these two adjoining parts fit each other exactly ; but after death they are separated by a space that varies according to the degree to which the heart shrinks up- wards. Thus in the body of a youth who died from hemorrhage after fever, and in that of a man who expelled two or three pints of blood from a cavity in the left lung, an inch of space intervened between the lower edge of the heart and that of the lower boundary of the front of the pericardium. In another instance that space was only the tenth of an inch. As a rule the space varied from a quarter to seven-tenths of an inch (in 38 of 44 in- stances) and its average measurement was nearly half an inch (0'46 inch). (Note 1.) The heart and the great vessels mainly occupy the centre of the chest, being pro- tected in front by the sternum and the adjoining costal cartilages. It is, how- ever, my present object, not so much to describe the relative bearings of those parts after death, as to indicate the varia- tion in the anatomical situation of the more important boundaries or landmarks of the healthy heart and great vessels ob- served by myself in different instances after death. The lower Boundary of the Heart.- In one instance, a woman who died from starvation, the lower boundary of the heart was situated behind the" ensiform cartilage an inch and a half below the lower end of the sternum (that term being restricted here and elsewhere to the manubrium and blade or osseous part of the sternum), while in another it was al- most as much (1-4 inch) above that end of the bone. Between these two extreme points this boundary occupied every va- riety of position. In one-fifth of the in- stances observed (15 in 71) the lower boundary of the right ventricle was just behind the lower end of the sternum, while in two-fifths of them it was above (30 in 71), and in two-fifths of them it was below (26 in 71) that end of the bone. (Note 2.) As we have already seen, the lower edge of the heart usually shrinks upwards after death for nearly half an inch, the extent varying from one inch to one-tenth of an inch. The position of the lower border of the front of the pericardium, which points out the position of the lower border of the heart at the time of death was indicated in four-fifths of the cases (55 in 71) in which the inferior boundary of the heart was observed after death. In one-fifth of these instances (11 in 55) the lower limit of the pericardium was on a level with the lower end of the sternum ; while in two-thirds of them (37 in 55) it was below that point, being situated be- hind the ensiform cartilage ; and in only one-eighth of them (7 in 55) was it above that point. We thus see that at the time of death, in the great majority of in- stances (40 in 59) the inferior border of the heart was below the lower end of the sternum, being situated behind the ensi- form cartilage. (Note 3.) The seat of the lower boundary of the apex in relation to the left fifth space is a more important landmark for the clinical observer than that of the lower boundary of the heart in relation to the lower end of the sternum. The lower edge of the heart at the apex was on a level with the lower edge of the left fifth cartilage in one-seventh of the instances observed (9 in 69), it was below that edge in two-fifths of them (26 in 69), and it was above that edge in almost one-half of them (34 in 69). In five instances the lower boundary of the apex was situated one inch above the lower edge of the fifth cartilage, and in four it was fully one inch below that edge. (Note 4.) The lower border of the pericardium just below the apex, which corresponds with the seat of the lower border of the apex at the time of death, was on a level with the lower edge of the fifth cartilage in one-sixth of the instances observed (9 in 55), was situated below that edge in three-fourths of them (41 in 55), and was above that edge in only one-eleventh of them (5 in 55). (Note 5.) We thus see that there was a general, but not a constant correspondence between the relation of the inferior boundary of the right ventricle to the lower end of the sternum, and that of the inferior bound- ary of the apex to the lower edge of the fifth cartilage, both at the time of death, and after death when the examination of the body was made. This correspondence would have been more constant but for variation in (1) the comparative height of the fifth cartilage and the lower end of the sternum, (2) the degree of inclination from above downwards and from right to 372 POSITION AND FORM OF THE HEART. left of the lower boundary of the heart, and (3) the extent to which the right ven- tricle is situated to the right and to the left of the middle line of the sternum. (1) In the great majority of instances (60 in 71) the inferior edge of the left fifth cartilage was lower in position than the inferior extremity of the sternum, to an extent varying from a quarter of an inch to an inch and a quarter; in five cases those two parts were on the same level; and in six the lower edge of the fifth car- tilage was higher by from a quarter to three-quarters of an inch than the lower end of the sternum. The height of the fifth cartilage in re- lation to that of the lower end of the sternum is influenced by (1) respiration, (2) abdominal distension, and (3) natural and acquired formation. (1) Inspiration raises and expiration lowers both the sternum and the fifth cartilage attached to the sternum, but as the cartilage has an additional movement of its own, during the double act of breathing, it is more low- ered during expiration and more raised during inspiration than the sternum. The artificial distension of the lungs after death elevates the fifth cartilage from the sixth to the third of an inch more than the cor- responding part of the sternum. If the chest is broad the left fifth cartilage is higher, and if the chest or the left side of it is narrow, the left fifth cartilage is lower in relation to the lower end of the ster- num than it would have been otherwise. (2) Abdominal distension raises, and ab- dominal collapse lowers both the sternum and the fifth cartilage, but the raising or lowering of the fifth cartilage under these circumstances is greater than the respec- tive raising or lowering of the sternum. (3) In some persons the fifth cartilage is naturally higher or lower than in others. Thus the fifth cartilage is sometimes in- tegrally attached to the sixth cartilage and it is restrained by and shares its movements. When this is so the fifth cartilage tends to be lower in relation to the lower end of the sternum than when that cartilage is free. In robust persons with ample chests the fifth cartilage is higher relatively to the sternum than in thin persons with contracted chests, in whom the cartilage tends to be low in position in relation to the end of the sternum. (2) In nearly all instances (67 in 70) the lower boundary of the heart inclined downwards from the auricle to the apex, in a direction from right to left. In one instance the lower boundary of the heart was an inch, and in another it was only the tenth of an inch lower at the apex than at the lower end of the sternum. Between these two extremes there was every variety, the average dip of the lower boundary of the heart from that point to the apex being about half an inch. (Note 6.) The inclination or dip of the lower boundary of the right ventricle ceased at the apex, and thence the lower boundary of the heart curved gently upwards. (3) The lower boundary of the heart usually extended from two inches to two inches and three-quarters to the left of the middle line of the sternum (in 43 in- stances in 65), but in one-third of the cases (20 in 65) it only extended from an inch and a quarter to an inch and three- quarters, while in five instances it extend- ed as much as three inches to the left of the middle line of the sternum. (Note 7.) The Top of the Arch of the Aorta.-The top of the arch of the aorta, which is in- dicated by the adjacent origin of the in- nominate and left subclavian arteries, forms the upper limit of the system of the heart and great vessels. The position of the top of the arch, like that of the lower border of the heart, is subject to great variety. In one instance the top of the arch was an inch and a half below the top of the manubrium, so that it was buried deep down in the chest and the innominate artery ditl not appear in the neck. In another, the top of the arch was seated in the neck, being half an inch above the top of the sternum, so that before the chest was opened the whole innominate artery was visible in the neck, coursing upwards and from left to right across the front of the trachea. The summit of the aorta occupied in different instances every variety of position between these two ex- treme limits. In five cases it was above, and in six it was on a level with the top of the manubrium ; while in seven, in- stead of being thus almost or quite visible in the neck, it was situated quite an inch below the top of the manubrium and the whole of the innominate artery -was shielded by that bone. In two-thirds of the instances (30 in 48) however, the top of the aorta occupied an intermediate place behind the upper half of the manu- brium, its average position being half an inch below the top of that bone. (Note 8.) In forty-eight instances the position both of the lower boundary of the heart and the upper boundary of the arch of the aorta was observed, and, as might have been looked for, there was a general correspondence in the position of these two boundaries in those cases in which they occupied respectively a very high or a very low position. Thus, of the five cases in which the top of the arch of the aorta rose above the top of the sternum, the lower boundary of the heart was situated above the lower end of the ster- num in three, at that point in one, and less than half an inch below it in one. Again, the top of the arch of the aorta THE HIGHER OR LOWER POSITION OF THE HEART. 373 was situated below the upper end of the manubrium in the whole of six cases in which the lower boundary of the heart was from half an inch to an inch and a quarter below the lower end of the ster- num. Again, of seven instances in which the top of the arch was deep in the chest, being more than an inch below the top of the manubrium, in three the lower boundary of the heart was below the lower end of the sternum, in one at that point, and in three above it. Here the correspondence of the upper and lower boundaries is rather indicated than kept up, but this correspondence can scarcely be recognized when we compare these boundaries with each other in those cases in which they occupied a less ex- treme position. (Note 9.) The Boundary-line between the Upper Border of the Heart and the Lower Limit of the Great Arteries. - The origin of the pulmonary artery and the top of the auricular portion of the right auricle may be regarded as the upper boundary of the heart and the lower boundary of the great arteries. The highest position of the origin of the pulmonary artery was at the top of the second cartilage, while that of the top of the auricle was a little higher or on a level with the first space. The lowest position of the origin of the pul- monary artery was the upper edge of the fourth cartilage, while that of the top of the auricle was a little less low, or on a level with the lower border of the third space. Between these two extreme limits the origin of the pulmonary artery and the top of the right auricle occupied every variety of position, but their favorite seat was at or on a level with the second space and the third costal cartilage, which was the situation of those parts in two-thirds of the instances (36 in 49 for the pulmon- ary artery; 43 in 63 for the top of the auricle). In the majority of instances there was but little difference between the height of the origin of the pulmonary artery and the top of the right auricle, the height of the two being identical in one-fourth of the instances (10 in 44), and the difference in their height being respectively less than the third of an inch or the third of the breadth of a space or cartilage in one- half of them (21 and 20 in 44). Of the remaining instances, in twelve the differ- ence of the height of those two parts varied from one-third to two-thirds of an inch or two-thirds of a space or cartilage, and in one the difference of their height amounted almost to an inch. As a rule, the origin of the pulmonary artery tended to behigher in position than the top of the right auricle, the former part being the higher of the two in twenty instances, and the latter part being the higher of the two in fourteen instances. (Note 10.) The varying position, higher or lower, of (1) the pulmonary artery, (2) the aorta, (3) the right ventricle, and (4) the right auricle, in relation to the costal cartilages and the spaces between them, and to the sternum will next be considered. The Pulmonary Artery.-A knowledge of the position of the pulmonary artery is important to the clinical worker, because it is near the surface of the chest, and be- cause the signs afforded by it reveal the condition of the cavities and valves of the heart, and the ease or difficulty with which the blood finds its way from and to those cavities, the lungs, and the body. Among those signs are, the character of the first sound, whether loud and sharp, or feeble and almost silent, or presenting a pulmonic murmur ; the character of the second sound, whether feeble or intense, blunt or sharp, or presenting a double sound, giving in quick succession the aortic and the pulmonic second sounds or the reverse, the latter sound being the louder of the two. The trunk of the pulmonary artery varied in length from three-quarters of an inch to two inches and a half. In more than a third of the instances (17 in 46) the artery was from an inch to an inch and a half in length, while in less than a third of them it was below (lo in 46), and in less than a third of them (14 in 46) it was above that length. The vertical measurement of the right ventricle from the origin of the pulmon- ary artery to the lower boundary of the heart, varied in these instances from two inches and a half to a little over four inches. The length of the ventricle thus measured was from three inches to three inches and a half in less than one-half of the cases (20 in 46). The proportion between the length of the pulmonary artery and the length of the right ventricle, measured from above downwards, presented great variety. In one instance the length of the artery was nearly equal to the length of the ventricle, that of the former being two inches and a half, that of the latter scarcely three inches; while in two others the vertical measurement of the ventricle was five times as great as that of the artery, the length of the latter in one instance being three-quarters of an inch, and that of the former being fully four inches. The aver- age length of the ventricle in relation to that of the artery was as three to one. As a rule, the length of the pulmonary artery regulated the proportion in length which that vessel bore to the ventricle ; thus in the whole of the fifteen instances in which the length of the pulmonary artery was less than an inch, the length of the right ventricle was more than three times that of the artery; while in the whole of the fourteen in which the artery 374 POSITION AND FORM OF THE HEART. was an inch and a half in length and up- wards, the length of the right ventricle was less than three times that of the vessel. (Note 11.) As we have already seen, the origin of the pulmonary artery varied in position from the second to the fourth cartilage, its usual situation being the second space and the third cartilage. The top of the pulmonary artery was in*one instance al- most as high as the clavicle, and in almost one half of the cases (25 in 63) it was sit- uated behind the manubrium or the first rib ; while in one case it was so low as to be almost on a level with the upper edge of the third cartilage. In more than one half of the cases (33 in 63) it was seated behind the first space or the second cartil- age. (Note 12.) The situation of the pulmonary artery during its course is regulated by the length of the vessel and by the position of its starting place and upper end. In one instance it was so high as to be entirely concealed by the manubrium, while in another it was so low as to be entirely covered by the third cartilage and third space. The artery was rarely limited in position to one space or one cartilage: thus in but one instance it only occupied the first space, and in but one it was quite covered by the second cartilage. The artery usually lay behind one space and one costal cartilage (35 times in 60), but in one-third of the instances (21 in 60) it extended to an additional space or cartil- age. In two-thirds of the instances it was present behind the second cartilage (43 in 60); in more than half of them it lay behind the first space (35 in 60), and in nearly as many behind the second space (32 in 60); while in one-fourth it was covered by the third cartilage (15 in 60), and in one-sixth by the manubrium (9 in 60). (Note 12.) When the pulmonary artery was long (it was so in 14 of 46 instances), its origin occupied, as a rule, a low position. Thus in sixteen instances the origin of the ar- tery was entirely above the second space, and in only two of these was it long, while in seven it was short. On the other hand, in thirty instances the pulmonary artery at the first part of its course was at or be- low the second space, and in twelve of them the artery was long, while in eight it was short. (Note 12.) The Arch of the Aorta.-The arch of the aorta is not, like the pulmonary artery, visible in its whole course from its root to its summit, being hidden at its root by the right auricle and ventricle. I shall, there- fore, not speak here of the whole of the ascending aorta, but of that portion of it which comes into view above the right auricular appendix and between it and the beginning of the pulmonary artery and the arterial cone of the right ventricle. The arch of the aorta, from the part in its course just spoken of where it first be- comes visible, to its highest point at the origin of the innominate and left carotid arteries, varied much in length. In two female subjects, one aged nine, the other a few years older, the arch was an inch and a half in length, but in the adult sub- ject its length ranged from an inch and three-quarters to three inches. The arch, measured from the lower to the higher points just named, was from just over two inches to two inches and a half in length in two-fifths of the instances (19 in 47), that being about the average or standard length; from an inch and three-quarters to two inches in more than one-fifth (11 in 47), and from two inches and a half to three inches in less than two-fifths of them (17 in 47). (Note 13.) Viewed in proportionate relation to the length of the body, measured approxi- mately from the chin to the pubes, the vertical measurement of the arch varied from one-seventh to one-fourteenth of the vertical measurement of the body thus taken, and in one-half of the instances (23 in 45) the length of the aorta was one- tenth that of the body. In three instances the vertical measure- ment of the arch of the aorta was the same as the vertical measurement of the right ventricle taken from the part at which the aorta was visible to the lower boundary of the organ. In tw'O instances the arch was longer than the ventricle in the proportion of ten to nine, but in the remainder the length of the ventricle was greater than that of the aorta, the relative proportion varying from 10 to 10T to 10 to 19T7, so that in the last example the ventricle was nearly twice as long as the arch. The average length of the arch in proportion to that of the right ventricle was about 10 to 14 (14 in 47). The variation in the proportionate length of the arch of the aorta and the right ventricle, although thus consider- able, is not nearly so great as the varia- tion in the proportionate length of the pulmonary artery and the right ventricle ; since that artery varied in length from more than one-half to less than one-fifth of the vertical measurement of the ventri- cle, while the arch was about the same length as the vertical measurement of the ventricle at one end of the scale, and was of half that length at the other end. There was some correspondence be- tween the length of the aorta and that of the pulmonary artery. Thus the pulmo- nary artery was short, long, or of medium length in two-fifths of the instances in which the aorta was respectively short, long, oi- of medium length (13 in 33). In the remaining instances (20 in 33) this strict proportion was not maintained, but in only two of them was the difference in THE HIGHER OR LOWER POSITION OF THE HEART. 375 the proportionate length of the vessels great, the aorta being long while the pul- monary artery was short. The position of the lower boundary of the heart in relation to the lower end of the sternum, whether above, at or below that point is, as a rule, governed to a con- siderable extent by the length of the arch of the aorta. Thus in nine instances in which the arch was short, measuring two inches or less, the lower boundary of the heart was above the lowrer end of the sternum in seven instances, and below that point in two. The other circum- stances that regulate the position of the lower boundary of the heart in relation to the lower end of the sternum are (1) youth; (2) the distension or collapse of the right ventricle ; (3) the length of the sternum; (4) the important influence of the higher or lower position of the ster- num, higher when the chest is ample, being of an inspiratory type, and lower when the chest is narrow and flat, being of an expiratory type; (5) the higher or lower position of the top of the arch of the aorta which is often ruled by (4) the lower or higher position of the sternum ; (6) the extent to which the heart shrinksupwards after death which is evinced by the space intervening between the lower boundary of the heart and the lower boundary of the front of the pericardium; and (7) the elevation or depression of the diaphragm, which is the most important influence in producing respectively the elevation or depression of the heart, and which may be caused by (a) the contraction or ex- pansion of the lungs, or (6) the distension or collapse of the abdomen. These points are illustrated by the two exceptional cases just cited, in which, although the arch of the aorta was short, the lower boundary of the heart was below the level of the lower end of the sternum. Both of these cases were quite young (1); in both the vertical measurement of the right ventricle was long, while in one of them that cavity was distended and large (2); in both of them the sternum was short, its length being less than four inches in one, while in the other it was four inchesand a half (3); again in one of them the sternum was high, the length of the neck being only two inches, that of the sternum four inches and a half, and that of the abdo- men fourteen inches, -while in the other instance in which the right ventricle was large, the sternum was low in position, the length of the neck being almost four inches, that of the sternum less than four inches, and that of the abdomen only ten inches and a half (4). In neither of these examples was the position of the lower boundary of the heart lowered owing to the low position of the top of the arch, for in one of them that point was above the top of the sternum and in the other it was a little way below it (5). In fact this in- fluence, which tended to elevate the lower boundary of the heart in relation to the lower end of the sternum was more than counter-balanced by the combined influ- ences of which I have just spoken, all working in the opposite direction so as to lower the inferior border of the heart. In further illustration of this point, the influence, namely, of the shortness or length of the arch in respectively raising or lowering the lower boundary of the heart, we find that of seventeen cases in which the aorta was long, measuring two and a half inches and upwards, in ten the lower boundary of the heart was below the level of the lower end of the sternum, in four it was at that point, while in only three was it above the lower end of the sternum. The three exceptional cases in which the lower boundary of the heart was above the level of the lower end of the sternum were adults of full size (1) ; the right ventricle was narrow and con- tracted in two of them (2) ; and in two the heart deviated to the left so that the lower border of the right ventricle was situated to the left of the lower end of the sternum, instead of being to the right, as is usual. The sternum was long in two of them, measuring in one case over seven inches (3); in all of them the ster- num was low in position, the length of the neck being five inches and a half, four inches, and three inches and a half respec- tively, while that of the abdomen was in each instance less than fourteen inches (4) ; in one of them the top of the arch was situated above the top of the sternum (5); in one of them the space between the lower limit of the heart and the lower limit of the front of the pericardium was nearly an inch, while in another it was fully half an inch in width, showing that the upward shrinking of the heart after death had been considerable (G); and finally one of them, that in which the space between the heart and the lower rim of the pericardium was small, the stomach was globose and much distended so as to push the heart upwards (76). In twenty-three cases the arch of the aorta was of intermediate length, or from a little over two inches to two inches and a half, and in these the lower boundary of the heart was in equal relative propor- tion above, at, and below the level of the lower end of the sternum. It is evident and is illustrated by what has just been said that if we group the cases as I have just done, according to the actual length of the arch of the aorta without relation to age or the dimensions of the body, we shall include some in- stances in which the arch of the aorta is relatively short or long with those in which it is respectively actually long or short. I have therefore grouped the 376 POSITION AND FORM OF THE HEART. whole cases anew, and according to the proportional length of the aorta in rela- tion to the length of the body. It will suffice here if I say that the results thus obtained are exactly confirmatory of those that I have just related, and show that the higher or lower position of the lower boundary of the heart in relation to the lower end of the sternum is to a consider- able extent governed by the proportional shortness or length of the arch of the aorta. They show those results indeed more strikingly, for the conflicting ele- ment of (1) youth has been removed. Two exceptional instances have been brought into the group in which the arch of the aorta was long in proportion to the length of the body, that were not in- cluded in the parallel group in which the arch was actually long. In these two examples the lower boundary of the heart was above the level of the lower end of the sternum, although the aorta was pro- portionally long. The heart was lifted directly upwards to a great extent in both of these instances, in one of them by very great enlargement of the liver, upwards, as well as downwards, owing to the presence of malignant disease in the organ, the sternum being in this case very long (6'8 inches); and in the other by excessive distension of the stomach and intestines owing to peritonitis, the ster- num in this instance being short (4'7 inches) and the top of the aorta being situated in the root of the neck, a third of an inch above the level of the top of the sternum (76). The Right Auricle.-The right auricle is, as a rule, hidden from observation by the couch of lung that is interposed be- tween it and the sternum and cartilages. It comes, however, to the surface in cases of pericarditis when the effusion into the sac accumulates in sufficient quantity to press aside that portion of lung with which the auricle is covered. With the exception of the important point just con- sidered, the right auricle cannot be recog- nized locally by the clinical observer, the condition of that cavity being in fact best told by the state of the veins in the neck. The right auricle measured from the top of its auricular portion to its lowest point, varied in length from one inch to four inches and a half. Its length was usually from two and a half to three and a half inches (in 41 of 62 instances). In one- fifth of the cases (12 in 62) its length was less than two and a half inches ; but one- half of these were youthful subjects (7 in 12). The vertical measurement of the right ventricle was longer than that of the right auricle in more than two-thirds of the cases in which the comparison was made (35 in 49); in one-fifth of them the two cavities were nearly or quite of equal length (10 in 49); and in one-twelfth of them the auricle was longer than the ven- tricle. (Note 14.) The auricular portion of the auricle, which during life laps, like a tongue, to and fro, from right to left and back again, was usually nearly on the same level as the top of the right ventricle, the top of the auricle being of the same height as that of the ventricle in ten instances, higher than that of the ventricle in four- teen instances, and lower in twenty. It was at the lower boundary that the right auricle failed. In one case, in which there was fatal hemorrhage, the auricle, which was quite insignificant in size, was only half as long as the ventricle. Usually, however, the auricle was shorter than the ventricle by from one-tenth to one-third of its vertical measurement (in 29 of 35 in- stances). The right auricle, from the variable ex- tent to which, on the one hand it receives blood, and on the other retains or parts with it before, during, and after death, and from its passive nature, is more vari- able in form and size than any other cavity of the heart. This point will be briefly illustrated when the lateral dimen- sions of the cavities are considered. The Hight Ventricle.-The vertical mea- surement of the right ventricle in relation to the pulmonary artery and the aorta has already been considered. The right ventricle, measured from the origin of the pulmonary artery to the lower boundary of the cavity, varied in length from two inches and three-quarters to four inches. In one-fifth of the instances (9 in 46) the length of the ventricle thus mea- sured was less than two inches, the ma- jority of these being youthful subjects (5 in 9); in nearly one-half of them (20 in 46) this measurement was from three inches to nearly three inches and a half; and in the remainder it was three inches and a half and upwards, being fully four inches in six of them. The variable di- mensions and form of the ventricle will be briefly noticed when its lateral measure- ments are considered. (Note 15.) The extent of the vertical measurement or length of the right ventricle produces a marked influence on the position of the lower boundary of the heart in relation to the lower end of the sternum. Thus, of the nine cases in which the ventricle was short, its lower boundary was above the level of the end of the sternum in five in- stances, and below that level in only one ; while of the sixteen instances in which the ventricle was long, in ten of them its inferior border was below the end of the sternum, while in only six of them was it above that point. It is, indeed, self-evi- dent that the lower border of the ventricle must be lower in position when the cavity increases, and higher when it lessens in size. POSITION OF THE HEART AND GREAT VESSELS. 377 The extent to which the upper part of the bony sternum covers the great arte- ries, and the lower part of it, the heart, is very variable. In one instance the great arteries occupied only the upper fourth of the sternum, while the heart occupied its lower three-fourths. In another instance this proportion ■was to a considerable ex- tent reversed, for the vessels lay behind the upper five-eighths of the bone, the heart itself being limited to its lower three-eighths. In three-fourths of the in- stances (39 in 52) the greater share of the sternum lay in front of the heart, but in one-fourth the greater share of the bone was given to the great vessels. On an average, the position of the heart was be- hind the lower four-sevenths, and that of the great arteries was behind the upper three-sevenths of the sternum. (Note 16.) (II.) The Position of the Heart and Great Vessels from Side to Side. Eelation of the Breadth of the Heart to the Breadth of the Chest.-The proportion- ate transverse diameter of the heart, com- pared with the transverse diameter of the chest, varied considerably. Thus in one instance, in which death was the result of hemorrhage, the width of the heart was less than one-third of the width of the chest, on a level with the lower end of the ensiform cartilage (3'2 to 10 inches); while in another instance the measure- ment across the heart was nearly two- thirds of that across the chest (5T inches to 8'2 inches). In a large number of the cases observed (39 in 65) the breadth of the heart was somewhat less than one-half of the breadth of the chest, the proportion varying from 10 to 4 to 10 to 5. In one-sixth of the instances (11 in 65) the width of the heart was less than two-fifths (10 to 3 to 10 to 3'9), and in one-third of them (15 in 65) it was more than one-half (10 to 5 to 10 to 6'2) of the width of the chest. The size of the chest from side to side did not appear to exercise any material influence on the proportional breadth of the heart, but the heart was more frequently of the average proportional width in those instances in which the chest was of medium breadth (9 to 9'9 inches) than in those in which it was either wide (10 to 12 inches) or nar- row (6 to 8'9 inches). Thus, the heart was of the average proportional breadth in five-sixth of the instances in which the chest was of the medium breadth (10 in 12); in one-half of those in which the chest was wide (12 in 22) ; and in two- thirds of those in which the chest was narrow (19 in 31). The heart was comparatively wide and comparatively narrow in equal numbers in those in- stances in which the chest was wide (6 of each kind in 22); while the organ was more frequently comparatively wide than narrow, in those in which the chest was narrow (wide in 8, narrow in 4, of 31). Great distension and great collapse of the abdomen produced a marked effect on the proportionate width of the heart in rela- tion to that of the chest. Thus, in fully two-thirds of the instances in which the heart was proportionally narrow, the ab- domen was distended (8 in 11), and in one- half of these the distension was very great (4 in 11) ; while in one of the three re- maining cases the abdomen was large, in one it was of moderate size, and in only one was it small. Then the reverse took place in those cases in which the heart was proportionately wide, since in only one-fifth of them was the abdomen dis- tended (3 in 15), and in but one of these was the distension very great. Disten- sion of the abdomen seemed to produce this effect by acting in two directions, one upon the chest, by widening it, the other upon the heart itself, by lessening it. The chest is widened because the dis- tended abdomen pushes the ribs outwards on either side, and elevates the lower bor- der of the chest in front and at each side ; and the heart is lessened because the dis- tended abdomen compresses the heart up- wards into the contracting space of the higher part of the cone of the chest, and so lessens the amount of blood in the organ. (Note 17.) The proportional size of the anterior transverse diameter of the combined right auricle and ventricle, compared with that of the left ventricle, exercises a marked effect on the proportional breadth of the heart in relation to the breadth of the chest. This might indeed be anticipated, for when the proportional width of the combined right auricle and ventricle is great in relation to the width of the left ventricle, the right cavities are distended ■with blood, and the whole heart is conse- quently large, measured from side to side. In more than one-half of the cases (7 in 12) in which the proportional breadth of the heart to that of the chest was great, the proportional breadth of the combined right auricle and ventricle to the left ven- tricle in front was very great, the former being about ten times wider than the lat- ter ; and in none of them was the propor- tional breadth of the right cavities small. Again, in almost one-half of the instances (5 in 11) in which the proportional width of the heart in relation to that of the chest was small, the proportional width of the right auricle and ventricle in rela- tion to that of the left ventricle was also small, the ratio being about 10 to 4. (Note 18.) Extent to which the Hewt occupied the Eight and the Left Sides of the Chest.-The extent to which the hea'rt occupied re- 378 POSITION AND FORM OF THE HEART. spectively the right and the left sides of the chest varied much in different in- stances. Thus in one example, the heart extended one inch and a tenth to the right and four inches to the left of a ver- tical line drawn down the middle of the sternum; and in another the organ ex- tended nearly two inches and a half to the right, and only two inches and a quarter to the left of that line ; while in two other instances the heart occupied the right and the left sides of the chest in exactly equal proportions. Thus, taking the two extreme cases, in one of them one-fifth of the heart occupied the right side, and four-fifths of it the left side of the chest; while in the other fully one- half of the heart was lodged in the right side, and less than one-half of it in the left side of the chest. There was every gradation of difference between these two extreme examples. In fully two-fifths of the instances (27 in 67) one-third of the heart or less was situated in the right side, and two-thirds of the heart or more, in the left side of the chest; while in fully two-fifths of them (28 in 67), three-fifths of the heart or less was seated in the left side, and two-fifths of it or more in the right side (literally 16 to 10). In twelve intermediate or standard in- stances, the heart was distributed to the right and to the left of the middle line of the sternum in the proportion respectively of ten and eighteen, and this was the average position of the organ in sixty- seven bodies, so that nearly two-thirds of the organ lay in the left side, and more than one-third of it in the right side of the chest. (Note 19.) The influences that cause the deviation of the heart towards the right or the left side of the chest, are (1) before all others, the difference in size of the right lung and the left; (2) the encroachment upwards of the liver or the stomach to an unusual extent on the right or the left side of the chest respectively; (3) the position of the patient before death on the right side or on the left, an occurrence that may take place in certain rare cases, such, for in- stance, as bed-sores and affections of one side of the chest; (4) the shrinking of the heart upwards after death, as evinced by the extent of the space intervening be- tween the lower boundary of the heart and the lower boundary of the front of the pericardium; (5) the shortening of the aorta; (6) the relative size of the heart and of its cavities, measured from side to side. There are doubtless other influences at work to produce the effect in question, but I have not discovered them. (1) Of the small number of instances (6 in 66) in which the heart swerved very far to the left, so as to occupy that side of the chest to a greater extent by from three to four times than the right side of the chest, the two lungs were equal in size in one-third (2 in 6), while the right lung ■was greater than the left in the remaining two-thirds. On the other hand, of the cases in which the heart was lodged equally in the right and the left sides of the chest (3 in 66), and those in which it bore only a little more to the left than the right side of the chest (12 in 66), the two lungs were of equal size in one-fourth, and the left lung was larger than the right in the remaining three-fourths. Thus in none of the instances in which the heart deviated greatly to the left was the left lung larger than the right; and in none of those in which the heart tended towards the right side of the chest was the right lung greater than the left. In the whole of the remaining instances, with a few exceptions, an analogous con- dition obtained, the right lung being the larger when the heart was lodged to an unusual extent in the left side of the chest, and the left lung being the larger when the heart was lodged to an unusual extent in the right side of the chest. (Note 20.) (2) The position of the upper surface of the liver, covered by the diaphragm, was higher in the right side of the chest than that of the stomach in the left side of the chest in all but a fraction of the instances observed (57 in 61). On an average, the liver at this situation was higher than the stomach by more than half an inch ('6 inch). In two-fifths of the cases (25 in 61) the heart occupied the left side of the chest to an unusual extent; of these, in nearly two-thirds the height of the liver in relation to that of the stomach was above the average (14 in 25); in nearly one-third it was below the average (7 in 25) ; and in a fraction it was at the aver- age (3 in 25). In all but one of the five instances in which the heart was very far to the left, the relative height of the liver was above the average. In one-fourth of the cases (14 in 61), the heart occupied the right side of the chest to an unusual extent, and in nearly three-fifths of these (8 in 14) the height of the liver was below the average, while in fully two-fifths of them (6 in 14) it was above the average. When the top of the liver encroached to an unusual proportional extent on the right side of the chest, it may be said that the unduly-elevated organ tended to dis- place the heart to the left. There were, however, a few remarkable exceptions to this rule. Thus, in one instance the heart occupied equally the right and the left sides of the chest, and yet the top of the liver rose higher by nearly an inch and a half into the right side of the chest than the stomach did into the left side of the chest. The reason of this was obvious. POSITION OF THE HEART AND GREAT VESSELS. 379 There was contraction of the right lung in this case, owing to phthisis, with the effect of drawing both the heart and the liver mainly into the space previously oc- cupied by the right lung. (3) I have no after-death evidence to show that the position of the patient on the right side or the left during the period preceding death caused the heart to occupy unduly the right or the left side of the chest. We know, however, that during life the heart falls towards the side on which the person lies. At the same time that side of the chest expands less during inspiration than the opposite side, owing to the restraint offered to the movement of the ribs that bear the weight of the chest, while, to compensate for the de- ficient expansion of the restrained side, the free side of the chest expands to an increased extent. After death, the or- gans, as a rule, retain pretty nearly the place they occupied during life, and the effect of position during life in displacing the heart more towards the right side or the left, is retained after death. (4) When the heart shrinks upwards, so as to leave a considerable space be- tween the lower boundary of the organ and the lower boundary of the front of the pericardium, the heart, as a rule, bears more towards the right than the left side of the chest. Thus the space below the heart was large in two-thirds of the cases in which that organ bore unusually to the right (8 in 12) ; and in only two-fifths'of those in which it bore unusually to the left (8 in 19). (5) I am of opinion that in those cases in which the heart shrinks thus upwards, and bears unusually to the right, the con- traction and shortening of the aorta is one of the principal agents that draws the apex and the body of the heart to the right as well as upwards. (6) The relative size of the heart and of its cavities, measured from side to side,, exercised much less influence than the relative size of the right and left lung, and the relative height of the liver and stomach, on the extent to which the heart occupied after death the right and left sides of the chest respectively. W hen the heart is large, the lungs necessarily make way for it, to the right and left equally if the development of the lungs is equal; but when one lung is ex- panded and the other is contracted, the heart when large encroaches more upon the contracted than the expanded lung, for that lung offers the least resistance. The stronger influence of the greater size of one lung overrides then the weaker in- fluence of the size of the heart. But it is evident that the size of the heart must produce an influence supplementing and modifying the influence of the greater size of one lung. When the heart is large it enhances the influence of the greater size of one lung, and the heart encroaches more on the side containing the contracted lung ; and when the heart is small it les- sens the influence of the greater size of one lung, and the heart encroaches less on the side containing the contracted lung. Thus in the large group of cases in which the heart occupied the left side of the chest to an unusual extent (1 to 3'9 to 1 to 2, in 23 in 60), and in the equally large group in which the heart was dis- tributed in the average proportion to the right and. left sides of the chest (1 to 1'5 to 1 to 1'9 in 23 in 60), the heart was large in fully one-fourth of the respective instances (6 in 23 and 7 in 23), while in no instance was the heart large in the group in which that organ occupied the right side of the chest. The heart was small in two of the three instances in which the organ occupied the right and the left sides of the chest to an equal extent. The heart is attached at the centre of the chest, behind, to the roots of the lungs by the pulmonary veins and pulmonary arteries; and above and in front, to the great arteries and the de- scending vena cava from which it is sus- pended. The heart, therefore, when it does not bear to the left or to the right owing to the greater or less size of the right or left lung, hangs directly down- wards from the points of its suspension at the centre of the chest, and tends to oc- cupy a central position, bearing equally to the right and to the left. Breadth of the Combined Bight Auricle and Ventricle in Belation to that of the Left Ventricle as seen in Front.-The breadth of the combined right auricle and ventricle in relation to the breadth of the left ven- tricle as seen in front, varied from 10 to 1 to 10 to 4^. Thus the right cavities occu- pied almost the whole front of the heart in some examples, and little more than two-thirds of it in others. Every shade of variation existed between these two extreme instances; but the average or standard proportion between the breadth of the right cavities and that of the left ventricles in front was as 4 to 1. (Note 21.) Breadth of the Bight Auricle.-The auric- ular portion of the right auricle varied in breadth from a little over half an inch (•55 inch) to two inches and a third (2'3 inches), its average breadth being one inch and a third (1'3 inch). (Note 22.) The body of the right auricle1 varied in 1 The right auricle is about half an inch wider, and the right ventricle is about half an inch narrower than the measurements given in this article. Those measurements have been necessarily taken from the right auriculo-ventricular furrow, which is the apparent boundary-line between the right 380 POSITION AND FORM OF THE HEART. breadth from a quarter of an inch to an inch and a half, its average breadth being four-fifths of an inch (8'1 inch). (Note 23.) The left edge of the auricular portion of the right auricle extended to the left of the left edge of the sternum in four in- stances ; it was placed nearer to the left than the right edge of the sternum in twenty-four cases ; it was situated about midway between the left and the right edge of the sternum in eight instances; and it was nearer to the right than the left edge of that bone in fourteen. (Note 24.) The right edge of the right auricle ex- tended to the right of the right edge of the sternum to an extent varying from a quarter of an inch to an inch and three- quarters, so that to that extent the auricle lay behind the right costal cartilages. The right auricle extended on an average from half an inch to a little over an inch to the right of the sternum. (Note 25.) The auricular portion of the right auri- cle was wider than the body of the auricle in all but two instances, in which instances their breadth was the same. As a rule, the auricular portion was wider than the body of the auricle in the proportion of ten to six and a half (10 to 6'4), but in two instances that portion was nearly three times as wide as the body of the auricle. (Note 26.) The proportional breadth of the auricu- lar portion of the right auricle varied from two-fifths to one-fifth of the breadth of the heart itself. The width of the heart was, on an average, nearly four times as great as that of the auricular portion of the right auricle. (Note 27.) The proportional breadth of the body of the right auricle varied from about a fourth (10 to 36) to a ninth (10 to 86) of the breadth of the heart. In one excep- tional case in which death took place from hemorrhage, the heart was twelve times as wide as the right auricle, that cavity being quite empty. The width of the heart was, on an average, nearly six times as great as the width of the right auricle. (Note 28.) Breadth of the Right Ventricle. - The breadth of the right ventricle1 varied from four-fifths (in 6 of 38 instances) to a little over one-half (in 11 of 38 instances) of the whole breadth of the heart. The average or standard breadth of the right ventricle was two-thirds of the breadth of the heart (10 to 15), and in one-half of the cases observed the proportional width of the right ventricle in relation to that of the heart was above (19 in 38), and in one- half of them it was below that average (19 in 38). (Note 29.) The breadth of the arterial cone of the right ventricle a little way below the origin of the pulmonary artery varied from four-fifths to two-fifths of the breadth of the right ventricle at its middle, the average width of the arterial cone being nearly three-fifths of that of the body of the right ventricle. As a rule, when the body of the right ventricle was wide or narrow in relation to the heart, the arte- rial cone was respectively narrow or wide in relation to the body of the right ven- tricle. (Note 30.) The vertical diameter or length of the right ventricle,1 measured from the origin of the pulmonary artery to the lower boundary of that cavity, was somewhat shorter than the transverse diameter or breadth of the ventricle in one-sixth of the cases (5 in 30). In the rest of them the length of the right ventricle was greater than its breadth. In one instance the length of the ventricle was to its breadth as 17'3 to 10, but the average or standard measurement of the length to the breadth of that cavity was as 4 to 3. (Note 31.) The breadth of the right ventricle in re- lation to that of the right auricle below its auricular' portion varied from 10 to 1'4 to 10 to 5'2, the average proportion being 10 to 3. (Note 32.) The actual breadth of the right ven- tricle in adults, without distinction of sex, varied from two to four inches. In three-fifths of them the width of the ven- tricle was from three to three and a half inches (in 14 in 24) ; in one-fifth of them it wras above three and a half inches ; and in two-fifths of them it was less than three inches. (Note 33.) In one instance the right ventricle ex- tended further to the right than to the left of a vertical line drawn down the middle of the sternum, but in every other instance the ventricle extended more to the left than to the right of that line. In one case, nine-tenths of the right ventri- cle was situated in the left side of the chest, and only one-tenth of it in the 1 As the breadth of the body of the right ventricle is about half an inch narrower than the measurements of that cavity given in this article, for the reason stated in the foot-note at page 379, the actual relation of the trans- verse diameter or width of the body of the right ventricle here stated to that of the conus arteriosus, and to the vertical diameter or length of the ventricle, is half an inch nar- rower than the proportional measurements here given. auricle and ventricle, but is situated half an inch to the right of the real boundary-line between those cavities. 1 The right ventricle is about half an inch narrower, and the right auricle is about half an inch wider than the measurements of those cavities given in this article, for the reason stated in the preceding foot-note. POSITION OF THE HEART AND GREAT VESSELS. 381 right side ; but, on an average, the ven- tricle extended nearly three times farther to the left than the right of the middle line (27 to 10). (Note 34.) The limits of the body of the right ven- tricle and of its arterial cone are indicated, (1) to the left by the position of the longi- tudinal furrow between the ventricles; and (2) to the right by the position of the transverse furrow between the right ven- tricle, including the right edge of the ori- gin of the pulmonary artery and the right auricle, including its auricular portion. (1) As a rule, the inter-ventricular furrow takes an oblique direction out- wards, or to the left from above down- wards, so that the ventricle occupies a wider space below than above (in 26 of 39 instances). In a small number of cases (6 in 39) the reverse takes place, and the furrow tends inwards, and then outwards with a peculiar double curve as it de- scends. In these instances the right ven- tricle was in a state of contraction, and the left ventricle was exposed to a large extent, while in those in which the sep- tum inclined markedly outwards during its descent, the right ventricle was dis- tended so as to cover all but a small por- tion of the left ventricle. The greatest inclination of the longitudinal furrow to the left was one inch, and its greatest in- clination to the right was half an inch (•45 inch). (Note 35.) In one instance, a case in which the right ventricle was contracted, the longi- tudinal furrow in its descent curved to the right, and the body of the right ven- tricle towards its left border was com- pletely shielded by the sternum; but in every other instance that cavity was covered in front to a greater or less ex- tent by the cardiac costal cartilages, to the left of the lower half of the sternum. In a small proportion of the cases (6 in 36) the right ventricle lay behind the costal cartilages from end to end, from the sternum, namely, to the ribs to which they are united; and in half of these (3 in 6) the ventricle extended to the left, beyond the cartilages and behind the ribs. In the majority of the cases (19 in 36) the longitudinal furrow extended either up to the ends of the cartilages, a little beyond them, or half an inch or less to the right of them, so that in all these cases the car- diac cartilages covered the right ventricle almost or quite from end to end. In the remaining instances (17 in 36) a consider- able portion of the cartilages, varying from less than an inch to more than an inch and a half ('7 to 1'7 inch) extended beyond the right ventricle. (Note 36.) The body of the right ventricle, start- ing from a vertical line drawn down the middle of the sternum, extended to the left in all the cases, from a little over half an inch ('6 inch) to almost four inches (3'8 inch). Between these two extreme instances there was every shade of differ- ence. In the great majority of the cases (35 in 52) the right ventricle extended from one inch and a half to two inches and a half to the left of the middle line of the sternum, and behind the cardiac car- tilages. (Note 37.) (2)1 The transverse or right auriculo- ventricular furrow was situated to the right of the right edge of the lower por- tion of the sternum, and behind the right costal cartilages, in fully two-thirds of the cases (3G in 51), at that edge in a fraction of them (3 in 51), and to the left of that edge, and therefore behind the lower por- tion of the sternum, in one-fourth of them (12 in 51). In one instance the right auriculo-ventricular furrow extend- ed an inch and a third (1'3 inch) to the right of the right edge of the sternum, so as to lie behind the right costal cartilages to that extent, and in five instances its right limit was situated behind the mid- dle line of the sternum. Between these two extreme limits there was every grada- tion in the position of the right auriculo- ventricular furrow. The left edge of the auricular portion of the right auricle gives, as a rule, very nearly the position of the right edge of the arterial cone of the right ventricle, where it is about to end in the pulmonary artery. The right edge of the arterial cone, starting from the tricuspid orifice, invariably inclines, as it ascends, from right to left. There was considerable difference in the degree of its inclination, which was measured by the distance be- tween the right limit of the auriculo- ventricular furrow and a line drawn downwards from the right edge of the pulmonary artery. The right edge of the arterial cone swerved as it ascended from right to left in one instance, a man, to the extent of two inches, and in another, also a man, to that of a little over half an inch ("6 inch). There was every variety of inclination between these extreme in- stances, but in the great majority of cases (34 in 51) the curved line of the right border of the arterial cone bent down- wards, with an inclination from left to right of from an inch to an inch and a half, the boundary line starting above from the right border of the origin of the pulmonary artery, and ending below in the auriculo-ventricular furrow. (Note 38.) Breadth and Position of the Pulmonary Artery.-As the origin of the pulmonary artery is the point of convergence towards * The transverse furrow, which is the ap- parent boundary-line between the right auri- cle and the right ventricle, is about half an inch to the right of the real boundary-line between those cavities. See note at page 379. 382 POSITION AND FORM OF THE HEART. which the right ventricle propels its blood, this is the natural place for examining the position of that artery. The pulmo- nary artery forms, indeed, the pointed apex of a triangle, the body of which is constituted by the front of the right ven- tricle, its base by the lower boundary of that cavity, resting on the central tendon of the diaphragm, its left side by the longitudinal furrow, and its right side by the auriculo-ventricular furrow.1 The breadth of the pulmonary artery varied from a little over half an inch ('6 inch) to a little under an inch and a half (1'45 inch). Between these two extreme limits, both of which occurred in men, there was every kind of variation in the breadth of the artery. The width of the artery depended as much on the amount of blood that it happened to contain as on the natural size of the vessel. In one- third of the cases (18 in 45) the breadth of the artery varied from three-quarters of an inch to less than an inch, and of these three were boys and four were young people; and in one-third of them (17 in 45) the breadth varied from an inch to an inch and a quarter, and of these the youngest was a girl of 16, the rest being adults. The pulmonary artery was wider than the aorta in twenty-seven cases, narrower than the aorta in eleven, and of the same width as the aorta in six. (Note 39.) In one instance the right border of the pulmonary artery at its origin lay two- thirds of an inch to the left of the sternum, and in another it was covered by the ster- num to the extent of an inch, so that a mere, rim of the artery ('25 inch) appeared in the second left space. Between these two extreme instances there was every degree of difference in the position of the origin of the pulmonary artery to the right or the left. In two-thirds of the cases (31 in 45) the pulmonary artery was situated partly be- hind the sternum, and partly behind the upper cartilages and spaces to the left of the sternum; but in one-third of them (14 in 45) the vessel lay entirely to the left of that bone, and behind the upper spaces and cartilages. Of those instances in which the artery lay completely to the left of the sternum, in three-fourths (11 in 14) the right bor- der of the vessel was on a line with or a little beyond the left border of the bone, and in the remainder (3 in 14) it was placed from one-third to two-thirds of an inch to the left of that bone. Of the in- stances in which the artery lay partly be- hind the sternum, partly behind the car- tilages and their spaces, in all but one- fifth (6 in 31) the vessel was situated to a greater extent behind the spaces than the sternum. In no single instance was the artery entirely covered by that bone. In the large majority of the cases, therefore, the greater part (in 25 of 45 instances), or the whole (in 14 of 45 instances), of the artery bore to the left of the sternum and presented itself behind the upper costal cartilages and their spaces from the first cartilage to the third space. (Note 40.) Breadth of the Left Ventricle. - The breadth of the left ventricle as it is seen in front where it extends from the septum between the ventricles to the left border of the heart, varied from almost half an inch ('4 inch) to almost an inch and a half (1*4 inch). The average width of the ventricle was four-fifths of an inch ('8 inch). The proportion that the width of the left ventricle at its anterior aspect bore to the width of the whole heart varied from less than one-tenth ('08 to 10) to more than three-tenths (3'2 to 10). As a rule, when the ventricle was actu- ally narrow, it was also proportionally narrow in relation to the breadth of the heart; and when the ventricle was actu- ally wide, it was also proportionally wide in relation to the breadth of the heart. The exceptions to this rule are so few that I need not give the details here. (Note 41.) Position of the Apex of the Heart.-The line of junction of the fourth and fifth ribs to their cartilages is a landmark of some clinical importance, for, aided by knowledge, this line may be pretty nearly ascertained during life. A downward bow is made by the descending curves of those ribs and of their cartilages, and their junction usually corresponds to the deepest part of the bow. The left bound- ary of the heart at the apex was situated in one instance an inch to the left, and in another instance an inch to the right of the junction of the fourth or fifth rib to its cartilage ; in five cases out of forty-two this left boundary was at that junction, in eighteen it extended to the left of it, and in six it was seated to the right of it. The relation of the lower anterior edge of the upper lobe of the left lung to the apex of the heart is a point of clinical value. The septum between the upper and lower lobes is situated a little way to the left of the apex of the heart, and this portion of the upper lobe is detached as it were from the body of the lung and dips downwards and forwards, so that it may devote itself to the protection of the apex around which it is folded, being situated outside, behind and in front of, above and slightly below the apex. A small tongue of lung, the existence of which I pointed out in 1844, frequently interposes itself between the front and under surface of the apex and the walls of the chest. This tongue of lung and the adjoining 1 Or rather by a line half an inch to the left of the furrow. See note at page 379. POSITION OF THE HEART AND GREAT VESSELS. 383 structure of the lower portion of the up- per lobe play backwards and forwards with the forward and backward play of the apex of the heart. When the apex comes forward towards the ribs and spaces during the contraction of the ventricle, tlie tongue of lung retracts; when the apex retracts, the tongue of lung expands; and thus those two structures interchange with and adapt themselves to each other during the movements of the heart and the lungs. This tongue of lung that thus laps round and in front of the apex was present in two-fifths of the series of cases under observation (24 in 61), was absent in one-half of them (31 in 61), and was just indicated in the form of an inward curve in one-tenth of them (6 in 61). This tongue was strongly marked in one- third of the instances in which it existed (8 in 24), was slightly marked in another third (9 in 24), and was of intermediate form in the remaining third (7 m 24). Besides these instances, this tongue was present in eighteen additional examples in my possession : in one-half of these it was large and pronounced (9 in 18), in four of them it was of medium size, and in four it was small. During and after death the apex con- tracts in one direction, or upwards and to the right towards the centre of the heart, and the left lung retracts in another di- rection or to the left. The heart is there- fore more exposed after death than dur- ing life. This especially applies to the apex of the heart. As a rule, however, in these cases, the apex and the adjoin- ing portion of the heart are still covered to a certain extent by lung (in 34 in- stances out of 58). In two of these in- stances the lung covered the heart from the apex towards the sternum to the ex- tent of two inches and a half, but in the rest of them the extent of lung in front of the apex varied in breadth from an inch and a quarter to the tenth of an inch. In one-sixth of the cases (9 in 58) the edge of the lung was on a line with or crossed the apex, and in one-fourth of them (15 in 58) it was situated to the left of the heart, so as to expose the apex. The space thus left between the lung and the apex varied from one inch to the eighth of an inch. (Note 42.) The Breadth and Position of the Ascend- ing Aorta.-The breadth of the ascending aorta varied from half an inch to an inch and a half (1'45), its average breath being nearly one inch (*96 inch). (Note 43.) The aorta was usually narrower than the pulmonary artery (in 27 of 44 cases), but it was sometimes wider than that ves- sel (11 in 44), and in a few instances (6 in 44), the two arteries were of equal breadth. When the aorta was less than an inch in width, it was very seldom wider than the pulmonary artery (in 2 of 36 cases); but when the aorta was an inch or more in breadth, it was more often the wider of the two arteries, in the proportion of nine to eight. (Note 44.) The ascending aorta was completely covered by the sternum in nearly one-half of the cases (19 in 45), and of these in- stances, in one-third the artery was cen- tral (6), in one-third (6) it inclined to the right, and in one-third (7) it inclined to the left. In one-third of the cases (15 in 45) the ascending aorta was visible to a greater or less extent to the right of the sternum, and in six of these the exposure of the artery to the right was great, the whole artery being brought into view in one case in which there was excessive disten- sion of the abdomen. In one-fourth of the cases (11 in 45), the ascending aorta was partially visible to the left of the sternum, but in only one instance did the breadth of the portion of the artery thus exposed amount to more than the third of an inch. (Note 45.) The Position of the " Root of the Aorta,"1 including the Orifice, Valve,2 and Sinuses of the Aorta.-I possess only seven illustra- tions of the position of the root of the aorta. They, however, show the aortic valve in a variety of situations, and as the anatomical relations of the "root of the aorta" to the root of the pulmonary artery, and to the visible portion of the ascending aorta are very definite, it is easy to infer the position of the aortic valve, when we know that of the pul- monic valve, and that of the ascending aorta. * I have adopted the term ' ' root of the aorta" at the suggestion of Mr. Marshall and with the approval of Dr. Sharpey. 2 Haller, writing in Latin, correctly desig- nates the valves of the heart under the term "valvulae," derived from "valvse," folding doors, thus-"valvulse semilunares," "val- vulse mitrales," "valvulae in quas annulum venosum diviserunt." Senac (Structure du Cceur), speaking of the valves of the heart, uses the terms "valvules tricuspidales, mi- trales, et sigmoides and Douglas, in his translation of Winslow, describes the "tri- cuspid valves," the "mitral valves," and the "semilunar valves." Portal was apparently the first to speak of the auriculo-ventricular valves in the singu- lar number, under the name respectively of "valvule mitrale" and "valvule triglochine," on the ground, long previously recognized by anatomists, that the flaps of each of those valves are attached to a valvular ring. The English word "valve" has been ap- plied by engineers and in common use to the mechanism, as a whole, for preventing the back-flow of fluid, and not to one or other of the flaps composing that mechanism. I have therefore, here and elsewhere, spoken of the semilunar flaps of the aortic or pulmonic valve, and not of the semilunar valves. 384 POSITION AND FORM OF THE HEART. The ascending aorta, as it mounts up- I wards, curves first to the right and then to the left. The upper and lower ends of the curve bear to the left, and the centre of the curve bears to the right. When, therefore, the visible portion of the as- cending aorta is situated far to the left or far to the right, the sinuses and valve of the aorta are also situated far to the left or far to the right, their bearing being always more to the left than that of the ascending aorta. The lower boundary of the pulmonic orifice corresponds with the upper boundary of the aortic orifice at the junction of the anterior and the left posterior flaps of the aortic valve. Nearly one-half of the root of the pulmonary artery is situated just above the left pos- terior aortic sinus, and more than one-half of it extends to the left of the root of the i aorta. The root of the aorta extends ob- liquely downwards to the extent of about one inch below, and fully half an inch to the left of the pulmonary artery, the ex- tent being greater or less in accordance with the oblique diameter of the root of the aorta. In one instance the greater part of the anterior aortic sinus was situated behind the second left space from its upper to its lower boundary, while the remainder of the root of the aorta was covered by the left border of the sternum. In this case the ascending aorta occupied the left half or three-fifths of the sternum, the right side of that bone being occupied by the descending cava, and the pulmonic valve was situated entirely to the left of the sternum behind the second cartilage and the upper third of the second space. In another instance the right border of the right posterior sinus of the aorta was present in the third right space close to the right edge of the sternum, and the whole of the rest of the root of the aorta was covered by the right three-fifths of the sternum, its left two-fifths being occu- pied by the arterial cone of the right ven- tricle. In that case the whole heart lay moie to the right than to the left of the median line, the ascending aorta extended ^bur-fifths of an inch to the right of the right edge of the sternum, and "four-fifths of the origin of the pulmonary artery, which was on a level with the third car- tilage, was covered by the sternum. In the first of these two cases, the situ- ation of the ascending aorta, and that of the origin of the pulmonary artery were high and much to the left, and the situa- tion of the root of the aorta was corre- spondingly also high and much to the left. In the second of them, the ascending aorta and the origin of the pulmonary artery were low in situation, and were placed very far to the right; and the root of the aorta was also low in situation, and was placed very far to the right. Of the remaining five instances, in two the root of the aorta was situated for one- fifth of its breadth in the second left space, and for four-fifths of its breadth behind the sternum on a level with the second space and the third cartilage. In two other cases, the proportion of the root of the aorta behind the sternum and to the left of that bone was about the same as in the two cases just quoted; but in one of them it was situated behind the third left cartilage and the upper third of the third left space; while in the other instance it was still lower, being on a level with the lower border of the third carti- lage, the third space, and the upper bor- der of the fourth cartilage. The root of the aorta, including, as I have said, in that term the orifice, valve, and sinuses of the artery, was oblique in direction in all instances. Its longest or oblique diameter ranged from one inch to almost an inch and a'half (14); its verti- cal diameter varied from *8 inch to T05 inch ; and its transverse diameter from -8 inch to 1'2 inch. In three instances the transverse and vertical measurements were equal; in two the transverse diam- eter exceeded the vertical; and in two the vertical diameter exceeded the trans- verse. Although the observation of the actual position of the root of the aorta in health has been limited to the seven cases just examined, yet we are able to infer its proximate position by the knowledge al- ready obtained of the situation of the right edge of the ascending aorta, and of that of the origin of the pulmonary artery. The origin of the pulmonary artery was in one case as high as the upper border of the second cartilage, and in another it was as low as the upper border of the fourth cartilage. In the former case the root of the aorta must have been on a level with the second cartilage and the upper portion of the second space, while in the latter case it must have been on a level with the fourth cartilage and the up- per portion of the fourth space. The usual position of the origin of the pulmo- nary artery was behind the secomI space or the third costal cartilage, and the usual position of the root of the aorta, following in the wake of its companion great artery, must have been on a level with the third cartilage and the third space. The ave- rage situation of the root of the aorta must therefore have been on a level with the lower portion of the third cartilage and the third space. In the seven cases just examined, the right edge of the ascending aorta was situated on a line to the right of the right edge of the root of the aorta, to an extent varying from the eighth of an inch to more than half an inch. In the same instances the left edge of the ascending aorta was situated on a line to the right of the left edge of the root of the aorta, to an extent varying from one-third POSITION OF THE HEART AND GREAT VESSELS. 385 (•3 inch) to three-fifths of an inch. The ex- tent to which the ascending aorta bore to the right in relation to the root of the aorta was governed by two circumstances: (1) the degree to which the ascending aorta was situated to the right or to the left: and (2) the distension or collapse of the artery. (1) The root of the aorta was situated further to the left in relation to the ascending aorta, when the position of' the ascending aorta was far to the left than when it was far to the right. (2) Fig. 47. Anterior aspect. Superior aspect. Inferior aspect. Posterior aspect of the heart. Showing the pulmonic and aortic valves closed ; the tricuspid and mitral orifices open. Period of the diastole of the ventricles. Fig. 48. Superior aspect. Inferior aspect. Showing the pulmonic and aortic orifices open ; the tricuspid and mitral orifices shut. Period of the systole of the ventricles. The root of the aorta was further to the left in relation to the ascending aorta when the breadth of the artery was great owing to distension, than when it was small owing to collapse. In one instance, a case with great in- testinal distension, the whole of the as- cending aorta was situated to the right of the sternum, and in that instance the greater portion of the root of the aorta must have been also situated to the right of the sternum. In another instance, the ascending aorta was situated to the ex- tent of more than one-half of its breadth to the left of the sternum, and in that instance the greater portion of the root of the aorta must have been also situated to the left of the sternum. VOL. II.-25 386 POSITION AND FORM OF THE HEART. it' ore-half of the cases (19 in 45), the wie of the aorta was covered by the sternum, and in most of these the greater part of the root of the aorta must have been also covered by the sternum, but its left border must have usually passed a little to the left of that bone, being situ- ated behind one of the cartilages or spaces close to the left edge of the sternum. Under these circumstances the average or standard position of the root of the aorta must have been behind the left two- thirds or half of the sternum on a level with the third cartilage and the third space, its left border being placed behind and below that cartilage at its articulation to the sternum. (Note 4G.) The Position of the Aortic Sinuses, and the Flaps of the Aortic Valve.1-The aortic orifice looks towards the apex of the ven- tricle in a direction to the left downwards, and slightly forwards. The aspect of the orifice is therefore oblique, its obliquity being usually quite as great from above downwards, as from left to right. When the heart bears unduly to the left, the downward obliquity of the aortic orifice is greater than when it bears unduly to the right. The root of the aorta, including the aortic orifice, valve, and sinuses, projects forwards, in front of the mitral valve and the cavity of the left ventricle, so as to in- terpose itself between the orifice of the pulmonary artery above and the tricuspid orifice below. The root of the aorta thus separates those two openings from each other, the conus arteriosus being situated in front of it. When a section is made through the auricles across the base of the heart, so as to expose the four great openings of the heart, the pulmonic, the aortic, and the tricuspid orifices, viewed in their natural position, are seen to range themselves in a line from above downwards, the mitral orifice being sit- uated behind the lower half of the aortic and the upper two-thirds of the tricus- pid orifice. This line is not, however, straight, but is somewhat convex, the convexity looking backwards, so that the pulmonic and tricuspid orifices which are situated at the upper and lower portions of the line are somewhat in advance of the aortic orifice, which occupies the central position., When the line of the three orifices is looked at in front, it is seen to take an oblique direction from above downwards, and from right to left, the pulmonic orifice at the upper end of the line being situated partly behind and chiefly to the left of the left edge of the sternum at the second left cartilage and space, and the tricuspid orifice being sit- uated behind the right half of the ster- num at its lower portion. The 11 Aortic Vestibule,'1 or Intervalvu- lar Space of the Left Ventricle.-When the semilunar flaps of the aortie valve meet together so as to shut the aortic aperture, they fall backwards into a short space that I have described in my "Medical Anatomy" under the name of the "inter- valvular space in the left ventricle." I have here, however, at the suggestion of Dr. Sharpey, adopted the appropriate name of the "aortic vestibule" for this space, which is well seen in the prepara- tion from which Fig. 49 was taken, in which the semilunar flaps of the aortic valve are seen through an opening cut in the anterior flap of the mitral valve. The aortic vestibule bends forwards and to the right from the upper part of the left ven- tricle, and forms the channel between the cavity of that ventricle and its outlet at the aortic aperture. The walls of the aortic vestibule are rigid and unyielding, and it therefore retains its size during every stage of the action of the heart. These walls are muscular in front and to the left, where they are lined by rigid fibrous tissue, and where the space is sit- uated immediately behind the conus arte- riosus of the right ventricle; fibro-cartil- aginous on the right, where they are formed by the central fibro-cartilage and " fibrous septum" of the heart; and fibrous behind, where they are formed by the base of the anterior flap of the mitral valve and the adjoining wall of the left auricle, upon which the posterior sinuses of the aortic valve are implanted. The aortic vestibule occupies the centre of the heart, and is surrounded by ail the more important parts of the organ. The conus arteriosus and the orifice of the pul- monary artery are in front of it; the tri- cuspid valve and right auricle are to the right of it; and the mitral valve and left auricle are behind it. During the ven- tricular diastole, when the left ventricle is of full size, the aortic vestibule is the narrowest portion or bent neck of the ven- tricle, and it then receives the flaps of the closed aortic valve which fall back into its cavity. During the ventricular sys- tole, on the other hand, when the ventricle has completely contracted upon its con- tents so as to present an almost solid mass, the aortic vestibule moves downwardsand to the left towards the apex, and becomes the widest part of the small remaining cavity, and the presence of this space then allows the mitral valve to remain closed up to the end of the systole by the pres- sure of the blood on its anterior flap. The " aortic vestibule, " as Mr. Marshall suggests, is a short conus arteriosus, since it corresponds in relative position and function, though not in shape or size, or in the structure of its walls, to the conus arteriosus of the right ventricle, immedi- ately behind which it is situated. These 1 See Figs. 47, 48, and 49. POSITION OF THE HEART AND GREAT VESSELS. 387 two analogous parts take opposite direc- tions in relation to each other, and re- spectively to the ventricle from which they spring and the great artery to which they proceed. The right conus arterioszis as- cends with a bearing to the left, and curves backwards to end in the pulmonary artery ; while the aortic vestibule or left conus arteriosus ascends with a bearing to the right and bends forwards to terminate in the root of the aorta. Those two great arteries, following the direction of the Fig. 49. Fig. 50. Aortic valve shut, seen in the aortic vestibule of the left ventricle, which parts are exposed by cut- ting a flap in the anterior cusp of the mitral valve and pinning it backwards. Other half of the heart represented in Fig. 51, showing the mitral and tricuspid valves and the fleshy septum (d) with its continuation in the form of a "fibrous septum," which, is also seen in the companion, figure. conus arteriosus from which they respec- tively spring, cross each other in their on- ward and upward course, so that the pul- monary artery proceeds backwards to the left and then to the right, while the as- cending aorta proceeds forwards to the right and then to the left. If the two cavities be looked at as a combined whole, each with its ventricle, its conus arteriosus, and its great artery, they resemble some- what the curious double oil and vinegar fiask that is met with so commonly in the most beautiful parts of South Germany. The central fibro-cartilage and " tendi- nous septum'1'1 of the heart form, as I have just said, the right wall of the aortic ves- tibule. The fleshy septum terminates at its base in a strong tendinous aponeurosis or fibro-cartilage, which forms a part of great importance in the structure of the heart, and which is well seen in the prep- aration from which Figs. 49 and 50 have been taken. The muscular septum (d) is, in fact, converted at this region into a fibrous septum; but while the muscular septum separates the two ventricles, the fibrous septum separates the left ventricle from the right auricle as well as from the top of the right ventricle. Higher up this fibrous septum is converted into the cen- tral fibro-cartilage, which corresponds to the central fibro-cartilage and bone of the heart of the ox (Fig. 52), and which is converted into bone in a human heart in my possession. The central fibro-car- tilage, as may be seen in Fig. 48, forms a firm bond of connection between the ten- dinous rings of the mitral and tricuspid orifices, the central or inner angles of the mitral and tricuspid valves, the right pos- terior sinus of the aorta, and the aortic vestibule. It also gives insertion to mus- cular fibres from the left and the right ventricles (Fig. 51 A), which, sweeping round from the left and the right respec- tively, blend together toward the base of the posterior longitudinal furrow, so as to form short central bands of fibres, which dip forwards at right angles to the circu- lar fibres, deepening as they advance, 388 POSITION AND FORM OF THE HEART. enter and go to form the septum and end in the central fibro-cartilage, which gives origin to numerous muscular fibres, to the inter-auricular septum, and the right and left auricles. During the ventricular sys- tole the central fibro-cartilage, and with it the aortic vestibule and all the adjacent parts, are drawn downwards and to the wards, forwards, and to the right of the orifice of the aorta, the right posterior flap of the aortic valve is much lower in position than the other flaps. Thus the lower boundary of that flap was in two instances half an inch lower than the lower boundary of either of the other flaps. In another example, in which the aorta was far to the right, the lower edge of the right posterior cusp was only a quarter of an inch lower than that of the left posterior cusp, but it was half an inch lower than the lower edge of the anterior cusp. The root of the aorta is buried in the centre of the heart, and is therefore en- circled by all the cavities of the heart and the two other great vessels. The cres- centic edge of the anterior sinus is at- tached throughout to the central fibro- cartilage which forms the summit of the interventricular septum. The anterior sinus is covered in front by the conus arte- riosus and, higher up, on the right side, to a varying extent, by the auricular portion of the right auricle, and on the left side by the pulmonary artery. The left and right halves respectively of the right and left posterior flaps of the aortic valve are attached at their junction, and along their lower border to the ante- rior cusp of the mitral valve, and to the aponeurosis that is continuous with that cusp. At this situation the two posterior sinuses of the aorta are in front of the left auricle. (Figs. 49 and 50.) The left half of the left posterior sinus is attached at its root to the muscular base of the left ventricle, and is covered, going from right to left, first by the auric- ular portion of the right auricle, and then by the inner or right wall of the pulmon- ary artery. The junction of the anterior to the left posterior flap of the aortic valve is usually a little in front of the junction of the posterior and the left ante- rior flaps of the pulmonary artery, so that a pin thrust through that artery at the junction of the flaps in question "into the aorta, appears about the tenth of an inch behind the junction of those aortic flaps ; but in one instance the pin, thus inserted, pierced through the junction of the aortic flaps as well as through that of the pul- monic flaps. The left or posterior coron- ary artery at its origin is, in one of my preparations, -25 inch from the left edge of the left posterior cusp, and -4 inch from its right edge, and I believe it will be found that this represents the usual posi- tion of the origin of the artery. The relations of the right posterior sinus of the aorta are of remarkable extent and importance. The centre and right side of the root of that sinus is firmly at- tached to or incorporated with the central fibro-cartilage and fibrous septum of the heart that crown the interventricular Fig. 51. Showing the muscular fibres unravelled of the left and right ventricles, b, Fibres from the left and right ventricles ^oing to the central fibro-cartilage of the heart, and forming a portion of the septum. left towards the apex by the contraction of the ventricular fibres inserted into the tendinous ring and especially into the central fibro-cartilage, which thus becomes the focus and movable pivot of the heart, which binds together all those important parts and gives to them a common move- ment. The setting of the orifice of the aorta is muscular anteriorly and to the left, and fibrous posteriorly and to the right. The muscular setting is made by the anterior half of the base of the left ventricle, and the fibrous setting by the anterior cusp of the mitral valve and its continuation to- wards the left auricle, and by the central fibro-cartilage. During the diastole the anterior cusp of the mitral valve divides the ventricle into two portions, each with its own aperture, an anterior or aortic portion, out of which the blood pours during the systole through the aortic ori- fice, and a posterior or mitral portion, into which the blood flows during the diastole through the mitral orifice. There is one anterior, and there are two posterior and lateral aortic sinuses. The right or anterior coronary artery springs from the anterior sinus, and the left or posterior coronary artery from the left posterior sinus. The right posterior sinus is sometimes called the intercoronary sinus. Owing to the obliquity down- POSITION OF THE HEART AND GREAT VESSELS. 389 septum. To the left of this attachment to the fibro-cartilage, the right aortic sinus is united, as we have just seen, to the anterior cusp of the mitral valve, and it is seated in front of the left auricle. To the right and in front of this attach- ment, it is closely connected with the inner or left angle of the tricuspid valve. The right wall of the right posterior sinus, as it advances to join the right edge of the anterior sinus, is covered first by the inner or left wall of the right auricle, and finally by the inner or posterior wall of the arte- rial cone of the right ventricle. This right aortic sinus is thus closely connected with every important part of the heart, except the pulmonary artery. The right and left ventricle, the right and left auricle, -the mitral and tricuspid valves are all of them attached to or in contact with it: and the central fibro- cartilage of the heart, as we have seen, with which the base of this sinus is incor- porated acts as a tie that binds together the allied movements of those parts.1 The descending vena cava also comes into contact with the upper portion of this sinus. Mr. Thurnam brought into notice, thirty-three years ago, the extensive and important bearings of the sinuses of the aorta, in especial relation to aneurism of those parts. It is customary for authors on anatomy, following the original error of the great Valsalva, unfortunately repeated by Mr. Thurnam, and more recently by that great anatomist, Henle, to describe the aortic sinuses as being two of them ante- rior, and one posterior. I have examined the heart in situ in many bodies, with re- gard to this point, and I have always found those sinuses and the corresponding flaps of the aortic valve in the position I have described, one being anterior, and two posterior. A little consideration as to the known relation of these sinuses to other parts, the position of which is well ascertained and admitted, will show that two of these sinuses are posterior and lateral, and that only one of them is an- terior. The right and left posterior flaps of the aortic valve are attached in about an equal degree to the anterior mitral cusp, as is shown in drawings and many hearts now around me, and in Dr. John Reid's figure.2 The anterior cusp of the mitral valve is on a level with the posterior wall of the root of the aorta, and it is therefore impossible that either of the aortic sinuses that are attached to that flap can be situ- ated at the anterior aspect of the aorta ; they must, indeed, both be posterior in position. Again, while the right or ante- rior coronary artery arises from the an- terior aortic sinus, the left or posterior coronary artery arises from the left poste- rior sinus; and while the right artery advances to the right of the pulmonary artery, the left artery passes to the left be- hind the pulmonary artery. Further, the origin of the left coronary artery is nearer to the left or anterior and lateral edge than to the right or posterior edge of the left posterior sinus. I might adduce other points in illustration of what I have advanced, but these facts, which speak for themselves, are sufficient.1 1 Valsalva's original drawing (V. Opera, tab. ii. fig. 1; see Fig. a), in which the anterior and left posterior sinuses with their respect- ive coronary arteries are represented in front of the root of the aorta, gives not a front but a side view of the aortic arch. The artery from which this drawing was taken shows the cut end of the vessel, and has evidently been removed from the body and placed upon its right side. The effect of this position would be to place the anterior and left pos- terior sinuses, each with its coronary artery, on the same anterior plane. Fig. b is a re- duced copy of a similar drawing of the arch of the aorta after its removal from the body, given by Lower (Tractatus de Corde, tab. i. fig. 4) in which the two coronary arteries, as in Valsalva's drawing, spring from the front of the root of the aorta. Nearly all the drawings of the root of the aorta that have been taken from the actual body, the artery being in situ (reduced copies of several of which drawings are given be- low), represent the sinuses in the position that I have described, two of them being pos- terior in situation and one anterior, and the right posterior sinus being the lowest of the three sinuses. I find it thus in Tiedemann's "Tabula Arteriarum," plate xix. (fig. e) ; John Bell's "Anatomy," vol. ii. p. 283 (fig. f); Charles Bell's Engravings of the Arteries, tab. ii. (fig. g) ; Mr. Quain's "Anatomy of the Arteries," anterior view, fig. 3, and pos- terior view, fig. 4, plate xlviii. (figs, h i) ; Pirogoff's " Anatomia Topographica," in eleven different views (figs, k l m n) ; and Braun's " Topographisch-Anatomisch Atlas" (figs, o p). Henle, in a much reduced figure of the aorta in situ, represents one anterior and two posterior sinuses (fig. q), but he gives a series of drawings of the heart and aorta after their removal from the body (one of which I have given on a reduced scale, fig. d) , in all of which the sinuses are represented and described as being two anterior and one posterior. Anatomists, including Morgagni and Senac in former times, and, as I have said above, the respected names of Thurnam and Henle in our own day, have as a rule described two of the sinuses of Valsalva and their corre- sponding coronary arteries as being anterior, and one of them, or that which is destitute of a coronary artery, as being posterior. On the other hand, Vesalius and P. Syl- 1 See Fig. 50. 2 " Cyclopaedia of Anatomy," vol. i. p. 588. See also Figs. 47, 48, and 49. 390 POSITION AND FORM OF THE HEART. The error has, I believe, arisen and been perpetuated from the custom of ex- amining these sinuses, not when the heart is in situ, but after it has been removed from the body. If the right ventricle with its arterial cone, and the ventricular septum are carefully removed without disturbing the position of the heart, and vius described the left coronary artery as arising from behind the posterior valve. Some authors give contradictory descriptions of the origin of the coronary arteries. Thus, Wins- low in one passage says that there are two coronary arteries, ' ' one of which is situated anteriorly, the other posteriorly" (vol. ii. p. 3); while elsewhere (p. 221) he says that "one of the vessels lies towards the right hand, the other towards the left, of the anterior third part of the circumference of the aorta." Portal ("Anatomie Medicale," vol. iii. p. 152) says that the left coronary artery arises from the left posterior portion of the aorta; but else- where (p. 51) he states that two of the valves are anterior and lateral and the third is pos- terior, and that the right and left coronary arteries are situated above the two anterior valves. The accurate Haller, " Element a Physio- logiae," iii. 345, speaking of the aortic valve, says: "Situs alequantum differ t, duae enim superior! loco ponuntur, altera anterior, pos- terior altera ; tertia inferior est. Earum ese, quae superiori loco ponuntur, sodales habent arterias coronarias, inferior nullum aortae ramum vicinum habet." Here that great anatomist has given a correct description of POSITION OF THE HEART AND GREAT VESSELS. 391 without injuring the anterior wall of the aorta at its origin, the true position of the aortic sinuses and of the flaps of the aortic valve may be readily observed. The right and left posterior aortic si- nuses advance forwards on either side, and finally curve gently inwards and forwards to complete the circle of the aorta by uniting at either end with the anterior sinus. The anterior portion of the left posterior sinus is concealed by the pul- monary artery, while the anterior portion of the right posterior sinus is readily ex- posed by pressing aside the auricular appendix. It is rather difficult to say which of the two posterior sinuses comes forward to the greater extent at their points of attachment to the anterior sinus; I think, however, that the right posterior sinus, which usually goes by the name of the posterior sinus, comes forward to a greater extent than the left posterior sinus, which usually goes by the name of the left anterior sinus. (Note 46.) The Position of the Mitral Valve.-In seven instances the size and position of the mitral valve are given, and in three of them accurate details of its structure are represented. These points are further illustrated by preparations and dissec- tions. (Note 46.) The setting of the mitral orifice is mus- cular in its two posterior thirds, and fibrous in its anterior third. In these re- spects the mitral and aortic orifices bal- ance each other. The setting of the mitral orifice is muscular behind, while that of the aortic orifice is muscular in front, the two openings being sepa- rated by the interposed anterior flap of the mitral valve and its short fibrous con- tinuation to the two posterior aortic si- nuses, and by the central fibro-cartilage of the heart. When the heart is boiled for a sufficient length of time this inter- posed fibrous partition softens and sepa- rates from its attachments, and the aortic and mitral apertures are thrown into one large irregular opening (see Fig. 52). The base of the ventricles then presents not four but three great apertures, the tricus- pid, the pulmonic, and the mitral-aortic. The apparatus of the mitral valve occu- pies the whole of the posterior part of the left ventricle, and when its anterior walls are removed, the whole of this apparatus is brought into view. The anterior cusp or flap of the mitral valve is alone visible in one of the three drawings giving the anatomical details of the valve, while in the two others the lower border of the posterior cusp is likewise brought into view. Fig. 52. Calf's heart boiled, showing the aortic (c) and mi- tral (d) orifices thrown into one by the removal of the mitral valve, the lower A being the central fibro-car- tilage, e the tricuspid orifice, and f the orifice of the pulmonary artery. The whole apparatus of the valve takes an oblique direction from right to left and downwards. The right end or base of the apparatus of the valve corresponds with Fig. 53. the situation of the flaps of the aortic valve and of the origin of the coronary arteries. In our own day, Pirogoff and Mr. Heath describe the sinuses as being one of them anterior and two of them posterior. Bourgery (fig. c) curiously figures the coronary arteries and their sinuses as being both anterior ; but he describes the anterior coronary artery as arising from the anterior sinus, and the pos- terior coronary artery from the posterior sinus. Showing the mitral orifice, the anterior flap of the mitral valve, and the right and left posterior flaps of the aortic valve. Diastole of the ventricles. the junction of the left auricle with the left ventricle, and its left end corresponds with the interior of the apex of the left 392 POSITION AND FORM OF THE HEART. ventricle. The apparatus of the valve thus forms a long triangle, its base being at the base of the ventricle, its apex at the apex of the ventricle, its upper side being slightly curved upwards or outwards, cords to the flaps, form the three compo- nent parts of the valve. (Figs. 53, 56, 57, 58, and "Medical Anatomy," Plate VI.) The convex base of the anterior flap of the mitral valve is attached on the one hand to the junction of the left ventricle to the left auricle, and on the other to the roots of the right and left posterior flaps of the aortic valve. This attachment of the mitral to the aortic valve is effected through the fibrous structure that extends from the base of one valve to the base of the other, and by the central fibro-cartil- age of the heart, which forms a triple bond of connection that ties the mitral, the aortic, and the tricuspid valves to each other. (Fig. 48.) When the mitral valve is shut, the an- terior flap of the valve presents a convex edge, shaped like a horseshoe, which falls back upon and fits like a lid into the pos- terior flap of the valve, which flap, being crescentic in shape, presents a concave edge.1 Each flap adapts itself to the other by a notched lip, made up of small hemispherical eminences. The eminences of one lip fill up the notches of the other lip. These eminences, thus seen on the auricular surface of the valve, are cells Fig. 54. Systole of the left ventricle. and its lower side being slightly bent in- wards or upwards at its middle. The flaps, the tendinous cords, and the papil- lary muscles, which are connected by the Fig. 55. Fig. 56. Mitral valve shut; auricular surface; anterior or convex and posterior or crescentic flaps; ventricular systole. Mitral valve shut; ventricular surface; anterior flap, with tendinous cords and papillary muscles ; two posterior flaps of aortic valve; ventricular sys- tole. when seen on its ventricular surface, and as these cells are distended with blood when the ventricle contracts, and are ex- actly maintained in their places by the tendinous cords and papillary muscles, the distended cells or eminences at the oppo- site lips of the valve adapt themselves to and press against each other during the systole, so as to shut the valve. (Figs. 48, 55, 56, 58.) The anterior flap is simple, and when closed is shaped like a three-quarters moon. The posterior flap is compound, and when closed is shaped like a quarter or crescent-shaped moon. The compound posterior flap is usually made up of one central and two lateral sub-segments, the latter being sometimes subdivided. These sub-segments adapt themselves so to each other, that the concavity of the crescentic border of the posterior compound-flap is preserved entire ; for it would have been impossible, by means of one simple fold of membrane, to fill up without a break the whole of the crescentic border. I need scarcely give a description of the arrangement of the tendinous cords in relation to the flaps of the valve, and of 1 Figs. 48, 55. POSITION OF THE HEART AND GREAT VESSELS. 393 the papillary muscles in relation to the cords and the flaps. It will be sufficient if I here say that they are so arranged that when the muscular walls of the ventricle contract, the papillary muscles, which are really semi-detached portions of those walls, also contract with equal steps ; that as the walls, shorten so as to approximate the base and the apex by a double move- ment to each other, the papillary muscles shorten to an exactly parallel degree ; and that thus while they hold the flaps of the valve, through the medium of the cords, in apposition, they steadily draw the whole valve towards the apex, and the apex towards the valve, to exactly the same extent that the base and apex of the ventricle are drawn towards each other. The mechanical arrangements are complicated, for there are many parts to be adjusted to each other ; but the prin- ciple on which those parts are adjusted to each other is simple, for it is by one sin- gle contraction of the whole single muscle of the left ventricle, made up in its com- ponent parts of walls, columns, and papil- lary muscles, that the base of the ven- tricle (including the mitral aperture and valve and the aortic aperture and valve) and the apex of the ventricle are approxi- mated steadily to each other during the systole. When the convex anterior flap of the mitral valve falls back upon and fills up Fig. 57. Fig. 58, Diagram of the shut mitral valve, with the anterior cusp A A in close contact with the posterior cusp (&, b). The tendinous cords and papillary muscles are shown, the direction of the current and pressure of the blood being indicated by arrows. Mitral valve shut; posterior flap, with tendinous cords and papillary muscles. the concave posterior flap of the valve, the anterior flap and its membranous con- tinuation to the left and right posterior aortic flaps form a smooth scooped channel or hollow, along which the blood flows noiselessly from the ventricle into the aorta during the systole. (Fig. 53.) The mitral orifice extends downwards, with an inclination to the left, immedi- ately behind and below the aortic orifice ; and, like that orifice, it looks towards the apex of the left ventricle, or to the left, downwards and slightly forwards. The line of direction of the mitral orifice, viewed from the front, is therefore from above downwards, with a slight obliquity from left to right. The upper and left boundary of the mitral orifice is about half an inch above the level of the lower edge of the right posterior flap of the aortic valve. The lower border of the mitral orifice is about three-quarters of an inch below the lower border of the aortic orifice. The upper or left edge of the mitral orifice is not so far to the left, while its lower or right edge is about as far to the right, as are the left and right edges respectively of the aortic orifice. The mitral orifice is situated deep behind the sternum, a little below the middle of that bone. Its upper or left boundary, in four instances, was on a level with the third cartilage, just within the left edge of the sternum ; and its lower or right boundary was on a level with the fourth cartilage, behind a line drawn down the middle of the sternum. This is probably higher than the average position of the mitral orifice after death. In one other case the top of the mitral orifice was on a level with the lower border of the second space, its situation otherwise correspond- ing to that in the cases just described. In two other instances, the mitral orifice was comparatively low and was situated unusually to the right, its upper border being on a level with the lower edge of the third cartilage or upper border of the fourth space, behind the middle line of the sternum, and its lower or right border being on a level with the lower portion of the fourth space, or the top of the fifth cartilage behind the right edge of the sternum. As a rule, the mitral orifice occupied a space behind the left half of the sternum, extending down- wards for more than one inch below the middle of the bone; but in occasional 394 POSITION AND FOKM OF THE HEART. cases it wTas present behind the right half of the bone. The tendinous cords and papillary muscles of the mitral valve, as they ex- tended to the left with an inclination downwards, retained, as a rule, their situation behind the space or cartilage that was on a level with their starting- point from the valve. Thus in the four instances in which the upper rim of the orifice was on a level with the third cartilage, the upper or left cords lay behind the third left cartilage, and the upper or left papillary muscle behind the third space ; and in the same instances the lower rim of the orifice was in two of them on a level with the third space, and in two of them on a level with the fourth cartilage ; and in these two sets of cases the lower or right cords and papillary muscle lay respectively behind the third space and the fourth cartilage, wfith a final dip to the space or cartilage below. In the other cases in which the position of the upper and lower edges of the mitral orifice were higher or lower in relation to the spaces and cartilages than in those just quoted, the upper and lower cords and muscles retained their bearing throughout in relation to the space or car- tilage on the level of which they started, until they also usually made a final dip so as to occupy a relatively lower position. In two of the instances there was a space of half an inch between the right and left papillary muscles, the width of the interior of the ventricle being an inch and a half; and in the other instance, in which the systole of the ventricle was more pronounced, the space between the muscles was the fifth of an inch, the width of the cavity being a little over an inch (1'2 inch). In one instance, in which the heart and all its parts lay unduly to the right, and in which the flaps, cords and muscles of the valve took a very oblique direction downwards, the right papillary muscle was situated behind the left border of the sternum and the sternal half of the fifth cartilage, and the left papillary muscle crossed the third cartilage and space mid- way between the sternum and the junc- tion of the cartilages to their ribs. This instance was throughout excep- tional in the position of the heart and all its parts, and the great vessels; but the other instances offer fair average exam- ples of the position of the mitral valve. I need not, therefore, further analyze addi- tional cases. It is sufficient to bear in mind that when the origin of the pul- monary artery is high or low in position, the aortic and mitral valves are also cor- respondingly high or low in position ; and that when the ascending aorta and the origin of the pulmonary artery are far to the right or far to the left of their usual situation, the aortic and mitral valves are also correspondingly far to the right or far to the left of their usual situation. The Tricuspid Valve.-The apparatus of the mitral valve occupies the whole of the posterior part of the left ventricle, but the apparatus of the tricuspid valve fills up the whole body of the right ventricle, the narrowing conus arteriosus being the only portion of the ventricle unoccupied by it. (Note 46.) The reason for this diffusion of the ap- paratus of the tricuspid valve and this concentration of that of the mitral valve is obvious. It depends on the form of the two ventricles and the relation to each other of their apertures of ingress and egress. The left ventricle is the central cavity of the heart, and is flask-shaped ; and its walls on a transverse section are shaped like a ring, and surround a circular space, the mitral valve being behind (see Fig.49). The right ventricle is applied upon the anterior and inferior walls of the left ven- tricle, which project into the cavity of the right ventricle and form its inner or pos- terior wall. The right ventricle on a transverse section is crescent-shaped, its inner w7all being convex, while the inner aspect of its outer wall is concave or an- gular, for it presents at its lower border and outer aspect a projecting angle. The whole cavity of the right ventricle looked at in front is triangular in form, the base of the triangle resting on the central ten- don of the diaphragm, its apex pointing to the top of the pulmonary artery, its right side being formed by the junction of the right auricle to the right ventricle and by the tricuspid orifice, and its left side by the septum between the ventricles. The three cusps of the tricuspid valve are visible when the cavity is opened, the anterior and inferior flaps being com- pletely exposed while the posterior flap is partially concealed (Figs. 59, 60, 61). The whole apparatus of the tricuspid valve, like that of the mitral valve, takes a direction from right to left; but while the apparatus of the mitral valve concen- trates itself as it recedes from the flaps, the papillary muscles pointing towards the apex, and the whole structure form- ing a long triangle, the apparatus of the tricuspid valve spreads itself out as it recedes from the flaps, like the rays of a fan. The anterior flap gives attachment at its upper edge to a group of cords which converge upon the small superior papillary muscle, which is incorporated with the posterior wall of the cavity at the lower portion of the arterial cone. The cords from the lower edge of the anterior flap con- verge upon the anterior papillary muscle, which muscle also sends a radiating series POSITION OF THE HEART AND GREAT VESSELS. 395 of cords that attach themselves to the upper and anterior edge of the lower flap of the valve. The anterior papillary muscle is not immediately connected either with the front or the back wall of the ventricle, but is attached intermedi- ately to both of them by fleshy columns. A strong and rather long column curves Fig. 59. Showing the tricuspid valve open, during the complete dilatation (diastole) of the right ventricle. Figs. 59, 60, and 61 are views of the interior of the right ventricle and of a portion of the left ventricle: A, anterior flap ; b, posterior flap ; c, inferior flap ; and d, one of the long sub-segments of the inferior flap of the tricuspid valve. F, anterior papillary muscle ; G, superior papillary muscle ; h h, inferior papillary muscles ; n, sub-segment occupying the angle between the anterior and posterior flaps of the valve ; o, conus arteriosus ; p, pulmonary artery ; r, upper or left papillary muscle, and B, lower or right papillary muscle belonging to the left ventricle and mitral valve. backwards to be attached by outspreading roots to the posterior wall of the ventricle near the septum ; while an interlacement of shorter and thinner columns advances forward and to the left, extending from the base of the anterior papillary muscle to the anterior wall of the ventricle, also near the septum (Fig. 59). Thus the roots of the anterior papillary muscle spread both backwards and forwards, the base of the muscle being, however, nearer to the front than the back of the ventricle. By this beautiful arrangement a purchase is given for this muscle to act upon the centre of the valve from the middle of the cavity. The inferior flap of the valve is not formed, like the anterior flap, of one sheet of membrane, but is a compound flap, which is subdivided into four or five sub- segments, two of which are longer than the rest, which, by meeting together and adapting themselves to each other, fill up the large rounded space of the tricuspid orifice, at its inferior portion. The cords from these sub-segments converge upon a series of papillary muscles that are con- veniently situated around the lower por- tion of the ventricle, some, or one, being seated in front, some below, and some be- hind. The inferior papillary muscles are attached, like the anterior papillary mus- cle, not immediately to the walls of the ventricle, but intermediately by interlacing fleshy columns. The posterior papillary muscles of this group, which are thus con- nected with the inferior flap of the tri- cuspid valve, are immediately attached to the inner or convex wall of the ventricle. The posterior flap is attached behind by a series of radiating cords to the inner walls of the ventricle, sometimes by 396 POSITION AND FORM OF THE HEART. means of small papillary muscles, some- times by the immediate insertion of the cords into the walls. The upper portion of the tricuspid ori- fice is narrow and angular, while its lower portion is wide and circular; and thus, Fig. 60. Showing the tricuspid valve shut during the early period of the contraction of the right ventricle. therefore, the simple anterior and poste- rior flaps, with the intervention of one anterior and one superior sub-segment, fill up the upper and narrow part of the orifice; while the inferior and compound sub-segments adapt themselves to the Fig. 61. Showing the tricuspid valve shut during the period of the complete contraction of the right ventricle, large and rounded inferior portion of the orifice. (See fig. 48, p. 385.) The whole of these segments of the valve meet together at the centre of the orifice, and hence arises the necessity for an array of papillary muscles, the points of which converge towards the centre of the valve, and that are attached at their POSITION OF THE HEART AND GREAT VESSELS. 397 roots by fleshy columns that connect them with both the outer and the inner walls of the ventricle. The tricuspid orifice is situated behind the lower portion of the sternum and in front of the mitral orifice and the left ven- tricle. The direction of the tricuspid ori- fice is from above downwards with a slight inclination from left to right. The upper boundary of the tricuspid orifice is immediately below the orifice of the aorta, and in front of the mitral valve. The four great orifices of the heart-the pulmonic, the aortic, the mitral, and the tricuspid-are situated in that order, one above another, the pulmonic orifice being the highest and the tricuspid the lowest. The lower portion of each of the first three orifices is lower than the upper portion of the orifice below it. Thus the pulmonic orifice, when looked at in front, covers the upper part of the orifice of the aorta on its left side ; the lower border of the aortic orifice is lower than the upper border of the mitral orifice; and in like manner, the lower two-thirds, or three-fifths, of the mitral orifice lie behind the upper half of the tricuspid orifice, the lower half of which is below the level of the lower edge of the mitral valve. The posterior aspect of the tricuspid orifice is attached to the anterior wall of the left ventricle, not on a level with the mitral orifice, but about half an inch nearer to the apex. The wall to which it is thus attached is convex, and the poste- rior surface of the tricuspid valve wThere it fits upon the left ventricle is therefore concave. The shape of the tricuspid ori- fice is, in consequence, angular above, concave behind, convex in front, and rounded and broad below. The tricuspid orifice thus maintains the crescentic form of the cavity of the right ventricle when a cross section is made through its walls. In five of the cases, the upper and left boundary of the tricuspid valve was situ- ated about the third of an inch to the left, and its lower and right boundary about a third of an inch to the right of a line drawn down the middle of the sternum. In two instances the lower and right boundary of the tricuspid valve extended to the right of the right edge of the ster- num. The right transverse or auriculo-ven- tricular furrow which corresponds with the right edge of the right ventricle, as I have already remarked, is situated about half an inch to the right of the right edge of the tricuspid valve, and when therefore we know the position of the furrow, we can infer the position of the right edge of the valve. As we already seen (page 381) the transverse furrow was situated to the right of the right edge of the sternum in nearly three-fourths of the cases (36 in 51), at that edge in three of them, and to the left of that edge, behind the right half of the sternum, in one-fourth of them (12 in 51); and it extended in one instance for an inch and a third to the right of the right edge, and was situated in five in- stances behind the middle line of the ster- num. The transverse furrow occupied every variety of position between these two extreme points. We may therefore infer that the right border of the tricuspid valve occupied every range of position between a line three-quarters of an inch to the right of the right edge of the lower portion of the sternum, and a line half an inch to the left of its middle line ; the average situation of the right border of the valve being behind the right edge of the sternum. In like manner we can infer approxi- mately the position of the lower border of the tricuspid valve if we know the posi- tion of the lower boundary of the right ventricle. We have already seen that the lower boundary of the right ventricle varied in situation from an inch and a half below, to an inch and a half (1'4 inch) above, the lower end of the sternum. The lower border of the tricuspid valve is from half an inch to nearly an inch above the level of the lower boundary of the right ventricle, and we may therefore infer that the lower border of the valve varies in position from a point nearly two inches above, to a point three-quarters of an inch below the lower end of the ster- num. The top of the tricuspid orifice and valve was situated on a level with the third cartilage in three cases, with the third space in one, and with the fourth cartilage in two; its lower edge being in those cases on a level respectively with the fourth cartilage, the fourth space, and the fifth cartilage. In each of those cases the upper edge of the tricuspid orifice and valve was lower, and its lower edge was much lower than the corresponding edges of the mitral orifice and valve. The tendinous cords and papillary mus- cles of the tricuspid valve, as they radiated to the left, slightly upwards, downwards and outwards, retained, as a rule, their situation behind the space or cartilage that was on a level with their starting- point from the valve. Thus, the inferior cords and muscles maintained their rela- tive position throughout, behind the fourth space or fifth cartilage, w'hich was on a level with the lower edge of the tri- cuspid valve, while the anterior group of cords and the anterior papillary muscles lay behind the fourth cartilage or the fourth space. The upper group of cords retained its relation to the third cartilage or space, or the fourth cartilage, on a level with which the upper edge of the valve was situated, but the superior papillary muscle radiated upwards to a somewhat 398 POSITION AND FORM OF THE HEART. higher relative position than that from which it started, so that, as, for instance, in two cases, the top of the valve being on a level with the third or fourth car- tilage, the superior papillary muscle was behind, respectively, the second or third space. In the remaining instance, that in which the heart was placed to an unusual extent to the right, the flaps of the valve were situated behind and to the right of the right portion of the sternum, the valve extending from the level of the upper edge of the fourth cartilage to that of the lower edge of the fifth. The tendinous cords, and the papillary muscles took an oblique direction downwards, and they were seated almost entirely behind the right half of the sternum. The position of the tricuspid valve cor- responds with the position of the right ventricle, the valve occupying about the lower two-thirds of the cavity. The Relation oe tiie Lungs to the Heart. The extent to which the lungs covered the heart varied much in different exam- ples. In two instances the heart was almost concealed by the lungs, the edges of which were separated over the lower portion of the right ventricle by a mere chink, which widened out to three-quar- ters of an inch at the inferior border of the heart. In other instances the lungs had receded from before the heart to such an extent that almost the whole organ and the great vessels were exposed to view, though in no instance were they entirely uncovered. The space where the heart comes to the surface, which is bounded above and at the sides by the lungs, and below by the liver and stomach, was sometimes trian- gular in shape (in 10 of 60 cases), but was usually four-sided (50 in 60). The superficial "cardiac space" was triangular in shape in the two instances just noticed in which that space was very small, the width at the lower boundary of the heart being three-quarters of an inch ; and in an instance of an opposite kind in which the base of the triangle, which always corresponded with the lower boundary of the heart, was four and a half inches wide. In this instance the lower boundary or base of the superficial space of the heart was wider than in any other. The base of the triangular super- ficial cardiac space presented every inter- mediate gradation of breadth between the extreme instances just noticed. This tri- angular shape is favorable to the covering of every part of the heart with lung except the right ventricle, for, while the anterior wall of the right ventricle was laid bare to a greater or less extent in these cases, as it was in every case under observation, in but one of them was the apex of the heart exposed, while in only two of them the right auricle, the aorta and pulmonary artery were also somewhat uncovered. The superficial cardiac space was in all these cases actually triangular in shape, the lower limit or base of the triangle being the lower border of the heart. If, however, the lower boundary of the heart had occupied a lower position in relation to the adjoining margins and the lower boundaries of the lungs, then that space would have been four-sided in shape in the majority of these instances (6 in 10); for in them the inner border of the left lung, after it had left the heart, curved in a downward direction. If, therefore, the heart had not shrunk upwards in these instances, the superficial cardiac space would, like the other cases, have been four-sided in shape. When, as is usually the case, the super- ficial space of the heart is bounded by four sides,1 the heart, which moulds for itself a place between and within the lungs, comes forward to the surface at that part where the organ is massive and its walls are powerful. The inner edge of the right lung descends in a straight line behind the sternum, but the edge of the left lung leaves the right lung, and deviates to the left at a variable point. This deviating edge of the upper lobe of the left lung, which is suspended like a curtain above the upper margin of the superficial space of the heart, describes a double curve, first convex, where it leaves the right lung, and then concave, where it begins to dip downwards to form the outer edge of the space. It then, as I have already observed, again tends to curve in- wards, and to form the tongue of lung that enfolds the apex of the heart. The breadth of the cardiac space, measured along its base at the lower boundary of the heart, varied from an inch and a half to four inches and a third (4'3 inch). The breadth of the lower boundary of the superficial cardiac space varied in three- fourths of the cases (37 in 50) from two to four inches; it was less than two inches in one-fifth of them (9 in 50), two-thirds of these being youthful, and it was above four inches in four of them. The superficial cardiac space was, as a rule, narrower at its upper than at its lower boundary (in 35 of 50 cases); but 1 I have grouped the remainder of the cases, amounting to fifty, under the common heading of those in which the superficial space of the heart was bounded by four sides, but in seven of these cases the space was al- most triangular in shape, and in a few other instances irregularity in outline modified the typical four-sided form of the space. THE RELATION OF THE LUNGS TO THE HEART. 399 sometimes this was reversed, the space being narrower below than above (in 10 of 50 cases). In a few instances (5) the space was of equal breadth above and be- low. The lower boundary of the superficial cardiac space measured less than three inches in all but one of those instances in which it was narrower than the upper boundary of that space. The inner borders of the right and left lungs were in contact with each other be- hind the upper portion of the sternum so as to cover the great vessels in three-fifths of the cases under examination (in 35 of 59). In the remaining two-fifths of the cases (24 in 59) a space varying in width from the eighth of an inch to an inch and a half was interposed between the inner borders of the right and left lungs at the upper part of the front of the chest. In one-third of these instances (7 in 24) the space between the edges of the lungs was less than the third of an inch, so that, practically, these cases may be added to those in which the edges of the lung were in contact, which brings up their propor- tion to three-fourths of the total number of cases observed (42 in 59). The point of separation and divergence of the left and right lungs in these cases, including those in which the lungs were nearly in contact, varied from the level of the first intercostal space to that of the fifth cartilage. In three-fourths of the cases this point of separation varied in position from the level of the second space to that of the fourth cartilage. In the seventeen cases in which the lungs were separated from each other over the great vessels to an extent ranging from almost half an inch to an inch and a half, the position of the point of diverg- ence of the right and left lungs varied from the level of the first cart ilages to that of the third, the level of the second car- tilages and second spaces being the more usual situation of the point of divergence in this group of cases. There was much variation in the rela- tive size of the right and left lungs. The two lungs were about of equal size in more than one-fourth of the cases (17 in 59), the right lung was larger than the left in nearly one-half of them (27 in 59), and the left lung was larger than the right in one-fourth of them (15 in 59). Although the right lung was so often larger than the left, yet the base of the left lung, was lower at the side than that of the right lung three times more often than the reverse, the bases of the two lungs being on the same level in one- fourth of the cases (14 in 57). When the right and left lungs met to- gether behind the upper half of the ster- num to form a covering over the great vessels, the margin of the right lung ex- tended to the left of a line drawn down the middle of the bone more often than that of the left lung extended to the right of that line in the proportion of 35 to 15, while in nine instances the edges of the two lungs lay in contact behind the mid- dle line of the sternum. Below the point of separation of the two lungs, while the left lung deviated, as we have seen, extensively to the left, the right lung usually (in 42 of 60 cases) de- viated at first very slightly and then more definitely to the right, so that at its lower anterior border the left inner margin of the right lung at the level of the lower boundary of the heart was usually situated to the right of the middle line of the ster- num, the extent to which it did so vary- ing from the tenth of an inch to an inch and three-quarters. In less than one- third of the cases (18 in 60) the left margin of the right lung, at or a little above, the level of the lower boundary of the heart, extended to the left of the middle line of the sternum. When the superficial cardiac space was small, measuring less than two inches across, the inner margin of the right lung extended to the left of the centre of the chest in three-fifths of the cases (10 in 18). When, however, the space was of medium size (2 to 3 inches wide), the right lung passed to the left of the middle line in less than one-fifth of the cases (4 in 21) ; and when the space was large (above 3 inches wide), the right lung extended thus to the left of the middle line over the superficial cardiac space in only one-tenth of the cases (2 in 21). The upper boundary of the superficial cardiac space, which is an important landmark to the clinical worker, is formed by the lower anterior border of the upper lobe of the left lung after it deviates from its point of separation from the right lung. I have already described the direction and nature of this curve. The margin of lung, which thus forms the upper boundary of the superficial car- diac space, lay immediately behind one or other of the left costal cartilages or their spaces, and it generally took the down- ward direction of the cartilage behind which it lay, or was somewhat more in- clined. It generally lay behind one car- tilage or space, from the point at which it left the sternum to the point where it curved downwards to form the left border of the superficial cardiac space. It some- times, however, took a more oblique di- rection downwards, and crossed from behind one cartilage to behind the next space below, and then, after crossing that space, it spent itself behind the next car- tilage below. The upper boundary of the cardiac space varied in position from the level of the second left costal cartilage to that of the fifth, but it was most frequently 400 POSITION AND FORM OF THE HEART. present behind the third or fourth carti- lage or the fourth space,being thus situated in three-fifths of the cases (35 in GO). In three of the cases the surface of the heart exposed below the lower edge of the left lung was a mere belt composed of the lower boundary of the right ventricle, this belt being from two inches to two inches and a half in diameter from side to side, and from a fifth to a little over one-half of an inch from above down- wards. The heart had been lifted up- wards behind the lungs by great disten- sion of the stomach and intestines in these three cases, and the front of the cage of the chest had been also lifted up- wards by the same agency, while the lungs had expanded downwards under the influence of the forward movement of the ribs. Extent to which the Surface of the Heart is Exposed. In every instance more or less of the right ventricle was uncovered. A very small portion of the right ventricle was exposed in the two instances in which there was a narrow longitudinal chink over the front of the heart, and in the three in which the exposed surface of the organ was a very narrow belt extending from right to left along the lower border of the ventricle. In nearly one-half of the cases (25 in 60) the right ventricle was the only part of the heart that was exposed at the super- ficial cardiac space. In five other cases the apex of the heart was the only addi- tional part brought into view by the late- ral withdrawal of the lung. In almost one-half of the cases (25 in 60) the apex of the heart was in contact with the walls of the chest, the pericardium intervening; and in one-third of them (19 in 60) the higher portion of the left ventricle was also exposed to a greater or less extent. In only one instance was the whole of the narrow anterior portion of the left ven- tricle laid bare. In the rest of the cases, more or less of the upper portion of the left ventricle was covered by the edge of the left lung where it overlaps the front of the heart. The right auricle was uncovered to a greater or less extent in one-fifth of the cases (11 in 59), and in all but three of these its auricular appendix was also ap- parent. In one instance the whole of the auricle was exposed. The tip of the au- ricle was just visible in eight additional cases. The whole of the ascending portion of the aorta was exposed to view in nine instances, and it was visible on its right side in three, on its left side in four, and at its middle in one. Thus the aorta was more or less exposed in nearly one-fourth of the cases. The whole of the pulmonary artery was laid bare in only one instance, but in eight other cases the right side of the ves- sel, and in five others the left side of the vessel, was respectively exposed. The arterial cone of the right ventricle was completely covered by the lungs in one- third of the cases (20 in 59). In certain cases (10) a very small portion of the cone was uncovered just below the point of separation of the right and left lungs. These cases may practically be added to those in which the cone was completely concealed, so that, with this reservation, it may be said that the cone was covered with lung in one-half of the cases (31 in 59). In several instances, only one-fourth of the arterial cone was exposed, while in one instance the whole of it was uncover- ed. Between these extreme cases there was every variety in the extent to which the cone was brought into view. FRONT VIEW; DUE ING LIFE. We have just seen that after death the healthy heart and great vessels, and the different parts composing them, present great variety in position; and that al- though perhaps in no two instances do those parts occupy precisely the same relative situation, yet in a considerable proportion of the cases, and within cer- tain limits, they present a standard or average position. During life in like manner the healthy heart and great vessels vary much in rela- tive situation, yet those parts, within cer- tain orderly limits, regulated and modified by the various demands of life, maintain a standard or average position. It is evident that during life, when the heart is at work and in motion, sending blood to and receiving blood from the lungs and every part of the frame, the position of the heart and great vessels is different from what it is when observed in the dead body. A knowledge of the position of the heart and the great vessels during life, when in active motion, is essential to the clinical worker, and not merely that of the anatomy of the dead organ. I shall here, therefore, endeavor to de- scribe the average position of the heart and great vessels in the living frame, from the study of the situation of those parts after death and during life, and of the movements of the heart when in action, and when influenced by respiration. When the exertions of the body are prolonged and powerful, the heart acts with corresponding power; it receives MOVEMENTS OF THE HEART. 401 and distributes more blood than when the body is at rest, and its size, and that of its great vessels, become enlarged. When, however, the body is in repose the heart's action is weakened ; it receives and sends out less blood, and its size and that of its great vessels are diminished. The used power and the size of the heart, and the supply of blood to and from the organ, strictly balance the actual demands of the body, whether in action or at rest. Under the like circumstances the lungs, answering to the demands on respiration, enlarge or lessen in size, and the volume of the cage of the chest is correspondingly larger or smaller, while the pitch of the diaphragm is lower or higher, so as di- rectly to depress or elevate the heart. As the result, therefore, of these changes, thus induced by respiration, the heart, when it enlarges during exertion, is low and deep, and when it lessens during rest, is high and superficial. In a corresponding manner, and for the same reasons, the heart is large, low, and deep in strong laboring men, while it is small, high, and shallow in weak youths of sedentary habits. In women and in children the heart is proportionally smaller and higher than in adult men : and in the scale of life, from infancy to old age, the heart tends proportionally to increase in size, and to become lower and deeper in position. In order that we may have before us the movements of the heart and great ves- sels during the varied exercises of life, I shall, before describing the position of those parts in the living body, give a brief account of the action of the heart, of the currents of blood through the cavities of the heart, and of the movements of the heart caused by respiration. Movements oe the Heart. (See Figs. 62, 63, 68, 69.) I have observed, with the valuable as- sistance of Dr. Broadbent, the movements of the heart in the dog and the donkey, when under the influence of chloroform; and from those observations, and the careful examination of the human heart in many subjects, I have constructed figures 62, 63, 68, and 69, representing the Fig. 62. Fig. 63. Front view. Side view. Th® continuous lines indicate the position of the outlines of the various parts of the heart during the systole of the ventricles ; the interrupted lines indicate the position of the same parts during the diastole of the ven- tricles ; the arrows point out the direction and extent of the movements of the walls of the heart during the systole. Fig. 62 shows the transverse, vertical, and. oblique measurements in millimetres during the systole and the diastole. heart in man in the opposite conditions of complete ventricular contraction and dila- tation. In figures 62 and 63, the direction and extent of the movements of the walls during the ventricular systole are repre- sented by arrows. The appearance of the heart in motion is very striking. The ventricles, during their systole, contract from all sides upon their own centre and become wrinkled, and the arteries and veins on their surface arc full and tortuous, while the auricles become purple, plump, and glistening. During the diastole, the aspect is re- vol. ii.-26 402 POSITION AND FORM OF TIIE HEART. versed. The ventricles enlarge and be- come smooth, their superficial vessels almost disappearing, while the auricles shrink, and become pale and wrinkled. The Systole of the Ventricles.-During the systole, the ventricles, when looked at in front, contract from all sides towards a given centre, which is situated on the right ventricle a little to the right of the septum, about midway between the origin of the pulmonary artery and the lower boundary of the ventricle, where it rests upon the diaphragm. The contraction of the right ventricle, owing to its position at the front of the heart, and its conse- quent complete exposure, is marked and vigorous. The whole right margin of the ventricle, at its juncture to the auricle, moves extensively from right to left; while its left margin, at the longitudinal furrow or septum between the ventricles, moves to a comparatively slight degree from left to right. At the same time the top of the ventricle, at the origin of the pulmonary artery, descends, while its lower border, where it rests on the diaphragm, ascends. The point of rest towards which these various movements converge corresponds closely with the attachment of the ante- rior papillary muscle. The right auricle and superior vena cava are distended, and the pulmonary artery is enlarged and lengthened simul- taneously with the contraction of the ven- tricle. The auricle, which just before was wrinkled, becomes full; and its auric- ular portion and left edge move rapidly inwards, and to the left, so as to replace the ventricle. The movement of the auricular portion is remarkable. It sud- denly enlarges and becomes purple, and its tip moves from the right to the left edge of the sternum, at the level of the third costal cartilage. The vigorous contraction of the left ventricle is only visible at its apex and along its left border, since the rest of the cavity is hidden by the right ventricle. The apex has a revolving movement, up- wards, forwards, and to the right. The left border of the ventricle, like the apex, moves forwards and to the right; but while the portion of the ventricle near the apex ascends, the portion near the base descends. The appendix of the left auri- cle, which during the diastole of the ven- tricle is scarcely visible, descends during the systole, and moves rapidly forwards and downwards, so as to replace the re- treating ventricles, and to fill up the angle between them and the pulmonary artery. When we remove the left ribs and look at the heart from the left side so as to obtain a profile view, the animal lying upon the back, we see that the whole left ventricle moves forwards during the sys- tole, the posterior wall advancing much more than the anterior ; and that the base of the ventricle descends, while the apex ascends, so that apex and base approxi- mate. It is difficult to fix upon the pre- cise zone of rest of the ventricular walls towards which the apex ascends and the base descends, but it is somewhere about the middle of the ventricle, nearer, per- haps, to the apex than the base. This region of stable equilibrium corresponds to a similar point of rest in the papillary muscles. Owing to this arrangement, the ventricles and their valves adjust themselves to each other during the ven- tricular contraction. The left auricle, like the right, enlarges during the systole, and as the base of the ventricle then descends and advances, the ventricular attachment of the swollen auricle descends likewise, apparently, as it were, pushing the base of the ventricle before it. When the left ventricle propels its con- tents into the aorta, the arch of the aorta is distended and lengthened, and its root, like that of the pulmonary artery, de- scends. The arch of the aorta enlarges both in length and breadth, and becomes tense and rigid. Its lateral enlargement is small, but its elongation is considerable; and its orifice, like that of the pulmonary artery, descends during the systole. During the systole, the auricles and great vessels enlarge, and descend into the place just left by the retreating ven- tricles ; there is, therefore, more blood at the base of the heart at the end of the systole than at the end of the diastole, ^ince, however, during the systole, both ventricles contract, the increase of the blood at the base probably balances its diminution towards the apex. During the pause which follows the dilatation of the ventricles, the blood continues to flow into the auricle, so that the amount of blood in the heart and great vessels is greater just before the ventricular systole than at any other period. Movements of the Papillary Muscles.- That I might observe the action of the papillary muscles, I removed the anterior wall of the right ventricle when the heart was beating in situ; and I found that the tip of the anterior papillary muscle of the right ventricle contracted towards the septum during the systole. I then removed the septum, so as to expose the two papillary muscles of the left ventricle, and I noticed that both the muscles, which during the diastole were wide apart, approximated and came close together during the systole. At the same time the muscles shortened towards their own centre, so that their tips and their tendinous cords descended to the left towards the apex of the ventricle, while their roots of attachment near the apex ascended to the right towards the base of CURRENTS OF BLOOD IN CAVITIES OF THE HEART. 403 the ventricle. The fixed point towards which the two ends approximated corre- sponded apparently to the zone of rest, or stable equilibrium, in the walls of the ventricle, towards which the base and the apex of the ventricle approximate during the systole. Action of the Mitral and Tricuspid Valves.-In order that I might see the movements of the mitral and tricuspid valves, I cut out the heart when beating vigorously, and immersed it in water. The ventricles contracted with force, and expelled the water from the great arteries during each systole. The jet from the aorta was six inches in length. The seg- ments of the mitral and tricuspid valves were seen to come together at their notched and bead-like margins, so as to close the valves during the systole, and prevent the efflux of a drop of liquid. At the beginning of each diastole the margins of the valves separated quickly from each other, so as to admit the flow of water freely into the cavity. Direction oe the Currents of Blood in the Cavities of the Heart. (See Figs. 64, 65.) In the left ventricle, the aperture of entrance, the mitral orifice, is contiguous to the aperture of exit, the aortic orifice, the two orifices being separated by a membranous septum consisting of the anterior flap of the mitral valve. In the right ventricle, the aperture of entrance, the tricuspid orifice is at a distance from the aperture of exit at the pulmonary artery, the two orifices being separated by the muscular channel of the conus arteri- osus. In the left ventricle the current of blood inwards, which descends during the diastole behind the anterior segment of the mitral valve, is parallel in direction to the current of blood outwards, which ascends during the systole in front of that segment. (Fig. 64.) In the right ven- tricle the current of blood inwards is at right angles to the current of blood out- wards, since the blood enters the cavity from right to left, and leaves it from be- low upwards (Fig. 65). During the sys- tole the stream of blood in the left ventri- cle takes a spiral direction towards the aortic orifice, in accordance with the direction of the aorta itself. The stream of blood in the right ventricle, as it as- cends, mounts over the bulging septum, being restrained by the concave anterior wall of the ventricle. This upward stream, which narrows as it ascends, thus takes the curved direction upwards, backwards, and inwards of the conus arteriosus and the pulmonary artery. In the left ven- tricle, the anterior segment of the mitral valve and the right and left papillary muscles, form a hollow channel for the stream of blood, which, as it ascends to Fig. 64. Fig. 65. Showing the direction of the currents of the blood in the left side of the heart. Showing the direction of the currents of the blood in the right side of the heart. the aorta, presses upon the under surface of the valve. In the right ventricle the stream of blood, as it ascends, sweeps onwards at right angles to the under sur- face of the tricuspid valve, and rushes between and across the papillary mus- cles, and through the tendinous cordage that connects the muscles to the flaps of the valve. 404 POSITION AND FORM OF THE HEART. The Movements oe the Heart caused by Respiration (See Figs. 66, 67.) During inspiration the diaphragm, in its descent draws downwards the fibrous sac and floor of the pericardium, and the whole of its contents. The heart rests upon the central tendon of the diaphragm which forms the floor of the pericardium, and it therefore necessarily rises and falls with the rise and fall of the diaphragm. The descent of the diaphragm is accom- panied by the advance of the anterior wall of the chest, which produces the corresponding expansion of the lungs anteriorly. The central tendon of the diaphragm forming the floor of the peri- cardium presents an inclined plane, upon which the heart glides forwards and down- wards during inspiration, under the com- bined influence of the descent of the di- aphragm and the forward movement of the ribs and sternum. Whatever be the cause of the altered level of the dia- phragm, whether it contracts and de- scends, as in inspiration, or is pushed downwards by fluid or tumors in the chest-whether it is raised during expira- tion, or pushed upwards by distension of the stomach and intestines, by fluid in the abdomen, by abdominal tumors, or by abscess or other affections of the liver ; whatever, in short, be the cause producing the ascent or descent of the diaphragm, a corresponding ascent or descent of the Fig. 66. Showing the position of the heart and great vessels in relation to the walls of the chest, and the lungs in a healthy man at the end of a forced expiration. heart must ensue. The only exception is the displacement downwards of the cen- tral tendon of the diaphragm by means of effusion into the pericardial sac, when the fluid interposes itself between the heart and the diaphragm, with the effect of pushing the diaphragm downwards and the heart upwards. An important part is played by the pericardium in the in- fluence of respiration on the position of the heart. The central tendon of the diaphragm forms the base of the pericar- dium, upon which the heart rests as upon a floor. The aponeurotic structure of the pericardium, which takes its origin from the central tendon, ascends so as to form a strong fibrous pouch which envelops the whole heart, and gives off a fibrous investment to each of the great vessels as they enter or leave the pericardial sac. Through the medium of this aponeurotic structure, the diaphragm, during its de- MOVEMENTS OF THE HEART CAUSED BY RESPIRATION. 405 scent, acts so as to draw downwards the great vessels simultaneously with the heart. The respiratory movements of the heart are vertical. The organ and all its parts and great vessels move downwards during inspiration, and move upwards during expiration. While, therefore, the vertical relations of the heart and great vessels to the parietes of the chest are altered, the lateral relations of the various parts of the heart and great vessels to each other are unaltered, and their relative positions to the surrounding organs are not mate- rially changed. While the diaphragm descends during inspiration, carrying with it the heart, the front and sides of the cage of the chest, formed by the ribs and sternum, ascend. The change in the position of the heart in relation to the ribs and sternum is, there- fore, doubled in extent by the twofold operation of the descent of the diaphragm and the heart simultaneously with the ascent of the cage of the chest. Inspiration, besides causing the descent of the heart, produces also a lengthening and general enlarg ,ment of the organ and its great vessels. The lengthening of the heart and its vessels tells with decreasing effect from below upwards. The descent of the great vessels in the neck is much, but not completely, restrained by the attach- ments of those vessels. The innominate, the left carotid and the subclavian arteries, and the ascending aorta are elongated and straightened to a considerable extent, and as less blood is sent into those vessels during inspiration than during expiration, they are lessened in width at the same Fig. 67. Showing the position of the heart and great vessels in relation to the walls of the chest, and the lungs in a healthy man at the end of a deep inspiration. Note.-The lower boundary of the heart ought to have been somewhat lower in this figure. time that they are increased in length. The enlargement of the cavities of the heart is limited to the right side. Tlie right auricle receives in increased quan- tity the blood which has been stored up in the hepatic and portal vessels and the great veins during expiration. The space in the vessels of the expanded lungs for the reception of blood is increased; the blood is sent with greater ease through the pulmonary artery from the right ven- tricle, in consequence of the enlargement of the pulmonary capillaries, and is at the same time sent in greater quantity from that cavity, because its supply of blood, derived from the auricle, is materially in- 406 POSITION AND FORM OF THE HEART. creased during inspiration. The vense cavse, the right auricle, the left ventricle, and the pulmonary artery are therefore enlarged both in length and width. The supply of blood to and from the right cavities of the heart, which is thus in- creased during inspiration, is then prob- ably associated with a corresponding diminution in the supply of blood to and from the left cavities of the heart. The blood is retained in the pulmonary vessels in augmented quantity during inspira- tion. We may infer that less blood is sent then into the left auricle, and we know that less blood is sent then into the system through the arteries from the left ventri- cle, than during expiration. The result of the various co-operating and contending forces which I have just considered are exhibited with, I believe, an approach to accuracy in Figs. 66 and 67, respecting the position of the heart and great vessels in relation to the cage of the chest and the lungs at the end of a forced expiration, and at the end of a deep inspiration. The greatest change in the relative po- sition of the heart during inspiration takes place at its lower boundary, the descent of which is equal to that of the central tendon of the diaphragm, or at least one inch. The upward movement at the same time of the lower end of the sternum and the adjoining cartilages is about one inch also. The resulting change in the relative position of the lower boundary of the heart and the ex- ternal walls ought to be, and I believe is, though I have not ascertained it by exact demonstration, about two inches. The ascertained change in the relative posi- tion of those parts is such, that the lower boundary of the right ventricle, at the end of expiration, is situated behind the lower end of the sternum, and at the end of inspiration, behind the lower end of the ensiform cartilage. The result during life, in a robust man, is that at the end of expiration, the impulse of the right ven- tricle may be perceptible to the left of the lower end of the sternum ; while at the end of inspiration it is to be seen and felt beating with considerable force over, below, and to the left of the ensiform car- tilage, or in other words, at the epigas- trium. The heart has in fact descended into the space previously occupied by the liver and stomach, and instead of being protected at the part spoken of by a bony framework, is at the end of a deep inspi- ration only covered to each side of the ensiform cartilage by the abdominal mus- cles. The apex of the left ventricle de- scends to the same extent during a deep inspiration, or from the fifth rib to the seventh costal cartilage. The impulse at the apex, which at the end of expiration is often felt beating with force in the fourth intercostal space, is at the end of a deep inspiration quite imperceptible. I need not go through the whole of the de- tails of the altered relative positions of the heart and great vessels in relation to the ribs and sternum during expiration, and at the end of a deep inspiration. They speak for themselves, and are exhibited in the accompanying figures. It will suf- fice, if I describe the altered bearings of the principal landmarks. A transverse boundary line drawn across the top of the right auricle and right ventricle corre- sponds with the attachment of the great vessels to the heart. This transverse line, which marks the position of the aorta above the right auricle, and the com- mencement of the pulmonary artery, ex- tends at the end of expiration across the second intercostal spaces, and the inter- vening portion of the sternum a little below the manubrium ; while at the end of in- spiration it crosses the lower boundary of the third intercostal spaces, and the visible commencement of the aorta makes a cor- responding descent behind the sternum. The top of the arch of the aorta which at the beginning of a deep inspiration is a little below the top of the manubrium, is, at the end of it, at or at a little above the lower end of that bone. The vertical and forward respiratory movements of the heart explain the dif- ference in the position of the heart in re- lation to the walls of the chest in weak persons with flat chests on the one hand, and in those who are full-chested and robust on the other. The relations of the heart and great vessels to the cage of the chest follow the type of expiration in the feeble, and the type of inspiration in the strong. Front View of the Heart and Great Vessels in a Healthy Man WITH A WELL-FORMED CHEST. (See Figs. 68, 69.) The heart and great vessels occupy the central region of the chest. The lower boundary of the right ventricle is situated behind the ensiform cartilage, and is about half an inch or more below the lower end of the osseous sternum and 1 All the works on the diagnosis of the dis- eases of the heart with which I am acquaint- ed, whether published in this country or in Germany, represent the lower boundary of the heart as being situated above the lower end of the sternum. Several of these works have evidently taken their figures from Luschka's well-known drawing, which gives undoubtedly an accurate view of the heart and the surrounding parts in the dead body from which it was taken. It gives, however, on that very account, an inaccurate view of FRONT VIEW OF THE HEART AND GREAT VESSELS. 407 the top of the arch of the aorta, at the origin of the innominate and left carotid arteries, is about half an inch or more be- low the upper end of the sternum. The breadth of the heart is about one- half of the breadth of the chest. The heart, at its extreme limits, extends for a little more than one-third of its breadth into the right side of the chest, and for a little less than two-thirds of its breadth into the left side of the chest, or in that proportion to the right and left of a verti- cal line drawn down the middle of the sternum. During the systole of the ventricles the proportion of the heart in the left side of the chest lessens, owing to the inward contraction of the left border of the left ventricle, while that in the right side of the chest increases, owing to the outward expansion of the right border of the right auricle. The boundary line across the sternum, between the upper border of the heart and the lower limit of the great vessels, is on a level with the third costal cartilages. The lower boundary of the heart ex- tends, with a slight inclination down- wards, from about half an inch below the lower end of the sternum to the fifth left space, just above or on a level with the upper edge of the sixth left cartilage. The lower boundary of the heart ascends during the systole of the ventricle, and descends during its diastole; it descends also during ordinary inspiration, and ascends during ordinary expiration for about the third of an inch. A deep in- spiration may bring down the lower border of the heart to the lower end of the ensi- form cartilage, and a forced expiration may raise it to or above the level of the lower end of the sternum. The left boundary of the heart at its apex is situated to the left of the junction of the fifth rib to its costal cartilage, and behind or to the left of a vertical line drawn downwards from the left nipple.1 The right boundary of the heart extends about an inch to the right of the right edge of the sternum. The Hight Side of the Heart.-The right cavities occupy the whole front of the heart with the exception of its left portion, -where the left ventricle comes into view from behind the right ventricle to the extent of an inch in breadth. The transverse or auriculo-ventricular furrow forms the external apparent separation between the right auricle and right ven- tricle. The auriculo-ventricular furrow sweeps backwards and forwards to so great an extent, to the left during the sys- tole, and to the right during the diastole, that it presents no fixed position during life, but ranges to and fro between certain limits. The upper end of the furrow may be situated at the left edge or at the mid- the relative position of the heart in the living man. I have just stated that the lower boundary of the heart is situated behind the ensiform cartilage, about half an inch or more below the lower end of the osseous sternum, and have done so on the following grounds:- (1) At the time of death the heart is raised by the elevation of the diaphragm during the final expiration. After death the heart contracts upwards towards its higher points of attachment, so as to leave an aver- age space of half an inch between the lower boundary of the heart and the lower boun- dary of the front of the pericardium; that space being the exact measure of the upward shrinking of the heart after death. The lower boundary of the heart was situated behind the end of the osseous sternum in one- fifth, and below that point in two-fifths of my cases, while it was above that point in two- fifths of them. The lower boundary of the front of the pericardium, which marks the position of the lower boundary of the heart itself at the time of death, was behind the lower end of the sternum in one-fifth, and below that point (being situated behind the upper portion of the ensiform cartilage) in two-thirds of my cases, while it was above that point in only one-eighth of them. (2) We have already seen (pp. 371, 372) that there is a general correspondence between the relation of the lower boundary of the right ventricle to the end of the osseous sternum, and the relation of the lower border of the apex of the heart to the inferior edge of the fifth costal cartilage and rib. The inferior edge of the junction of the fifth cartilage and rib was on a lower level than the end of the sternum by from a quarter of an inch to an inch and a quarter in 60 out of 71 cases, was on the same level in 5, and was about that level in 6 instances. It is evident that, with few exceptions, the apex-beat could not be felt in the fifth space if the lower boundary of the heart were situated above the end of the sternum. (3) The lower edge of the anterior portion of the right lung at its left border corresponds, as a rule, with the lower boundary of the heart at the same situation. In six cases the lower edge of that portion of the right lung was behind or on a level with the lower end of the sternum; in three it was above that point to the extent of half an inch; and in twenty it was below that point to an extent varying from a quarter of an inch to an inch and a half, or, in one exceptional case, two inches. We may therefore infer that the lower boundary of the heart was situated in two-thirds of these cases behind the ensiform cartilage, in one-fifth of them behind the lower end of the osseous sternum, and in only one-tenth of them above that end of the bone. 1 I have made comparatively few observa- tions as to the position of the left nipple in relation to the junction of the adjoining ribs to their cartilages and the left boundary of the heart at its apex. 408 POSITION AND FORM OF THE HEART. die line of the sternum, on a level with the third cartilage ; and its lower end may be placed a little below and to the right of the lower end of the sternum, being be- hind the sternal end of the seventh car- tilage, but it may extend for fully half an inch to the right of this position. The transverse furrow thus crosses behind the lower half of the sternum obliquely from left to right, and from above downwards. The upper third of the transverse furrow forms a true line of separation between the auricular appendix and the arterial cone of the right ventricle ; but the lower two-thirds of the furrow lie about half an inch to the right of the tricuspid orifice Fig. 68. Showing the position and relative size of the various cavities of the heart and of the great vessels during the ventricular systole in a healthy, well-formed man. Note.-The fifth cartilages were unusually high in the body from which figures 68 and 69 were taken. SYSTOLE. and the line of division between the right auricle and the right ventricle. The right transverse or " auriculo-ventricular" fur- row is not therefore at this part of its course a true line of separation between the right auricle and ventricle, but is thrown half an inch to the right of that line by the presence there of the right coronary vessels, and the couch of fat in which they are imbedded. The Right Auricle.-The right auricle is broad above, where it widens out into the auricular appendix, especially during the systole, and lies behind the middle of the sternum, reaching from its right often to its left edge, on a level with the third cartilages ; and it is narrow below, where it appears to come to a point at the lower end of the transverse furrow, to the right of the lower end of the sternum. The real or internal breadth of the right auri- cle is, as I have just explained, greater than its apparent or external breadth along the line of the transverse furrow. When, therefore, the lower portion of that furrow is situated a little to the right of the sternum, the lower portion of the tricuspid orifice is covered by the lower FRONT VIEW OF THE HEART AND GREAT VESSELS. 409 end of the sternum, a little to the right of the middle line of that bone. The right boundary of the auricle extends be- hind the right costal cartilages for about an inch beyond the right edge of the ster- num. The right auricle undergoes more change in form during the action of the heart than any portion of the organ. During the systole of the ventricles the auricle retains its length, but it becomes twice as wide, and its whole surface, instead of being pale and wrinkled, is purple, plump, and glistening. The ventricular border moves extensively to the left, so as to pass from the right margin to the middle line Fig. 69. DIASTOLE. Showing the position and relative size of the various cavities of the heart and of the great vessels during the diastole of the ventricles in a healthy, well-formed man. of the sternum, while its right border expands a little to the right. There is a slight descent of the upper and lower bor- ders of the right auricle during the con- traction of the ventricles. During the diastole of the ventricles these appear- ances and movements are reversed. The Hight Ventricle.-The right ventri- cle forms the solid muscular front of the heart, and is flanked to the right by the right auricle, and to the left by that small portion of the left ventricle that comes into view in front of the heart, and forms its left border. The right ventricle, when exposed to view in front of the heart, presents a pyr- amidal shape. The base of the pyramid is formed by the lower boundary of the ventricle, which rests on the central ten- don of the diaphragm, and extends, with a slight obliquity downwards and from right to left, from the right auricle to the apex of the left ventricle ; its upper border is crowned by the pulmonary artery, which forms the apex of the pyramid; its left border is formed by the longitudinal fur- row, which divides the right from the left ventricle ; and its ostensible right border by the transverse furrow which appa- rently separates the right auricle from the right ventricle, the actual separation of those two cavities at the tricuspid orifice 410 POSITION AND FORM OF THE HEART. being situated, as I have just stated, about half an inch to the left of the trans- verse furrow. The right ventricle, in its vertical diam- eter or length, extends from the third left cartilage to the sixth, which are the car- diac cartilages. In its transverse diame- ter, or breadth, the right ventricle extends from the transverse furrow, at or to the right of the right edge of the sternum be- low, and somewhat to the right of the left edge of the sternum above, to the anterior longitudinal furrow, which is situated be- hind or a little to the right of the junction of the left costal cartilages to their ribs from the third to the fifth. The length or vertical measurement of the ventricle is greater than its breadth or transverse measurement in the propor- tion of about four to three. The body of the ventricle forms about the lower two- thirds of the cavity extending from the fourth left cartilage to the sixth, and the conus arteriosus forms about the upper third of the cavity extending from the third left cartilage to the fourth. The arterial cone of the right ventricle nar- rows from below upwards until it ends in the pulmonary artery, and the breadth of the cone a little below the origin of the pulmonary artery in relation to that of the body of the right ventricle, is in the proportion of nearly three to five, or in other words, the width of the cone is nearly three-fifths of the width of the body of the right ventricle. Owing to the arterial cone being so much narrower than the body of the right ventricle, especially at its right border, the transverse furrow extends further to the left at its upper than at its lower bor- der by more than an inch. In conse- quence of this great deviation towards its upper end the transverse furrow presents a double curve, which, looking to the right, is concave above, where the rounded auricular appendix fits into the hollow profile of the arterial cone ; and convex below, where it is situated half an inch to the right of the tricuspid orifice. The' longitudinal furrow takes a down- ward direction, with a slight inclination to the left, this inclination to the left in- creasing rapidly towards the lower end where it approaches the apex. In con- sequence of this, the longitudinal furrow also presents a double curve, which, look- ing to the left is convex above, concave below. The deviation to the left of the lower end of the longitudinal furrow is caused by the deviation to the left of the cavity of the right ventricle as it ap- proaches the apex of the heart. The fur- row between the ventricles turns to the left at its inferior extremity, and, so to speak, cuts through the apex of the heart. The apex of the heart is thus composed of the apex of the left ventricle and the ad- joining left end of the lower border of the right ventricle. During the contraction of the right ventricle its four sides approximate to- wards a point of rest or stable equilib- rium, which is situated on the anterior wall of the cavity, over or close to the attachment of the anterior papillary mus- cle, a little to the left of the longitudinal furrow, and slightly nearer to the lower than the upper border of the ventricle. The movement of the transverse furrow to the left is extensive, and that of the longitudinal furrow to the right is slight; the downward movement of the upper border at the origin of the pulmonary artery is considerable, and the upward movement of the lower border of the ven- tricle is somewhat less. The right bor- der of the conus arteriosus moves less to the left than the right border of the ven- tricle at the tricuspid orifice. At the same time the surface of the ventricle be- comes wrinkled, and its coronary vessels start out from the surface and become tortuous. During the dilatation of the ventricle the reverse movements take place, its surface becomes smooth, glisten- ing, and rounded, and the vessels on its surface cease to be prominent. (See Fig. 62, page 401.) The Left Ventricle.'-The left ventricle, where seen in front, comes into view to the left of the right ventricle, and forms the convex left border of the heart. The left ventricle forms here a comparatively long, narrow slip, extending from the third left space down to the fifth, and from the longitudinal furrow behind or to the right of the junction of the corresponding ribs to their cartilages, to the left border of the heart, which reaches up to or just beyond the left nipple. This visible an- terior portion of the left ventricle is of the greatest width at and below its middle, behind the fourth space and the fifth car- tilage. Above and below this region the ventricle narrows, coming to a point at the apex below, and above bearing to the right, where it is finally hidden by the ap- pendix of the left auricle. The breadth of the anterior visible portion of the ven- tricle at its widest part is about one-fifth of the breadth of the heart. The apex of the heart occupies the fifth space, its lower border being situated just above or behind the upper edge of the sixth cartilage and rib, and its left border being at or a little beyond a vertical line drawn down from the nipple. During the contraction of the left ven- tricle the right and left borders of its visi- ble anterior portion both move a little to the right, its base and upper portion de- scend, and its lower portion and apex ascend, both portions moving forwards and to the right. (See Fig. 63, page 401.) The Appendix of the Left Auricle is situ- FRONT VIEW OF THE HEART AND GREAT VESSELS. 411 ated behind the third left cartilage close to its junction with the third rib, and fills up the angle or space between the upper end of the left and right ventricles, at the top of the longitudinal furrow, and the left boundary of the origin of the pul- monary artery. The left auricular appendix is much more prominent and extensive during the contraction of the ventricles, when its right and lower borders move respectively considerably to the right and downwards, and its left and upper borders move ob- liquely to the right and slightly down- wards, than it is during the dilatation of the ventricles, when the auricular appen- dix shrinks inwards upon itself. The Great Vessels.-The great vessels lie side by side, the ascending aorta being in the centre, the pulmonary artery to the left, and the superior vena cava to the right, behind the upper portion of the sternum and the adjoining costal car- tilages, at and above the level of the third cartilage. J1 he Arch of the Aorta.-The root of the aorta, including the aortic orifice, valve, and sinuses, is hidden in the centre of the heart. The ascending aorta comes into view just above the appendix of the right auricle, on a level with the third costal cartilages, and is covered by the sternum, the right border of the artery being situ- ated behind or a little to the left of the right edge of the sternum; and its left border, which is partially covered by the right border of the pulmonary artery, being about a quarter of an inch or less to the right of the left edge of the ster- num. As the arch of the aorta ascends, it bears to the left, and at the point where it gives origin to the innominate artery, it is exactly behind the middle line of the sternum. From this point the transverse aorta ascends slightly until it gives origin to the left carotid artery, whence it curves backwards and slightly downwards, with an inclination to the left, and gives off the left subclavian artery, the last of its three great branches. The left carotid arises just within a line drawn downwards from the sternal end of the left clavicle, and the left subclavian just without that line. The part at which the innominate and left carotid arteries take their origin is the highest point of the arch, and is situ- ated about three-quarters of an inch or rather less below the top of the manu- brium, as far as the breadth of the in- nominate artery to the left of a line drawn down the middle of that bone, and in front of the lower portion of the body of the third or the upper portion of that of the fourth dorsal vertebra, which corre- sponds with the third dorsal spine, which is situated midway between the spines of the scapula?. The transverse aorta, as it curves backwards, to the left and down- wards, rests first on the front and left side of the trachea, and then upon the left side of the oesophagus, and is situated between the manubrium, just to tlie left of the middle line, from three-quarters of an inch or less below the top of the bone down to its lower end in front, and the left side of the body of the fourth and the upper portion of the fifth dorsal vertebra behind. The relations of the transverse aorta to the manubrium in front are very variable, but those to the dorsal vertebrse behind are less so. The deep left border of the descending portion of the arch may be seen in a front view, and this border is situated in suc- cession behind the left and lower portion of the manubrium, near its junction to the first rib, the first space and the sternal portion of the second left costal cartilage, and the adjoining portion of the sternum. The relations of this important portion of the arch will be considered when the side and back views of the heart and great vessels are described. The ascending aorta just above the right auricular appendix descends slightly during the contraction of the ventricles ; but the top of the arch, at the origin of the innominate and left carotid arteries, is scarcely moved during the contraction of the heart. Inspiration causes the de- scent of the ascending and transverse aorta and its great branches. This de- scent is slight during ordinary breathing, but is considerable on a deep inspiration. The inspiratory descent of the arch of the aorta is much less than that of the root of the aorta and heart. The Pulmonary Artery.-The origin of the pulmonary artery is situated behind the upper portion of the third left carti- lage, and its top lies behind the second left cartilage. As the artery ascends to the left of the ascending aorta, it occupies the second left space and cartilage for four-fifths of its breadth, and is covered by the left border of the sternum for the remaining fifth. The pulmonary artery, at its origin, is situated just above and within the appendix of the left auricle ; and, as it proceeds on its course, it makes for the hollow of the arch of the aorta, through which it sends its right branch. Its direction is therefore much more from before backwards than from below up- wards. The remaining course of the ar- tery cannot be seen in front, and will be considered when the side and back views of the heart and great vessels are de- scribed. During the contraction of the right ven- tricle the pulmonary artery descends at its origin to a considerable extent, and the higher parts of the artery also de- scend, but less and less from below up- wards. At the same time the whole artery enlarges and lengthens. The pul- 412 POSITION AND FORM OF THE HEART. monary artery descends also during in- spiration, but to a less extent than the body of the right ventricle, and less at its upper part than at its origin. The Superior Vena Cava.-The supe- rior vena cava receives the right and left innominate veins a little below the level of the top of the arch of the aorta, behind the right portion of the manubrium, mid- way between the upper and lower end of the bone. The right innominate vein descends behind the sternal end of the right clavicle, and the left innominate vein crosses in front of the three great arteries, just at or above their origin from the arch of the aorta. The superior vena cava descends immediately to the right of the sternum behind the first space, the second cartilage and the second space, and it opens into the right auricle behind the third right costal cartilage. The superior vena cava descends slight- ly at its point of entrance into the right auricle during the contraction of the ven- tricle. It descends also during the inspi- ration, but to a greater extent. The Relation of the Lungs to the Heart in Front.-The lungs cover the great ves- sels and the whole of the heart except the more prominent portion of the right ven- tricle which is behind the cardiac car- tilages. The inner margins of the right and left lungs in front meet together behind the upper two-thirds of the sternum, the right lung, as a rule, passing to the left of the centre of the sternum, so as to encroach somewhat on the left side of the chest. The inner margin of the left lung sepa- rates from that of the right lung, and diverges to the left on a level with the fourth left costal cartilage. Thence the lower border of this portion of the lung extends to the left, lying behind the lower edge of the fourth cartilage or the upper border of the fourth space, and in front of the body of the right ventricle. Before this border of the lung reaches the longi- tudinal furrow and the junction of the cartilages to the ribs, it curves down- wards, crossing within the fourth space and the fifth cartilage, where it again curves to the right, so as to form a hollow space for the lodgment of the apex of the heart. After crossing the fifth space the inner margin ends in the lower border of the upper lobe, which is situated behind the upper edge of the sixth cartilage and rib, where it soon ends in the septum that divides the upper from the lower lobe of the left lung. Owing to the outward and inward curve thus made by the inner margin of the left lung where it crosses the heart to form the left and lower bor- der of the superficial cardiac space, a re- markable tongue of lung is formed by the inner and lower borders of the upper lobe of the left lung. This tongue of lung, owing to its free position just in front of the interlobular septum, wraps round the apex of the heart, being above, below, outside and in front of it, so as to adapt itself to every movement of the apex. When the apex advances it recedes, when the apex recedes it advances, and thus it allows free play to the apex at the same time that it softens the impulse of the apex upon the walls of the chest, and shields it, when it becomes again flaccid, and retires within its nest. The inner margin of the right lung, after that of the left lung has deviated to the left, continues its course downwards, behind the sternum, being nearer to the left than the right edge of that bone. It thus completely covers the transverse fur- row, the right border of the right ven- tricle, and the tricuspid orifice. This inner margin of the right lung inclines to the left before it reaches the lower boun- dary of the heart, where it soon ends in the lower margin of the right lung ; which margin lies at first behind the upper part of the ensiform cartilage, then crosses be- hind the sternal portion of the seventh and sixth right cartilages, and afterwards takes its course to the right, behind or just above the sixth cartilage. It is evident, from what has just been stated, that the lungs are moulded by a natural adaptation to the form and struc- ture of the heart and great vessels. They thus cover the soft and yielding right auricle, which requires the additional pro- tection of the soft covering in which it is thus imbedded ; they thus cover the great vessels, which do not advance so far for- wards as the body of the heart; they thus cover the circuit of the ventricles around the three sides of the superficial cardiac space ; and they thus leave uncovered the most prominent and powerful portion of the right ventricle. Obeying this law of adaptation, the inner margin of the right lung extends inwards and to the left along its whole length, more than that of the left lung extends to the right; for the greater prominence of the pulmonary artery, of the conus arteriosus, and of the centre of the right ventricle, parts that are situated to the left of the middle line of the ster- num, offers resistance to the free inward expansion to the right of the margin of the left lung. On the other hand, the less prominence of the ascending aorta, the soft and yielding character of the right auricle and its appendix, and the less prominence of the right border of the right ventricle, parts that are situated behind and to the right of the sternum, allow and even invite the more free inward expan- sion to the left of the inner margin of the right lung. The inner margins of the lungs, in short, advance freely where they FRONT VIEW OF THE HEART AND GREAT VESSELS. 413 meet with the least resistance, and stop or even recede where they meet with the greatest resistance. The Orifices and Valves of the Heart and the Great Arteries.-The orifices and valves of the heart may be considered in two orders: (1) As they are superficial or deep in situation, when the pulmonic and tricuspid orifices and valves would come first, and then the aortic and mitral ori- fices and valves; and (2) as they are ranged from above downwards, when the pul- monic orifice and valve come first in order, then the aortic, then the mitral, and last the tricuspid orifice and valve. I shall consider them in detail according to the first and most natural of those orders, namely, the superficial and deep orifices and valves, which are also the orifices and valves of the right or anterior and the left or posterior cavities. After doing so, I shall briefly indicate them, for the sake of their common connection, in their order, from above downwards. The orifice of the pulmonary artery is the highest of the four orifices, and its anterior portion is situated mainly behind the third left cartilage, its right border being covered by the adjoining edge of the sternum. During the systole of the ven- tricles the anterior portion of the orifice of the pulmonary artery descends into the third space. The root of the pulmonary artery con- sists of two anterior sinuses and one pos- terior sinus, and its valve consists of two flaps in front and one behind, each in its own sinus. The position of the anterior flaps is higher than that of the posterior flap. The anterior or superficial convex wall of the right ventricle is much longer than its posterior or internal convex wall, owing to its outer wall being a section of a much larger sphere than its inner one. When, therefore, the right ventricle con- tracts, its anterior and outer wall shortens and draws downwards the anterior flaps of the pulmonic valve to a much greater extent than the posterior and inner wall shortens and draws downwards the pos- terior flap. The result is that when the right ventricle is in a state of complete contraction, the anterior and posterior flaps of the pulmonic valve are nearly on the same level; and that when the ven- tricle is in a state of distension the anterior flaps may be an inch higher than the pos- terior flap. This is well seen in several of Pirogoff's vertical sections. The tricuspid orifice, is the lowest as well as the most superficial of the four orifices, and is separated from the orifice of the pulmonary artery by the conus arteriosus of the right ventricle. In a healthy active man with a well-formed chest, the tricuspid orifice is situated be- hind the lower fourth of the sternum to *he right of the middle line of that bone, its upper border being on a level with the lower edge of the fourth cartilage, and its lower border being behind the lower end of the sternum, and the articulation to it of the right sixth cartilage. The tricuspid orifice is situated about half an inch to the left of the right trans- verse auriculo-ventricular furrow. It is impossible to assign accurately a fixed position to the tricuspid orifice, owing to its extensive movement to the left during the contraction, and to the right during the dilatation of the right ventricle. The limits of the range of this movement may, however, be defined to the right by a line a little to the right of the sternum, and to the left by a line a little to the left of the middle line of that bone, the orifice play- ing backwards and forwards behind, and to the right of the right half of the lower portion of the sternum. The position of the flaps, the tendinous cords, and the papillary muscles of the tricuspid valve have been already de- scribed in detail.1 It will, therefore, be sufficient to say here that the papillary muscles radiate like a fan upwards, out- wards, and downwards from the cords and flaps of the valve ; that the superior papillary muscle, when present, ascends behind the fourth cartilage ; that the an- terior papillary muscle takes the direction outwards of the fifth cartilage ; and that the inferior papillary muscles descend be- hind the sixth cartilage. The root of the aorta,2 including its ori- fice, valve and sinuses, occupies the space between the pulmonic and tricuspid ori- fices. The root of the aorta, and the aor- tic vestibule, which is the channel or chamber with rigid walls that leads to it from the cavity of the left ventricle, pro- ject forwards in front of that cavity and of its mitral orifice, so that the orifice of the aorta, covered by the posterior wall of the conus arteriosus, interposes itself, as has just been stated, between the pul- monic and tricuspid orifices. By this arrangement the aortic orifice advances more nearly to the front of the chest, the shallow conus arteriosus being in front of the orifice, and the deep cavity of the right ventricle being below it. Hence the murmur of aortic regurgitation, and an intensified aortic second sound, and coin- cident doubling of that sound, are heard loudly over and to the left of the middle third of the sternum in front of the arte- rial cone and the root of the aorta ; and feebly over and to the left of the lower third of the sternum, in front of the cavity of the right ventricle. The root of the aorta is somewhat overlapped above and 1 See pages 394-398. 2 I have already described the anatomical relations of the root of the aorta. (See pages 383-386.) 414 POSITION AND FORM OF THE HEART. to the left by the root of the pulmonary artery, and is situated accordingly below and to the right of the pulmonic oritice, behind the left half or three-fifths of the sternum, on a level with the third space, the left portion of the aortic orifice ex- tending beyond the sternum so as to lie within that space. The upper and left border of the aortic orifice, especially during the diastole, is seated behind the lower portion of the third cartilage, near the sternum ; and its lower and right border, especially during the systole, is situated behind the middle line of the ster- num, on a level with the upper portion of the fourth cartilage. The root of the aorta descends consid- erably and moves to the left, so as to ap- proach towards the apex during the con- traction of the left ventricle, and at the same time the apex moves to a less degree upwards, and to the right, so as to ap- proach towards the aortic orifice. The mitral orifice is situated partly be- hind and partly below the level of the aortic orifice? its upper third or upper two-fifths being behind, and its lower two-thirds or three-fifths below the level of that orifice; and partly behind and partly above the level of the tricuspid ori- fice, its lower two-thirds or three-fourths being behind, and its upper third or fourth being above the level of that ori- fice. The mitral orifice is seated behind the left half of the sternum, at the upper two-thirds of the lower third of that bone, on a level with the fourth cartilage, the fourth space, and the upper portion of the fifth cartilage. It is impossible to assign a fixed position to the mitral orifice, for it, like the tricuspid orifice, plays to and fro during the contraction and dilatation of the ventricles. The limits of its move- ment may, however, be approximately defined by a line a little to the right of the middle line of the sternum on the one hand and a line corresponding to the left edge of the sternum on the other. I have already described the anatomical rela- tions of the mitral valve,1 and it will therefore be sufficient to state here that the left or upper and the right or lower papillary muscles, starting from their at- tachments through their tendinous cords to the flaps of the valve, concentrate themselves towards their roots at the apex, instead of radiating from the flaps upwards, outwards, and downwards, as in the instance of the tricuspid valve. The left or superior papillary muscle usually follows the course of the fourth cartilage and space, and the right or in- ferior papillary muscle that of the fifth cartilage, both muscles dipping down- wards towards the lower cartilage or space as they approach the apex. It may be gathered, from what has just been said, that each ofithe higher orifices overlaps in position the orifice immedi- ately below it. Thus the pulmonic orifice at its lower or right edge is situated to a slight extent in front of the upper and left edge of the aortic orifice ; the right pos- terior or lower flap of the aortic valve is situated in front of the upper third or two-fifths of the mitral orifice; and the lower two-thirds or three-fourths of the mitral orifice is behind the corresponding upper portion of the tricuspid orifice. The position of the orifices and valves of the heart in relation to the deeper parts of the heart and of the chest, and to the spinal column, will be considered when the side and back views of the heart and great vessels are described. The Position of the Heart and Great Vessels in Robust and Fee- ble Persons. (See Figs. 66, 67, 68, 69, 70.) We have just seen that respiration ma- terially alters the position of the heart and the great vessels, and that at the end of a deep inspiration the lower boundary of the heart may be two inches lower in relation to the walls of the chest than at the end of a forced expiration. Thus, the lower boundary of the heart is situated behind or even above the lower end of the sternum at the completion of a forced ex- piration ; while it may be situated at the lower end of the ensiform cartilage at the termination of a deep inspiration. Again, the top of the arch of the aorta may be situated behind the upper end of the ma- nubrium at the end of a forced expiration, and behind its lower end on the comple- tion of a deep inspiration. This great change is produced by a double agency, acting in opposite direc- tions : one, the descent of the diaphragm which lowers and lengthens the heart and great vessels, and lengthens the lungs by lowering their base; the other, the ascent and advance of the walls of the chest in front. This combined downward move- ment of the heart and arteries, and up- ward movement of the sternum and car- tilages, doubles the effect on the position of the organ in relation to the cartilages and sternum. In robust persons, who lead an active and laborious life, the amount of reserved air constantly in the lungs is great, the chest is high, deep, and broad, and the heart and arteries are low in position in relation to the anterior avails of the chest. In such persons the chest and its organs present the form and position of inspira- tion, and they have therefore the inspira- tory type of chest. (See Figs. 66, 67, 68, 69.) 1 See pages 391-394. POSITION OF THE HEART AND GREAT VESSELS 415 In feeble persons, on the other hand, Who lead an indoor sedentary life, the amount of reserved air constantly in the lungs is small, the chest is flat and nar- row, and the heart and arteries are high in position in relation to the anterior walls of the chest. In such persons the chest and its organs assume the form and position of expiration, and they present the expiratory type of chest. (See Fig. 70.) over the front of the chest, that of the right ventricle being sometimes trans- ferred, as I have just said, to the epigas- trium, and the apex beat is lost, being enveloped in the folds of the enlarged lung. In such persons, also, the top of the arch of the aorta is low in position, being perhaps situated quite an inch be- low the top of the manubrium. The position of the lower boundary of the heart and the summit of the arch of the aorta being unusually low, the position of every part of the heart and the great arteries is also correspondingly low. It is not necessary to describe the situation of the various anatomical points in detail, but it will be well to name that of the leading landmarks of the heart and great arteries. The boundary-line across the third car- tilage that indicates the upper border of the right auricle and ventricle and the lower limit of the great arteries may be shifted downwards to the level of the fourth cartilages. The position of the origin of the pulmonary artery in front being thus given, that of the aperture and valve of the aorta, being a degree lower and to the left, may be inferred, it being situated behind and a little to the left of the left half of the sternum, on a level with the fourth cartilage and the fourth space. The mitral and tricuspid orifices in their descending order take each of them a lower position, the mitral orifice being situated behind the lower fourth of the sternum, its upper boundary being on a level with the fourth space and its lower border, a quarter of an inch above the lower end of the sternum ; and the tricuspid orifice being behind the lower sixth of the sternum and the upper por- tion of the ensiform cartilage. In feeble, thin persons, of sedentary oc- cupation, or in those who have only re- cently recovered from illness, the lower boundary of the heart may be situated behind the lower end of the sternum, or somewhat higher, and its apex may be present behind the fifth left cartilage, and may be felt, therefore, beating, not in the fifth, but in the fourth space. Each lung at the same time lessens at its base, and shrinks away from before the body of the heart, uncovering the apex and the left ventricle, the whole of the right ventricle, and a portion of the auricular appendix, of the pulmonary artery, and even of the ascending aorta. The heart's impulse is, therefore, diffused to an unusual extent over the front of the central part of the chest, from the second space to the fourth, and from the right of the lower portion of the sternum to the apex, being felt not only over the apex, but with considerable force over the right ventricle, where it is usually feeble or absent. A double pul- sation may also be often felt over the pul- Fig. 70. Showing the heart and great vessels in relation to the front of the chest and. the lungs in a slender youth with a small chest. In robust persons, such as sailors, mi- ners, laborers, and smiths, the lower boundary of the heart may be situated quite an inch below the lower end of the sternum, so that the heart may be felt beating in the epigastrium to the left of the ensiform cartilage and the apex of the heart may be situated behind the sixth left cartilage or space. The lungs at the same time enlarge forwards and down- wards, so as to interpose themselves be- tween the heart and the walls of the chest, all but a small space bounded above by the fifth cartilage, on the right by the en- siform cartilage, and on the left by the sixth and seventh cartilages near their attachment to the sternum. The heart's impulse is, therefore, quite imperceptible 416 POSITION AND FORM OF THE HEART. monary artery, feeble and soft with the first sound, but sharp and sudden with the second sound. In such persons also the top of the arch of the aorta is high, being situated behind or even above the top of the manubrium. The position of the other parts of the heart and great vessels is correspondingly high. The boundary-line between the upper border of the right auricle and ven- tricle and the lower limit of the great arteries may be on a level with the mid- dle of the second space, behind which the origin of the pulmonary artery may be seated. The orifice and valve of the aorta, being a stage lower and to the left, may be on a level with the lower portion of the second space and the third carti- lage, behind the left half of the sternum. The mitral orifice may be situated behind the left half of the sternum, behind and just below the central portion of the bone, its upper border being on a level with the upper edge of the third cartilage, and its lower border with that of the upper edge of the fourth cartilage ; and the tricuspid orifice may be situated behind the right half of the sternum just below the centre of the bone, so that its upper border may be on a level with the lower edge of the third cartilage or the upper portion of the third space, while its lower border may be on a level with the fourth space. In many well-formed women of active, healthy habits, the heart and great ves- sels maintain their proper position. But this is not so in the large class of women who work indoors with the needle, and in whom the chest is wont to be flat, the po- sition of the heart being high. The effect of tight stays is to lessen the descent of the diaphragm, and to in- crease, for the sake of compensation, the expansion and elevation of the upper part of the front of the chest. In such per- sons a double and opposite effect may be produced. The lower boundary of the heart in relation to the lower end of the sternum may be high, but the top of the aorta in relation to the higher costal car- tilage may be low. In children of both sexes the position of the heart in relation to the Avails of the chest is high. inch and a half below the lower end of the sternum. In this instance the top of the manu- brium was on a level with the middle of the body of the third dorsal vertebra, and the lower end of the sternum was on a level with the upper border of the ninth vertebra. The middle of the sternum corresponded in level to the lower portion of the body of the fourth vertebra; the lower end of the manubrium, to the lower portion of the fifth vertebra ; and the top of the lower third of the sternum, to the middle of the body of the seventh dorsal vertebra. The ensiform cartilage was of great length, measuring nearly 3 inches (2'8 inches), and its lower end was about on a level with the upper border of the body of the twelfth dorsal vertebra. This drawing and Plate X. of the same work show well the great anatomical im- portance of the somewhat neglected ensi- form cartilage, especially to the clinical worker. The front of the diaphragm, and the floor of the pericardium, which is formed by the central tendon of the dia- phragm, take their origin in part from the tip of the ensiform cartilage by means of a strong slip of muscular fibres. The lower boundary of the pericardium and of the heart, and the lower boundary of the diaphragm, and with it that of the cavity of the right side of the chest and the right lung, may be brought down on a deep inspiration almost to the extremity of the ensiform cartilage, when that point forms the lower boundary of the chest. In this drawing, the lower boundary of the peri- cardium and the lower margin of the right lung were situated an inch above the end of the ensiform cartilage, and nearly two inches below the lower end of the sternum, and the lower boundary of the heart at the apex, as I have already remarked, was an inch and a half below the level of the lower end of the sternum. The top of the arch of the aorta at the adjacent origin of the innominate and left carotid arteries was in this instance four-fifths of an inch (-8 inch) below the top of the manubrium, and was on a level with the upper portion of the body of the fourth dorsal vertebra. The lower end of the descending por- tion of the arch of the aorta was in front of the upper portion of the body of the sixth dorsal vertebra, and was on a level with a point a little below the lower end of the manubrium. The top of the pulmonary artery was a little higher in position than that of the lower end of the descending portion of the arch of the aorta just described ; the ori- gin of the pulmonary artery was three- quarters of an inch below the centre of the sternum, and within the third space, and was on a level with the lower portion of the body of the seventh vertebra; and the SIDE VIEW; AFTER DEATH. LEFT SIDE. (Fig. 71.) The ninth plate of my Medical Anat- omy represents a side view, looked at from the left side, taken from the body of a robust well-formed man. In this body the lower boundary of the heart was sit- uated behind the ensiform cartilage, an SIDE VIEW: AFTER DEATH. 417 pulmonary artery occupied in its ascent the upper portion of the third space, the third cartilage, and the second space. The top of the appendix of the right auricle was nearly half an inch below the centre of the sternum, and on a level with the cartilage between the sixth and sev- enth vertebrae. The top of the appendix of the left auricle, and the upper boundary of the left ventricle, which would be a little above the lower boundary of the orifice of the aorta, were about on a level with the middle of the body of the seventh dorsal vertebra behind, and the top of the lower third of the sternum, or about the fourth costal cartilage in front. The lower boundary of the left auricle, which would nearly correspond with the lower boundary of the mitral valve, was in front of the top of the ninth vertebra, and on a level with a point a quarter of an inch above the lower end of the sternum. The lower boundary of the posterior part of the left ventricle was in front of the top of the tenth dorsal vertebra, and about on a level with a point four-fifths of an inch below the lower end of the sternum ; while the lower boundary of the left ven- tricle at the apex was on a level with the lower portion of the body of the tenth dorsal vertebra, and with a point about an inch and a half below the lower end of the sternum. RIGHT SIDE. The tenth plate of my Medical Anat- omy represents a side view, looked at from the right side, taken from the body of a strong man with a well formed chest of the inspiratory type. In this body the heart was distended with water, and the lower boundary of the swollen right ven- tricle was situated behind the ensiform cartilage, three-quarters of an inch ('7 inch) above the tip of that cartilage, and an inch and a half (1'4 in.) below the lower end of the sternum. The top of the manubrium in this in- stance corresponded in level with the lower border of the body of the second dorsal vertebra ; the lower end of the sternum, with the lower border of the ninth vertebra; the middle of the ster- num at the level of the third cartilage, with the body of the sixth vertebra ; the lower end of the manubrium, with that of the fifth vertebra ; and the upper border of the lower third of the sternum corre- sponded in level with the body of the seventh dorsal vertebra. The commencement of the superior vena cava in this instance was on a level with a point below the middle of the man- ubrium in front, and with the body of the fourth dorsal vertebra behind; and the termination of the vein in the right auri- cle was in front of the cartilage between the sixth and seventh vertebrae, and on a level with a point half an inch below the middle of the sternum, and with the third space. The top of the appendix of the right auricle was on a level with the middle of the sternum and the third cartilages in front, and the body of the sixth dorsal vertebra behind ; the attachment of the lower boundary of the appendix to the body of the right auricle, at the trans- verse furrow, which corresponds closely to the upper boundary of the tricuspid valve, was on a level with a point an inch and a quarter above the lower end of the sternum in front, and the upper border of the eighth dorsal vertebra behind ; and the lower boundary of the right auricle, which corresponds closely to the lower boundary of the tricuspid orifice, was on a level with a point half an inch below the lower end of the sternum in front, and the upper portion of the tenth dorsal vertebra behind. The origin of the pulmonary artery and the upper boundary of the right ventricle were on a level with a point half an inch below the centre of the sternum and the third space in front, and with the lower border of the sixth vertebra behind ; and the lower boundary of the right ventri- cle in front was situated behind the ensi- form cartilage, an inchand a half (1'4 in.) below the lower end of the sternum, and three-quarters of an inch above the tip of the ensiform cartilage in front, and about on a level with the lower border of the body of the tenth dorsal vertebra behind. The lower boundary of the right ventricle was about three-quarters of an inch higher behind than in front. The lower boundary of the pericardium was about an inch and three-quarters be- low the lower end of the sternum, and about half an inch above the tip of the ensiform cartilage. Although I possess other drawings showing a side view of the heart and the other internal organs, these are the only ones that give the relation of the heart and its various parts to the walls of the chest in front and the spinal column be- hind. Both of these drawings were taken from the bodies of men of a robust frame, with a chest of the inspiratory type, and with a heart well developed and low in position. The relations of the heart to the front of the chest in all their variety have been already abundantly illustrated, and its relations to the spinal column will be further described when the position of the heart and great vessels looked at from the back is considered. Pirogoff gives numerous sections, both vertical and hori- zontal, showing the position of the various parts of the heart and great vessels in re- lation to the anterior walls of the chest vol. ii.-27 418 POSITION AND FORM OF THE HEART. and the spinal column, and I therefore refer the reader to the notes describing those sections and two others that are fig- ured in Braun's work. (Note 40; Note 47.) where they are situated immediately be- hind the left auricle and the base of the left ventricle. By the distribution also of the fibrous pericardium to the veins en- tering, and the arteries leaving the sac, and to the branches of those arteries in the neck, the central tendon of the dia- phragm, when it descends during inspi- ration, draws intermediately upon the whole of those vessels so as to save them from dragging immediately upon the heart itself. SIDE VIEW; DURING LIFE. In a Healthy Man with a well- formed Chest. left side. (Fig. 71.) The heart and great vessels occupy the space in the centre of the chest, between the sternum in front and the bodies of the dorsal vertebrae behind. The margins of the lungs fill up the unoccupied spaces in front of* the great vessels and the heart; and the oesophagus and descending aorta are interposed between the heart and the bodies of the vertebree behind. It is evident that in the recumbent pos- ture and during the ventricular systole, the heart would press backwards upon the oesophagus and the descending aorta so as to render swallowing difficult, and to in- terfere with the flow of blood to the lower part of the body, unless the heart were supported by some special contrivance. Such support is to be found in the walls of the pericardial sac. The floor of the pericardium is formed by the central ten- don of the diaphragm, which is suspended in its place, in the middle of the partition between the chest and the abdomen, by means of the great converging circuit of the muscular fibres of the diaphragm, arising from the ensiform cartilage and the ribs; and is supported firmly from be- low by the liver and stomach. The heart rests upon the floor of the pericardium, formed by the central tendon of the dia- phragm, and this supplies a smooth in- clined plane, upon which the heart glides forwards and downwards during inspira- tion, and backwards and upwards during expiration, so as to adapt itself to the va- rious modulations of respiration. The strong fibrous walls of the pericardium arise from the central tendon of the dia- phragm. Those walls are endowed with a fibrous structure which is of special strength posteriorly, where it is firmly in- corporated with the coats of the pulmo- nary veins as they enter the pericardium. A fibrous covering is also contributed by the pericardium to the inferior and supe- rior veme caves where they enter the sac, and to the pulmonary artery and ascend- ing aorta where they leave the sac. In virtue of this arrangement the posterior wall of the pericardium supports the heart forwards and prevents it from making pressure upon the aorta and oesophagus, Fig. 71. Side view, looked at from the left side, showing the heart and great vessels in relation to the walls of the chest and the spinal column. The lower boundary of the heart is on a level with the lower end of the upper third of the ensiform cartilage and the upper edge of the sixth costal cartilage in front, and with the upper edge of the tenth dorsal vertebra behind. The top of the arch of the aorta, at the origin of the innominate, and the left carotid arteries, is on a level with the top of the middle third of the manubrium in front, and the lower edge of the body of the third or the upper edge of that of the fourth dorsal SIDE VIEW. DURING LIFE. 419 vertebra behind. The horizontal bound- ary-line that divides the upper border of the heart from the origin of the pulmonary artery and the ascending aorta, is on a level with the third cartilage in front, and the body of the sixth dorsal vertebra be- hind. The heart therefore extends down- wards from the body of the sixth dorsal vertebra to that of the tenth, and from the third costal cartilage to the sixth ; and the great arteries extend upwards from the body of the seventh to that of the third or fourth dorsal vertebra behind, and from the level of the third cartilage to the top of the middle third of the manu- brium in front. The left auricle and ventricle occupy fully as great a proportionate amount of space at the left side of the heart as the right auricle and ventricle do at the front of the heart. The left ventricle occupies by much the largest share of the left side of the heart, and its double-convex cone- shaped outline is completely exposed to view from its base to its apex when the left side of the chest is looked at. The transverse furrow, which divides the left ventricle from the left auricle, follows a direction from above downwards and somewhat backwards. The left auricle rests behind on the descending aorta and the oesophagus; and that auricle, the transverse groove, and the mitral orifice are situated in front of the seventh and eighth dorsal vertebrae and the upper border of the ninth ; and on a level with the sternal end of the third and fourth costal cartilages, the fourth space, and the upper edge of the fifth cartilage in front. The upper border of the left ventricle is nearly as high as that of the left auricle, but the lower boundary of the left ventri- cle which extends down almost or quite to the upper border of the tenth dorsal vertebra, is considerably lower than that of the left auricle, which reaches down to the lower border of the eighth or upper border of the ninth vertebra. The left auricle and ventricle take a direction from behind forwards, to the left and down- wards, and as they have a similar inclina- tion to that of the ribs, they, as well as the transverse furrow between them, are covered throughout by the fourth, fifth and sixth ribs. The left auricle and ven- tricle start from the back of the centre of the chest in front of the bodies of the seventh, eighth, and ninth dorsal verte- brse, and the left ventricle crosses from the back to the front of the chest with a definite leaning to the left, so that its apex points at the left fifth space. The left auricular appendix and the left pul- monary veins, where they enter the auri- cle at its higher part, are situated in front of the adjoining portions of the bodies of the seventh and eighth dorsal vertebrae and their intervening cartilage, and on a level with the third and fourth costal car- tilages and the third space in front. The anterior longitudinal furrow pre- sents a convex outline, looking forwards towards the pulmonary artery at its upper third, and towards the right ventricle at its lower two-thirds ; and a concave out- line looking backwards and downwards towards the left auricular appendix and the left ventricle. The upper end of this furrow is in front of the body of the seventh dorsal vertebra and behind the third costal cartilage or space, and the lower end of the furrow at the apex of the heart is situated behind the lower border of the fifth space, and is on a level with the body of the tenth dorsal vertebra behind. During the ventricular systole, the left ventricle and auricle change remarkably in form, size, and position (Dig. 63). The ventricle contracts and shortens, and the auricle expands and lengthens to a great extent. The base of the ventricle and the adjoining edge of the auricle, the trans- verse furrow and the mitral orifice ad- vance to a considerable extent forwards, to the left and downwards away from the spinal column and towards the apex of the left ventricle. The apex at the same time moves forwards, upwards and to the right, towards the base, so that the base and apex of the ventricle both approxi- mate towards each other, and towards a zone of rest in the walls of the ventricle, situated nearer to the apex than the base. The anterior wrall of the ventricle, at the anterior longitudinal furrow, advances forwards and becomes more convex; while the posterior wall of the ventricle also advances forwards, but to a much greater extent, especially at its middle, where it becomes hollow, the apex point- ing downwards ; so that the posterior w7all of the ventricle, previously convex, be- comes concave towards the apex and con- vex at the base, thus presenting a double curve. All the systolic movements of the left ventricle converge forwTards, towards the point of rest on the surface of the right ventricle, about its middle and near the septum. During the ventricular systole the left auricle becomes greatly distended and ex- pands upwards, forwards and downwards, along its upper, anterior and lower bor- ders respectively, the amount of move- ment of the auricular appendix being greater than that of the transverse fur- row. The posterior wall of the auricle which rests on the back of the pericar- dium remains stationary. The right ventricle extends in front from the third cartilage to the sixth, and from the middle of the sternum to the lower portion of the upper third of the ensiform cartilage, and is on a level be- hind with the body of the seventh dorsal 420 POSITION AND FORM OF THE HEART. vertebra at its upper boundary, and with the upper portion or middle of the body of the tenth dorsal vertebra at its lower boundary. During the systole of the ventricles, the right ventricle advances, while the upper portion of its walls contracts downwards and the lower portion of its walls con- tracts upwards, those movements con- verging towards a point situated near the longitudinal furrow and the attachment of the anterior papillary muscle. The pulmonary artery conceals the as- cending aorta in the first half of its course, when we look at the left side of the heart. By removing the fat between the pul- monary artery and the left auricular ap- pendix, the left posterior sinus of the aorta and the left or posterior coronary artery are brought into view, deep behind and beyond the posterior surface of the pulmonary artery. The mode in which the pulmonary artery in its progress back- wards, and the ascending aorta in its progress upwards, cross each other, is now well seen. When the arch of the aorta is looked at in front, it does not present the appearance of an arch, since the left border of the ascending aorta is situated almost in front of the deep right border of the descending aorta; and the pulmonary artery covers the left edge of the ascending and almost the whole of the descending aorta, the deep left edge of which is alone visible in front. When, however, the left side of the arch of the aorta is looked at, its arched form is at once apparent, the ascending aorta form- ing the front, the descending aorta the back, and the transverse aorta the top of the arch. The pulmonary artery as it ascends makes for the hollow of the arch of the aorta, through which it sends its right branch, audits direction is therefore much more from before backwards than from below upwards. The origin of the pulmonary artery is situated just behind the third left car- tilage, and is on a level with the body of the seventh dorsal vertebra. The upper boundary of the pulmonary artery, at the top of its point of bifurcation, which is also its most posterior portion, is situated in front of the lower portion of the body of the fifth, or the upper portion of that of the sixth dorsal vertebra, and on a level with the second costal cartilage; and the left and right branches of the pul- monary artery are situated in front of the body of the sixth dorsal vertebra, on a level with the second space. The pulmonary artery in its course from before backwards and upwards presents a convexity on its anterior and upper sur- face, and a concavity on its posterior and lower surface, and is on a level with the third left cartilage and the second space. The posterior sinus of the pulmonary ar- tery is somewhat lower in position than the two anterior sinuses, and is situated behind the upper portion of the third spaee. The left bronchus separates the left pulmonary artery from the left pul- monary veins. During the systole of the ventricles, the whole pulmonary artery lengthens and enlarges. The origin of the artery moves to a considerable extent downwards and forwards, the higher parts of the artery sharing this movement, but to a less and less extent from below upwards. The two anterior sinuses of the pulmonary artery descend more during the systole than its posterior sinus, so that the ante- rior or higher valves are then more nearly on a level with the posterior or lower valve than during the diastole. The arch of the aorta, like the pulmo- nary artery, lengthens and enlarges dur- ing the systole, so that the whole arch widens. The orifice of the aorta, which is situated at the centre of the heart, moves to a considerable extent down- wards and to the left, the direction of its movement, like that of the mitral valves, being towards the apex. The walls of the ascending aorta also move down- wards, but to a less and less extent from below upwards. The position of the ascending, trans- verse, and descending portions of the arch of the aorta in relation to the sternum, the adjoining parts, and the spinal column has already been described. The pulmonic, the aortic, and the mi- tral orifices and valves are situated in their relative position on an inclined plane, each being one above and behind the other in the order named, the orifice of the pulmonary artery being the highest and most anterior, the mitral orifice the lowest and most posterior, and the aortic orifice holding an intermediate position. The upper and anterior boundary of the pulmonic orifice and valve is behind the third costal cartilage and on a level with the lower third of the body of the sixth dorsal vertebra; and the lower boundary of the mitral valve is on a level with the fifth cartilage, and is situated in front of the lower border of the body of the eighth or the upper border of that of the ninth dorsal vertebra. The aortic orifice, being a stage lower than the pulmonic orifice, by which it is overlapped, is in front of the body of the seventh dorsal vertebra, and the intervertebral cartilage just be- low it. The mitral orifice is in front of the same intervertebral cartilage, the body of the eighth and the upper border of the body of the ninth dorsal vertebra. The position of the sternum and costal cartilages in relation to those valves need not be here repeated. The position that I have assigned to SIDE VIEW : DURING LIFE. 421 the various parts of the heart and great arteries is that which usually exists in a healthy, well-formed man, but those parts change in position during the systole and diastole of the ventricles, and during in- spiration and expiration, in the manner and to the extent that I have already de- scribed. In those who are robust and possess a broad and deep chest of the in- spiratory type, the position of the heart and arteries and of all their parts are lower, while in those who are slender and possess a narrow and flat chest of the ex- piratory type, the position of those parts is higher, than in the average man whom I have taken as an example. During in- spiration the whole of the anterior walls of the chest ascend considerably, but the spinal column, owing to the deepening of the dorsal arch, descends to a small but definite degree, the descent of the upper being greater than that of the lower dor- sal vertebrae, some of the lowest of which are stationary. While, therefore, during respiration, the change in the position of the cartilages and sternum in relation to the heart and arteries is doubled by the inspiratory ascent of those cartilages dur- ing the descent of the heart, and by the expiratory descent of those cartilages during the ascent of the heart; the slight respiratory movement of the dorsal ver- tebrae is in the same direction as the movement of the heart, that of both of them being downwards during inspira- tion, and upwards during expiration. The result is, that the position of the heart and great arteries in relation to the bodies of the dorsal vertebrte during respiration is more stable than their position in rela- tion to the sternum and cartilages. For a twofold reason, the position of the great arteries in relation to the superior dorsal vertebra? changes less during respiration than the position of the heart in relation to the lower dorsal vertebrse. The first reason is the greater respiratory move- ment downwards and upwards of the higher than of the lower vertebrse. The second reason is the attachment of the descending aorta by means of the inter- costal arteries to the spinal column, as well as that of the great branches of the arch to the head, neck, and arms, which hold the movements of the great arteries in check. The heart itself, on the other hand, is suspended so freely in the centre of the chest that it yields without re- straint to every definite influence, being thus moved readily upwards and down- wards by respiration, and by the disten- sion and collapse of the abdomen, and from side to side by changes in position, or by effusion into or tumors in the chest, or by contraction or expansion of either lung singly. RIGHT SIDE. The position of the heart and great vessels viewed from the right side is much more simple than that of their position viewed from the left side. When the right side of the heart is looked at, the right auricle and ventricle, the descend- ing vena cava, the ascending aorta, and the pulmonary artery are visible, but every other part is concealed. The rela- tive position of the lower boundary of the heart, of the top of the arch, and of the boundary-line separating the great vessels from the heart is necessarily the same on the right side of the chest as on the left side. The upper boundary of the right ventricle is on a level with the body of the seventh, and its lower boundary with that of the tenth dorsal vertebra. The right ventricle occupies the anterior por- tion of the space between the sternum and the spinal column; and the right auricle, including its appendix, occupies the posterior portion of that space; so that its posterior surface is situated in front of the right side of the bodies of the dorsal vertebrte from the seventh to the upper portion of the tenth, the right pulmonary arteries and pulmonary veins and the right portion of the left auricle being interposed. The tricuspid orifice is the most an- terior and the lowest in position of the four orifices of the heart and great ves- sels, and is separated from the spinal column by the left ventricle and auricle. The tricuspid orifice is situated, as we have already seen, behind the right half of the lower fourth of the sternum, and is on a level with the bodies of the eighth and ninth dorsal vertebrae. The descending vena cava is situated to the right of the ascending aorta and on a deeper plane. The commencement of the vein, at the confluence of the two in- nominate veins, is on a level with the body of the fourth dorsal vertebra, and it enters the right auricle behind its appen- dix in front of the body of the seventh dorsal vertebra, the right pulmonary artery being just above its termination, the superior right pulmonary vein just below it, and the oesophagus just behind it or to its left. The vein, as it descends, rests upon the right side of the trachea near and at its bifurcation, and upon the right bronchus. 422 POSITION AND FORM OF THE HEART. ventricle from base to apex ; anteriorly, the lower surface of the right ventricle ; and intermediately, the posterior longitu- dinal furrow. The lower boundary of the left ventricle is on a level with or higher than the spine of the ninth and the upper portion of the body of the tenth dorsal vertebra ; the top of the arch of the aorta at the origin of the innominate and left carotid arteries is in front of the spine of the third and the lower edge of the body of the third or the upper edge of that of the fourth dor- sal vertebra, or it may be somewhat higher ; and the boundary line between the heart and the great arteries, at the lower border of the division of the right and left pulmonary arteries and the upper border of the left auricle, is in front of the spine of the fifth and the lower border of the body of the sixth dorsal vertebra. The level of the boundary line between the heart and the great arteries is some- what higher behind, where it follows the line of the lower border of the division of the pulmonary artery, than it is either in front or at the sides, where it follows the line of the origin of the pulmonary artery or that of the top of the right auricle. The Left Auricle and Ventricle.-The left auricle and ventricle maintain the same relation to each other and to the spinal column at the back of the chest that the right auricle and ventricle do to each other and to the sternum at the front of the chest, but each portion of the left side of the heart bears more to the left be- hind, than the corresponding portion of the right side of the heart does in front. The left auricle at its upper and pos- terior portion, which includes the auricu- lar appendix, is central, being situated in nearly about equal proportions to the right and left of the middle line of the spinal column. The auricular appendix, which is a semi-detached wing of the auricle, leaves the body of the auricle at its left upper corner and advances for- wards and to the left, so as to fill up the deep furrow between the pulmonary artery and the base of the left ventricle. The lowest portion of the left auricle lies en- tirely to the right of the middle line of the spine, while the left ventricle lies al- most completely to the left of it, and the transverse furrow where it separates the two cavities occupies an intermediate position, its upper portion lying consider- ably to the right, and its lower portion slightly to the left of the middle line of the spine. The left auricle at its anterior aspect lies, when at rest, almost entirely to the right of the middle line of the chest, but its left boundary moves to the left of the middle line when the ventricles con- tract, and to the right of that line when they dilate. The transverse furrow takes an oblique direction from above down- BACK VIEW; AFTER DEATH. I made observations some years ago on the position of certain parts of the heart and great vessels in relation to the spines of the dorsal vertebras in eleven different bodies. The top of the arch of the aorta was situated in front of a point below the spine of the second dorsal vertebra in one instance, just above the spine of the third dorsal vertebra in seven instances, and below the spine of that vertebra in three instances. In other words, in one instance the top of the arch was in front of the upper portion of the body of the third dorsal vertebra, in seven cases it was in front of its lower portion, and in three it was in front of the body of the fourth dor- sal vertebra. The lower boundary of the left ventricle was on a level with the spine of the ninth dorsal vertebra in one in- stance, with a point just above that spine or below that of the eighth vertebra in eight cases, with the spine of the eighth vertebra in one, and above it in one. In other words, the lower boundary of the left ventricle varied in position from the level of the lower edge of the body of the eighth to that of the upper third of the tenth dorsal vertebra. In five instances the upper boundary of the left auricle was on a level with the spine of the fifth dor- sal vertebra (in one), or just above that spine (in one), or just below that spine (in three); and its lower boundary was on a level with (in one), above (in one), or below (in three) the spine of the seventh dorsal vertebra. In other words, the upper border of the left auricle was situated in front of the upper part of the seventh dorsal vertebra, or just above it, and its lower border in front of the body of the eighth vertebra.1 BACK VIEW; BERING LIFE. In a Healthy Man with a well- formed Chest. (See Fig. 72.) When the back of the heart and great vessels is exposed, the left cavities of the heart are brought into view, the lower boundary of the left ventricle resting upon the lloor of the pericardium, which con- ceals the under surface of the heart. When the floor of the pericardium is withdrawn, the under surface of the heart is visible from behind. The under sur- face of the heart inclines from behind downwards and forwards, and it presents posteriorly, the lower border of the left 1 Note 46 ; Note 47. BACK view: after death. 423 wards and from right to left, and as it sweeps to and fro, from one side to the other and back again, during the contrac- tion and dilatation of the ventricle, it occupies a position in front of the spines of the fifth, sixth, and seventh, and the bodies of the seventh and eighth dorsal vertebrae, and the upper part of that of the ninth. The heart is attached to the roots of the lungs by the entrance of the right and left pulmonary veins into the upper part of the left auricle at either side of the spine. The left pulmonary veins are as a rule higher in position, and enter the auricle nearer to the centre of the spine than the right, while the right lower pulmonary vein is larger and lower in position than the left, the right lower vein being sometimes double. The greater size of the lower lobe of the right lung compared with that of the left, evi- dently accounts for the greater size of the right lower pulmonary veins. The higher position of the left side of the auricle, owing to the presence on that side of the base of the ventricle, and the general inclination downwards of the heart, its longitudinal parts following the line of the longitudinal furrows from right to left, and its transverse parts following the oblique direction of the transverse furrow from left to right, explain, I consider, the Fig. 72. Back view, showing the heart and great vessels in relation to the spinal column, the ribs, and the diaphragm. lower position of the right than the left pulmonary veins. The pulmonary veins have, in short, more room to deploy on the right side of the left auricle, where no object interferes with their freedom, than on the left side of the auricle at its upper angle, where the veins and the auricular appendix .are pushed up into a corner by tHe close proximity of the upper border of the left ventricle. The downward incli- nation from left to right of the upper boundary of the left auricle, between the left and right pulmonary veins, although quite definite, is very much less than the 424 POSITION AND FORM OF THE HEART. downward inclination from left to right of the posterior transverse furrow. The right pulmonary veins are on a level with the spines of the fifth and sixth dorsal vertebrae, and the two left pulmonary veins, holding a higher position, are re- spectively just above the level of those two spines. The left ventricle lies to the left of the spinal column, and extends in a direction to the left downwards and forwards, from its base at the back of the chest where it is in front of the spinal column on a level with the sixth and seventh dorsal spines, to its apex at the front of the chest .where it is behind the fifth left inter- costal space. The upper boundary of the left ventricle is more rounded and more inclined from above downwards than its lower boundary along the line of the pos- terior longitudinal furrow, where it is more nearly straight and horizontal. The posterior and left border of the mitral orifice is situated about or fully half an inch to the left of the posterior transverse furrow. This orifice looks towards the apex of the left ventricle, or in a direction to the left, forwards and slightly downwards. Its superior or left angle is a little behind the auricular ap- pendix, on a level with a point above the spine of the sixth, and with the. middle of the body of the seventh dorsal vertebra, and about half an inch, more or less, to the left of the middle line of the spine. Its inferior or right boundary is on a level with the spine of the seventh, and the lower portion of the body of the eighth dorsal vertebra, and with a point between the scapulae, just above their lower angles, and a little to the left or right of the mid- dle line of the spine. The space between the mitral orifice and the apex of the left ventricle is occupied by the flaps of the mitral valve, their tendinous cords, and the papillary muscles, the apparatus of the mitral valve occupying the space at the back of the left ventricle between its base and its apex. The apparatus of the mitral valve is always in action. The transverse furrow and the mitral orifice oscillate to and fro extensively, moving to the left, forwards, and slightly downwards towards the apex during the contraction of the ventricle, and in the reverse direction during the dilatation of the ventricle (see Fig. 63, p. 401). The mitral portion of the left auricle and the base of the left ventri- cle necessarily share in the movements of the mitral orifice and of the transverse furrow in extent and direction, but the movements of the walls of both cavities, as they recede from the orifice, gradually lessen, and at a zone or transverse circuit of stable equilibrium around each cavity, the walls both of the auricle and ventri- cle maintain a state of rest. This zone of rest in the left ventricle is probably more near to its apex than its base, while the position of the zone of rest in the left auricle is probably to the left of and just below the termination of the right and left inferior pulmonary veins. The apex moves towards the zone of rest of the ventricle during the contraction of that cavity, but the upper and right boundary of the left auricle moves away from, or to the right of the zone of rest of the auri- cle during the dilatation of that cavity. Thus during the systole of the ventricle there is a movement, both of the base and the apex of the cavity towards a com- mon centre, tending to its complete con- traction ; while during the same period the auricle dilates in all directions, and its left and right portions both diverge from the zone of rest of the cavity. The movement of expansion to the left, for- wards and downwards, of the mitral por- tion of the auricle, is much greater than the movement of expansion to the right and upwards of the right portion of the auricle. During the contraction of the left auricle and the expansion of the left ventricle, the reverse movements take place at the mitral orifice, the transverse furrow, and both cavities at all points. The play of all these parts is constant, and they are a-lways undergoing a series of regulated and co-ordinate changes in po- sition. For this reason, although the range of movement of each part, as far as we know it, can be assigned within cer- tain limits, yet the exact position of each part cannot be stated.1 The position of the mitral orifice, which is oblique in direction from above down- wards, and from left to right, is, as I have just said, in front and to the left of the fpines of the sixth and seventh dorsal vertebrae, and between the scapulae, a little above their lower angles. This region forms a landmark for the position of the mitral orifice and valve over the dorsum. The left ventricle is situated to the left of this region, and extends below its level. During the diastole of the ven- tricle, the stream of blood from the auricle into the ventricle pours across this region in a direction from right to left, forwards and somewhat downwards. To the right of, and rather above this region, is situ- ated the left auricle; and in cases of mitral incompetence, the reversed stream of blood pours across this region from left to right and somewhat upwards, as it regurgitates from the left ventricle into the left auricle. In cases of mitral regurgitation, one 1 I have frequently observed the movements of the heart in animals at the front and the side but never at the back of the organ, so that the movements of the left auricle de- scribed above have been derived from infer- ence and not from observation. BACK VIEW: AFTER DEATH. 425 might be led, a priori, to expect that the mitral murmur would be always audible over the back at the region of the mitral orifice, or midway between the scapulae, just above the level of their lower angles. This is, however, not usually the case, and especially when the mitral murmur is soft in character, the lungs and chest are of full size, and respiration is free. This is, I believe, to be explained by the great space that intervenes, owing to the pres- ence of the vertebrae, between the mitral orifice and the ear when applied over that region, by the extent to which the lungs envelop the heart and fill the chest back- wards, and by the position of the descend- ing aorta and the oesophagus between the mitral orifice and left auricle in front and the spinal column behind. When, how- ever, the mitral murmur is grave, vibrat- ing or musical in character and loud, and when the lungs and chest are contracted and respiration is limited, then the mitral murmur is audible over the back at the region of the mitral valve, and in many cases with great intensity. The Hight Auricle and Ascending Vena Cava.-The inferior and posterior portion of the right auricle, and the entrance of the ascending vena cava into that portion of the auricle are situated at the back of the heart. The right auricle is here separated at its upper boundary from the lett auricle below the entrance of the lower right pulmonary vein by a septum, which often makes but little mark ex- ternally. The lower boundary of the right auricle is defined by the continua- tion backwards of the posterior transverse furrow between the base of the left ven- tricle and the right auricle, until it reaches the posterior longitudinal furrow. The posterior and inferior portion of the right auricle thus fills up the angle formed be- tween the lower border of the left auricle and the base of the left ventricle poste- riorly. This angle is formed by the down- ward prominence and thickness of the mus- cular wall of the left ventricle at its base. The ascending vena cava penetrates the diaphragm on a level with the eighth or ninth dorsal spine, where it is situated nearly half an inch to the right of the descending aorta, and of the middle line of the spine ; and after ascending to the extent of an inch or less, it enters the right auricle on a level with the seventh dorsal spine, about three-quarters of an inch to the right of the descending aorta. The Under Surface of the Heart; the Longitudinal Furrow and the Hight Ven- tricle.-The posterior longitudinal furrow divides the left ventricle behind from the right ventricle in front, on the under sur- face of the heart, and when that organ rests upon the floor of the pericardium, the transverse furrow and the right ven- tricle are hidden. When, however, the floor of the pericardium is lowered so as to bring into view the under surface of the heart, which inclines from behind, for- wards and downwards, the posterior lon- gitudinal furrow, and the under surface of the right ventricle beyond and in front of it, are rendered visible. The posterior longitudinal furrow, resting upon and adapting itself as it does to the floor of the pericardium, is comparatively hori- zontal in direction ; but it is slightly con- vex near the base of the ventricle, owing to the shoulder formed there by the mus- cular walls. During the contraction of the ventricle, when its base and apex approximate, the transverse furrow changes in direction both toward the base and the apex. The furrow then be- comes more convex than before at the base, because the base of the ventricle itself becomes more convex, and it turns or twists downwards in a peculiar manner towards the apex, because the apex itself twists downwards, so as to form a con- cavity towards that end. The longitudi- nal furrow then presents, therefore, an outline with a double curve. The posterior longitudinal furrow at its auricular extremity comes very close to the posterior border of the heart, and I think that it is visible from behind at that point, even when the heart rests upon the floor of the pericardium. Thence the furrow advances forwards and to the left to the apex of the heart, where it divides the left ventricle from the right, and where it joins the anterior longitudinal furrow. The under surface of the heart con- tracts gradually from its auricular portion or base, where it is wider than at any other part, to its apex, where it is nar- rower than at any other part. The under surface of the right ventricle is thus tri- angular in form, the base of the triangle being at the auriculo-ventricular furrow, and its apex at the apex of the heart. The posterior longitudinal furrow which is straight, forms the posterior side of the triangle, and the lower boundary of the right ventricle, which is somewhat con- vex, forms its anterior side. This lower boundary of the right ventricle at the front of the heart, which is on a level with the body of the tenth and the spine of the ninth dorsal vertebra, is lower in position than the lower border of the left ventricle at the back of the heart, which is situated in front of the cartilage be- tween the bodies of the ninth and tenth dorsal vertebrae, or a little lower, and is on a level with the space between the eighth and ninth dorsal spines. The apex of the heart is lower in posi- tion than the lower boundary of the right ventricle, and is on a level with the body of the tenth, and with a point above the spine of the ninth dorsal vertebrae, and with the lower angle of the left scapula. 426 POSITION AND FORM OF THE HEART. The Great Vessels.-The position of the boundary line between the upper border of the heart and the lower limit of the great vessels is, as I have already stated, higher at the back than at either side or in front. The boundary line dividing the upper border of the left auricle from the lower border of the right and left pul- monary arteries is situated in front of the cartilage below the body of the sixth and the spine of the fifth dorsal vertebra ; and the lower end of the descending portion of the arch of the aorta and of the vena cava, where it is lost behind the right pulmonary vein, are nearly on the same level. The great arteries of the neck, the de- scending portion of the arch of the aorta, through the medium of the transverse and ascending portions of the arch, the right and left pulmonary arteries, and the right and left pulmonary veins, form in succession a series of central attach- ments for the heart, which are situated, so to speak, in tiers one below the other. To these must be added, but on a differ- ent plane, the descending vena cava. The heart is suspended forwards and down- wards from these various attachments. Two of them, those formed by the pul- monary veins and the pulmonary arteries, connect the heart intimately with the roots of the lungs, so that the roots of the lungs and the heart at that position enjoy a common movement of descent during inspiration, and of ascent during expira- tion, a degree of movement that is mea- sured by the respiratory movements of descent and ascent of the larynx. The descending portion of the arch is maintained at its lower end in a fixed position in relation to the spinal column by the sixth intercostal arteries. The higher intercostal arteries, those which go to the third, fourth, and fifth inter- costal spaces, arise in succession from the descending portion of the arch, in front, in their descending order, of the fifth and sixth dorsal vertebra?. These vessels all ascend from their point of origin to the spaces they respectively supply, the higher arteries making a greater ascent than the lower ones, because they have to reach a higher point in relation to their respective origins ; and the right arteries mounting upwards to a greater extent than the left arteries, because they arise from a lower part of the aorta, owing to the right side of the descending portion of the arch being otherwise occupied by the passage behind it of the oesophagus, and under and in front of it, of the right bronchus. The intercostal arteries to the sixth spaces pass directly to the right and left from their point of origin. It is evident, therefore, that the lower end of the de- scending portion of the arch, which is braced down to the spinal column by the direct origin of the sixth intercostal arteries, is more fixed in position than its upper part, the intercostal arteries from which have a free ascent, and where the oesophagus is interposed between the artery and the spine ; that the descending portion of the arch has less range of movement than the transverse portion, the great arteries from which are com- paratively long and capable of being put on the stretch ; and that the ascending portion of the arch enjoys a still more free play of movement than the trans-, verse portion, for it is weighted at its root by the heart, and it is long, curved, and free from vascular connections. The descending portion of the arch lies in front of the left half of the bodies of the fourth and fifth dorsal vertebra;, and that of the upper border of the sixth, on a level with the third and fourth, and the space between the fourth and fifth dorsal spines, and with the interscapular space at and below the spines of the scapula*. This region forms a landmark at the back for the position of the descending portion of the arch of the aorta ; over this region direct and even regurgitant aortic mur- murs, especially if they are loud, grave, and musical, are often audible, and that with great intensity ; and in this region, the signs of aneurism of the descending aorta most frequently betray themselves. It is sufficient if I allude here to the effect in such cases of the pressure of aneurism affecting this artery on the left recurrent laryngeal nerve, which winds underneath this portion of the arch on its way to the larynx ; on the oesophagus, where it passes behind the artery ; on the left bronchus, where it passes underneath it; on the left pulmonary artery, which is situated in front of the artery ; on the bodies of the vertebra?, upon which it rests ; and on the intercostal nerves that pass between and to the left of those ver- tebrse. I have already described the position of the transverse aorta. The right and left pulmonary arteries are situated in front of the body of the sixth and the spine of the fifth dorsal vertebra, and they, as I have just said, form one of the two great points of attachment of the heart to the roots of the lungs. The principal points of clinical interest with regard to those arteries is the one I have just alluded to in relation to the pressure of aneurism of the descending aorta on the right or left pulmonary artery, which interferes with the supply of blood to the lungs; of the analogous effect of aneurism of the trans- verse aorta, below which the division of the pulmonary artery is situated ; of an- eurism of the ascending aorta on the right pulmonary artery, which often leads to secondary affections of the right lung ; and on the effects of the pressure of an NOTES. 427 intra-thoracic tumor or enlarged bron- chial glands on either of those arteries. The right pulmonary artery is some- what lower in position than the left pul- monary artery, in the same way and for the same reasons that the right pulmo- nary veins are lower than the left pul- monary veins. The descending vena cava is seen from behind, winding round the right side of the ascending aorta; and its great affluent, the left innominate vein, lies in front of the upper border of the transverse aorta and the great arteries that spring from it. Aneurisms of the ascending aorta tend therefore to make pressure on the descend- ing vena cava so as to impede or arrest the flow of blood through that vein to the heart, and the same may be said with regard to the effects of the pressure of aneurisms of the transverse aorta in im- peding or arresting the flow of blood through the left innominate vein. The descending aorta, being attached by the intercostal arteries to the spinal column, is situated in front of the bodies of the dorsal vertebrae at their centre and left side, and it is therefore interposed between the mitral orifice and the base of the left ventricle in front and the spine behind. The oesophagus lies in front of the right side of the spinal column until it reaches the bodies of the eighth, ninth, and tenth dorsal vertebree, which are on a level with the seventh, eighth, and ninth dorsal spines, where it gradually passes over the front of the aorta. It is thus interposed between the left auricle and the right side of the spinal column, and finally between the base of the left ventricle in front and the aorta and spinal column behind. The right and left lungs at the back of the chest fill up the deep hollow in front of the angles of the ribs, and their inner margins overlap respectively the right and left borders of the bodies of the dor- sal vertebra?. The lungs at the back and both sides completely envelop the heart and great vessels, with the exception of those parts that lie at the very centre of the chest, in front of the anterior portion of the bodies of the dorsal vertebrse. NOTES. Note 1.-Pirogoff, in his valuable "Anato- mia Topographica;" Braun, in his beautiful ' 'Topographisch-Anatomischer Atlas;' ' and Le Gendre, in his "Anatomie Chirurgicale Homo- lographique," give drawings taken from sec- tions of the frozen dead body representing the position of the internal organs. In this and the following notes I shall briefly describe the position of the heart as it is represented in those various drawings. I may remark that many of these drawings are evidently not of the size of nature. Pirogoff represents vertical sections of twelve different bodies, the section being made either through the centre of the sternum in front and the spinal column behind or to the right or left of the centre. In these instances the front of the pericardium was lower in position than the front of the heart to an extent vary- ing from "8 or *9 inch to -02 inch. Between these two extreme instances there was every variety of difference from -2 inch to -7 inch, the average extent to which the front of the pericardium was lower than the front of the heart being *4 inch, or less than half an inch. These drawings of Pirogoff represent, which mine do not, the relation of the whole under surface of the heart to the floor of the pericar- dium. In two of them, the whole lower sur- face of the heart, including both ventricles and the longitudinal furrow between them, rested upon the pericardium ; while in one of these, with healthy organs, the front of the pericardium was *7 inch, and in another with, ascites it was -35 inch below the front of the right ventricle. In the latter case the fluid in the abdomen pressed the pericardium up- wards into close contact with the heart, and elevated that organ. In four other cases the right ventricle rested upon the pericardium, while in all of these the interventricular fur- row was separated by fluid from the pericar- dium from -2 in. to *65 in., and in three of them the left ventricle was higher than the pericardium from '3 in. to *4 in. In the six remaining cases, a film of fluid, varying from •1 in. to *5 in., separated both ventricles and the longitudinal furrow from the pericardium; in two of those cases the separation of the two surfaces was equal throughout; in two it was greater at the furrow than the ventri- cles, and greater below the left ventricle than the right; and in two it was greater below the right ventricle than the left. Note 2.-Pirogoff represents the exact posi- tion of the lower boundary of the front of the heart in relation to the lower end of the bony sternum in five instances in which a vertical section was made through the centre of the sternum in front and the spinal column be- hind. In two of these instances the lower boundary of the heart was above the lower end of the sternum to an extent varying from •8 in. to *7 in., and in three of them it was below the lower end of the sternum to an ex- tent varying from one inch to half an inch. He also gives thirteen cross sections of the body that show whether the lower boundary of the heart was higher or lower than the lower end of the sternum. In one instance the lower border of the heart was very much below, and in another it was very much above the lower end of the sternum. The latter case stood alone. The section was made through the lower margin of the nipples and the middle of the third space, and only a small piece of the ventricles towards the apex remained frozen in the pericardial fluid; the heart being absent from behind the cen- tre of the sternum. The stomach and the oesophagus were enormously distended with. 428 POSITION AND FORM OF THE HEART. food, and both the stomach and the liver rose high into the cavity of the chest, above the level of the section. In eight other cases the section was made, as in this one, through the third cartilage, in nine others through the fourth, and in four others through the fourth space; and in all of these, amounting to twenty-one, the heart was present in the sec- tion of full size. Braun gives vertical sections of the body through the centre of the sternum and the spine in two instances, in one of which the lower boundary of the heart is half an inch above, and in the other is an inch and a third below the level of the lower end of the Sternum. Note 3.-The position of the lower boun- dary of the pericardium in relation to the lower end of the sternum is represented by Pirogoff in the two groups of sections, vertical and transverse, referred to in Note 2. In two of the vertical sections the lower boun- dary of the front of the pericardium was above the level of the lower end of the sternum from the tenth to the third of an inch, and in three of them it was below the lower end from 1*2 in. to '88 in. In the thirteen cross sec- tions the lower border of the pericardium was above the level of the lower end of the sternum in only one case, and below it in twelve cases. Note 4.-Pirogoff represents the position of the apex in relation to the fourth, fifth, and sixth spaces and cartilages in the two groups of vertical and transverse sections. In one of the vertical sections, a case of ascites, the apex was situated in the fourth space; in another, it was situated behind the fifth rib, and in a third behind the sixth rib; while of the cross sections, in five the apex was situ- ated in the fifth space, in five behind the fifth cartilage, and in one behind the fourth carti- lage or the third space. Five vertical sec- tions also represent the relation of the lower boundary of the right ventricle to the carti- lages and spaces, at a point intermediate be- tween the lower boundary of the sternum and the apex; in two of these the inferior margin of the right ventricle was behind the seventh cartilage, in one behind the sixth cartilage, in one behind the fifth space, and in one be- hind the fifth cartilage. Note 5.-Pirogoff, in the three vertical and eleven cross sections referred to in Note 4, shows the relation to the cartilages and spaces of the lower boundary of the pericardium be- low the apex. In two of the three vertical sections representing the apex, the inferior border of the pericardium was lower than the inferior border of the apex from two-thirds of an inch (*7 in.) to half an inch ('4 in.) ; and in the remaining one the pericardium fitted close upon the apex. In two of these cases the lower boundary of the pericardium below the apex was behind the sixth cartilage, and in the third, that affected with ascites, be- hind the fifth cartilage. In three of the cross Sections the lower boundary of the pericar- dium below the apex was situated behind the sixth cartilage, in five of them it was behind the fifth space, in two behind the second car- tilage, and in the remaining one behind the fourth cartilage. In two of the five vertical sections in which the relation of the lower border of the right ventricle to the cartilages and spaces is shown, the lower boundary of the pericardium below the ventricle was situ- ated behind the seventh cartilage, in two be- hind the sixth space, and in one behind the sixth cartilage. Note 6.-Pirogoff gives a series of deepen- ing sections made downwards and from side to side, presenting a front view of the organs. In two of the more superficial of these sec- tions there was an inclination of two thirds of an inch (-7 in.) from right to left extending from the lower boundary of the right auricle to the apex of the heart. In a third section, a case of ascites, there was no inclination, the apex being on the same level as the lower border of the right auricle. When the sec- tions deepened, the inclination was still main- tained, but the dip from auricle to the apex was less great. Thus in three sections in which the lower border of the left ventricle was exposed, the dip from auricle to apex was respectively one-half (-4 in.), one-third (•3 in.), and one-sixth (-15 in.) of an inch, the latter section being progressively deeper than the former. In like manner, but with a different effect, in two other sections of the case of ascites, the lower boundary of the apex was higher than that of the auricle, in one section by the fifth of an inch ('2 in.), and in a deeper section by half an inch (-5 in.) Note 7.-Pirogoff shows the extent to which the heart extends to the left of the middle line of the sternum in four (or five) vertical, and in eighteen (or seventeen) cross sections. The heart extended to the left of the centre of the sternum from two inches to two and three-quarters (2'8 in.) in two-thirds of these cases (14 in 22) ; from an inch and a third (1'4 in.) to an inch and three-quarters (1'85 in.) in one-third of them (7 in 22); and three inches and a third (3'4 in.) in one additional instance. Note 8.-Pirogoff indicates approximately the position of the top of the arch in five ver- tical and four cross sections. In two of the vertical sections the top of the arch appeared to be respectively a quarter and a tenth of an inch above the top of the manubrium, on a level in one with the top of the second, and in the other with the top of the third dorsal vertebra. In the three other vertical sec- tions the top of the arch was three-quarters of an inch (-6 to '8 in.) below the top of the manubrium, and on a level with the lower portion of the third dorsal vertebra. In one of the four cross sections the top of the arch at the origin of the innominate and left carotid arteries was on a level with the lower edge of the sterno-clavicular articulation, and with the lower border of the second or upper bor- der of the third dorsal vertebra: while in three of them it was on a level with the first space, and in the individual cases respectively with the lower border of the second, the lower border of the third, and the upper border of the fourth dorsal vertebra. Braun gives two vertical sections, in one of which the top of the arch of the aorta was from a quarter to NOTES. 429 halt an inch below the top of the manubrium and on a level with the third dorsal vertebra, while in the other it was more than an inch below the top of the sternum and on a level with the fourth vertebra. Note 9.-The lower boundary of the heart was from two-thirds of an inch (-6 in.) to an inch below the lower end of the sternum in Pirogoff's three vertical sections in which the top of the aorta was three-quarters of an inch (•6 in. to -8 in.) below the top of the manu- brium ; and was an inch and a quarter below the end of the sternum, reaching, indeed, to the tip of the ensiform cartilage in Braun's case, in which the top of the aorta was more than an inch below the top of the sternum. On the other hand, the lower boundary of the heart was three-quarters of an inch (-8) above the lower end of the sternum in one of Pirogoff's cases, in which the top of the aorta was above the top of the sternum, and was fully half an inch above that bone in Braun's case, in which the top of the aorta was from a quarter to half an inch below the top of the sternum. Note 10.-Pirogoff shows in his vertical sections the position of the origin of the pul- monary artery in eight instances, and that of the top of the auricular portion of the right auricle in seven. The origin of the pulmo- nary artery was situated behind the second cartilage in one instance, and behind the fourth cartilage in another ; in three cases it lay behind the third cartilage, and in one behind the second space ; while in two it lay from two to two and a half inches below the top of the manubrium. The top of the right auricle was seated behind the second carti- lage in two cases, behind the third cartilage in two, and below the top of the manubrium from an inch and a half to an inch and three- quarters in three. In one of the instances in which it lay behind the third cartilage, it was three inches below the top of the manubrium. Note 11.-In five of Pirogoff's vertical sec- tions referred to in Note 10 the vertical length of the pulmonary artery and the right ventri- cle is shown. In two cases the vertical length of the pulmonary artery was about half an inch, and in these two cases the vertical length of the right ventricle was respectively three inches (3'2 in.) and two and a third (2*3 in.). In the three other cases the verti- cal length of the pulmonary artery was about one inch ( 9 in., 1*05 in., 1'2 in.), that of the right ventricle in those cases being about three inches (2 8 in., 3'1 in., 3'5 in.). In the three latter cases, in which the pulmo- nary artery was relatively long, the length of the ventricle to that of the artery was as three to one; while in the two others in which the vessel was short, the ventricle was from four and a half to six times the length of the artery. Note 12.-In one of Pirogoff's transverse sections, referred to in Note 11, the top of the pulmonary artery was situated just above the second cartilage, and the artery, in its short upward course ('4 in.), was covered by the second cartilage ; in another, the top of the artery lay behind the third cartilage, and the artery ascended within the third space. In the three other cases the artery took an intermediate and average position within the second space, its top being seated behind the second cartilage, and its origin behind the third cartilage, or, in one instance, the sec- ond space. The origin of the pulmonary artery was the lowest in position, being behind the fourth cartilage, in the one among these five cases in which the vessel took the longest upward course (1'2 in.) ; while on the other hand, the origin of the artery was the highest, be- ing behind the second cartilage, in the one in which the vessel was the shortest ('4 in.). Note 13.-The arch of the aorta, measured from the point at which it came into view above the right auricle to the adjacent origin of the innominate and left carotid arteries, in Pirogoff's vertical sections, varied in approxi- mate vertical length from about one inch to more than two inches (about 2'2 in.), its av- erage length being about an inch and a half. In two cases, in which the vessel was short (about 1 in.) the vertical length of the arch, from the point at which it came into view, was less than that of the heart, measured, from the same point, in the proportion of 10 to 25 ; while in three cases, in which the ves- sel was long (1'8 in., 2 in., 2'2 in.), the ratio of the length of the vessel to that of the heart was about 10 to 18. Note 14.-Pirogoff shows the vertical length of the right auricle in six sections. In three of these the length of that cavity was two inches and three-quarters (2'6 in., 2'7 in., 2'8 in.); and in three it was from three inches and a third to almost four inches (3'3 in., 3'4 in., 3*8 in.). Note 15.-Pirogoff represents the vertical length of the right ventricle in eleven cases. In two of these the cavity was two inches and a third (2'3 in.), and in one it was four inches in length. There was considerable variation in the other cases between these limits, the average length of the cavity in the eleven cases being three inches. Note 16.-The great vessels occupied the upper half of the sternum, and the heart its lower half, in two of Pirogoff's and in one of Braun's sections. In one of Braun's sections the great vessels lay behind the upper third of the bone, and the heart beat behind its lower two-thirds ; in three of Pirogoff's sec- tions the great arteries were covered by the upper three-sevenths of the sternum, and the heart by its lower four-sevenths (1'5 in. to 2'1 in.; 2'7 in. to 3 in.; 1'4 in. to 2-3 in.) ; while in one of Pirogoff's the great vessels oc- cupied the sternum to a greater extent than the heart in the proportion of eight to seven (3-l in. to 2-7 in.). Note 17.-The width of the healthy heart was one-half of the width of the chest in two of Pirogoff's cross sections (7'8 in. to 3'9 in. and 7'2 in. to 3'5 in.) ; it was one-third of that of the chest in four of them (7'4 in. to 2'4 in., 9'4 in. to 3'2 in., 9'2 in. to 3'2 in., 7'2 in. to 2'6 in.), and in six of them the proportion between the width of the heart and that of the chest varied from 10 to 3'9 to 10 to 4-6. In no instance was the breadth of the healthy heart greater in proportion than 430 POSITION AND FORM OF THE HEART. one-half of that of the chest. In this respect Pirogoff's cases differ from mine, for, as I have said above, in one-third of my cases the width of the heart was greater than one-half of that of the chest (10 to 5 to 10 to 6'2). This may partly be accounted for that in Pirogoff's drawings the section was not as a rule made across the widest part of the heart, and that the breadth of the heart was meas- ured from precisely opposite points ; whereas in mine the measurement was taken from the point of the heart furthest to the left, which was near the apex, to the point of the heart furthest to the right, which was about the middle of the right auricle; and I need scarcely say that these points were never precisely opposite to each other. Note 18.-In some of Pirogoff's sections the right ventricle and auricle were proportion- ally broad in relation to the front of the left ventricle when the heart itself was wide in relation to the width of the chest, while the right cavities were relatively narrow when the heart itself was relatively narrow. In other instances, however, it was the reverse, the heart being relatively narrow or wide, when the right cavities were respectively relatively wide or narrow. Note 19.-In one of Pirogoff's cross sections the heart extended one inch and a tenth into the right side of the chest, and nearly three inches (2-8 in.) into its left side; while in another of them the heart occupied the right side of the chest for a little less than two inches (1'85 in.), and its left side for a little more than two inches (2-15 in.). In one of these extreme instances nearly three-fourths of the heart occupied the left side, and over one-fourth of it the right side of the chest; while in the other more than one-half of the organ lay in the left side, and less than one- half of it in the right side. In twenty-five cross sections nearly two- fifths of the heart occupied, on an average, the right side, and fully three-fifths of it the left side of the chest (10 to 17). These sec- tions were made across the heart at all levels, from just below the origin of the great vessels to a little above the lower boundary of the organ. In at least four instances more sec- tions than one were made through the same body at different heights, and in these in- stances the heart, as a rule, lay more to the right in the higher than in the lower sections. This was due to the greater proportionate prevalence of the right auricle in the higher and middle sections; and of the right and left ventricles in the lower sections of the heart. There were, however, three marked exceptions to this rule, which seemed to be due to the greater extension of the right auri- cle to the right at its middle than at its higher region. Note 20.-The right lung was more devel- oped in front than the left in eight out of nine cases, in which two-thirds of the heart or more occupied the left side, and one-third of it or less the right side of the chest; and the development of the two lungs was about equal in seven out of eight cases in which two-fifths of the heart or more lay in the right side, and three-fifths of it or less in the left side of the chest, the right lung being, however, larger than the left in the two ex- ceptional cases. Note 21.-The breadth of the combined right auricle and ventricle in relation to that of the left ventricle as seen in front in fifteen of Pirogoff's cross sections, varied from 10 to 1'4 to 10 to 4'4, the average proportion being 10 to 3'3. Note 22.-The auricular portion of the right auricle varied in breadth in Pirogoff's cases from nearly an inch and a half (1'4 in.) to four-fifths of an inch (#8 in.), its average breadth in ten cases being one inch. Note 23.-The body of the right auricle varied in breadth in Pirogoff's cases from nearly an inch and a half (1*4 in.) to the fifth of an inch (-2 in.), its average breadth in twenty-one cases being two-thirds of an inch ("66 in.). Note 24.-The left edge of the auricular portion of the right auricle extended almost to the left edge of the sternum ('1 in. from left edge) in one instance; almost or quite to the centre of the sternum, so as to lie behind its right half, in four instances; and in one instance it was covered by the right third of that bone. Note 25.-The right edge of the right auri- cle extended to the right of the right edge of the sternum from the third of an inch to an inch, and, on an average, for two-thirds of an inch in sixteen of Pirogoff's cross sections. Note 26.-The auricular portion of the right auricle was from one-third to two-thirds wider than the body of the auricle in five hearts represented by Pirogoff. Note 27.-The width of the heart in ten of Pirogoff's sections varied from a little more than twice (22 to 10) to almost four times as great as that of the auricular portion of the right auricle; the heart being on an average fully three times as wide as the auricular appendix. Note 28.-The heart was from three to nine times wider than the exposed portion of the body of the right auricle in twenty of Piro- goff's cases; the heart being on an average nearly six times as wide as the auricle. Note 29.-The breadth of the right ventri- cle varied from four-fifths (10 to 12-5) to a little less than one-half (10 to 20'5) of the breadth of the heart in twenty-one of Piro- goff's drawings, sixteen of which were from cross sections of the body, and five from front views of the heart. The average breadth of the right ventricle in these drawings was two-thirds of the breadth of the heart (10 to 15), and in one-half of them (10 in 21) the proportionate width of the heart was at or above, and in one-half of them (11 in 21) it was below that average. The average pro- portionate breadth of the right ventricle in relation to that of the heart was 10 to 16 in the sixteen cross sections, and 10 to 14 in the five front views of the heart. Note 30.-The breadth of the upper part of the conus arteriosus varied from one-half (10 to 20) to four-fifths (10 to 17'2) of the breadth of the right ventricle at its middle, in Piro- goff's five front views of the heart; the aver- age width of the conus arteriosus being in those NOTES. 431 cases fully three-fifths of that of the right ventricle (10 to 18'6). Note 31.-The length of the right ventricle was equal to that of its breadth in one, and was greater than that of its breadth in four of Pirogoff's five front views of the heart, the average proportion of the length to the breadth of the right ventricle being in those four cases as 5 to 6 (10 to 11'75). Note 32.-The breadth of the right ventricle in relation to the right auricle in Pirogoff's five front views of the heart varied from 10 to 2'2. Note 33.-The breadth of the right ventri- cle varied from an inch and two-thirds (1'65 in.) to nearly three inches (2'9 in.) in sixteen of Pirogoff's cross sections, its average breadth being just over two inches (2'1 in.); while in his five front views of the heart, its breadth varied from two inches and a half to three and a third, its average breadth being almost three inches (2'9 in.). The cross sections were somewhat reduced in size, while the front views appeared to be of the natural dimensions. Note 34.-In one of Pirogoff's sections the right ventricle extended further to the right than the left of the middle line of the sternum 1'4 in. to 1' in. to left) ; in one it occupied the right and left sides of the chest in equal proportions (1'2 in. to 1'2 in.) ; but in four- teen other sections the right ventricle ex- tended more to the left than the right of the vertical centre of the sternum. In two in- stances six-sevenths of the ventricle lay to the left, and one-seventh of it to the right of the central line; but on an average, two- thirds of the ventricle occupied the left, and one-third of it the right side of the chest. Note 35.-In three of Pirogoff's five front views of the healthy heart, the longitudinal furrow during its descent took a direction slightly to the left or outwards during its whole course, so that it was about half an inch more to the left at its lower than its up- per portion; but in two of them the furrow curved first to the right for the third of an inch ('3 in.), and then to the left for, in one instance, the same, and in the other for a greater extent (-5 in.). Note 36.-In one of Pirogoff's cross sections the right ventricle extended for only a quar- ter of an inch to the left of the sternum; but in every other instance that ventricle was covered to a greater or less extent by the costal cartilages. The exact extent to which they were so is not indicated, but I judged that in one-fifth of the cases (5 in 16) the right ventricle extended almost as far to the left as the junction of the cartilages to their ribs ; that in one-fourth of them (4 in 16) the ventricle was covered by the two sternal thirds of the cartilages ; that in two of them it extended to midway between the sternum and the ribs; and that in one-third of them (6 in 16) it was only covered by the sternal third of the cardiac costal cartilages. Note 37.-The body of the right ventricle extended to the left of the middle line of the sternum from four-fifths of an inch ('85 in.) to two inches (2'1 in.), and on an average for an inch and a half (1'45 in.), in sixteen of Pirogoff's cross sections. Note 38.-The right auriculo-ventricular furrow, starting from the right edge of the origin of the pulmonary, as it descended, ex- tended to the right to an amount varying from one inch to one inch and four-fifths, and on an average for an inch and a half (1'45 in.), in Pirogoff's five front views of the healthy heart. Note 39.-The breadth of the pulmonary artery at its origin varied from an inch to an inch and a half, and was on an average an inch and a quarter, in Pirogoff's five front views of the healthy heart; and in the same cases the breadth of the pulmonary artery a little above its origin varied from three-quar- ters of an inch to an inch and a quarter, and was on an average about one inch. The pul- monary artery was wider than the aorta in four of these instances, and narrower than the aorta in one of them. Note 40.-The right edge of the pulmonary artery was covered by the sternum to the ex- tent of the third of an inch in one instance, and the tenth of an inch in another, and the remainder of the artery, amounting to three- fourths of its diameter in one instance ('8 in., •11 in.), and six-sevenths of its diameter in the other, occupied the second left space or the second costal cartilage. Note 41.-The approximate breadth of the left ventricle as seen in front of the heart varied from almost half an inch (-4 in.) in two instances to an inch and one-fifth (1*2 in.) in three cases, and was on an average three-quarters of an inch in nineteen of Piro- goff's cross sections and five of his front views of the heart. The proportion that the width of the left ventricle at its anterior aspect bore to that of the whole heart in those cases varied from one-eighth (10 to 1'25) to one- third (10 to 3'2). Note 42.-The apex was covered by the inner margin of the left lung to the extent of from half an inch to three-quarters in three of Pirogoff's cross sections, and to the extent of the tenth and the fifth of an inch respect- ively in two of them; while in two others the outer edge of the lung was not covered by the lung, which, however, was close to it; and in one other instance the apex was completely exposed, the left edge of the lung being '6 in. to the left of the apex and '3 in. to the left of the outer left border of the pericardium. Note 43.-The ascending aorta varied in breadth from three-quarters of an inch ('7 in.) to an inch and a fifth (1'2 in.) in Piro- goff's five front views of the healthy heart, its average breadth being one inch. Note 44.-The aorta was narrower than the pulmonary artery in four and wider in one of Pirogoff's cross sections. Note 45.-The ascending aorta was covered by the sternum in four of Pirogoff's five cross sections showing that vessel, and of these in- stances, in three the artery was central and in one it inclined to the right. In the re- maining case the ascending aorta extended a quarter of an inch to the left of the sternum, being present to that extent within the left second space. Note 46.-Pirogoff, whose work is rich in illustrations of the root of the aorta, including 432 POSITION AND FORM OF THE HEART. its valve and sinuses, represents those parts in eight cross sections, five vertical sections, made through the sternum or cartilages in front, and the spinal column or adjoining ribs behindhand two vertical sections made from side to side. In the eight cross sections the root of the aorta, including its sinuses and the flaps of its valve, was in part covered to a very varying extent by the sternum, and was in part situated behind the corresponding cartilage or space to the left of the sternum. In one of them four-fifths of the artery lay behind the sternum ('8 in.), and one-fifth of it extended to the left of that bone ('2 in.) ; while in one of them only one-fifth of the ves- sel ('8 in.) was covered by the sternum, while four-fifths of it occupied the adjoining third left space. There was every gradation be- tween these two extreme instances ; and, on an average, less than three-fifths of the root of the aorta lay behind the left portion of the sternum, and more than two-fifths of it be- hind the corresponding left cartilage or space. The upper part of the root of the aorta, in- cluding its sinuses and the flaps of its valve, was situated in two of the cross sections on a level with the second space, its lower portion being on a level with the third cartilage ; in three of them its upper portion was on a level with the middle or lower edge of the third cartilage, its lower portion extending to a greater or less extent to the level of the third space; in one of them its lower border was on a level with the upper half of the third space ; and in two of them its upper portion was on a level with the third space, at and above its middle, while its lower portion ex- tended to the level of the upper part of the fourth cartilage. In an additional cross sec- tion made through the third space the lowest portion of the right posterior flap of the aortic valve remained, showing its attachment to the anterior flap of the mitral valve. Pirogoff shows the root of the aorta, in- cluding its sinuses and the flaps of its valve, in five vertical sections, of which, (1) two sections were made through the left costal cartilages in front, close to their articulation to the sternum, and the ribs behind near their attachment to the transverse processes of the vertebrae ; (2) one through the left side of the sternum and the fifth and sixth cartilages near their attachment in front, and the bodies of the vertebrae behind; and (3) two through the eentre of the sternum and ensiform cartilage in front, and that of the spinal column behind. The relations of the anterior and left pos- terior flaps of the aortic valve were shown in three of those sections (1, 2), and those of the three flaps, including in addition the right posterior flap, in two others (3). In one section the top of the angle of junction of the anterior and left posterior flaps was situ- ated behind the left third cartilage, in one of them the tenth of an inch (•! in.) below its upper edge, and in another of them the third of an inch ('3 in.) above its lower edge. In two of them the lower boundary of the section of the aortic valve was half an inch (-5 in. and *45 in.) below the lower edge of the third cartilage or about the middle of the third space. As, however, in these instances the right posterior flap had been removed, the lower boundary of the valve and of the origin of the aorta must have been about half an inch lower than the lowest point of the sec- tion, or behind the upper portion of the fourth left costal cartilage. In the third in- stance (2), in which also the inferior flap had been removed, the top of the angle of junc- tion of the two superior flaps lay behind the sternum, three-quarters of an inch ('7 in.) below the lower end of the manubrium, or about on a level with the lower border of the second space; and the lowest portion of the section through the aortic valve was situated behind the sternum an inch and a half (1'5 in.) below the lower end of the manubrium, or about on a level with the top of the third space, so that in this instance the lower boundary of the aortic valve would be about on a level with the lower border of the third space. In these three cases the measurement of the section of the aortic valve, the lower portion of those valves being removed, varied from two-thirds of an inch in one instance (•6 in.) to almost an inch (-9 in.) in two in- stances. In the two remaining sections, how- ever, in which the whole valve was exhibit- ed, its measurement from above downwards amounted to a little over an inch (1'1 in.) in one instance, and to an inch and a half (1'5 in.) in the other. In one of these cases, in which the lower boundary of the heart was four-fifths of an inch (-8 in.) above the lower end of the sternum, the upper boundary of the aortic valve was situated about half an inch (-4 in.) above the middle of the sternum, or about on a level with the second space, and its lower boundary about three-quarters of an inch ('7 in.) below the middle of the sternum, or about on a level with the lower edge of the third cartilage or upper border of the third space. In another case, in which the lower boundary of the heart was situated behind the ensiform cartilage, about an inch (•95 in.) below the lower end of the sternum, the upper boundary of the aortic valve was situated behind the sternum four-fifths of an inch ('8 in.) below the middle of the bone, or about on a level with the lower edge of the third cartilage or upper border of the third space, and the lower boundary of the valve was situated behind the sternum, fully two inches (2'2 in.) below the middle of the bone, and two-thirds of an inch (-65 in.) above its lower end, or about on a level with the fifth cartilage. Keeping out of view this unusual case, it may be said that in Pirogoff's sections, on an average, the root of the aorta, including its sinuses and the flaps of its valve, was situated on a level with the third cartilage and the third space. Mitral Valve.-In one of Pirogoff's verti- cal sections the top of the mitral valve vvas fully half an inch ("55 in.) and in another of them it was a third of an inch ("3 in.) above the lower border of the right posterior flap of the aortic valve. In three other sections, the right inferior flap of the aortic valve had been removed, the other flaps being retained ; and in one of these sections the top of the mitral valve was the third of an inch, in another it NOTES. 433 was the fifth of an inch ('2 in.), and in the third it was about the tenth of an inch above the lower edge of the left posterior flap of the aortic valve. The lower border of the mitral valve was about an inch below the lower border of the left posterior or the anterior flap of the aortic valve in the three instances in which the right posterior flap had been removed ; and it was from fully half an inch to fully three- quarters of an inch below the lower edge of the right posterior flap in the two other in- stances. In one of Pirogoff's front vertical sections the top of the mitral valve was fully half an inch ('6 in.) above the level of the lower border of the right posterior flap of the aortic valve. In two of Pirogoff's vertical sections, and probably in a third, the top of the mitral valve was about half an inch ('6 in.) below the level of the middle of the sternum, but it was an inch and three-quarters below that point in another instance in which the lower boundary of the heart was an inch below the lower end of the sternum. In one of Pirogoff's vertical sections the top of the mitral valve was on a level with the lower edge of the third cartilage; and in three of them it was behind the third space, these occupying respectively the upper, the middle, and the lower portion of that space. If we combine the cases in which the vertical section was made through the cartilages with those in which it was made through the sternum, and estimate in the latter cases the approximate relative position of the valve to the cartilages by its position in relation to the sternum, we find that in two cases the top of the mitral valve was on a level with the lower portion of the third cartilage; in three, with the upper third of the third space; in two, with the middle or lower portion of the third space; and in one, with the fourth space. In one of Braun's vertical sections (a wo- man aged 25), in which the lower boundary of the heart was half an inch above the lower end of the sternum, the top of the mitral valve was half an inch ('4 in.) below the centre of the sternum; and in another section (a soldier aged 21), the lower boundary of the heart was an inch and a fifth (1*2 in.) below the lower end of the sternum, and the top of the mitral valve was nearly an inch and a half (1'4 in.) below the middle of the sternum. The lower border of the mitral valve was situated an inch and a half above the lower end of the sternum in one vertical section, and in two it was as low as half an inch above that point; while in three other verti- cal sections it was on a level with the fourth space, and in two with the fifth cartilage. If we group the two sets of cases together, it may be estimated that in four of them the lower end of the valve was behind the fourth space, and in four behind the fifth cartilage. In one of Braun's vertical sections, from a woman aged 25, in which the lower boundary of the heart was half an inch above the lower end of the sternum, the lower boundary of the mitral valve was an inch and a half (1*4 in.) above that end of the bone; and in another, from a soldier aged 21, in which the lower boundary of the heart was an inch and a fifth below the lower end of the sternum, the lower border of the mitral valve was less than half an inch (*4 in.) above the end of the bone. Pirogoff represents nine cross sections through the second space, the whole of which were above the mitral valve; four through the third cartilage, two of which were above the mitral valve, and two were made through the upper part of the valve; eight through the third space, one of which was above and one below the mitral valve, while five were made through the upper portion of the valve, and one through the middle of the mitral orifice; nine through the fourth cartilage, of which two were made through the upper por- tion and two through the middle of the valve, while five were made below the valve; six through the fourth space, of which one was made through the top of the valve, and three through its middle, while two were made be- low the valve; and seven through the fifth cartilage, of which six were below the valve, and one was made through the middle of the mitral orifice. It is self-evident that, in these cases, the top of the mitral valve occupied the space or cartilage above that in which the section passed through the middle of the mitral ori- fice, and that the top of the valve was rela- tively still higher in those cases in which the section was made below the mitral valve. Estimating the position of the top of the mitral valve approximately in these sections cm this view, I consider that the upper boun- dary of the valve was situated in one case on a level with the second space ; in nine, on a level with the third cartilage; in two, with the third cartilage or third space; in nine, with the third space; in two, with the third space or fourth cartilage; in three, with the fourth cartilage; in six, with the third carti- lage or space or the fourth cartilage; and that in one instance the top of the mitral valve was on a level with the fourth space. In these cases, on the basis of the calcula- tion just made, it may be approximately esti- mated that the average position of the top of the mitral valve was about on a level with the upper half of the third intercostal space. In the same transverse sections, on a simi- lar approximate calculation, the lower border of the mitral valve was situated about on a level with the third cartilage in one instance; the third space in six instances; the fourth cartilage in two; the fourth space in four; the third space, fourth cartilage, or fourth space in six; the fifth cartilage in four in- stances ; and below that cartilage in one. The average position of the lower boundary of the mitral valve in these cases appears to me, from as close an estimate as I can make, to be about on a level with the lower edge of the fourth cartilage and the upper border of the fourth space. Pirogoff represents the mitral valve or ori- fice in seven cross sections, and in all of them the anterior wall of the mitral orifice was situated more to the right than its posterior wall to an extent varying from one-third (*35 in.) to four-fifths (• 8 in.) of an inch. VOL. II.-28 434 POSITION AND FORM OF THE HEART. In four of these sections the mitral orifice was situated behind the left half of the sternum ; and in three of them it was placed partly behind the left portion of the sternum, partly behind the cartilages and spaces to the left of that bone. In no instance was the anterior wall or border of the mitral valve seated to the right of the middle line of the sternum. Tricuspid Valve.-In two of Pirogoff's ver- tical sections the top of the tricuspid valve was nearly the third of an inch ('3 in.), and in two others it was nearly half an inch (-4 in. and *45 in.) below the level of the top of the mitral valve. The lower border of the tricuspid valve was below the level of the lower border of the mitral valve from half an inch, in the first two cases noted above, to three-quarters of an inch (*65 in. and -75 in.) in the other two cases. The top of the tricuspid valve was situated, in one of Pirogoff's vertical sections, half an inch, and in two of them one inch, below the centre of the sternum; in another in- stance it was an inch above the lower end of that bone. In one of Braun's vertical sec- tions, in which the lower boundary of the heart was high, the top of the tricuspid valve was on a level with the centre of the sternum. The top of the tricuspid valve was on a level with the top of the third space in one vertical section, with the fourth space in another, and with the fifth cartilage in a third instance. The lower border of the tricuspid valve was one inch above the lower end of the sternum in two of Pirogoff's vertical sections, and an inch and a half above that point in one of Braun's vertical sections, in which the lower boundary of the heart was above the lower end of the sternum ; and it was a third of an inch ('3 in.) below the lower end of that bone in two of Pirogoff's sections, in which the inferior boundary of the heart was behind the middle of the ensiform cartilage. The lower border of the valve was on a level with the fourth space in one of Pirogoff's sections, and with the sixth cartilage in two of them. Pirogoff represents four cross sections through the third cartilage, all of which were above the tricuspid valve; eight through the third space, four of which were above that valve, three were made through its upper portion, and one below it; nine through the fourth cartilage, of which three were above the valve, one was made through its middle, three through its lower portion, one through the bottom of the valve and one below it; six through the fourth space, of which one was above the valve, three through its upper por- tion, one through its lower portion, and one below it: and seven through the fifth carti- lage, of which one was made through the middle of the tricuspid orifice and six be- low it. Estimating approximately the position of the top of the tricuspid valve in these cross sections, I consider that the upper boundary of the valve was situated on a level with the second space, or third cartilage in one in- stance ; with the third cartilage or space in two; with, the third space in seven; with the third space or fourth cartilage in ten; with the fourth cartilage in three; with the fourth cartilage or space in four; and with the fourth space in two. I think that we may estimate that in these sections the top of the tricuspid valve was on an average situated behind the lower portion of the third space, or the upper edge of the fourth cartilage. In the same cross sections, and on a similar approximate calculation, the lower border of the tricuspid valve was about on a level with the third cartilage in one instance; with the third space in one; with the third space or fourth cartilage in one; with the fourth car- tilage in one; with the fourth cartilage or space in six ; with the fourth space in seven ; with the fifth cartilage in three; and with the fifth cartilage or space or lower in ten. The approximate average position of the lower boundary of the tricuspid valve in these transverse sections appears to me to be about on a level with the lower portion of the fourth space, or upper portion of the fifth cartilage. Pirogoff represents the tricuspid orifice in eleven cross sections, and in all of them the anterior edge of the tricuspid orifice was more to the right than its posterior edge to an ex- tent varying from a quarter (-25 in.) to four- fifths (-85 in.) of an inch. The left edge of the tricuspid valve was situated more to the right than the right edge of the mitral valve in six of seven instances in which the section went through both valves, to an extent varying from the tenth to the third ('3 in.) of an inch; while in the seventh instance the left edge of the tricuspid was immediately in front of the right edge of the mitral valve. In five of the eleven sections the tricuspid valve was situated behind the right half of the sternum; in one of them it was behind the right third of that bone; in one it lay partly behind the right portion of the sternum and partly to the right of it; in two it was central, occupying equally the right and left sides of the sternum, and in the remaining two it lay to the left of the middle line of that bone. Note 47.-Pirogoff shows the relation of the sternum and costal cartilages in front to the vertebra behind in twelve antero-poste- rior vertical sections and in sixty-two cross sections. In five of the vertical sections the top of the sternum was on a level with the lower border of the body of the second or the upper border of the third dorsal vertebra, or the cartilage between these two vertebrae; in one of them it was on a level with the top of the fourth dorsal vertebra; and in one of them, an instance that stands alone, it was, accord- ing to Pirogoff's description, on a level with the upper portion of the first dorsal vertebra. This description is, however, evidently an accidental error, and I, therefore, for the first, read the second vertebra. In Braun's two vertical sections the top of the sternum was on a level with the cartilage between the second and third dorsal vertebra. NOTES. 435 I examined eleven human skeletons in the Museum of the Royal College of Surgeons, with the valuable assistance of Mr. Wright, of the Museum, and I found that in eight of them, including one in the Hunterian Mu- seum, the top of the manubrium was on a level with the second dorsal vertebra,1 the point varying from its upper to its lower bor- der ; and that in three of them it was on a level with the first dorsal vertebra. In two of Pirogoff's vertical sections the top of the sternum was on a level with the lower border of the third rib, near the spine, in one of them it was on a level with the up- per border of the fourth rib, and in one it was above the level of the first rib. In this last instance there was evidently an acci- dental error. The lower end of the osseous sternum was on a level with the middle of the eighth dor- sal vertebra in two of Pirogoff's vertical sec- tions, in one of which the sternum and ribs had been elevated by a large accumulation of fluid in the abdomen; in one of them it was on a level with the middle of the ninth verte- bra, and in one with the cartilage between the ninth and tenth vertebrae. In Braun's two sections the lower end of the sternum was on a level respectively with the middle and lower border of the ninth vertebra. In one of the skeletons in the Museum of the Royal College of Surgeons the lower end of the sternum was on a level with the sev- enth dorsal vertebra, in one with the carti- lage between the seventh and eighth verte- brae, in three with the middle of the eighth vertebra, in two with the cartilage between that vertebra and the ninth, and in three with respectively the top, middle, and lower border of the ninth vertebra, the last instance being the skeleton in the Hunterian Museum. The middle of the sternum which corre- sponds with its articulation to the third cos- tal cartilages was on a level with the middle of the fifth dorsal vertebra in one of Pirogoff's vertical sections, with the cartilage between the fifth and sixth vertebrae in two of them, and with the middle of the sixth vertebra in another of them, and in Braun's two sec- tions. The bottom of the manubrium which cor- responds with the second cartilage and with the lower end of the upper third of the sternum was on a level with the lower half of the body of the fourth dorsal vertebra in two of Pirogoff's vertical sections, and in two of them and in Braun's two sections with the middle of the fifth vertebra. The lower end of the middle third of the sternum which corresponds as a rule with its articulation to the fourth costal cartilages was on alevel with the lower half of the body of the sixth dorsal vertebra in two of Piro- goff's vertical sections and with the middle of the seventh vertebra in two of them and in Braun's two sections. In one of Pirogoff's cross sections the sternum at the junction to it of the first costal cartilages was on a level with, the up- per border of the body of the fourth dorsal vertebra ; in four of them the sternum at the spaces between the first and second cartilages was on a level respectively with the upper and lower borders of the second vertebra and the upper border of the third; the sternum was on a level-at the second cartilage, in three instances, with the fifth vertebra;-at the second space, in eight instances, with re- spectively the fourth, fifth, and sixth verte- brae-at the third cartilage, in four instances, with the top of the fifth vertebra in one and with the seventh in three;-at the third space, in eight instances, with respectively the cartilages between the fifth, sixth, sev- enth, and eighth vertebrae, and with the bod- ies of the seventh, eighth, and ninth verte- brae ; at the fourth cartilage, in ten instances, with respectively the cartilages between the sixth, seventh, eighth, and ninth vertebrae, and with the seventh and eighth vertebrae and the top of the ninth;-at the fourth space, in six instances, with the cartilages between the sixth, seventh, eighth, and ninth vertebrae, and with the bodies of the seventh and eighth;-at the fifth cartilage, in eight instances, with respectively the lower border of the seventh vertebra, the upper border of the tenth, and the two intermediate verte- brae ;-at the fifth space, in two instances, with respectively the eighth and tenth verte- bra ; and finally, in four instances, the lower end of the osseous sternum or base of the en- siform cartilage at the sixth cartilage, was on a level respectively with the lower third of the ninth vertebra, the cartilage between that and the tenth, and the upper border of the body of the eleventh dorsal vertebra. The lower boundary of the front of the heart was situated in one of Pirogoff's vertical sections on a level with the middle of the body of the eighth or, according to an evi- dently erroneous reference, the seventh dor- sal vertebra, behind, and the sixth cartilage in front; in two of them on a level with the cartilage between the eighth and ninth ver- tebrae ; in three of them with the top, and in one of Braun's sections with the middle of the ninth vertebra ; and in one of Pirogoff's sec- tions with the lower border, and in one of Braun's with the middle of the body of the tenth vertebra. In the last two instances the lower boundary of the heart was situated be- hind the ensiform cartilage, an inch below the lower end of the sternum, in another in- stance it was half an inch below, and in two others from half to three-quarters of an inch above the lower end of the sternum. The lower boundary of the pericardium was on a level in one of Pirogoff's vertical sections with the cartilage between the sev- enth and eighth dorsal vertebrae ; in three of them with the cartilage between the eighth and ninth vertebrae ; in one with the upper, and two with the lower portion of the ninth, and in one with the top of the eleventh ver- tebra. In these cases the lower boundary of the pericardium was situated from a third of an inch above to fully one inch below the lower end of the sternum, and from a third of an 1 The body of the dorsal vertebra is referred to here and elsewhere, unless it is otherwise specified. 436 POSITION AND FORM OF THE HEART. inch above the level of the sixth cartilage to that of the lower portion of the seventh car- tilage. The top of the arch of the aorta was about on a level with the upper portion of the body of the third dorsal vertebra in three of Piro- goff's vertical sections, and with its middle in one of his and in one of Braun's sections, and with respectively the top and middle of the fourth vertebra in one of Pirogoff's and the other of Braun's vertical sections. In these seven cases the top of the arch of the aorta was about on a level with a point vary- ing from a quarter of an inch above the top of the manubrium to an inch and a half be- low it. In one of Pirogoff's cross sections the top of the arch, at the origin of the innomi- nate and left carotid arteries, was in front of the upper portion of the third dorsal verte- bra, and in two of them the arch a little be- low its top was on a level respectively with the lower border of the third and the upper border of the fourth vertebra. The top of the pulmonary artery was on a level with the cartilage between the fourth and fifth dorsal vertebrae in one of Pirogoff's vertical sections, with the space between the fourth and fifth ribs near the vertebrae in another of them, with that between the fifth and sixth ribs near the space in a third in- stance, and in a fourth with the lower border of the seventh rib at the same situation. In these four cases the position of the top of the pulmonary artery varied from the level of the middle of the second left cartilage to that of the lower border of the third. The origin of the pulmonary artery was on a level with the body of the fourth dorsal vertebra in one instance, and with respect- ively the lower border of the fifth and the upper border of the sixth vertebra in two others of Pirogoff's vertical sections; and it was on a level with the top of the sixth ver- tebra or the cartilage above it in four of Piro- goff's cross sections. The lower boundary of the body of the left ventricle, not including its apex, in three of Pirogoff's vertical sections was respectively on a level with the middle of the eighth, the top of the ninth, and the two upper fifths of the tenth dorsal vertebra. The lower boundary of the body of the left ventricle was on a level with the upper bor- der of the ninth vertebra in one of Braun's vertical sections, and with the cartilage be- tween the ninth and tenth vertebrae in the other. The section passed through the left ventri- cle a little above its lower border at the apex in Pirogoff's cross sections, in one instance on a level with the cartilage above the ninth vertebra, in another of them on a level with that vertebra, in two others with the carti- lage below it, and in one on a level with the upper portion of the tenth vertebra. The upper boundary of the root of the aorta, including its orifice, valve, and sin- uses, at the attachment of the angle of junc- tion of the anterior and left posterior flaps of the aortic valve, was situated in one of Piro- goff's vertical sections as high as the upper third of the fourth vertebra, in two of them it was in front of the sixth, and in one of them the upper portion of the seventh verte- bra. The lower boundary of the root of the aorta, including the aortic orifice, valve, and sinuses, was on a level in two instances with respectively the middle and lower borders of the sixth vertebra, in one with the upper third of the seventh, and in one with the lower border of the eighth vertebra. In one of Braun's vertical sections the upper boun- dary of the root of the aorta was in front of the cartilage between the fifth and sixth ver- tebrae, and its lower boundary was in front of the cartilage between the sixth and sev- enth vertebrae ; and in his other vertical sec- tion the lower boundary of the root of the aorta was on a level with the lower border of the seventh vertebra. The upper portion of the aortic valve, including the anterior and left posterior flaps and sinuses, was situated in three instances in front of the cartilage above the sixth vertebra, and the top and middle of that vertebra; in six instances in front of the top of the seventh vertebra or the cartilage above it; and in one in front of the body of that vertebra. The lower portion of the aortic valve, or its right posterior flap, was situated in four in- stances in front of the middle or top of the seventh vertebra or the cartilage above it, and in one in front of the middle of the eighth vertebra. The upper boundary of the mitral valve was situated in six of Pirogoff's vertical sec- tions in front respectively of the middle of the sixth dorsal vertebra, the cartilage between the sixth and seventh vertebrae, the seventh vertebra, and in one instance the eighth; and its lower boundary was situated in three of his vertical sections in front of the eighth, and in one it extended down to the top of the lower third of the ninth vertebra. In one of Braun's vertical sections the mitral valve ex- tended from the level of the cartilage below the sixth vertebra down to that of the upper third of the eighth, and in the other it ex- tended from the cartilage below the seventh vertebra down to the upper third of the ninth vertebra. The mitral valve was situated in front of the cartilage above the seventh dorsal verte- bra in two of Pirogoff's cross sections, the seventh vertebra in probably nine of them, the cartilage between that vertebra and the eighth in two of them, and in front of the eighth vertebra in four of them. The upper boundary of the tricuspid valve was situated in seven of Pirogoff's vertical sections on a level respectively with the up- per and (in a case of ascites) lower borders of the sixth dorsal vertebra, the cartilage be- tween that vertebra and the seventh, and the upper border of the seventh vertebra, the lower portion of the eighth vertebra, and the cartilage below it. The tricuspid valve in one of Braun's sections extended from the level of the top of the seventh vertebra to that of the middle of the eighth. The tricuspid valve was on a level with the eighth vertebra in five instances, with the cartilage below it in two, and with the ninth vertebra in two. MALPOSITIONS OF THE HEART. 437 sion of the lung. This may be so in some cases, but as a rule the unusual descent of the heart, like that of the base of the lungs, is caused by the unusual descent of the diaphragm. The lower boundary of the right ventricle is brought down- wards into the epigastrium, so that it is situated behind and to each side of the ensiform cartilage. In that position, and to the left of it, the heart is not covered with lung, and it is therefore in contact with the ensiform cartilage, with the neighboring margin of the seventh left costal cartilage, and with the intermedi- ate abdominal muscles, the pericardium MALPOSITIONS OF THE HEART. The displacements of the heart may be conveniently divided into the Vertical, Lateral, Forward, and Backward dis- placements. The Vertical Displacements of the Heart. Cases in which the Heart is Low- ered.-The cause of the vertical lower- ing of the healthy heart is in all cases, with the exception of aneurisms of the arch of the aorta, an unusual lowering of the diaphragm. Pulmonary emphysema, bronchitis, and spasmodic asthma; croup, laryngitis, and laryngismus stridulus; col- lapse of the stomach and intestines ; and aneurism of the arch of the aorta-all tend to lower the heart. To these may be added certain cases of mediastinal tumor, and pleuritic effusion into the left side during the middle period of its increase. Pulmonary Emphysema, Bronchitis, and Spasmodic Asthma.-In Pulmonary Em- physema the right cavities of the heart and the pulmonary artery are greatly en- larged. The right ventricle often com- pletely covers the left ventricle. The diaphragm is remarkably low, its standard position being often lower than it is in health at the end of the deepest possible inspiration. The enlargement of the lungs is so extensive that they cover the heart within the chest; and they are con- sequently everywhere interposed between the heart and the walls of the chest, with the exception of the border of the seventh costal cartilage (Fig. 73). The heart is invariably enlarged, the enlargement be- ing almost limited to the right side. The venee cavse and right auricle are usually distended and of great size ; the right ventricle is so much increased in volume that it almost or altogether conceals the left ventricle, its walls being hardened and hypertrophied; and the" pulmonary artery is greatly increased in length and breadth. Notwithstanding the enlarge- ment of the heart, its impulse is imper- ceptible over the walls of the chest; and in some cases its sounds are so muffled that they are scarcely audible over the usual cardiac region owing to the great development of the lungs in front of the heart. In no instance, however, is the heart absolutely covered by the dilated lungs. The central tendon of the dia- phragm descends almost or quite to the level of the lower end of the ensiform car- tilage, and necessarily draws downwards the enlarged heart. It is customary to speak of the displacement of the heart downwards as being caused by the expan- Fig. 73. Position of tha heart and great vessels in Pulmon- ary Emphysema. The heart is displaced downwards, and is covered with the over-developed lungs. The apex-heat is imperceptible, but the impulse of the right ventricle is seen and felt in the epigastrium. intervening. The result is that, as Dr. Stokes has pointed out, the impulse of the right ventricle may be felt in the epigas- trium; and as the right ventricle is hyper- trophied, " the heart may be felt pulsat- ing with a violence that we would not ex- pect from the examination of the pulse at the wrist, which is often small and feeble, while the impulses of the right ventricle are given with great strength."1 The form of the chest, the great expansion of the lungs, the low position of the dia- phragm, and the enlargement, elongation, 1 Dr. Stokes on the Diseases of the Chest, p. 178. 438 POSITION AND FORM OF THE HEART. and lowering of the heart and great ves- sels, all correspond, though to an exagge- rated degree, with the condition of those parts at the end of the deepest possible inspiration in health. The presence of the impulse and sounds of the heart over the epigastrium, and their absence over the walls of the chest, are the signs that often first direct attention to the morbidly enlarged condition of the lungs. In cases of severe bronchitis, the dia- phragm is invariably lowered, the right cavities of the heart are enlarged, and the lungs are amplified. In those cases, there- fore, as in emphysema, the heart is low- ered, its impulse is obliterated over the intercostal spaces by the interposition of the lung, and the beat of the right ventri- cle is felt and seen in the epigastrium. The extent to which the heart is enlarged, lowered, and covered by lung is by no means so great in bronchitis as in emphy- sema. When, as is often the case, the patient affected with emphysema is attacked by bronchitis, the extent to which the heart is lowered, and enveloped by the lungs is increased. During an attack of spasmodic asthma, the diaphragm descends, the lungs are expanded to the utmost, and the impulse of the right ventricle is lowered into the epigastrium, just as in cases of true pul- monary emphysema. After the seizure is over, its effect upon the size of the lungs and the position of the heart does not im- mediately disappear. Gradually, how- ever, the organs resume their healthy size and position. The asthmatic seizure that often attacks those affected with emphy- sema, is accompanied by an excessive am- plification of the lungs and descent of the impulse; but in such patients the lungs and heart do not regain their normal size and position after the cessation of the at- tack, and in this important respect true spasmodic asthma is to be distinguished from the asthmatic seizure of a person affected with true pulmonary emphysema. Croup, Laryngitis, Laryngismus Stridu- lus.-In all those cases in which there is excessive narrowing of the fauces, larynx, or trachea so as to contract the channels through which air is admitted into the lungs and render inspiration exceedingly difficult, the inspiratory efforts are labori- ous but ineffectual. Every muscle of res- piration is brought into powerful action. The diaphragm descends as low as possi- ble. The lungs are consequently length- ened and the heart is drawn downwards. As air, in spite of the labored breathing, can scarcely enter the air tubes, the lungs, being lengthened downwards, instead of expanding, collapse during inspiration, and the walls of the chest fall inwards. The lungs recede from before the heart, which is in immediate and extensive con- tact with the walls of the chest as well as with the ensiform cartilage. The heart is, therefore, in such cases to be felt beat- ing with force over and to the left of the lower sternum and in the epigastrium. Collapse of the Stomach and Intestines.- When the abdomen is unusually spare, the stomach and intestines being com- paratively or quite empty, the abdominal organs shrink downwards, and the dia- phragm is permanently lowered. This was well seen in the poor woman from whom fig. 74 was taken. She had been unable to swallow owing to cancer of the oesophagus for a fortnight before her death. Her emaciation was extreme. The stomach and intestines were abso- lutely empty of gas as well as of food. The liver, though not enlarged, had dropped downwards, so that its lower border rested on the bones of the pelvis. The diaphragm necessarily followed the liver and stomach in their descent, and as the result, the lungs at their base, and the heart where it rested on the dia- phragm, were unusually lowered, and both organs were remarkably lengthened. The elongation of the ascending aorta and the pulmonary artery was very marked. This was an extreme case, but in all instances of abdominal collapse, the dia- phragm descends in exact proportion to the descent of those organs upon which it rests, and the lungs and heart are length- ened downwards to a corresponding .de- gree. In some of those cases the transfer of the impulse from the intercostal spaces to the epigastrium may give rise to the suspicion of pulmonary emphysema on the one hand, or aneurism of the abdomi- nal aorta on the other. In emphysema the chest is unduly developed, and the abdomen, instead of being retracted, is usually of more than average size. In aneurism of the lower thoracic or higher abdominal aorta, the impulse or pulsation in the epigastrium is strong during expi- ration, but it lessens and even disappears during a deep inspiration. In cases of abdominal collapse, it is the reverse, for the impulse in the epigastrium becomes lower and stronger when the patient takes a deep breath. Aneurism of the Arch of the Aorta.-One would have expected a ptriori that aneur- isms affecting the arch of the aorta, espe- cially when they are of large size, would cause considerable displacement of the heart downwards. Dr. Townshend saw an instance of aneurism of the arch thrust- ing the heart downwards, so that it pul- sated in the epigastrium.1 I possess drawings taken from thirteen cases of aneurism of the arch of the aorta. In one of these the lower boundary of the right ventricle was situated more than an 1 Cyclopaedia of Medicine, ii. 391. THE VERTICAL DISPLACEMENTS OF THE HEART. 439 inch below the lower end of the sternum. In four there was effusion of blood into the left pleura, displacing the heart to the right. In the remaining seven instances the lower boundary of the right ventricle was from one-third to three-quarters of an inch below the lower end of the sternum. It is clear that in the majority of these Fig. 74. Position of the heart and great vessels in a case with Collapse of the Stomach and Intestines. The heart is displaced downwards, and covered with lung to the fifth cartilage. The apex-beat is present in the fifth space, and perhaps in the sixth, and the impulse of the right ventricle is seen and felt in the epigastrium. cases, although the aneurism was in nearly all of them large, varying from three to five inches in diameter, the de- scent of the heart into the epigastrium was definite, but not proportionately great. In two of the instances there was cylindrical aneurism or dilatation of the ascending aorta. In these the transverse diameter of the aorta was only two inches, while its vertical measurement was four inches. They must, therefore, be included with the others in estimating the influence of aneurism of the arch of the aorta in displacing the heart down- wards. The aneurismal sac displaces not so much the whole heart as those parts of 440 POSITION AND FORM OF THE HEART. it upon which it makes immediate pres- sure, and which are subjected thereby to compression. This applies especially to the aneurisms of the ascending aorta, which amount to nine among my cases. In all of these the right ventricle, and in most of them the right auricle, were com- pressed from above downwards, the com- pression starting from a point at the top of the transverse furrow between those cavities, where the aorta comes into view. The difference in the vertical diameter of the right ventricle below the part in ques- tion and just below the pulmonary artery, amounted in one instance to two inches, the actual measurements being respec- tively three and five inches. As a rule the difference was much less, but this was mostly due to the right ventricle being compressed downwards in its whole breadth by the sac. In five of the cases the auricular appendix was displaced downwards and to the right. The downward displacement of the apex in aneurism of the arch of the aorta is not considerable, being in fact mainly due to coexisting hypertrophy of the left ventricle. That condition, however, is not usual, except in those cases of cylin- drical aneurism or dilatation of the ascend- ing aorta, in which there is free aortic re- gurgitation, when the left cavity is greatly enlarged, and when the descent of the apex is much more due to that cause than to the aneurism. Mediastinal Tumors.-Dr. Bennett gives a case of mediastinal tumor, which will be more fully noticed at page 449, in which there was considerable displace- ment downwards and to the right of the heart, which was seen and felt beating in the epigastrium. Pleuritic Effusion into the Left Side.-In the middle period of these cases, when the fluid is steadily increasing, but has not yet reached to its height, there is dis- placement downwards and to the right of the heart, which may be felt beating in the epigastrium. A full account of such cases, and an explanation of their phe- nomena, will be found at page 443. Cases in which the Heart is Raised.-Abdominal enlargement from gastro-intestinal distension, ascites, the presence of gas in the cavity of the abdo- men, abdominal tumors, ovarian dropsy, aneurism of the abdominal aorta at the cseliac axis, and enlarged liver and spleen, all tend to elevate the heart. To these may be added certain cases of mediastinal tumors. We have just seen that when there is collapse of the abdomen the diaphragm descends, drawing after it the heart and lungs. When there is distension of the abdomen, whatever be the cause, the re- verse of this takes place. The diaphragm is raised, the cavity of the chest is short- ened, and the heart and lungs are elevated and compressed upwards. Distension of the Stomach and Intestines. -By far the most frequent, distressing, and often fatal cause 0/ the elevation of the diaphragm and compression upwards of the heart and lungs, is the distension of the stomach and intestines with gas. The effect of this condition is well shown in Fig. 75, which was taken from a youth affected with diabetes, who, for months before his death, suffered from great abdo- minal distension. The cavity of the chest was materially lessened. The lower ribs, especially on the left side, were pressed outwards so as to restrain their move- ments, and the whole cage of the chest was elevated in front and at the sides. The heart and lungs were compressed up- wards and lessened in size, so as to im- pede respiration and circulation. When the abdomen is enlarged, it is enlarged in two directions, one outwards and downwards by the expansion of the walls of the abdomen, the other upwards by the elevation of the diaphragm. When the abdomen is extremely distended, the whole cavity becomes oval in form, or shaped like a balloon; the outer part of it presses outwards, and the upper part of it presses upwards. The cage of the chest is raised by this double movement of distension upwards and outwards. The wide irregular cone formed by the upper part of the swollen oval abdomen, acting upon the lower ribs, forces them asunder to the right and to the left, and lifts up the whole front of the cage of the chest. The more important effect of this disten- sion of the abdomen is to lift up the dia- phragm, and with it the heart at the cen- tre of the chest, and the right and left lung on each side of it. When these organs are thus raised, as the walls of the chest in front of them, by which their relative position is measured, are raised also, the apparent elevation of the heart is much less than its real elevation. The heart and great vessels are compressed upwards, and displaced somewhat to the right, so that the heart takes a central position in the chest, while the great ves- sels often bear unduly to the right. The shape of the heart is altered. It is short- ened from below upwards, and is propor- tionally though not actually widened. Its apex is especially tilted upwards, and in- stead of being, as in health, lower than the inferior boundary of the right ven- tricle at the end of the sternum, is higher than that point by from a third to one- half of an inch. It is to be observed that the heart and lungs are compressed up- wards into the highest part of the cavity of the chest, and as that cavity is a cone narrowing from below upwards, those organs, to their great additional incon- THE VERTICAL DISPLACEMENTS OF THE HEART. 441 venience, are pushed up into the narrow- est part of the space that they naturally occupy.1 Intestinal distension is usually present in peritonitis, and it becomes in many cases the most distressing symptom. As Dr. Stokes has shown, muscles are para- lyzed by inflammation. The inflamed muscular coat of the intestines, being paralyzed, yields before the gaseous dis- tension, which is no longer restrained by the peristaltic contraction of the intes- Fig. 75. Position of the heart and great vessels in cases with Distension of the Stomach and Intestines. The heart is displaced and compressed upwards, its impulse being present in the second and third spaces, and perhaps in the fourth. wards to a greater degree than in those cases of abdominal distension in which the diaphragm retains its power. Dis- tension of the stomach and intestines is very frequent in the dying. It was pres- ent to an excessive degree in either the stomach or intestines, or both, in 63 out of 122 dead bodies observed by me indis- criminately ; and in 28 of these the stom- ach and intestines were very much dis- tended. In such cases the abdominal distension, which is usually one of the tines. In peritonitis, abdominal respira- tion is suspended and the diaphragm is passive. It therefore yields without re- sistance to the upward pressure exerted upon it by the distended intestines, and the heart and lungs are compressed up- 1 For additional details as to this subject, see a lecture by the author on the " Influence of Distension of the Abdomen on the Func- tions of the Heart and Lungs," in the British Medical Journal for August 2, 1873, p. 108. 442 POSITION AND FORM OF THE HEART. secondary effects of the original disease, produces compression of the heart and lungs, and thereby often hastens death or becomes its immediate cause. The intro- duction of the oesophageal tube from above, or of O'Beirne's tube from below, or the insertion of a small aspiration tube through the abdominal walls into the stomach, will in some of these cases give vent to the flatus and so produce material relief. Many persons, especially those who have become stout, are subject to habitual distension of the stomach and intestines, with the effect of compressing the dia- phragm upwards, curtailing its power to descend freely during inspiration, and so encroaching on the cavity of the chest. Those so affected do not, in many in- stances, suffer when they are at rest, but on any exertion respiration becomes hur- ried and difficult and the circulation of the blood is impeded. Such persons gen- erally present themselves in two classes. One class complain of shortness of breath, the other of pain or distress in the heart when they make exertion, especially after a full meal. In many cases of an- gina pectoris, the distress is most easily excited after food. Some stout people are unusually subject to distress in breathing or in the heart, or both, from compara- tively slight distension of the abdomen. In these persons the cavity of the abdo- men is naturally incapable of great ex- pansion owing to its walls being firm and resisting. The abdominal fulness, when it passes certain limits, cannot make way forwards and outwards, and the result is that the diaphragm is pushed upwards, and the lungs and heart are soon subject- ed to a distressing amount of pressure. In dyspeptic persons, the most distress- ing symptoms induced by the fulness of the stomach after food are often referred to the heart. This is apt to be the case also whenever the stomach is greatly dis- tended. The reason is obvious: the stomach is immediately subjacent to the heart, the diaphragm being interposed, so that the heart, in fact, rests upon the stomach. Whenever, therefore, the stomach is greatly swollen by an accu- mulation of gas and food, the heart is compressed upwards in an especial man- ner, and the distress experienced is often, therefore, almost limited to the heart. I do not, of course, lose sight of the addi- tional physiological influence exerted by the stomach upon the heart through the medium of the eighth pair of nerves. Ascites.- In ascites, the accumulation of the fluid is gradual. The patient is usually in bed, and the distress in breath- ing and in the heart experienced by the patient, owing to compression of the heart and lungs, is by no means proportionate to the amount of the distension. Indeed, those cases of ascites that suffer great distress in the organs of the chest usually have in addition distension of the stomach and intestines as well as enlargement of the liver. When this is so, a small amount of fluid in the peritoneal cavity will produce serious discomfort, and the removal even of a little of it by tapping will give immediate and unusual relief Some years ago I had a patient in St. Mary's Hospital who was affected with aortic and mitral regurgitation. The heart was enlarged and the pericardium was adherent. He breathed with diffi- culty, owing to the great size of the abdo- men, which was produced by the triple combination of great enlargement of the liver, distension of the stomach and in- testines, and ascites. The quantity of urine was scanty, being about eleven ounces daily. The amount of fluid in the peritoneal cavity was small, but with the view of affording relief, tapping was re- sorted to. The intestines were so near the surface that an incision was made in the parietes of the abdomen, and the trochar and canula were introduced in a downward direction. At first only half a teaspoonful of fluid escaped, but by pass- ing a female catheter through the canula, so as to press the intestines gently away from the end of the tube, about ninety ounces of serum were withdrawn. The relief to breathing was complete. The urine, before so scanty, now began to flow freely, and from fifty to eighty ounces were passed daily. By drawing off the fluid the extreme distension was relieved, and the ligature, so to speak, on the cir- culation, caused by the compression of the heart, was removed. Ultimately the fluid reaccumulated, and the patient died. The result was unfavorable, but the case was none the less instructive, for it dem- onstrated that the encroachment of the abdomen upon the chest checked the cir- culation of the blood, and so prevented the free secretion of urine. In all cases of abdominal distension the seat of the impulse of the heart is a ready and exact measure of the extent to which the cavity of the abdomen encroaches up- wards on the cavity of the chest. The progress of such distension, whether on the ascending or descending scale, may be exactly ascertained by noticing the vary- ing position, upwards or downwards, of the impulse of the heart. It must, how- ever, be borne in mind, that, when the heart and lungs are raised by distension of the abdomen, the walls of the chest in front of those organs is raised also, and that the apparent elevation of the heart, measured by its relation to the walls of the chest, is much less than its real ele- vation. Escape of Gas into the Cavity of the Ab- domen.-The escape of gas into the cavity THE LATERAL DISPLACEMENTS OF THE HEART. 443 of the abdomen, owing to perforation of the stomach or intestines, produces rapid distension of that cavity and great eleva- tion of the diaphragm and the heart and lungs, with the effect of inducing great distress in breathing and difficulty in the action of the heart. Abdominal Tumors, even when they are of considerable size, rarely produce any material disturbance either in the action of the heart or in the performance of res- piration. Ovarian Dropsy.-The same may be said of cases of ovarian dropsy, even when the sac is of very large size, and rises up- wards so as to encroach on the chest, un- less that affection be accompanied by in- testinal distension. In the female the walls of the abdomen are capable of great forward expansion, and the result is that large ovarian cysts as well as the gravid uterus at full time tend rather to pro- trude forwards so as to distend the ab- dominal parietes anteriorly, than to rise upwards so as to elevate the diaphragm and encroach upon the heart and lungs. Simple Enlargement of the Liver and Spleen.-When the liver is universally en- larged, even when it assumes a very great size, it does not rise upwards, so as to raise the diaphragm and compress the heart and lungs, but it tends to grow downwards, so as to displace the stomach and intestines. The same may be said of the spleen in cases of leucocythemia, even when that organ attains to a very large size. The result is, that simple enlargement of the liver or spleen does not as a rule encroach upon the chest so as to produce serious disturbance in the functions of the heart or lungs. It is quite otherwise when the upper part of the right lobe of the liver is occu- pied by large abscesses or hydatid cysts or malignant growths. These morbid condi- tions produce a peculiar displacement of the heart upwards and towards the left subclavicular region, and I shall there- fore consider them under the lateral dis- placements of the heart. Mediastinal Tumor.-Dr. Bennett1 gives a case of mediastinal cancer involving the bronchial glands and spinal column, in which the heart was found displaced, being drawn upwards. During life there was very little impulse to be felt or seen imme- diately to the left of the sternum just above the nipple. The Lateral Displacements of the Heart. Pleuritic effusion, empyema, and pneu- mo-thorax of one side of the chest ; hem- orrhage into either cavity of the chest from the rupture of an aneurism of the aorta; thoracic tumors; aneurisms of the arch of the aorta ; aneurisms of the abdominal aorta at the cieliac axis ; and large abscesses or hydatid cysts or ma- lignant tumors in the upper part of the liver; all tend to displace the heart towards the side of the chest opposite to that which is affected. Contraction or cirrhosis of one lung with adhesions of the pleura tends to displace the heart towards the affected side. To these may be added lateral curvature of the spine and con- genital transposition of the viscera. The lateral or transverse displacements of the heart, which are sometimes called dislocations, unlike the displacement of the heart upwards by the encroachment of the cavity of the abdomen upon that of the chest, do not as a rule produce much distress in the heart itself or disturbance of the circulation. The lateral displace- ments of the heart are, however, valuable and decisive indications of disease, since by the evidence they afford they often render our diagnosis accurate and certain. Pleuritic Effusion, Empyema, Pneumo- thorax.-The effusion of serum into either cavity of the chest, owing to pleuritis, acute or chronic, is the usual cause of the lateral displacement of the heart. When extensive effusion takes place into the left side, the heart is pushed over towards or into the right side of the chest, as may be seen in fig. 76. This figure, unlike the others,does not repre- sent an actual case, but is a diagram, made from drawings of six cases, one of effusion of serum into the pleura, one of empyema, and the four others of exten- sive effusion of blood into the left pleura from the rupture a thoracic aneurism. In one of these the clot measured three pints and a half. The displacement of the heart from the increasing effusion of fluid into the pleura is usually gradual. It may, however, be rapid, and Dr. Walshe states that thirty- six hours will sometimes suffice for the heart's impulse to find its way beyond the right nipple. When the quantity of fluid is so small as to occupy only the back part of the left side of the chest, the heart is scarcely displaced. When the fluid in- creases the left ventricle and its apex are at first thrown a little forwards, and towards the centre of the chest. The pressure of the effused fluid is not made directly upon the heart, but upon the strong fibrous sac of the pericardium, and through its medium, upon the heart. If the heart had no sac of its own, and was present without restraint in, say, the left cavity of the chest, it would not be forced forward and to the right when the left cavity of the chest is fiiled with fluid, but it would, I consider, gravitate backwards owing to its own dead weight, and sink to 1 Intrathoracic Tumors, p. 127. 444 POSITION AND FORM OF THE HEART. the back of the cavity, just as the liver sinks to the back of the fluid in cases of ascites. The presence of the pericardium completely prevents such a state of things. The accumulated fluid distending the left cavity of the chest presses equally in every direction. It displaces the ribs backwards, forwards, and especially out- wards, so that they draw the lower end of the sternum somewhat to the left; it dis- places the left wing of the diaphragm, the spleen, stomach, and left lobe of the liver downwards and to the right; and it displaces the pericardium and the heart and great vessels inwards and to the right. The lower end of the pericardium at its Fig. 76. Position of the "heart and great vessels in cases of Pleuritic Effusion info the. Left cavity of the Chest. The heart is displaced into the right side of the chest, its impulse being felt in the third, fourth, and fifth spaces. attachment to the central tendon of the diaphragm is stretched downwards by the traction upon it of the lowered left wing of the diaphragm to which it is attached by its central tendon. The apex forms throughout the lowest part of the heart, and it describes a seg- ment of a circle or arc as it sweeps round from its natural position in the left side of the chest to the position of extreme deviation to which it may attain in the right side of the chest. When the apex describes this curve, instead of being raised by the resistance offered by the ab- dominal organs, it is lowered during the first two-thirds of its course. The reason for this is obvious. The fluid in the left pleura, which displaces the pericardium and the heart to the left, displaces at the same time, as I have just explained, the left wing of the diaphragm and its central tendon and the subjacent organs down- wards, forwards, and to the right. Under these circumstances, as the central tendon THE LATERAL DISPLACEMENTS OF THE HEART. 445 icrming the base of the pericardium is lowered, there is a free space downwards into which the apex of the heart, sus- pended from the arch of the aorta, neces- sarily drops, so that it may be felt beating in the epigastrium over, beyond, and even below the ensiform cartilage. At length, however, the heart, as it advances further into the right side, meets with increasing resistance from the solid convexity of the liver; and the heart, consequently, again rises, so that it is at length about as high on the right side as it is in health on the left. The displaced heart may indeed at- tain to a higher position if it deviate still farther to the right, when, as in a case of Wintrich's,1 it may approach the axilla, and be felt beating from the second to the fourth spaces. Information of some diagnostic value is to be obtained by observing the position of the heart in comparatively early stages in cases of pleuritic effusion, at a time when the impulse of the apex has already moved from its natural position and is on its way towards the central line. To quote Dr. Stokes, we observe, first, that the apex strikes in a situation about mid- way between its natural position and the upper portion of the ensiform cartilage.2 It is not, however, until the apex beat presents itself in the epigastrium that much notice is taken of the altered po- sition of the heart. In four of my cases of displacement of the heart towards the right from effusion into the left side of the chest, the apex presented itself in the epi- gastrium, being in one of these behind the lower end of the ensiform cartilage, and in two behind its middle. As Dr. Town- shend remarks, in speaking of empyema in the left side, the heart is thrust from its natural position down into the epigas- trium, where it may be seen and felt beat- ing. There is no difficulty in distinguish- ing the impulse of the apex from that of the right ventricle in the epigastrium. When the latter is present the whole heart has been lowered, owing to the low- ering of the diaphragm. This may occur, as we have already seen, in cases either of pulmonary emphysema, or croup, or with collapse of the stomach and intes- tines, when the presence of pulmonary resonance over the left side will at once enable us to distinguish the case. In cases of pleuritic effusion the existence of dulness, and in those of pneumothorax the presence of amphoric resonance, over the whole of the left side, and the absence of impulse to the left of the sternum, will generally suffice to ma'ke the case clear. Cancerous tumors occupying the whole of the left side may also give rise to dis- placed impulse and to general dulness on percussion, when that disease cannot be distinguished from pleuritic effusion or empyema on those grounds alone. In cases of pneumonia of the whole of the left lung, it is possible that owing to the enlargement of the pneumonic lung from consolidation and the development of the right lung to compensate for the disable* ment of the left lung, the impulse of the apex may disappear from the walls of the chest, while that of the right ventricle may descend into the epigastrium. In such cases, however, the impulse is com- paratively slight, and it always extends rather to the left than the right of the ensiform cartilage, while in cases of pleu- ritic effusion the impulse is usually strong and marked, and tends rather to the right than the left side of that cartilage. As soon as the seat of the impulse disappears from the left side of the chest and extends to the right of the sternum, every diffi- culty of the kind just stated vanishes. As the heart passes over from the left to the right side of the chest it gradually and necessarily turns over upon itself, hinging, so to speak, upon the vessels by which the heart is attached to the lungs and the system, so that the right auricle is hidden, all but the top of its appendix, and instead of the right ventricle being in front of the left ventricle, all but its left border, it is the reverse, for the left ventricle hides a large portion of the right ventricle (see Fig. 76). The part of the right ventricle exposed is, however, not that near the apex, but that near the pul- monary artery. The ascending aorta and pulmonary artery change their direction ; they move to the right at their respective origins, but higher up they are retained in their places, the arch of the aorta at the end of its transverse portion, and the pulmonary artery at its bifurcation. The aorta and pulmonary artery, therefore, present not a front but a profile view, with a direction to the right. I published a case with a diagram show- ing the position of the internal organs in the "Provincial Medical Transactions" for 1844 (p. 162), in which effusion in the left side of the chest was limited to the lower two-thirds of the bavity, owing to the upper lobe of the left lung being ad- herent down to the third rib. In this case the heart was simply displaced to the right, the front of the organ being still occupied by the right ventricle, and its right and left sides by the right auricle and the left ventricle. This case shows that the heart does not turn over upon itself so as to present the left ventricle in- stead of the right in front, unless the fluid presses upon the left side of the peri- cardium for its whole length, so as to bear upon the great vessels as well as upon the body of the heart. 1 Krankheiten der Respirationsorgane. 2 Dr. Stokes on the Diseases of the Heart and Lungs, p. 500. 446 POSITION AND FORM OF THE HEART. The impulse to the right of the sternum is sometimes limited to the fourth and fifth intercostal spaces, while sometimes it is also present over the third and even the second space. In the latter case the impulse is double, and is due to the pul- sation, followed by the second beat coin- cident with the second sound of the pul- monary artery or aorta, or both. When pulsation is present in the first, second, and third right spaces, and also in the normal position to the left of the sternum, the case is one of aneurism of the aorta ; and the distinction of this impulse or pul- sation from that of displaced heart pre- sents therefore no difficulty. Wintrich1 states that sometimes, when the effusion is in the left side, the heart is displaced backwards (and to the right) being covered by lung, when the displace- ment of the heart can by no means be dis- covered. He saw one such case in which an able clinical physician mistook the disease for pericarditis with very great effusion. When effusion of fluid takes place into the right cavity of the chest, the heart is displaced towards the left side. As the impulse, however, is already seated on that side, the change in position of the impulse of the heart is not nearly so marked or diagnostic as in cases in which the heart is displaced to the centre or right side of the chest, owing to effusion into the left side. Important information, however, is to be obtained in such cases from the position of the impulse on the left side. In a patient under my care who had extensive effusion into the right pleura, the impulse was felt in the sixth space, two inches farther to the left, and some- what lower than the natural position. In two cases of seropurulent effusion in moderate quantity into the right pleura, of which I possess drawings, the heart was displaced to the left, and lowered to a slight extent. In one the apex of the heart was situated behind the seventh rib, more than an inch to the left of the natural site, and nearly an inch lower. In the other, the displacement of the heart downwards and to the left also ex- isted, but to a less degree. Since the above was in type I have seen three cases of extensive effusion of fluid into the right side of the chest. In two of these cases the apex-beat was felt as far to the left as about the seventh rib, the position of the impulse being somewhat lower than natural. In the third case, a young woman, whom I saw through the kindness of Dr. Wane, the amount of fluid in the right side of the chest was very great. The impulse of the heart was not perceptible to the right of the mamma, but prevailed along its upper left border from the third or fourth to the seventh space where it was unusually low in situation. There was a double impulse over the great arteries at the left upper border of the mamma, and doubling of the second sound, the second of the two sounds being that made in the pulmonary artery. There was also a loud mitral murmur around the region of the apex. A large quantity of fluid was drawn off, by means of a glass syringe through a fine tube, by Mr. James Lane, who performed the same operation for the two other cases. I watched the position of the impulse when the fluid was being withdrawn, and noticed that it soon disappeared from the seventh space, and more slowly from the sixth, the beat moving steadily to the left and somewhat upwards. When the full amount of fluid had been withdrawn, the impulse was present in the fourth and fifth spaces, and perhaps in the third, being situated to the right of the mamma. The doubling of the second sound at once disappeared, and later I believe that the mitral murmur also vanished. In the drawing of an instance of great cylindri- cal dilatation or aneurism of the ascend- ing aorta, in which there was considerable effusion of fluid in the right side of the chest, the heart, which was greatly en- larged and lowered in position, was dis- placed to the left as far as the ribs would allow, the apex extending to the seventh space, fully twro inches below the level of the lower end of the sternum. In two cases related by Dr. Gairdner1 of effusion into the right pleura, the apex- beat in both was displaced to the left; in one (p. 329) the impulse probably re- tained its usual level, being displaced about one inch to the left. In the other (p. 354', before paracentesis, the apex- beat was felt in the fifth space, one inch and a half to the left of the normal site ; after the operation it was present in the fourth space. In this case the impulse was probably lowered. Dr. Townshend, who was the first to observe the displace- ment to the left in such cases, felt the apex striking against the stethoscope be- tween the fourth and fifth ribs in the axilla in two cases of empyema of the right side.2 It is evident, then, that when considerable effusion takes place into the right side the apex-beat is always pushed further to the left, and that it is usually lower, sometimes on the same level as, and sometimes higher than the natural position. 1 attribute the lowered position of the impulse to two causes, the displace- ment downwards of the central tendon of the diaphragm by the effusion, and the inspiratory lowering of the diaphragm to 1 Krankheiten der Respirationsorgane, p. 255. 1 Clinical Medicine. 2 Cycl. of Med. vol. ii. p. 38. THE LATERAL DISPLACEMENTS OF THE HEART. 447 enlarge the left lung, and so to compensate for the disuse of the right lung. I do not find that the displacement of the heart from empyema differs in any respect from that caused by the effusion of serum into the pleura. In pneumothorax of the left side, the displacement of the heart is the same as in cases of fluid effusion into the pleura. In general, fluid is combined with the air in those cases, but air without fluid will produce displacement of the heart, and it must do so when it is in sufficient quan- tity to distend the sac of the pleura, press down the diaphragm, and so push the pericardium and the heart over to the opposite side. Dr. Douglas Powell1 re- lates a case in which the right side of the chest was filled with air, and the right border of the heart was situated to the left of the left sterno-clavicular line. Wintrich2 states that displacement of the heart takes place in pneumothorax as in pleuritic effusion; the only difference being that in pneumothorax the heart is more frequently displaced from before backwards. Hemorrhage into either Cavity of the Chest from the rupture of an aneurism of the aorta displaces the heart, as a rule, to the opposite side, in the same manner, and to the same extent, the quantity of fluid being alike, as in cases of pleuritic effusion. Two circumstances, however, tend to modify this result, one, the size and position of the aneurismal sac; the other, the lessening of the size of the heart that may be induced by the hemor- rhage. Mr. Sidney Coupland3 gives a case in which a diffuse aneurism of the thoracic and abdominal aorta ruptured into the left cavity of the chest, which contained twenty-four ounces of clot. During life the apex was tilted upwards, and was felt beating in the fourth space, one inch within, and on a line with the left nipple. Contraction or Cirrhosis of the Lung with Adhesion of the Pleura.-When pleuritis with effusion, whether chronic or acute, ends in the permanent condensation of the lung, fibroid thickening of the pleura, and binding adhesions, the whole of the affected side contracts and the ribs are crowded together. That side of the chest, however, is not obliterated ; it is still much larger than the condensed lung, and the result is that if, for instance, the right be the affected side, the heart is permanently drawn over into the right side. Dr. Stokes was the first to draw atten- tion to the displacement of the heart to the right side, in consequence of the ab- sorption of an effusion into the right pleura.1 When the left is the affected side, the heart may be drawn quite over into the left side, the right auricle being situated to the left of the median line. This is well seen in Fig. 77, which was taken from a man in whom, owing to the com- plete contraction of the left lung, the heart entirely occupied the left side of the chest in front, no portion of the left lung being interposed between the heart and the walls of the chest. The heart is raised towards the infra-clavicular region and the axilla, and the ribs fit closely upon the heart from the second to the fifth. In this man the impulse must have extended from the first intercostal space to the fourth. It may be observed that here also, as in displacement of the heart into the right side, the heart revolves upon itself and turns over, but in the reverse direction. In displacement into the right side, the left ventricle and auricle are situated in front, the right ventricle being partially and the right auricle all but its tip being wholly concealed. In displacement to the left, the right ventricle entirely hides the left side of the heart. The aorta and pulmo- nary artery are twisted to the left, both venae cavae are completely exposed when the right lung is turned aside, and are situated behind the sternum, and the whole heart seems to turn to the left upon the two venae cavae as upon a hinge or pivot. In cirrhosis of either lung the heart is drawn towards the affected side. Dr. Hilton Fagge2 relates a case of cirrhosis of the right lung in which the impulse was seen and felt two inches below and one inch to the left of the right nipple. The heart deviated more to the right dur- ing life than after death, when the apex was two inches to the left of the middle line, being situated between the fifth and sixth (cartilages); and one-half of the heart was to the left, and one-half of it was to the right of the middle line. Dr. Greenhow3 gives a case of contraction of the right lung, the precise condition of which was unknown, observed by him during life, in which the heart was dis- placed very far to the right and upwards, and was felt beating in the third and fourth spaces over an area of three inches by three and a half, of which the right nipple formed the central point. Dr. Wilks4 communicates a case of cir- rhosis of the left lung, in which that lung was contracted and hard, and had to be 1 Path. Trans, xix. 77. 2 Krankheiten der Respirationsorgane, pp. 344, 347. 3 Path. Trans, xxiv. 54. 1 On the Diseases of the Chest, p. 501. 2 Path. Trans, xx. 35. 3 Ibid. xix. 159. 4 Ibid. viii. 39. 448 POSITION AND FORM OF THE HEART cut out. The right lung was enlarged, and was the only organ observable on removing the sternum. The heart was drawn towards the left side, "owing to the pericardium being firmly united to the pleura." Dr. Bastian1 gives an analysis of thirty cases of cirrhosis derived from various sources. The heart was much displaced towards the affected side in twelve of these, and slightly in three; while in three of them there was no displacement, and in the remaining twelve there was no notice of the position of the heart. When the left bronchial tube is oblite- rated by compression, by its own con- Fig. 77. Position of the heart and great vessels in a case with Contraction of the Left Lung. The heart and great vessels are drawn completely over into the left side of the chest, so that it is much farther to the left and higher in situation than in the healthy chest. They are partially covered by the right lung, but not at all by the left, and the impulse of the heart is present in the second, third, and fourth spaces, and perhaps in the fifth. traction, or by the admission of a foreign body, the left lung shrinks, the left side contracts, and the heart is displaced towards the clavicle and axilla, exactly as in cases of complete contraction with adhesions of the left lung. Dr. Stokes publishes a case of Dr. Mayne's of aneu- rism arising from the front of the trans- verse portion of the arch of the aorta, which extended downwards towards the left lung, compressing and flattening the left bronchial tube. The left side of the chest was less than the right by two inches, the ribs were crowded together, and the heart was displaced towards the left axilla.1 There are many cases of partial con- traction of a portion of the upper lobe of the left lung, whether from phthisis, cir- rhosis of the lung, gangrene of the lung, or other cause, in which the upper part 1 Dr. Stokes on Diseases of the Heart and Aorta, p. 566. 1 Path. Trans, xix. 47. THE LATERAL DISPLACEMENTS OF THE HEART. 449 of the heart and the great vessels, espe- cially the pulmonary artery, are drawn upwards and to the left towards or into the former seat of the contracted portion of the lung. In such cases the presence of the pulmonary artery, elevated in posi- tion and drawn to the left, may be imme- aiately ascertained by its peculiar double impulse. I cannot say that I have strictly observed the analogous displacement of the ascending aorta towards the seat of the upper lobe of the right lung, in cases of contraction of that lobe, but I have noticed cases of this class in which the vessel evidenced itself by very loud super- ficial first and second sounds, which com- municated themselves to the ear, if not to the hand, like a double shock or impulse. Dr. Stokes has given an interesting ac- count of the displacements of the heart from the diminished volume of the lung, in his work on Diseases of the Heart, p. 458. Intra-thoracic Tumors.-Large cancer- ous growths in the cavity of the chest, when they press upon the heart without penetrating into its structure, necessarily displace it in the direction of the pressure. The heart is simply pushed aside by the tumor, and its displacement is in no way influenced by the relation of the heart to the central tendon of the diaphragm. "In the year 1856 I saw," writes Dr. Cockle, in his paper on intra-thoracic can- cer, " a case of intra-thoracic cancer occu- pying the whole of the left side of the chest, and encroaching slightly on the right side, in which the*tumor carried the heart before it as far as the right nipple. The impulse was felt pulsating between the second an 1 third ribs, and down to, and at a late: period beyond, the right nipple." Dr. Bennett1 relates the case, commu- nicated to him by Dr. Sutton, of a little girl, in whom the entire left side was oc- cupied by a mass of medullary cancer which had pushed the heart considerably to the right. During life the heart was displaced and was felt beating at the right nipple. The diagnosis was " very great effusion into the left pleural cavity and the chest was twice punctured. In a case published by Dr. Andrew,2 in which a large malignant growth occupied the upper lobe of the left lung, the heart was displaced downwards and to the right. Dr. Bennett3 gives a case of can- cer of the anterior and posterior mediasti- num involving the anterior portion and root of the right lung on which the heart was pushed downwards and towards the right side, so that rather more than half of the organ was to the right of the me- dian line. A fortnight before death there was manifest and considerable displace- ment of the heart, which was beating in the epigastrium. Dr. Douglas Powell1 relates a case in which the left cavity of the chest was occupied by a solid mass, displacing the heart to the right, and the lung posteriorly. After death it was found that this tumor was intimately con- nected with the heart at its left and pos- terior aspects. I might cite other cases of intra-thoracic tumor, published by Dr. Townshend, Boerhaave, quoted by him, and others, in which the heart was dis- placed. On the other hand, cases are recorded in which there was little or no marked displacement of the heart, although the extent of the disease was great. Dr. Graves and Dr. Stokes2 have pub- lished a well-known instance of this dis- ease, in which there was found, in place of the right lung, a solid mass, weighing more than six pounds. It encroached upon the left side of the chest, enveloping and nearly concealing from view the peri- cardium, great vessels, and trachea. Not- withstanding the extent and position of the disease, the heart pulsated in its natu- ral situation. Dr. Wilks describes a case in which the ■whole right lung was converted into one mass of medullary cancer, which pro- truded into the pericard'um, ran along the great vessels at the base of the heart, and pierced the auricles of the organ it- self. The superior cava v as almost de- stroyed by the cancer, the inferior vena cava was closely surrounded by it but was free, the right pulmonary artery was a mere slit in the midst of it, and it had entered the heart through the pulmonary veins. There is no notice of displacement of the heart, although it is stated that the sounds of the heart were very feeble. Dr. Quain3 exhibited before the Patho- logical Society an encephaloid mass of the size of a large cocoa-nut, which was sit- uated between the root of the left lung and the heart. When the patient was first seen, six weeks before his death, the heart was little displaced. Afterwards effusion took place into the left side, and the heart became much displaced towards the right side. It is evident from these cases, that a large intra-thoracic tumor occupying one side of the chest may in some instances displace the heart into the opposite side, while in other instances, in which the tumor is equally large, there may be no displacement of the heart whatever. The reason is obvious. In those instances in 1 Path. Trans, xxiv. 28. 2 Dr. Stokes on the Diseases of the Chest, p. 371. 3 Path. Trans, viii. 54. 4 Intra-thoracic Growths, p. 100. 2 Path. Trans, xvi. 51. 3 Loc. cit. p. 92. vol. ii.-29 450 POSITION AND FORM OF THE HEART which there is no displacement, the cancer penetrates or surrounds the organ, with- out pushing it aside. It is evident, then, that the displace- ment or non-displacement of the heart, and the mode and extent of its displace- ment, in instances in which there is com- plete dulness of one side, may sometimes help us to discover whether the case is one of intra-thoracic cancer or of simple effusion into the pleura. Large abscesses, hydatid cysts, or malig- nant tumors in the upper or convex portion tf the Liver.-The patient from whom Fig. 78 was taken was affected with jaundice. On post-mortem examination several large abscesses were found in the upper portion of the liver, where it ascends into the right side of the chest. He also had peri- tonitis, and excessive intestinal disten- sion. The whole diaphragm was raised, and with it the heart was pushed upwards Fig. 78. Position of the heart and great vessels in a case with Large Abscesses in the Upper portion of the Liver. The heart and great vessels are displaced extensively upwards and to the loft towards the left axilla, so as completely to occupy the left side of the chest. The impulse is present in the second and third left spaces. and to the left in a remarkable manner. The liver encroached upon the right side of the chest to such an extent that its highest point was on a level with the lower edge of the second rib. The con- vexity of the liver consequently encroached on the left side of the chest as well as the right, and carried the heart, resting upon its upper surface, completely over into the upper portion of the left side of the chest. If this figure be compared with Fig. 75, DISPLACEMENT OF THE HEART FORWARDS. 451 in which the diaphragm is excessively raised by means of distension of the stomach and intestines, it will be seen that while in both the diaphragm is raised to an excessive degree, there are important points in which they differ ma- terially from each other. In that figure as well as in this we find that the abdo- men is distended, the diaphragm is pushed upwards, the lower ribs are prom- inent, and the heart and lungs are pressed upwards and lessened in size, being en- croached on by the abdominal organs. In universal distension of the abdomen, the heart, while it is compressed upwards, retains a central position, as it rests on the central tendon of the diaphragm. It deviates rather to the right than to the left. But in those cases in which there are large abscesses or hydatid cysts, or cancerous growths in the upper portion of the liver, the heart, as it is pushed up- wards, deviates extensively to the left, and occupies a space to the left of the up- per half of the sternum, behind the first, second, third, and fourth ribs. It is to be remembered that in this case there was peritonitis and great intestinal dis- tension, consequently the compression of the heart upwards was effected by a double cause. The deviation of the heart to the left side of the chest from extensive abscesses in the upper portion of the liver, differs thus from the deviation caused by effusion of duid into the right side of the chest- in effusion into the right side of the chest, the heart and the impulse at the apex are either lowered or only slightly raised; while in cases with abscesses in the up- per portion of the liver they are pushed upwards, being above the fourth rib. The position of the heart in enlargement of the liver from abscess, and in great contraction and adhesions of the left lung, corresponds very closely. (Compare Figs. 77 and 78.) In both the heart and great vessels are situated behind the sec- ond and two or three upper ribs, in both the heart is pushed entirely into the left side, the venae cavae being behind the sternum. But in the following respects they differ. In enlargement of the liver from abscesses, the anterior aspect of the heart is unchanged ; the left upper ribs are widened apart and the ribs on both sides are raised and pushed outwards; the dulness on percussion is more exten- sive on the right side than the left, espe- cially behind, and the heart and its im- pulse scarcely appear below the fourth rib. In contraction of the left lung, these conditions are reversed. The heart turns upon the venae cavae as upon a hinge over towards the left, the right auricle and both venae cavae being completely exposed, and the left ventricle being hidden by the right; the ribs are crowded together, the whole of the left side of the chest being contracted ; there is dulness on percussion over the whole left lung, while the whole right side of the chest is very resonant, the area of resonance being increased, owing to the encroachment of the right lung upon the left side of the chest to the left of the sternum; and the impulse of the heart is felt down to the fifth rib. Extensive effusion in the pericardium in acute pericarditis is an additional cause of displacement of the heart towards the axilla. Of this displacement I shall speak in the article on pericarditis. Displacement of the Heart Forwards. Dr. Hope relates a case in which the thoracic aorta, extending from an inch below the left subclavian artery down to the diaphragm, was enlarged into an aneurismal sac which lay across the spine, and projected on the right side three inches beyond the vertebra? without reaching the ribs, while on the left it ex- tended to the ribs, causing destruction of three and caries of two or more of them, and at last formed a considerable tumor on the back. This tumor necessarily compressed the heart forwards against the front of the chest. The impulse of the heart was exceedingly vigorous, and was double, consisting of a diastolic as well as a systolic impulse, each of a jog- ging character. It was agreed that fliere must be considerable hypertrophy of the heart to account for so strong an impulse, and yet the organ was found by Mr. Caesar Hawkins, who drew up the autopsy, only "slightly enlarged and thickened."1 Dr. Hope quotes without reference, a case mentioned by Dr. Todd, in which the heart was pushed forward and outwards, and, as it were, compressed against the ribs by an enormous aneurism of the tho- racic aorta. The sounds of the heart were so modified by this compression as to lead to the erroneous diagnosis of con- centric hypertrophy. I possess a drawing taken from a case of extensive aneurism of the abdominal aorta at the coeliac axis, in which the aneurismal sac extended upwards, behind the diaphragm, in front of the lower dor- sal vertebra?, so as to displace the heart forwards and probably somewhat up- wards. Displacement of the Heart Backwards. When abscesses or tumors form in the anterior mediastinum, behind the lower 1 Dr. Hope on the Diseases of the Heart, p. 447. 452 LATERAL OR PARTIAL ANEURISM OF THE HEART. portion of the sternum, the heart must be displaced backwards. The displacement of the heart back- wards is also induced by the very extensive effusion that gradually takes place into the pericardium in cases of chronic pericarditis, Wintrich states, as we have already seen, that sometimes when there is pleu- ritic effusion in the left side, the heart is displaced backwards and to the right, so that its displacement can by no means be discovered. LATERAL OR PARTIAL ANEURISM OF THE HEART. Thomas Bevill Peacock, M.D., F.R.C.P. Under this term it is proposed to treat of the partial or lateral sacculated dilata- tions, in contradistinction to the general enlargements of the cavities of the heart, to which, and especially in France, the term aneurism has also been applied. The partial aneurisms differ, however, from the lattes forms of the disease, not only because they involve only a portion of the parietes of the cavity, but also in that the structure of the muscular walls is always more or less altered in the seat of disease. The real aneurismal tumors affect only the left cavities of the heart, the left ven- tricle and auricle, or the corresponding arterial and auriculo-ventricular valves. The immunity thus possessed by the right cavities has been variously explained "by different writers. Breschet, who thought that the aneurismal dilatation was almost always, if not invariably, situated near the apex of the left ventricle, and that its production was due to the laceration of the inner portions of the ventricular walls, supposed that the non-occurrence of the disease in the right ventricle was owing to the greater relative power of its walls at the apex. Dr. Thurnam referred the freedom of the right ventricle from dis- ease to the peculiar action of the valves at the right auriculo-ventricular orifice, by which, when the ventricle becomes dis- tended, the aperture is incompletely closed so as to allow the reflux of the blood into the right auricle. He also contended that the term aneurism should be restricted to the dilatations of the cavities of the heart through which arterial blood circulates; while the term varix should be applied to the similar enlargements of the venous cavities, so as to maintain the analogy between the affections of the two sides of the heart and those of arteries and veins. Rokitansky considers the dilatations of the right side of the heart as not truly aneurismal, and ascribes the occurrence of the real aneurisms only on the left side to the greater frequency of endocarditis in that situation. There seems good rea- son to believe that the proneness to in- flammation of the lining membrane of the left cavities, is mainly influential in caus- ing the occurrence of aneurism on the left and not on the right side of the heart; but it is also probable that the greater tension to which the walls of the left ven- tricle are exposed, with the variations of pressure exerted by the column of blood in the arteries, materially conduces to the dis- ease. Certainly when from any cause any portion of the parietes is rendered less re- sistant and more readily expansible, the pressure of the blood will tend rapidly to expand the weaker part so as to form a distinct sac. In the following notice I shall treat first of aneurisms of the left ventricle, then of those of the left auricle, and lastly of val- vular aneurisms. ANEURISM OF THE LEFT VENTRICLE. The occasional occurrence of partial aneurismal dilatations of the heart simi- lar to those which are of such frequent occurrence in the arteries, was first shown by the case recorded by Galeatti in 1757; and it is a curious coincidence that in the same year the condition was brought to the knowledge of John Hunter by the oc- currence of a case, the preparation of which is contained in the Museum of the Royal College of Surgeons, and of which the description was found by Dr. Thur- nam1 in his MS. Catalogue. In 1759 a case of the kind occurred to Walter, which was published in 1785,2 and in 1793 an- 1 Med.-Chir. Trans, vol. 21, 1838. 2 Nouv. Mem. 1'Acad de Berlin. ANEURISM OF THE LEFT VENTRICLE. 453 other specimen preserved in Dr. Hunter's Museum, was described by Dr. Baillie and figured by him in the plates which appeared in 1799. Corvisart met with a case in 1796, which was published in 1806. Hodgson described one in 1815,' Zannini in 1816,2 Rostan in 1820,3 and Shaw in 1822? Sir A. Cooper, in his Lectures pub- lished by Tyrrell in 1825, said that he had met with three cases of which two were contained in the Museum of St. Thomas's Hospital. In 1827 the first memoir on the subject was published by Preschet,5 in which the particulars of ten cases were collected, including one communicated to him by Cruveilhier in 1816, two by the Berards which appeared in a Paris The- sis, and one by Dance, together with the case of the celebrated Talma and the de- scription of a specimen in the museum of the Faculty by Breschet himself. In the same year two other cases of the kind were described by Adams in Dublin,6 and by Johnson in this country.7 In 1830, Dr. Elliotson, in his Lumleian Lectures, described another case, of which the preparation is now in the Museum at St. Thomas's, and referred to sixteen cases as on record at that time. In 1829 two additional cases were narrated by Bignardi and Reynaud,8 in 1832 a third was published by Hope, and in 1833 a fourth by Lobstein. In 1834 a notice of the subject was given by Ollivier,9 in which he referred to the cases collected by Breschet, together with those of Adams, Bignardi, and Reynaud. In 1835, Dr. Thomas Davies referred to the disease, and stated that there were two specimens in the Museum of the late Mr. Langstaff. In the same year, Bouillaud treated of the subject in a section of his work, detailing the more important obser- vations recorded by Breschet and Olli- vier, with two more recently published cases by Choisy and Petigny. In 1838 Dr. Thurnam contributed a memoir to the Medical and Chirurgical Society,10 which was then completely exhaustive of the subject and still leaves little to sup- ply, and affords the best description of the pathology of these affections which has appeared. In this memoir he re- lated seven new cases, of which three were drawn from the MSS. of John Hun- ter in the possession of the Royal College of Surgeons. He further referred to five other specimens previously undescribed, which he had found in different museums. In 1842 a short notice of the subject was published by Rokitansky, in his work on Pathological Anatomy ; and in 1843, Dr. Craigie contributed to the Edinburgh Medical and Surgical Journal a valuable memoir,1 detailing the particulars of twen- ty-two of the cases up to that time re- corded, all of which had, however, been previously referred to by Dr. Thurnam, together with a very interesting example which had occurred in his own practice. In 1846 a case was described by myself ;4 in 1850, Dr. Halliday Douglas3 related the particulars of four cases ; and in 1852, M. Cruveilhier discussed the subject in his Pathological Anatomy, illustrating his views by reference to various examples which had fallen under his own notice. Since the publication of Dr. Thurnam's memoir, numerous observations have been placed on record, so that I have had no difficulty in collecting forty-three fresh cases, together with brief notices of others not fully reported. Of this number four- teen are contained in the Bulletins of the Societe Anatomique of Paris, two in the Memoires of the Societe de Biologie, and sixteen in the Transactions of the Patho- logical Society. With the cases collected by Dr. Thurnam, fifty-eight in number, those on record must at present exceed one hundred, and I have seen references to several others, the particulars of which I have not been able to obtain. Nature and Mode of Origin.-Breschet, as the name, false consecutive aneurism^ which he gave the affection, indicates, re- garded the real aneurisms of the heart as originating in rupture or ulceration of the lining membrane of the ventricle and some portion of the muscular walls, the result of softening from inflammation or atheroma. Reynaud showed that in his case the dilatation originated in disease of the endocardium; and Cruveilhier pointed out that in some cases the whole of the structures of the ventricular walls were dilated, - and apparently in con- sequence of the muscular fibres having undergone conversion into a fibroid struc- ture, which was less resistant to pressure and more readily admitted of expansion. Dr. Thurnam to some extent adopted the views of the pathologists who had preceded him, and contended, that, while the aneurisms did in some cases originate in rupture or softening of the lining mem- brane and muscular walls of the ventricle, they more frequently were connected with 1 Diseases of Arteries and Veins, p. 84. 2 Italian Translation of Baillie's Morbid Anatomy. 3 Sur les Rupt. du Cceur, Obs. v. 4 Manual of Anatomy, vol. i. p. 251. 5 Rep. G6n. d'Anat, tome 3me p. 181. 6 Dublin Hospital Reports, vol. iv. 7 Med.-Chir. Rev. vol. xv. 8 Journal Hebd. de Med. 9 Diet, de Med. tome viii. p. 303. 10 Transactions, vol. xxi. In Dr. Thurnam's paper references will be found to all the cases here named, published up to the period of its appearance. i Vol. lix. p. 381. 2 Edin. Med. and Surg. No. 169. 3 Monthly Jour, of Med. Sc. 454 LATERAL OR PARTIAL ANEURISM OF THE HEART. the changes in the endocardium and mus- cular substance pointed out by Reynaud and Cruveilhier, and consisted in dilata- tions of the whole of the structures con- stituting the parietes of the ventricle. He also thought that these changes were probably often referable to inflammation, and that in some cases the formation of coagula in the cavity of the ventricle might cause the expansion of the ven- tricular wall in the seat of deposition. He further contended that the aneurisms of the heart presented all the several forms which are met with in similar affec- tions of arteries. Rokitansky regards the aneurisms of the heart as always depend- ing upon inflammatory processes, either of an acute or chronic character. In the first or acute form of the affection, the disease originates in recent inflammation of the endocardium and probably also of the contiguous muscular substance, and the consequent laceration or breaking down of the inflamed surface under the pressure of the blood. In the other variety, the dilatation is the more remote result either of inflammation of the endocar- dium and a somewhat thick layer of the muscular substance, or of the whole thick- ness of the wall of the ventricle during endo- and peri-carditis. In this form the muscular fibres become replaced by fibroid structure, the endo- and peri-cardium are blended with the altered tissue, and the parietes become expanded under the pres- sure of the blood. The first of these forms corresponds therefore with the false consecutive aneurism of Breschet; the second with the true aneurism of Rey- naud, Cruveilhier, and Thurnam. While adopting Rokitansky's views as to the inflammatory origin of the cardiac aneu- risms, there is no reason to deny the cor- rectness of the analogy contended for by Dr. Thurnam, between their various forms and the different varieties of arterial aneu- risms. It is, however, very doubtful how far the coagulation of the blood in the cavities of the heart gives rise to partial dilatation. Such coagula form, it is well known, chiefly on the right side, in which the aneurismal dilatation does not occur ; and the clots which Dr. Thurnam has de- scribed and figured, might as probably have originated in the already dilated part as have given rise to the dilatation. It is obviously only by the examination of incipient aneurismal sacs, or those of small size, that we can form a correct judgment as to their original modes of development. Confining his assertion only to such cases. Dr. Thurnam states that of twenty-eight out of the fifty-eight cases which he collected, twenty-two origi- nated in dilatation of the structures en- tering into the composition of the walls of the heart; while in six there was solution of continuity of the endocardium and inner stratum of muscular fibres. Of the forty-three cases which I have myself col- lected, in thirteen the data are imperfect or the disease is very far advanced; of the remaining thirty, in twenty-five the sac was lined by endocardium, which is stated to have been opaque, thickened, indurated or ossified in eleven cases;- and in four the lining membrane was de- stroyed. In sixteen of these cases the subjacent muscular structure had under- gone the fibroid degeneration and was more or less attenuated, in one of them to such an extent as to present only a trace of the altered tissue ; in five the muscular substance was thinned but not otherwise altered ; and in seven cases it was wholly wanting and the sac was only bounded by the endo- and peri-cardium. Both series of facts, therefore, show that in the cases in which satisfactory opin- ions as to the mode of origin of the sacs can be formed, they are usually at first of the true form, or that in which all the structures are expanded. From several specimens which I have had the opportunity of examining, either in the recent state or as preparations, the following may be stated to be the progres- sive changes in the development of the true aneurisms. 1. In the earliest stages in which the affection can be recognized, we observe thickening and opacity of the endocar- dium, with slight dilatation of the corre- sponding portion of the walls of the ven- tricle, and attenuation of the muscular substance without any marked alteration of its texture. 2. In a more advanced stage there is thickening and opacity of the endocar- dium, and conversion of a more or less thick stratum of the muscular substance into a dense, yellowish or whitish colored fibroid tissue intermixed with the muscu- lar structure. The parietes of the ventri- cle in the seat of disease have become more atrophied, and the cavity presents a more marked dilatation. 3. At a still later period, together with the thickening and opacity of the endo- cardium, this membrane becomes inti- mately blended with the subjacent tissue, so as to be no longer separable from it. The muscular substance throughout the whole or the greater part of the thickness of the ventricular parietes, is converted into dense, pale-colored fibroid tissue. The attenuation of the walls of the ven- tricle is greater, and the dilatation of the corresponding portion of the cavity, if occupying the outer surface of the heart, occasions a more or less marked promi- nence externally. While these changes are in progress in the parietes of the ventricle, others are proceeding in its interior. The dilated portion of the cavity becomes, especially ANEURISM OF THE LEFT VENTRICLE. 455 if it be somewhat circumscribed and bounded by a tolerably defined margin, the seat of coagula. These are at first thin, loose, and dark colored, subsequently they become more firm and paler ; and at length the sac is found more or less com- pletely filled by coagula, of which the outer portions are distinctly laminated and decolorized, and often adherent to the altered endocardium. As the partial dilatation of the ventricular cavity in- creases and forms a more or less decided prominence externally, the visceral peri- cardium becomes implicated in the dis- ease. At first it is only slightly opaque and presents a rough surface, from the existence of small granular concretions of flbrine; these become thicker and coalesce, and finally constitute a distinct layer of false membrane ; and at length adhesions are formed between the visceral and re- flected pericardium over the seat of the aneurism, or more rarely uniting the whole or a large portion of the mem- branes ; often also, when there are not entire adhesions, the surface of the heart displays large white patches. In the cases in which there are evidences of the existence of more general pericarditis, it seems probable that the alterations in the ventricular walls upon which the aneuris- mal dilatation depends, have, as stated by Rokitansky, proceeded from without, and have involved the inner portions of the parietes secondarily. With the gradual expansion of the aneurismal sac, the lining membrane and part or the whole of the muscular layers may be eroded or destroyed, so that the cavity may come to be bounded by the pericardium, with or without a portion of altered muscle; the aneurism thus assum- ing the "false consecutive''' form. Pathologists have within the last few years described the occurrence of fibrinous deposits in the walls of the heart. The Pathological Transactions contain various instances of the kind, originating either in acute inflammatory action, or resulting from an altered condition of the blood. In some cases this fibrinous material may undergo imperfect organization, giving rise to the fibroid degeneration of the muscular tissue which, as above shown, so frequently precedes the formation of the true aneurisms. In other cases the deposit breaks down and destroys the in- volved tissue, so as to give rise, under the pressure of the blood, to a kind of sac, to which the term "false aneurism'1'' may be applied. It should, however, be stated that Roki- tansky regards the acute or originally false form of aneurism, as of decidedly less common occurrence than that in which the whole of the tissues are ex- panded, and his conclusions are confirmed by the observations of others. Various cases originating in the former mode are, however, on record. One such was re- ported by Dr. Pereira, in which the cavity was situated at the base of the septum of the ventricle ; and another is related by Mr. Shillitoe and myself in the Pathologi- cal Transactions. In both these cases there was considerable disease of the ad- jacent parts and the patients rapidly sank ; and such is probably generally the case in similar instances. It is by no means uncommon in connection with endocarditis of the aortic valves to find smaller or larger excavations in the ven- tricular walls at the base of the septum, which, were life sufficiently prolonged, might probably become aneurismal sacs. Cases of the kind have at different times been exhibited at the Pathological Society by the late Mr. Avery,1 Dr. Bennett,2 and myself.3 In some cases it has been supposed that an extravasation of blood, or the forma- tion of an abscess in the substance of the ventricular walls, producing a laceration or erosion extending into the cavity, may give rise to the formation of an aneurismal sac; and instances affording examples of aneurisms probably so originating have been referred to by Cruveilhier. I have also myself described a case in which, in connection with general pericarditis, an abscess had formed in the septum of the auricles, which opened into the base of the left auricle and origin of the aorta. In this instance the aortic valves were also extensively involved and the patient died rapidly, but it apparently formed an instance in which an abscess in the car- diac walls might have been followed by aneurism. The case is more fully reported by Dr. Craigie, in whose practice it oc- curred. It is also highly probable that in some cases lacerations of the internal por- tions of the muscular walls of the ventri- cle connected with fatty degeneration, may lead to the formation of the false consecutive aneurisms. I have already mentioned the conclu- sions deduced from the cases analyzed as to the parts constituting the walls of the sacs. Dr. Thumam has also given par- ticulars of their contents. He states that in twenty-three cases they contained a greater or less amount of laminated co- agulum; in nineteen simple amorphous clots ; and in twenty-three cases they had been found empty. Of my own series of cases, nineteen contained old coagula, which were more or less decolorized, lami- nated, and in some cases adherent to the lining membrane of the sac ; three dis- played old and recent clots combined: and seven contained only recent coagula. The 1 Path. Trans, i. p. 72. 2 Ibid. p. 59. 3 Ibid. ii. p. 49. 456 LATERAL OR PARTIAL ANEURISM OF THE HEART. condition of the sac has not been reported in most of the remaining cases. In twenty- one of the first collection of cases the aneurismal walls, and especially when the sacs formed distinct tumors, had been strengthened by adhesions of the peri- cardium ; in other instances there were loose false membranes on the pericardium without adhesions ; and in seven cases the layers of pericardium were universally adherent. In the second series, eleven out of thirty in wdiich the condition of the pericardium is named in the reports, dis- played adhesions over the projections of the aneurisms ; in live there were white patches and adhesions in the seat of dis- ease or elsewhere ; in one the adhesions were almost entire ; and in three instances the two layers of pericardium were uni- versally attached. Seat of Disease.-M. Breschet supposed that the aneurismal sacs were nearly al- ways situated at the apex of the left ven- tricle. Dr. Thurnam was led to qualify this opinion, and showed by the analysis of the cases which he collected, that, while the partial dilatations are of more frequent occurrence at the apex than elsewhere, they do occur in all parts of the ventricular walls. Of fifty-seven cases in which the description was complete, in twenty-seven the sac was situated at or near the apex ; in twenty-one in different parts of the base ; in fifteen in the intermediate parts of the ventricle ; and in three in the sep- tum. Of forty-two of the more recent cases, in fourteen the sacs were situated at the apex ; in eleven near the base ; in eight in the middle of the ventricle, at the anterior, outer, or posterior part; and in six in the septum. In three instances there were two or more sacs in the same case. In one of them one sac was situ- ated at the apex, and another on the left side ; in a second, one aneurism was at the apex, the other in the septum ; in the third, one sac was situated partly in the septum and partly in the anterior wall, another was situated posteriorly in the septum, and a third occupied the middle of the external wall. Both these enumer- ations concur in showing that the most frequent situations for the aneurismal sacs are first the apex, then the base, and lastly the external wall and septum. The greater liability to the occurrence of aneurisms at the apex of the ventricle is supposed by M. Breschet to be owing to the relative thinness of the parietes in that situation, exposing them to rupture during the active contraction of the heart. It is, however, more probably owing to the tissues being readily involved in in- flammatory action, extending from the peri- or endo-cardium, when, as at the apex, those membranes are more nearly in contact, than when the layer of mus- cular structure is of greater width. The portions of the ventricle near the base are probably commonly affected, from the fre- quency of endocarditis of the aortic valves, leading to induration and thickening, and so to more or less obstruction to the flc,w of blood from the ventricle. Under these circumstances there is a tendency to ex- cavation beneath the aortic valves, which may proceed to the extent of forming a distinct aneurismal sac. In some cases the disease is situated in what has been termed the " undefended space," the space which intervenes between the base of the ventricular septum and the convex sides of the left and posterior semilunar valves. This ordinarily is only closed by the endo- cardium of the left ventricle, and by a layer of fibrous tissue, a thin layer of mus- cle, and the endocardium of the right ventricle. Being thus imperfectly pro- tected, the space is readily expanded under any unduly distending force, and a sac is formed which will protrude into the right cavities about the auriculo-ventric- ular aperture. When in Vienna a year ago Rokitansky showed me one or two cases of the kind ; one was exhibited at the Pathological Society during the last session, by Dr. Hare, and I have found the condition myself. In some cases por- tions of the ventricular wall in this situa- tion may be congenitally deficient, and a column of blood flowing from the left ven- tricle may distend and dilate the folds of the tricuspid valves, as shown in a speci- men in the Museum of the Royal College of Surgeons. In other cases, the excava- tion may occupy some other portion of the base of the ventricle beneath the aortic valves, and a channel may be formed leading into a small aneurismal sac, situ- ated external to the origin of the aorta ; and such sac may be still further prolonged so as to open above into the aorta. Cases of this kind were first described and fig- ured by Dr. Hope, though he supposed that the aneurisms originated in connec- tion with the aorta and only opened into the ventricle. I have described two cases of the kind in the Pathological Transac- tions, and a similar one is also related by Dr. Bristowe. Aneurism at the base of the ventricle may also rupture into the right auricle or pericardium, Rokitansky mentions having seen a case in which both these results occurred. When the sacs form in the external wall of the ven- tricle, they may open into the left auricle or may burst into the left pleura, as in a case referred to by Sir A. Cooper. When seated in the septum they may press upon the right auricle and ventricle and open into one or other of those cavities, espe- cially the right ventricle, as in the case related by Dr. Pereira, one existing in the Museum of St. Thomas's Hospital, and one referred to by Rokitansky. In cases of this kind a form of aneurism results, ANEURISM OF THE LEFT VENTRICLE. 457 which, as pointed out by Dr. Thurnam, is analogous to the " spontaneous varicose aneurisms" of authors. Form and Size.-Aneurisms of the heart may be either circumscribed or diffused ; or, in other words, the apertures by which they communicate with the ventricle may be more or less constricted ; or the cavity of the aneurism may gradually extend from that of the ventricle without any obvious line of separation. The sacs, when situated at the apex, are more gen- erally of the diffused form; those at the base, and in other parts of the ventricle, are more commonly circumscribed. In the first series of cases the sacs are in- ferred to have been circumscribed in twenty-five cases, and diffused in nine- teen. As far as can be ascertained from the reports of the more recently published cases, it appears that of thirty-seven cases, twenty-five were circumscribed and twelve diffused. The size of the sacs also varies accord- ing to the seat and duration of the dis- ease. At the base and in the septum the sacs rarely attain any great size ; on the contrary, when developed in the external wall or at the apex, they may form tu- mors of considerable magnitude or may even equal the dimensions of the heart itself. The acute forms of aneurism also appear, as might be expected, not to at- tain the dimensions of the more chronic cases. Dr. Thurnam states that in his cases the sacs might, in nine instances, be compared to nuts, in twenty to walnuts, in seven to fowls' eggs, in fourteen to oranges, and in nine their size almost or quite equalled that of the healthy heart itself. In thirty of the cases which I have myself collected, in four .the aneurisms are simply stated to have been small; in five they are compared to hazel nuts or filberts ; in two to walnuts ; one is said to have been large enough to hold a plover's egg, one to hold a pigeon's egg, and six are compared to bantam's or smaller or larger fowl's eggs. One sac is said to have been as large as a nutmeg, another as a plum; one is reported to have been capable of holding the whole end of the thumb, another to have been as large as an apple, and a third as a small orange. Two are described as being large. In one case, in which there were two distinct cavities, both were the size of walnuts; in a second one was as large as a hen's egg, the other as a walnut. In a third there were three cavities, the largest the size of a nut. In several cases the cavi- ties contained one or more loculi, and in one there were three large pouches pro- jecting from the main cavity. Strife of other parts of the Pericardium and Heart.-The frequency of alterations in the pericardium and endocardium and in the walls of the ventricle in the seat of the aneurismal swellings, has already- been referred to. It must also be men- tioned that the occurrence of thickening, opacity, and induration and ossification of the endocardium and pericardium, and the fibroid transformation of the muscular substance, are by no means confined to the immediate seat of disease. These changes often involve a considerable por- tion of the heart, and especially of the left auricle and ventricle. In addition to these morbid conditions, also, the effects of more recent inflammation are frequent- ly found. Hemorrhagic pericarditis oc- curred in one of the first collection of cases ; and in the recent series, pericardi- tis, with or without old adhesions and white patches, is recorded to have been found in four cases. In two also of the cases, blood was found in the pericardium, and in a large proportion of both series there was serous effusion in conjunction with general dropsy. In two cases also of the latter collection there were evidences of recent endocarditis, and in several in- stances fatty degeneration of the muscular structure had occurred in different parts of the heart. In five of Dr. Thurnam's cases there is stated to have been disease of the mitral valves, in three of the aortic valves, and in one of both sets, and in only eight cases are the valves expressly stated to have been healthy. In my own cases, the valves are stated to have been healthy in only five cases. The aortic valves are re- ported to have been diseased in seven instances, the mitral in two, and both sets in three, and in two or three other in- stances the aneurismal sacs were so sit- uated as to have interfered with the action of the auriculo-ventricular valves. It must necessarily follow that the state of the whole heart is affected to a greater or less extent in these conditions, which ne- cessarily lead to alterations in the size of the cavities and in the thickness of the walls. From the first series of cases it was inferred that there was general dila- tation of the organ in three cases, dilata- tion with hypertrophy in three, dilatation of the left ventricle only in two, hyper- trophy in two, and dilatation with hyper- trophy of both ventricles in nine. In only ten cases was the heart reported to have presented no other lesion than the aneu- risms, and in three only was it stated to have been positively healthy. In the more recent collection the heart appears to have been greatly enlarged in seven cases; there was great enlargement, but especially hypertrophy and dilatation of the left ventricle in twenty cases ; dilata- tion of the left ventricle in two ; and dila- tation of the right ventricle in one. In two cases the separation of the two sides of the heart was imperfect from the aper- tures having formed in the fold of the fora- 458 LATERAL OR PARTIAL ANEURISM OF THE HEART. men ovale. In three cases the coronary arteries were diseased ; and in six there existed more or less atheroma, calcifica- tion, dilatation, or aneurism of the ascend- ing portion of the aorta. Of the whole number of cases, excluding from con- sideration six in which the reports are imperfect as to the general condition of the heart, there is not one in which there was not some alteration in the state of the heart or pericardium, in addition to the aneurism. In one case the heart is in- deed said to have been of natural size, but in that instance there was recent pericar- ditis and an acute aneurism. The shape of the heart is stated to have been frequently altered by the presence of the aneurismal swellings. In some it had an unusually wide or globular form; in others there was a bulging of the aneu- rismal sac, separated by a more or less distinct furrow from the other portion of the ventricular wall; and in yet other cases there were obvious tumors project- ing from the surface of the organ. These were sometimes only of small size so as to be compared to a small nut or thimble ; in others they were of considerable mag- nitude, and were separated from the walls of the heart by a distinct constriction or neck. In one specimen contained in the Museum of St. Thomas's Hospital, prob- ably one of those referred to by Sir A. Cooper, there is a tumor with thin parietes as large as an ordinary heart projecting from the anterior surface of the organ, and separated from it by a neck which is not half the circumference of the tumor itself. The existence, however, of an obvious tumor or irregularity on the surface of the heart depends upon the seat and size of the aneurismal sac. At the base the tumors are generally, if not always small, and do not form projections which can be detected till the parts around are dis- sected away. Aneurisms in the septum also can produce no marked alteration in the general form of the organ ; but those on the anterior, outer, and posterior walls, if at all of large size, necessarily occasion either some general bulging or form a dis- tinct tumor. Of fifty-four aneurisms it is inferred that only thirty-five were attended by tumor. State of other Organs of the Body.-The condition of the other organs of the body is not recorded by Dr. Thurnam, prob- ably from the histories of the cases which he collected being defective in these par- ticulars. I regret also that I am not able to supply satisfactory information from the reports of the more recent cases. I find, however, that in a large proportion of them there was more or less general dropsy, and that serous effusion had oc- curred in one or both pleural cavities and in the peritoneal sac. In one of the cases the fluid in the pleura was bloody, the lungs being also engorged in the same case. In two cases there were signs of recent pleurisy, and in eight the visceral and parietal pleurse were attached by old adhesions. In eight cases there was pul- monary apoplexy, emphysema, bronchitis, or pneumonia, and in one of the latter cases the lung was gangrenous. In one instance there were tubercles in the lungs, and in another old syphilitic disease of the larynx. The liver is reported to have been small and pale in one case; fatty in one; and congested, enlarged, granular or indu- rated in eight cases. The spleen was large in two cases, small in one, and soft- ened and containing fibrinous or purulent deposits in one. The kidneys were en- gorged in four cases ; granular, atrophied, cystic, or otherwise diseased in six: and. contained purulent deposits in one. Symptoms and Cause of Death. - It is impossible to point out any symptoms which can, in the present state of our knowledge, be regarded as characteristic of the lateral or partial aneurisms of the heart; and, indeed, it is doubtful whether any such symptoms will hereafter be as- certained. This will readily be under- stood when the frequency with which the affection is associated with valvular dis- eases and with alterations in the size of the cavities and thickness of the walls of the heart is considered. On analyzing the reports which have been published, it appears that in several cases the condi- tion was only detected on post-mortem examination, in the bodies of persons who were not known to be suffering from any form of cardiac disease, and were sup- posed to be previously in good health. In by far the largest proportion of cases, however, twenty-two out of twenty seven, there is a history of prolonged indisposi- tion, not unfrequentlj commencing with acute rheumatism or m some inflamma- tory affection of the thoracic organs, and characterized by the usual symptoms of cardiac disease. Difficulty of breathing, and sense of suffocation and oppression at the chest; pain in the region of the heart, at the sternum, and at the epigastrium ; palpitation and tumultuous action of the heart, and irregularity of the pulse ; with cough, expectoration, and dropsical symp- toms. are generally mentioned as having jeer present. Not unfrequently, also, the sounds of the heart are stated to have been replaced by morbid murmurs, but these appear to have been chiefly, if not wholly, referable to coincident valvular affections. The only symptoms, indeed, which can be regarded as at all of a spe- cific character are pain and sense of weight in the region of the heart, which appear to be more constant attendants on these forms of diseases than on any other ANEURISM OF THE LEFT VENTRICLE. 459 kind of organic affection of the heart. It must, however, be concluded, that, at the present time, the diagnosis of these affec- tions cannot be effected during life, and it is indeed doubtful whether it will be ever possible, with any exactitude, to diagnose them. The cause of death is also often not clearly stated in the reports which have been published. It appears, however, that of the cases collected, in three the patients died suddenly, and probably from syn- cope, without any obvious reason being detected for the occurrence. In two, death resulted from cerebral congestion and convulsions. In one, from more acute disease supervening upon old laryngeal affection. In one from bronchitis, two from pneumonia, one from pleurisy, and in one from phthisis. In two cases the patients sank from coma and other symp- toms connected with disease of the kid- neys. In four instances death resulted from the rupture of the sac and the escape of blood into the cavity of the pericardium ; in four from the rupture of an aneurism of the ascending aorta into the pulmonary artery. In two cases the patients died from extensive disease of the aortic valves connected with endocar- ditis ; combined in one with the opening of an acute aneurism into the left auricle and very nearly externally, and in the other with purulent deposits in different organs. In the remaining seventeen, out of the twenty-five cases in which the par- ticulars are given, it appears that death resulted from the progress of the general and dropsical symptoms and the affec- tions of different organs superinduced by the cardiac defects. Of the cases pre- viously analyzed, the cause of the death was assignable in twenty-four. In twelve of them death was sudden : in three from syncope, in six from rupture of the sac into the pericardium, in one into the left pleura, and in one from rupture of the heart itself. In four, the patients died of apoplexy or paralysis, and in one from epistaxis. In nine cases death ensued from the progress of the cardiac symp- toms, and six from other coincident com- plications. Rokitansky mentions the case of a boy of twelve years of age, in whom a small aneurism at the base of the ven- tricle, after having first formed a connec- tion with the right auricle, opened into the pericardial sac. It thus appears that there are on record eleven cases in which the aneurismal cavities have terminated by rupture. In most of them the affection proved sud- denly fatal. Such was the result in the instance of General Kidd, a gentleman of seventy-three years of age, whose case is related by Dr. Johnson, and who was found dead in his bed. Here the aneu- rism was of small size, and was situated near the base of the ventricle. In a case related by Dr. Wilks, a girl twelve years of age, died suddenly when playing, and an aneurism about the size of a walnut was found about the middle of the ante- rior wall of the left ventricle near the septum. In other instances, however, life has been prolonged for some short time after the occurrence of the rupture. Thus, in the case related by Galeatti, the symptoms indicating the rupture ap- peared about a week before the fatal termination ; and in one which I have myself related, blood appears to have es- caped into the cavity of the pericardium, not, however, by a distinct rupture, five days before death ; more rapid extravasa- tion having been prevented by adhesions between the layers of pericardium at the seat of disease. In some cases the aneurism may be regarded as having undergone a partial natural cure. M. Cruveilhier has de- scribed cases in which the process of dila- tation seems to have been arrested and the sac had been converted into bone, or more properly speaking, in which creta- ceous matter had been deposited in its walls. In a case recorded by Dr. Wilks1 the cure appears indeed to have been almost complete. A man, fifty-two years of age, of very intemperate habits, died of phthisis, and on examination after death, the heart and pericardium were found adherent to the diaphragm at the apex. In this situation there existed a hard calcified tumor, about the size of a pigeon's egg, which contained layers of decolorized coagulum. The cavity com- municated with that of the ventricle by an aperture of about the same size as the sac itself. The edges of this aperture were smooth, and the membrane lining the sac was continuous with the endocardium of the ventricle. No history of the case could be obtained ; but there is no doubt that the sac was aneurismal,. and that the progress of the disease had been entirely arrested some time before the death of the patient. Age and Sex of the Subjects of the Dis- ease.-Dr. Thurnam found the sex as- signed in forty of the cases which he collected, and of them thirty were males and ten females, and he points out the difference which this proportion displays to the frequency of aneurismal affections of the arteries in the two sexes. The facts which I have brought together show a still larger proportion of cases in fe- males-the numbers being thirty-nine- twenty-five males and fourteen females. The ages of the patients in the first series of cases ranged from eighteen to eighty- one, and were pretty evenly distributed 1 Path. Trans, vol. viii. p. 103. 460 LATERAL OR PARTIAL ANEURISM OF THE HEART. throughout the middle and later periods of life, though somewhat more frequent between twenty and thirty, and in ad- vanced life. The more recent cases dis- play a tolerably equal distribution from early to advanced age, and are given in the following table :- nethy, Burns, and Hodgson, and, more recently, others have been placed on rec- ord by Sir A. Cooper, Elliotson, Hope, Chassaigniac, and Virchow, &c. Dr. Thurnam refers to eleven cases, including a further notice of one previously men- tioned by Dr. Thomas Davies. Since the date of his memoir there have been four or five other cases published. Of these one is related by Dr. Fenwick,1 another by Mr. Prescott Hewitt,2 a third by Dr. Bristowe,3 and one by myself.4 The so-called aneurisms of the auricle consist of dilatations containing coagula and fibrinous deposits of the sinus and auricular appendix, or both. They may either involve a considerable portion of the walls of the cavity and pass gradually from the undilated part without any ob- vious constriction or separation ; or they may form distinct sacculated expansions. In the largest proportion of instances the sinus has been the seat of the disease, and the aneurism has been of the diffused form. In the cases, however, of M. Chas- saigniac and Virchow, and in that of Dr. Fenwick, the cavity was distinctly cir- cumscribed. Most generally, also, the disease has been found in connection with some, and often very marked, ob- struction at the left auriculo-ventricular aperture ; but in the instances named the valves were free from disease. The case of Dr. Fenwick was further interesting from there having existed during life a loud systolic sound audible at the apex, which was clearly due to the obstruction caused by the aneurismal swelling. In two of the cases referred to, those of Mr. Prescott Hewitt and Dr. Bristowe, the right auricle was greatly dilated as well as the left, and the cavity contained coagula; in the former instance, appa- rently of similar character to those in the left auricle-in the latter, however, only the usual amorphous clots. Partial ex- pansions of this kind should not, however, have the term aneurisms applied to them; but to maintain the analogy between the similar affections of the arteries and veins, the dilatations of the right side of the heart should be termed varicose. Aneurisms of the Valves.-A dila- tation of the mitral valve, to which the term aneurism may properly be applied, was described by Morand in 1729; another ■was mentioned by Laennec and Fizeau at the beginning of this century. Sir A. Cooper, also, in 1825, referred to a case then and still existing in the Museum of St. Thomas's Hospital, and two other in- stances of the kind have been more fully A-ge. Males. 14 and 16 .... . 2 21 to 30 .... . 4 31 to 40 .... • 4 41 to 50 .... . 4 51 to 60 .... . 3 61 to 70 .... . 3 71 to 77 .... . 2 Between 60 and 70 . . 1 Not stated .... . 2 25 Age. Females. 12 and 15 .... . 2 21 to 30 .... . 4 31 to 40 .... . 0 41 to 50 .... . 0 51 to 60 .... . 0 61 to 70 .... . 4 71 to 77 .... . 2 Between 60 and 70 . . 0 Not stated .... . 2 14 The most noticeable circumstance in this enumeration is the very early age at which the cardiac cases occur as compared with different forms of arterial aneurism ; this being explained by the frequent origin of the disease in endocarditis, and the frequency of endocarditic affections, as complications of rheumatism, in early life. It would have been interesting to have given some more satisfactory infor- mation as to the influence which rheuma- tism exercises, either immediately or more remotely, in the production of the partial aneurisms of the heart. The re- ports of the cases are, however, very im- perfect on this point; but they clearly indicate that the aneurisms are not un- frequently connected with rheumatism. They appear also to be very commonly predisposed to by habits of dissipation and intemperance, both causes which we know are very influential in the causation of other forms of cardiac disease. Aneurism of the Left Auricle.- An instance of dilatation of the left auri- cle with deposition of coagula in the dilated part, the result of an injury, was related by Dionis in' 1716.1 With this exception, however, the condition does not appear to have been noticed till the beginning of the present century, when cases of the kind were related by Aber- 1 Lancet, Feb. 1846. 2 Path. Trans. 1848-50, vol. ii. p. 194. 3 Ibid. xi. 1859-60, p. 65. 4 Ed. Med. and Surg. Journal, 1846. 1 L'Anat. de 1'Homme, p. 713. ANEURISM OF THE LEFT VENTRICLE. 461 related by Dr. Thurnam though pre- viously noticed by others, of which one occurred in the practice of Sir Thomas Watson at the Middlesex Hospital. More recently specimens have been described by Cruveilhier, by Mr. Prescott Hewitt,1 Dr. Habershon,2 Dr. Ogle,3 and myself;4 and the affection has been noticed by Rokitansky in his Pathological Anatomy. Aneurisms may occur both in the aortic and mitral valves. Of their mode of origin in the former situation a very in- teresting example is contained in the Mu- seum of St. Thomas's Hospital. In one of the aortic valves there exists a small distinctly-marginated sac, which would have contained a small bean ; in a sec- ond, there is one of somewhat less size, and in the third there is simply a deposit of fibrine in one part of the fold and a very slight dilatation in the same seat. It is evident that the last is the result of inflammatory action, and indicates the first stage in the production of the small aneurisms which exist in the other valves. Dr. Chevers has shown that in cases of contraction of the outlet of the ventricle and expansion of the inlet, whether rela- tive or absolute, the aortic valves have a tendency to bulge at their most dependent parts. If this be unattended by any de- posit of fibrine, the fold ultimately gives way in the weakened portion; if, how- ever, the valve be strengthened by a de- posit of fibrine, the bulging may increase till a distinct sac is produced. A very characteristic example of the kind was exhibited by myself at the Pathological Society. In the mitral valve the disease is, I be- lieve, always found in the free fold. The dilatation may occupy merely a small part of the valve, or may be of large size, so as to involve a large portion of the fold. lu some cases the disease seems to originate in the protrusion of the endo- cardium of the left ventricle, through the fibrous structure of the valve, so as to come in contact with the lining mem- brane of the left auricle. In other cases all the coats are dilated. In both in- stances the sacs generally project into the cavity of the left auricle, and sometimes the base of the sac gives way, and an opening is produced in the valve as if a piece of the fold had been punched out. The sacs may vary in size from one which would lodge a pea or bean or filbert, to one capable of holding a pigeon's egg. Of the former size the cases of Mr. Prescott Hewitt and myself afford instances. Of the latter, the specimen in the Museum of St. Thomas's, referred to by Sir A. Cooper, is a most remarkable example. In several cases two or more sacs have been found in the same valve. These small aneurisms of the mitral valve not unfrequently occur in cases of aortic val- vular obstruction, and I have described one which was found in a case of rupture of the aortic valves. The sacs may con- tain laminated coagula, and in one of the cases described by Mr. Keith, a portion of the valve was entirely wanting, and a small sac was produced by a fibrinous coagulum being attached on the auricular side. These affections are not only interest- ing pathologically, but may be of prac- tical importance, as both at the aortic and mitral valves they may give rise to the symptoms and signs of incompetency. I have before referred to a specimen which exists in the Museum of the Royal College of Surgeons, in which the current of blood flowing through a congenital aperture existing at the base of the ven- tricular septum has expanded portions of the tricuspid valves, so as to form small sacs or aneurisms; and I have seen a similar condition of the tricuspid valve in a recent case of malformation of the same kind. 1 Path. Trans, vol. iii. p. 78. 2 Vol. ix. p. 117. 8 Ibid. vol. vi. p. 156. 4 Vol. iii. p. 71. 462 ADVENTITIOUS PRODUCTS IN THE HEART. ADVENTITIOUS PRODUCTS IN THE HEART. By Thomas Bevill Peacock, M.D., F.B.C.P. the dissection was a man twenty-one years of age. Dr. Macmichael,1 in 1826, detailed the history of a man of thirty- five, who died at the Middlesex Hospital with dropsy and other symptoms of car- diac disease, and in whom the lungs and bronchial glands were found tuberculous, and the pericardium, especially at the base, studded with tuberculous deposits. In 1834, M. Sauzier, as quoted by Bouil- laud,2 found in a man thirty-four years of age, who died with abscess from caries of the sternum after accident, the lungs, pancreas, and pleura tuberculous, and in the substance of the auricles there were two tubercles, and around them the peri- cardium was adherent. The most re- markable case of the kind is, however, that related by Dr. Townsend in 1852.' In this instance a large mass described as tuberculous was connected with the left auricle, and had compressed that cavity and the entrances of the pulmonary veins, so as to give rise to extreme distension throughout their course ; tubercles existed in the bronchial glands but not appa- rently in the lungs. The subject of the disease was a man sixty-two years of age, who died after an illness of twelve months. Since this time a case has been recorded by the late Dr. Baly in the Pathological Transactions.4 It occurred in a prisoner at Millbank, sixteen years of age, who died with symptoms of subacute fever and head affection, after an illness of about ten days, and tubercular masses were found in the substance of the brain, and small tubercles in the lungs, bronchial glands and intestines. A yellow rounded mass, the size of a man's thumb, pro- jected from the inter-auricular septum into the cavities of the right and left auri- cles, the two projections being parts of the same tuberculous mass which was situated in the septum. Dr. Quain also mentions that there were tubercular de- posits in the pericardium in a Bosjesman girl, who died of tuberculosis.5 TUBERCLE IN THE HEART AND TUBERCULAR PERICARDITIS. Laennec' when alluding to accidental products says, that he had only three or four times met with tubercles in the sub- stance of the heart ; and when speaking of chronic pericarditis, he remarks, that a tuberculous eruption may sometimes be developed in the false membrane and may thereby convert the acute into chronic disease, as frequently happens in pleurisy and peritonitis, and he states that he had met with two cases of the kind. In this passage, Laennec indicates the forms in which tuberculous deposits are found in the heart; in one of these they take place in the substance of the organ; in the other on the surface, in connection with inflammation of the pericardium. The former is certainly a very rare condition. Louis2 says that in 112 dissections of phthisical persons he did not meet with a single instancs of the existence of tubercle in the substance of the heart. Roki- tansky3 also speaks of the extreme rarity of the affection ; and in the records of 116 post-mortem examinations of persons who had died of phthisis which I have ana- lyzed, I do not find more than two or three cases in which tubercle is said to have been found in the heart. The re- corded instances of such deposits being at all of serious importance are also very few in number. The first writer who alludes to cases of the kind is, I believe, Dr. Baillie,4 who in his "Morbid Anatomy" says that he " once saw two or three scrof- ulous tumors growing from the cavity of the pericardium, one of which was nearly as large as a walnut. They consisted of white soft matter, somewhat resembling new cheese," and he adds that " the peri- cardium is a very unusual part for any scrofulous affection;" and in his "Dis- section,"5 in alluding to the same case, he further says that both lungs were studded with tubercles, and the right in a state of suppuration in places. The subject of 1 London Medical and Physical Journal, vol. Ivi. (N.S. vol. i.) p. 119. 2 Maladies du Coeur, 2me edit, tome ii. p. 442. 3 Dublin Journal, vol. i. 1852, p. 176. 4 Path. Trans, vol. iii. 1850-51, 1851-2, p. 34. 5 Path. Trans, vol. ii. 1848-49, 1849-50, p. 182. 1 Diseases of Chest, Forbes's trans. 4th edit. 1834, pp. 586 and 623. 2 Sydenham Society's Trans. 48-50. 3 Ibid. vol. iv. p. 210. 4 Morbid Anatomy, and works by Wardrop, 1825, vol. ii. p. 9. 5 Works by Wardrop, vol. i. p. 220. TUBERCLE IN THE HEART AND TUBERCULAR PERICARDITIS. 46o The second form of tuberculous deposit which occurs in connection with inflam- mation of the pericardium, is by no means so rare as that which has just been men- tioned. The first instance of the kind that is recorded is probably that by Cor- visart,* and another was figured by Cru- veilhier, and is further alluded to in the General Pathology more recently pub- lished. The pericardium adhered inti- mately to the heart, and in these adhe- sions a thick and continuous layer of tuberculous matter was deposited, and this enveloped the vessels and had de- stroyed the muscular structure of the auricle. M. Fauvel, as quoted by Aran,2 and by Rilliet and Barthez in their work on diseases of children, met with a case of tubercular pericarditis in a child six years and a half old, who died with dropsy and symptoms of disease of the heart. The pericardium was entirely adherent, the heart was considerably enlarged, and its surface was studded by whitish-yellow friable nodules, some of them the size of a nut, and as numerous behind as in front. The internal surface of the right ventricle displayed similar depositions everywhere except at the septum. Since this time the occurrence of tuberculous deposits in connection with pericarditis has been made the subject of a special memoir by Sir G. Burrows,3 in which he details three cases which he supposes to be examples of the affection ; and in two of them-one of which occurred in his own practice, the other under the care of the late Dr. Baly-the inference was con- firmed by post-mortem examination. More recently, Dr. Bristowe has described three other cases in the Pathological Transactions,4 and such instances cannot indeed be very uncommon. Cruveilhier says that he has many times met with tubercles, in connection with false mem- branes, in children with tuberculous lungs.5 Louis also refers to such cases, and details the particulars of one in his memoir on pericarditis.6 Otto7 mentions having twice seen the condition in chil- dren, and Dr. Walshe8 states that it is displayed in one of Dr. Carswell's drawings contained in the collection to illustrate morbid anatomy at University College. I have myself met with three cases of the kind, two while Pathologist of Edinburgh Infirmary and one at the Victoria Park Hospital. Tubercular deposits in the pericardium bear a close resemblance to the similar disease of the arachnoid, pleura and peri- toneum. They may be of very small size, mere specks, or may attain the dimensions of a cherry-stone, filbert, or walnut. In consistence they are generally soft, and they are usually of a grayish or yellowish color. In one of my own cases, the tu- bercles, which were thickly spread over the attached and reflected pericardium, varied in size from that of a pin's head to a cherry-stone. In another, while there were very small masses of yellowish tubercle thickly studied over the surface of the heart, there were also laminated false membranes, in some places a quarter of an inch, in other parts fully half an inch in thickness, and the middle layers of this deposit were of a yellowish color, soft and granular, and closely resembled what is commonly called tuberculous in- filtration. In the third case the tubercu- lous deposit assumed the form of small granulations of a grayish color, the two layers of pericardium being entirely at- tached by cellular adhesions. The affec- tion in two of Dr. Bristowe's cases con- sisted of small miliary granulations, in one with patches more closely set together in places ; in the other there were both separate tuberculous masses and laminae of considerable size. In the cases which have fallen under my own notice the deposits were situated beneath the serous membrane, and in one of them there were masses which were more deeply imbedded in the substance of the ventricles and which were only ex- posed on section. One of these cases also, it will be observed, displayed tubercle in the centre of a thick layer of false mem- brane covering the heart, thus correspond- ing with the observations of Laennec and Cruveilhier. The different writers who have alluded to this subject have agreed in asserting that tuberculous affections of the heart are only met with in connection with similar deposits in other parts of the body, and the cases which have been re- corded entirely confirm that view. The most frequent coexistence is with tubercle in the bronchial glands, or in the lymph- atic glands of the mediastinum. In two of the cases which I have myself seen, though occurring in persons twenty-eight and sixty-seven years of age, there was tuberculous deposit only in the bronchial glands and heart; though the general rule is, as is well known, that, after early life, if tubercle be found in any part of the body it also exists in the lungs. In the third case, the subject of which was a girl thirteen years of age, no tubercle was found anywhere else. In this instance 1 3me 6dit. Paris, 1818, p. 26. 2 Aran, Arch.. Gen. de Med. 4me serie, 1846, tome xi. p. 181. 8 Med.-Chir. Trans, vol. xxx. 1847, p. 77. Vol. xii. 1860-61, p. 63. 5 Traite d'Anat. Path, tome iv. serie 1862, p. 684. 6 Revue Medicate, 1826. 7 Path. Anat, by South, 1831, p. 258. 8 Diseases of Heart, 1862, p. 357. 464 ADVENTITIOUS PRODUCTS' IN THE HEART. there was also slight mitral valvular dis- ease. In Sir G. Burrows' case the lungs, pleura, bronchial glands, peritoneum, and spleen were tuberculous; and in Dr. Baly's there were tubercles and ulcers in the intestines and lungs. In one of Dr. Bristowe's patients there was tuberculous perforation of the intestines; in a second, there was tubercle in the mediastinum ; and in the third, in the brain, lungs, pleura, spleen, and mesentery. The oc- casional occurrence of tuberculous de- posits in the heart with similar affections of the bronchial glands and mediastinum, and in some cases when the lungs are en- tirely free, led Cruveilhier to suggest that possibly the affection of the glands might be secondary to that of the heart; but this supposition is scarcely in accordance with the advanced disease of the lungs which is reported to have existed in other instances. Laennec supposed that the tubercles in cases of this description were the result of the inflammation, and were situated in the false membrane; the latter is, however, certainly not usually the seat of the deposit, and Sir G. Burrows is much more probably correct in regarding the pericarditic affection as the effect of the irritation set up by the deposit under the membrane. Indeed, the first class of cases, in which the tubercles are situated deeply in the substance of the heart or under the endocardium and assume the form of separate tumors, cannot be re- garded as essentially distinct from the second, in which the tubercles are more superficial. The absence of adhesions in some of the latter class of cases seems conclusively to show that the inflamma- tory exudation is at least generally sec- ondary. The tuberculous deposits in the heart occur under the same circumstances as those which attend similar affections in other parts of the body ; they may be found in both sexes, and at all ages, but they are more common in comparatively early life. The age and sex of the subjects of some of the cases referred to are as follows :- cially if they assume the subacute form and are not attended by any large amount of liquid effusion, they may be suspected to be connected with tubercular deposits. It must, however, be borne in mind that pericarditis, having no connection with tubercle, may occur during the progress of phthisis. The inference as to the tu- bercular origin of such cases is therefore by no means decisive. CANCER. Cancerous deposits in the heart are of more common occurrence than tubercle. Dr. Walshe,1 writing in 1846, says that he had readily found twenty-five cases re- corded ; and more recently, in a paper in the Pathological Transactions,21 collected the particulars of forty-five, including in this number two which had fallen under my own notice. The earliest published examples of the disease were, I believe, those of Andral and Bayle in 1824.3 The cases of cancerous deposit in the heart may be classed into four series: First, Cases of primary cancer, in which the disease exists only in some part of the organ. These are of extremely rare oc- currence ; of the forty-five cases referred to, only two were expressly stated to have been instances of the kind,4 though in the reports of seven others, no mention was made of the existence cf cancer in any other part of the body. Secondly, Cases in vhich the disease occurred coincidently and probably simul- taneously, in the heart and in different parts of the body, and especially in parts adjacent to the heart. This form, though still rare, is more common than the other. Thirdly, Instances in which the disease first appears in parts adjacent to the heart, - the bronchial or mediastinal glands, the lungs, or the glands around the larynx and in the neck,-and thence spreads so as to involve the pericardium and the large vessels at the base of the heart or the auricles. Cases of this kind are not uncommon, though less frequent than those of the next series. Fourthly, By far the largest proportion of cases of cancerous diseases of the heart occur secondarily to the deposit of cancer in some distant organ. Of the forty-five cases, twenty were of this description; the primary disease being seated in dif- ferent cases in the eye, the cheek and bones of the face, the lower lip, the breast and axillary glands, the ribs and pleura, Males . years. " . . 13 " " . . 16 " " . . 19 " " . .21 " " . . 24 " " . . 34 " " . . 36 " " . . 62 " . . 62 " " . . 67 " Females . 14 years. " . 20 " " . 28 " 1 Nature and. Treatment of Cancer, p. 368. 2 Vol. xvi. p. 99, 1864, 1865. 3 Revue MSdicale, 1824, tome Ire, p. 268. 4 Ollivier, Traite de la Moelle Epiniere, 3me edit., 1837, tome ii. p. 164; Segalas, Rev. Med. tome iv. 1825, p. 247. In several of the cases of tubercular pericarditis the evidences of effusion in the pericardium had been observed during life. When such signs arise in persons who are obviously tuberculous, and espe- SIMPLE AND OTHER CYSTS. 465 the abdominal organs, the inguinal glands, the uterus, vagina, labia, the penis and testes, and the upper and lower extremi- ties. The heart may be affected by cancer in different forms. Thus, of the cases col- lected seven are reported to have been cases of scirrhus, four of melanosis, and twenty-five of encephaloid. The deposit also may assume either the form of dis- tinct masses or tubera, or it may be infil- trated into the tissue, or occur on the surface. The first form is the most common, especially when the deposits are second- ary. The masses in different published cases are compared in size to peas or beans, to almonds or chestnuts, or to hen's eggs or oranges; and they may be only one, two, or three in number, or they may amount to a dozen or more,1 and in one very remarkable case it is stated that they were so numerous that the examiner ceased counting them after enumerating six hundred.2 The most frequent seat of the disease seems to be the right auricle and ventricle, though the tumors may also occur, either alone or otherwise, in other parts of the organ. Generally they are situated beneath the attached pericardium; more rarely be- neath the endocardium ; and still more rarely in the substance of the auricles and ventricles or in the septa. The deposits may only slightly project above the adja- cent surface, or they may form distinct and nearly separate tumors, the mass being only attached to the part from which it projects by a narrow pedicle. In the Museum of St. Thomas's Hospital there is a specimen of medullary growth from the left auricle, which is almost entirely detached from the lining membrane. In some cases the masses are reported to have pressed upon the cardiac cavities or apertures, so as to interfere with the transmission of the blood or with the action of the valves. More rarely the disease assumes the form of infiltration, and when this is the case, the structure of the heart may be only slightly affected, or it may be exten- sively and completely destroyed. In one instance it is stated that not more than a twelfth of the organ was free from the de- posit.3 In the third form of disease the heart is found enveloped in a cancerous mass, which produces entire adhesion of all parts of the pericardium. This is, I be- lieve, of very unfrequent occurrence. A case of the kind has, however, been de- scribed and figured by Dr. Bright in the Medico-Chirurgical Transactions.1 A second is related by Dr. Kilgour,2 in the " London and Edinburgh Journal of Medi- cal Science and a third was described by myself in the paper in the Pathological Transactions before referred to.3 In only two or three of the recorded cases is the cancer stated to have been softened or ulcerated, and the nature of one of them may be doubted. In one in- stance, however, a cancerous mass situ- ated near the origin of the anterior coro- nary artery had softened and caused per- foration of the arterial coats and the escape of blood into the cavity of the pericardium.4 Cancerous deposits in the heart do not appear to be generally productive of any special symptoms by which their presence can be detected during life. In some cases, when there was disease of the adja- cent organs, there were signs of pressure on the large vessels and of interference with the circulation of the blood ; and in three or four other instances the forma- tion of the deposits on the surface of the heart occasioned inflammation of the pericardium which was recognized by the usual signs during life. Of this I have myself seen two instances. Most usu- ally, however, there are no symptoms by which the affection of the heart is indi- cated, and the condition is only detected on post-mortem examination. In the case under my own care which has been mentioned-notwithstanding that the ex- istence of a tumor in the chest was ascer- tained a considerable time before the pa- tient's death, and that the patient's father was said to have died of cancer of the heart, and thus attention was particularly directed to the state of the organ-no symptoms indicating the heart to have been involved were detected. SIMPLE AND OTHER CYSTS. Lancisi mentions having seen a cyst containing thick matter (meliceris) in the 1 Exposition d'un cas remarkable de Mala- die Cancereuse (Paris, 1825), quoted by Dr. Churchill in London Med. and Phys. Journal, vol. Ivii. (N. S. vol. ii.), 1827, p. 280. 2 Case of Dupuytren, quoted by Cruveilhier in Essai sur l'Anat. Path. Paris, 1816, vol. i. pp. 86-87. 3 Rilliet; Bullet, de la Soc. de Mgd. 1813, No. 5, tome iii. p. 357. A very marked case of cancerous infiltration with masses in the mediastinum, which occurred in a patient of vol. ii.-30 Dr. Barker's, at St. Thomas's Hospital, is described, by Dr. Bristowe in the Path. Re- ports, vol. vii. The specimen is preserved in the Museum, x. 67. ' Vol. xxii. 1839, p. 15. 2 Vol. iv. 1844, p. 828. 2 Vol. xvi. 1864-65, p. 100, Case 1. The specimen is preserved in the Victoria Park Hospital Museum. 4 M. Broca, Bullet, de la Soc. Anat. 25me, annee 1850, p. 253. 466 ADVENTITIOUS PRODUCTS TN THE HEART. substance of the heart, and other writers describe the occasional occurrence of cysts of different kinds in the heart or pericar- dium. Thus Cruveilhier refers to hsema- toid cysts as occurring in the pericardium and other serous surfaces, but does not detail any instance of the kind ; and I do not know any recorded case except that reported by Dr. Ogle in the Pathological Transactions for 1857 and 1858.1 In this instance a large cyst was found beneath the pericardium covering the posterior surface of the right ventricle. It had firm and thick walls, and contained lami- nated coagulum with brownish granular material. The layers of pericardium were adherent, and there were old and thick adhesions of the right pleura, with some similar coagulum in its sac. No connection could anywhere be traced be- tween any of the cavities of the heart and the cyst; and Dr. Ogle supposes that probably the blood had escaped from one of the branches of a coronary artery ; and that having first lodged in the pericar- dium, it had subsequently ruptured into the pleura. The cavities of the heart were rather large, the lining membrane of the right auricle was thickened and opaque, and the coronary arteries were in various places rigid. The specimen was removed from a man fifty-five years of age, who died with symptoms of cardiac disease and dropsy, and who had been ill for two years ; but no decided history of any attack to which the condition of the heart could be ascribed appears to have been obtained. The condition of the coronary arteries is in favor of Dr. Ogle's supposition, but it may be open to ques- tion whether the cysts might not have originated in acute hemorrhagic inflam- mation of the pericardium and right pleura. Certainly in some cases the appearance of a cyst is produced by the remains of a pericarditic effusion; the two layers of serous membrane becoming adherent, ex- cept in one portion, where a cavity con- taining pus or serum still exists. A spe- cimen of this kind was exhibited at one of the meetings of the Pathological Society. ENTOZOA. In the works of the earlier writers on morbid anatomy, cases are referred to in which the heart is stated to have con- tained worms. Such reports are, how- ever, generally entitled to little credit, though of late years hydatid cysts have, in various cases, been found in different parts of the heart. Probably the earliest recorded instance of the kind is that men- tioned by Morgagni,1 of a man seventy- four years of age, who died in the hospital at Padua ; but of whose previous state no further history was obtained than that he had not suffered from any of the usual symptoms of cardiac disease. A tumor about the size of a cherry was found at the posterior surface of the heart near the apex. It was half imbedded in the sub- stance of the organ, and "on puncturing it a small quantity of clear fluid escaped, but a more turbid humor remained, and was only evacuated on laying it open. In so doing a small piece of membrane escaped. This displayed white, and, as it were, mucous particles, and a particle of tendinous hardness." The whole was included in a dense sheath. Dupuytren,2 at the beginning of the present century, placed a similar case on record. It oc- curred in a female forty years of age, who died in one of the Paris hospices, whose body was dissected in the anatomical school. No history of the case during life was obtained. The right auricle was very greatly dilated, and on its inner sur- face, under a smooth membrane, were found numerous cysts which nearly filled the cavity. About the same time a third case was related by Dr. Trotter;3 it oc- curred in a boy fourteen years of age, on board one of her Majesty's ships, who had been very livid and subject to dyspnoea and palpitation : a large cyst, containing several loose hydatids, was found in the right auricle, and two similar bodies were also contained in the ventricle. Two cases of the kind are contained in the Transactions of the Medical and Chi- rurgical Society ; one of these, which was published in 1821, occurred in a boy of ten, who died suddenly without having been previously ill, and the case is imper- fectly related by Mr. David Price.4 The other was communicated by Mr. Evans® in 1832. The subject of the disease was a delicate female, forty years of age, who was suddenly seized with pain in the prsecordia and difficulty of breathing, and died in a few days. The pericardium displayed an effusion of lymph and serum; and a considerable tumor was situated at the apex of the heart and projected into the right ventricle, filling a fourth of the cavity. The tumor proved to be a cyst containing numerous hydatids, varying in size from a pea to a pigeon's egg. A 1 Alexander's Translations, vol. i. p. 583. Letter xxi. Art. 4. See also Letter iii. Art. 26, p. 60, where it is said a white membrane protruded like a hydatid. 2 Journal de Corvisart et Leroux, tome v. annee xi. p. 139. 3 Medical and Chemical Essays, 1795, p. 123. Case of a Blue Boy. * Vol. xi. p. 274. 5 Vol. xvii. p. 507. * Vol. ix. p. 165. ENTOZOA 467 plate is given of the specimen, which is stated to be preserved in the Museum of St. Bartholomew's Hospital. In 1838, Mr. Smith of Bristol published a somewhat similar case,1 which occurred in the prac- tice of a surgeon at Warminster. The subject of the disease was a female, whose age is not stated, and who died after an illness of three hours. A large hydatid was found in the right ventricle, and must have obstructed the entrance of the blood into the pulmonary artery. The more recent writers on cardiac dis- eases and on pathological anatomy very generally refer to cases of hydatid cysts found in some portion of the heart. An- dral2 says that he has seen three instances of the kind. In one a tumor, the size of a walnut, was imbedded in the substance of the left ventricle ; in another a cyst, as large as a nut, w'as attached by a small pedicle to the lining membrane of the right ventricle ; and in the third, three cysts, the size of nuts, were imbedded in the substance of the heart. The cysts were transparent except at one point which was white and could be made to protrude like a head from the centre, and he was thus led to regard them as cysti- cerci. Rokitansky3 relates the case of a woman, twenty-three years of age, who died suddenly, and a tumor the size of a hen's egg w'as found at the upper part of the interventricular septum, and pro- truded into both ventricles. On the right side the cyst had burst, and the contained hydatid had become impacted in the conus arteriosus, so as to obstruct the entrance into the pulmonary artery. In another instance, in a soldier thirty-five years of age, who also died suddenly, a tumor of the size of a duck's egg was found in the upper part of the septum and correspond- ing portion of the left ventricle behind. The sac contained fibrinous coagula mixed with portions of acephalocyst. The sur- faces of pericardium were adherent in the seat of the tumor. M. Aran,4 in a paper on these and other forms of tumor of the auricles, published in 1846, relates a case which occurred to M. Dupaul, in a female twenty-three years of age, who died sud- denly after her confinement, and on ex- amination a hydatid cyst in the left auri- cle was found to have ruptured on both sides, so as to allow of the escape of blood from the auricle into the pericardiac cav- ity. It was evident that the tumor had been developed under the endocardium of the auricle. Mr. II. Coote, in 1854,' found a large cyst in the walls of the left ven- tricle of a subject under dissection at St. Bartholomew's Hospital, and he refers to a second specimen as existing in the mu- seum, doubtless the case of Mr. Evans before referred to. In addition to the cases now mentioned several will be found re- ported in the Pathological Transactions by Dr. Budd,2 Dr. Wilks,3 Dr. Ilabershon,4 &c., and one, which occurred in a patient of my own at St. Thomas's Hospital, is re- lated by Dr. Hicks and myself.5 I have also had the opportunity of examining a specimen exhibited by the late Mr. Ward, at one of the earlier meetings of the so- ciety.6 In Mr. Ward's case the subject of the disease was a man, twenty-two years of age, who died shortly after having sus- tained an accident: the cyst was about the size of a French walnut, and was situated at the posterior and upper part of the left ventricle, beneath the superficial muscu- lar fibres. My own patient was a boy of eighteen, who died after an illness of about thirteen months : the cyst, about the size of a walnut, was partially im- bedded in the muscular substance of the right ventricle, but did not project into the cavity. In the sixth volume of the Transactions,7 there is a description of a case in which a patient at the Colney Hatch Asylum died suddenly when under excitement, and after death two cysts, one of which had ruptured, were found beneath the attached pericardium. The precise nature of the cyst in some of the above cases is not clear. The de- scription given of that related by Mor- gagni is supposed by Laennec conclusively to indicate the hydatid to have been a cysticercus; and both Andral and Roki- tansky speak of having met with cysti- cerci in the substance of the heart. Most generally, however, the cysts appear to be those of the echinococcus. Such is stated to have been the case in the instances re- lated in the Pathological Transactions, 1 Med. Times and Gazette, xxix. p. 156. 2 Vol. x. p. 80. 3 Vol. xi. p. 71. 4 Vol. vi. p. 108. 5 Vol. xv. p. 247. 6 Vol. i. p. 225. Dr. Walshe mentions in his work on Diseases of the Heart, &c. (3d edit. 1862, p. 65), that a specimen is figured in one of Dr. Carswell's drawings, and that a hydatid, the size of a pigeon's egg, situated in the interventricular septum, is contained in University College Museum. In the Mu- seum of St. Thomas's Hospital there is in addition to the specimen described by Dr. Hicks and myself (x. 68) another (x. 64) in which the cyst, as large as a duck's egg, is situated at the apex. 7 P. 114. See Report on the case by Dr. Wilks. 1 Lancet, vol. ii. p. 628. 2 Path. Anat, by Townsend and West, vol. ii. p. 348. 3 Path. Anat., Sydenham Society's Trans, vol. iv. p. 208. 4 Arch. Gen. de Med. 4me serie, tome xi. p. 187. 468 ADVENTITIOUS PRODUCTS IN THE HEART. though the bodies were not always met with. The Trichina, on the other hand, is usually considered not to be found in the heart. This is, however, denied by Dr. Cobbold,1 who says that all the differ- ent forms of larvae occur in the heart, but they do not stay there, the firmness of the muscular texture interfering apparently with the development of the worm in that situation. The same writer gives some calculations of the relative frequency with which the echinococcus is found in the heart and in other organs. Thus he states that Droaim, of 373 cases in which these cysts were found in some part of the body, met with them in the heart in ten cases; and Dr. Cobbold, of 136 cases, found echi- nococci in the heart or pericardium in nine instances. The most common situa- tions for the cysts appear to be the right auricle and ventricle, but no part of the organ is free from them ; cases being re- corded in which the walls of the left ven- tricle were affected ; and, it will be ob- served also, the interventricular septum. The cysts may be developed beneath the pericardium or endocardium, or in the substance of the muscle. According to the situation which they occupy is their tendency to grow, so as to protrude ex- ternally or internally ; and they may ulti- mately rupture into the pericardium or into one of the cavities of the heart. In the former situation they may give rise to acute pericarditis, or to adhesion of the surfaces of the membrane covering the projecting portion. In the latter the loose hydatids may escape into the cavity and produce fatal obstruction to the cir- culation of the blood. In one case, it will be observed that a cyst ruptured both ex- ternally and internally, and so allowed of hemorrhage into the cavity of the peri- cardium. The hydatids in the heart appear fre- quently to be solitary, not occurring in any other structure of the body. Such seems to have been the case in the in- stances related by Morgagni, Dupuytren, Dr. Trotter, Mr. Smith, and Mr. Coote, in one of those by Rokitansky, and in the cases described in the Pathological Transactions by Dr. Budd and Dr. Hab- ershon, and probably also in that of Mr. Ward. On the other hand, in the second case of Rokitansky there were three sep- arate cysts in the liver. In the case of Dr. Wilks, there was also a cyst in the liver ; and in my own case, in addition to the cyst in the right ventricle, there were numerous hydatids in the liver, spleen, omentum, right kidney, and lungs; and portions of cysts were expectorated dur- ing life. It will be seen that in the cases referred to the hydatids occurred in persons of both sexes and of all ages. It may also be observed that there are no certain signs by which their presence in the heart can be detected during life. In some cases they have been found without hav- ing been preceded by any indications of defect in the circulatory organs ; in other instances they have occurred in persons who have died after longer or shorter ill- nesses, with symptoms clearly pointing to some cardiac disease. In cases of the latter description, if there were evidences of hydatids in some other part of the sys- tem the suspicion might be entertained that the cardiac symptoms were due to the development of hydatid cysts in some part of the heart. In my own case there was nothing observed during life which at all indicated that the heart was the seat of disease. FIBRINOUS DEPOSITS : SYPHI- LITIC AFFECTIONS OF THE HEART. The substance of the heart is not un- frequently the seat of fibrinous deposits. These may occur either as the result of acute inflammation of the muscular struc- ture, myocarditis, with or without peri- and endo-carditis; or they may be con- nected with an altered condition of the blood, leading to the effusion of fibrine into the muscular structure, in the same way as such effusions occur in other organs, the spleen or kidneys, or as the blood coagulates in the vessels them- selves. When deposited the fibrinous material may soften and allow of the par- tial destruction of the walls of the heart, so as to constitute a false lateral or partial aneurism ; or it may undergo an imper- fect organization, being converted into fibroid tissue, and this, being less resist- ant than the natural muscle, may yield to the pressure of the blood, and a true partial aneurism be formed. Closely al- lied to these deposits are those which occur in the substance of the heart in connection with constitutional syphilis. Corvisart, struck with the remarkable re- semblance sometimes presented by vege- tations on the valves of the heart to syphilitic warty growths on the external organs of generation, suggested that in some such cases the vegetations might have a syphilitic origin ; and he detailed several cases which lie regarded as sup- porting this idea. His views have not, however, been generally adopted; and Laennec in particular, considering the frequency of venereal affections and the comparative rarity of such vegetations, expressed his decided dissent from the supposition. More recently, however, writers have attached more importance to the suggestions of Corvisart. Dr. Julia, 1 Entozoa, 1864, p. 275. FIBRO-CARTILAGINOUS AND OSSEOUS DEGENERATION. 469 of Cazeres,1 has published several cases in which vegetations on the endocardium were found in persons who were known to have recently had syphilis and pre- sented other indications of the disease ; and in two of these cases there were small patches of ulceration on the surface or in the substance of the heart, lie also re- fers to a case published in 1778, which, though often quoted as an example of ulcerated cancer of the heart, is doubtless an instance of syphilitic ulceration. The case was reported by M. Carcassone to the Academie de Medecine, and occurred in a female of dissipated habits, twenty- two years of ago, who was an inmate of the Ilouse of Refuge at Perpignan. Iler illness, which followed upon chancres, was characterized by weight and pain in the region of the heart, and rapidly proved fatal; after death a large ulcer with in- durated base was found on the anterior surface of the heart. More recently cases have been recorded by Ricord, Lebert, and especially by Virchow.2 The latter writer has indeed made the syphilitic affections of the heart the subject of a special memoir, of which a translation has been published as a separate work in French.3 In this country several com- munications of a similar kind have re- cently appeared in the Pathological Trans- actions, chiefly by Dr. Wilks. The syphilitic affections of the heart re- semble the similar degeneration of mus- cular structure in general. They consist of fibrinous exudations into the connective tissue, which may either soften and sup- purate, forming ulcers or small abscesses; or they may be converted into masses of hardened fibroid tissue, causing a puck- ered appearance resembling a cicatrix on the surface, and are generally combined with thickening and induration of the covering and lining membranes. In the first case described by Virchow, it is stated that a portion of the organ near the base of the posterior fold of the mitral valves, for the space of about an inch and a half, was occupied by a whitish-colored hard mass, and the intra-ventricular sep- tum was also similarly degenerated to the depth of from a quarter to half an inch. The endocardium was nearly cartilagin- ous, and tendinous cords passed deeply into the substance of the heart; the mus- cular structure had undergone the fatty degeneration, and the surface of the ven- tricle was marked by callous tuberosities. Under the microscope in the points of a white color and tendinous structure, the muscular fibres had disappeared and were replaced by fibrous tissue. At the apex of the heart there was a slight dilatation, indicating the commencement of an aneu- rism. FIBROCARTILAGINOUS AND OSSEOUS DEGENERATION. Under these terms, authors have de- scribed changes which are not of uncom- mon occurrence. Corvisart has related a case in which he states that the walls of the left ventricle were at least an inch in width, and much hardened. "At the apex, up to a certain point and through- out its thickness, the muscular structure was cartilaginous. The fleshy bodies also had acquired a remarkable hardness, ap- proaching that of cartilage."1 This oc- curred in a man sixty-four years of age, who died after an illness of about two years' duration characterized by dyspnoea, dropsy, and other cardiac symptoms. The state of the pericardium is not mentioned, but the mitral valve was also cartilagin- ous. The condition here described was alluded to by Laennec, and has been more fully illustrated by Cruveilhier.2 The transformation may either be gene- ral or diffused, extending over a consider- able portion of the heart; or it may be partial and limited to a small part. The diffused or more general change is chiefly seen in the parietes of the right ventricle, occurring in cases where the orifice of the pulmonary artery, the pulmonic circula- tion, or the left auriculo-ventricular aper- ture is obstructed, so as to subject the affected part to long-continued distension. This condition, which is well known to all pathologists, has recently been made the subject of a paper by Sir W. Jenner.3 The other or partial form is seen in the walls of the left ventricle, and especially at the apex or outer wall. When existing to a marked degree, it is generally com- bined with some dilatation of the cavity in the seat of the transformation, and not unfrequently with bulging of the walls ; and it has been regarded by Cruveilhier as the first step towards the formation of the true lateral or partial aneurisms. A view somewhat similar is also maintained by Rokitansky. In the slighter forms of the degenera- tion, such as occur in cases where the change is diffused, the structure of the heart is much coarser than usual, the al- tered parts have a yellowish color and a peculiarly hard leathery feeling, and re- sist when cut by the knife. The more i Gaz. AUd. de Paris, 1845, No. 52, p. 845. 2 Archiv. fur. Path. Anat, und Phys, etc., 1864, p. 468. 3 Le Syphilis Constitutionelle, par M. Ru- dolphe Virchow, traduit de l'Allemand par le docteur Paul Picard, Paris, 1860. i 3me ed. 1818, p. 171, obs. 28. 2 Trait6 d'Anat. Path. Gen. tome iii. 1856, p. 601. 3 Med.-Chir. Trans, vol. xliii. 1860, p. 199. 470 ADVENTITIOUS PRODUCTS IN THE HEART. advanced degrees of the transformation are only seen in cases in which the disease is limited in extent, and under such cir- cumstances the muscular structure may be almost entirely replaced by dense white fibrous material. This, as before men- tioned, is generally only found at the apex of the left ventricle, but it may occur over a large portion of the outer wall, or in the interventricular septum and fleshy bodies; and Cruveilhier says that he has seen the change affecting fully a third of the mus- cular substance of the organ. The mode in which the transformation is effected probably varies in different cases. Cruveilhier supposed that it was a slow change, by which the cellular tis- sue in the muscular substance became thickened and indurated, and replaced the atrophied contractile tissue. Rokitansky refers the change to inflammation ; and there can be no doubt that inflammatory action, affecting the peri- and endo-car- dium or both these membranes, and in- volving to a greater or less extent the interjacent muscular substance, does in some cases give rise to the alteration. This is shown by the very general occur- rence of thickening and induration of the investing membranes, or of adhesion of the visceral and reflected layers of the pericardium, in cases in which the mus- cular structure is transformed. The rela- tive thinness of the muscular substance of the heart at the apex affords apparently the explanation of the greater frequency of the change in that situation ; and the proneness to endocarditis on the left side accounts for the more marked changes being only found in the walls of the left ventricle. In other cases the change is probably due, as pointed out by Sir W. Jenner, to long-continued congestion of the sub- stance of the heart, causing slow hyper- trophy and induration of the connective tissue and secondary atrophy of the mus- cular fibres. This seems the mode in which the diffused and general induration of the walls of the right ventricle is pro- duced, though there does not appear to be any adequate reason why it should be so frequently confined to the right side. In yet other cases the transformation is probably the result of the imperfect or- ganization of fibrinous material, which, in connection with an altered condition of the blood, is effused beneath the investing membranes or in the substance of the heart. These effusions are not of unfre- quent occurrence and generally co-exist with similar depositions in the spleen, kidneys, &c. Whatever be the mode in which the disease commences, the subse- quent changes correspond, the connective tissue becomes greater in quantity and more solid, and by its contraction com- presses the muscular structure and so leads to its atrophy, and in some instances to its entire disappearance. It is not, pro- perly speaking, a degeneration or trans- formation of the muscular substance, but the replacement of the muscle by fibrous tissue. The older writers frequently speak of the conversion of portions of the heart into bone, or of bones being found in the substance of the heart, and most patholo- gists have met with cases of the kind. When such formations do not occur in connection with chronic pericarditis or in old false membranes, and are not trace- able to the calcification of the fibrous structures around the orifices or in the valves, they take place in portions of the muscular substance which have under- gone the changes now described. Such formations are not, however, to be re- garded as truly bony, though they may be very hard, thick, and of large size. They consist indeed only of granules of calca- reous matter, deposited in the altered tis- sue, without any of the elements of true bone structure. POLYPOID GROWTHS. Most writers on cardiac pathology men- tion polypoid growths as occurring in the different cavities of the heart. There can, however, be no doubt that many of the cases which have been described as of this1 description were only instances in which decolorized coagula were adherent to the lining membrane. Such may be concluded to have been the nature of the bodies described by Dr. Ryan2 and Mr. Stewart,3 which have been frequently re- ferred to by authors. In other instances, however, it may be inferred that the for- mations observed were new growths. Such apparently were the polypi described by Mr. Reeves, Mr. Mayo,4 and Mr. Wil- kinson King,5 and by MM. Puisaye6, Du- breuil,7 Choisy,8 and Bouillaud.9 Most of these cases have been collected by M. Aran, in a memoir published in 1846.10 Two other similar cases are described by Dr. Wilks11 and Mr. Birkett,12in the Patho- 1 Case of M. Renauldin ; Corvisart, p. 175. 2 Med. Gaz. vol. iii. 1829, p. 336. 3 Ed. Med. and Surg. Jour. vol. xii. 1817, p. 182. 1 Outlines of Human Pathology, 1836, p. 472. 5 Lancet, 1842, vol. ii. p. 428. 6 Gaz. M6d. de Paris, 1843, p. 270. i Ibid. p. 512. Two cases, one of which is quoted by Bouillaud. 8 Revue Medicale, 1833, tome ii. p. 425, quoted by Aran, p. 278. 9 Vol. ii. p. 170, obs. 105. 10 Arch. G6n. de M6d. 4me sSrie, tome xi. 1846, p. 274. 11 Vol. viii. p. 150. , 12 Vol. i. p. 224. POLYPOID GROWTHS. 471 logical Transactions, and one has fallen under my own notice. The true polypoid growths appear gen- erally to occur in the left auricle, and to be most usually attached to the fibrous zone of the auriculo-ventricular valves. Sometimes they are connected with some other part of the walls of the cavity, or are found in the right auricle or either ventricle. When in the former situation, they frequently project through the au- riculo-ventricular aperture into the cavity of the left ventricle. They vary consider- ably in size in different instances. Some have been compared to partridge's or pigeon's eggs or to walnuts; others to hen's eggs; and yet others are stated to have filled the cavity from which they sprang. Most usually they assume a pyri- form or cordate shape, and are attached to the walls of the cavity by a more or less constricted pedicle. The surface of the growths is sometimes smooth, some- times nodulated or studded with vegeta- tions ; and most generally they are cov- ered wholly or in part by the endocardium, this, especially at the root, being thick- ened and indurated. They may consist of a simple growth, or, on the contrary, may be composed of different portions. The precise nature of the bodies is not clear in the accounts of several of the published cases. Mr. Burns says, in ref- erence to that which he has described, that it was dense, laminated, and fully organized, and closely resembled the po- lypi of the nose. Mr. Mayo is in doubt whether the specimen he mentions was to be regarded as a slowly growing polypus, or a medullary sarcomatous growth. In the case which occurred at the Middlesex Hospital,1 the structure of the tumor is compared to the spleen; in that of M. Puisaye the growth is stated to have been fungous, and to have had the aspect and consistence of gelatine; and in those of M. Dubreuil, the tumors are called fibrous or albugineous. Dr. Wilks and the re- porters on his case described the tumor as fibrous, and Mr. Birkett regards the specimen he exhibited as fibroid. The growths are included by Mr. Aran under the general term of "Tumeurs fongeuses sanguines." The specimen which fell under my own notice was about the size of a walnut; it was attached to the auricu- lar surface of the mitral valve, was of a rounded form with a short and thin pedi- cle, and was studded on its upper surface with vegetations or granulations. It was apparently covered by endocardium throughout, and was of a pearly white color and obviously fibrous structure. The subject of the disease was a young woman who was insane and died of gangrene of the extremities, but had not during life presented any symptoms attracting atten- tion to the heart. The mode of origin of these growths probably varies in different cases. In some instances they may be simply ad- herent clots which have become organ- ized ; in others they probably originate in inflammatory exudations in the subserous cellular tissue. Indeed, this would ap- pear to be the most usual mode of origin of the polypoid growths, for, as before stated, they generally spring from the fibrous tissue of the left auriculo-ventricu- lar aperture and valves, and are usually covered by the endocardium. As might be expected, the cavities in which these bodies are developed are ordinarily con- siderably dilated ; and similar effects are produced on other parts of the heart to those which would result from obstruc- tions of any other kind in the same situa- tion. The polypoid growths have been met with at various ages and in both sexes, and generally in persons, who, for a longer or shorter time, have presented obvious symptoms of cardiac disease. When, as in most of the cases on record, the bodies obstruct the orifices of the heart or interfere with the action of the valves, they give rise to the ordinary effects of valvular disease, which manifest themselves by the usual signs. In one very interesting case, quoted by M. Aran from the " Annali Universali " for 1844,1 a pulsating tumor was observed for a con- siderable period before the death of the patient, on the left side of the upper part of the sternum, between the cartilages of the second and third ribs; and this ulti- mately attained a considerable size. After death a tumor was found to occupy the upper and anterior part of the heart, and proved to be connected with the left auricle. The pericardium was inflamed and covered with recent exudation. The precise situation and character of the tumor is not clear from the description. M. Aran2 also quotes from Schmidt, a case in which a hollow body was found filling the right auricle, passing through the auriculo-ventricular aperture, and com- municating with the cavity of the aorta by an opening between the sigmoid valves. 1 Lond. Med. Gaz. vol. xv. (1834-35), vol. i. p. 671. 1 Supra, obs. x. p. 275. 2 Obs. xviii. p. 287. 472 PNEUMO-PERICARDIUM. PNEUMO-PERICARDIUM. By J. Warburton Begbie, M.D. Tins is the term employed to designate the presence of air in the cavity of the pericardium, and may be applied to that condition, whether or not the signs of in- flammatory action in the sac are present. There exist three different ways in which an accumulation of air in the pericardial sac may be determined : 1st. Such may be the direct product of the irritated mem- brane itself. It is admitted that, occa- sionally, air is produced in the cavities of the pleura and peritoneum, when these are the seat of inflammatory action, and if this be the case, there can be no reason why the same formation should not occur within the pericardium. Dr. Stokes has recorded an instance of this nature, in which, although recovery happily oc- curred, and the diagnosis must therefore be regarded as inferential rather than de- monstrative, the opinion expressed by him seems alone tenable. " I could form," he says, " no conclusion but that the peri- cardium contained air in addition to an effusion of serum and coagulated lymph. " 1 2d. Air may result from the decomposi- tion of fluid in the pericardium. Laennec and other observers have not only pointed out the physical signs which in their opinion indicate the existence of this lesion, but the former, more particularly, has in all probability greatly exaggerated the frequency of its occurrence. The effusion of fluid and air into the peri- cardial sac, in the opinion of Laennec, is a phenomenon likely to occur in the last stages of all diseases, and its existence he believed himself able to recognize both by percussion and auscultation. " L'epan- chement liquide et aeriforme a la fois du Pericarde pent avoir lieu dans l'agonie de toutes les maladies. Il m'est arrive quel- quefois de l'annoncer a une resonnance plus claire du has du sternum, survenue depuis pen de jours, ou a un bruit de fluc- tuation determine par les battements du coeur et par les inspirations fortes. "2 In a case recorded by M. Bricheteau, to which reference is made in Bouillaud's work, " Traite des Maladies duCoeur," as well as in a note by Andral to his edition of Laennec's Treatise, and which is also alluded to by Dr. Stokes and Dr. Walshe, the diagnosis of air as well as fluid exist- ing in the sac of the pericardium was made during the life of the patient, and depended chiefly on the presence of a peculiar sound with the heart's action, a sound compared by Bricheteau to that produced by a water-wheel (" 1'eau agitee par la roue d'un moulin"), while on ex- amination after death the pericardium was found to be occupied by a peculiar fluid of very fetid character, air escaping with a whistling sound when the sac was opened. Acknowledging, however, the occasional occurrence during life of Pneu- mo-pericardium, as the result of decom- position in fluid occupying the sac, it is manifest that this source of the lesion is of much greater frequency as a post- mortem occurrence. Laennec, indeed, has acknowledged this, for after alluding to Pneumo-pericardium as of common existence in autopsies, he adds, "Et surtout de ceux (cadavres) qui out ete gardes pendant un certain temps." 3d. Air may reach the pericardium from a distance, through perforation, and the establishment of a communication be- tween its cavity and that of any hollow organ normally containing air. Thus the sources of the air may be various, and the event may further be the result of direct injury or of disease. A very remarkable illustration is mentioned by Dr. Walshe, in which a communication was established between the oesophagus and pericardium, in an attempt to swallow a long blunt instrument, a juggler's knife-the case terminated fatally.1 A case of traumatic Pneumo-pericardium, unattended by in- flammation and resulting in complete re- covery, is given by Dr. Austin Flint, to whom it was related by Dr. Knapp of Louisville. "■The patient was stabbed with a knife, which penetrated the pleural cavity and perforated slightly the peri- cardium. A splashing sound with the heart's action was immediately heard, which continued for a few days and dis- appeared. The symptoms and signs, sub- sequently, did not denote pericarditis, but the patient had pleurisy, which was fol- lowed by considerable contraction of the 1 Diseases of the Heart and Aorta, p. 21. 2 Traits de 1'Auscultation mediate: Des Maladies du Coeur-Du Pneumo-Pericarde, chap, xxiii. 1 Diseases of the Heart. See pp. 46 and 271. PNEU MO-PERICARDIUM. 473 left side. The splashing sound in this case," continues Dr. Flint, "was fairly attributable to the presence of air and probably a little blood within the pericar- dium."1 Whether the inference that no inflammation of the Pericardium succeeded the injury in this instance be correct or not, there can be no doubt that the ordi- nary result of a perforation of the sac, whether by wound or by communication established between it and any organ con- taining air, is pericarditis. Dr. Walshe observes in regard to the latter: "Now Pneumo-pericarditis must exist tempo- rarily, be it for ever so few minutes, as the sole result of perforative communica- tion between the pericardial sac and any hollow viscus containing gas ; but in this isolated state it has never been observed, pericarditis having supervened before clini- cal examination has been made.'1'' After the operation of Paracentesis Pericardii and injections of iodine into the sac, physical signs have been discov- ered precisely similar in character to those met with in traumatic cases. Such resulted in the memorable instance re- corded by the late M. Aran under the title, "Pericardite avec epanchement, traitee avec succes par la ponction et 1'in- jection iodee." Of communication established between the Pericardium and neighboring organs through the progress of disease, and per- mitting the entrance of air into the cavity of the former, several instances have been recorded by different writers. Dr. Graves has furnished a remarkable example of communication by fistulous opening be- tween the stomach and an hepatic ab- scess on the one hand, and the peri- cardium on the other.2 Dr. M'Dowel exhibited to the Pathological Society of Dublin the morbid appearances in a case of communication established between a cavity in the left lung and the pericar- dium.3 The writer has placed on record the history of a very interesting case, in which disease of a cancerous nature pri- marily affecting the oesophagus, subse- quently involved adjacent organs, giving rise to pericarditis with effusion, and ulti- mately by perforation led to Pneumo- pericardium. When the close anatomical relationship of oesophagus to the pericar- dium, the former lying in the posterior mediastinum in contiguity with the pos- terior portion of the pericardium for nearly two inches, is considered, it will be seen how, in their conditions of disease likewise, the one is very apt to influence the other. In the instance now specially referred to, a careful scrutiny had led to the opinion that rupture of the oesopha- gus where in contact with the pericar- dium, and affected by cancer, had taken place, and, as a result of the perforation, that the passage of air into the pericardial sac had occurred. Post-mortem exami- nation confirmed the correctness of the diagnosis. On opening the chest, the pericardium, marked by the pressure of the ribs, bulged forwards, and on being punctured air escaped. Several ounces of dark-brown fetid fluid existed in the sac: lymph, recent in its deposition, and of yellowish color, coated the inner surface of the membrane. Cancerous ulceration, and destruction to a considerable extent of the wall of the oesophagus existed, cor- responding to its usual point of contact with the pericardium.1 In the diagnosis of Pneumo-pericar- dium, of Pneumo-hydropericardium, and Pneumo-pericarditis, reliance may reason- ably be placed on the physical signs as determined by percussion and ausculta- tion. Laennec, who, as already observed, exaggerated the frequency of the occur- rence of air in the pericardial sac before death, speaks of three signs to be expected when air and fluid exist in the pericar- dium. 1. Unusual resonance over the lower part of the sternum: 2. Fluctua- tion sound ("bruit de fluctuation") audi- ble with the action of the heart, and on deep inspiration. 3. This specially relat- ing to the diagnosis of simple Pneumo- pericardium, that is, without fluid effu- sion, or inflammatory product; the heart's sounds being heard at a distance from the chest. Upon this sign the distinguished inventor of auscultation placed very great reliance. Dr. Stokes, whose entire ob- servations on the subject of Pneumo-peri- carditis are most instructive, noticed the fact of the heart's sounds being heard at a distance in a case which he has record- ed ; he remarks, however, that this indi- cation did not exist in the instances of Dr. Graves and Dr. M'Dowel, already alluded to. Auscultation over the region of the heart, when practised by the writer in the case which fell under his own ob- servation, revealed the probable existence of air and fluid in the pericardial sac, by the extraordinary guggling sound which accompanied the heart's action-a sound which cannot, he thinks, be better de- scribed than as a churning splash. Dr. Stokes gives the following description of the sounds which he observed:-"They were not the rasping sounds of indurated lymph, or the leather creak of Collin, nor 1 A Practical Treatise on the Diagnosis, Pathology, and Treatment of Diseases of the Heart. By Austin Flint, M.D. 2 Clinical Lectures, edited by Dr. Neligan. Edition of 1864, page 616. 3 See Dr. Stokes's work, p. 23, also p. 35; and Dr. Walshe's work, p. 271. 1 Observations in Clinical Medicine, by J. Warburton Begbie, M.D. Edinburgh Medical Journal, 1862. 474 PERICARDITIS. those proceeding from pericarditic with valvular murmurs, but a mixture of va- rious attrition murmurs with a large crepitating and guggling sound, while to all these phenomena was added a distinct metallic character. In the whole of my experience I never met so extraordinary a combination of sounds. The stomach was not distended by air, and the lung and pleura were unaffected, but the re- gion of the heart gave a tympanitic bruit de potfele on percussion, and I could form no other conclusion but that the pericar- dium contained air in addition to an effu- sion of serum and coagulable lymph." The phenomena on auscultation and per- cussion thus graphically described by Dr. Stokes, will receive a farther value as in- dicating the existence of Pneumo-pericar- ditis, if in addition there be noticed, as was done by Dr. Walshe in the singular case of traumatic communication between the oesophagus and pericardium, a dull or tympanitic sound over the precordial re- gion, according to the position assumed by the patient. Even without this indi- cation, and in default of a metallic char- acter attaching itself to the cardiac sounds, as noticed by Dr. Stokes, the diagnosis of Pneumo-pericarditis, or, to be still more explicit, of Hydropneumo- pericarditis, may be made from observing a guggling or churning splash sound with the heart's action limited to the cardiac region, with which more or less of tympa- nitic precordial resonance on percussion is associated. These signs will be still more available, if the guggling sound has been noticed to succeed a distinct friction sound, and the tympanitic has replaced a dull percussion note. It is satisfactory to note that the phe- nomena to which attention has now been called, and which serve to indicate the existence of a very serious lesion, are not necessarily of a fatal import. In Dr. Stokes's case, as already noticed, recovery resulted, and in the instance of Pneumo- pericardium, traumatic in origin, noticed by Dr. Knapp, and recorded by Dr. Flint, the termination was equally gratifying. We may indulge the hope that the records of medicine may yet contain other exam- ples of a similar nature. PERICARDITIS. By Francis Sibson, M.D., F.R.S. CLINICAL HISTORY OF PERICAR- DITIS AS IT OCCURRED IN THE AUTHOR'S PRACTICE IN ST. MARY'S HOSPITAL. Inflammation of the surface of the heart and the lining of the pericardial sac occurs so very rarely by itself, and is so generally one of the attendant affections of a general disease, such as acute rheu- matism, Bright's disease, and pyaemia or the secondary inflammations; or of a local affection, such as aneurism of the aorta or cancer ; or of a local injury; that we cannot practically regard it as a dis- tinct disease. Pericarditis is, indeed, with very rare exceptions, one of the in- flammations attendant upon those dis- eases or injuries. Pericarditis occurs so much more fre- quently in acute rheumatism than in any other disease, that I shall first consider the affection as it exists in connection with that disease ; and in so doing shall examine the proportion of my cases of acute rheumatism that were affected with Pericarditis, and shall describe the pro- gress of that affection in those cases. RHEUMATIC PERICARDITIS. I possess notes of 326 cases of acute rheumatism that were admitted under my care into St. Mary's Hospital during the fifteen years ending in the autumn of 1866. This number does not include four- teen patients in whom it was doubtful whether the affection was acute rheuma- tism or acute gout. One-fifth of those cases1 (63) were at- tacked with Pericarditis, which was ac- 1 In two of those cases (59, 61) the evidence of pericarditis was slight and perhaps doubt- ful, but I am of opinion that in both of them the affection existed though in a slight and transient form. The numbers thus given here and elsewhere refer to the individual cases of Pericarditis as they occur in my records, so that the reader may trace for him- self each of those cases as it appears from part to part of this analysis. SEX, AGE, AND OCCUPATION IN ACUTE RHEUMATISM. 475 companied in all but nine instances (54) by endocarditis, and fully one-third of them with simple endocarditis (108), while in only one-fourth of them was there no evidence of either endocarditis or pericar- ditis (79). There was, however, an inter- mediate group, amounting nearly to one- fourth of the whole number (76), in which endocarditis, though not established, was either threatened or probable, the signs of that affection being either transient or imperfect. I think that we may class this intermediate group arbitrarily into two divisions, and consider that in one- half of them there was endocarditis, and that in the other half there was no endo- carditis. If we add the cases of pericarditis that were also affected with endocarditis (54) and half of those in which endocarditis was threatened or probable (38), to those in which simple endocarditis was present (108), we shall find that in my patients inflammation of the interior of the heart (200) was fully three times as frequent as inflammation of the exterior of the heart (63). This summary, otherwise stated, stands thus:- Cases of acute rheumatism with Pericarditis 63 Cases in which the Pericar- ditis was accompanied by endocarditis 54 Cases of simple endocarditis . 108 Cases of threatened or probable endocarditis 76 Cases in which there was no sign of endocarditis 79 Total number of cases of acute rheumatism 326 I.-Sex, Age, and Occupation in Acute Rheumatism in especial RELATION TO PERICARDITIS. Sex.-Acute rheumatism affected the female sex somewhat more frequently than the male sex in the proportion of 168 to 158. Pericarditis attacked 35 male and 28 female patients, so that nearly one in four of the former (35 in 154), and only one in six of the latter (28 in 166) were affected by it. Endocarditis was also present in 31 of the male and 23 of the female pa- tients affected with pericarditis. Simple endocarditis, on the other hand, attacked 47 male and 61 female patients, while, in addition, endocarditis was threatened or probable in 32 male and 41 female patients. The cause of the greater proportional frequency of Pericarditis, usually accom- panied by endocarditis, in the male sex, and of simple endocarditis in the female sex in these cases, will, I think, be in part explained by the influence of age and occupation on acute rheumatism and its complications. Aye.-One-half of the male (17 in 34)' and more than one-half of the female pa- tients (17 in 27)' affected with Pericardi- tis, were below the age of 21: while two- fifths of the male (13 in 34j and only one- seventh of the female patients (4 in 27) were above the age of 25. If we group these two classes of cases separately in relation to age, and compare them with each other, we find that acute rheumatism attacked 70 male and 77 female patients below the aye of 21, and that of these 17 of each sex were affected with Pericarditis, combined with endocar- ditis in all but one or two cases, and 25 of the males and 32 of the females with sim- ple endocarditis ; that in 12 of the males and 20 of the females endocarditis was threatened or probable, and that in 15 of the males and in only 8 of the females there was no sign of inflammation of the heart, within or without. On the other hand, we find that acute rheumatism affected 53 men and 53 women abovethe aye of 25, and that of these 13 men (13 in 53 or one-fourth) and only 4 women (4 in 53 or one-thirteenth) were affected with Pericarditis which was usually ac- companied by endocarditis, and 13 men and 17 women with simple endocarditis ; that in 11 men and 11 women endocardi- tis was threatened or probable ; and that the residue, or 16 men and 21 women, gave no sign of inflammation of the heart. The accompanying Table shows the proportion in which endocarditis and Pericarditis were absent or present in the cases of acute rheumatism, and the influ- ence of age and sex in the proportionate production of those affections of the heart in that disease. 5 The age of one of the 35 male patients and that of one of the 28 female patients was not stated. 476 PERICARDITIS. Male Female .... No Endocarditis Endocarditis threatened or probable. Endocarditis Pericarditis. Total. Threatened. ; Probable. Total. 42 )7 37 $ ' 9 { (jo 37 $ ™ $ 113 5 J 13 34 J 42 r6 fl J108 35 ' m 28 j 63 1'^8 ) nAg 168 Ages. | Male. | Female | Total. | Male. | Female. | Total. Male. Female. Total. Male. Female Total. | Male. | Female. Total. Male. Female. Total. Male. Female. Total. 10 to 15 5 3 8 2 1 3 0 11 2 2 4 10 9 1 19 6 3 9 23 | 17 40 10 to 20 11 5 16 9 14 23 14 5 10 18 28 15 23 38 11 14 25 47 60 107 21 to-25 10 8 18 6 9 15 4 0 4 10 9 19 8 11 19 4 6 10 32 34 66 26 to 30 8 13 21 3 5 8 2 0 2 5 5 10 8 6 14 5 1 6 26 25 51 31 to 40 5 4 9 6 5 11 0 0 0 6 5 11 4 10 14 6 2 8 21 21 42 41 to 50 3 3 6 0 1 1 0 0 0 0 11 1 0 1 2 0 2 6 4 10 51 and - 0 1 1 0 0 0 0 0 0 0 0 0 0 1 1 0 1 1 0 3 3 ? 0 2 2 1 0 1 12 3 112 1 1 2 3 4 7 Total.... 42 37 79 26 37 63 8 5 13 34 42 76 47 61 108 35 28 । 63 158 ^168 . 326 We thus see that in these cases of acute rheumatism, inflammation of the heart, grouping together those in which it at- tacked the interior and the exterior of the organ, affected the young below 21 (91 in 147) more frequently than the adult above 25 (47 in 106); that the heart was more fre- quently free from signs of inflammation in the adult above 25 (37 in 106), and espe- cially in women (21 in 53), than in the young below 21 (24 in 147), and especially in girls (8 in 77); that endocarditis was threatened or probable as often in the young below 21 (32 in 147) as in the adult above 25 (22 in 106) ; and, this being the point to which I would especially call attention that Pericarditis-while it af- fected the two sexes in nearly equal pro- portions below the age of 21, the male patients (17 in 70) a little more frequently than the female patients (17 in 77)-at- tacked men above the age of 25 (13 in 53) three times more frequently than women above that age (5 in 53). Occupation.-The study of the influence of occupation on the occurrence of acute rheumatism and on the production of in- flammation of the heart, both outside and in, throws light in two directions, one on the influence of sex, the other on that of age in producing those affections. The accompanying Tables show (I. pages 478-81) the influence of occupation in acute rheumatism in relation to age ; the presence or absence of endocarditis and Pericardisis ; the degree of the affec- tion of the joints, and that of the heart: and (II. pages 482-5), for the sake of com- parison, of ages (1) of 1000 patients, taken consecutively, with an occasional break, from my hospital books, affected with all other internal diseases besides acute rheu- matism and acute gout, and (2) of 326 cases of acute rheumatism with its attend- ant Pericarditis and Endocarditis, in re- lation to occupation. I take female domestic servants first, since they formed nearly one-third (101 in 326) of the whole number of those of both sexes, and nearly three-fifths of those of the female sex (101 in 168) who were affected with acute rheumatism. Among those patients affected with other dis- eases than acute rheumatism, female ser- vants formed one-fifth of the whole num- ber (204 in 1000) and two-fifths of the female patients (204 in 453). Nearly two- thirds of the female patients affected with acute rheumatism were below the age of 21 (57 in 100), while of those affected with other diseases, only one-third were below that age (64 in 195, or 33 per cent.). The influence of that employment in causing Pericarditis and endocarditis in acute rheumatism, especially below the age of 21, is remarkable. Of the wfliole number of 101 servants only 13-one- eighth-presented no sign of inflamma- tion of the heart, wdiile one-fifth of them (19) were attacked with Pericarditis, ac- companied in all but one instance with endocarditis also, and two-fifths of them (43) with simple endocarditis, while in the remaining fourth part (26) endocardi- tis was either threatened or probable. Servants formed fully two-thirds of the whole of the female patients affected with Pericarditis complicated usually with en- docarditis (19 in 28), and with simple en- docarditis (42 in 60); and three-fifths of those in whom endocarditis was threat- ened or probable (26 in 42): while they formed only one-third of those who gave no sign of affection of the heart (13 in 37). The influence of age in inducing inflam- mation of the heart in servants affected with acute rheumatism is still more re- markable. Of the whole number of ser- vants (101) attacked with that disease, 57 were below the age of 21. In only 3 of these was there no mark of affection of the heart, but one-fourth of them (14) were attacked with Pericarditis, all of whom had endocarditis also, and nearly one-half of them (25) with simple endo- carditis, while endocarditis was either SEX, AGE, AND OCCUPATION IN ACUTE RHEUMATISM. 477 threatened or probable in the remaining 15. Three-fourths of the servants at- tacked with Pericarditis and endocarditis (14 in 19), and three-fifths of those with simple endocarditis (26 in 42) were below the age of 21, while only one-fourth of those who were quite free from symptoms of heart affection were below that age (3 in 13). Girls engaged in the hard labor of a servant, at work, at a tender age, from morning to night, when attacked with this disease to which they are so subject, are all but certain to have in flanimation of the heart without or within. Servant-girls below the age of 21, keeping in view their time of life and constitution, are more ex- posed to the causes of acute rheumatism and its attendant inflammation of the heart than persons of any other class. They are growing, their frame is not yet knit, they are sensitive to cold and wet, and they are subject to palpitation. Be- fore all, in these young women their joints are not yet perfected, the ends of the bones forming them being still united to their shafts by cartilage ; their growth is active so that the blood circulates in them freely; their structures are sensi- tive ; and while they are supple, and their play is free and lively, they are tender and do not bear undue pressure ; they are liable to strains, are unequal to labor and fatigue,and are easily affected by draughts, and by exposure to wet and cold, espe- cially after undue and prolonged exertion. Then the labor of these poor girls, espe- cially in hard places of service, is great and constant; they carry weights up and down stairs, often in lofty houses ; they are constantly on foot, standing rather than walking, so that full pressure is con- tinuously made on the joints ; or what is worse, they are kneeling sometimes on cold and even wet stone floors, hard at work, scrubbing and brushing. The joint affection was, as a rule, more severe in servants suffering from acute rheumatism than in the rest of those so affected, the joints being attacked with severity in one-half of the servants (49 in 101), and a little over one-third of the rest (91 in 225). Among those servants who suffered from Pericarditis, the joint affec- tion was severe in fully three-fourths (15 in 19), and in a large proportion of these (6) it was very severe. If we compare these cases with the rest of the servants affected with acute rheumatism, we find that the severity of the joint affection rose in the scale in exact proportion to the severity of the heart affection. The joint affection was severe in less than one-third (4 in 13) of those servants who prfesented no sign of inflammation of the heart, while it was so in a little over a third (9 in 2G) of those in whom endocarditis was threatened or probable, and in one-half of those who were attacked with simple en- docarditis (21 in 42) ; while, as 1 have just said, it was severe in three-fourths of the cases with Pericarditis (15 in 19). In the servants who were attacked with Pericarditis, the severity of the joint affec- tion bore a strict relation to tlie severity of the heart affection in the great majority of the cases. In one-third of them (6 in 19) the joint affection was very severe; and in the whole of these the heart affection was very severe, while in one of them it was fatal. In nearly one-half of these patients (9 in 19) the joint affection was severe in the second degree, and in two-thirds of these (6 in 9) the heart affection was severe ; in two cases it was rather severe ; and in one it was slight. In three pa- tients the joint affection was rather severe, and of these the heart affection was severe in one, rather so in a second, and not so in a third. The last case is a notable exception to this rule. The attack in the joints was slight, but the attack at the heart was very severe, and proved fatal. 478 PERICARDITIS. TABLE I.-ACUTE OCCUPATION IN RELATION TO AGE, THE DEGREE Male Patients. Patients in whom There was no indication of Endocarditis. Endocarditis was threatened or probable. Number. Years. Joint affection. Number. Years. Joint affection. Out-of-door Employments. Engaged in laborious employments in the open air, including labor- ers (17), gardeners (5), brick- layer, brickmaker, sawyer (in tw<ce), mason, dustman, carter, plasterer, seaman, smiths (4), butchers (6), carpenters (4) 9 - 2 a;t. 20 1 " 24 2 " 26 to 27 2 " 32 " 37 2 " 42 " 46 1 severe 6 rather sev. 2 not severe f 3 set. 20 nJ 4 " 22 to 25 ] 1 " 26 " 29 t 3 " 31 " 38 6 severe 4 rather sev. 1 not severe Engaged in employments chiefly on foot, in the open air, includ- ing porters(4), watchman, errand boys (4), milkmen (2), hawker, cowkeeper, out of work - "on tramp" (1) C 2 set. 10 to 12 7 J 3 '* 16 " 20 ' 1 1 " 28 t 1 " 38 1 severe 3 rather sev. 1 not severe 1 slight 1 doubtful 2 1 " 14 1 " 21 2 rather sev. Employed with horses and in sta- bles, including grooms (6), riding- master, horsekeeper, coachmen (9), cabmen (5) 7 - r 2 set. 19 1 " 23 2 " 26 1 " 38 . 1 " 43 3 severe 4 rather sev. 7 • 4 " 16 " 19 2 " 21 " 24 1 " 27 4 severe 3 rather sev. Total of those employed in the above laborious out-of-door employments 23 - f 2 at. 10 to 12 7 " 16 " 20 2 " 23 " 24 5 " 26 " 28 4 " 32 "38 . 3 " 42 " 46 5 severe 13 rather sev. 3 not severe 1 slight 1 20 - r 1 " 14 7 " 16 " 20 7 " 21 " 25 2 " 26 " 29 L 3 " 31 " 38 10 severe 9 rather sev. 1 not severe Painters (3), plumber, gas-fitter... 2 1 set. 17 1 " 26 1 rather sev. 1 not severe 2 1 " 16 1 " 21 1 severe 1 rather sev. Commercial traveller >. In-door Employments. Including servants (12), bakers(3), paperhanger, French - polishers, (4), boot and shoemakers (3), " shopman," greengrocer, drap- ers (4). cheesemonger, slop cut- ter, tailor, teacher, silversmith, chairmaker, bath-attendant, and two others 7 - I 1 set. 14 2 " 16 to 18 2 " 25 L 2 " 27 " 28 3 severe 2 rather sev. 1 not severe 1 slight 9 ■ C2 " 19 1 " 25 3 " 29 3 " 33 " 37 1 very severe 4 severe 4 rather sev. Waiters (6), potmen and barmen (5) 8 1 set. 19 6 21 to 23 1 " 40 2 severe 5 rather sev. 1 not severe 1 " 21 1 rather sev. Schoolboys (5) .... .... .... Had no employment, including one discharged trom the navy (12) .. 2 set. 14 to 15 1 rather sev. 1 slight 2 5 1 " 14 ( 1 not stated 1 severe 1 slight Occupation no stated SEX, AGE, AND OCCUPATION IN ACUTE RHEUMATISM. 479 RHEUMATISM. OF JOINT AFFECTION, AND THAT OF HEART AFFECTION. Patients in whom there was Simple Endocarditis. Pericarditis, usually with Endocarditis (54 in 63). Total No. Years. Joint affec'n. No. Years. Joint affec'n. No. Years. Joint affec'n. Heart affec'n. 15- f6 set. 16 to 20 4 " 21 " 24 3 " 26 " 29 .2 " 35 " 38 10 severe 5 rather sev. 10- fl set. 17tol9 1 " 22 " 24 4 " 27 " 28 3 " 31 " 39 Ll " 42 4 very sev. 4 severe 2 rather sev. 1 fatal 3 very sev. 2 severe 3 rather sev. 1 not severe 45s fl2 set. 17 to 20 10 " 21 " 24 10 " 26 " 30 10 " 31 " 40 . 3 " 42 " 46 4 very sev. 21 severe 17 rather sev. 3 not severe 3 1 " 12 1 " 17 1 " 22 1 severe 1 not severe 1 slight 2 [1 " 17 1 " 25 1 severe 1 not severe 2 severe 14- f 4 " 10 " 14 5 " 16 " 20 3 " 22 " 25 1 " 28 1 " 38 3 severe 5 rather sev. 3 not severe 2 slight 1 doubtful 8- f3 " 18 " 20 2 " 21 1 " 26 1 " 33 "38 .1 " 42 2 severe 5 rather sev. 1 not severe 1 " 22 1 severe 1 severe 23- f 9 " 16 " 20 6 " 21 " 24 4 " 26 " 28 2 " 33 " 38 . 2 " 42 " 43 10 severe 12 rather sev. 1 not severe 26- r i " 12 10 " 16 " 20 7 " 21 " 24 4 " 26 " 29 3 " 33 " 38 1 " 42 13 severe 10 rather sev. 2 not severe 1 slight 13- r2 " 17 " 19 3 " 22 " 25 4 " 27 " 28 3 " 31 " 39 L1 " 42 4 very sev. 6 severe 2 rather sev. 1 not severe 1 fatal 3 very sev. 5 severe 3 rather sev. 1 not severe 82- f 4 " 10 " 15 26 " 16 " 20 19 " 21 " 25 15 " 26 " 30 13 " 31 " 40 . 5 " 41 " 46 4 very sev. 34 severe 34 rather sev. 7 not severe 2 slight 1 doubtful 1 " 35 1 very sev. 1 severe 5- r 2 " 16 " 18 I " 21 1 " 26 1 " 35 1 very sev. 1 severe 2 rather sev. 1 not severe 1 " 18 1 severe 1 very sev. 1 " 18 1 severe 9- f5 " 18 " 19 1 " 22 2 " 29 " 30 1 " 38 4 severe 3 rather sev. 2 not severe .3. f2 " 14 8 " 17 " 20 1 " 23 1 " 38 Ll " 50 6 severe 4 rather sev. 2 not severe 1 slight 1 fatal 2 very sev. 4 severe 4 rather sev. 2 not severe 1 slight 38- r 3 " 14 17 " 16 " 20 5 " 21 " 25 7 " 27 " 30 5 " 33 " 38 1 " 50 1 very sev. 17 severe 13 rather sev. 5 not severe 2 slight 3 " 27 " 30 1 rather sev. 1 not severe 1 " 39 1 severe 1 rather sev. 12- f 1 " 19 7 " 21 " 23 2 " 27 " 30 1 " 39 1 " 40 3 severe 7 rather sev. 2 not severe 3 " 9 "15 2 rather sev. 1 not severe 2 " 11 " 15 1 rather sev. 1 not severe 1 severe 1 rather sev. 5 " 9 " 15 3 rather sev. 2 not severe 6 " 9 " 15 3 severe 3 rather sev. 2 " 14 " 15 2 rather sev. 1 rather sev. 1 slight 12 11 " 9 " 15 1 not stated 4 severe 6 rather sev. 2 slight 1 not stated 1 rather sev. 2P " 26 ( 1 not stated 2 rather sev. 1 severe 1 rather sev. 3 1 " 26 2 not stated 3 rather sev. 480 PERICARDITIS. TABLE I -ACUTE Female Patients. Patients in whom There was no indication of Endocarditis. Endocarditis was threatened or . probable. Number. Years. Joint affection. Number. Years. Joint affection. Active In-door Employments. Servants 13 3 at. 19 to 20 4 " 21 " 25 6 " 26 " 30 4 severe 5 rather sev. 4 not severe 26 - f 1 tet. 15 14 " 16 to 20 4 " 22 " 2i 3 " 26 " 30 3 " 31 " 40 1 not stated 9 severe 11 rather sev. 6 not severe Cooks (5), charwomen (2), nurses (5), laundresses (9), washer- woman f 2 at. 26 to 28 R J 1 " 36 I 2 " 42 " 50 L 1 " 52 2 severe 1 rather sev. 3 not se"ere 7 - r 3 at. 19 to 20 2 " 21 " 24 1 " 26 1 " 40 3 severe 4 rather sev. Sedentary In-door Employments. Needlewomen (3),milliners, dress- makers (3), tailoress, shoebiuder, shoemaker 4 1 at. 20 2 " 26 1 " 49 1 severe 2 rather sev. 1 not severe 1 at. 44 1 rather sev. Kept a stall 1 at. 21 1 severe Married women, without special occupation, including 2 widows.. 8 3 at. 25 2 " 28 to 30 3 " 36 " 40 4 severe 2 rather sev. 2 not severe c 2 at. 25 5 J 1 " 30 1 1 " 32 1 not stated 2 severe 3 rather sev. Of no occupation 5 3 at. 13 to 15 1 " 16 1 " 25 1 severe 1 rather sev. 2 not severe 1 slight 2 1 at. 6 1 " IS 1 severe 1 rather sev. Occupation not stated at. 29 1 rather sev. Male Patients-total 42 - 5 at. 10 to 15 11 " 16 " 20 10 " 21 " 25 8 " 26 " 30 5 " 31 " 40 3 " 41 " 46 10 severe 22 rather sev. 6 not severe 3 slight 1 doubtful 34 - f 2 at. 14 10 " 16 to 20 10 " 21 " 25 5 " 26 " 30 6 " 31 » 3.8 1 not stated 1 very severe 16 severe 15 rather sev. 1 not severe 1 slight Female Patients-totals .... 37 - f 3 at. 13 to 15 5 " 16 " 20 8 " 21 " 25 13 " 26 " 30 4 " 31 " 40 3 " 42 " 50 1 " 52 12 severe 12 rather sev. 12 n >t severe 1 slight 42- f 2 at. 6 to 15 18 " 16 " 20 9 " 22 " 25 5 " 26 " 30 5 " 31 " 40 1 " 44 2 not stated 16 severe 20 rather sev. 6 not severe Grand total of the Male and Female Patients 79 - r 8 at. 10 to 15 16 '■ 16 " 20 18 " 21 " 25 21 " 26 " 30 9 " 31 " 40 6 " 41 " 50 1 " 52 22 severe 31 rather sev. 18 not severe 4 slight 1 doubtful 76 - 4 at. 6 to 14 28 " 16 " 20 19 " 21 " 25 10 " 26 " 30 11 " 31 " 40 1 " 44 3 not stated 1 very severe 31 severe 35 rather sev. 7 not severe 1 slight 4 of these cases died SEX, AGE, AND OCCUPATION IN ACUTE RHEUMATISM. 481 RHEUMATISM-(Continued). Patients in whom there was Simple Endocarditis. Pericarditis, usually with Endocarditis (54 in 68). Total No. Years. Joint affec'n. No. Years. Joint affec'n. No. Years. Joint affec'n Heart affec'n. 43- 4rei.l2tol5 21 " 16 " 20 10 " 21 " 25 4 " 26 "30 3 " 31 " 40 . 1 " 55 2 very sev. 19 severe 13 rather sev. 7 not severe 1 slight 1 doubtful 1 ret.15 13 " 16 to 20 4 " 21 " 25 1 " 26 6 very sev. 9 severe 3 rather sev. 1 not severe 2 fatal 8 very sev. 6 severe 2 rather sev. 1 not severe 101- 6 ret.12 to 15 51 " 16 " 20 22 " 21 " 25 14 " 26 " 30 6 " 31 " 40 1 " 55 1 not stated 8 very sev. 41 severe 32 rather sev. IS not severe 1 slight 1 doubtful 4 1 " 21 1 " 27 2 " 33 " 40 2 severe 2 slight 5^ r 1 " 20 1 " 21 1 " 35 1 " 60 L 1 not stated 1 severe 2 rather sev. 1 not severe 1 doubtful 1 severe 2 rather sev. 1 not severe 1 slight 22- r 4 " 19 " 20 4 " 21 " 25 4 " 26 " 30 5 " 31 " 40 2 " 42 " 50 2 " 52 " 60 1 not stated 8 severe 9 rather sev. 4 not severe 1 doubtful 4 1 " 18 3 " 31 " 38 3 rather sev. 1 not severe 1 r 2 " 18 " 20 2 " 26 3 " 31 " 38 2 " 44 " 49 1 severe 6 rather sev. 2 not severe 1 " 33 1 severe 2 1 " 21 1 " 33 2 severe 2 1 " 30 1 " 40 1 severe 1 rather sev. 2- 1 " 24 1 " 34 1 very sev. 1 rather sev. 1 severe 1 slight f 6 " 24 " 25 .J 4 " 28 " 30 6 " 34 " 40 1 not stated 1 very sev. 7 severe 7 rather sev. 2 not severe 7 5 " 13 " 15 1 " 18 1 not stated 3 severe 3 rather sev. 1 not severe 2 " 13 " 14 1 severe 1 slight 1 very sev. 1 slight ['ll " 6 " 15 3 " 16 " 20 1 " 25 _ 1 not stated 6 severe 6 rather sev 3 not severe 1 slight 1 " 29 1 rather sev. 47- '10ret. 9 to 15 15 " 16 " 20 8 " 21 " 25 8 " 26 " 30 4 " 33 " 38 1 " 42 1 not stated 20 severe 20 rather sev. 6 not severe 1 slight 35- 6ret.ll to 15 11 " 16 "20 4 " 22 " 25 5 " 27 " 28 6 " 31 " 59 2 " 41 " 50 u 1 not stated 5 very sev. 14 severe 11 rather sev. 4 not severe 1 slight 2 fatal 6 very sev. 12 severe 11 rather sev. 2 not severe 2 slight 158- '23 ret. 9 to 15 47 " 16 " 20 32 " 21 " 25 26 " 26 " 30 21 " 31 " 40 6 " 41 " 50 3 not stated 6 very sev. 60 severe 68 rather sev. 17 not severe 6 slight 1 doubtful 61- 9ret.l2tol5 23 " 16 " 20 11 " 21 " 25 6 " 26 " 30 10" 31 "48 1 " 55 1 not stated 2 very sev. 26 severe 22 rather sev. 9 not severe 1 slight 1 doubtful 28- r 3 " 13 " 14 14 " 16 " 20 6 " 21 " 25 1 " 26 2 " 34 " 35 1 " 60 1 not stated 7 very sev. 11 severe 7 rather sev. 2 not severe 1 doubtful 2 fatal 9 very sev. 9 severe 4 rather sev. 2 not severe 1 slight 1 doubtful 168- ("17 " 6 " 15 60 " 16 " 20 34 " 21 " 25 25 " 26 " 30 21 " 31 " 40 4 " 42 " 50 3 " 52 " CO 4 not stated 9 very sev. 65 severe 61 rather sev. 29 not severe 2 slight 2 doubtful L - -iSOl ri9«t. 9 to 15 38 " 16 " 20 19 " 21 " 25 14 " 26 " 30 14 " 31 " 41 1 " 42 1 " 55 . 2 not stated 2 very sev. 46 severe 42 rather sev. 15 not severe 2 slight 1 doubtful CO 9ret.ll to 15 25 " 16 " 20 10 " 21 " 25 6 " 26 " 30 8 " 31 " 40 2 " 41 " 50 1 " 60 2 not stated 12 very sev. 25 severe 18 rather sev. 6 not severe 1 slight 1 doubtful 4 fatal 15 very sev. 21 severe 15 rather sev. 4 not severe 3 slight 1 doubtful 326- ' 40ret. 6 to 15 107 " 16 " 20 66 " 21 " 25 51 " 26 " 30 42 " 31 " 40 10 " 41 " 50 3 " 55 " 60 7 not stat'd 15 very sev. 125 severe 129 rath. sev. 46 not severe 8 slight 3 doubtful 1 1 of these cases died. 2 5 of these cases died (1 from Bright's disease). VOL. II.-31 482 PERICARDITIS. TABLE II. Ages of I.-1000 Patients affected with ale other Internal Diseases except Acute Rheumatism, with its attendant Pericarditis and Endocarditis, and Male Patients. Below the Age of 21 Years. From 21 to 25 Years. (Other diseases except acute Workers out of rheumatism and acute gout d°"rs' r Acute rheumatism. . . . Laborious em- L Ditto with pericarditis . . ploymeuts . [pitto with simple endocard. _ Acute gout f Other diseases except acute ) 1 rheumatism and acute gout j Acute rheumatism .... Workers on foot - J Pericarditis L Endocarditis Acute gout 'Other diseases except acute ) rheumatism and acute gout $ f Acute rheumatism .... Workers among J | horses Pericarditis [.Endocarditis .Acute gout 'Other diseases besides acute ) rheumatism and acute gout $ Painters, plum- _ p Acute rheumatism .... ^els • ' " ■< Pericarditis (-Endocarditis .Acute gout 'Other diseases besides acute ) rheumatism and acute gout $ rAcute rheumatism.... In-door employ- j | ments . . . -( Pericarditis [.Endocarditis .Acute gout 'Other diseases besides acute ? rheumatism and acute gout $ Waiters, bar- f Acute rheumatism .... men, and one J commercial | -4 Pericarditis traveller . . (.Endocarditis .Acute gout 'Other diseases except acute ) rheumatism and acute gout s Of no occupa- B } tion and at S r Acute rheumatism .... school ... J pericar(iitis . (.Endocarditis ( Other diseases except acute ) rheumatism and acute gout 5 1 Acute rheumatism .... Total of Male , 1 Pericarditig Patients . Endocarditis L Acute gout 21, or 10 per cent, of those ) whose ages are stated, $ 12, or 26-6 per cent. J1, or 8-3 per ct. at that age.1 [ 1, or 10 per cent, of whole.2 $ 6, or 50 per cent of that age. ( 6, or 40 per cent, of whole. 0 6, or 17'7 per cent. 9, or 64 per cent. 5 1, or 11 per cent, at that age. J 1, or 50 per cent, of whole. j 2, or 22 per cent, at that age. j 2, or 66'7 of whole. 0 1, or 1'5 per cent. 9, or 39 per cent. 0 $ 3, or 33-3 per ct. at that age. | 3, or 37-2 per cent, of whole. 0 2, or 5 per cent. 2, or 40 per cent. 0 0 0 20, or 16-3 per cent. 20, or 52'5 per cent. J 10, or 50-6 per ct. at that age. ( 10, or 77 per cent, of whole, j 5, or 25 per cent, at that age. { 5. or 55-2 per cent, of whole. 0 2, or 16-6 per cent. 2, or 15-3 per cent. i 1, or 50 per cent, at that age. | 1, or 50 per cent, of whole. 0 0 37, or 100 per cent. 16, or 100 per cent. 4, or 25 per cent, at that age. 9, or 56-6 per ct. at that age. 89, or 17 per cent. 70, or 45 per cent. $17, or 21-3 per ct. at that age. / 17, or 51'5 per cent, of whole. S 25, or 35-7 per ct. at that age. [ 25, or 54-3 per cent, of whole. 0 31, or 15 per cent. 10, or 22-2 per cent. 1, or 10 per cent, at that age. 1, or 10 per cent, of whole. 4, or 40 per cent, at that age. 4, or 27 per cent, of whole. 2 4, or 11-7 per cent. 3, or 21-4 per cent. 1, or 33-3 per ct. at that age. 1, or 50 per cent, of whole. 1, or 33'3 per ct. at that age. 1, or 33-3 per cent, of whole. 0 4, or per cent. 6, or 26 per cent. 11, or 16-6 per ct. at that age. ( 1, or 10J per ceut. of whole. 2, or 30-9 per ct. at that age. 2, or 25 per cent, of whole. 1 9, or 22 per cent. 1, or 20 per cent. 0 0 0 20, or 16-3 per cent. 5, or 13-5 per cent. 1, or 20 per cent, at that age. 1, or 7'7 per cent, of whole. 1, or 20 per cent, at that age. 1, or 11 per cent of whole. 2 2, or 16-6 per cent. 7, or 54T per cent. 0 0 0 0 0 0 0 70, or 13'4 per cent. 32. or 20-8 per cent. 4, or 12 per cent, at that age. 4, or 12 per cent of whole. 8, or 24'2 per ct. at that age. 8, or 17'4 per cent, of whole. 1 Here and elsewhere in these columns add after " age" of those with acute rheumatism who were so affected and who were engaged in the class of employments indicated in the column headed Male Patients." 2 Hero and else where in these columns " whole" applies to the whole number of all ages of those with acute SEX, AGE, AND OCCUPATION IN ACUTE RHEUMATISM. 483 TABLE II. Acute Rheumatism and Acute Gout, and II.-326 Patients affected with III.-58 Patients affected with Acute Gout, in relation to Occupation. Above 25 Years. Age and Occupa- tion NOT STATED. Total. - 55, or 75 per cent. Age not stated 14 221 Qr 5 40'4 per cent, of the males. ( 22-1 per cent, of the whole.1 23, or 51 per cent. 45 nr j 29 percent, of the males. ( 14 per cent, of the whole. 8, or 35 per cent, at that age. 10 t Or 22 per cent, of those with 8, or 80 per cent, of whole. ( acute rheumatism. 5, or 21 per cent, at that age. 15 i Or 33'3 per cent, of those with 5, or 33 per cent, of whole. } acute rheumatism. 13 • • 15 24, or 70'6 per cent. ..4 38 O ) 6-9 per cent, of the males, ( 3-8 per cent, of the whole. 2, or 14-3 per cent. • • 14 0 $ 9 per cent, of the males. ( 4'3 per cent, of the whole. $ Or 14 per cent, of those with ( acute rheumatism. 0 ) Or 21-4 per cent, of those with ( acute rheumatism. 2 .. 2 61, or 93 per cent. ..3 69 0 $ 12-6 per cent, of the males. ( 6-9 per cent, of the whole. 8, or 35 per cent. .. 23 Qr )14'8 per cent, of the males. r ( 7'1 per cent, of the whole. 1 ( Or 4-3 per cent, of those with • • • • ( acute rheumatism. 3, or 37 per cent, at that age. f Or 35 per cent, of those with 3, or 37-5 per cent, of whole. ( acute rheumatism. 14 15 30, or 73 per cent. .. 41 0r 5 9*5 per '-ent. of the males. r ( 4'1 per cent, of the whole. 2, or 40 per cent. 5 0r $ 3-2 per cent, of the males. ( 1'5 per cent, of the whole. 1, or 50 per cent, at that age. 1 Or 20 per cent, of those with ac.rh. 4 .. 4 83, or 67-4 per cent. .. .. 6 129 O < 23-6 per cent, of the males. ( 12'9 per cent, of the whole. 13, or 34 per cent. .. 38 q t 24*5 per cent, of the males. ( 11-4 per cent, of the whole. 2, or 15'3 per cent, at that age. 13 i Or 35 per cent, of those with 2, or 15'3 per cent, of whole. ( acute rheumatism. 3, or 23 per cent, at that age. ) Or 24-3 per cent, of those with 3, or 33-3 per cent, of whole. ( acute rheumatism. 11 • • 13 8, or 66-6 per cent. .. 12 o < 2'2 per cent, of the males. ( 1'2 per cent, of the whole. 4, or 30'6 per cent. .. 13 0r 5 8'4 per cent, of the males. ( 4 per cent, of the whole. S1, or 25 per cent, at that age. ) Or 8*3 per cent, of those with / 1, or 50 per cent, of whole. ) acute rheumatism. $ 2, or 50 per cent, at that age. $ Or 16'6 per cent, of those with ( 2, or 100 per cent, of whole. ( rheumatism. 3 3 0 • • 38 0r $ Pe>" cent, of the males. ( 3-8 per cent, of the whole. 0 O $ 11 per cent, of the males. ( 5-3 per cent, of the whole. 0 4 Or 24 percent, of those with ac.rh. 0 .. 9 Or 53 per cent, of those with ac.rh. 361, or 69-4 per cent. Age not stated 27 547 $ 52, or 33'7 per cent. + 1 occupa- ) Age (?) 1+2 occ. 1 4 155 + 3 occ. ) ( tion not stated. ( not stated ( ( not stated $ 12, or 25 per cent, at that age. S Age (?) 1+1 occ. ) $ 33 + 2 occ. ) 12, or 36'3 per cent, of whole. ( not stated ( ) not stated ) 13, or 25 per cent, at that age. S Age (?) and occ. ) ) 46 + 1 occ. ( 13, or 28'2 per cent, of whole. ( not stated 1 $ ( not stated J 47, + 1 occupation not stated. i Age (?) - 3 occ. ) ( not stated j 52 1 rheumatism whose ages were stated, and who were so affected, who were engaged in the class of occupations indicated in the column headed Male Patients." 1 Here and elsewhere in this column " whole" applies to the whole number of patients of both sexes. 484 PERICARDITIS. TABLE II.-Continued. Female Patients. Below the Age of 21 Years. From 21 to 25 Years. Servants . . . - 'Other diseases except acute ) rheumatism $ Acute rheumatism .... Pericarditis . Endocarditis 64, or 32'8 per cent, of those ) whose ages are stated. $ 57, or 57 per cent. t 14, or 24'5 per ct, at that age.1 / 14, or 73'7 per ct. of the whole.2 j 25, or 44 per cent, at that age. ( 25, or 58-5 per cent, of whole. 60, or 30-8 per cent. 22, or 22 per cent. 4, or 18-2 per ct. at that age. 4, or 22-2 perct. of the whole. 10, or 45'5 per ct. at that age. 10, or 23'2 per ct. of the whole. Other In-door active em- ployments . . 'Other diseases except acute 1 rheumatism and acute gout J Acute rheumatism .... Pericarditis Endocarditis Acute gout 1, or 1*4 per cent. 4, or 18'2 per cent. 0 0 0 9, or 12-5 per cent. 4, or 18'2 per cent. S 1, or 25 per ct. at that age. ( 1, or 25 per ct. of the whole. 1, or 25 per cent. 0 Sedentary in- door employ- - ments . . . 'Other diseases except acute ) rheumatism j Acute rheumatism .... Pericarditis Endocarditis 1, or 2-7 per cent. 2, or 22-3 per cent. 0 $ 1, or 50 per cent, at that age. ( 1, or 25 per cent, of whole. 5, or 13-8 per cent. 0 0 0 Married women without spe- cial employ- ment. . . . 'Other diseases except acute ) rheumatism ..... 5 Acute rheumatism .... Pericarditis Endocarditis 3, or 4-3 per cent. 0 0 0 9, or 12-6 per cent. 6, or 37-5 per cent. < 1, or 16-6 per ct. at that age. 1, or 50 per ct. of the whole. Out-of-door em- ployment. Kept a stall. . ' 'Other diseases except acute ) rheumatism J Acute rheumatism .... Pericarditis .Endocarditis 0 0 0 0 0 1, or 50 per cent. 0 0 Of no occupa- tion, includ- ing girls at school . . . Other diseases except acute ) rheumatism J Acute rheumatism .... Pericarditis ..;.... .Endocarditis 57, or 100 per cent. 14, or 93 per cent. 2,or 14-4 per ct. at that age. 6, or 43 per cent, at that age. 0 1, or 7 per cent. 0 0 Total offemale patients . . ' 'Other diseases except acnto ) rheumatism and acute gout J Acute rheumatism .... Pericarditis Endocarditis Acute gout 126, or 29 per cent. 77, or 47'2 per cent. J17, or 22 per cent, at that age. ( 17, or 63-3 per ct. of the -ijvhole. $ 32, or 41-5 per ct. at that age. j 32, or 53'3 per ct. of the whole. 0 83, or 19 per cent. 34 6, or 17-6 per ct. at that age. 6; or 22-2per ct. of the whole. 11, or 32-3 per ct. at that age. 11, or 18-3 per ct. of the whole. 0 Grand Total of Male and Female Pa- tients . . . 'Other diseases except acute ) rheumatism and acute gout $ Acute rheumatism • . . . Pericarditis Endocarditis Acute gout 215, or 22-5 per cent, of the whole with ages stated. 147, or 46'7 per cent. J 34, or 33 per cent, at that age. t 34, or 56-6 per ct. of the whole. $ 57, or 38'8 per ct. at that age. ( 57, or 53 per ct. of the whole. 0 153, or 16 per cent, of whole, with ages stated. 66, or 20'8 per cent. 10, or 15 per ct. at that age. 10, or 16-6per ct. of the whole. 19, or 28-8 per ct. at that age. 19, or 18 per ct. of the whole. 5 1 Here and elsewhere in these columns add after " age" of those with acute rheumatism who were so affected and who were engaged in the class of employments indicated in the column headed " Male Patients." 2 Here and elsewhere in these columns " whole" applies to the whole number of all ages of those with acute AGE, SEX, AND OCCUPATION IN ACUTE RHEUMATISM. 485 TABLE II.-Continued. Above 25 Years. Age and Occupa- tion NOT STATED. Total. 71, or 36-4 per cent. Age not stated 9 204 0 $ 42 per cent, of the females. ( 20'4 per cent, of the whole. 21, or 21 per cent. .. 1 101 0r $ 60-5 per cent, of the females. ( 31 -3 per cent, of the whole. 1, or 4-7 per cent, at that age. ) $ Or 18'8 per cent, of those with 1, or 5-2 per cent, of whole. $ • • • • ( acute rheumatism. 8, or 38 per cent, at that age. i $ Or 42'5 per cent, of those with 8, or 18 per cent, of whole. $ - - ( acute rheumatism. 62, or 86-1 per cent. .4 5 77 n 515 per cent, of the females. 13, or 62 per cent. 3, or 37-7 per cent, at that age. ) 3, or 75 per cent, of whole. J .. 1 1 22 5 ( 7'7 per cent, of the whole. 0 $ 13'7 per cent, of the females. ( 6'8 per cent, of the whole. $ Or 22'7 per cent, of those with 3, or 75 per cent. 4 ( acute rheumatism. $ Or 18 per cent, of those with - - 3 ( acute rheumatism. 31. or 84-5 per cent. 1 38 nv $ 8'4 per cent, of the females. ( 3-8 per cent, of the whole. 7, or 77'7 per cent. 9 n $ 5'4 per cent, of the females. 0 0 ( 2-8 per cent, of the whole. 3, or 43 per cent, at that age. ) C Or 44-4 per cent, of those with 3, or 75 per cent, of whole. $ ( acute rheumatism. 59, or 83 per cent. 0r $ 16-3 per cent, of the females. • • .. 4 75 ) 7'5 per cent, of the whole. q $ 10-2 per cent, of the females. ( 5'3 per cent, of the whole. 10, or62-5 per cent. • • 4 • 1 17 1, or 10 per cent, at that age. ) $ Or 11-8 per cent, of those with 1, or 50 per cent, of whole. $ • • • • 2 ( acute rheumatism. 5 2, or 20 per cent, at that age. ) $ Or 11-8 per cent, of those with ( 2, or 100 per cent, of whole. 5 2 ( acute rheumatism. 2, or 100 per cent. 0 5 0 4 per cent, of the females. •• 2 ) 0'2 per cent, of the whole. q $ 1'2 per cent, of the females. 1, or 50 per cent. 2 ( 0'6 per cent, of the whole. 0 0 1, or 100 per cent, at that age. .. 1 Or 50 per cent, of those with ac.rh. $ 12'5 per cent, of the females. 0 • • 4 4 57 ( 5-7 per cent, of the whole. 0 1 16 0 $ 9'6 per cent, of the females, j 5 per cent, of the whole. 0 2 Or 12-5 per ct. of those with ac. rh. 0 .. 1 7 Or 44 per cent, of those with ac. rh. 225, or 51'8 per cent. 19 453 53 -|- 1 occupation not stated. 3 J 167 4-1 occ. 1 4, or 7-5 per cent, at that age. ) I not stated $ 4, or 15 per cent, of whole. $ • - • 4 28 17, or 32-7 per cent, at that age. i 17, or 28'3 per cent, of whole. $ • • 4 4 61 3 4. 3 $ 586, or 61-4 per cent, of those ) 1000 ( with ages stated. $ 46 \ 104 4- 2 occupation not stated, or $ Age (?) 54-2 occ. ) ) 322 4- 4 occ. ) ( 32-8 per cent. / not stated. ( not stated $ ( 16 4- 1 occupation not stated, or < 15-4 per cent, at that age, or ( 26'6 per cent, of the whole. i Age (?) l-|-2 occ. ) * not stated. 5 5 61 -|- 2 occ. 1 ( not stated 5 J 30, or 29'4 per cent, at that age. $ Age (?) 14-I occ. ) $107 4-1 occ. 1 ( 30, or 28'3 per cent, of whole. ( not stated. ( not stated 5 S Age and occ. not ) $ 55 + 3 occ. 5 ( stated 3 $ ( not stated $ rheumatism whose ages were stated and who were so affected, who were engaged in the class of occupations indicated in the column headed ' Male Patients. ' 1 Here and elsewhere in this column " whole" applies to the whole number of patients of both sexes. 486 PERICARDITIS. The accompanying Tables show (1) the proportion in which female domestic ser- vants affected with acute rheumatism were attacked by endocarditis and Peri- carditis, and the influence of age in the proportionate production of those affec- tions of the heart in that disease; and (2) the relation of the degree of the joint affection to the degree of the heart affec- tion in those cases. 1. Degree of the Joint Affection in Servants affected with Acute Rheumatism, in relation to Age and Heart Affection. Joint Affection. No Endocarditis. Endocarditis threatened or probable. Endocarditis. Pericarditis. Total. Grand Total. | Below 21. | 21 to 25. | Above 25. i Below 21. 21 to 25. Above 25. 7 age. Total. | Below 21. | 21 to 25. । Above 25. | Below 21. 1 21 to 25. 1 1 Above 25. Total. | Below 21. | 21 to 25. Above 25. ? age. Very severe.. 0 0 0 0 0 0 0 0 0 2 0 0 2 5 1 0 6 7 1 0 0 8 Severe 1 0 3 4 5 0 4 0 9 10 5 4 19 7 1 1 9 23 6 12 o 41 Rather severe 1 3 1 5 7 3 1 1 12 7 4 1 12 2 1 0 3 17 11 3 1 32 Not severe... 1 1 2 4 3 2 1 0 G 5 0 2 7 0 1 0 1 9 4 0 18 Slight 0 0 0 0 0 0 0 0 0 1 0 0 1 0 0 0 0 1 0 o o ] Doubtful .... 0 0 0 0 0 0 0 0 0 0 0 1 1 0 0 0 0 0 0 1 0 1 Total.... 3 4 6 13 15 5 6 1 27 25 9 8 42 14 4 1 19 57 22 21 1 101 2. Degree of the Joint Affection in Servants in relation to the degree of the Heart Affection in the cases of Rheumatic Pericarditis. Degree of the Joint Affection. Degree of the Heart Affection. Total Degree of the Joint Affection. Fatal. Very Severe. Severe. Rather Severe. Not Severe. Slight. Very severe 1 5 0 0 0 0 6 Severe o 1 5 2 0 1 9 Rather severe 0 0 1 1 1 0 3 Not severe 1 0 0 0 0 0 1 Heart affection .. 2 6 6 3 1 1 19 I will now briefly consider the occupa- tions of the remaining female patients who were attacked with acute rheumatism. I have thrown into one group the cooks, charwomen, nurses, and laundresses, who numbered altogether 22. Of these 5 had Pericarditis, 4 of whom had endocarditis also, and 4 had simple endocarditis ; in 7 endocarditis was threatened or probable ; and in 6 the heart gave no evidence of being affected. Of the whole number less than a fifth were younger than 21 (4 in 21'). Of the five cases with Pericarditis, in one the attack was severe but transient, and in that patient the joint affection was severe. In two others the heart affection was rather severe, and in the remaining two it was slight, while in none of these was the joint affection severe. Nine of the women followed sedentary employments, using chiefly the needle ; and in none of these was there Pericar- ditis ; four of them, however, had endo- carditis. The married women numbered 17, and of these only two had Pericarditis and endocarditis, one severely, the other slightly. In. both the joint affection was rather severe. Of the remainder, 2 had simple endocarditis, and 5 were threat- ened with it, while one-half (8) gave no sign of heart affection. These patients were all older than 23. Sixteen of the female patients had no occupation, only one of whom was above the age of 20. Only two of them had Pericarditis, one of whom had endocar- ditis also ; in one of these the heart affec- tion was fatal, in the other it was severe ; and in one of them the joint affection was severe, while in the other that ended fatally it was so only to a moderate de- gree. Seven of these cases had simple endocarditis and 2 were threatened with it; while 5 of them presented no indica- tion of endocarditis. These cases, taken as a whole, show that those women who followed at a ma- ture age occupations as laborious as the young servants, were affected in but a moderate proportion with Pericarditis, and that in a comparatively mild form. They also show that those of tender age who followed no occupation were not at- tacked with inflammation of the heart with anything like the same frequency as young female servants. We thus see, in 1 In one of the 22 cases belonging to this group the age of the patient is not stated. AGE, SEX, AND OCCUPATION IN ACUTE RHEUMATISM. 487 brief, that in acute rheumatism affecting the female sex, youth with labor is nearly always attacked or threatened with endo- carditis or Pericarditis, or both; that youth without labor is thus attacked -with comparative infrequency; and that ma- ture age with labor is attacked less fre- quently and much less severely with in- flammation of the heart than youth with labor. The male patients give us two great illus- trations. One of these is supplied by those working indoors, and they naturally run in the same grooves as the female patients, who were, all but two, occupied indoors. The other is supplied by those following out of door occupations ; and they stand completely apart in kind of labor, age, and character of disease, as well as in sex, from the female patients, whose cases have just been considered. I have brought the male patients work- ing indoors including ten servants, into one group, numbering 37. In several features this group presents a remarkable agreement as regards age and the fre- quency of heart affection, and especially of Pericarditis, with the important and large analogous group of female servants. Thus in each group more than half of the patients were below the age of 21 (of the male patients 19 in 37, of the female ser- vants 57 in 100) ;* in each, the proportion of cases with Pericarditis was great, amounting among the males to one-third (13 in 37), among the female servants to one-fifth (19 in 101); in each three-fourths of those thus affected with Pericarditis were below the age of 21 (10 of the 13 male patients, and 14 of the 19 female servants); in each the proportion of those in whom the heart presented no sign of inflammation was small, amounting to one-sixth of those male patients (6 in 37), and one-eighth of the female servants (12 in 101); and in each few of the patients whose hearts were thus unaffected wrere below the age of 21, amounting to fully one-third of those male patients (3 in 7), and to one-fourth of the female servants (3 in 13). Here, however, this close parallel ends, since among the patients affected with acute rheumatism above the age of 25, Pericarditis attacked the men working indoors more frequently (2 in 13) than the female servants (1 in 22), and among those with Pericarditis, less than one-half of the males (6 in 13), and almost as many as three-fourths of the females (15 in 19) were attacked with severity; while the proportion of cases affected or threatened with simple endocarditis was much smaller among the male patients (9 and 9 respectively in 37) than the female servants (42 and 26 in 101). Looking at these two sections of the patients in their larger and more vital re- lations, it is evident that in both sexes the same causes produce, under like con- ditions, the same effects; and that a very large proportion of the young persons who work on foot indoors during many hours daily, are attacked with inflammation of the heart when affected with acute rheu- matism, while a very small proportion are thus attacked of the men and women of mature age who are engaged in the same manner. If we looked solely to the kind of em- ployments just considered it would be natural to infer that overwork indoors in young people of both sexes was the main cause of acute rheumatism and of its at- tendant Pericarditis and endocarditis. While, however, as we have just seen, the whole of the female patients with oc- cupations -were engaged indoors, save two poor women who each kept a stall, only about one-fourth of the male patients worked indoors. The larger proportion of the male pa- tients affected with acute rheumatism, amounting nearly to three-fifths (82 in 154), excluding tliose working with lead, worked out of doors. More than one-half of these (45 in 84) were engaged in hard labor. Pericarditis attacked nearly one- fourth of these patients (10 in 45). We here find, what is at first sight an unex- pected result, that of these laborious workers out of doors thus attacked with Pericarditis only one in ten was below the age of 21; whereas of the male indoor workers thus affected, fully three-fourths (10 in 13) were below that age. If we look at those of older age, we find the scale exactly reversed; since of those laboring out of doors four-fifths (8 in 10) were above the age of 25; while of those working indoors only one-sixth (2 in 13) were above that age. We here, I con- sider, find the explanation, that I prom- ised when considering age, of the twofold fact, that the male cases of Pericarditis usually combined with endocarditis out- number the female cases by one-fifth (35 to 28) ; and that the number of the men so affected above the age of 25 is three times as great as that of the women so affected (men with Pericarditis 13 in 53, women 4 in 53). I think we may infer from these facts that excessive labor in the open air in men of mature age is a frequent cause of acute rheumatism hav- ing a strong tendency to Pericarditis. Male patients with acute rheumatism, whose occupation was chiefly on foot, such as watchmen and porters; and those em- ployed with horses and in stables,whose habits make them liable to gout, includ- ing coachmen, cabmen, and grooms ; did not suffer from Pericarditis so frequently as those who were engaged in hard labor: 1 In one of the 99 female servants affected With acute rheumatism, the age of the pa- tient is not stated. 488 PERICARDITIS since of those working on foot only one seventh (2 in 14) and of those employed with horses only one-twenty-third (1 in 23), while of those whose work was labo- rious, nearly one-fourth (10 in 45) were thus attacked. These facts support the view that Peri- carditis tends to attack men of mature age affected with acute rheumatism when their work is hard, but not when it is comparatively easy. It remains to me to speak of two other classes of employments, painters and plumbers on the one haud, and waiters and barmen on the other, who tend to have gout much more frequently than acute rheumatism. I find, however, that 11 waiters and barmen and 5 of those working with lead were attacked with acute rheumatism. One of each of those classes was attacked with Pericarditis, both of whom were above 30 years of age. Seven of the waiters and barmen and two of the workers in lead presented no sign of heart affection. These were all but one below the age of 24, and in none of them was the great toe affected. It would thus appear that when bar- men, painters, or workers among horses, whose employments tend to induce gout, are attacked with acute rheumatism, es- pecially when young, they do not tend to have Pericarditis or endocarditis. II.-The Affection of the Joints in Rheumatic Pericarditis. The inflammation of the joints and the inflammation of the heart in acute rheu- matism form one disease. We know that in a certain proportion of the cases the heart shows no sign of being touched by the disease, and here and there perhaps in a very rare instance the heart is at- tacked with inflammation when the joints are free from it. The unity of the two phases of the disease, the external phase, in the joints, and the internal in the fibrous structures of the exterior and the interior of the heart being established, we have to inquire what was the relative in- tensity of the inflammation of the joints and the inflammation of the heart in my cases of acute rheumatism, and especially in those affected with Pericarditis. We have just seen that in servants at- tacked with acute rheumatism, the joint was, as a rule, only of moderate severity when the heart gave no signs of being affected ; that the joint affection was more severe when the heart was threatened or probably attacked with endocarditis ; and that the severity of the joint affection in- creased in a direct ratio with the in- creased certainty and severity of the heart affection; the joint affection being greater when simple endocarditis was ac- tually present than when it was threat- ened or probable, and much greater when the heart was attacked with both endo- carditis and Pericarditis. I find that the same rule applies to the whole body of the cases of acute rheuma- tism ; as may be seen in the accompanying Table, showing the degree of intensity of the joint affection in relation to the ab- sence or presence of endocarditis and Pericarditis in cases of acute rheumatism. Degree of intensity of the Joint Affection in relation to the absence or presence of Endocarditis and Pericarditis in cases of Acute Rheumatism. Joint Affection. No Endo- carditis. Endocarditis threatened or probable. Endocarditis Pericarditis. Total. Female servants. Other em- ploym'nts Very severe 0 1 2 12 15 - 8 = 7 Severe....... 22 32 46 25 125 - 41 = 84 Rather severe . 34 35 42 18 129 - 32 = 97 Not severe 18 7 15 6 46 - 18 = 28 Slight 4 1 2 1 8 - 1 = 7 Doubtful 1 0 1 1 3 - 1 = 2 Total 79 76 108 63 326 -101 =225 Thus the joint affection was severe in one-fourth (22 in 78)' of those patients in whom the heart gave no sign of inflamma- tion ; in two-fifths (32 in 7G) of those in whom endocarditis was threatened or probable ; in more than two-fifths (48 in 107)' of those affected with simple endo- carditis, and in three-fifths (37 in 62)2 of those who were attacked with Pericardi- 1 The degree of the joint affection was not stated in one of the 108 cases belonging to this group. 2 The degree of the joint affection was not stated in one of the 63 cases belonging to this group. 1 The degree of the joint affection was not stated in one of the 79 cases belonging to this group. AFFECTION OF THE JOINTS IN RHEUMATIC PERICARDITIS. 489 tis, all but 9 of whom (54) had endocar- ditis also. The inflammation of the joints was very intense in 12 of the 37 patients with Peri- carditis, usually coupled with endocardi- tis, in whom the inflammation of the joints was severe, whereas in only 3 of the 184 patients in whom simple endocarditis was present or threatened, and in none of the 79 in whom the heart gave no evi- dence of being affected, was the joint affection of this great degree of intensity. Table giving the actual number of the Joint Affection in relation to the degree of Heart Affection in 621 cases of Rheumatic Pericarditis. Joint Affection. Heart Affection. Fatal. Very severe. Severe. Rather severe. Not severe, or slight. Total. The joint affection was very severe in 12 cases Of these the heart affection was fatal in " very severe in " " severe in " " rather severe in The joint affection was severe in 25 cases Of these the heart affection was fatal in " very severe in " severe in " rather severe in .. " " not severe in .... 6 7 3 113 22 3' 2' 12 25 The joint affection was rather severe in 18 cases Of these the heart affection was fatal in " " very severe in " '' severe in " " rather severe in " " not severe 2, or slight 3 in The joint affection was not severe 6, or slight 1 = 7 Of these the heart affection was fatal in " very severe in " severe in " rather severe in " not severe or slight in "o' "i* 2 0 5 2 6' 4 18 7 The joint affection was not described (?) in 1 In this case there were no signs of Endocarditis. Of the total of the above 63 cases of Pericarditis, the heart affection was fatal in The heart affection was very severe in " " severe in " rather severe " " not severe or slight in Total number of cases.... 4 15 21 15 1 64 In the cases of Pericarditis, there was a close correspondence in severity between the inflammation of the joints and the inflammation of the heart. The above Table shows in detail the degree of the joint affection in relation to the degree of the heart affection in sixty-two cases of Rheu- matic Pericarditis.1 The joint affection was very severe in 12 cases, and in three- fifths of those cases (7) the heart affection was very severe, being fatal in one; in one-fourth of them (3) it was severe ; and in only one-sixth of them (2) was it of moderate severity. The joint affection was severe in 25 cases, and in one-third of those cases (9) the heart affection was very severe ; in less than one-half of them (11) it was severe, and in one-fifth of them (5) it was of moderate severity, or slight. If we combine these two groups of cases, amounting to 37, that were 1 In 1 of the 63 cases of Rheumatic Pericar- ditis the condition of the joints is not de- scribed. 2 In these 2 cases the signs of Endocarditis were absent or doubtful. 3 In 2 of these cases the signs of Endocar- ditis were absent or doubtful. 4 In 1 of these cases the signs of Endocar- ditis were absent or doubtful. 5 In this case Endocarditis was absent or doubtful. 1 In one of the 63 cases of Pericarditis the joint affection was not described. 490 PERICARDITIS. marked by the severity of the joint affec- tion, we find that in four-fifths of them (30) the affection of the heart was severe, while in one-fifth of them (7) it was not severe or only moderately so. Endocar- ditis was present in all but two of the 30 cases in which the affection both of the joints and the heart was severe; while the signs of endocarditis were either ab- sent or doubtful in 4 of the 7 cases in which the affection of the joints was severe, while that of the heart was either of moderate severity or slight. If we examine those cases, amounting to 26, or two-fifths of the whole number, in which the degree of the joint affection was below the line of severity, we find that in 18 of them the affection of the joints was only of moderate severity, while in 7 of them it was slight; and that in two-fifths of these (10) the heart affection was severe, while in three-fifths of them (15) it was either slight or of moderate severity. We find, then, that in the 37 cases of Pericarditis in which the joint affection was more severe, the heart affection was more severe in four- fifths (30) and less severe in one-fifth (7) ; while in the 25 cases of Pericarditis in which the joint affection was less severe, the heart affection was more severe in two-fifths (10) and less severe in three- fifths (15). III.-The Degree of the Joint Af- fection DURING THE ACME OF THE Effusion into the Pericardium. When the exterior of the heart is at- tacked by inflammation in cases of acute rheumatism, the distress and oppression in the region of the heart and in the chest is often so great as to call the pa- tient's attention away from the seat of suffering in the joints. At the same time the physician or the clinical clerk is so much interested in the state of the central organ that he readily overlooks that of the joints. I find that in 12 of the 45 cases given in the accompanying plans (see pages 478, 479), the condition of the joints was not reported during the acme of the pericardial effusion, and in one other case the joint affection was not noted until the attack of Pericarditis had declared itself. The state of the joints during the period of the acme of the inflammation of the exterior of the heart, marked by the ex- tent of fluid in the pericardium being then at its height, is shown in 32 of the 45 patients under examination. These cases divide themselves naturally into two groups; in one of these, amounting to 12, the Pericarditis was at its acme at the time of admission, or on the follow- ing day ; while in the remaining 20 cases the effusion into the pericardium reached its acme after the admission of the pa- tient. In the latter set of cases, the in- tensity of the joint affection had been, as a rule, modified and lessened by rest and soothing treatment, and, especially in four-fifths of the cases, by opium given at repeated intervals; while in the former set of cases in which the pericarditis was at its height at the time of admission, the joint affection had been, as a rule, some- what aggravated by the removal of the patient from home to hospital. The set of cases, therefore, that were admitted with pericarditis at its height show the natural relation of the degree of the joint affection to that of the heart affection during the period of the acme of the dis- ease, in a manner less affected by other influences than the set in which the peri- carditis came on and reached its height after admission. The inflammation of the joints was severe at the time of admission in more than one-half of the patients (7 in 12) who came in with the Pericarditis at its height, and in six of these seven cases the joint affection was of about equal severity before admission and at the time of the acme of the effusion into the pericardium ; while in one of them the joints were less severely affected before than during the period of the height of the Pericarditis. In two-fifths of this group of cases (5 in 12) the joint affection was not severe when the Pericarditis was at its height, at the time of admission or on the next day, and in three and perhaps in four of these the inflammation of the joints was more severe before admission than after it and during the period of the acme of the effusion into the pericardium. The remaining case stands alone, since in it, although the affection of the heart proved fatal, that of the joints was but slight, both before and after admission. The second group consists of twenty cases in which the effusion into the peri- cardium reached its acme after admis- sion ; and it will be seen that the relation of the joint affection to the heart affection was very different in this group from what it was in the former one in which the patients came in when the Pericarditis was at its height. The inflammation of the joints was more severe at the period of the acme of the peri- cardial effusion than before that period in one-fifth of these cases (4 in 20), and it was of equal severity during the two periods in one other case. The affection of the joints became less severe during the period of the acme of Pericarditis than before that period in three-fourths of these cases (15 in 20). Four-fifths of these patients (12 in 15) PREVIOUS ATTACKS OF ACUTE RHEUMATISM. 491 took repeated doses of opium, with less- ening joint affection during the acme of Pericarditis, while only one of the four patients with increasing joint affection during the acme was placed under the influence of opium. It is evident that if we look only to the first group, or only to the second group of these cases, we should arrive at opposite conclusions with regard to the relation of the degree of the joint affection to that of the heart affection during the acme of Pericarditis. Thus the joint affection lessened during the acme of the disease in one-third of the first group (4 in 13) and in three-fourths of the second group (15 in 20). The influence of repeated doses of opium evidently told on the second group of cases, and the movement of the patients from their homes to the hospital, on the first group of cases, to modify the relation of the joint affection to the heart affection. I think that we may safely draw an in- ference midway between these two ex- treme illustrations, and consider that in about one-half of the cases of Pericarditis the joint affection was of equal severity during the period of the acme of the dis- ease, and before that period ; and that in about one-half of them the joint affection became less severe when the Pericarditis was at its height. The general conclusion may be drawn from this inference, that the joint affection tends to lessen in sever- ity when Pericarditis is at its height in about one-half of the cases. IV.-Time in the Hospital. The accompanying Table shows the average time that the patients remained in the hospital in relation to the absence or presence of endocarditis or pericarditis in acute rheumatism :- Time in the Hospital in relation to the absence or presence of Endocarditis and Pericarditis in cases of Acute Rheumatism. In the Hospital. No Endocarditis. Endocarditis threatened or probable. Endocarditis Pericarditis. Total. From 6 to 20 days 33 22 14 7 76 " 21 " 30 " 23 21 31 8 83 " 31 " 50 " 15 21 37 16 89 Over 50 days 3 8 21 28 60 An uncertain number of days . 2 2 3 4 11 Total 76 74* 106* 63 319* * Since this table was drawn up, seven cases have been added, making the total number 326. The time that the patient remained in the wards measures the duration and severity of the disease. Two-fifths of the patients in whom the heart gave no sign of being affected, left the hospital before the end of the third week (33 in 76), three-fourths of them during the first month (56 in 76), and one-fourth of them after the first month (20 in 76). Those who had Pericarditis usually accompanied by endocarditis remained in the wards for a much longer period, since only one- ninth of them (7 in 63) left the hospital before the end of the third week, and one- fourth of them (15 in 63) during the first month, while three-fourths of them re- mained in the hospital longer than a month (48 in 63), and one-half of them more than fifty days. Those with simple endocarditis remained in the house much longer than those whose hearts were healthy, but not nearly so long as those with Pericarditis usually combined with endocarditis. V.-Occurrence or Non-Occurrench OF ONE OR MORE PREVIOUS ATTACKS of Acute Rheumatism. The following Table shows the pro- portion in which the patients affected with acute rheumatism had been previ- ously attacked by that disease in fully three-fourths of the patients (243 in 319 cases). Less than one-third of those who gave no sign of endocarditis (23 in 76) and nearly one-half of those who were affected with endocarditis (48 in 106), had suffered from one or more previous attacks of acute rheumatism ; so that in my cases the occurrence of a previous attack evidently favored the presence of endocarditis. This did not, however, appear to be the case with pericarditis, for only one-third of the cases with that affection had been previously attacked by acute rheumatism. The previous occur- rence of acute rheumatism implies in a certain proportion of the cases the pres- 492 PERICARDITIS. ence of valvular disease of the heart, a condition that promotes the occurrence of endocarditis in acute rheumatism. It is open to inquiry why valvular disease should have more frequently influenced the production of endocarditis than of pericarditis in my cases. Occurrence or Non-occurrence of Previous Attacks of Acute Rheumatism in relation to the Absence or Presence of Endocarditis and Pericarditis. Joint Affection. No Endocarditis. Endocarditis threatened or probable. Endocarditis. Pericarditis. Total. No previous attack 37 23 31 26 117 No note of previous attack . . 16 17 27 16 76 One previous attack .... 17 24 35 15 91 More previous attacks than one . 6 10 13 6 35 Total 76 74* 106* 63 319 * Since this table was drawn up, seven cases have been added, making the total number 326. VI.-The Time of the First Obser- vation of Friction Sound and of THE BEGINNING OF RHEUMATIC PERI- CARDITIS in Relation to the begin- ning OR RELAPSE OF THE AFFECTION OF THE JOINTS. In a large proportion of the cases of acute rheumatism affected with Pericar- ditis, friction was heard over the heart either at the time of admission or very soon after it. Thus in more than one- third of the total number of the cases, the rubbing noise was noticed on the day that they entered the hospital (22 in 63) ; in all but one-half of them (29 in 63) it was heard on that or the following day ; and in fully two-thirds of them (41 in 63) it was observed either at the time of admis- sion or during the three days following it. In nine-tenths of the whole number of cases affected with Pericarditis (55 in 63) the frottement was distinguished during the first nine days of the patient's resi- dence in the hospital. These facts do not, however, point out how soon Pericarditis occurred after the commencement of the attack of acute rheu- matism. To ascertain this we must add the number of days from the commence- ment of the attack to the time of admis- sion, to the number of days from that time to the period at which the to-and- fro sound was heard. This plan answers with those cases in which the friction sound was observed on or after the third day from the date of admission, since in all but four of them the heart had been previously examined. It does not, how- ever, apply to those patients in whom the frottement was detected during the day of admission or on the next day, since in those cases we do not know how long the rubbing sound may have been in existence before the patient came in. This applies to one-half of the patients affected with rheumatic Pericarditis, since they had suffered from acute rheu- matism for a period varying from two days to three weeks before entering the wards. These cases are, however, of use in showing how early in the disease, and how late, Pericarditis may declare itself by friction sound in full play. Thus out of the twenty-nine cases in which frotte- ment was heard during the first two days, more than one-fourth (8 in 29) had been affected with acute rheumatism for a period of from two to four days ; while on the other hand one-fifth of them (6 in 29) had been ill for from two to three weeks before admission. If we bring together the whole of the 63 cases of Pericarditis, we find that in one-sixth of them (10 in 63) the rubbing sound was audible as early as from the third to the sixth day after the commence- ment of the disease ; while in one-half of them (30 in 63) that sound was audible on or before the eleventh day of the illness. In only seven of the cases did the heart affection show itself so late as the twenty- fifth day, and from that to the sixty-third after the onset of the acute rheumatism. These facts point, I think, to the con- clusion that in a certain small proportion of the cases, amounting perhaps to one- eighth (8 in 63) the onset of the inflam- mation both of the exterior and the inte- rior of the heart took place at the very commencement of the disease, and at the same time with the onset of the inflam- mation of the joints. It is scarcely needful to say that the first appearance of the rubbing sound is later than the beginning of the inflamma- tion of the surface of the heart. In this respect, the inflammation of the outside of that organ corresponds with the in- flammation of the joints, since, as in in- flammation of the joints, pain and ten- derness precede exudation and swelling, so in Pericarditis, in at least some in- stances to which I shall now refer, pain ENDOCARDITIS IN RHEUMATIC PERICARDITIS. 493 and exquisite sensitiveness over the heart preceded the notable increase of effusion into the pericardium and the existence of a rubbing sound. In five of the cases in which friction sound was heard on the day of admission (13, 15, 44a, 53, 61), pain had existed over the region of the heart, or in the left side, or in the chest, for one or more days before the patient entered the hospital. In one of these cases (44a) pain was pre- sent over the heart from about the begin- ning of the illness, the precise time of which is not stated. In nearly one-half of the patients in whom the frottement was heard for the first time from one to fifty-three days after admission (16 in 39), there was pain over the region of the heart or in the chest from one to seven days before the rubbing noise was observed. In seven (51, 8, 26, 28, 50, 29, 5) of them the pain was noticed one day ; in three (57, 56, 23), two days ; in one, three days (14) ; in two, four days (55, 36) ; in two, six days (123, 30) ; and in one, seven days (20) before the first observation of the friction sound. The patient (24), in whom friction sound was heard on the fifty-third day after admission, presented a chain of symptoms interesting in two points of view, one, that the attack of Pericarditis was immediately preceded by a relapse of the joint affection; the other, that pain over the heart preceded the frottement. The patient was a laborer, aged 27, and had almost passed through a severe attack of acute rheumatism with endocarditis, resulting in permanent injury to the mi- tral and aortic valves. On the 36th day, he, being stronger and of better color, was allowed to get up. On the 42d his gene- ral health was good, his pains were di- minished, and he walked about. On the 45th he felt stiffness in the right hip-joint on walking, that joint having been affected for eight months previously ; and on the 48th the pain in the hip was worse, though he was otherwise free from complaint, and his appetite was good. On the 50th day, however, his neck was stiff, and he had flying pains about the knees ; and on the next day his face was flushed, he per- spired copiously, and complained of great pain over the region of the heart and pal- pitation. On the 52d he suffered from a terrible pain in the neck and head, the wrists were swollen and painful, and the heart's action was so loud that the mitral and aortic murmurs wTere inaudible ; and on the following day a loud and harsh double friction sound was heard over the heart. Here the attack of Pericarditis im- mediately followed the relapse in the joint affection, and the pain over the heart preceded the rubbing sound by two days. In four other cases in which the friction sound appeared some time after admis- sion, the Pericarditis followed closely upon a relapse of the joint affection. In one of these (36), a woman, aged 20, who was motionless on admission from the affection of the joints, the pain was worse on the 6th day, she was still powerless on the 7th from the pain in the joints, and on the 8th a harsh grating frottement, chiefly systolic, was heard over the apex of the heart. In another patient (3), a man, aged 26, who was re-admitted with a severe relapse of the affection of the joints six days after leaving the hospital, the hands and hips were better on the 5th day after his readmission, but on the 8th there was again pain in the hip, and on the 9th there was excessive pain and ten- derness in the fascia of the thigh. On the next day (the 10th) there was pain, and increased dulness on .percussion over the heart, and a double friction brush was audible at the apex. In a third case (30), a man, aged 31, all the joints were swollen and painful when he came in, but were so much better on the 8th day that they only pained him when he moved. The pain in the joints returned, however, on the 9th, being better next day, when a harsh double friction sound was audible over the heart. In the last case of this group (17), a female servant, aged 20, the joints were painful and swollen on admission, they were less so on the 4th day, and on the 7th they were almost of the natural size. On the 9th a little pain returned in the joints and there was oppression over the heart. On the 13th the pain had in- creased and she suffered much in the chest, the first sound being rough and prolonged. On the 16th there was a mur- mur all over the heart, which was the seat of pain; and on the 17th a soft double friction sound was established over the region of the pericardium. To these cases must be added one of a series that were treated by rest during the years 1866-68. In this patient, a man, aged 20, the pain in the joints, which was considerable on admission and which lessened on the 4th day, again increased in the arms and neck on the 5th, when a pain, beginning at the lower portion of the breast bone, shot through the region of the heart to the back. This symptom and pain in the region of the apex were relieved by leeches. The joints also im- proved. but on the 10th, after he had been using his hand, pain returned in the fin- ger, and on the 14th. the next report, Pericarditis had fully declared itself. VII.-The Presence or Absence oe Endocarditis in Rheumatic Peri- carditis. I. Cases where Endocarditis was present. - There was evidence of inflammation in the interior of the heart in all the cases excepting nine (54 in 63). 494 PERIC ARDITIS. The heart was healthy at the time of the attack in 46 of the cases with endo- carditis, and the mitral, or mitral and aortic valves were crippled by previous disease in the remaining 8 cases, including one just alluded to (24) in which Pericar- ditis followed a relapse of the affection of the joints, the aortic and mitral valves having become affected during the earlier part of the attack of acute rheumatism. A tricuspid murmur was alone present in 3 of the 46 cases of endocarditis: in two of these cases that murmur was per- sistent, and in one of them it disappeared. These cases were comparatively free from serious symptoms, the heart affection being severe in only one instance, and the inflammation of the joints being very severe in another. The proportion of cases of this class with simple tricuspid murmur, was much smaller in these cases of combined endocarditis and Pericarditis than in those of simple endocarditis ; 1 in 18 of the former, as we have just seen (3 in 54), and 1 in 8 of the latter (13 in 108) being thus affected. The mitral valve was affected in 42 of the 46 patients with Pericarditis in whom endocarditis attacked the heart when pre- viously healthy, in 6 of whom the aortic valve was affected as well as the mitral. The aortic valve was attacked in one other case in which the mitral valve was not involved. I have divided these 43 cases with mitral (36), aortic (1), and mitral and aortic (6) incompetence into three groups ; in the first group, containing 16 cases (11 mitral, 5 mitral and aortic incompetence), valvular disease was finally established, or, in two instances, the disease proved fatal when the murmur was in full play ; in the second group, which numbered 8 cases with mitral regurgitation, the mur- mur was lessening when the patients were discharged; while in the third group, amounting to 19 (17 mitral, 1 aortic, and 1 mitral and aortic incompetence), the murmurs disappeared on the recovery of the patients from acute rheumatism, and the heart was restored to a healthy condi- tion. The accompanying Table shows the re- lation of the degree of the affection of the joints and that of the affection of the heart to the occurrence and degree of en- docarditis in cases of acute rheumatism affected with Pericarditis. If we compare the cases of endocarditis thus combined with Pericarditis, with the cases of uncomplicated or simple endocar- ditis, we find that valvular disease was finally established, that the murmur les- sened in intensity, and that the murmur finally disappeared in nearly the same proportion in the two sets of cases. Thus in 70 cases of simple endocarditis, either mitral '53), aortic (10), or mitral and aortic (7) incompetence was present. If we divide these cases, like those with Pericarditis and endocarditis, into three groups, we find that in the first group containing 28 cases (16 mitral, 5 aortic, and 5 mitral and aortic incompetence) valvular disease was finally established, or, in two instances, the disease proved fatal; in the second group, which num- bered 11 cases (11 mitral incompetence), the murmur was lessening when the patients were examined for the last time ; while in the third group, amounting to 31 cases (24 mitral, 5 aortic, and 2 mitral and aortic incompetence), the murmur had disappeared on the recovery of the patients from acute rheumatism, and the heart became again healthy. A tricuspid murmur was alone audible in 13 addi- tional cases of simple endocarditis: in 7 of these the murmur disappeared, but in 6 of them it was still audible when the heart was listened to for the last time. I am of opinion, notwithstanding the remarkable correspondence in the effects of the inflammation of the valves in the three parallel groups of each of these two sets of cases, that when inflammation at- tacks the interior of the heart alone, it is less likely to induce permanent valvular disease, that when the heart is inflamed without and within. This, I think, is a priori self-evident, and it is supported by two pieces of clinical evidence that I shall now adduce. (1) Disease of both the mi- tral and aortic valves, which is the most extensive form of valvular disease, was established in 5 of the 43 cases affected with both endocarditis and Pericarditis, and in 5 only of the 70 cases affected with simple endocarditis. (2) Simple endocar- ditis was present in 28 out of 74 cases of acute rheumatism that were treated by me in St. Mary's Hospital on a careful and rigid system of rest. Valvular dis- ease of old standing existed in 7 of those patients, and a recent mitral murmur, accompanied in one instance by aortic incompetence, affected the remaining 21 cases. The heart regained its healthy condition in 14 of these patients, the mur- mur was lessening or doubtful in 4 of them on their recovery from acute rheu- matism, and valvular disease was estab- lished in 3 only of the whole series of 21 cases. The inflammation both of the joints and the heart was more often severe in those cases in which the valves became permanently diseased, than in those in which the recovery of their function was complete. The heart affection was severe in 12 of the 16 cases in which the valves were permanently disabled, being fatal in two and very severe in six of them; while it was severe in 13 of the 19 in which the valves were restored to health, being very severe in four of them. The relative in- ENDOCARDITIS IN RHEUMATIC PERICARDITIS. 495 tensity of the joint affection was even I greater than that of the heart affection ; ! since, in the former class of cases, it was j severe in 12 of the 16 in which the organ became diseased, and in only 10 of the 19 in which its recovery was perfect. PERICARDITIS WITH AND WITHOUT ENDOCARDITIS. Relation of the degree of the Heart Affection and the Joint Affection to the occurrence and degree of Endocarditis. I Very severe. Severe. Rather severe. | Not 1 severe. Slight. Doubtful. Total. j With Endocarditis. Tricuspid murmur permanently established 2 Heart affection Joint affection 1 1 2 •• 2 2 Tricuspid murmur Heart affection i 1 disappearing on recovery .... Joint affection 1 1 Tricuspid murmur Total number 3 Heart affection Joint affection •• 1 1 1 2 i 3 3 Mitral regurgitation, ending in mitral valve disease 11 Heart affection Joint affection 1 5 4 1 4 2 3 2 11 11 Aortic and Mitral regurgitation, ending Heart affection i 1 3 5 in established disease of both valves Joint affection 1 3 1 5 Mitral and Mitral-aortic regurgitation . ending in established valve disease 16 Heart affection Joint affection 2 6 5 4 7 2 4 2 :: 16 16 Mitral regurgitation lessening on recovery 8 Heart affection Joint affection 1 3 3 2 2 i 2 1 1 8 8 Mitral regurgitation disappearing on recovery .... Aortic regurgitation 17 Heart affection Joint affection Heart affection 4 2 8 7 1 4 6 1 2 17 17 1 disappearing on recovery .... Joint affection 1 1 Mitral-aortic regurgitation 1 Heart affection 1 1 disappearing on recovery .... Joint affection 1 1 Mitral, Aortic, and Mitral-aortic regurgitation . disappearing on recovery .... 19 Heart affection Joint affection 4 3 9 7 7 1 2 19 19 Mitral valve-disease of old standing . Mitral-aortic valve-disease of old standing (1 recent) 5 3 Heart affection Joint affection Heart affection Joint affection 1 1 1 3 1 2 1 1 1 1 i 5 5 3 3 Mitral and Mitral-aortic valve disease of old Heart affection 1 4 2 1 8 standing Joint affection 2 3 8 i 8 Total number of cases of Pericarditis accom- ■ 54 3 15 19 11 3 3 54 panied by Endocarditis 10 21 17 5 1 54 Endocarditis absent or doubtful Cases without signs of Endocarditis । Heart affection ' Joint affection 1 i 2 3 1 1 1 1 6 5 Cases in which the signs of Endocarditis were Heart affection 3 T doubtful Joint affection i 1 1 3 Total number of cases in which Endocarditis was absent or doubtful । Heart affection ; Joint affection 1 *2 2 4 4 1 1 1 1 i ? 5 Grand total of cases of Pericarditis . i Heart affection [ Joint affection 4 15 12 21 25 15 18 4 6 4 1 i? 63 63 There was mitral regurgitation in the whole of the group of cases, amounting to 8, in which there was previous valvular disease, in three of which the aortic valves were also incompetent. The heart affec- tion was severe in the whole of these cases save one, and the joint affection was so in five of them. The all but universal pres- ence of inflammation within the heart in patients of this class, supports the in- ference that in acute rheumatism, old standing valvular disease, by throwing additional labor on the organ, tends to produce endocarditis and pericarditis, and to increase the severity of the inflamma- tion of the heart, both within and with- out. II. Cases in which Endocarditis was ab- sent or doubtful.-The signs of endocarditis were absent or uncertain in only 9 of the 63 cases of Pericarditis. In five of these patients no murmur was audible ; in one there is no note that a murmur could be heard, and in the remaining three the ex- istence of a murmur was doubtful. One of these cases proved fatal, and the affec- tion of the heart was severe in two and of moderate severity or slight in the remain- 496 PERICARDITIS. ing six patients. The joint affection was severe in six of these cases. Classification of the cases of Pericarditis, ■-I have classified the cases according to the presence or absence of endocarditis, and subdivided those with endocarditis into the groups which have just been de- scribed and which are specified in the fol- lowing scheme :- I. Cases of Pericarditis in which Endocarditis was present . . . .54 A.-Cases with Endocarditis attacking the healthy heart ... 46 1.-Cases with tricuspid regurgitation 3 a.-Cases in which the regurgitation became permanent after recovery from acute rheumatism . ... 2 c.-Cases in which the regurgitation disappeared on recovery 1 -Cases with mitral (36), aortic (1), and mitral-aortic (6) re- gurgitation ......... 43 a.-Cases in which the regurgitation became permanent after recovery from acute rheumatism (mitral 11, mitral- aortic 5) ......... 16 b.-Cases in which the regurgitation lessened after recovery (mitral 8) ......... g c.-Cases in which the regurgitation disappeared after recovery (mitral 17, aortic 1, mitral-aortic 1) . . .19 B.-Cases with Endocarditis attacking a heart already affected with mitral (5), or mitral-aortic (3) valve-disease .... 8 II. Cases of Pericarditis in which Endocarditis was absent (6) or doubtful (3) 9 Total number of cases of Pericarditis . . • . .63 VIII.-Sketch of the Progressive Changes that take place in the Heart and Pericardium during THE PROGRESS OF PERICARDITIS. We cannot rightly understand the symp- toms and signs of Pericarditis unless we keep in the mind's eye the changes that are going on in the heart and pericardium, and the surrounding organs during the periods of the beginning, increase, and acme, the decline and ending of the dis- ease. I shall, therefore, before discussing the symptoms and signs of the disease that were present in my cases, give here a slight sketch of the more important mor- bid changes, in so far as they make them- selves appreciated during life, and shall afterwards describe some of those changes more fully when the consideration of the symptoms and signs of the affection seems to call for it. When the surface of the heart becomes inflamed, a blush of fine vessels, consist- ing of a velvety network, appears on the surface of the organ, and especially over the larger coronary vessels at the base and septum of the ventricles. The inner sur- face of the pericardial sac, wherever it rests upon the inflamed heart, kindles also into a blush of fine vessels. The inflam- mation caught from the heart on the inner lining of the sac, spreads rapidly to the fibrous structure of the pericardium, and through it may even often extend to the surface of the pleura covering the sac. The inflammation of those parts tells upon the nerves distributed to them. The sur- faces of the heart and sac, instead of being smooth and glistening, become dull and velvety ; and fluid is poured out and lymph exudes from the inflamed surfaces. The liquid in the pericardium increases rapidly. At first it falls into the back part of the sac, but as it increases in quantity it makes a space for itself between the floor of the pericardium, which it de- presses, and the lower surface of the heart, which it elevates, and it gradually dis- tends the pouch in every direction, dis- placing the lungs to each side in front, pushing the central tendon of the dia- phragm, the stomach, and the liver down- wards, and pressing backwards, when the distension from the fluid becomes great, upon the bifurcation of the trachea, the left bronchus, the oesophagus, and the aorta. The fluid at the same time reacts upon the heart so as to compress the auri- cles, the vense cavse, the pulmonary veins, and the ascending aorta ; and to displace the apex and body of the organ and its great arteries upwards and forwards, owing to the extensive interposition of the fluid between the lower surface of the heart and the floor of the pericardium. The lymph is poured out upon the sur- faces of the heart and the sac. Where those two surfaces touch each other, the soft lymph is drawn into threads and lit- tle pointed ridges and prominences, and wrought into a network, so that when AFFECTION OF THE HEART. 497 ridges or prominences are present on the heart, ridges or prominences are present on the inner surface of the pouch lying upon it, and when a network of lymph covers the heart, a network of lymph lines the corresponding sac. The constant play of expansion and contraction of the heart alternately stretches and relaxes its coat- ing of lymph, so that its surface resembles a honeycomb in structure. The heart, elevated by the fluid between the under surface of the ventricles and the base of the pericardium to a degree pro- portioned to the amount of the fluid, leaves the broader part of the chest below, and ascends into the narrower part of the chest above. The lungs, and especially the left lung, are consequently displaced from before the swollen sac and the heart, and the front of the right and left ventri- cles, including the apex and the great ar- teries, beat with some force against the higher costal cartilages and intercostal spaces, and the adjoining portion of the sternum, with which they come into close contact. Owing to the narrowing com- pass of the portion of the chest in which the heart is then situated, and the with- drawal of the lung from before the organ, its impulse is both elevated and widened outwards, so that it is felt beating strongly in the second and third, or third and fourth left spaces, according to the amount of the effusion, the apex-beat being felt above, and beyond the nipple ; instead of the impulse, as in health, being felt gently in the fourth and fifth spaces, the apex- beat within the nipple-line. When the pericardium is distended to the utmost, its sac becomes pyramidal or pear-shaped, the apex or narrowest part of the pyramid pointing upwards, behind the lower por- tion of the manubrium and to the left of it, the base of the pyramid bearing down- wards and extending across the ensiform cartilage from the sixth right costal car- tilage to the lower border of the sixth left cartilage at its attachment to the rib. The fluid rapidly fills the sac, and often reaches its acme in two, three, or four days ; but it soon begins to lessen,, and in from four to six additional days it usually returns to its healthy amount. At the same time the heart descends and comes again in contact with the lower end of the sternum and the top of the ensiform car- tilage, the fifth space, the sixth costal cartilage, and the diaphragm. In most instances slight threads of adhesion form between the sac and portions of the right auricle, and often also between the sac and the apex and interventricular septum, that being the portion of the front of the heart that presents the least movement during the action of the ventricles. These soft threads of adhesion are generally drawn out, by the oscillating movements of the heart, until they at length yield, and break away, but sometimes perma- nent adhesions form, which may be par- tial or universal. IX.-Over-Action of the Heart in Acute Rheumatism as a Cause of Endocarditis and Pericarditis ; and (in illustration), Over-Action of the Limbs, Local Injury, and other Influences, as Causes of Acute Rheumatism with Affec- tion of the Heart. In a small number of my cases of rheu- matic Pericarditis, the inflammation of the heart commenced soon after laborious, or violent action of the organ. A woman (12), aged 26, a servant, was attacked, seven days before admission, with great pain in the soles of her feet. On the following day the pain continued, and proceeded up the legs to the knees and hips, so as to confine her to bed. On the third day she was seized with violent palpitation of the heart, and pain below the lower part of the sternum. On ad- mission her countenance was flushed and anxious, the pulse was 160, and there was pain on pressure over the region of the heart, which was beating with great force. A friction sound was perceptible at the apex with each beat, but indistinctly, owing to the violent action of the organ. The breathing was hurried. Eight leeches were applied over the region of pain, and next day her aspect was better, the action of the heart was natural, the area of dulness on percussion over the region of the pericardium was greatly enlarged, reaching as high as the second cartilage, and friction sound was audible over the whole front of the heart, where the pain was only slight. After this the heart's action became feeble, irregular, and intermittent, but it regained its regu- larity in eighteen days. The friction sound lasted for about three weeks, and a mitral murmur became permanently es- tablished. Another patient (24), already referred to, a laborer, aged 27, came in with acute rheumatism and endocarditis, presenting first mitral and then aortic regurgitation, both of which became established. He was allowed to get up on the 36th day. On the 48th he looked well, but pain in the hip, a trouble of old standing, had in- creased in severity. On the 50th the right side of his face was swollen and flushed, and he complained much of stiff- ness in the muscles of the neck, and next day of great preecordial pain and palpita- tion, the heart acting strongly and rapidly. On the 52d he was seized with terrible pain in the neck and head, and the heart's action was so loud that the endocardial murmurs were rendered inaudible, and on VOL. IL-32 498 PERICARDITIS. the 53d he suffered from acute pain about the prsecordia, the left cartilages were arched, precordial dulness extended up to the third space, and a loud and harsh double friction-sound was heard over the front of the heart. II is attack was of unusual severity, but the rubbing sound had disappeared on the 68th day after his admission, and on the 83d he was walking about. A third case (17), a servant girl, aged 20, who was affected with permanent mitral disease owing to a previous attack, was admitted on the fifth day of her ill- ness with severe joint affection, the heart being rapid and its sounds loud. Next day its action was very tumultuous, its impulse was strong, and its sounds were ill-defined, loud, and harsh. Leeches were applied to the chest, and the bleed- ing from one of the bites could not be re- strained. On the 3d the sounds of the heart were softer; on the 13th the first sound was more rough, on the 16th the impulse was very much diffused, and a murmur was audible over the front of the heart, and next day friction sound was heard over that region and Pericarditis in a severe form was fully established. After this the heart's action became irregular and intermittent, and she looked and felt anxious and depressed. A long, severe and varying illness followed. On the 55th day she seemed to be sinking, though she thought herself better. On the 58th day she kept nothing on her stomach, but on the 59th she felt better and looked much brighter. Smallpox, however, then in the wards, declared itself on the 62d day, and on the 63d she died. In the first and second of these cases the heart continued to act with increased force during the period of the onset of the Pericarditis; but in the first of them this condition gave way after the application of leeches to irregular action of the heart, which lasted for eighteen days. In seven or eight other cases the impulse of the heart was strong during the early period of the inflammation of the exterior of the heart. As a rule, however, the impulse of the heart was feeble when first observed during the attack of Pericarditis. The condition of the impulse of the heart dur- ing Pericarditis will, however, be consid- ered under its proper heading. If we look at these cases, and especially the first and second of them; combine with them the six others already given in which Pericarditis followed closely upon a relapse in the joint affection, brought on often by getting up too soon ; and add to these the relation that existed in my cases of acute rheumatism, between the severity of the joint affection and the presence, character, and severity of the heart affec- tion, the joint affection being slight in the majority of cases without signs of endo- carditis, severe in the majority of cases with simple endocarditis and still more severe in the great majority of cases with Pericarditis and endocarditis ; the severity of the heart affection corresponding, as a rule, with the severity of the joint affec- tion ; we must, I consider, conclude that we may have here not a mere lifeless chain of passive links, but a living succes- sion of active events, one giving birth to the other. Exposure to cold and wet, combined with undue labor or exertion, give the first impulse,-the start, to the affection of the joints. When the joint affection is severe, it may call forth exces- sive labor or even tumultuous action of the heart. In acute rheumatism, inflam- mation attacks the fibrous structures, especially if those structures are unduly strained, and the increased action of the heart may therefore, I consider, induce inflammation of the fibrous tissues of that organ, such inflammation being propor- tioned in severity to the augmented action of the heart. This interesting subject derives larger illustration from the influence, already considered, of sea;, age, and occupation in the production of acute rheumatism, accompanied, in proportion to the sever- ity of the affection of the joints, by in- flammation of the heart within and with- out. I need only here again refer to the large number of young female servants, in whom the ends and shafts of the bone are as yet only united by cartilage, who are attacked by acute rheumatism in a severe form ; and the very large propor- tion in which those cases have endocar- ditis or Pericarditis, or both, the heart being subject, in those overworked young women, to undue action and palpitation. In illustration of the influence of over- action of the heart in producing inflam- mation of the interior and the exterior of that organ, I shall give here a brief sum- mary of the influence of local injury, scar- let fever, chorea, abscess, and general illness in the production of acute rheuma- tism with endocarditis and Pericarditis, including those cases of acute rheumatism in which a relapse of the joint affection, followed by Pericarditis, was induced by the too early use of the limbs, when the recovery was almost but not quite perfect. Two influences usually combine to pro- duce acute rheumatism ; one, exposure to wet and cold; the other, the over-use of certain limbs and joints. The part imme- diately in use is usually the part first attacked, while the joints that take the greatest share in the permanent labor of the patient are generally those visited by the disease with the greatest severity and duration. Thus, among the coachmen admitted under my care, one was first AFFECTION OF THE HEART. 499 attacked in the right thumb, the knees being afterwards affected ; another was seized badly in the right arm, and then in the left; a third in the wrist and hands; and a fourth in the hands, and especially the middle finger, the arms, and then the knees, the affection of the fingers being obstinate; in a fifth the back and hips were the seat of pain ; and in the sixth the ankles, knees, hands, and hips were all involved. If we take the carpenters, we find that one of them was attacked in the arms, wrists, and elbows ; another, who was in search of work, in the arms, back, ankles, and knees ; and a third was seized, when walking, with pain in the knees, the ankles, shoulders and arms being afterwards affected. Young female servants, for to them I must here again refer, who usually work too hard, whose joints are not yet perfect, being still in a state of active growth, are for the most part first attacked in the feet and ankles, that is to say, the parts that more immediately tread the ground. The knees usually then suffer, or perhaps earlier, at the same time as the feet and ankles ; and afterwards the wrists, hands, arms and shoulders, in succession, share in the affection. The knees, which gen- erally bear not only the internal pressure of standing, but also the external pres- sure of kneeling when at work, are as a rule, more constantly and deeply affected, and for a longer period, than any other joint. The effect of past labor is, so to speak, stored up in the knees, which are therefore in these cases more affected in acute rheumatism than any other joint. Under the combined influence, then, of exposure and overwork, rheumatic in- flammation is set up in the joints, and under the combined influence of the dis- ease thus established, and overwork of the heart, rheumatic inflammation is estab- lished in that organ. In a small but important group of my cases, acute rheumatism followed local in- jury. The first of these, a stonemason, fell from a scaffold on his back. He had pain in his back and legs, and could not stand. On the 5th day he had a pro- fuse sour perspiration, and his finger and elbow-joints were red, swollen, and pain- ful. The hips, knees, and shoulders were afterwards attacked, and he probably had endocarditis, the first sound being pro- longed, while the second was followed by a soft murmur. The second patient was admitted under Mr. Lane's care for a slight injury, and was attacked on the fourth day with pain in the chest and in- flammation of the wrist and ankles. On the 7th he was transferred to my charge with acute rheumatism, mitral murmur, and Pericarditis. A third patient, a dust- man, hurt his back by carrying a sack of flour. The pain in the back was in- creased by his getting wet; and this was followed by acute rheumatism. A fourth patient was attacked with the disease in the wrists 32 days after breaking his leg. A fifth came in with acute rheumatism five days after leaving the surgical ward ; and a sixth, who was admitted with en- docarditis and transient Pericarditis, had received a kick in the groin five weeks previously, and since then had been sub- ject to pain in the loins. In some of these cases the disease appeared to be directly, and in others to be indirectly, caused by local injury. These cases and others given below are allied to those previously given, in which the too early use of a limb, during the period of convalescence from acute rheu- matism, produced inflammation in the used joint, a relapse of the affection in the other joints, endocarditis and Peri- carditis, ending in permanent crippling of the valves of the heart. The whole of these results, the latter of them so per- manently injurious, started from the re- newed focus of the disease in the single joint thus affected for the second time. Through what means is this diffusion and transmission of the disease effected ? Is it by a blood poison ? Is it by a change in the fibrous structures of the limbs and the heart ? Or is it by reflex influences, transmitted through the afferent nerves, locally acted upon in the inflamed joint or injured part, and sent back through the vaso-motor or other nerves distributed to the fibrous structures of the joints and the heart ? The local character of the injury inducing this general effect,. and the quickness with which the effect is in- duced, would appear to forbid the material agency of either blood poison or change in the tissues; and would tend to throw us upon the transmission of influences through the nerves for an explanation of these remarkable effects,-effects not less remarkable, but rather more so, that they are open to daily observation; or must we look for some other explanation than any of these here suggested ? We cannot, however, limit ourselves to the points of view just sketched in our in- quiry into that many-sided disease, acute rheumatism, with its attendant inflam- mation of the heart; and I would here briefly state the other influences that have been apparently at work in the origin of the disease, besides overwork and ex- posure on the one band, and local injury on the other. In three of my patients the disease was associated with scarlet fever, one of whom had Pericarditis in the hospital, one out of it. The latter was the son of a medi- cal friend, who detected symptoms of acute rheumatism just as the scarlet fever was declaring itself, and by which the acute rheumatism was suspended. When, 500 PERICARDITIS. however, the eruption had ceased and desquamation was going on, endocarditis and Pericarditis, the offspring of the original rheumatism, declared themselves. This case did well, and though a mitral murmur existed for some time, it at length disappeared. In the two other cases, acute rheumatism followed a chill caught by too early exposure after the scarlet fever had disappeared. In several of my cases, chorea has given place to acute rheumatism or the reverse. In one patient, a girl, acute rheumatism passed into chorea, for which she was ad- mitted. After a time the choreal move- ments were for a period suspended by the renewal of acute rheumatism. I do not here speak of that terrible complication, the occurrence of serious local choreal and tetaniform symptoms in connection with rheumatic endocarditis and Pericarditis, complications to which I shall soon refer. In three patients the acute rheumatism was preceded by recent abscess, in one of them in the axilla, in another in the peri- neum, and in a third in the tonsil; and in a fourth case, abscess in the neck ex- isted some time before the supervention of the rheumatism. Sore throat appeared for from one day to three weeks before the occurrence of acute rheumatism in thirteen cases, in- cluding the case of abscess in the tonsil just quoted. Two of these patients had Pericarditis; three had simple endocar- ditis ; in three endocarditis was threat- ened ; and five gave no sign of heart affection. In eleven patients, pain in the chest, sometimes accompanied by cough, ex- isted for from one day to two or even three weeks before the development of acute rheumatism. I refrain from pursuing this important collateral subject farther in this place. X.-Pain. I.-Pain over the Region of the Heart and Pericardium. Pain over the region of the heart and pericardium showed itself in six different ways: 1. Over the front of the organ ; 2. On pressure at the same place ; 3. In the epigastrium, chiefly on pressure ; 4. Over the back of the heart, when it was excited by swallowing and by eructation ; 5. After eating; and, 6. Pain shooting through the heart, evidently anginal in character. 1. The pain over the front of the heart extended usually from the right of the sternum at its lower two-thirds to the left nipple; it was more or less continuous, and was complained of in three-fourths of the cases (48 in 63). This pain came on in one-fourth of the patients affected with it (9) before the friction sound was heard, and in a greater number (16, including 5 in which the pain and the friction sound were both present on the day of admis- sion) at the time that the sound was first audible. In a few instances (7) it wa.s felt soon after the appearance of the rubbing sound. It was either relieved, suspended, or removed by the application of leeches. It was complained of in about one-fourth of the cases (8) at the time the effusion was at its height, but usually re- lief, which was permanent, came at that time. In two instances (15, 51) of re- apse, the second, and in one (44a) even a third, wave of increase of pericardial effu- sion was preceded by a second, and in one even a third attack of pain over the heart; but in three cases the pain came late in the period of the relapse, and when the effusion was declining. In scarcely any instance did the pain over the heart con- tinue during the whole period of the du- ration of the friction sound, and in only two or three of the cases did it last over the first half of that period. When the pain comes on with the first blush of the inflammation on the surface of the heart, before it has spread to the inner surface of the pericardial sac, and before friction sound is audible, it may be inferred that it is seated in the sentient nerves distrib- uted to the surface of the heart. When, however, the pain strikes over the heart at the same time as the appearance of the friction sound, and still more when it comes on at a later period, it is generally, I believe, seated in the pericardial sac, and especially in the pleura covering the sac. The accompanying table gives a resume of the period of the occurrence of pain over the region of the heart in relation to the time of the appearance of friction sound in the eases of Pericarditis (see page 501). 2. If the pain over the heart is increased or excited by pressure over the region of the organ, it may, with an approach to certainty, be attributed to inflammation of the pleura, especially if the pain on pressure is complained of, not before, but at the time of or after the first presence of friction sound. Pain on pressure over the heart occurred in one fourth (14 in 63) of the whole num- ber of cases affected with acute rheuma- tism, and in one-third of those who suf- fered from continuous pain in the region of the heart (11 in 38). In two only of these cases was the pain excited by pres- sure before the friction sound was audi- ble, and in these the pain was probably excited over the surface of the inflamed heart. In one-half of the patients the pain on pressure and the rubbing sound appeared on the same day, and in the rest PAIN OVER THE REGION OF HEART AND PERICARDIUM. 501 the pain was preceded by the friction sound. In most or all of these cases, the pleura covering the pericardiac sac, or the fibrous structure of the sac itself, was the probable seat of the suffering. In one-half of those patients (7 in 14) the skin over the region of the pericar- dium was tender and sensitive, so much so indeed, in some instances, as to forbid the slightest manipulation over the chest, and to make a proper examination of the heart impossible until this exquisite sen- sibility was subdued by the application of leeches or of belladonna liniment with chloroform. In the majority of the cases the pain was deeper than the skin, and was not excited unless actual pressure was made. In three of the patients the pain was only felt when pressure was made over the re- gion of the heart; but in all the others continuous pain already existed over that region, and was intensified by the pres- sure. In one or two instances the suffer- ing and distress of the heart were so great as to drown all other complaints ; but in three others, as I have just said, the pain was only brought into play when pressure was exerted. Between these two oppo- site extremes, there was every shade in the extent, variety, and constancy of the pain. Period of the occurrence of Pain over the region of the Heart and Pericardium in relation to the time of the appearance of Friction Sound in cases of Rheumatic Pericarditis. Pain over the region of heart and pericardium, including pain over the epigastrium. Cases. Pain on pressure over the region of the heart. * * or t No endo- carditis. Total. Pain over heart and friction sound on ) day of admission J Pain over epigastrium and friction 1 sound on day of (in one day after) > admission, included above . . . J Pain over heart before admission, I friction sound on admission . . . ) Pain over heart before appearance of ) friction sound ) Pain over epigastrium before appear-1 ance of friction sound, included > above J Pain over heart and friction sound f occurring on same day . . . . $ 5 4 4 9 2 11 Appearing before ) friction sound J Appearing same 1 time as friction > sound . . .) Appearing after 1 first indication > of friction sound J Appearing after 1 friction sound > had ceased . . ) 1 4 2 1 8 2 1 3 1 * 1 2 1 1 2 7 4 1 14 Pain over epigastrium, and friction 1 sound occurring on same day, not > included above * Pain over heart coming on after fric-) tion sound had been observed . . J Pain over epigastrium coming on after ) friction sound had been observed, > not included above ) Ditto, included above Pain over heart appearing shortly) before relapse (renewed increase of ( fluid in the pericardium) not in- j eluded above J Ditto, included above Pain over epigastrium before relapse Pain over heart late in period of re- ) lapse, not included above. . . . ) Ditto, included above Pain over heart at the time of acme ( of Pericarditis $ Pain over heart shortly before time ) of acme of Pericarditis ) Pain of epigastrium at time of acme ) of Pericarditis $ Ditto before acme of Pericarditis . Ditto after acme of Pericarditis . . 3 7 2 8 1 1 1 1 2 8 2 6 4 4 Explanation of Symbols. * mitral disease, f aortic disease. 502 PERICARDITIS. 100 90 80 70 60 50 40 30 20 10 P UI Cases in which j-1 murmur was established. Cases in which „ murmur les- sened on re- Cases in w was previi Cases M* P UI W 00 - Cases > with a $ hich the 1 nisly hea wit mit orti 33. 19 n. 11 •oporti - covery. Cases in which £ murmur dis- I-1 appeared on recovery. h Enc ral, ac c mur Q p m cases. 8 cas< pain. 7 pai on per cent. leart Ithy. ocarditis. »rtic, or m mur. js of Peric Cases w z cases witn previous valve-disease. i-B K 33. n. of c UI Pain eg Cases in which Endocarditis was absent or doubtful. cases, pain, s with IVER THE ' 63 cas 44 pa pain c . 0 H O Total cases of Pericarditis. M Q b* CD ® F s° ION OF - " O 3 P ® c. a; J* B ® 5' • " Hn Total cases of Simple Endocarditis. the Heart. B , 1 Total cases of Endocarditis threatened or probable. cases. 1 pain. >f the 1 79 cases. 1 pain epigas'm leart. 1-3 or 0 Total cases without indications of Endocarditis. S to Grand total cases of Acute Rheuma- tism. ►d o ►- UI £ cd . m 63 50 h side P 3 - ® 'O ►g £. £ 2. P Total cases of Pericarditis. ses. i of t, est. ortio jASES wi 3 E. C; - •B S' to © ; cases, pain of eart, , chest, r cent. § 5 Total cases of Simple Endocarditis. eh Pain of i 76 33 h side of ca and Total cases of Endocarditis threatened or probable. cases, pain of leart, , chest. ,ses wit' chest. Seart, Side •eg; "'-t Total cases without sign of Endo- carditis. b ~ CD o S' £ S- i IlSS ses. i of t, test. T he d Chest 326 152 h side art, Grand total cases of Acute Rheuma- tism. u* ~ CD *d n £2.£ g § ® 5 * S3 ? *+ 2> ' 10( 90 80 70 60 50 40 30 20 10 PAIN OVER THE REGION OF HEART AND PERICARDIUM. 503 3. Pain was present over the epigastric region, frequently increased and some- times induced by pressure, in one-fourth of the patients with rheumatic pericar- ditis (16 in 63), and in nearly two-fifths of those who suffered from pain over the region of the heart (14 in 38). It would appear curious, at first sight, that pain over the pit of the stomach should be a marked feature in so many cases of Peri- carditis. When, however, we consider that in health the lower boundary of the heart is situated behind the upper third of the ensiform cartilage, and that the pericardial sac, when distended with fluid in Pericarditis, dips downwards so that its lower boundary may be on a level with the point of that cartilage, or perhaps even below it, we see how natural it is that pain should be excited by pressure over the epigastric region. This epigastric pain appeared in only two cases before the supervention of fric- tion sound. Those two patients, how- ever, suffered from a renewal of the pain after the commencement of the rubbing sound, consequently in every case the suf- fering over the pit of the stomach was complained of either at the time of the first observation of the friction sound (7 in 16, including 4 in which the pain and the friction sound were both present on the day of admission), or from one to sev- eral days later (9 in 16). In one-third of the cases (6) the epigas- tric pain appeared at the time when the effusion into the pericardium was at its height, and when the sac bulged down- wards into the epigastric space ; and in four of them it was complained of before, and in four of them after, the effusion had reached its acme. In all these cases the disease had reached a stage in which the heart was separated by the intervention of fluid from the floor of the pericardial sac, which is formed by the central tendon of the diaphragm. The pain in the epigas- tric region in these cases, especially when it is increased or excited by pressure, is therefore seated not in the surface of the heart, but in the lower portion of the pericardial sac. It is natural to suppose that the branches of the phrenic nerve must be the immediate seat of the pain, but the exact anatomical distribution of the phrenic nerve has not yet been ascer- tained. These questions suggest them- selves : is this pain seated in the fibrous tissue, the pericardial surface, or the peri- toneal surface of the affected diaphragm- atic portion of the sac ? Peritonitis affecting the central tendon of the diaphragm has been noticed in few or no fatal cases of Pericarditis, but indi- rect evidence of its existence has been supplied in rare instances by the discovery of partial adhesions of the spleen and liver to the diaphragm in cases with ad- herent pericardium. We may, however, I think, fairly infer that the pain on pres- sure below or at the side of the ensiform cartilage is in these cases due, not to peri- tonitis, but to inflammation of the fibrous structure and pericardial or inner surface of the central tendon of the diaphragm, where it form the floor of the pericardial sac, and the lower and anterior portion of that sac. The distribution of the nerves to the pericardium, like that of the phrenic nerve, has not yet been ascertained, and this interesting clinical question therefore invites the attention of the phy- siologist. 4. In three of the patients affected with rheumatic Pericarditis deep pain was felt between the shoulder-blades, and in one of them this pain was increased by the act of swallowing. Pain in the chest was excited in three cases of swallowing, and in two others it was complained of there after eating. Another patient complained that the ascent of wind from the stomach gave much pain over the posterior region of the heart. In all these instances, amounting to nine, the suffering must have been seated in the back of the in- flamed pericardium, being either constant or induced by local pressure, due to swal- lowing or eructation. In several other cases it is stated that pain was seated in the back, but it is impossible to say, from this description, whether the pain was situated in or near the pericardium or lower down. 5. Pain and fulness after eating was complained of by one patient, and I think it likely that the suffering in this instance was excited by the pressure made by the distended stomach over the lower and back part of the pericardium. We thus see that in a large proportion of my cases affected with rheumatic Peri- carditis, pail! was felt over the heart, fre- quently in front of the pericardial sac, and occasionally behind and below it, the pain being usually fixed, sometimes in- creased by pressure, and less often excited by it. 6. The heart was attacked with a shoot- ing pain, more or less violent, associated either with faintness or failure in the action of the organ, and evidently anginal in character, in four of my patients affected with rheumatic Pericarditis. In two of these cases the heart, already crippled by valvular disease, was attacked with inflammation within and without, but in the others the Pericarditis and en- docarditis seized upon the virgin heart, the valves being previously healthy; one of these two cases proved fatal, and in the other valvular disease became established. In the fatal case (4), a man, aged 27, a carpenter, a darting pain passed now and 504 PERICARDITIS. then from the heart to the right side on the day of his admission. This pain was relieved by leeches, the application of which was followed by faintness. On the 3d his limbs started when he fell asleep ; on the 6th he was seized with delirium and trembling; and on the 7th, the day of his death, he was noisy and restless, and was continually moving his lower jaw. Another patient (15), a servant girl, suddenly became very faint on the even- ing of the 10th day, when she was suf- fering from a relapse of Pericarditis, and was attacked with great pain over the heart. This pain returned on the even- ing of the 12th, when it was also felt be- tween the shoulders. One (3) of the two remaining patients had old standing aortic and mitral dis- ease, and suffered from pain over the region of the heart on the 10th day, when friction-sound appeared. On the 16th day, when the Pericarditis was at its height, when I was examining him, he cried out as if from pain, beginning over the stomach, and begged to be raised up, the dyspnoea becoming extreme, the face being flushed, the perspiration pouring oft it, the lips somewhat livid, and his countenance being expressive of extreme anxiety. He was immediately raised up, and having a towel placed behind him, was as it were slung in it, when he took a little port wine and fell asleep. The other patient (17), ayoung woman, affected with mitral disease, was attacked on the 17th day, when the Pericarditis was at its acme, with great pain over the sternum and the whole front of the chest, the pain passing through to the back. She ultimately died on the 63d day, with smallpox, which attacked her when in a state of extreme exhaustion. If we add to the cases in which there was continuous pain over the region of the heart (38) those others not so affected in which ct, there was pain on pressure over the heart (3) ; 6, pain over the epi- gastric region (2); and c, pain at the back of the pericardium on eructation (1) ; we find that in 44 of the 63 cases of Pericar- ditis, or in 70 per cent., there was pain over the heart or pericardium. II.-Pleuritic Pain in the Side. Pain in the side was complained of in one-half of the cases of rheumatic Peri- carditis (31 in 63). Pain was present over the region of the heart and pericar- dium also in all but 4 of these patients. The pain was limited to the left side in 19 cases, and to the right in only 5, while it attacked both sides in 6 instances. There were, besides the pain, other symp- toms or physical signs of pleurisy in all but seven of the patients thus aliected. Pleuritic friction sound was heard in nearly one-half of those cases (15 in 31) and in five others there was tenderness on percussion over the seat of pain. In a large proportion of the cases the pain was increased or excited by a deep breath (18 in 31), and in four of these it was catch- ing. The pain was induced by coughing or laughing, stooping or moving in four- teen instances, and in three it was "pleu- ritic" or cutting. The first complaint of pain in the side was made after the appearance of the friction sound in 19 of the 31 cases that suffered in this manner; the pain and the friction sound appeared together in seven patients ; and the pain occurred before the friction sound in five. In one, of the five, and three of the seven patient- just spoken of, the pain aftected both sides, having appeared at a late period in one side, and at a period actually or comparatively early in the other. The pleurisy that induced the pain in the side which came into play either with or after the friction sound, was due to two causes; one the extension of the inflammation through the fibrous struc- ture of the pericardium to the pleura covering it; the other, the occurrence of pulmonary apoplexy with its attendant pleurisy. The more frequent appearance of the pain, and the greater spread of the pleu- risy on the left side of the chest than the right, is, I conceive, due in many in- stances to the greater extent to which the inflamed pericardium occupies the left side of the chest than the right, and the great displacement backward of the left lung, and especially its lower lobe, by the distension of the pericardial sac. Per- haps the pressure of the distended peri- cardium on the left bronchus increases the tendency of the left lung to inflamma- tion. In one of the five patients that were seized with pain in the side before the supervention of the friction sound, the pain came on at the first onset of the dis- ease, and at the same time as the affec- tion of the joints three days before admis- sion. I think it likely that this case was attacked with pleurisy and acute rheuma- tism affecting the joints at the same time, the pleurisy being, however, rheumatic in its nature, like the joint affection in this instance, and like the Pericarditis in the other cases. We may have, in short, in these cases, rheumatic pleurisy, just as we may have rheumatic Pericarditis. In another of these cases (20), the pa- tient, a married woman, aged 24, was at- tacked with pain in the joints the day after being wet through, and a week be- irregularity and failure of action of heart. 505 fore admission. She came in with very severe pain in the left side, which had existed for some days, and which was somewhat reduced by leeching. On the 6th day after admission she suffered much in the left side, and a pleuritic friction sound was audible just below the seat of pain. Friction sound from Pericarditis was heard over the region of the heart for the first time on the same day. In this case the pleurisy preceded the Pericarditis by ten days. Pain in the side was, in proportion, twice as frequent as in Pericarditis usually accompanied with endocarditis as in sim- ple endocarditis ; one-fourth of the latter (26 in 108), and, as we have just seen, one-half of the former (31 in 63) being thus affected. A similar proportion of such cases existed among the patients who were threatened with endocarditis, of whom rather more than one-fourth were affected with pain in the side (17 in 63). None of the thirteen cases classed under the heading of "probable endocar- ditis" suffered from pain in the side, and only three of those who were attacked with acute rheumatism ami had no endo- carditis, complained of pain in that re- gion (3 in 71). The pain more frequently attacked the left side than the right in the cases of endocarditis in the proportion of 14 to 6; but among those threatened with endocarditis, the two sides were af- fected in nearly equal numbers, the right side being rather more often attacked than the left in the proportion of 7 to 6. III.-" Pain in the Chest." "Pain in the chest" was present in 30 of the 63 cases of rheumatic Pericarditis. The pain thus described is so indefinite in situation-that it may be seated either at the centre of the chest or at its sides, either over the pericardium or the pleura. Fortunately, to guide us to the actual seat of suffering, the "pain in the chest" was attended in all but two instances with other pain, either over the heart, or in the side, or in both regions. Thus in all but four of the thirty cases, pain was present over the region of the heart or the epigastrium ; in all but nine, in the side ; and in one-half of them (16 in 30) it was situated both over the heart and in the side. In fully one-half of the cases (17 in 30) the pain in the chest was itself associated with symptoms of pleurisy, in the way of being increased or caused by deep breath- ing, or coughing, or it was accompanied, in two instances only, by pleuritic friction sound. There were symptoms of pleurisy in eight of the nine cases in which pain of the chest was not associated with pain of the side, and I think those eight cases may be added to the 31 in which pain in the side was actually present, thus bring- ing their number up to 39 in 63 cases of rheumatic Pericarditis. On the other hand, there were four cases with pain in the chest in which there was no notice of pain in the heart, and I think that these four cases may probably be added to those in which the presence of cardiac pain is stated; thus bringing the total number so affected up from 44 to 48 in 63. Eleven patients suffered from pain in the chest, either previously to admission or before friction sound was audible. In the greater number of these I think that the pain was seated over the region of the heart, and was not due to pleurisy. And I find, giving strength to this view, that in all of these but two, pain was described as being present over the heart. It would be futile to compare the rela- tive frequency of pain in the chest ih Peri- carditis, and in the other various groups of cases in acute rheumatism, since to do so would be to compare unlike conditions under the same name. But it will be in- structive to compare the proportion of cases attacked with pain over the heart, in the side, and in the chest, combined together, with those in which there was no such pain, in cases of acute rheuma- tism with Pericarditis and endocarditis, and with and without simple endocarditis. The accompanying table, and graphic scheme, will show this comparison, the one by study, the other at a glance (see pages 501-502). In those affected with Pericarditis, most of whom had endocarditis also, four- fifths had pain in the heart, chest, or side, and one-fifth had no such pain; in those with endocarditis nearly six-tenths had such pain and over four-tenths had none ; in those threatened with endocarditis, less than one-half had pain, and more than one-half had none ; and in those who gave no sign of endocarditis only one-tenth suffered from this kind of pain, and nine-tenths had no internal pain, thus nearly reversing the proportion that we find in cases affected with Pericarditis. XI.-Irregularity and Failure of the Action of the Heart. Faint- ness. ' We have already seen that in two of the patients the action of the heart, which was powerful and tumultuous be- fore the occurrence of Pericarditis, be- came at a later period feeble, irregular, and intermittent, this state being accom- panied by a look of great anxiety and de- pression. We have also seen that the four patients who were attacked with pain shooting through the heart, experi- enced faintness or failure in the action of the organ (p. 503). 506 PERICARDITIS. In the following case death took place from syncope. A female servant, aged 25, came in on the 7th day of her ill- ness, with difficult, hurried breathing, which was relieved when she was raised, great pain in her chest, cough, which had continued from the 2d day of the attack, mucous rattle, slightly rusty phlegm, a sensation of choking, difficulty in swallow- ing, and great anxiety. The joint affec- tion was slight, and apparently limited to the shoulder. Pericarditis, with friction sound and great effusion, was at its height. She was very ill throughout, perspiration being profuse, the voice husky, the face flushed and anxious, and breathing laborious. Iler face was brighter, and she breathed with ease from the 7th day to the 13th, when her appetite was improving ; but at two hours after midnight, in the early morn- ing of the 14th, when attempting to turn on her side, she became quite pulseless, her face turned livid, and she frothed at the mouth. After taking some wine she gradually recovered. An hour later the sounds of the heart were muffled, and the rubbing noise, which had been harsh, loud and dry on the previous day, could not be detected. In another hour she had a similar attack, in which she died. There were 18 ounces of fluid in the peri- cardium, the heart was covered with honeycomb lymph, and there were patches of pulmonary apoplexy in the left upper lobe. Faintness occurred as a symptom in several of the cases, but in none, besides those alluded to and that just given, did it appear in a threatening form. Although, as we have already seen, in a few cases the action of the heart was unusually strong during the early period of Pericarditis, yet even then, or rather when the attack was first observed, the impulse of the heart was more frequently feeble than strong, and this was especially the case during the remaining course of the affection. Feebleness, irregularity, and even fail- ure of the heart's action, may evidently be induced in these cases by several influ- ences working separately or together, and by the exhaustion of the nervous and general forces induced by the accumulated effect of those influences, all tending to lower and exhaust the power of the heart, and even, as in the case just told, to arrest its action. Among such influences are, the pain and inflammation of the joints when severe, extensive, and prolonged; the pain in the heart and pericardium, the side, and the chest; the existence of endocarditis with its immediate and re- mote consequences ; the presence of pre- vious valvular disease ; the grave influ- ences exerted by great distension of the pericardium, which,-by compressing the vense cavre, the pulmonary veins, both auricles, and the aorta, impedes the sup- ply of blood through the vense cavse and pulmonary veins to both sides of the heart, and through the aorta to the sys- tem, and causes the accumulation of blood in the lungs,-by pressing upon the bifur- cation of the trachea and the left bron- chus, and by lessening the size of the lungs, seriously embarrasses respiration- and by compressing the oesophagus, ren- ders deglutition difficult; and the exist- ence of congestion of the lungs, of pul- monary apoplexy and pleurisy, due to one or more of the causes just named. Besides these, there are two important influences that may induce feebleness, irregularity, and perhaps even failure of the action of the heart; one, the inflam- mation of the superficial muscular fibres of the heart; the other, the inflammation of the nerves situated at the surface of the heart and great vessels. Inflammation of the superficial muscular fibres of the heart, which sometimes occurs in pericar- ditis, paralyzes the affected fibres. This paralysis of the inflamed fibres must in itself embarrass the action of the heart, especially when we consider that those superficial fibres turn inwards by a double entrance at the apex, to become the inner- most fibres of the left ventricle, where they end in the papillary muscles of the mitral valve. But this influence cannot be limited to those fibres, but must extend in a varying degree to the other muscular structures of the organ so as to interfere with the exercise of their power ; just as inflammation of certain limited fibres of a voluntary muscle, say the biceps, while it paralyzes those fibres, interferes with the exercise of the whole muscle. The many and important nerves situ- ated at the surface of the heart and great vessels may be more or less involved in the inflammation affecting those parts in Pericarditis. That accurate physiologist, Dr. Burdon Sanderson, remarks, "that nothing is known either as to the anatomi- cal distribution of nervous elements in the hearts of mammalia, or as to the func- tions which they perform. "1 When, how- ever, we consider that electrical or other excitation of the vagus retards the con- tractions of the heart, and if it is strong enough, arrests the organ in diastole, and in the dog, lessens arterial pressure, while division of the vagi produces acceleration of the contractions of the heart, and in the dog, increased arterial pressure ; that the lower cervical ganglion of the sympa- thetic exercises an accelerating influence, not always in action, on the contractions of the heart; and that in the frog, the ganglion cells contained in the heart are 1 Handbook for the Physiological Labora- tory, p. 263. DIFFICULT AND QUICKENED RESPIRATION. 507 the springs of its automatic movement; and that the surface of the heart is rich in nerves connected with the vagi, the sym- pathetic and the intrinsic ganglia of the heart, and that those nerves are therefore locally affected by the inflammation in Pericarditis; we must, I consider, con- clude that this affection exercises in such cases an important influence, either to stimulate or to injure those nerves and so to accelerate or retard the contractions of the heart, to excite or, more frequently, depress the powers of the organ, and to increase or diminish arterial pressure. It is for the pathologist to ascertain, by direct experiment, the effect of the inflammation or irritation of the nerves on the functions of the heart. It is right that I should mention an- other depressing influence on the action of the heart in Pericarditis, accidentally due, in the case about to be referred to, to treatment. In one case (17) already given at page 498, the loss of blood due to irre- pressible hemorrhage from a leech-bite seemed to produce serious irregularity of the action of the heart. XII.-Difficult and Quickened Respiration. Respiration was disturbed to a marked degree in 49 of the 63 patients affected with rheumatic Pericarditis; it was slightly or not at all affected in 3, and in 11 its character was not recorded. The Pericarditis was severe in 2 only of the 11 cases in which the state of the respira- tion was not noticed, and in none of the 3 in which the breathing was but slightly affected ; but the attack was severe in 37 of the 49 patients in whom the respiration was markedly disturbed. The respiration was rendered difficult and quick by three or four local causes: first, in order of time, the inflammation of the heart, without and within, and of the pericardial sac, including the central ten- don of the diaphragm, and the accom- panying pain in the heart, the sac, and the diaphragm, with the consequent re- straint imposed upon the movements of the latter; after this, the distension of the pericardial sac with fluid, which greatly enhanced the severity of the symp- toms ; and, at a later period, the super- vention of pleurisy with its attendant per- manent pain and stitch in the side, or of pulmonary apoplexy, often accompanied by pleurisy. The breathing is hurried, and rendered laborious by distension of the pericardium, often so as to demand a raised posture, owing to two causes, one, the encroachment of the swollen sac upon both lungs, and especially upon the lower lobe of the left one ; the other, the direct pressure, backwards and upwards, exerted by the fluid in the tense pericardium on the trachea at its bifurcation, and on the left bronchus, a pressure that is materially relieved by the erect posture, and still more by the forward attitude which throws the volume of the liquid forwards and downwards towards the diaphragm and away from the trachea. There was great distress, difficulty, and rapidity of respiration in 24 of the cases of rheumatic Pericarditis, and in one-half of them it is recorded that the patient was raised or propped up. The attack was fatal in 4 of those patients, and se- vere in 18, being very severe in 11. One of those cases, a sawyer, aged 26, who had aortic and mitral valve- disease of old standing, came in feeling low and anxious, and was delirious at night. On the 5th day he was better, the respirations being 20 in the minute ; but on the 10th he had pain and friction sound over the heart, and the respirations rose to 30 in the minute. The dulness over the pericardium increased, and reached its acme on the 19th. On the 16th he was seized with extreme and urgent dyspnoea, which was relieved when lie was raised. The respirations were 70 during the at- tack, and fell after it to 35 ; on the 18th they varied from 36 to 44, and on the 21st, when the pericardial dulness had greatly lessened, they had fallen to 28 in the minute. A man whose case I have already given, had Pericarditis with rubbing sound, on the 53d day, the pericardial effusion being at its height on the 57th. On the 55th the respirations were 44 in the minute, and he had extreme difficulty in breathing, which was relieved by the up- right posture. On the 58th the pericardial effusion had lessened, the respirations had fallen to 24, and he breathed easily in the recumbent posture. Another patient, a servant girl, breathed 32 times in a minute on admission, as well as on the 7th day when leeches were applied over the region of the heart. On the 8th friction sound appeared, and the effusion was at its height next day, when the respirations were 52, and on the 10th her head and shoulders were propped up. On the 11th the effusion had lessened, and her breathings numbered 40. On the 14th there was pleuritic pain, followed by friction sound, and the respirations rose to 48 ; but on the 20th, when there was no pain in the chest, they had fallen to 24. In the following case, a female ser- vant, the breathing rose in frequency a second time during a second wave of in- creased pericardial effusion. On the 6th the respirations were 28 in the minute; on the 7th they were 40 ; on the 9th fric- tion sound was heard over the heart, and on the 10th the pericardial dulness was at 508 PERICARDITIS. its height. On the 12th the effusion had lessened ; she was in a raised position breathing more freely, 40 times in a minute; but on the 17th the fluid in the pericardium had again attained to the full; she had pulmonary apoplexy and pleurisy, and the respirations mounted up to 66 ; but next day, with a renewed dim- inution of the fluid, there was a renewed lowering of the respirations to 44. I would gladly illustrate this point by additional cases, but shall limit myself to one more instance that shows the effect on the breathing of pulmonary apoplexy and pleurisy in cases of rheumatic Peri- carditis. A young man was admitted with pain in the chest and shortness of breath. On the second day friction sound was heard, and pericardial effusion had already reached its acme; leeches gave relief, and the breathing was more free; but on the 6th he had a stitch in the side, and the respirations numbered 60 in the minute ; on the 8th, when he was easier, they were 46 ; but on the 13th pulmonary apoplexy was established, and they had risen to 72. On the 17th he had diph- theria, the respirations being 50; on the 28th this was nearly well, and he raised little phlegm, the respirations being 36, and on the 35th they were 28. We thus see that with pain over the heart and pericardium, the breathing is hurried and distressed, while it is slack- ened and relieved with the relief of the suffering; that with the rise and fall of Pericarditis, with the increase, the acme, and the decline of pericardial effusion, we have an increase, an acme, and a decline in the number of the respirations ; that a second wave of increase in the amount of pericardial effusion, leads to a second wave of increase in the number of the respirations ; and that the respirations are also again accelerated, if, in the later progress of the case, pleurisy should spring up from the spreading of the peri- cardial inflammation; or if pulmonary apoplexy should declare itself, especially if combined, as it usually is, with notable pleurisy. XIII.-Difficulty in Swallowing. There was difficulty or pain in swallow- ing in 13 of my cases of rheumatic Peri- carditis. I have already spoken of cases in which the act of deglutition caused pain over the back of the inflamed pericardium, generally complained of, however, in the chest, by the pressure of the morsel of food upon the inflamed structures during its descent along the oesophagus, where it passes behind the affected region. The difficulty in swallowing, of which I now speak, occurs when the pericardial sac is distended to the full with fluid, and is caused by the compression of the oesophagus between the swollen sac and the spinal column. When the effused fluid lessens, the pressure diminishes, and swallowing becomes easy ; but it becomes again difficult when a relapse takes place and the effusion again increases. When the patient lies flat, the weight of the fluid in the pericardium falls back- wards with full pressure upon the oesopha- gus, and deglutition becomes more diffi- cult ; when, however, he is raised into the sitting posture, and especially if he leans forwards, the volume of the liquid tends forwards and downwards, and swallowing is more easy. A servant girl, aged 16, who had been ill about three weeks, came in suffering much both in the joints and the chest. Iler breathing was laborious and very rapid ; she looked anxious ; dulness was increased over the pericardial region, and a soft friction sound was audible over the heart on pressure. On the 3d day the amount of effusion in the pericardium had reached to its acme ; swallowing was diffi- cult, breathing was accelerated, her face was livid and anxious, she had pain in the epigastrium increased by pressure, and the veins of the neck were full. On the 5th she still had much difficulty in deglutition, but on the 8th the pericardial dulness had lessened all round, and she swallowed much more easily. On the 9th she was more bright and lively, the pericardial dulness had lessened much, but pain came in catches over the heart. On the evening of the 10th she had a re- lapse, she became suddenly faint, her lips turned blue and dusky, and she had great pain over the heart, which was soon re- lieved, but difficulty in swallowing re- turned. Next day the dulness over the pericardium had again increased, and the difficulty in swallowing was very great. On the 12th she was still very ill, but she could swallow more easily, and on the 15th the effusion into the pericardium had again lessened, and she was better. The friction sound was audible until the 17th day. She improved daily and gained strength. The poor female servant, who died from sudden failure in the action of the heart, whose case I have just related, on the day of her admission, when the amount of effusion into the pericardium was great, swallowed more easily when the shoulders were raised than when she was lying flat. One patient, a female servant, had a fourfold attack of difficulty of swallow- ing ; on the second day after admission, from great distension of the pericardium, the effect being heightened by shortness of breath ; on the 4th from diphtheria ; on the 7th from a renewed increase in FULNESS OF THE VEINS OF THE NECK. 509 the effusion owing to a relapse, there being great distress in the chest; and on the 11th to a slighter degree from a second relapse with increase of the pericardial effusion. This case recovered perfectly without valvular mischief, after passing through an attack of pneumonia or rather pulmonary apoplexy and pleurisy. Each patient presents some peculiarity in the way in which deglutition is affected ; but I shall only allude here specially to two more cases; one of them, a youth, could not swallow solids readily, but could drink freely ; the other, a coachman, aged 22, sometimes when drinking had a spasm which stopped his breath before he could swallow. The possibility that diphtheria may be the cause of the difficulty of swallowing must not be overlooked. It was, as we have seen, the intervening cause, in my case (44a), with double relapse, and it was the cause of dysphagia in another patient (55), a young man of 18, a com- mercial traveller, who had diphtheria on the 6th day after the cessation of friction sound, and the 16th after admission. XIV.-Loss of Voice. In the case fatal from syncope, a female servant, to whom I have several times alluded, on the 5th day after admission the voice was husky, and she spoke in a whisper, but she could, with a great effort, speak aloud. She was less husky on the 5th, and on the Sth her voice was more natural. This case tends to support the view that the left laryngeal recurrent nerve may become so affected by the con- tiguous inflammation as to paralyze the larynx. XV.-Effects on the Pulse of Rheumatic Pericarditis. The pulse obeys the same law as the respiration under the influence of the dis- ease ; it rises in number, like the respira- tions, as the disease rises in intensity, is at its greatest rapidity when the disease is at its acme, and falls in number as the disease declines. The increase in the rate of the pulse is not as a rule in propor- tion to the increase in the number of the respirations. During the early stage of the inflammation of the heart, when pain is generally felt and friction sound is audible over the organ, the pulse usually mounts up to 90,100, or even 120, while the respirations increase to from 30 to 40 in the minute, so that at this early period the ratio of the pulse to the breathing is in number as about three to one, instead of maintaining the healthy standard of about four to one. When the amount of the effusion into the pericardium reaches its height, the pulse is usually quicker than it is during the early stages, and on rare occasions it becomes very much quickened, reaching even to 160. More often, however, the pulse is not more rapid at this the stage of the acme of the disease than it is dur- ing its early period. The breathing, as we have just seen, is almost always more quickened and laborious at the time the fluid in the pericardium has reached to its height than at any previous period, so that then the ratio in number of the pulse to the respiration is often two or two and a half to one, instead of main- taining the healthy ratio of four to one. At a later period, when the effusion is les- sening, and the inflammation of the peri- cardium is coming to an end, the pulse, like the respiration, falls in number. At this stage, however, in severe cases, one or other, or even both of the two secondary affections, pleurisy and pulmonary apo- plexy, that quicken the respirations quicken also the pulse, when the num- bers of both, and the proportion that they bear to each other, are as a rule nearly the same that they were during the early period of the attack, the ratio of pulse to respiration being usually three to one. In considering the effects of rheumatic pericarditis on the pulse and respiration, I have separated from each other the advance, the acme, and the decline of the disease, and the two secondary influences, pleurisy and pulmonary apoplexy. In nature, however, those stages melt into each other, and those various causes com- bine and operate together to produce the hurry and distress of breathing and the quickening of the pulse of which I have just spoken. XVI.-Fulness of the Veins of the Neck from Distension of the Peri- cardial Sac. In several of the cases of rheumatic pericarditis there was fulness of the veins of the neck, sometimes with pulsation, during the period that the effusion into the pericardium was at its height, and the sac was distended to the utmost. The fulness of the veins of the neck pre- sent at this period must, I consider, be mainly due to the resistance offered to the return of the blood through the vense cavee into the right auricle, owing to the yielding inwards of the thin walls of that cavity before the pressure of the fluid con- tained in the swollen pericardium. The fluid exerts also direct pressure upon the thin walls of the descending vena cava, which carries on the latter part of its course for the extent of an inch within the pericardial sac. The ascending cava, on 510 PERICARDITIS. the other hand, sustains this pressure to a considerable extent by being short and very large, and by possessing walls thickened by fibrous structure derived from the central tendon of the diaphragm. We may, indeed, measure the degree of the distension of the pericardial sac by the degree of the distension of the veins of the neck. This compression inwards of the right auricle must be looked upon as one of the most serious consequences of pericardial distension, for it materially lessens, or in extreme cases may almost tend even to cut off the supply of blood to the right side of the heart, the lungs, the left side of the heart and the system. The walls of the left auricle, being thicker, do not yield so readily as those of the right, but the compression of the left auricle and of the pulmonary veins by the fluid in the distended pericardium pro- duces its own special mischief by imped- ing the flow of blood from the lung, thus often inducing pulmonary apoplexy. From this joint compression of the sister auricles flows a succession of consequences to which I need not here allude in detail, but which in their turn tend to produce weakening and intermission of the heart, a feeble irregular pulse, and even death from syncope. I shall have occasion by- and-by to speak of the support that the thin walls of the auricles and veins de- rive from the coating of lymph with which they are covered, and which enables them to bear much of the pressure to which they are then subjected. One patient, a servant girl, after being ill for a week and affected severely in the joints for two days, came in breath- ing hurriedly, suffering from pain over the region of the heart, and in great distress. There was dulness over the pericardium from the second space to the sixth, and a loud, harsh friction sound was heard over all that region. The left jugular vein was distended and did not empty during inspiration ; next day the amount of effu- sion had lessened, she improved rapidly, and the friction sound ceased on the ninth day, when a mitral murmur de- clared itself. In another servant, whose case, already referred to, proved fatal, the veins on the right side of the neck pulsated strongly, while those on the left side did so to a less extent, as they did not fill or empty themselves so completely. She died in a fit of syncope on the 14th day. Eighteen ounces of fluid were found in the pericar- dium, and several patches of pulmonary apoplexy were diffused through the upper lobe of the left lung. Another fatal case, a carpenter, who died delirious on the eighth day, presented pulsation in the neck on the second day after admission, when the pericardial effu- sion had reached its acme. This pulsa- tion was partly in the carotids but was chiefly venous and was more marked on the right side of the neck, the veins on that side being fuller than those on the left. On the third day the upper boun- dary of the region of pericardial dulness was lower, having descended from the third to the fourth costal cartilage, and the venous pulsation was not so percepti- ble. I will name two other cases of this class: one, a man who came in with an anxious expression of face : on the fifth day friction sound was heard over the heart, and on the seventh he presented extensive double venous pulsation in the neck : the other, already related, a girl who came in with rheumatic pericarditis, and in whom the veins of the neck were full during expiration on the third day, when the pericardial effusion was at its height and deglutition was difficult. There was visible pulsation of the jugu- lar veins in three of the patients who had been affected with valvular disease of some standing before being attacked with rheumatic pericarditis. In these cases, the venous pulsation was evidently due to the valvular affection. XVII.-Appearance and Expression of the Face during the course of Pericarditis. The face was flushed, dusky or very pallid, or its expression was one of anx- iety or depression, in 43 of the 03 patients affected with rheumatic pericarditis. In six other cases it is stated that the aspect had improved, although there is no pre- vious description of the face. There was thus a marked change in the appearance of the patient in four-fifths of the cases (49 in 63). The face is not mentioned in the remaining thirteen cases, and in one only of these was the attack severe, while it was so in thirty-six of the patients in whom its appearance was notably altered. The face was similarly affected in three- fifths of the patients attacked by endocar- ditis (60 in 108), in less than one-half of those who were threatened with endocar- ditis (27 in 59), and in one-fourth only of those who presented no sign or symptom of endocarditis. The appearance of the face was less and less profoundly altered in these patients, as the class to which they belonged became less and less affected in the heart, and still less in the class made up of those who gave no evidence of affection of that organ. The face was flushed in 19 of the 63 cases of rheumatic pericarditis. Perspira- tion was copious in all but three of these, the perspiration often standing in beads upon the face. The flush, instead of being limited to the cheeks, was diffused over those parts that are usually white APPEARANCE AND EXPRESSION OF THE FACE. 511 even in persons of the most rosy hue, the forehead, namely, the eyelids, the nose, the white skin of both lips, and the chin. I never noticed the color spread at the first blush from feature to feature, but it seemed to tint them all at once. Thus the face was pallid on the day of admis- sion in a fatal case already quoted by me, and on the following day it was flushed all over. But the flush which at first seemed to suffuse the whole face usually vanished step by step ; the pink skin of the upper and lower lips first becoming white, then the nostrils and, in succession, the eye- lids, the chin, the brow, and the cheeks in several of my cases. The face was pale during the period of the friction sound in nine cases. One of these,a female servant,was very pallid and sallow, the features being pinched, when admitted with pericarditis ; while on the following day, the face was rather flushed, and the fever seemed to be greater. Another case, a servant girl, aged 20, admitted with peri- carditis,was flushed on the second day, but on the third, when the fluid in the pericar- dium had reached its acme,deglutition was difficult, and she was depressed, pallid, and weak. The face was twice as often flushed (19 times), as pale (9 times), dur- ing the attack of pericarditis. I have been unable to discover clinical reasons for the difference in these cases of the hue and color of the face. The clinical his- tory of the pallor of the face induced by rheumatic pericarditis is illustrated by a case, the physical features of which I published in 1844 ;* a youth, aged 16, was admitted into the General Hospital near Nottingham, on the 17th of November, 1842, under the care of Dr. Williams, suf- fering from acute rheumatism, with peri- carditis. His countenance was pale, and his surface generally was also pale. On the third day after admission, the general symptoms were milder, although the ex- tent of pericardial dulness had not les- sened, and the face was less pallid, the lips being red. On the sixth, the follow- ing is my report: " The gums are slightly tender, his general appearance improves, the hue of the skin is clear, and rather red ; the reflex influence of disease in con- tracting the capillaries being removed." He made a complete and rapid recovery. In this case, the general surface was pale as well as the face ; but in the cases under analysis, my notes do not, as a rule, de- scribe the hue of the body. The aspect was dusky, muddy, or glazed in sixteen, and the expression of the face was anxious or depressed in thirty-five of the patients affected with pericarditis. I would here briefly compare these numbers with the numbers of those thus affected in the other cases of acute rheu- matism. The face was notably flushed in one- fifth of the cases with simple endocarditis (19 in 108), one-eighth of those threatened with endocarditis (8 in 63), and in one- twentieth of those giving no sign of endo- carditis (4 in 79). The aspect was dusky or muddy in one-tenth of those with sim- ple endocarditis (10 in 108), in one of those threatened with endocarditis (1 in 63), and in one of those who gave no evidence of endocarditis (1 in 79). The expression was anxious or depressed in one-fourth of those with simple endocarditis (25 in 108), in one-sixth of those threatened with that affection (10 in 63), and in one-twelfth of those who presented no sign of inflamma- tion of the heart (6 in 79). I have drawn up these numbers from a careful examination of my case books, and they present an accurate return of the symptoms there recorded. These cases are however necessarily reported with varying degrees of minuteness, and the more severe cases, attracting the greatest interest, are naturally observed and re- lated with greater care than those that present no unusual features. These must therefore be taken not as the actual, but the approximate numbers. Keeping this in view, it must be felt, from what I have said, that rheumatic pericarditis with endocarditis, and to a less degree simple endocarditis, produce a remarkable change on the complexion, aspect, and expression of the face. The attention is at once drawn to the heart by the altered countenance. When the in- flammation of the heart is established, the varying hue and expression of the face tell, with remarkable accuracy, the vary- ing state of the powers of the heart, and of the double inflammation with which the organ is affected. When the tide of effusion into the peri- cardium has reached its height, as I shall illustrate in the next section, the hue of the face is usually more dusky and livid, and its expression more anxious than at any other time; but when the tide has fairly turned, and, the effusion having lessened, the inflammation ceases to be active, the face becomes often quite sud- denly cheerful, while its hue becomes clear; the eye at the same time, instead of being heavy and charged with blood- vessels, becomes bright and clear. After this, if there is no relapse, the powers rally with remarkable quickness and free- dom, and the appetite returns. This state is very different from the convales- cence of fever, which passes through its period of improvement slowly and with scarcely perceptible steps. In a patient, to whom I have already alluded, whose heart acted strongly and 1 Prov. Med. Trans., vol. xii., 1844, p. 532. 512 PERICARDITIS. rapidly at the time of the first onset of the inflammation, the right side of the face was swollen and flushed, evidently under the influence of the attack of pericarditis. What are the causes of this remarkable influence of inflammation of the exterior and interior of the heart on the face ? There are probably more causes than one at work to produce the flushing or pallor present in pericarditis. The mode- rate elevation of temperature present in all cases of inflammation is probably con- nected with flushing of the face, either as a cause, or rather as a common effect. The question must here be put, what is the cause of the moderate elevation of temperature in cases of inflammation? Is it from general relaxation of the arteries, with elevation of temperature, owing to the influence of the inflammation on the afferent nerves of the part affected ? such influence being conveyed to the vaso- motor centre in a manner analogous to that in which relaxation of arteries and elevation of temperature is produced on one side of the head and face by the divi- sion of the sympathetic on that side of the neck, or by the pressure of that nerve by an aneurism of the arch of the aorta. This influence would, of course, only ac- count for the moderate rise of temperature in local inflammation, and does not touch the question of the cause of the increased heat in fevers or in cases of acute rheu- matism with delirium. Putting this cause aside, which applies to every case of inflammation, I would suggest that one great cause of the flush- ing or pallor of the face in pericarditis is the influence of the inflammation on the afferent nerves at the surface of the heart and great vessels, which, being depressed or stimulated, may induce reflex dilatation of the arteries of the head, with flushing of the face, or reflex contraction of the arteries of the head with pallor of the face. I suggested this in principle as the cause of the pallor in the Nottingham case in my note-book in 1842, and am still disposed to do so. In aneurism of the arch of the aorta, pressure on the branches of the sympathetic of one side causes re- laxation of the arteries and elevation of temperature on the corresponding side of the head and face. I consider that a parallel effect would result from the exci- tation or the injury of the sympathetic and sensory nerves, and perhaps of other nerves having, say, a vaso-inhibitory property distributed to the seat of the in- flammation of the heart and great vessels in pericarditis ; contraction of the arteries of the head and face with pallor being produced on the one hand, and relaxation of those arteries with flushing and perspi- ration on the other. In one case only, just referred to, was there flushing and perspiration notably limited to one side of the face. It is natural, however, to ex- pect that as the inflammation affects the nerVes of both sides in pericarditis, both sides of the face should be equally affected, as it was indeed in all but one of my cases of pericarditis affected with pallor or flushing of the face. I would here remark that as the reflex contraction or dilatation of the arteries with pallor or flushing, from excitation or injury of the sympathetic or sensory nerves is continuous, it differs essentially from the reflex movements of the muscles caused by the excitation of an afferent nerve, such movements being necessarily short and intermittent, the withdrawal and renewal of the stimulus to the afferent nerve being needful for their reproduction. In short, the reflex vaso-motor current is continuous, while the reflex excito-motor current (of the muscle) is interrupted. The increased contraction of the arteries caused by the excitation of a sensory or sympathetic nerve appears to be due to the increased discharge of nervous force directly from the vaso-motor centre when that centre is thus stimulated by the ex- citation of those nerves. That 'centre would indeed seem to require, for the ex- ercise of its proper functions, to be rein- forced and stimulated through the sym- pathetic nervous system, and probably by the blood circulating in the arteries, when we consider that the division of the left splanchnic in the rabbit may lower the arterial pressure from 90 millimetres to 41, that excitation of the divided nerve may raise the pressure to 115 millimetres, and that division of the other splanchnic may further lower it to 31 millimetres.1 I would here remark that similar effects are produced by analogous causes in pneumonia, and especially in pneumonia of the upper lobe, when the face, besides being congested, presents a dusky hue and a powerless expression that speak of the profound influence exercised upon it by the disease. In this disease also, as in pericarditis, with the turn of the tide of the inflammation and with the removal of its products, the veil is as it were lifted away from the countenance; and a pa- tient, one day under the weight of the inflammation, with an aspect dark, de- pressed and anxious, presents on the next day, with the removal of the exudation from the affected air-cells, and the renewal of their respiration, a face clear and clean, and an expression bright and cheerful. The eye is every now and then reported to have been dull, and heavy in appear- ance during the attack of pericarditis, its minute vessels being congested ; but it is more frequently described as becoming 1 Ludwig and Cyon, quoted by Dr. Burdon Sanderson : " Handbook for the Physiological Laboratory," p. 249. NERVOUS SYSTEM IN RHEUMATIC PERICARDITIS. 513 bright and clear when the effusion into the pericardium was lessening, and the inflammation was becoming inactive and only present in the shape of its results. I had not, until quite recently, made any close observation of this organ, but in one of the last cases of acute rheumatism with endocarditis treated by me in St. Mary's Hospital, I found that during the acme of the disease, when the face was flushed, dusky and anxious, the conjunctiva was crowded with small vessels which ended a very short distance from the cornea, so that round the clear of the eye there was a white zone or ring edged by fine converg- ing vessels. When the inflammation ceased to be active, and the face, in keep- ing with this improvement, became clear and cheerful, the eye became bright, and the vessels crowding the conjunctiva less- ened in number, so that the ball of the eye became again white. This organ re- quires careful observation in cases of rheumatic pericarditis and endocarditis. XVIII.-Condition of the Face when the Pericardial Distension was at its Height. When the pericardium is distended to the full with fluid, under the three-fold influence of (1) what may be termed the " fluid" pressure, induced by the disten- sion of the sac bearing with varying force, outwards upon the oesophagus and trachea, the left bronchus, the lungs, es- specially the left, and the diaphragm; and inwards on the descending vena cava, the right and left auricles, and the pul- monary veins; (2) inflammation involv- ing the nerves distributed to the surface of the heart and the great vessels ; and (3) inflammation of the superficial mus- cular fibres of the heart itself; as we have seen, point by point, pain may be present around and within the heart, over the pericardial sac and the pleura ; swallowing may be difficult ; the voice may be hoarse or reduced to a whisper; the action of the heart, which at the be- ginning of the attack is often forcible, may become feeble and intermitting, or even altogether fail; the respirations may be hurried and laborious, often so as to compel the raised and forward posture; the pulse may be rendered weak and ir- regular and be quickened, though not in the same proportion, as the breathing, the ratio of the pulse to respirations being two or three and a half to one, instead of, as in health, four to one ; and the veins of the neck may be swollen and pulsating. The last effect of the over-distension of the pericardium that I shall illustrate is that upon the circulation of the head and face. A female servant whose case has already been alluded to was admitted with acute rheumatism and pericarditis of great severity. On the third day, I found that the pericardium was distended to the full, she complained of a sensation of choking, swallowing was difficult, the countenance was anxious, the face was livid and perspiring profusely, and the veins of the neck were full. On the sixth day the pericardial dulness had lessened all round, her face was less dusky, and her aspect had improved. On the tenth, in the evening, she suddenly came over faint, the lips being blue, and the face dusky; but in a few hours the face, though still anxious, lost its dark hue and the lips became again red. Next day it was found that the pericardial effusion had again increased. The fluid, however, soon again diminished. On the twelfth her aspect had again improved, on the fifteenth her face was flushed, and on the sixteenth it was of good color, and its ex- pression was no longer anxious. Here, twice over, the effusion in the pericardium reached its acme, and under the influence of its pressure and the inflammation of the organ, the heart faltered, the venous blood was delayed in its passage, the arterial blood was with difficulty supplied, the face and neck became charged with venous blood, and the lips became livid ; and here, twice over, the pressure was re- moved by the lessening of the fluid, when the color returned to the face and the ex- pression of anxiety disappeared. XIX.-Affections of the Nervous System in Rheumatic Pericarditis. Dr. Davis, of Bath, in the year 18081 published three cases of acute rheuma- tism, two of them being affected with pericarditis, and one with endocarditis. One of the cases of pericarditis, which was observed in 1785 by Dr. IIay garth- who curiously does not mention this im- portant case in his "Clinical History of the Acute Rheumatism," published in 180G-was affected with moaning, rest- lessness, and delirium ending in death. The other case of pericarditis, a young lady, who was under the care of Dr. Da- vis, had great heats, with perspiration, screaming, and the most violent jactita- tion of the body, "occasioned by the ex- treme anguish which she felt in the region of the heart." She was perfectly sensi- ble throughout, and died after the disease had lasted twenty-six days. The patient with endocarditis was affected with want of sleep and violent delirium, for nine days, at the end of which time she died. 1 "An Inquiry into the Symptoms and Treatment of Carditis," by John Ford Davis, M.D. vol. n.-33 514 PERICARDITIS. In a series of important clinical contri- butions, Corvisart, Mr. Stanley, Dr. Aber- crombie, Dr. Macleod, Andral, Dr. La- tham, Dr. Bright, Dr. Mackintosh, M. Bouillaud, Sir Thomas Watson, Sir George Burrows, and Dr. Kirkes, have described cases of pericarditis, some connected with acute rheumatism, but many not so, in which delirium, coma, convulsions, tem- porary insanity, chorea and choreiform movements, or tetaniform symptoms and rigidity, and even actual tetanus were present. These observations suggested to several of those authors, including Andral and Dr. Bright, a close connection amounting even to cause and effect, between pericar- ditis and the affections of the nervous sys- tem associated with it. The affections of the nervous system in cases of rheumatic pericarditis, and acute rheumatism are always serious, often fatal, and comparatively rare. Recent observations have shown in many of those cases the presence of a very high temper- ature, delirium and coma, ending in death. I shall therefore, in inquiring into the clinical history of those associated af- fections, examine those cases admitted into St. Mary's Hospital under my care during the twenty years that I have held office, and all the published cases that I can find of this class. I have brought together from various sources, 180 cases of acute rheumatism with affections of the nervous system, more than one-half of which had pericar- ditis (92 in 180). The temperature of the body was recorded in one-third of the total number of cases (61 in 180) ; and al- though these cases were observed at a much more recent period than those in which the temperature was not recorded, I shall examine the more recent series of cases first, for they throw light upon the old series of cases.1 Cases of Acute Rheumatism with Affections of the Nervous Sys- tem, in which the Temperature of the Body was Observed. Dr. Sydney Ringer published in the year 1867, three cases of acute rheuma- tism with pericarditis, in which the tem- perature rose before death respectively to 109-2°, 110-8°, and 110'0°.2 These three patients had delirium, followed by coma and death, and one of them was under the care of Dr. Reynolds as early as May, 1862. Dr. Kreuser related in 1866' three fatal cases, of acute rheumatism in which the temperature rose respectively to 109-4°. 110"2°, and 110-4°, and these three pa- tients were affected with delirium, and one of them with coma also. More recently an important series of cases of this class have been communi- cated by Dr. Hermann Weber in an im- portant paper, Dr. Murchison, Dr. Bur- don Sanderson, Dr. Greenhow, Dr. Southey, Dr. Henry Thompson, Dr. Me- ding, Mr. Anderson, Dr. Wilson Fox, whose work on the treatment of hyperpy- rexia is of great value, and Dr. Andrews. I have brought together from these and other sources, sixty-two cases of acute rheumatism, affected with coma, delirium, chorea, or convulsive choreiform, or te- taniform symptoms, in which the temper- ature was observed during the progress of the illness. Of the sixty-one cases in which the ner- vous system was affected, and the tem- perature was ascertained-I. twenty-seven had pericarditis ; II. thirteen had simple endocarditis ; and, III. twenty-one were free from pericarditis, endocarditis being absent or doubtful. I.-Cases with Pericarditis in which the Nervous System was affect- ed, and the Temperature, gener- ally VERY HIGH, WAS OBSERVED. SUMMARY. A.1 Had coma without delirium, maxi- mum temp. 110° . . .1 A3 Had delirium followed by coma, temp. 110-8°-104-6° . . .11 A4 Had delirium followed by stupor, temp. 106°-103° .... 1 Had delirium and convulsive move- ments, temp. 107°-110'2° . . 1 -B' Had uncomplicated delirium, temp. 110-40-103° 9 Had delirium with general stiffness, temp. 103-2-102-2° ... 1 Had temporary or partial coma, temp. 101-8°9-9-3° . . .2 Cl Had chorea, temp. 101-5° . . 1 Total . . . .27 The temperature of the body was ob- served in twenty-seven cases of rheumatic pericarditis with affection of the nervous system, and was very high in three-fifths of them (15 in 27), their highest tempera- ture varying respectively from 106-8° to 115-8°. Five of these cases were placed in a cooling bath, when their tempera- ture, then at the highest, was ascending [' The Tables which here follow are omit- ted in the present edition, on account of their bulk and complication.-H.] 2 Medical Times and Gazette, 1867, ii. 378. 1 " Medicinisches Correspondenz-Blatt des Wurttembergischen ar tzlichen V ereins, ' ' ban d xxxvi. p. 105. TEMPERATURE IN NERVOUS COMPLICATIONS. 515 rapidly, with the effect of arresting its rise, cooling the body, and, in four in- stances, leading to the recovery of the pa- tient. The bath was employed also in two cases in which the temperature was 105° and 105'5° respectively, with the effect of cooling the body; but as the ascent of the thermometer was neither rapid nor very high, those cases can scarcely be included with those of hyper- pyrexia. The temperature was 104'6® and 105'3° respectively in two cases dur- ing the period of delirium, but was not observed during that of coma, and I therefore think that both those cases may be included with those of hyperpyrexia- which bring their number up to seventeen, or two-thirds of the total number of cases with Pericarditis. Seven of the remaining ten cases, or one-fourth of the total number, had a high, but not very high, temperature, varying from 103° to 106°, so that these cases would rank, as regards the heat of the body, with fever or pyrexia. The tempe- rature was only moderately high in the three remaining cases, or one-eighth of the total number, varying from 99'3° to 101-8°. A1 Profound coma, without delirium, was present in one case; A3, 4, delirium that passed into coma in eleven cases, into stupor in one case, and into convul- sive movements in one case; B, uncom- plicated delirium was present in nine cases, one of which had Bright's disease; and delirium with stiffness of jaws, neck, and limbs occurred in one case. Tempo- rary coma occurred in one case, and semi- consciousness in another, both with albu- men in the urine; and C1 chorea and slight continuous contraction of certain muscles existed in one case. A' The case of coma without delirium, a woman, was under the care of Dr. Wil- son Fox,1 with acute rheumatism and Pericarditis. The temperature was about 102° on the morning of the fourteenth day of illness, and had risen to 108'4° at 9.15 P. M., when she became entirely uncon- scious, and to 109'1° at 9.50 P. M., when she was put into a bath at 96°, and ice was applied to her body. She was uncon- scious, pulseless, and cyanotic, her respi- rations were irregular, gasping, and ster- torous, and she appeared to be dying. In half an hour her temperature had fallen to 106'2°, when the pulse became percep- tible, and she showed signs of conscious- ness. In ten more minutes the tempera- ture was 103'6°, and she was taken out of the bath, and twenty minutes later it had fallen to 100'1°, when she could speak, and had imperfect consciousness. After various oscillations, this patient recov- ered. I relate this case here briefly not to illustrate the treatment, but to show that profound coma became established when the temperature was excessively high, and that consciousness was restored when the body was cooled. A3 Ten cases, in which delirium was followed by coma, and in which the bath was not used, proved fatal, but one such case recovered after the employment of the bath. Delirium appeared at a temperature of from 103° to 104'8° in eight of the eleven cases in which coma was preceded by de- lirium, the temperature in six of these being at or above 104° when the dis- turbed state of mind was first noticed. In three of these cases delirium was still present when the thermometer was as high as from 107° to 108°, and in one of them when it was as low as 99'6°. Profound coma declared itself when the temperature had risen from 109° to 109'4° in five of the eleven cases in which com- plete unconsciousness followed delirium, when the thermometer stood at 108'4° in one of them, at 106'8° in another, and at 106'6° to 107'6° in another, in which the coma, not profound, was transient. In several of these cases it was noticed that the temperature rose between the supervention of coma and death. The delirium was violent in five of those eleven patients who passed from delirium into coma, two of whom got out of bed ; was active in three of them ; and resembled delirium tremens in two, while in another the manner was strange and excited, and the sentences were discon- nected and incoherent. The transition from a state of violent or active delirium to coma was usually grad- ual. Muttering replaced active delirium in three instances, the muttering delirium being accompanied by restlessness in two of them. A state of semi-consciousness, accompanied by moaning in one and by restlessness in the other, intervened in two cases between the period of delirium and that of coma; and two other cases passed from delirium to a state almost of unconsciousness, and from that to coma. Violent delirium ceased abruptly after venesection in one patient, who was quiet for a short time, but soon passed into a state of perfect unconsciousness. The duration of the delirium was very various in the different cases, lasting in one case about three-quarters of an hour, and in another eight days. The delirium was more frequent by night than by day, and lasted from one to four nights in four cases in which it was scarcely observed during the day. The period of coma varied much less than that of the delirium, lasting from a quarter of an hour to seven hours in nine of the eleven cases with delirium and 1 "Treatment of Hyperpyrexia," by Dr. Wilson Fox, p. 2. 516 PERIC ARDITIS. coma. In one of the remaining cases, the duration of the coma was prolonged, death being delayed, and in another of them consciousness was restored, and re- covery was established, by the use of the bath. The two cases were fatal in which de- lirium preceded semi-stertorous breath- ing, with violent spasmodic movements of the whole body in one instance, and profound stupor in the other. The tem- perature in the former case rose to 110'2° before death, but in the latter it was never higher than 106°. Dr. Murchison favored me with the leading features of that case. Bl Delirium without coma or other im- portant modifications affected nine cases of acute rheumatism with pericarditis. These cases divide themselves naturally into two groups ; in the first group, con- sisting of four, the delirium was of the usual character, and the temperature was very high, varying from 107'3° to 110'5°, and was kept in check in two of them by the cooling bath; while in the second group, containing four cases, the tempera- ture was not so very high, varying from 103'3° to 105'3°. The delirium was ac- companied by tremor, and usually by hal- lucinations, and a general condition resem- bling delirium tremens. The remaining case of delirium belongs to neither of these groups, since the delirium was slight, and gave way to general emaciation, ending in death. Delirium was present throughout in one of the four cases with very high tempera- ture, and in that patient it ranged from 103° to 105'6°, and ascended to 107'4° during the last ten hours. Death was sudden. The second case, a coachman who had lived well, was under the care of Dr. Wilson Fox.1 His temperature was 107°, his pulse 100-108, respiration 44-45. At 2 A. M. he was put for twenty- five minutes into a bath at 89° to 86°, when his temperature fell from 107° to 103 T°, and he became perfectly conscious. Fifteen minutes after the bath his tem- perature had fallen to 98°, when his pulse was 84, respiration 20, and he was per- fectly rational and conscious. The peri- carditis in this case was of unusual dura- tion and severity. The bath, the wet-pack, or the ice-bag was employed during the next six days to keep down the tempera- ture, which had a strong tendency to rise. This patient recovered. In another case, a man, the temperature was lowered by the bath from 108'2°, when he was de- lirious, to 103'8°, when he could answer questions rationally. A second bath low- ered his temperature from 105° to 102°, and thirty-five minutes after his removal from it, to 98'7°, when he was quiet. Ue recovered slowly.1 One of the four patients with tremor, hallucinations, a state resembling delirium tremens, and a temperature not exces- sively high, who was under the care of Dr. Southey, was an intellectual, nervous man, and a drinker of beer. His tongue and hands were at a temperature of 10o° ; he was placed in a bath at 71° for ten minutes, when he felt cold, talked ration- ally, and thought it the queerest treatment for rheumatism. He was wet-sheeted whenever his temperature rose to 104°, when he was always delirious. He died with bronchial symptoms. Sir William Gull saw the case, and suggested that it indicated the association of acute rheuma- tism with delirium tremens.2 The next case resembling delirium tre- mens was a poorly nourished, pale man. The bath lowered his temperature on the first occasion from 104-3° to 99'8°, and on the second from 105'3° to 101'6°, when he was rational, and aftei' the second bath he had visits sardovicus^ his limbs were tremulous, and he remained delirious until the fourteenth day (temp. 103'4° to 100'2°). After this he steadily improved.3 Dr. Southey favored me with the notes of an- other case of this class, a poorly nourished, anaemic man, a coachmaker, who had been ill ten days. When admitted (temp. 103°), his tongue was tremulous, and he per- spired profusely. On the fifth day he had pericarditis; on the seventh night, con- stant muttering delirium ; and next day an abrupt manner. On the ninth, after a delirious night, his hands were tremu- lous. On the seventeenth day his skin was hot and dry, temp. 103'8°; and the activity of his mind resembled what is observed in delirium tremens, but he had no horrors. The ice-bag was applied to his head on the eighteenth, and as he was sleepless, he had 30 grains of chloral, after which he slept for four hours. On the following day he was conscious, had pain in the knees and shoulders, perspired less, and looked better, but still had some tremulousness and jactitation. His respi- ration and temperature steadily fell, and he gradually recovered. The fourth case was a constable, who ten years before had been unconscious after a kick. His highest temperature was 103'3°, but it rarely exceeded 102°. In the course of his illness he had delirious nights, choreal movements of the left hand, on one occasion tremor of the right hand, hallucinations, and frequent rolling of his head from side to side. He im- 1 Dr. Andrews, "St. Bartholomew's Hos- pital Reports, x. 338. 2 Lancet, 1872, ii. 562. 3 Dr. Andrews, " St. Bartholomew's Hos- pital Reports," x. 350. 1 "Treatment of Hyperpyrexia," p. 10. TEMPERATURE IN NERVOUS COMPLICATIONS. 517 proved slowly, but remained for some days incoherent and childish in manner.1 B1 Delirium with stiffness of jaws, neck, back and limbs, occurred in a patient of Dr. Bristowe's, a bargeman, aged 21, with slight acute rheumatism, pericarditis, and endocarditis.2 Two cases, one affected with temporary unconsciousness, the other with stridor and semi-consciousness, were under my care in St. Mary's Hospital. They had albumen in the urine, and were both fatal. The first case had previous aortic and mitral valvular disease. The second had a presystolic murmur, and mitral and tri- cuspid systolic murmurs, and the inspec- tion after death showed pericarditis, but- ton-hole contraction of the mitral valve, and acute Bright's disease of the kidneys. C1 Choreal and continuous contraction of some muscles occurred in the following case, a delicate, excitable girl, aged eleven, for observing which I am indebted to Mr. Saunders. When I first saw her, about the tenth day of her illness, a loud peri- cardial friction sound prevailed over the whole front of the chest, extinguishing all other heart-sounds. Ten days later, temp. 101 '5°, she took little notice, bent and ex- tended her right arm and hand irregular- ly, but bent the hand backwards on the forearm, flexed the fingers, and pointed the right great toe downward, by the con- tinuous, but not constant, contraction re- spectively of the flexors and extensors of the forearm and the muscles of the calf. The face was still, the tongue protruded itself steadily and for long ; her body was quiet, and speech was limited. During the night she alarmed her mother by screaming violently, throwing herself about the bed, and tossing her head from side to side. After about twenty minutes she became quiet and fell asleep. Four days later she had a return of pain and swelling in the right knee, friction sound was barely audible over the heart, and the movements of the right arm had lessened and were more simply those of ordinary chorea. The affection of the joints during the early period of the attack of acute rheu- matism was severe in three-fifths (15 in 27), and of moderate severity in one-third of the patients (8 in 27), not severe in two I instances, and in one, the condition of I the joints was not described. The affec- [ tion of the joints disappeared, or was much lessened in severity at the time of the delirium, coma or chorea in all those cases (20 in 27) in which the condition of the joints is described. In thirteen cases the affection of the joints was well at the period in question ; in four it was slight, and in three it was not severe. The invariable subsidence of the inflam- mation of the joints in these cases, when affection of the nervous system takes place, shows that there is some connection between the appearance of the one affec- tion and the disappearance of the other. The improvement of the inflammation of the joints generally coincides with im- provement of the general symptoms, unless the heart is inflamed. We may therefore, I think, infer that the presence of trouble in the nervous system, whether accompanied or not by a very excessive rise in temperature, has a distinct associa- tion with the lessening of the affection of the joints. The perspiration, before the nervous system was affected, in these cases was noted in ten of the fourteen cases with coma, stupor or convulsions preceded in all but one instance by delirium, and dur- ing that early period it was profuse in seven, and moderate or slight in three of those ten cases. The perspiration was observed in eleven of the fourteen cases just noticed during the period of delirium or coma, when it was absent in three, slight in four, moderate or considerable in two, and profuse in two of these eleven cases. The perspiration was noted both before and during the period of the delirium or coma in nine of those fourteen cases. In eight of those nine patients, the tempera- ture was excessively high at the time of the delirium or coma, and perspiration was then absent or lessened. In one case with delirium, the highest temperature observed was only 103'8°, and perspira- tion, previously moderate, was then pro- fuse. The perspiration was observed during both periods in four of the nine cases in which delirium was present without coma or stupor, and was profuse in those four cases during the early period of the dis- ease. One of those patients had on pre- vious days perspired freely, but the skin became dry when the temperature rose to 107'3°. In another of them, the skin pre- viously perspiring, felt hot and dry when delirium appeared at a temperature of 103'8°. The perspiration remained pro- fuse in two cases during the period of delirium with hallucinations and tremor, the temperature being then respectively 105° and 102°. Both of those patients were predisposed to affections of the ner- vous system. Dr. Wilson Fox justly re- gards the cessation of perspiration while the temperature is still high as a symp- tom of very great gravity. It would ap- pear from what I have just stated, that the cooling influence of the perspiration may have kept down the temperature in the three latter cases, while in the ten former cases the want of that cooling in- fluence may have allowed the tempera- 1 Dr. Greenhow, Clin. Soc. Trans, vii. 172. 2 Path. Trans, xxiv. 518 PERICARDITIS. ture to rise unchecked when heat was supplied from within by the rapid com- bustion of the tissues of the body during the disease. The presence of a miliary eruption or sudamina was noticed in nearly one-half of the cases (12 in 26). The Pericarditis was of average inten- sity or severe in eleven and slight in three of the fourteen cases with coma, stupor, or convulsions, in all of which but one the more grave affection of the nervous sys- tem was preceded by delirium. In seven of the nine cases with uncomplicated de- lirium, the pericarditis was of average severity, and in two of them it was slight. The pericarditis was of average severity in the remaining three patients, in none of whom was the temperature above 101'5°, none of them having transient coma, one of them coma, and the other choreal symptoms. We shall be better able to consider whether the presence of pericarditis had any influence in producing the excessive rise of temperature in cases with " hyper- pyrexia" when we have inquired into the whole chain of cases, those namely with- out as well as those with that affection. Endocarditis was present in nearly one- half of these cases, with pericarditis and affection of the nervous system (11 in 26), was absent in almost as many (9 in 26), and was doubtful or not noted in the few remaining cases (5 in 26). Convulsive, Choreiform and Tetaniform Movements.-Movements of a convulsive, choreiform or tetaniform kind affected nine of the twenty-four patients with acute rheumatism and pericarditis in whom the temperature was observed, including the case just related in which choreal symptoms were present without delirium. Besides these, two patients affected with delirium had distinct risus sardonicus. One of these patients, a shopman in a cigar shop, aged 28, had in the morning muttering delirium, and a temperature of 107°. In the afternoon he had violent spasmodic movements of the whole body, his respirations were semistertorous, his temperature was 110'2°, and an hour later he died.1 Another of them, a female ser- vant, being violently delirious, temp. 107'8° F., was bled, and became, as I have already stated, abruptly uncon- scious. Then succeeded a peculiar series of irregular muscular movements of the hands and arms, with chattering and grinding of the teeth, and convulsive move- ments of the jaw, or trismus. Fully two hours later, after being in the bath, when she had cooled down to 104°, she had an attack of clonic spasms of the muscles of the arms, lasting some minutes.1 There were muscular twitchings of the limbs in three patients when in a state of uncon- sciousness. One patient, a police-constable, aged 23, who, ten years previously, had been unconscious from a kick in the mouth, after little sleep, had wandering, much jactitation, constant movement of the lingers of the left hand, tremors of the right hand, and subsultus. Two days later there was also frequent rolling of the head from side to side. His tempera- ture was not above 102°.2 Another pa- tient, a woman aged 29, also rolled her head from side to side, contracted her brows, and distorted her face into various grimaces. Iler temperature was 107 '8°.3 One patient, a man aged 23, on the even- ing before he died, temp. 105'4°, was very delirious, and rolled violently about the bed, so that he required to be held down. This violence quickly passed away, and he then lay half unconscious and moan- ing loudly. Symptoms of a more or less tetaniform character, that is to say, with continuous rigidity or contraction of muscles, ap- peared in five of the cases. Dr. Wilson Fox's patient, already sketched at page 516, after the bath, temp. 100'6°, had at times spasms of rigidity of the muscles of the lips and neck, but not of the limbs. Another patient, a gardener, seven hours before death, became incoherent, and within ten minutes, unconscious ; his lips pouted and rubbed incessantly over the teeth, and his whole.voluntary muscles twitched con- stantly.4 The third is that of Dr. Wilson Fox just referred to, with chattering and grinding of the teeth, and convulsive movements of the jaw, or "trismus."5 The fourth case is Dr. Greenhow's, already noticed, with choreal movements of the left hand. When that hand was turned on to its back,6 there were con- stant twitching movements of the hand and fingers, and the forefinger became flexed towards the palm. The fifth case is my own, already related at page 517, with choreiform movements of the right arm. Her right hand was bent back- wards, her right fingers were flexed, and her right toe pointed downwards, owing to the continuous contraction of the cor- responding sets of muscles, which offered steady resistance when put on the stretch. 1 Dr. Fox, "Treatment of Hyperpyrexia," 44. 2 Dr. Greenhow, Clin. Soc. Trans, vii. 175. 3 Dr. Sydney Ringer, Medical Times and Gazette, 1867, ii. 380. 4 Mr. Anderson, British Medical Journal, 1871, i. 529. 5 Loc. cit. p. 48. 6 Loc. cit. p. 174. * Dr. Murchison, Clin. Soc. Trans, i. 32. ACUTE RHEUMATISM WITH SIMPLE ENDOCARDITIS. 519 These five cases seem to suggest a com- bination of convulsive, choreiform and tetaniform movements. The question naturally arises, were the cases presenting choreiform movements associated with endocarditis ? The an- swer to that is, however, as regards these cases, definitely in the negative, for en- docarditis was absent, or not observed, in those cases, excepting to a slight and doubtful degree in one of those with mus- cular twitching. Endocarditis was, how- ever, present in Dr. Wilson Fox's case with spasms of rigidity of the muscles of the lips and neck. I shall again briefly consider these cases when I return to the important question of the association of pericarditis with tetaniform and chorei- form movements. Tremor was present in seven of the cases, all of which have been already alluded to. II.-Cases with Simple Endocarditis in which the Nervous System was AFFECTED AND THE TEMPERATURE, GENERALLY VERY HIGH, WAS OB- SERVED. SUMMARY. A3 Had delirium followed by coma, temp. 104'4°-110'2° . . .4 A2 Had delirium and convulsive move- ments, temp. 111'6° . . . 1 B' Had uncomplicated delirium in three, temp. 108'5°-lll'4°; in two, temp. 102'8°-103'9° . . 5 B2 Had delirium, cerebral embolism and hemiplegia, temp. 103° . 1 B3 Had delirium and chorea (minute cerebral embolism) temp. . . 1 Had high temperature without notice of delirium, temp. 105'8° (ice-bag) . 1 Total . . . .13 The nervous system was affected in thirteen cases of simple endocarditis in which the temperature was observed. The majority of these cases, like that of those affected with pericarditis, presented an excessively high temperature ; and in three of the whole number the tempera- ture, when undergoing a rapid ascent, was arrested in its rise, lowered, and kept down by the use of the cooling bath or the external application of the wet sheet and ice. The temperature was as high as from 108'5° to 111'6° in three-fifths of the cases (7 in 13) ; and in the one of those cases in which the temperature was the lowest, 108'5°, the vigorous use of ice- cold water within and without arrested the rise of temperature and induced its permanent lowering, followed by the re- covery of the patient. In one patient the temperature was checked at 105'8°, and brought down by the bath ; and in an- other the thermometer was at 104'4° dur- ing the period of delirium, but was not employed during that of coma. In four of the cases the temperature was only of a moderate height, being from 103'9° to 102'3° ; and we may therefore infer that fully two-thirds of the cases with simple endocarditis (9 in 13) in which the nerv- ous system was affected, had " hyperpy- rexia." A2'3 Twelve of the thirteen cases had delirium, which passed into coma in four instances, ended in convulsive movements in one, Bl was without complication in five, was associated with B2 cerebral em- bolism and hemiplegia in one patient, and with B3 minute cerebral embolism and chorea in another. In one instance, in which the temperature was high (105'8°), there was no note of delirium. A3 One of the four cases in which de- lirium passed into coma was a delicate, ailing woman. On the seventh day her temperature in the morning was 102°, but it rose in the evening to 109'5°, when she was comatose. For want of a bath, she was taken downstairs, placed, doubled up, in a washing-tub containing water at 80° cooled to 62°, and cold water was ladled over her body. Spasms soon came on, which were more and more continu- ous until she was taken out of the bath in one of them after being there for forty- five minutes, while her temperature had fallen to 100'3°. Towards midnight she was much convulsed, the teeth closing firmly on the lower lip and drawing blood. On the tenth day the temperature rose to 105T°, she was again put into the tub for fifty-eight minutes, and at the end of that time was taken out in a state of well- marked opisthotonos, which passed off gradually in about two hours. She died on the twelfth day.1 Bl Three of the four cases with de- lirium without coma had high tempera- tures, 111'4°-108'5° ; while in two the temperature was comparatively low, 103'9°-102'8°. One of the patients with delirium and high temperature was a female servant aged 22. On the eighth day of treatment, temp. 108'5°, her sen- sorium was much disturbed, and her skin, which hitherto had been moist and some- times covered with sweat, was dry. Cold was used energetically. Ice-cold water and cloths were applied freely to the body, and ice-water enemata were given every half-hour. In an hour's time she breathed more freely, her head was re- lieved, and the pulse fell. At half-past six in the evening her temperature was 98'6°, skin perspiring, mind clear, and she felt like a new-born person. Two 1 Dr. Andrews, "Bartholomew's Hospital Reports," x. 346. 520 PERICARDITIS. days later she sat up in bed, and took food with appetite.1 In the two cases with comparatively low temperature the delirium was only present during the night. The tempera- ture was 103'9° in the daytime in one of these patients, and 100'4° in the other. Convulsive movements affected four of the thirteen patients belonging to this group with endocarditis. The affection of the joints was severe in eight and was rather severe in one of the thirteen cases with simple endocarditis before the period of delirium or coma; while it was absent in two and not severe in three; and its condition was doubt- ful in four of those cases during that period. Perspiration was profuse in five and ab- sent in one of the cases of simple endocar- ditis before delirium set in ; and it was absent in two, slight in one, probably profuse in one, and doubtful in two of those cases after the appearance of de- lirium, while it was profuse in another patient who was delirious when admitted and whose temperature never rose above 102'8°. III.-Cases in which there was no Pericarditis, Endocarditis being ABSENT OR DOUBTFUL, IN WHICH THE Nervous System was affected, and the Temperature, generally VERY HIGH, WAS OBSERVED. SUMMARY. A3 Had delirium followed by coma, temp. lll'l°-105'8° . . .6 A4 Had delirium followed by somno- lence, temp. 106°.... 2 Bl Had delirium uncomplicated, temp. 110° to 100'4° . . . .10 Very high temperature without de- lirium, temp. 110'8°-106'3° . 2 Twitching of limbs, temp. 102° . . 1 Total . . . .21 Twenty-one cases had no pericarditis, endocarditis being absent or doubtful; and the majority of these cases, like that of those with pericarditis and with simple endocarditis, presented an excessively high temperature; and in five of the whole number the temperature, when undergoing a rapid ascent, was arrested in its rise, lowered, and kept down by the use of the cooling bath, the wet sheet, or ice. The temperature was as high as from 106° to 111'2° in three-fifths of the cases (T2 in 21), being kept down in the one of those in which it was the least high by the use of the cooling bath. In one-fifth of the cases (4 in 21)," the highest ascertained temperature varied from 106° to 103'4°, and in these the cooling bath was not employed. In one-fourth of the cases (5 in 21), the highest temperature varied from 102° to 100'4°. From this summary it would appear that three-fifths of these cases of acute rheumatism with- out pericarditis, endocarditis being absent or doubtful, in which the nervous system was seriously affected, had hyperpyrexia. Pericarditis was absent and endocar- ditis was absent or doubtful, as we have just seen, in twenty-one cases of acute rheumatism in which there was affection of the nervous system and the tempera- ture was ascertained. A3 In six of those cases delirium gave place to coma, and in one of these the delirium reappeared ; A4 in two delirium passed into somnolence. B1 Delirium without coma was present in ten cases. Two patients had very high temperature without delirium, one of whom was restless and talked when asleep, and the other had vomiting and dyspnoea ; and in one there was twitching of the limbs and body without delirium, the temperature not rising above 102°. A3 The whole of the six cases in which delirium passed into coma were fatal. The delirium was present in these pa- tients when the temperature varied from 102'2° to 108'4°, and coma replaced the delirium in five of them at a temperature ranging respectively from 108° to 110°. The highest temperatures observed in these cases towards or at the time of death was from 109'5° to 111'1°. In a case in which delirium gave place to coma and that again to delirium, the temperature about the period of coma was 104°, but eight hours before death it was 105.8°.1 The delirium was violent or active in four of these six patients, three of whom got out of bed or tried to do so ; and in two of them it was muttering or quiet. The duration of the delirium varied much in these cases. In one patient the delirium continued for four days, in an- other two; in one it lasted four hours, and in another, the most interesting of the series, after it was slight for one day, it became muttering for half an hour. The duration of the coma was more constant. It lasted for from an hour to an hour and a half in four cases, and in one for four hours, while in one there was alternate delirium and coma for two days. A4 In two cases delirium passed into drowsiness. One of these, a dull, corpu- lent woman, aged 32, was strange in man- ner (temp. 103'4°) on the eighth day after admission, and had low muttering deli- rium. At 2 A. M. on the following night 1 Dr. Meding, Archiv der Heilkunde, xi. 467. 1 Lebert, " Klinik des acutens Gelenkrlieu- matismus," p. 55. ACUTE RHEUMATISM WITHOUT PERICARDITIS. 521 (temp. 105'3°) she awoke restless ; and at 5 A. M. (temp. 106°) she was dull and somnolent. She was put for twenty min- utes into a bath at 90° to 81°. When in the bath she felt comfortable, but at length she complained of cold (temp. 102°). After this her temperature never rose above 104'7°, she had bronchitis and pneumonia for some days, and finally re- covered. I was favored by Dr. Murchison with notes of the other case of this class. A lady, aged 35, stout, was attacked with acute rheumatism. At the end of ten days her joints were better, but she be- came sleepless and delirious. Opium, chloral, and bromide of potassium only made her worse. Her pulse was 108, weak ; temp. 102'5°. She gave no signs of peri- or endo-carditis, and had head- ache. The following is the report of her case ten days later: " The temperature has been as high as 106°, but is now only 101°. She is heavy and drowsy, but has been very noisy and delirious. Respira- tion is quick and irregular-cerebral. She swallows well. Pulse 64. Heart seems still sound. Urine is made in bed. There are bed-sores, and she has some pains in the joints." She died next day. R1 There was delirium without coma in ten cases. In three of these the tem- perature was very high, being 110° in a fatal case; and 108'2° and 107° respec- tively in two that recovered after the use of the cooling bath ; in one of these the temperature, rarely above 104'6°, once rose to 105°, and this case died in spite of the repeated use of the bath ; while the remaining six cases had the comparatively low maximum temperatures respectively of 104'5°, 103'4°, 101'2°, 101'1°, 101'1°, and 100'4° ; and of these the first case (temp. 104'5°) and that in which the tem- perature was the lowest (100'4°), a case with Bright's disease, died, while the four others recovered. The duration of the delirium was very various in different cases, having ended in death in one instance in two hours and a half, and being prolonged with interrup- tions in another for twenty-nine days, the high temperature being kept down and lowered and the delirium from time to time suspended by the cooling effects of a succession of twenty baths. As I have just said, in two of the three cases with delirium and very high tem- perature, the temperature was kept in check by the cooling bath. One of these cases, a youth, on the morning of the fourth day of treatment, muttered to him- self but could be roused, temp. 107'8°, and at 7.45 temp. 108'2°. After being half an hour in a bath at 76°, his tem- perature was 101°, and half an hour later 98'8°, when he fell asleep, and awoke in a perfectly conscious state. In the eve- ning, a second bath again lowered the temperature from 105'8- to 98°, when he perspired freely and slept. After this the temperature never rose above 99'8°, and he recovered.1 The second case, a wo- man, with a temperature of 107°, was put into a bath at 90° cooled to 42°. Her temperature was lowered to 97'5°, and her mind became clear.2 One patient, a man, who had been a free liver, presented throughout from time to time profuse sweating, variable deli- rium, tremor of hands, subsultus, and twitchings of the face, and a temperature varying from 104'4° to 106'4°. The use of the cooling bath invariably lowered the temperature, restored the patient from a state of delirium to one of consciousness, and caused a subsidence of the other nerve-symptoms, tremor, subsultus, and facial spasms. This condition lasted for twenty-nine days, during which time twenty baths were employed, five of them in one day for a combined period of over five hours, and the patient finally died, the temperature at the instant of death being 104'2°.3 Among the six cases with delirium in which the temperature was not very high, varying from 104'5° to 100'4°, two died and four recovered. One of these cases, with a temperature of 103'5°, was a great beer-drinker. His hands were tremulous, he wandered dur- ing the day, was very noisy towards the evening, when he screamed out much, continued in a state of variable delirium for fourteen days, and finally recovered.4 The highest temperature observed in the four remaining cases with delirium was 101'4° and 100'4° respectively. Two of them had albumen in the urine, and the other one had obstinate diarrhoea, and was delirious when the diarrhoea was checked. There were three cases of hyperpyrexia in which there was no delirium. One of these was a man whose temperature rose to 106'3°. He had previously been deaf and very restless. Under the influence of a cooling bath his temperature fell to 101 '8,° and later to 99'8°. After the bath his deafness left him, and he did well.5 Another case, a woman aged 24, was sud- denly seized with dyspnoea and vomiting, which continued until death ; a short time before which event her temperature was 110 '8°.6 Convulsive Choreiform and Tetaniform Movements.-Twitchings were present in 1 Dr. Weber, Clin. Soc. Trans, v. 186. 2 Sir William Gull, Lancet, 1872, ii. 562. 3 Dr. Greenhow, Clin. Soc. Trans, vi. 7. 1 Dr. Johnson, Lancet, 1867, i. 6 Dr. H. Thompson, Medical Times and Ga- zette, 1873, i. 269. 6 Dr. Ogle, Lancet, 1876, ii. 154. 522 PERICARDITIS. four of the twenty-one cases that form this group, in which there was no peri- carditis and endocarditis was absent or doubtful. The twitchings affected the body in one instance, the limbs and fea- tures in another, the muscles of the face for a long period in another, whenever the temperature rose; and in a fourth, the features occasionally twitched with a sardonic grin. In one case the patient was restless and moved his arms about ; but, perhaps with this exception, there were no notable choreiform or tetaniform movements in any of the cases. In two cases there was tremor-in one, of the trunk and limbs, in the other, of the hands. Twitching movements were present in four of the twenty-six cases with peri- carditis, in one of the eleven cases with simple endocarditis, and as we have just seen, in four of the twenty-one cases in which there was no pericarditis and endo- carditis was absent or doubtful. Twitch- ing movements were therefore distributed in nearly equal proportion in those three groups of cases, and were therefore not due to pericarditis. Twitchings were present in eight cases with hyperpyrexia, and it is therefore probable that they were associated with the very high tem- perature. This is borne out by a case of Dr. Greenhow's, in which twitchings came on, and were again and again re- newed when the temperature became very high, and were again and again almost or quite suspended by the cooling bath. In the remaining case with twitchings, a man who was under my care, the tem- perature was never above 102°. On the fifth day, temp. 100'2°, he had muscular twitchings all over the body, which con- tinued for several days, and reappeared on the twenty-eighth day. There was albumen in the urine on both occasions when the twitchings were present. Ilis recovery was slow. There were choreiform or tetaniform symptoms - or both - in seven of the twenty-four cases with pericarditis, but in only one of the eleven cases with simple endocarditis, and in none of the twenty cases in which there was no pericarditis, endocarditis being absent or doubtful. The question how far the cho- reiform and tetaniform movements ob- served in these cases was connected with pericarditis will be considered when we review the larger series of cases of acute rheumatism with and without pericar- ditis in which the temperature was not observed. The affection of the joints during the early period of the disease was severe in ten, and moderately so in five of the twenty-one cases in which there was no pericarditis and endocarditis was absent or doubtful. The affection of the joints was more severe before than during the delirium or other affection of the nervous system, in all but three cases, in which the joint-affection was equally severe dur- ing the two periods. In two of these three exceptional cases the temperature never rose above 102°, in one of these the delirium was only present during the night, and in the other there was no de- lirium, but twitchings were present for a short time during the early days of the illness. Perspiration.-The state of the skin is described in one-half of the cases belong- ing to this group (10 in 21), and all of these had profuse perspiration before the nervous system became affected. In seven of those cases there was either no per- spiration, or it was much lessened during the period of delirium. In three cases, perspiration was equally copious during the two periods. In three of these cases the skin, which had been perspiring pro- fusely before the excessive rise of tem- perature, and the occurrence of delirium, was hot and dry when the temperature was 110° to 111'1°; coma was present, and death approached. These clinical facts correspond with those which, as we have already seen, occurred in the analo- gous cases affected with pericarditis. One of the cases in which there was no affec- tion of the heart was observed by Mr. Anderson night and day. This patient, of a nervous, excitable temperament, a laborer, aged 29, had a hot, dry skin, and rambled during the night for four suc- ceeding nights ; but during the three in- tervening days his skin was covered with a profuse acid perspiration, and his mind was unaffected. On the morning of the fourth day his manner was wild and ex- citable, not unlike that of a patient in the early stage of delirium tremens, and his skin was hot and dry, and covered with a miliary eruption. After a bath, he sprang out of bed, ran into the grounds, and struggled violently. Uis temperature at that time was 107°, and later in the even- ing, ten minutes before his death, it was 110'3°. Dr. Greenhow's case, already referred to at page 518, offers a contrast in some respects, but not in others, to Mr. Ander- son's case. In this man, perspiration was absent with delirium at a tempera- ture of 104'8°, and was absent without delirium after the bath at 100'2°, and was present afterwards with obscured in- tellect and intermediate temperatures. Perspiration, which is not present at ordinary temperatures, is indeed an in- dex of the internal production of great heat, and a safety-valve for carrying away a large portion of that heat. When per- spiration takes place from an exposed skin in a dry air-in motion-its evaporation ACUTE RHEUMATISM WITHOUT PERICARDITIS. 523 tends to keep down the heat. In these patients, however, lying, as they do, in their own perspiration, covered by bed- clothes, in a still air saturated with mois- ture, evaporation can do comparatively little towards cooling the body. We must look, then, to some other in- fluence than evaporation to account for the cooling effect of perspiration in acute rheumatism. Such an influence we find in the welling out of hot liquid from every part of the body-a liquid charged with a portion of the surplus heat generated by the rapid combustion or disintegration of the internal structures in that disease. It is self-evident, that if the temperature of the body be 103° or 104°, the fluid poured out from the body must likewise have a temperature of 103° or 104°, and that this fluid during its steady universal expulsion must carry away with it a cor- responding proportion of the heat gen- erated within, and so tend to keep down the temperature of the whole of the struc- tures that compose the body. If, on the other hand, the skin is dry, the chemical heat generated in the rap- idly-changing tissues tends not to escape, and may be stored up in accumulating quantities in the blood and the tissues, with the effect of producing an exces- sively high temperature, or "hyperpy- rexia." Respiration.-I have not made an anal- ysis of the rate of respiration in cases of acute rheumatism with affection of the nervous system, with and without high temperature. One well-observed and well- treated case of hyperpyrexia is sufficient for our present purpose, which is to illus- trate the influence of an excessively high temperature of the body on the one hand, and of the cooling of that body on the other, on the frequency of respiration. In Dr. Wilson Fox's case, already related at page 516, when the temperature of the body was 107°, the patient was delirious, and the respiration was 45 in the minute, but when the patient's body had been cooled down by the bath to 98°, the mind was clear, and the respiration was 20 in the minute. It is evident, therefore, that during hy- perpyrexia, the cooling effect of respira- tion is stimulated to its highest degree by the excessive heat of the "body, but that this cooling effect is quite inadequate to keep down the temperature of the body below that of hyperpyrexia. There were some conditions common to the three sets of cases - those namely with : 1, pericarditis ; 2, simple endocar- ditis ; 3, without pericarditis, endocardi- tis being absent or doubtful-and I shall now briefly notice those conditions. Restlessness affected a considerable pro- portion of the patients before the occur- rence of delirium. Six of the twenty-seven cases with pericarditis ; three of the thir- teen cases with simple endocarditis ; and ten of the twenty-one cases that had no pericarditis, endocarditis being absent or doubtful, were thus affected with restless- ness. A miliary eruption or sudamina ap- peared in a considerable number of the cases, being noticed in twelve of the twenty-seven cases with pericarditis; in three of the thirteen cases with simple endocarditis ; and in eight of the twenty- one cases in which there was no pericar- ditis and endocarditis was either absent or doubtful. An abundant secretion of urine took place in a few of the cases, at the time of the great rise in temperature. The urine was very abundant under those circumstances in three of the twenty-seven cases with pericarditis ; in three of the thirteen cases with simple endocarditis ; and in two of the twenty-one cases in which there was no pericarditis, endocarditis being either absent or doubtful. Diarrhoea^ sometimes profuse and offen- sive, was present when the temperature was very high in seven of the twenty- seven cases with pericarditis; in four of the thirteen cases with simple endocar- ditis ; and in five of the twenty-one cases in which there was no pericarditis, and endocarditis was either absent or doubtful. Excessively high temperature or 11 hyper- pyrexia" in acute rheumatism with and without pericarditis. We have just seen that in sixty-one cases of acute rheuma- tism in which the temperature of the pa- tient was observed, the nervous system was affected, and we shall now inquire how many of them presented an exces- sively high temperature, and what was the influence of pericarditis in those cases of hyperpyrexia. The temperature was excessively high, ranging from 106'8° to 111T° in thirty-one of those sixty-one cases, and was arrested during its rise when it was at from 105° to 106'3° by the use of the cooling bath, or cold externally, in six cases. In three of those six cases, the tendency of the temperature to rise was great, but in three of them it was not so. The temperature was not observed during the period of coma or the last hours of life in three fatal cases in which the tem- perature was 104'6°, 104'8°, and 105'8° respectively at the time of the last obser- vation, and I consider that these three cases and three of the six in which the high temperature was kept in check by the bath, ought to be added to the thirty- one cases in which the temperature was very high, thus bringing up the number of those with "hyperpyrexia," to thirty- seven of the total number of sixty-one 524 PERICARDITIS. cases. Thus estimated, we find that sev- enteen of the twenty-seven cases with pericarditis, nine of the thirteen with sim- ple endocarditis, and eleven of the twen- ty-one without pericarditis, endocarditis being absent or doubtful, either had, or were threatened with "hyperpyrexia." Among these thirty-seven cases of hyper- pyrexia, one had coma without delirium, twenty-one, delirium followed by coma, or, in one instance, stupor, two, delirium with convulsive movements, ten, uncom- plicated delirium, and three had neither coma nor delirium. The case of simple coma, and all but one of the twenty-one cases in which delirium passed into coma, were affected with ac- tual (18) or threatened (3) hyperpyrexia. The temperature observed soon rose above 106° in three cases with delirium and stu- por, but in one of these it was kept down and lowered by the cooling bath, while in both the cases which ended fatally with convulsive movements, the temper- ature was very high. Of the twenty-four cases with uncomplicated delirium, only two-fifths had hyperpyrexia (10 in 26). Coma preceded by delirium is, as we have just seen, the typical effect of rheu- matic hyperpyrexia, and one-half of those with hyperpyrexia and coma preceded by delirium, had pericarditis (10 in 20). From these clinical facts it would appear that hyperpyrexia attacked cases of acute rheumatism almost as frequently when they had pericarditis, as when they were not so affected (17 in 27 with pericarditis, 20 in 37 without pericarditis). When we consider that pericarditis usually attacks only one in every five or six cases of acute rheumatism, we must multiply the cases of pericarditis with hyperpyrexia by five or six if we would make a parallel com- parison between those cases with peri- carditis and those without it. It would appear from this that the presence of pericarditis in a case of acute rheumatism increases the chance of the occurrence of hyperpyrexia with delirium and coma, in the proportion of four or five to one. An important case successfully treated by Dr. Wilson Fox by the cold bath had pericarditis in its worst form. The dul- ness or percussion over the region of the pericardium filled the whole left front of the chest from apex to base. In that case the tendency to the renewed excessive rise of temperature after it had been brought down again and again, by the cold bath, the ice-bag, or the wet-pack, continued until the seventh day; when the pericardial dulness fell to the first rib mid-sternum, and the tendency to the increase of temperature lessened. It is a clinical fact that here the renewed rise of temperature continued so long as the pericarditis was severe, and gave way when the pericarditis gave way, and it is probable that the continued severity of the pericarditis had an influence in keep- ing up the tendency to the rise of temper- ature. It must, however, not be lost sight of that as a rule, cases of acute rheuma- tism with pericarditis are in all respects worse than those without it, and that, not only at the time of the pericardial inflam- mation, but usually also before it. It be- comes therefore a question whether or not the same severity of the acute rheu- matism itself that brought the pericardi- tis into existence brought also the exces- sively high temperature with its attendant delirium and coma into existence, the two affections being affiliated, and due to a common cause. The occurrence of a high temperature of the body in cases of acute rheumatism, corresponds in essential features with the high temperature observed in sunstroke, in certain exceptional cases of tetanus, and in injuries to the cervical portion of the spinal marrow. In sunstroke the temperature varies from 112° to 105*5°, the skin is hot and dry, coma supervenes, preceded occasionally by delirium, and death tends to ensue unless the tempera- ture of the body is lowered by cold.' The temperature in tetanus, though variable, does not as a rule rise to a very great height. Wunderlich, however, gives a case in which it attained to 44'75° C. (112*55° F.) before death.2 This instance resembled in all its main features the cases of hyperpyrexia in acute rheuma- tism. The patient, before the time of the fatal rise of heat, was very restless; had profuse perspiration and an abundant miliary rash ; then came on delirium, night trembling, contracted pupils, and death. Wunderlich, without giving any reason for it, gives the name of rheumatic tetanus to another but less extreme case of the same kind. Injury of the spinal cord from the fourth to the sixth cervical vertebra from fracture or caries of the spinal column has induced an excessively high temperature in several cases published since the first observation to that effect by Sir Benjamin Brodie.3 The symptoms in these cases closely resemble those of hyperpyrexia in acute rheumatism, but in only one of them was it stated that the final and fatal coma was preceded by delirium. One of Dr. Hermann Weber's two cases was a 1 Dr. Levick, " Pennsylvania Hospital Re- ports," 1868, p. 371; Dr. Gee, Gulstonian Lectures on Pyrexia, Brit. Med. Journal, 1871, i. 302; Dr. Maclean on Sunstroke, Reynolds' "System of Medicine," i. 661. 2 Wunderlich, Archiv der Heilkunde, ii. 3 Sir Benjamin Brodie, Med.-Chir. Trans, xx. 118 ; Reineke, Berliner Klinische Wor- terbuch, 1869, 113, 301; Billroth, Archiv fur Klin. Chirurgie Langenbeck, ii. 482. SUMMARY OF CASES OF ACUTE RHEUMATISM. 525 youth, who could walk supported, but like a drunken man, and could move his arms twenty minutes after the accident, which caused fracture and incomplete dislocation of the third, fourth, and fifth cervical vertebrse. He voided urine fre- quently and in great quantities. An hour after admission his temperature was 100 '4°. Two hours and a-half after the accident he passed liquid motions un- consciously, had occasional convulsive twitches in the arms and legs, his skin was slightly moist and hot, and his tem- perature was 109'58°. Four and a-half hours after the accident there was com- plete coma, and his temperature was 111°, and it was Ill'S0 at the time of death, eight hours after the accident.1 Dr. Burdon Sanderson, who has favored me with the use of the manuscript notes of his lectures delivered at Manchester, gives an account of experiments made by him in which the cervical portion of the spinal cord was injured. He found that there was no increase of temperature for two hours after the injury to the cord* but that at the end of that time it began to rise and to rise rapidly, attaining a very great elevation, 42° C. or 107'6° F., or higher than that of fever. Dr. Burdon Sanderson considers that this experiment shows conclusively that the process of which the higher temperature is the out- come, must consist in a gradual modifi- cation of those processes on which heat production depends, must have as wide a localization as they, and cannot therefore be attributed to any sudden interruption of the relation between the centre and the periphery of the nervous system. These experiments correspond remarkably with Dr. Hermann Weber's case just reported. Cases in which the temperature of the body was below that of hyperpyrexia.-We have just seen that of the sixty-one cases of acute rheumatism associated with affec- tion of the nervous system in which the temperature was observed, in thirty- seven there was actual (31) or threatened (6) "hyperpyrexia." In the remaining twenty-four cases, the maximum tem- perature of the body observed in the dif- ferent instances varied from 99'3° to 106'3° temp. Ten of the twenty-seven cases with pericarditis, four of the thir- teen with simple endocarditis, and ten of the twenty-one without pericarditis, and in which endocarditis was absent or doubtful, belong to this group in which the temperature was not excessively high. In twelve of these twenty-one cases, the maximum temperature varied in the dif- ferent cases from 103° to 106°, and in nine of them from 99'3° to 102'8°. A considerable proportion of those who were attacked with delirium at compara- tively low temperatures were either habitual drinkers, or of a nervous tem- perament, or had been subject to anxie- ties and privation, or to lowering diseases, or had received injuries affecting the ner- vous system, and in several of those cases the affection was closely allied to delirium tremens; several such cases occurred among those affected with pericarditis. This was so in Dr. Southey's two cases with pericarditis,referred to at page 516, in Dr. Greenhow's case, given at page 517, in Dr. Murchison's two patients, quoted at page 521, and in a patient of my own. To these must be added the case with which Dr. Southey favored me since the above was written, given at page 516, and two of Dr. Andrew's cases. Most of these cases had pericarditis. Cases of Acute Rheumatism with Affections of the Nervous Sys- tem IN WHICH THE TEMPERATURE OF the Body was not observed. There were 119 cases of acute rheu- matism with affections of the nervous system in which the temperature was not observed. Of these 65 had pericarditis; 16 had simple endocarditis ; and 38 were free from pericarditis, endocarditis being absent or doubtful.1 [* Several tables under this heading and under Pericarditis have been omitted, as they are too complicated in their arrangement to be followed by the ordinary reader, and as the results deducible from them are fully stated in the text.-H.] 1 Dr. Hermann Weber, Clin. See. Trans, i. 163. 526 PERICARDITIS. Summary of cases of Acute Rheumatism, with Affections of the Nervous System, in which the temperature was not observed. With Pericar- ditis. Simple Endocar- ditis. No Peric. Endocard, absent or doubtful. Total. .A1-Coma with delirium or convulsions . 3 0 2 5 .A2- " with convulsions . 2 1 2 5 H3- " preceded by delirium .... 5 0 8 13 A*-Stupor preceded by delirium .... 0 0 2 2 A -Had Coma or Stupor. Total .... 10 1 14 25 Had Semi-consciousness 1 1 Bx-Delirium, uncomplicated ..... 21 8 14 42 B2 " passing into temporary insanity II 5 3 20 " with chorea or choreiform or tetani- ) form symptoms ... $ 5 2 7 " Total ...... 16 5 5 27 B3-Delirium, with chorea and choreiform move-1 ments, not including those with temporary > 4 o 1 5 insanity ......} B4-Delirium with tetaniform movements, not in- 1 eluding those with temporary insanity . j B -Delirium without Coma. Total 43 13 21 77 Delirium. Totals (including those with coma) 48 13 31 92 Cx-Chorea without delirium ..... 7 7 C2-Choreiform movements (jactitation), without ( delirium ...... ) C3-Tetaniform symptoms, without delirium . 2 2 D-Had slight fit ....... 1 1 E -Had embolism, hemiplegia .... 1 1 F-Had Paraplegia....... 2 2 G-Had agitation and prostration .... 1 1 Total ....... 65 16 38 119 I.-Cases affected with Peri- carditis. There were sixty-five cases of acute rheumatism with pericarditis, in which the nervous system was affected. (A.) Ten of these had coma, of which (A1,) three had uncomplicated coma ; (A2,) two had coma with convulsions ; and (A3,) in five the coma was preceded by delirium. (B.) Forty-three cases had delirium with- out coma ; of these (B1,) twenty-one had uncomplicated delirium, one of which had "symptoms of inflammation of the brain," and one apparently had pyaemia ; (B2,) sixteen, of which five had choreal or tetaniform symptoms, had temporary insanity, lasting from two weeks to three months, or in three instances, insanity was cut short by death; (B3,) four had chorea or choreiform movements, and (B4,) two had tetaniform symptoms with- out temporary insanity. (C1.) Eight of the cases had chorea or choreiform move- ments, and (C2,) two had tetaniform symptoms without delirium. (D.) One of them had a slight fit with ptosis. II.-Cases affected with Simple Endocarditis. There were sixteen cases of acute rheu- matism with simple endocarditis, in which the nervous system was affected, exclud- ing cases of ordinary chorea, but includ- ing cases of chorea rapidly fatal, or with delirium. (A2.) One of these cases had coma with convulsions, associated with acute Bright's disease from embolism. (A3.) One had delirium ending in coma, with embolism of the minute cerebral arteries. (B.) Twelve of them had delirium with- out coma, of these (B1,) seven bad un- complicated delirium; and (B2,) five passed into a state of temporary insanity, lasting from three weeks to four months. (C1.) One had chorea ending rapidly in death. (E.) One had embolism with hemiplegia. COMA DELIRIUM. 527 III.-Cases in which there was no Pericarditis and Endocarditis WAS ABSENT OR DOUBTFUL. There were thirty-eight cases of acute rheumatism without pericarditis, endo- carditis being absent or doubtful, in which the nervous system was affected, exclu- sive of cases of ordinary chorea. (A.) Twelve of these had coma or stupor, of which, (A1,) two had uncomplicated coma, (A2,) two had coma with convul- sions, (A3,) in eight the coma was pre- ceded by delirium ; and there were also (A4,) two cases in which delirium passed into stupor. (B.) Twenty of the cases had delirium including two with "cere- bral rheumatism," and one that had pus in the pia mater ; of these (B',) .fourteen had uncomplicated delirium; (B2,) five passed into temporary insanity, two of which had chorea also ; (B3,) one had chorea ; and (B',) one had tetanic spasms. (F.) Two of the cases had paraplegia. (G.) One of the cases had agitation and prostration ending in rapid death. A.-Coma. I.-Cases with Pericarditis. A1.-Un- complicated Coma.-Three cases with Pericarditis had coma without convul- sions or delirium, all of which proved fatal. A2.-Coma with Convulsions.-In the two cases of coma with convulsions, death was speedy. A3. - Coma preceded by Delirium.-Four of the five cases in which delirium passed into coma, died ; and one recovered. One of the cases passed rather into stupor than coma. The duration of the coma in these cases was variable and uncertain, and that of the delirium lasted for from one or two nights to nine or ten days, II. - Cases with Simple Endocarditis. A2.-Coma with Convulsions.-One fatal case of coma preceded by convulsions had simple endocarditis with embolism of the spleen and kidneys, the coma and convul- sions being evidently associated with acute Bright's disease.1 III.-Cases without Pericarditis, Endo- carditis being absent or doubtful. A1*2.- Coma without and with Convulsions.- There were four fatal cases of coma with- out delirium among the cases without pericarditis, endocarditis being absent or doubtful, two of them having convulsions. In three of them death was very rapid, and in one coma, coming on after convul- sions, lasted for twelve hours before death. These cases did not differ materially in character and history from those with coma and pericarditis. A3. - Coma and Delirium.-Coma was preceded by delirium in eight fatal cases that presented no sign of affection of the heart. The delirium was more frequent by night than by day, being present in three of the cases from two to five or six nights, while it was absent in the daytime, and it lasted in the other five cases from two to four or five days. The coma, as a rule, soon ended in death. In one-half of the cases, or four, the delirium became violent, and in the other half, its character was not de- scribed. These cases do not differ materially in essential character from those with peri- carditis that were affected with delirium and coma. There were, however, ner- vous symptoms in the form of agitation, twitchings, and choreiform and tetaniform movements in a much greater proportion of those with pericarditis than of those not so affected. A4.-Delirium and Stupor.-One of the two cases in which delirium preceded stupor recovered after the employment of the wet sheet, and the other died. B.-Delirium. B1.- Uncomplicated Delirium.-1. Cases with Pericarditis.-Twenty-one of the sixty-five cases with rheumatic pericardi- tis had uncomplicated delirium, includ- ing one with " symptoms of inflammation of the brain," and one with probable pyaemia. Eleven of these cases died and ten recovered. The duration of the delirium varied much. The delirium was more active by night than by day, and in five cases was present from one to three or four nights, but was absent during the day. In the rest of the cases it lasted from for a few hours to four or five days. The delirium was noisy or violent in eleven instances, moderate in four, and slight in five cases. One case, a female servant, felt much better at the evening visit, but a quarter of an hour later became delirious, with loud continuous cries. A varied treat- ment, including wet packing, was em- ployed, and she recovered. Another case, a workman in Messrs. Guinness's Brewery, drank largely of their XX porter besides whiskey. He had pericarditis, and " delirium tre- mens," and recovered after taking opium.1 2. Cases with Simple Endocarditis.- Seven of the sixteen cases with simple 1 Frerichs, " On the Diseases of the Liver," New Sydenham Soc. Edition, vol. i. p. 164. 1 Dr. Graves, "Clinical Lectures on the Practice of Medicine," vol. i. p. 531. 528 PERICARDITIS. rheumatic endocarditis had uncompli- cated delirium. Three of these cases died and four recovered. The duration of the delirium varied from, for a single night in one patient, to at least nine days in another. It was present more often, and, as a rule, with greater violence by night than by day. In four of the cases the delirium was active or violent, in one the delirium was wan- dering, and in another, it was accompa- nied by somnambulism. One of these cases was observed by Dr. Boisragon and Mr. Tudor, and reported by Dr. Davis, and is, so far as I have dis- covered, the first case in which endocar- ditis was well described. Three of the cases of endocarditis with delirium were under my own care, and of these, one died and two recovered. 3. Cases without Pericarditis, Endocar- ditis being absent or doubtful.-Fourteen of the thirty-eight cases without pericar- ditis, endocarditis being absent or doubt- ful, had uncomplicated delirium. Ten of the fourteen cases died, and four re- covered. The duration of the delirium varied much in the different cases. It prevailed more during the night than the day. In three instances it was only present during the night for from one to three nights. In one case the delirium was only present for a quarter of an hour before death, in four cases it existed for one day, and in four others from two to five or six days. The delirium was violent or lively in five of the cases, and five were simply " de- lirious." These cases corresponded in essential features with those that had delirium with pericarditis. " Hyperpyrexia" in cases of acute rheu- matism without and with Pericarditis in which the temperature was not observed.- The ten fatal cases belonging to the last group of fourteen with delirium, the twelve with coma and the two with stupor, all of which had neither pericarditis nor endocarditis, evidently belong to the im- portant group of cases of acute rheuma- tism with hyperpyrexia. All of those twenty-four cases except one with stupor, died, and that patient recovered after the external use of the wet sheet. The ten cases with coma, and the eleven fatal cases that recovered under the use of wet packing that had uncomplicated delirium among the patients with pericarditis, and three fatal cases of delirium with simple endocarditis, may also be ranked among the cases of hyperpyrexia. According to this estimate, twenty-two of the sixty-five cases with pericarditis, three of the six- teen with simple endocarditis, and twenty- four of the thirty-eight without pericar- ditis or notable endocarditis, in which the temperature was not observed, were affected with "hyperpyrexia." These forty-nine cases corresponded in their broad features as regards coma, de- lirium, and death with those cases of " hyperpyrexia" in which the tempera- ture was observed. As in those also so in these, in the few cases where these conditions were observed, the affection of the joints ceased when the delirium ap- peared, and the perspiration, copious during the earlier stages, was absent or much lessened during the stage of deli- rium or coma, when the skin was usually dry and hot. Convulsive, choreiform, and tetaniform movements in the cases with hyperpyrexia.- There was an important difference in the two sets of cases with and without peri- carditis, as regards the presence of con- vulsive, choreiform, and tetaniform symp- toms in combination with the far more important symptoms of "hyperpyrexia." Convulsive movements, jactitation, agi- tation, choreiform movements without ac- tual chorea, and tetaniform symptoms ap- peared more frequently in the cases of coma or delirium with pericarditis, than in those without pericarditis. Involuntary move- ments of the muscles occurred in one, and general agitation in three of the twenty-five cases of hyperpyrexia that had neither pericarditis nor notable endocarditis. A convulsive fit occurred in one, jactitation of the limbs or body in two, tetaniform symptoms in two, and great general agi- tation in three, of the twenty-two cases with hyperpyrexia that had pericarditis. Besides these eight instances of convul- sive, choreiform, or tetaniform affections among the fatal cases of coma and deli- rium with pericarditis, there were two with jactitation, and one with twitchings of the muscles of the face, among the cases of delirium with pericarditis that were not fatal. Four of the eleven cases with pericarditis thus affected with con- vulsive, choreiform, or tetaniform move- ments had endocarditis, three had no endocarditis, and in four the presence of endocarditis was doubtful. We have already seen that among the cases of "hyperpyrexia," in which the temperature was observed, choreal and tetaniform symptoms occurred much more frequently among those with, than among those without, pericarditis ; while on the other hand twitching movements were as frequent among those without, as among those with, pericarditis. Delirium resembling Delirium Tremens.- Among the cases of delirium in acute rheumatism without pericarditis or evi- dent endocarditis as among those pre- viously analyzed with pericarditis, there are several that present symptoms partly allying them to delirium tremens-partly to the delirium of rheumatic hyperpy- TEMPORARY INSANITY. 529 rexia, and that are associated with pre- vious habits of drinking, or with some affection of the nervous system. One of these patients, a hard drinker, complained of being unable to see, called out "thief," rushed out of bed and fell down. After this he struggled with two attendants, and then dropping back, died. All this took place in less than a quarter of an hour.1 Two of my own patients belong to this class, one of whom recovered, the other died. One was a stout florid waiter, aged 40, who perspired profusely, slept but lit- tle, and became very violent. On the seventh night he slept with an opiate, lie recovered rapidly. The patient who died was a barman, aged 23, who was rather restless, and hurried in speech on the day after admis- sion, became more restless on the third day, and died suddenly. B2.-Temporary Insanity with Taci- turn Melancholy and Halluci- nations. B2. I.-Cases with Pericarditis.-1The series of cases that I have now to con- sider present a remarkable succession of symptoms. In eleven cases of acute rheumatism with pericarditis, delirium, usually desponding and taciturn, often with hallucinations, came on when the heart was inflamed; but instead of pass- ing away quickly, this sombre delirium lasted for from two or three weeks to three months. Of these eleven cases of temporary insanity, ten recovered, and one died ; eight of those cases were fe- males, six below the age of twenty, and three were males. All but one of these patients were affected with endocarditis as well as pericarditis. The duration of the insanity varied considerably, and the return to a healthy state of mind was gradual, and never sharp. The temporary insanity lasted for above a fortnight in three cases; for about a month in three; for two months in one ; for ten weeks in one patient, whose mind was not yet clear at the end of that time ; and one died with her in- tellect still confused at the end of two months. The prevailing feature of the delirium was a state of taciturn melancholy. Only one patient, a young woman, the fatal case, was at times in wild delirium, at times taciturn and almost idiotic, and at times quite rational.2 Eight of the pa- tients were taciturn, and two others were confused in mind or speech. Four of them had hallucinations; one saw her mother at her side ; one a knife and poi- son ; one was followed and insulted, and then reached out his hand as to an old friend; and one complained of vermin. Another patient had delusions. Two of my patients belong to this series of cases. One of these, a potman, aged 21, on the seventeenth night after his ad- mission was in a state of partial stupor and delirium. On the following day he answered no questions, and as he would not take food, stimulants were given by enemata. On the twenty-sixth day he again took food, but he continued to be taciturn. On the thirty-ninth day he re- covered the powers of nature, was up on the forty-seventh, and left on the seventy- fifth day, his heart-sounds being healthy. The other case, a laborer, with endo- pericarditis, had a vacant, torpid, and wandering mind for three weeks, which followed an attack of hemiplegia from embolism affecting the right side, with loss of speech, which was apparently a mixture of aphasia and a taciturn charac- ter of mind. On the tenth day his face wras paralyzed on the right side, and the pupils were irregular. On the thirteenth he would not or could not speak, but muttered slightly, and tried to get out of bed. He improved daily and his speech returned, but his expressions were inco- herent. On the thirty-eighth day he had more command over his articulation, and on the forty-second had almost regained the use of his right side. He improved steadily, and on the seventy-second, day he went out well, the heart-sounds being healthy. Besides the eleven cases just spoken of with temporary insanity of a taciturn melancholic type, there were five others in which a similar condition was associ- ated with chorea or choreiform move- ments (in 4) or with tetaniform symptoms (in 1). Three of these cases were fatal, and two of them recovered. The whole of the five cases were below the age of twenty-one, and two of them were male and three were female patients. All of them had endocarditis as well as pericar- ditis. The affection lasted in one of the two that recovered about a month, and in the other for a shorter period. The three fatal cases died respectively in about twenty-three, sixteen, and nine days after the beginning of the mental trouble. One of those patients was taciturn, then deli- rious, and finally had the most violent choreiform movements, ending in death. Another fatal case had difficult utterance, incoherence, tossing of the head from side to side, and choreiform spasms which put on the character of the most violent con- vulsions. A third case spoke loud and low, after, in succession, being excited and stubborn, weeping, seeing a dead 1 Trousseau, "Lectures on Clinical Medi- cine" (New Sydenham Soc.), vol. i. p. 513. 2 Sir Thomas Watson, loc. cit. ii. 307. vol. ii.-34 530 PERICARDITIS man, and grimacing as in chorea : death took place an hour after an attack of uni- versal convulsions. One of the two cases that recovered had a rather childish ap- pearance ; her answers were sometimes irrelevant, sometimes rational, and she had choreal movements of the right arm and leg. The last case had delirium with tetanic spasms ; at first he had an excited man- ner, with wild rolling of his eyes, then furious delirium, followed by firm clench- ing of the hands, sleep, and a more tran- quil state. After this he was idiotic and violent by turns, until the twenty-eighth day after the first disturbance of the mind, when he became tranquil. These sixteen cases with taciturn mel- ancholy, often with hallucinations, lasting for from three weeks to three months, and then usually getting well, present a group of conditions that seem to separate them from the twenty-one cases of delirium that were not followed by coma, and the five that were so. In those cases the de- lirium was often violent, generally active, sometimes muttering ; in these it was melancholic and taciturn. In those cases the delirium was often exclusively by night and was then almost always most noisy ; in these it was present day and night, though it was usually more active by night. In those cases the delirium lasted for from one or more hours to five or six nights and five days ; in these it lasted for from three weeks to three months. In those cases perspiration was generally profuse before the appearance of the delirium, the skin usually becoming hot and dry as the temperature rose to the fatal height; in these perspiration was only noted as being profuse in two cases, and slight in one. In those cases death was the natural result; in these, all but one of the eleven without chorea recov- ered, while three of the five with chorea died. In those endocarditis was absent in three-fifths of the cases (11 in 32) with coma and delirium, but three more of those cases probably had endocarditis ; in these endocarditis was present in all but one. We saw that in the two sets of cases, in one of which the temperature was, and in the other, was not observed, delirium pre- sented itself in two forms : (1) one, and the leading form, of delirium with hyper- pyrexia, ending in death ; (2) the other, the secondary form, with a less high tem- perature in which a condition resembling delirium tremens associated itself with and modified the delirium of hyperpy- rexia, often occurring in persons who had been intemperate, anxious, nervous, or in want, and ending generally in recovery. In these cases of temporary insanity with taciturn melancholy we have clini- cal evidence of a third kind of delirium, differing from the two other kinds of which we have just spoken. These cases resemble in some of their symptoms, cases of insanity with settled taciturn melancholy ; but from those they differ in this essential point, that while in those the insanity is obstinate, often in- deed for life ; in these the insanity comes definitely to an end in from two or three weeks to three or even four months. The features, then, that characterize these cases of temporary insanity are youth and previous good health ; or in a few cases intemperate habits ; the absence of hyperpyrexia ; the existence of endo- carditis ; the settled though varying and even intermittent character of the taciturn delirium, which is present, though modi- fied, by day as well as by night; and the dying out of the affection in a limited period. These conditions point, not to a rapidly progressive and varying cause, which marks hyperpyrexia, which is kept in check or suspended by a perspiring skin, or the external use of cold, and is promoted by a hot dry skin ; but to a con- tinuous cause, that is excited during the height of the disease, but that varies in operation for from two weeks to three months after the acute rheumatism and the acute stage of the endocarditis have passed away. In one of my own cases there was embolism, evidenced by the loss of power in the right side, and taci- turn aphasia, in combination with endo- carditis ; and it appears to me that in embolism of the minute cerebral arteries of the convolutions, we have a series of conditions that correspond with those occurring in the whole of these remark- able cases. Embolism of the cerebral arteries comes on with endocarditis, and arrests for a time the circulation of the blood through the parts of the brain sup- plied by the affected vessels ; its effects remain after the acute stage of the origin- ating endocarditis has passed away ; and, if death does not cut short the clinical history of the case, those effects usually gradually lessen and disappear in from two or three weeks to several months, unless the extent of the plugging of the vessels be such as to cause extensive soft- ening of the part of the brain supplied by those vessels. I therefore consider that to embolism we may have to look for the explanation of these cases. We shall find other instances of a like nature among the cases without pericarditis, in which endocarditis was present, and in those also in which it was doubtful or absent. B2.-II. Cases with Simple Endocarditis. -Five of the sixteen cases that had endo- carditis without pericarditis were affected with delirium of a desponding type with taciturn melancholy. Two of these died and three recovered. In addition to these five cases with taciturn melancholy, there TEMPORARY INSANITY. 531 was another analogous case of embolism of the basilar artery, with headache and agitation, and in the evening apoplectic symptoms, right hemiplegia, and difficulty of speech.1 As this case did not survive the first great attack, I shall not add it to the rest. The length of time that the mind was disturbed varied in the different cases from three weeks to four months; one of the fatal cases lasted twenty-three days, and another two months; while those that recovered were affected for one, two, and four months respectively. Four of them were restless; three were taciturn, especially during the night; another an- swered slowly ; and the fifth case in a low voice ; three had hallucinations, including one of those that were also taciturn, and two would get out of bed. Three of them were desponding or melancholy ; one was apathetic ; and the remaining one, a fatal case, was for ten days in a state of quiet delirium, and afterwards preserved a dogged silence. Two of them were con- fused ; and one of them was violent. If we compare these five cases of temporary insanity, with simple endocarditis; with the sixteen cases of the same class with pericarditis and endocarditis, we find that the two sets of cases correspond in their main features. Both had disorder of mind, by day as well as by night, though with greater accentuation at night in those with simple endocarditis ; in both early restlessness, obstinate silence, mel- ancholy, apathy, and hallucinations pre- vailed ; and in both the affection of the intellect commenced during the attack of acute rheumatism, and of the accompany- ing endocarditis, and lasted for a variable period after the acute affections had ceased. As we have just seen, five out of the sixteen cases, or one-third, with simple endocarditis, not including the fatal case of embolism, difficult speech, and right hemiplegia, and another case with em- bolism of the minute cerebral arteries and delirium that died on the eleventh day ; and sixteen of the sixty-five with pericar- ditis, all but one of them having endo- carditis also, or one-sixth, were thus affected with taciturn melancholy lasting for a limited period after the cessation of the acute affection. We may, I think, consider that the existence of endocarditis in so large a proportion of such cases adds to the probability of embolism being the cause of the temporary insanity. Since the above was written Dr. Broad- bent has favored me with his notes of an important case of acute rheumatism and endocarditis, with chorea and delirium, in which there was capillary cerebral em- bolism. I have also met with a case ob- served by Dr. Dickinson of acute rheu- matism and endocarditis with delirium, and minute cerebral embolism, and red softening of some of the convolutions; and with another case of chorea and endocar- ditis with delirium and minute cerebral embolism. These three cases afford direct evidence of the association of embolism of the minute arteries of the convolutions of the brain with delirium. Dr. Broadbent's patient, a laundryman, aged 17, when attacked, had severe affec- tion of the joints, and was light-headed ; two days later his right limbs twitched and jumped, and he was delirious. On admission, after being ill a week, he seemed stupid, had to be spoken to loudly, his an- swers were confused, his articulation was indistinct, and his limbs still twitched, but especially on the right side. T. 103°. During the two following nights he had no sleep, was very delirious, talked, screamed, and jumped out of bed. He slept after a dose of chloral, but was soon pale and prostrate, and died on the fourth day after his admission. Recent loose clots were found in the minutest arteries and capillaries of the corpora striata and of some of the convolutions. B2.-III. Cases without Pericarditis, Endocarditis being absent or doubtful.- Five of the thirty-eight cases in which there was no pericarditis, and endocarditis was absent or doubtful, or one in eight of the whole number, became delirious dur- ing the acute stage of the disease, and re- mained of unsound mind for two months and a half in one, and for about a month in four instances. Two of these patients were also affected with choreiform move- ments. Four of these were men, and one was a girl, aged 16. Two of the men had been at one time drunkards, one of them had suffered in health from losses and ex- cesses, and the other man was a servant, and probably lived generously. The speech was affected in all of them. One stammered, one answered slowly, one was taciturn, one refused to answer, and the girl did not reply to the question put to her, but spoke of something else. Two of them had hallucinations; one was de- spondent ; another, after being noisy, be- came sulky ; one was morose by day, and had lively delirium. One, with clioreal movements, after being confused and de- lirious in paroxysms, became so continu- ously ; and the fifth, also having chorea, was strange in manner. In none of these five cases was there any notable sign of endocarditis, and the dis- turbed state of mind and speech could not therefore be attributed to embolism. B2. Temporary Insanity-General Sum- mary.-There were altogether twenty-one cases of acute rheumatism with temporary insanity ; and six of delirium, usually of the low melancholy type, in which the in- 1 Bouillaud, "Maladies du cceur," vol. i. p. 405. 532 PERICARDITIS. sanity was cut short by death. Of these twenty-seven cases, sixteen had pericar- ditis, six simple endocarditis, and five had apparently neither pericarditis nor endo- carditis. Four-fifths of the cases had endocardi- tis (21 in 27), and one-fifth of them gave no evidence of endocarditis (6 in 27). I have already given clinical reasons for thinking that the temporary insanity may have been due to embolism of the minute cerebral arteries in those cases with endo- carditis, and direct evidence that in two cases that condition coincided with de- lirium. In six of those cases with endocarditis the temporary insanity, delirium, or mel- ancholy was associated with chorea, and their clinical history would seem to sug- gest that in those cases the temporary insanity and the chorea were due to a common cause acting perhaps on different parts of the nervous centre. This view is strengthened by Dr. Tuck well's impor- tant remarks on Muscular Chorea and its probable connection with Embolism. This memoir is illustrated by a case1 in which there were two large patches of red softening affecting the cortex, and in one of them the white substance also, of the right hemisphere of the brain. The arte- rial branches leading to one if not both of these softened patches were occluded by coagula, and very fine granular particles were dotted along the small bloodvessels in the softened cerebral gray matter. This patient, a boy, was attacked with chorea nine days before admission, and became delirious during the first night after it. On the third day he had wild maniacal delirium, and furious choreic movements. This wild state soon quieted itself, but was renewed on the eighth night, and on the ninth day he became comatose and died. More than one-half of the cases were below the age of twenty-one (14 in 27), and of these all but one had endocarditis, while one-third of them were above the age of twenty-five (9 in 27) and of these nearly one-half (4 in 9) presented no sign of endocarditis. Although the majority of these cases, and especially those with endocarditis, ■were young people of previously good health, yet a small but definite group of the cases form an important exception to this typical series. Six of the cases, all men, were either known to be of habits of intemperance, or were of occupations in ■which such habits are possible. Three of those male patients were drunkards or given to excess, and of the rest, one was a policeman, one a man-servant, and the sixth was a postboy. Four of these pa- tients, all of whom recovered, presented no sign of endocarditis, and the two others had endocarditis. The question arises here, Whether the temporary insanity in these four men who had not endocarditis, one of whom had chorea also, may have been due to thrombosis or the spontaneous collection of fibrine in the minute arteries of the convolutions ? I simply put this as a question, but in support of the possibility of this condition I find an important case that was closely observed by Dr. Charlton Bastian during life and after death. The patient was a strong man, a gate porter, who had been accustomed to drink a great deal of late, and was attacked with ery- sipelas of the head and face following a fall, when he cut his head on the curb- stone. He became violently delirious, was then quieter, became comatose at night, and died early on the following morning. The heart was healthy ; the pia mater and brain were abnormally vascular; the consistence of the brain was good. Minute embolic masses were present in the small arteries and capil- laries of the brain in every specimen looked at.1 B' & C ', 2, '.-Chorea and Chorei- form AND TETANIFORM MOVEMENTS, WITH AND WITHOUT DELIRIUM, IN Cases of Acute Rheumatism, with ESPECIAL REFERENCE TO PERICAR- DITIS. The occurrence of chorea without deli- rium in cases of acute rheumatism when connected with endocarditis will be con- sidered when we inquire into that affec- tion. The present inquiry will be limited to (1) cases of chorea and of choreiform movements with delirium, or ending in sudden death, occurring in acute rheuma- tism with or without pericarditis ; and (2) cases of chorea and choreiform movements without delirium, occurring in acute rheumatism with pericarditis ; and in in- quiring into these cases, I shall briefly include the cases of combined chorea and temporary insanity that have already been considered. B2 & C, 2.-I. Cases with Pericarditis. -Chorea occurred as a definite accompa- nying affection in six instances with deli- rium, and in seven without delirium ; and choreiform movements not amounting to definite chorea occurred in twro instances with delirium and in one instance with- out delirium among the sixty-five cases of acute rheumatism affected with pericar- ditis now under examination. In addi- tion to these cases so affected, there were six patients with pericarditis who had 1 British and Foreign Medico-Chirurgical Review, xl. p. 506. 1 Path. Trans, xx. 8. CHOREA WITH AND WITHOUT DELIRIUM. 533 delirium, or coma, or both, as the princi- pal affections, and who had choreiform movements as a subsidiary affection. There were thus twenty-two cases of rheumatic pericarditis with chorea or choreiform movements, not including sev- eral who had also tetaniform symptoms. The thirteen cases with chorea, and two of the three with limited choreiform movements, were below the age of twenty- one, nine of these being girls and six youths. The remaining case with limited choreiform movements was a man aged 22. Nine of these sixteen choreal cases died and seven recovered. Thirteen of these cases, including the whole of those with delirium, had endo- carditis as 'well as pericarditis; in two cases endocarditis was probable, and in one it was absent or doubtful. In eight of the cases the chorea ap- peared after the commencement of the pericarditis; in seven of them the two affections probably came into existence about the same time ; and in one excep- tional case, recorded by Dr. Ormerod, the chorea appeared first, then the pericar- ditis, and finally the affection of the joints, thus reversing the usual order of succession of those affections. The chorea appears to have continued up to the time of death in most of the fatal cases when the pericarditis was active ; but the reports of several of them are, in this respect, imperfect. The relation of the termination of the chorea to that of the pericarditis varied much in the cases that recovered. In one case the choreic movements were violent on the day that the frottement dimin- ished, and were absent four days later. In another case the chorea improved with the improvement of the state of the heart.1 A patient of my own made objectless movements with his hands when the peri- carditis was at its acme; and two days later those movements ceased. In a boy with pericarditis, violent chorea appeared when the rheumatic and cardiac affec- tions rather suddenly disappeared. Six days later with return of pain in the joints the chorea ceased.2 In another patient, a girl, chorea appeared four days after the disappearance of friction sound.3 Partial choreiform movements, usually of short duration, appeared in six of the cases that were affected with delirium with and without coma, and in all of them the movements appeared when peri- carditis was present. The character of the choreiform move- ments was peculiar in some of the cases. Two of the patients rolled the head from side to side ; one smacked his lips, an- other pursed his mouth, a third snapped, grimaced, and cried out; two moved the left hand and arm constantly ; and in five the spasmodic movements of the body were very violent, so that in three of them personal restraint was demanded. In one of those five patients, on the sec- ond and third days, the spasms put on the character of the most violent convul- sions. The cases of chorea with delirium presented considerable variety ; and sev- eral of them, as we have already seen, had temporary insanity. Five of the eight cases with delirium were fatal, and three recovered. The duration of the cases varied consider- ably. The five fatal cases died at various periods from the fourth to the sixteenth day of the delirium. Of the three that recovered, one had delirium for a month, one had chorea for three weeks, and in one, a man under my care, quick and needless movements of the hands, and occasional muttering, lasted two or three days. B3.-II. Cases with Simple Endocarditis. -No case of chorea with delirium, and only one with rapid death, occurred among the cases of acute rheumatism with endocarditis. B3. - III. Cases without Pericarditis, Endocarditis being absent or doubtful. - I have already given two cases of this class with chorea and delirium that were affected with taciturn melancholy of lim- ited duration. The third case, a girl, aged 14, also had chorea and delirium.1 B3. Cases with Choreiform Movements in which those movements were partial and of secondary importance,and occurred in patients already included among those with delirium or coma. B3. - I. Cases with Pericarditis.- Six cases with deli- rium, one of which had coma also, among the sixty-five cases of rheumatic pericar- ditis had movements of a choreiform char- acter for a single day in the course of the disease. Three of these patients died and three recovered. Four of them were male and two were female patients, and of these, five were above the age of twenty- five, and only one below that of twenty- one. B4, C3.-Cases with Tetaniform Move- ments sometimes associated with Choreiform Movements.-I. Cases with Pericarditis.- In a small but important group of cases tetaniform symptoms occurred in connec- tion with rheumatic pericarditis. Seven of the sixty-five cases of pericarditis had tetaniform movements, or continuous con- traction or rigidity of muscles, of greater or less intensity. Some of these affections 1 Guy's Hospital Reports, vi. 1841, pp. 420, 421. 2 Mr. Land, Lancet, 1873, i. 38. 3 Dr. Kirkes, Trans, of the Abernethian Society, 1850, p. 57. 1 Tungel, loc. cit. 18G0, p. 125. 534 PERICARDITIS approached in their severity and charac- teristic form to tetanus, others could only be indistinctly associated with that disease. The first case was an excitable man, aged 19, a gardener, who had, when first seen, twitching of the muscles, and of the right side of the face, increased by speaking. He had increasing agitation, indistinct articulation, and a difficulty in opening his mouth, which he closed with a snap. After this he threw his head from one side of the bed to the other, his convulsions resembled tetanus and opis- thotonos, and his distress in swallowing was like that in hydrophobia. Four days later he rolled his eyes, ground his teeth, and smacked his lips ; and he died ex- hausted by laborious spasm and probably by want of sustenance. His brain was vascular, and there was questionable soft- ening around a vascular spot in the spinal cord opposite the first dorsal vertebra. There was pericarditis and endocarditis.' The next case, an over-worked girl, aged 19, at a late period of its history, seemed to plunge almost at once into the tetani- form condition. She rolled her eyes wildly, had furious delirium, and violent tetanic spasms with firm clenching of the fingers. After a week the delirium sub- sided, but she talked incessantly and inco- herently, and was half maniacal, half idiotic up to the forty-sixth day, but from that time her progress to recovery was steady.2 The third case, a youth, had pericarditis, but no endocarditis, inflam- mation of the kidney, occasional deli- rium, and slight opisthotonos ; and on the eleventh day he died.3 The two following cases, both of which were fatal, were under my own care. The more important case was a youth aged 17. On the eighteenth day, the left side and the tongue were affected with choreiform movements, which extended, with stiffness, to both arms. On the thirty-eighth the left arm, which still jerked and shook about, was rigid, the forearm being bent on the arm, the hand on the forearm. On the forty-seventh day, stiffness of the neck appeared, and he moved his arm with difficulty ; and on the following day he died. He had both pericarditis and endocarditis. In this case the rigidity of the limb points to an affection of the nervous centre, probably due to embolism. The other case, a man aged 27, a car- penter, came in with pericarditis at its acme, and endocarditis. On the third day he frequently slumbered and, as the eyes were half-closing, the arms and legs started. On the evening of the seventh day he was restless, and not quite rational, trembled, and kept moving his lower jaw and biting his lips. Half an hour later he was more noisy, and knocked about, still shaking his jaw. His pupils were dilated and very sluggish, and at eleven o'clock he died. I can find no notes of his post- mortem examination. The two remaining cases with tetani- forin symptoms belong to the group of cases of endo-pericarditis with delirium and coma. One of these, a young man, had pain in his right temple, followed by wild delirium. During the night general convulsions came on in occasional spasms of a tetanic character, and in the inter- vals he lay in a state of coma. He re- mained in this condition for three or more days, when he died.1 The remaining case, a young woman, became restless and flighty on the sixth day of her illness, and next day pericarditis and endocarditis de- clared themSblves. She then became very violent. T'he right arm and leg were never still; at times, however, this state became aggravated into one of general convulsions of a tetanic character. She continued thus for nine days, the convul- sions being incessant. On the twelfth day she became comatose, after jumping up and falling out of bed with her forehead on the floor. She finally recovered. Pericarditis - neither Rheumatic nor from Bright's Disease-accom- panied by Affections of the Ner- vous System. An important series of cases of pericar- ditis in which there was neither acute rheumatism nor, so far as was directly ascertained, Bright's disease, have been published from time to time by Rostan, Dr. Abercrombie, Dr. Bright, Bouillaud, Andral, and Sir George Burrows. The cases of this class that I have gathered together from the records of various observers, and from the note- books of St. Mary's Hospital amount to twenty-six. These cases present examples of the whole series of affections of the nervous system that have been observed in cases of rheumatic pericarditis, with the excep- tion of those with temporary insanity, and these were possibly represented by one fatal case that had obstinate taciturnity. Among these twenty-six cases, (A1) one had coma without delirium ; (A3) four had delirium and coma, the delirium in two of them preceding, and in two of them following the coma ; one had delirium and convulsions; (B1) eleven had uncompli- cated delirium which was slight and of short duration in seven of them ; and of 1 Dr. Yonge; Dr. Bright, Guy's Hospital Reports, v. (1840) p. 276. 2 Dr. Fuller, loc. cit. 201. 8 Dr. Fuller, loc. cit. 289. 1 Sir Thomas Watson, loc. cit. ii. 306. AFFECTIONS OF THE NERVOUS SYSTEM. 535 those without delirium, (C,2) three had chorea or choreiform movements; (C3) two had tetanus, and (D) one had slight convulsions. The affections of the ner- vous system in these cases of pericarditis, instead of being similar in character were thus very various. A1. Coma.-The patient with coma was a woman who was suddenly seized with complete loss of consciousness, remained in this state four days, and died. Peri- carditis was the only appreciable lesion. A3. Coma with Delirium.-Among the four cases with coma associated with de- lirium, in two instances the delirium, as usual, preceded the coma, while in two the delirium followed the coma. One of the former class, a boy, aged 12, affected with pysemia, was delirious, and after a night without sleep, became unconscious and died in the afternoon. Pericarditis was associated with small deposits of pus in the walls of the heart, the fibres of which were soft and almost black.1 The other case in which delirium was followed by coma, presented tetaniform symptoms. A woman aged 26, was admitted soon after a false conception in a state of deli- rium and obstinate taciturnity. After this she frequently reversed her head backwards, had convulsive movements of the face, and the arms presented from time to time a rigidity almost tetanic. On the fifth day the arms when raised fell as if paralyzed, she became comatose, and died in the evening. Pericarditis was the only morbid state discovered after death.2 Three of these cases may have been affected with "hyperpyrexia." There is, however, no indication that their tempera- ture was raised. In the other patient, a house-painter, in whom the coma preceded the delirium, I think that Bright's disease, not noticed after death, when the kidneys were not examined, was the probable cause of the fatal conditions spoken of.3 The patient with delirium and convul- sions was a schoolboy with evident pyse- mia, who had, in the opinion of all who saw him, severe inflammation of the brain. His brain was healthy, but his pericar- dium was inflamed, and innumerable small patches of pus oozed from among the muscular fibres of the heart.4 The case with convulsions without delirium was also a boy, aged 7, who had pain in the left side and the epigastrium, and on awaking next morning was seized with slight convulsions, sank into a low ex- hausted state, and died in half an hour. There was universal pericarditis, and when the heart was cleared from its soft gelatinous envelope, it was covered with small irregular granulations.1 B1. Delirium without coma or other complications was present in eleven cases of pericarditis not occurring in acute rheumatism or Bright's disease. The most important of these cases was a man aged 36, under the care of Sir James Alderson. Three and a quarter pounds of dark amber-colored fluid were found in his pericardium, the heart being covered and the sac lined with a thick honeycombed layer of new membrane. The supra-renal capsules, especially the right one, were enlarged with tubercular deposit. He had excessive distress and pain over the heart, the whole front of the chest was dull on percussion, and the impulse and sounds of the heart were ab- sent. From the presence of these signs Sir James Alderson concluded that his patient was affected with pericarditis. On the twenty-second day after admission he became delirious, and on the twenty- fifth he was maniacal, and died. Another case of this class was a shoe- black, aged 67, who had delirium, with great loquacity. He raised himself sud- denly, went to the window to breathe, re- turned to bed, lay down, and soon died. There was extensive pleurisy on the left side, spreading to the pericardium, which contained a pound of purulent liquid; the walls of the heart being soft and its fleshy substance yellow.2 A third case, a man, had pericarditis associated with pysemia, following an operation for stric- ture. Seven of the remaining cases of this series presented only slight delirium, and may be conveniently grouped together. One, who had pleuro-pneumonia and pericarditis, recovered.3 Another had slight delirium and fever, and pericar- ditis. One had empyema and pericar- ditis. Two cases under my care were delirious the day before death. One had pysemia, and purulent dots were scattered through the fleshy substance of the heart; the other had empyema of the left side, and pericarditis. In the two remaining cases the delirium appeared a short time before death ; one had extensive phthisis of the right lung and a vast cavity, the other had empyema of the left side, the pericardium being inflamed and thicken- ed. In all these cases the delirium ap- peared to be quite as much connected with the disease upon which the pericar- ditis had grafted itself as upon the peri- carditis itself, and in most of them it was little more than the wandering of mind 1 Mr. Stanley, Med.-Chip. Trans, vii. 322. 2 Andral, Clinique Medical, i. 25. 8 Bouillaud, loc. cit. i. 319. 4 Dr. Latham, London Medical Gazette, iii. 129, p. 209. 1 Dr. Abercrombie, Trans. Edin. Med.-Chir. Soc. i. 1821-24. 2 Corvisart, loc. cit. p. 239. 3 Bouillaud, loc. cit. i. 3G7. 536 PERICARDITIS incident to illness of so lowering and fatal a character. The remaining patient of this group, a coachman, aged 51, and a drunkard, who was under the care of Dr. Chambers, pre- sented a condition resembling delirium tremens. He had extensive pleuro-pneu- monia of the left lung, and pericarditis. Two of these cases with brief delirium, were under the care of Sir James Aider- son, and two under that of Dr. Chambers. C,2. Chorea and Choreiform Movements. -Two cases of non-rheumatic pericarditis had chorea, and four presented move- ments of a choreiform character. C*. Chorea.-One of the cases, a well- grown girl of 15, had chorea for six weeks before admission, and on the twenty-sev- enth day after it was suddenly seized with obstructed respiration followed by a con- vulsive fit, and died. There was pericar- ditis, and the mitral valve was somewhat thickened, but the endocarditis was not noted. The other case, a little girl, was under my own care. She was brought to the hospital in her mother's arms, in great distress. She presented prominence over the region of the pericardium, dul- ness on percussion extending up to the clavicle, and a pericardial friction sound. There was evidence also of pleurisy of the left side. Choreal symptoms appeared in the face, beginning in the corrugator su- percilii, on the third day after admission, and chorea was established on the fifth day. On the ninth day she was much quieter; her face was pale, her lips "were blue, and the veins of the neck pulsated, being full during expiration and during the ventricular systole ; and a loud mitral murmur was audible at the apex. She died on that day, but I have found no notes of the examination after death. C2. Choreiform Movements.-Four cases of non-rheumatic pericarditis presented in the course of their illness movements of a choreiform character. These cases hold an intermediate place between those with well-developed chorea, and those with regularly repeated local convulsive movements. The most important case ought perhaps to be included among those with chorea, but it developed certain characteristic symptoms of the choreiform type, that are rarely or never present in uncomplicated chorea. This patient, a young lady, after a fortnight of extreme restlessness, and a good deal of delirium, fell into a state resembling chorea with convulsive agitation of the limbs, con- stant motion of the head, and wild rolling of the eyes. Cold was applied to the head, her symptoms subsided in a few days, and she gradually recovered. Three months and a half after the commence- ment of her illness she took cold, became suddenly worse, and died on the seventh day. The pericardium was universally adherent to the heart by lymph, and a depositof lymph covered its outer surface.1 The other three cases, all fatal, of non- rheumatic pericarditis were reported by Corvisart, and the most remarkable symp- tom was a state of extreme agitation amounting to jactitation. They all had pleurisy as well as pericarditis, and one had pneumonia also. One of them had delirium, in another the mind was affect- ed, and in the third disturbance of the in- tellect -was not noted. C3. Tetaniform Symptoms and Tetanus. •-Two of the cases of non-rheumatic peri- carditis were affected with tetaniform movements, or rather with actual tetanus, some of the symptoms of which were un- usual. One of these cases was a boy who when admitted had cramps, and a threat of suffocation. His fingers, arms, and forearms, his legs, and feet were strongly bent, and the muscles of his limbs and abdomen and his masseters were so hard that they felt like touching a stone, espe- cially during the paroxysms. A warm bath and cold affusion gave great relief, and the paroxysms of suffocation ceased half an hour later. After this the jaws were slightly closed, he had a return of the suffocation, especially when he drank, and occasional cramps. On the fifth day he had a cold bath by accident, and was seized with cramp when in the bath. He had spasmodic contractions of great in- tensity on the following day, and died in a paroxysm of suffocation. There were two ounces of pus in the pericardium, the surface of which was injected.2 The other patient with tetanus was a gentleman of middle age who, when first seen, was suffering from a violent spas- modic contraction of his limbs. On the fifth day he had cramps of his extremi- ties and occasional spasmodic rigidity of the whole body, which "was sometimes bent backwards, being supported by the occiput and the heels in a state of com- plete opisthotonos. During the night his spasms were so severe that he could scarcely be kept in bed, and he died sud- denly on the following day. He had peri- carditis, and the brain and spinal cord were healthy.3 I have ranked these cases with those of tetanus because they presented universal rigidity of the limbs and body ; which, in the first case, extended to the masseters ; and in the second, caused, during the paroxysms, complete opisthotonos. There were, however, certain conditions in which they both differed from ordinary tetanus. In neither of them did the affec- tion commence with trismus, and in the ' Dr. Abercrombie, Trans, of Med.-Chir. Soo. of Edin. i. 1 2 Bouillaud, loc. cit. i. 333. 3 Dr. Mackintosh, Practice of Physic, ii. 25. AFFECTIONS OF THE NERVOUS SYSTEM. 537 second case its presence is not mentioned. In both of them at the outset of the at- tack the muscles of the extremities were involved ; and in the first of them, be- sides cramps of the legs, the fingers, arms and forearms were strongly bent. In tet- anus I need scarcely say that the reverse conditions prevail, for trismus is usually the earliest symptom, and the affection of the limbs is comparatively late, while that of the hands and arms is usually slight, the extensor muscles being more affected than the flexors. In tetanus the advance of the disease is steadily progressive, but there was a suspension of the spasmodic contraction of the limbs in both of these cases. Dr. Bright describes a case of tetanus occurring in a man affected with inflam- mation of the pleural surface of the right side of the pericardium, involving the phrenic nerve, in which there was no pericarditis. In this instance the tetanus advanced rapidly through its usual pro- gressive course. On the first evening he complained of difficulty in opening his mouth, and swallowed with a convulsive catch. During that night his teeth were completely closed, and next morning he could get nothing into his mouth, and could not even swallow his saliva. There were slight indications of opisthotonos, and spasmodic action of the muscles of the back. In the afternoon there was no relaxation of the spasm ; he had several epileptiform seizures, during which his face was purple, his eyes stared, and his whole body was convulsed. He rambled occasionally, and died twenty-four hours after the first seizure of dysphagia. Dr. Bright suggests that in this case tetanus may have been caused by the phrenic nerve being involved in the seat of the inflammation.1 Convulsive Movements, Chorea, and Cho- reiform and Tetaniform Symptoms in Cases ff Acute Rheumatism with and without Pericarditis, and in cases of Non -Rheumatic Pericarditis, in which BrighVs Disease was Absent. Summary. Convulsive Movements. -I do not consider here cases of coma with convulsions, of which there were five, three with and two without pericar- ditis, one with and three without endo- carditis, which was probably present in the remaining instance ; nor those with convulsions associated with albuminous urine, of which there was but one pa- tient, affected with both pericarditis and endocarditis. There were altogether nineteen patients with convulsive movements among the whole series of 180 cases of acute rheu- matism with affection of the nervous sys- tem ; twelve of whom had pericarditis and seven had no pericarditis, while eight or perhaps nine of them had endocarditis. Fourteen of these cases had twitchings of the limbs or face, and of these, eight had pericarditis, and five endocarditis. From this resume it is evident that al- though these convulsive movements are probably influenced, and may in some in- stances have been caused by the co-exist- ence of pericarditis or endocarditis ; yet they may, and often do occur quite inde- pendently of either of those affections, and in the absence of both of them. Hyperpyrexia (actual in seven cases, inferred in four) was present in eleven of the nineteen cases with convulsive move- ments or twitchings. In Dr. Greenhow's important case, given at page 521, twitch- ings of the face were generally present when the temperature ranged from 102'1° to 106'2°, but they were suspended by the cooling bath, and returned after removal from the bath. The general affection of the nervous system varied in the different cases with convulsive movements and twitchings. In one patient a convulsive fit preceded coma without delirium. In seven cases there was delirium followed by coma. In four of these, twitchings occurred during the delirium ; while in two of them, twitchings, and in one, convulsive move- ments, accompanied the coma. Convul- sive movements of the whole body in one instance, and of the face in another, fol- lowed delirium and preceded death. There were general convulsive movements in one, and twitchings of the face in two cases of uncomplicated delirium. There were twitching movements in four cases with chorea and delirium, in one of which there was also a state re- sembling tetanus and opisthotonos. In these four cases the twitchings were prob- ably choreiform in character. In one of the two remaining cases, a slight fit with ptosis preceded death by a few hours ; and in the other twitching was present with albuminuria. Convulsions were present in three, and convulsive agitation of the limbs in one, and of the lips or face in two of the twenty- six cases of non-rheumatic pericarditis, in which there was no Bright's disease. Chorea, and Choreiform, and Tetaniform Symptoms. Chorea.-Twenty-one of the 180 cases of acute rheumatism with affec- tions of the nervous system had chorea. Fifteen of those patients with chorea had pericarditis, six had no pericarditis; while fourteen of them had endocarditis; three had no endocarditis; and in three of them, endocarditis was probable or doubt- ful. Pericarditis and endocarditis at- tacked three-fifths of these patients con- jointly (13 in 21). It would appear from this, at first sight, as if pericarditis favored or influenced the production of chorea, 1 Med.-Chir. Trans, xxi. 4. 538 PERICARDITIS. thus apparently supporting the view of Dr. Bright that the more frequent cause of chorea in conjunction with rheumatism is inflammation of the pericardium, the irritation being probably communicated thence to the spine through the phrenic nerve.1 This view is apparently strength- ened by the history of several of the cases in which the chorea and the pericarditis ap- peared, improved, and disappeared simul- taneously. On the other hand, in one case, chorea preceded pericarditis, and in at least two others it came into play when the pericarditis was vanishing. The united presence of inflammation without and within the heart in so many of these cases, complicates the question as to the influ- ence of pericarditis on the production of chorea; and these clinical statistics favor the view that endocarditis may be the cause of the chorea, quite as much as that pericarditis may be its cause. I will not pursue this question in this place farther, excepting to repeat that in Dr. Broad- bent's and Dr. Tuckwell's important cases of chorea and delirium, there was embo- lism of the most minute cerebral arteries, associated with endocarditis. These two cases seem to show that it is possible that in some of the above cases also, chorea may have been associated with minute cerebral embolism due to endocarditis. I have already illustrated the possible or probable connection of temporary insanity in cases of acute rheumatism with endo- carditis and minute cerebral embolism,, or with minute cerebral thrombosis, the con- volutions being affected ; and five of these cases of chorea had also temporary in- sanity, in three of which there was endo- carditis, while in two there was no endo- carditis. , Chorea was present in two cases of non- rheumatic pericarditis without Bright's disease. In one of these the onset of the chorea preceded, and in the other fol- lowed, that of the pericarditis. In one of those cases endocarditis was also present, and in the other it was doubtful. Choreiform Movements. Jactitation. - Chorea, as we have just seen, affected twenty-one of the 180 cases of acute rheu- matism with affection of the nervous sys- tem. Besides these there were fourteen cases that had choreiform movements without definite chorea. One patient moved automatically, as in chorea, and another made objectless movements with his hands. Both of these cases had endo- pericarditis. Eight patients were affected with jactitation, which was general in six instances, and limited to the right or left side in two. The whole of these patients had pericarditis, while endocarditis was present in three of them, was absent in one, and probably absent in four. There was extreme jactitation of the whole body in three cases of non-rheu- matic pericarditis, probably without endo- carditis, observed by Corvisart; two of these had pleurisy, and the other one pleuro-pneumonia ; those affections in two of the cases being the probable cause of the pericarditis. The invariable presence of pericarditis and the frequent apparent absence of en- docarditis in these cases of general jacti- tation, would appear to point to pericar- ditis as a possible cause of that condition, and perhaps by inducing reflex move- ments. Agitation.-Fourteen of the cases with affection of the nervous system in which the temperature was not observed had agitation, which is a condition allied to general jactitation, which was also present in two of them. 1 find no express men- tion of agitation in the sixty-one cases in which the temperature was observed. Five of the fourteen cases with agitation had pericarditis ; eight of them had endo- carditis ; while five of those cases had neither endocarditis nor pericarditis. Ten of the cases with agitation died and four recovered. Holding of the Head from side to side.-A peculiar, regularly repeated rolling of the head from side to side occurred in eight of the 180 cases of acute rheumatism with affection of the nervous system. Five of these cases had well-developed chorea, and two others had limited choreiform movements. Six of these cases had peri- carditis, while five of them had endocar- ditis, and in one its presence was doubt- ful. All of them had either endocarditis or pericarditis. This peculiar oscillating movement of the head, though generally connected in these cases with chorea or choreiform movements, is not, so far as I know, ever present in ordinary chorea, and it forms, therefore, a feature of differ- ence between those cases and these. One patient, who had endo-pericarditis, de- lirium, and coma, rolled violently about the bed so that he required to be held down. Choreiform movements were present in four cases of non-rheumatic pericarditis without Bright's disease. In one of these the state resembled chorea, there being convulsive agitation of the limbs and constant motion of the head, with deli- rium ; in another patient there was slight convulsive agitation of the face ; and in two other cases there was violent general jactitation. I'etaniform Symptoms and Tetanus.- Thirteen, or if the presence of " risus sar- donicus" alone be included, fifteen cases presented symptoms of a tetaniform nature. In eight of those cases the tetaniform symptoms were general. Some of these 1 Med.-Chir. Trans, xxii. 15. PHYSICAL SIGNS OF RHEUMATIC PERICARDITIS. 539 had also chorea, or choreiform move- ments. In one such case the choreal convulsions put on a character resembling tetanus and opisthotonos, and the distress in swallowing was not unlike that in hydrophobia. Another case had opistho- tonos and tetanic spasms ; and a third had slight opisthotonos. Three other cases had spasms or convulsions of a tetanic character, which were accompa- nied in one instance by firm clenching of the hands. One patient under my care had stiffness of the neck ; and rigid jerk- ing and shaking about of the left arm; the forearm, at a later period, being bent on the arm, the hand on the forearm. The eighth case, a woman, had a tempe- rature of 109*5, and after being put into a tub of cold water was attacked with tonic spasms. Two cases had spasms of rigidity of the muscles of the neck, in one after being cooled in the bath from t. 109° to 103*6°, and two had stiffness of the neck, one of which has been already alluded to. One patient who was violently delirious at a temperature of 107*8° to 109°, after being bled, immediately passed into a state of unconsciousness, and was attacked with trismus, and convulsive movements of the jaws, hands, and arms. Two cases were affected with stiffness of the jaw ; which was accompanied in one of them by swelling of the temporo-maxillary articulation ; this being the patient just spoken of who was seized with tonic spasms after the bath ; and who closed her teeth firmly over her lips, drawing blood. Another patient, a man, was con- tinually moving his lower jaw and biting his lip ; and another, also a man, kept incessantly pouting his lips and rubbing them over his teeth. One patient, spoken of above, with spasms of rigidity of the neck after the bath, had also spasms of rigidity of the lips. Another case with opisthotonos and tetanic convulsions, closed the lips in snaps before, and smacked the lips after having convul- sions. " Risus sardonicus" was observed in five cases, in three of which there were, and in two there were not, other tetani- form symptoms. Of the above thirteen cases w*ith tetani- form symptoms, not including the two with simple "risus sardonicus," ten had endo-periearditis, one had pericarditis, endocarditis being absent, in one both of those affections were doubtful, and in one they were both absent. These clinical facts make it probable that pericarditis or endocarditis, or both, may sometimes be concerned in the production of tetaniform symptoms. Other influences were, how- ever, at work connected with hyperpy- rexia in some of the cases. Thus trismus appeared in one patient just alluded to who became unconscious after being bled, the temperature rising from 107*8° to 109°; and in three cases the tetaniform symptoms came into play after the exces- sive temperature had been cooled down by the bath. We have already seen that in one case of non-rheumatic pericarditis ending in coma, the arms presented occasionally a rigidity as of tetanus ; and that in two other cases of the same kind, there was actual tetanus of a peculiar type. These three fatal cases had no endocarditis. Andral, in commenting on the first of these cases, or that with occasional rigidity of the arm, and delirium ending in coma, asks whether the cause of the affection of the nervous system in these cases is not in the inflammation of the pericardium itself? We have already seen that Dr. Bright looks to the communication of an influence from the inflamed pericardium, through the phrenic nerve to the spine, as a cause of choreal and tetaniform affections. I would here remark that tetanus may be caused by a wound and by exposure to cold, and there is nothing therefore incon- sistent, so far as I can see, in the idea, that it may be caused also by an internal inflammation affecting local nerves, and through their channel acting on the spi- nal marrow. Tetanus is not, so to speak, an inter- mittent contraction of the muscles of the reflex type, but a continuous contraction of the muscles, due to the direct continu- ous action of the spinal cord. In tetanus, as Dr. Lockhart Clarke has shown, there are areas of disintegration in the spinal cord. In traumatic tetanus, the cause of the affection is the injury to the nerve, and in these cases the nerve must carry from its periphery to its centre an influ- ence that sets into action the disintegra- tion of the cord. If the inflammation of the peripheral ends of the nerves of the pericardium excites tetanus, it would per- haps do so in some such manner as that just suggested. The cases of tetanus and tetaniform affection associated with peri- carditis, though striking are very rare, and we may fairly ask whether in those cases in which the two affections coin- cided, some other cause may not have been at work to induce the tetanus. I know of no instance in which tetanus was induced by any other internal inflamma- tion, and if this be so, it is not easy to see why pericarditis or pleurisy affecting the phrenic nerve should be the only internal inflammations capable of inducing that affection in its typical or modified form. THE PHYSICAL SIGNS OF RHEU- MATIC PERICARDITIS. In every case of rheumatic pericarditis there is an increase in the amount of 540 PERICARDITIS fluid in the pericardium, and a layer of ridged, roughened, or honeycombed lymph is spread over the opposing sur- faces of the heart and the pericardial sac. The amount of the fluid poured into the sac is made known by the extent of dul- ness on percussion, the prominence of the sternum and costal cartilages, and the widening of the intercostal spaces over the region of the pericardium, and by the position of the impulse; while the pres- ence of lymph covering the heart and lining the sac is told by a friction sound. Effusion of Fluid into the Pericardium in Rheumatic Pericarditis.-.Although in the prescribed order, the examination of the chest by the eye and the application of the hand rightly precede that by percussion I shall here reverse tliis order, and begin with percussion, for by it we really judge of the extent of the fluid in the sac. The pericardium of an adult man with a healthy heart is capable of holding from fourteen to twenty-two ounces of fluid, and that of a boy of from 6 to 9 years old, about six ounces, when the sac is distended Fig. 79. Fig. 80. Pericardium not distended. Pericardium artificially distended with fifteen ounces of fluid. to the full by injecting water into it by a syringe, through an opening made in the anterior wall of the pericardium. The effect of this artificial distension of the pericardium on the size, form, and position of the sac and on the situation of the surrounding parts is shown in the accompanying figures (79, 80). The peri- cardium, thus distended, is pyramidal or pear-shaped. It is formed, so to speak, of a larger and a smaller sphere, the smaller one resting on the top of the larger. The larger and lower sphere contains the heart, the ascending vena cava, and the pulmonary veins ; and the smaller sphere holds the great vessels. The distended sac occupies the whole centre of the chest, filling up the space between the sternum PHYSICAL SIGNS OF RHEUMATIC PERICARDITIS. 541 in front and the spinal column behind; and extending across the chest from a little within the right nipple to a little beyond the left nipple. The whole sac is lengthened ; its smaller end reaches up- wards almost to the top of the sternum ; and its floor, being formed by the central tendon of the diaphragm, presents a large spherical prominence that bulges down- wards into the abdomen, occupies the epigastrium, and reaches as low as the tip of the ensiform cartilage and the lower edge of the sixth costal cartilage. The enlarged and swollen sac displaces all the organs and parts surrounding it. In front it separates the two lungs from each other, so as to uncover the pericardium in front of the heart and great arteries. It pushes forwards the two lower thirds of the sternum, the ensiform cartilage, and the adjoining costal cartilages, especially the left, from the third to the sixth ; and by counter-pressure backwards it compresses the oesophagus, the descending aorta, the bifurcation of the trachea, and the left bronchus between itself and the bodies of the vertebrae upon which those parts rest. It displaces the lungs to either side and backwards ; and the central tendon of the diaphragm where it forms the floor of the pericardium, the stomach, and the left lobe of the liver downwards. The artificial distension of the pericar- di um closely corresponds in general form with its natural distension from pericar- ditis, when the amount of the effusion has reached its acme. I have already sketched at page 496 what I believe to be the usual course of the increase of the effusion from the beginning of an attack of pericarditis to the period of its acme. When, how- ever, the inflammation of the pericardium has existed for some time, the walls of the sac, so thin, tough, and firm in health, become comparatively thick, soft, and yielding; and as the sac cannot expand to a material degree either upwards to- wards the neck, or downwards towards the abdomen, it yields sideways and back- wards, and widens to the right and espe- cially to the left, so as to encroach on both lungs, but more seriously on the left lung; as may be seen in the accompanying figure^ which is taken from a case of chronic pericarditis of long standing, in which the sac contained three pounds and a quarter of fluid (fig. 81). When thus distended, the sac seems to occupy the whole front of the chest; and it com- pletely conceals the left lung, which is pushed backwards and compressed by it so that comparatively little air is admitted into that lung at its lower and posterior part; this effect being increased by the compression of the left bronchus. There is another effect of this disten- sion of the pericardium to which I have already alluded, its inferred effect namely upon the heart itself. The muscular walls of the ventricles are so thick, and their action is so powerful, that the direct effect of the fluid pressure upon them can- not be very great. But the pressure of the fluid tells inwards upon the weak and unresisting walls of the auricles, the vena cava descendens within the pericardium, and the pulmonary veins, so as to com- Fig. 81. Case of nericarditis inKhichone sac contained 3J lbs. of fluid. The patient was under the care of Sir James Alderson. press and lessen those vessels and the auricles, and to resist and impede the cur- rents of blood, on the one hand from the system along the cava, and on the other from the lungs along the pulmonary veins. This partial blocking of the double stream from the system and the lungs to the heart lessens the contents of the organ, and tends to diminish the size of its cavi- ties. At the same time the supply of blood to the aorta is lessened, and the ascending aorta is therefore also com- pressed by the fluid. The pulmonary artery, however, owing to the obstacle to the flow of blood through the lungs, tends to resist the pressure of the fluid in the swollen sac, and to remain distended. While, however, this influence on the part of the fluid pressure of the distended pericardium is at work compressing the auricles and veins; a second influence is 542 PERICARDITIS. at work, also set up by the inflammation, to counteract the first influence, and to shield to some extent the weaker parts of the heart. The auricular appendices shrink at an early stage, and the walls of the auricles and veins are thickened and somewhat protected from the pressure of the effused fluid by a leathery coat of mail in the shape of the roughened and honeycombed coating of lymph that clothes and strengthens the feeble natu- ral walls of those parts. Thus the double march of the inflammation supplies at the same time a compressing fluid, and a sus- taining covering of lymph. The distension of the pericardium with fluid produces two other effects on the heart. 1. The heart is heavier than the fluid in which it plays, and its ventricles consequently tend to sink backwards so that the left ventricle rests upon the pos- terior wall of the pericardium, just as the liver sinks backwards when the abdomen is distended with fluid in cases of ascites. 2. The other effect of pericardial disten- sion on the heart is the lifting or tilting upwards of the organ within the sac. The heart is attached by its great vessels to the posterior and upper parts of the sac, and the whole organ, therefore, tends to shrink upwards and gravitate backwards towards its points of attachment. At the same time the accumulating fluid which occupies in volume the space between the lower surface of the heart and the central tendon of the diaphragm, displaces the organ upwards into the higher part of the pericardium. The natural effect of this gravitation, shrinking, and upward displacement of the heart, owing to the great accumula- tion of fluid in the sac, would be, I con- ceive, if not modified by other agencies, to cause a layer of fluid to be interposed between the front of the heart and the anterior walls of the chest. Practically however we find that this is not usually the case over the mass of the ventri- cles ; for with one or two rare exceptions we can always feel the impulse of the heart beating sometimes with force, some- times with a thrill, in the second and third, or third and fourth left spaces, ex- tending from the edge of the sternum to above and beyond the nipple. A layer of fluid is, however, evidently interposed between the lower portion of the front of the heart and the anterior walls of the chest. The reasons for the presence and pul- sation of the heart in the upper intercos- tal spaces when the pericardium is distend- ed, I believe to be, firstly, the distension of the pulmonary artery, and to a less ex- tent, of the right ventricle, owing to the difficulty with which the blood flows through the lungs; and, secondly, the raised position of the heart, which having left the broader space of the chest below, where it enjoyed free play, occupies its narrower space above, where the heart and pericardium are as it were grasped between the walls of the chest in front and the bodies of the vertebrae behind. The result is that under the combined influence of the elevation of the heart; the distension of the pericardium; and the contracted area of the upper part of the chest in which the heart is lodged, the left lung is displaced from before the or- gan and the right and left ventricles, and the apex and the great arteries beat against the higher intercostal spaces with which they come into direct contact. In consequence of the withdrawal of the lung from before the heart, and the nar- rowing compass of the portion of the chest in which the organ is situated, its im- pulse besides being raised, is also widened outwards, so that the apex beats against the third or fourth space, at or above the level of the left nipple, where it extends beyond the nipple line. Although the upper portion of the right ventricle is in immediate contact with the walls of the chest, I am satisfied that a portion of the fluid effused into the sac is interposed between those walls and the lower portion of the right ventricle over its anterior surface. We shall afterwards see that the im- pulse is raised in position when the fluid in the pericardium increases, and is low- ered in position when that fluid dimin- ishes, so that under these circumstances the varying amount of the fluid is told by the varying position of the impulse. Cases that form the subject of this inquiry into the physical signs of pericarditis.- I possess notes of 44 of my 63 cases of rheu- matic pericarditis, of the increase, acme, and diminution of the quantity of fluid in the pericardium, as shown by the enlarg- ing and lessening area of the dulness on percussion over that region ; the progres- sive changes in the position of the im- pulse ; and the variations in the tone, in- tensity, and area of the friction sound ; all of which signs are at once the effects and the witnesses of tiie advance and de- cline of the inflammation. I shall now briefly analyze, point by point, these par- allel effects in those cases. Percussion. The enlarged Area of Dulness on Percus- sion over the Pericardium, caused by the Increase of Fluid in the Sac.-In 22 of the 44 cases under examination, the increased amount of fluid in the pericardium, as indicated by the extended area of dulness over that region, had already at the time of its first observation reached its acme, PERCUSSION. 543 and from that time, the amount of fluid with its area of dulness steadily declined. One of these cases had a relapse and proved fatal on the 14th day. In the remaining 22 cases the period of the greatest distension of the sac was pre- ceded by a gradual increase, and was fol- lowed by a more gradual decrease, in the amount of the fluid; the periods of in- crease, acme, and decrease of the amount of fluid, being shown by the correspond- ing gradual enlargement, greatest area, and lessening of the region of dulness on percussion over the pericardium. In 11 of these 22 cases there was a single rise and fall of the tide of the effusion ; but in the 11 remaining cases there was a re- lapse, and the amount of effusion, after lessening considerably, again increased and attained to a second acme. In five of those cases, indeed, there was a second relapse, so that the fluid in the pericar- dium presented a third, and in one of them even a fourth wave of increase. The duration of the whole period of in- crease of dulness on percussion over the region of the pericardium varied much in different patients. Of the 22 cases in which the region of dulness had attained to its greatest area at the time of the first observation, the average duration of the increased dulness from the effusion into the pericardium was eight days, the ex- treme duration varying from three days on the one hand, to seventeen on the other. The average duration of the pe- riod of increased dulness in the 11 cases in which there was a gradual increase, sin- gle acme, and a decrease in the amount of fluid effused into the pericardium, amount- ed to fully eight days, the extreme varia- tion ranging from four to thirteen days. The average duration of the whole period of increased pericardial dulness was more than twice as long in the 11 cases of re- lapse, as in the cases with a single acme, since in them it amounted to eighteen days, the extremes varying from fourteen to twenty-four days. The increase of fluid in the early stage was usually rapid. In one-half of the cases in which this increase was watched, the area of dulness had reached its maxi- mum, on the second or third day after the first observation (11 in 22), and in all but two or perhaps three of the remainder, on the fourth or fifth day. The early ad- vance of the dulness was, as a rule, more slow in those patients who suffered from a relapse than in those who did not do so. The time during which the effusion into the pericardium remained at its height was, as a rule, very short, In 39 of the 44 cases the region of dulness extended over its greatest area for about a single day. It may have lasted longer, but on the next examination, made usually on the following day, but sometimes later, the tide had turned and the extent of dul- ness had lessened. The acme of the peri- cardial dulness lasted two days in three of the remaining cases, and three days in two of them. The period of the decrease of the effu- sion in the pericardium was much longer than that of its increase, its average dura- tion having been, as we have already seen, eight days in the 22 cases in which the effusion was at its acme on the first examination. We thus see that the period of the ad- vance of the effusion, dating from the time of its first observation in the early stage, usually lasted about three days ; that the period of the acme of the effusion was usually observed during only one day ; and that the period of the decline of the effusion generally lasted about eight days. The fluid in the pericardium begins to increase on the first day of the inflamma- tion ; but, as it necessarily gravitates backwards during the early stages, the effusion does not appear in front until it has accumulated so as to occupy the natu- ral hollow at the back of the sac, and the space between the lower surface of the heart and the floor of the pericardium. Dulness on percussion over the region of the pericardium therefore does not declare itself until the inflammation has lasted for a day or two. I have no exact indi- cations telling how soon the fluid ad- vances to the front of the heart in suffi- cient quantity to push aside the lungs. That it must, however, have been rapid in certain cases is I think shown by the instance given on next page. The effusion had reached its acme in one patient three days after the beginning of the attack of acute rheumatism; and the increased cardiac dulness was ob- served for the first time on the fifth or from that to the seventh day after the beginning of the illness in nine cases. Pain attacked the heart in three cases the day before, and in one three days before the first appearance of increased dulness over the pericardium; and from one to four days before the effusion had reached its acme in eight other cases. Friction sound, like increased pericar- dial dulness, is not present at the first blush of pericarditis, and in my cases the two signs usually appeared at the same time. Thus they did so in 16 of the 22 cases in which the dulness on percus- sion was detected in the early stage; while in only one of those cases did the first brush of the friction sound precede, and in the remaining five it followed the onset of the increased pericardial dulness. The upper boundary of the pericardial dulness when first observed, was limited by the space between the third and fourth left cartilages in 11 out of 22 cases, by the fourth cartilage in three cases, and by the 544 PERICARDITIS. Fig. 82. Fig. 83. Figure 82, from a youth aged 17, affected with rheumatic pericarditis, who recovered in nine days from the time of his admission. Period of the rapid increase of the effusion into the pericardium, just before the occurrence of its acme. The effusion completely distended the sac. Day of admission. The pericardial effusion distends, lengthens, and widens the sac, to the same extent and with the same effect as when the healthy pericardial sac is artificially distended witli fluid (see figs. 79, 80, p. 540). The swollen pericardium is pyramidal or shaped like a pear, as in figure 80. Its smaller and higher portion (1, 1) contains the great arteries ; and its larger portion is occupied above (2, 2) by the heart, and below (3, 3) by the great volume of fluid which accumulates between the under surface of the heart and the floor of the pericardium. The distended pericardium displaces the lungs upwards, and to each side; and the dia- phragm, liver, and stomach downwards : and the fluid in the sac compresses the auricles; and that in the lower portion of the sac, between the under surface of the heart and the floor of the pericardium, elevates the heart. Owing to the displacement of the lungs from before the pericardium, the whole of the anterior surface of the heart and great arteries is exposed, including the right auricle and ventricle, the apex and front of the left ventricle, the ascend- ing aorta within the pericardium and the pulmonary artery ; and, owing to the elevation of the heart by the fluid, that organ presses and rubs with increased force against the walls of the chest in front of it; the anterior surface of the heart at its lower portion is, however, separated from the sternum and cartilages by a thin layer of interposed fluid. This explanation, and that which follows, given once for all, will apply to figures 83 ; 86, p. 551 ; 88, p. 553; 91, p. 559 ; and 94, p. 576, which represent, each of them, the single, or first or second acme of the pericardial effusion. There is prominence over the region of the pericardium, the left costal cartilages and ribs from the third to the eighth being raised and moved outwards. The region of dulness on percussion over the distended pericardium ("pericardial dulness," see the black space) indicates the extent of the pericardial effusion; has the pyramidal or pear- shaped form of the distended sac; and extends from a little above the lower end of the manubrium, where it displaces the lungs, down almost to the tip of the ensiform cartilage, where it intrudes on the epigastrium. The lower and larger portion of the region of pericar- dial dulness over the heart and the great body of the effusion is more than twice the width of its upper and smaller portion over the arteries. This narrow upper portion forms there- fore a peak which gives to the region of pericardial dulness its pear-shaped form, and which rises high behind the sternum, and occupies the lower portion of the manubrium. The wider portion of the region of pericardial dulness bears chiefly to the left; and its upper border, starting from the foot of its narrower portion, is on a level with one of the higher left costal cartilages or spaces. The upper and left boundary of the region of pericardial dulness is therefore indented ; and its upper border is much higher behind the manubrium, than behind the adjoining left costal cartilage or space that may form its higher limit. The higher and narrower region of pericardial dulness (1, 1) over the ascending aorta and pul- monary artery, is about two inches in width, and is situated behind the sternum, on a level with the first and second spaces, and for about half an inch to the left of it in those spaces. The lower, larger, and wider region of pericardial dulness that extends over the heart itself PERCUSSION. 545 (2, 2) and over the accumulated fluid that occupies the depending portion of the sac below the heart, and that bulges downwards into the epigastric space (3, 3), extends from the upper edge of the third left costal cartilage, and the corresponding portion of the sternum, down to the lower edge of the sixth left cartilage, and almost to the tip of the ensiform carti- lage ; and from about an inch to the right of the lower half of the sternum, to half an inch or more to the left of the nipple. The lower border of the fifth cartilage, and a line running thence across the sternum to the fourth right space, probably forms the lower boundary of the heart (2, 2), and the upper boundary of the depending space (3, 3) occupied by the volume of the fluid distending the pericardial sac. The impulse of the heart occupies the third and fourth left spaces (see the curved lines in those spaces), and extends in the latter space to just beyond the nipple; and the pulsation of the pulmonary artery is felt in the first and second spaces to the left of the sternum; where the first impulse is followed by a sharp second stroke, which is synchronous with the loud second sound of the pulmonary artery, and which gives the effect of a double impulse, one systolic and gradual, the other diastolic and sharp. Figure 83, from the same patient as figure 82. Period of the acme of pericardial effusion. Third and fourth days after admission. The explanation of pericardial effusion and dulness given with figure 82, applies also to this figure. The pericardial effusion, which distended the sac on the day of admission (see fig. 82) has steadily increased in quantity since then, so that the whole pericardium has become enlarged, and has yielded sideways, and especially to the left; but it has not lengthened from above downwards. In this patient, therefore, the region of pericardial dulness (see the black space) during the acme is unusually wide, and especially along its left border; this increased width being fully as great above over the great vessels (1, 1), as lower down over and below the heart (2, 2, 3, 3). The left boundary of the region of pericardial dulness over the great arteries (1, 1) extends about an inch to the left of the sternum, in the first and second spaces ; while the left boundary of the large region of pericardial dulness over and below the heart, extends fully half an inch to the left of the mammary line (2, 2, 3, 3). In all other respects, except the increase of the dulness to the left, the region of pericardial dulness corresponds with figure 82, taken on the day of admission. The apex of the left ventricle seems in this case to be behind the fourth left rib or space, and the lower boundary of the heart probably extends along the upper edge of the fifth left cartilage, and across the corre- sponding portion of the sternum ; the heart having been much elevated by the increase of the fluid, which interposes itself between the anterior surface of the heart at its lower border and the walls of the chest. The prominence over the region of the pericardium has increased. The impulse is peculiar ; it is felt beating (4th day) from the first to the third left costal cartilages, while the third and fourth spaces are retracted during the systole (see the curved and straight lines in those spaces). These movements give to the impulse the appearance of an undulation. The interposition of the fluid between the apex and lower border of the front of the heart and the walls of the chest has combined with the elevation of the organ to raise the impulse. For later views of this case see figures 84, 85, p. 549. third cartilage in seven cases. In one patient only did the dulness on its first observation reach as high as the second space. The increase of the region of dulness over the pericardium was sometimes grad- ual, sometimes rapid. In rare instances the gradual ascent was slow and irregular. As a rule, however, the ascent was rapid. The contour of the area of dulness on percussion over the pericardium when swollen with fluid in acute rheumatism corresponds very closely with the outline of the sac when distended with water after death. (See figures 79, 80, p. 540). In a paper in the Provincial Medical Transactions I gave illustrations of the area of pericardial dulness in which the boundary lines of the effusion were ascer- tained with care, and I here give figures of those cases (figs. 82, 83, p. 544; 84, 85, p. 549; 86, 87, p. 551; 88, 89, p. 553); and elsewhere, views taken from a case of pericarditis in St. Mary's Hospital, which show the same point during various stages of the affection. (See figures 90, 91, p. 559; 92, 93, p. 575; 94, p. 576.) The form of the region of pericardial dulness changes as its area increases, its upper boundary being then on a higher level over the sternum than over the costal cartilages, instead of being, as in health, on the same level. The pericar- dial dulness, at the same time, extends further downwards in the manner shown in the figures just referred to, so as to in- trude on the abdomen, and to replace the liver and stomach to a degree proportion- ate to the amount of the effused fluid. When the increase of fluid in the peri- cardium reaches its height, and the sac is completely distended, the area of dulness over the affected region is pyramidal, or, more exactly, pear-shaped, and it extends over and beyond the heart, and in front of the great vessels. The inner borders vol. ii.-35 546 PERICARDITIS. of the right and left lungs are pushed to each side by the distended sac, so as to expose the whole of the heart and the great vessels. The region of dulness over the great vessels extends upwards from the level of the third cartilages, sometimes as high as across the middle of the manubrium, or within an inch of the top of the sternum, but more usually to a little above the junction of the manubrium with the long bone of the sternum, or about two inches below the upper end of the bone. This space of dulness over the aorta and pul- monary artery extends across the whole width of the sternum and reaches some distance to the left of it, in the first and second spaces. The area of the region of dulness over the heart itself and the lower portion of the distended pericardium, may extend across the chest from an inch or more to the right of the lower portion of the ster- num to an inch beyond the left nipple; and from above downwards from the second cartilage to the lower edge of the sixth cartilage. The extreme measure- ment from side to side of the whole region of pericardial dulness may vary from four and a half to six inches, anil somewhat diagonally from above downwards, from five and a half to seven inches. The lower portion of the region of dul- ness, from side to side, for the extent of about two inches from above downwards, is situated below the lower boundary of the heart; and is entirely occupied by the effused fluid, which here, as I have before shown, displaces the heart upwards, and the diaphragm, stomach, and liver down- wards to an extent corresponding to the amount of the effusion. The width of the region of pericardial dulness in front of the great arteries is usually about two inches, and this region usually ascends above the upper boundary of the heart to an extent varying from one inch to an inch and a half. This upper region of pericardial dulness over the great arteries, which is two inches wide, is much narrower than the great re- gion of dulness over the heart itself, which at its upper portion is above four inches wide, the greater width of the cardiac portion of the region of dulness being gained chiefly to the left. This sudden widening of tlie area of pericardial dulness from distension of the sac gives that area a peaked form above, and an indented outline along its left upper border, that distinguish it from the equally high and extensive area of cardiac dulness due to adherent pericardium and valvular dis- ease, when the heart is enlarged in all directions and especially upwards and to the left, and when the upper left border of the region of cardiac dulness presents a very gradual inclination downwards and to the left without a break. (Compare figure 88 with figure 89, p. 553.) This pear-shaped outline of the region of dul- ness over the pericardium is quite charac- teristic, and indicates with certainty the presence of extensive effusion into the sac. Among the forty-four cases, the upper boundary of the region of dulness when the effusion had reached its acme was over the first space or second cartilage in ten cases, over the second space in twenty- two, and over the third cartilage in twelve. In those cases that suffered a relapse, the first acme was as a rule higher, and the second, and still more the third acme were lower than the single acme in cases that had no relapse. If the position of the upper boundary of the pericardial dulness over the cartilages and their spaces is known, the whole area of the region of dulness over the pericar- dium may be inferred with considerable accuracy ; since the whole outline of that area shrinks when its upper boundary is lowered, and widens when it is raised. In this respect with certain definite reser- vations, the upper border of the region of pericardial dulness over the cartilages and spaces to the left of the upper half of the sternum, serves to measure the whole area of dulness and to define its complete outline; just as the ebb and flow of the tide, or the rise and fall of a flood indi- cated on a measuring post, will tell any one accurately acquainted with the coast, or the contour lines of the country, the exact area over which the land is covered by water. If the upper boundary of pericardial dulness reach to the second space, the contour line defining the dulness extends -to within an inch of the top of the ster- num ; an inch beyond the right edge of the lower half of that bone; and more than an inch below its lower end, where it may descend as far as the tip of the ensiform cartilage; to the lower edge of the left sixth cartilage; and about an inch beyond the left nipple. (See figures 88, p. 553 ; 91, p. 559.) If the upper mar- gin of dulness be limited by the third space, the boundary line extends-across the sternum on a level with the third costal cartilages; to the right edge of that bone ; and to fully half an inch below its lower end; to the upper edge of the sixth cartilage ; and to the left nipple. (See figures 84, p. 549; 90, p. 559.) The lungs, the diaphragm, the liver, and stomach are all correspondingly displaced, to a greater degree all round when the upper limit of dulness is over the second cartilage ; and to a lesser degree all round when that limit is over the third space. The intermediate position of the upper PROMINENCE OVER THE REGION OF THE PERICARDIUM. 547 edge of dulness over the other cartilages and spaces gives an intermediate outline of the whole area. The restrictions to this rule are due to age and sex, to previous affections of other organs, to valvular disease of the heart of old standing, to coinciding affections of the lungs, especially the left lung, to the duration of the attack of pericarditis and the occurrence of relapses, to accompany- ing endocarditis, to the progress of the disease, and to its terminations, whether in complete restoration to health, the valves being intact, in valvular disease, or in pericardial adhesions. These re- strictions are numerous in appearance, but practically they seldom interfere with the rule just stated of the corre- spondence of the whole area of dulness with the boundary of a particular part of it. The rule that the region of pericardial dulness in rheumatic pericarditis enlarges over corresponding areas in different cases, holds good in young persons of both sexes, and in women. In men, however, the bony framework of the chest is larger, the lungs are more ample and cover the heart to a greater extent, and the dia- phragm is lower than in boys, youths, or women. The result is, that in men both the upper and lower boundaries of the region of pericardial dulness are lower than in the classes just spoken of. Thus the upper boundary of dulness during the acme was over the third cartilage in 8 out of 14 cases of rheumatic pericarditis in men ; while in the whole of those of the female sex so affected, except one, that boundary was above the third cartilage. In nearly one-third, or 3 in 11 of the male youths with rheumatic pericarditis, the upper boundary of the region of dulness during the acme was over the third car- tilage. This is due to the fact that in the male sex, the lungs at a comparatively early period are more largely developed than in the female sex. When rheumatic pericarditis attacks a heart enlarged from previous valvular disease, the pericardial sac, being more ample, is capable of containing a larger amount of fluid, and the region of peri- cardial dulness is of greater relative width than when the affection attacks the virgin heart. If the lower lobe of the left lung shrinks, owing to the combined effect of the com- pression of that lobe and of the left bron- chus by the swollen sac, and of pleurisy with or without pulmonary apoplexy, a condition of things by no means unusual, the whole area of pericardial dulness tends towards the left, and its left border comes into direct contact with the ribs at the side. Changes in the Form of the Outline of Pericardial Dulness caused by Variations in the Progress and Termination of the Affec- tion.-If the attack lasts long, the peri- cardial sac, as I have already stated, be- comes softened, it yields sideways, and becomes widened to the left and right, while it is not proportionally lengthened above and below (see figure 81, p, 541). This is especially to be noted when re- lapses take place, and when the effusion, after lessening in quantity, again in- creases. (See figure 94, p. 576.) If the affection passes quickly through its stages, and the recovery is perfect, the heart being restored to health, the changes of the increase, the acme, and the decline of the pericardial effusion and of the area of pericardial dulness pass through the course I have described. (See figures 82, 83, p. 544; 84, 85, p. 549.) If, however, the heart becomes enlarged owing to the establishment of valvular disease, the lessening and disappearance of the effusion are delayed, and the area of dulness is somewhat widened and lowered, especially towards the left. If along with valvular disease, adhe- sions of the heart are established, the whole organ is enlarged, upwards, down- wards, and sideways. The outline of the area of dulness loses its characteristic pear-shaped form, and its peaked outline over the great vessels gives place to a gradual widening of that area from above downwards, that corresponds with the en- larged outline of the heart itself. (Com- pare figure 88 with figure 89, p. 553.) Prominence over the Region of the Pericardium. Increased dulness on percussion over the region of the pericardium is the only reliable sign of the increase of fluid in the sac. Increased prominence of the costal cartilages over the heart, with widening of the spaces between them, form, how- ever, a secondary sign of some interest and value. In my paper before alluded to, I state that the distension of the pericardial sac by fluid, besides displacing the surround- ing organs, pushes forward the sternum, elevates the costal cartilages from the second to the seventh, widens the spaces between the cartilages and ribs from the second to the sixth or seventh, pushes outwards the sixth left rib, and causes some degree of prominence over the left side. This condition was observed with care in one or more of the cases of pericarditis examined by me in the Nottingham Hos- pital. I find that prominence over the region of the pericardium was noticed by me in 19 of 63 cases of rheumatic pericar- ditis under my care in St. Mary's Hos- pital. More than three-fourths of those 548 PERICARDITIS. patients (15 in 19) were males, while only 4 were females. The cardiac prominence is obscured in women by the mamma ; that sign having been observed in only one-seventh of the female cases of rheu- matic pericarditis (4 in 27), while it was noticed in nearly one-half of the male cases (15 in 36). The increased prominence over the re- gion of the heart was usually noticed when the effusion into the pericardium was at its height, and it lessened when the effu- sion declined. In the greater number of the cases (12 in 19), the prominence over the region of the heart is described in general terms, but in seven its area was specified. In one of these it extended from the second cartilage to the sixth; in two, from the third to the sixth; in three, from the third to the fifth ; and in the re- maining one, from the fourth cartilage to the sixth. In these cases the cartilages yielded to the distension of the sac, and were dis- placed by it forwards and upwards ; with the good effect of somewhat relieving the pressure exerted by the swollen sac on those important structures, the bifurca- tion of the trachea, the left bronchus, the oesophagus, and the aorta, that are situ- ated between the back of the pericardium and the bodies of the dorsal vertebrse. The prominence over the cardiac region caused by the forward pressure of the en- larged pericardium, points out that a seri- ous counter-pressure backwards is exerted at the same time on the three vital tubes that I have just named, which convey air to the lungs, and especially the left lung, food to the stomach, and blood to the lower half of the frame. Indeed, the true value of this sign is that its presence re- veals to us at the surface, the existence of deep and serious pressure on important internal parts, a pressure that is aug- mented when the superficial prominence increases, and that is relieved when that prominence lessens. It is to be remarked that at the same time that the sternum and cartilages over the region of the distended pericardium are rendered prominent with the effect of somewhat lessening the pressure of the swollen sac upon the bifurcation of the trachea, the left bronchus, the oesophagus and the aorta-the dorsal portion of the spinal column deepens itself and curves backwards so as to afford increased space for the swollen sac, and those important tubes that are compressed by it. At the same time the patient sits up, and even leans forward, so as to allow of the gravi- tation downwards and forwards of the fluid in the pericardium. By this attitude, and the deepened spinal curvature, in- deed, the pressure of the distended sac upon those vital parts is materially les- sened, breathing and swallowing are ren- dered less difficult, and blood is supplied through the descending aorta with greater freedom to the body and lower limbs. The Position of the Impulse of the Heart in Cases of Pericarditis. When the amount of fluid in the peri- cardium has increased so as to enlarge the area of dulness on percussion over the region of the heart, the seat of the im- pulse is raised and extended outwards. I gave figures of three cases of pericar- ditis with great increase of fluid in the sac, in my paper on the position of the in- ternal organs, in which the impulse was present in the third and fourth spaces, in- stead of occupying its usual position in the fourth and fifth spaces. In that paper, attention was I believe called for the first time to the elevation of the impulse in cases of pericarditis with effusion into the sac. In thirty-seven of the forty-four cases of rheumatic pericarditis, the exact posi- tion of the impulse during successive visits is stated, in five others the impulse is described, but its situation is not speci- fied, and in the remaining two the im- pulse was almost or quite imperceptible. In examining these cases I shall study the position of the impulse from two points of view, (1) the elevation of its lower boundary; (2) its diffusion into the higher intercostal spaces during the pe- riod of the increase of fluid in the peri- cardium. (1) The Elevation of the Lower Boundary of the Impulse.-In fourteen cases, the ex- tent of dulness on percussion over the re- gion of the pericardium increased, and the effusion attained to its acme after the first observation ; and in twelve of these the impulse occupied a higher position at the time of the acme than at that of the first observation, while in two its position was unchanged. In twenty-two of the patients the amount of fluid in the pericardium was at its greatest height or acme at the time of the first observation ; and as the effusion les- sened, in eighteen of these the lower boundary of the impulse fell, in three it was stationary, and in one it became higher in position. We thus see that in thirty of these thirty-seven cases of rheumatic pericar- ditis,' the lower boundary of the impulse was raised in position when the amount of effusion in the pericardium was at its acme. POSITION OF THE IMPULSE OF THE HEART. 549 Fig. 86. Fig. 87. Figure 86 from a housemaid aged 17, affected with rheumatic pericarditis. Period of the first acme of pericardial effusion, fifth day after admission. The explanation of pericardial effusion and dulness given with figure 82, page 544, applies also to this figure. The pericardial effusion extends less to the left and more to the right than in figure 83, page 544 (acme of pericardial effusion), add is of about equal extent in the two figures from above downwards. The heart, which is enlarged, is elevated by the fluid, but to a less degree than in figure 87, its lower boundary being probably situated behind the lower border of the fifth cartilage, and just above the lower end of the sternum. The whole front of the heart is exposed, including the right auricle and ventricle, the apex and front of the left ventricle, the ascending aorta within the pericardium, and the pulmonary artery. The region of pericardial dulness (see the black space) extends from a little above the lower end of the manubrium and the second left space, down to the tip of the ensiform cartilage, and the middle of the sixth cartilage; and from a little over an inch to the right of the lower half of the sternum, to a little beyond the left mammary line. The area of dulness includes (1, 1) the region of the great arteries ; (2, 2) that of the heart; and (3, 3) that of the volume of the effused fluid below the heart, and projecting downwards into the epigastric space. The impulse is less elevated than in figure 83 (acme), being situated in the second, third, and fourth spaces. (See the curved and circular lines in those spaces.) The friction sound (represented by zigzag lines, the systolic lines being thick, the diastolic thin), is heard, double, over the whole length of the sternum, being audible, with pressure over its tipper third (the great arteries), and without pressure over its lower two-thirds; and is also audible with pressure from the third to the fifth left cartilages (right ventricle) ; and over, but not beyond the apex of the left ventricle. A loud mitral murmur is audible extensively to the left of the heart. Figure 87 from the same patient as figure 86. Period of the decrease of the pericardial effusion after the first acme. Eighth day after admission, third after the acme-for the sounds. Eleventh day after admission, sixth after the acme-for the pericardial effusion and dulness, and impulse. The pericardial effusion has lessened considerably, but is still present in considerable quan- tity. The right ventricle and the apex and front of the left ventricle are completely exposed; and the left border of the right auricle, and the lower portions of the ascending aorta and pulmonary artery, are also brought into view. The heart (2, 2), which is enlarged, has dropped down into its natural place, and even extends beyond that place, at its lower and left boundaries. The amount of effusion between the under surface of the heart and the floor of the pericardium (3, 3) is very small. The region of pericardial dulness (see the black space) has lessened considerably in area; it extends from between the second spaces, behind the sternum, down to the lower third of the ensiform cartilage; from the third left space to the upper border of the sixth cartilage; and from the right edge of the sternum to a point an inch beyond the left mammary line. There is reason to believe that adhesions have formed at the apex, so that the latter boundary ig 550 PERICARDITIS. in three it was felt over the third carti- lage. The existence of previous valvular dis- ease, owing to the increased size of the heart in such cases, exercised a marked influence on the position of the lower boundary of the impulse, and as a rule lessened or prevented its ascent during the acme of the effusion. Thus, of five pa- tients of this class, all of whom had affec- tion of the mitral valve, and one of them of the aortic valve also, in two the lower boundary of the impulse occupied the sixth space, in two the fifth space, and in one it was seated in the fourth space. If we deduct from the thirty-seven cases these five with valvular disease, which are exceptional both in their nature and as regards the influence of the effusion on the seat of the impulse, we find that in only one of the remaining thirty-two pa- tients was the lower boundary of the im- pulse as low as the fifth space during the acme of the effusion. These cases of previous valvular disease are exceptional in another point of view. In three of these five patients the position of the lower boundary of the impulse was not higher during the acme of the effusion than at other times. If we deduct these five cases from the thirty-seven under review, we find that in only three of the remaining thirty-two cases was the posi- tion of the lower boundary of the impulse unchanged during the acme of the effusion, while in twenty-nine of them it was defi- nitely higher than in health. Extent to which the Lower Boundary of the Impulse was liaised, when the Effusion into the Pericardium was at its Height or Acme.-In the twelve patients in whom the acme of the effusion was reached after the first observation of increased dulness on percussion, and in whom the lower boundary of the impulse was then ele- vated, the impulse at its lower boundary ascended two spaces in two instances (compare figure 90 with figure 91, p. 559), a space and a half in one, one space in six, and less than a space in three cases ; and it descended after the acme two spaces in five instances, one space in five, less than a space in one, and in the remaining case its descent was not observed. In the eighteen cases in which the effu- sion had attained to its acme at the time of the first observation the lower boundary of the impulse subsequently descended two spaces in three patients, one space in thirteen, one rib's breadth in one, and half a space in one case. If we combine these thirty cases in one group, we find that the lower boundary of the impulse was higher during the acme of the effusion than in the natural state by two spaces in eight cases, by one space in nineteen, and by less than a space in three cases. Time occupied during the Ascent and the Descent of the Lower Boundary of the Im- pulse in connection respectively with the In- crease the Acme, and the Decline of the Fluid in the Pericardium.-In the twelve cases in which the impulse at its lower boundary ascended to its highest point after the first observation, and during the period of the increase of the pericardial effusion, the time occupied by its ascent was from one to two days in nine cases, and from four to six days in three cases. The lower boundary of the impulse fell from its highest position to its natural one in from one to two days in ten cases, in from three to nine days in eighteen, and in sixteen days in two out of a total of thirty cases. The ascent of the lower boundary of the impulse was therefore more rapid than its descent. Delation between the Extent of the Effusion in the Pericardium, and the Height of the Loicer Boundary of the Impulse. - The clinical facts just given show that the lower boundary of the impulse was raised by the increase of the fluid in the pericar- dium ; and we find, therefore, as a rule, a relation between the extent of the effusion and the height of the impulse in these cases of pericarditis. But this rule is re- versed in a small group of exceptional cases, amounting to seven, in which the upper limit of the effusion was as high as the first space or the second cartilage; while the lower boundary of the impulse was present in the sixth space in one, in the fifth space in two, in the fourth space in three, and in the third space in only one of these cases. Three of these pa- tients in whom the impulse was low had valvular disease of old standing, a condi- tion that, as I have already shown, pre- vents or lessens the ascent of the impulse. (2) The Diffusion of the Impulse over the Higher Intercostal Spaces during the Acme, and Decline of the Fluid in the Pericardium. •-In three-fifths of the cases (22 in 37) the impulse, at the time of the acme of the effusion, extended upwards above its lower boundary to the extent of one or more of the higher intercostal spaces. In more than one-half of these cases the im- pulse was felt beating as high as the second space (12 in 22), while in less than one-half of them its upper limit was the third space (10 in 22). The extent to which the impulse was felt in the higher spaces was naturally regulated by the position of its lower boundary. Thus, the impulse was bounded below by the fourth space in ten cases, and in eight of these it extended up to the third space or carti- lage, and to the second space in only two ; while in eight other patients the impulse, which was bounded below by the third space or cartilage, spread upwards to the second space. According, therefore, to the degree to which the impulse was POSITION OF THE IMPULSE OF THE HEART. 551 Fig. 86. Fig. 87. Figure 86 from a housemaid aged 17, affected with rheumatic pericarditis. Period of the first acme of pericardial effusion, fifth day after admission. The explanation of pericardial effusion and dulness given with figure 82, page 544, applies also to this figure. The pericardial effusion extends less to the left and more to the right than in figure 83, page 544 (acme of pericardial effusion), and is of about equal extent in the two figures from above downwards. The heart, which is enlarged, is elevated by the fluid, but to a less degree than in figure 87, its lower boundary being probably situated behind the lower border of the fifth cartilage, and just above the lower end of the sternum. The whole front of the heart is exposed, including the right auricle and ventricle, the apex and front of the left ventricle, the ascending aorta within the pericardium, and the pulmonary artery. The region of pericardial dulness (see the black space) extends from a little above the lower end of the manubrium and the second left space, down to the tip of the ensiform cartilage, and the middle of the sixth cartilage; and from a little over an inch to the right of the lower half of the sternum, to a little beyond the left mammary line. The area of dulness includes (1, 1) the region of the great arteries ; (2, 2) that of the heart; and (3, 3) that of the volume of the effused fluid below the heart, and projecting downwards into the epigastric space. The impulse is less elevated than in figure 83 (acme), being situated in the second, third, and fourth spaces. (See the curved and circular lines in those spaces.) The friction sound (represented by zigzag lines, the systolic lines being thick, the diastolic thin), is heard, double, over the whole length of the sternum, being audible, with pressure over its upper third (the great arteries),,and without pressure over its lower two-thirds; and is also audible with pressure from the third to the fifth left cartilages (right ventricle) ; and over, but not beyond the apex of the left ventricle. A loud mitral murmur is audible extensively to the left of the heart. Figure 87 from the same patient as figure 86. Period of the decrease of the pericardial effusion after the first acme. Eighth day after admission, third after the acme-for the sounds. Eleventh day after admission, sixth after the acme-for the pericardial effusion and dulness, and impulse. The pericardial effusion has lessened considerably, but is still present in considerable quan- tity. The right ventricle and the apex and front of the left ventricle are completely exposed; and the left border of the right auricle, and the lower portions of the ascending aorta and pulmonary artery, are also brought into view. The heart (2, 2), which is enlarged, has dropped down into its natural place, and even extends beyond that place, at its lower and left boundaries. The amount of effusion between the under surface of the heart and the floor of the pericardium (3, 3) is very small. The region of pericardial dulness (see the black space) has lessened considerably in area; it extends from between the second spaces, behind the sternum, down to the lower third of the ensiform cartilage; from the third left space to the upper border of the sixth cartilage; and from the right edge of the sternum to a point an inch beyond the left mammary line. There is reason to believe that adhesions have formed at the apex, so that the latter boundary i» 552 PERICARDITIS. not pericardial but cardiac. The region of dulness over the great arteries (1, 1) is still very marked but has materially lessened ; that over the heart (2, 2) being still extensive; and that over the depending portion of the pericardial effusion between the under surface of the heart and the floor of the pericardium (3, 3) being very narrow, indeed a mere strip. The impulse of the apex is felt in the sixth space, considerably to the left of the nipple. The position of the impulse elsewhere is not mentioned in the report, but I have given it in the figure as being present in the fourth and fifth spaces, because three days later, at the time of the second acme, it was felt in those spaces, as well as in the second and third spaces. (See the circles and curved line in those spaces.) The friction sound (see the zigzag lines, systolic thick, diastolic thin) on the seventh day had increased considerably below and to the right, and lessened above and to the left. It was audible over the sternum from below, but not above, the level of the second spaces, and thence down to the tip of the ensiform cartilage; to the right of the lower half of the sternum; and over the left cartilages, from the third to the seventh, where it extended about two inches below the heart; but it was inaudible over the region of the apex, where there were probable adhesions. For the later views of this case, see figures 88, 89, p. 553. raised by the increased amount of fluid in the pericardium, it was felt beating in the second and third spaces, or the third and fourth spaces, instead of, as in health, the fourth and fifth spaces. In these cases there were two agencies at work: one, the increase of fluid in the pericardium, which elevated the heart and its impulse both at their lower and upper boundaries into the contracted space at the higher part of the chest, and caused the heart to beat against the left upper spaces ; the other, the enlargement from distension of the right ventricle and especially of the pulmonary artery, owing to the difficulty with which the blood passes through the lungs from the com- bined effect of the pressure upon the auricles by the fluid in the swollen sac, and the existence of endocarditis with mitral regurgitation. The enlarged right ventricle and pulmonary artery displace the lungs, and pulsate, the former against the third, the latter usually against the second space ; and in that space the double beat of the artery is then felt, the first being feeble, the second sudden and like a shock, coinciding with a feeble first and intensified second sound heard over the same situation. When the heart is much raised, it is evident that the conus arteri- osus must sometimes occupy the second space, the pulmonary artery being ele- vated into the first space. After the acme, when the amount of the fluid in the pericardium lessened, the position of the impulse, as we have just seen, as a rule descended at its lower boundary, but it generally retained its place at its upper boundary. Sometimes, indeed, the impulse extended upwards as well as downwards during the period of the lessening of the effusion. The clinical facts that I have just re- lated as to the extension of the impulse into the upper region during the succes- sive periods of the increase, the acme, and the decrease of the effusion into the pericardium; while its lower boundary steadily rose during the increase, and fell during the decrease of the fluid, are to be traced I consider to a succession of causes. I have just considered tlie two agencies that are at work to extend the impulse into its higher region during the periods of the increase and acme of the effusion ; the increase namely of the pericardial fluid elevating the heart into the con- tracted space of the chest above ; and the enlargement of the right ventricle and pulmonary artery from obstruction to the flow of blood through the lungs. During the decline of the fluid the first of these influences is reversed, for the heart de- scends into its natural place, where it beats with comparative freedom ; but the second influence, the enlargement of the right ventricle and pulmonary artery from obstruction through the lungs, often re- mains in full force to retail?the impulse in its higher position ; and this influence is frequently added to by other causes that have a like effect. These additional influences include the thickening and matting of the inflamed pericardium ; the possible adhesion from pleurisy of the left lung to the pericardium at its upper border; and the deficient or absent ex- pansion of this portion of the lung from adhesion and other causes, such as pul- monary apoplexy, and the imperfect gen- eral use of the left lung. These views derive additional confirmation from the fact that in all the cases save one in which the impulse extended over the higher spaces during both the acme and the decline of the effusion, there was en- docarditis with mitral incompetence, and in several of them, aortic incompetence also. Position of the Impulse after the Decline of the Pericardial Effusion during the Later Stages of Rheumatic Pericarditis; and after its Cessation.-When the effusion disap- pears and the heart resumes its natural position, and when the lungs again cover the great vessels and the upper part of the organ in front, the impulse as a rule de- scends into its natural position, and is again felt in the fourth and fifth spaces. In those patients in whom the heart be- POSITION OF THE IMPULSE OF THE HEART- 553 Fig. 88. Fig. 89. For previous views of this patient see figures 86, 87, page 551. Figure 88, from a housemaid aged 17. Period of the second acme of pericardial effusion owing to a relapse of pericarditis. From the fourteenth to the eighteenth day after admission, from the tenth to the fourteenth day after the first acme (figure 86), and from the third to the seventh day after the period of decrease of the effusion illustrated in figure 87. The period of the acme lasted four days. The explanations of pericardial effusion, prominence and dulness, given with figure 82, at page 544, apply also to this figure. The pericardial effusion has increased again to a very great extent. The heart is consider- ably enlarged, and is probably adherent at the apex; its lower boundary is therefore much lower than during the first acme, figure 86, and apparently reaches down to the sixth carti- lage, and the middle of the ensiform cartilage. The effusion has increased very much, espe- cially upwards, downwards, and to the right; but owing probably to adhesions at the apex, it has been stationary or has lessened in area at the left side-compared with its amount and area during the period of decrease of the effusion after the first acme shown in figure 87. The effusion extends much higher and more to the right than during the first acme (figure 86), but it is of the same extent at its lower and left boundaries in this as in the first acme. The area of the effusion was much wider in relation to its length, and especially towards the left, in the single acme shown in figure 83, owing to the enlargement of the sac from long- continued distension, than it is in this instance, in which the expansion of the sac to the left has been apparently stopped by the probable adhesion of the apex and front of the left ven- tricle. The whole front of the heart and great arteries is exposed, including the right auricle and ventricle, the apex and front of the left ventricle, and the ascending aorta and pulmonary artery. The region of pericardial dulness (see the black space), corresponding to the pericardial effu- sion, extends very high, or to within an inch of the episternal notch ; far to the right, or nearly two inches to the right of the sternum; low down, or below the tip of the ensiform cartilage; and owing probably to adhesions at the apex, proportionately less far to the left, or fully half an inch to the left of the mammary line. The region of dulness over the arteries is unusually high and narrow. Its width on the first day of the acme was little more than one inch; but it had increased to about two inches on the fourth day, when its upper border was not quite so high as on the first day of the acme at its upper part. The impulse is extensive but not strong, the double pulsation over the pulmonary artery being felt over the second and third spaces; and the impulse of the heart, over the third, fourth, and fifth spaces, where it extends beyond the nipple (see the curved lines and circles in those spaces). The lower boundary of the impulse has therefore been elevated from the sixth space to the fifth since the period of the decrease of the effusion following the first acme, shown in figure 87; it is, however, lower in this second acme than it was in the first acme, when it occupied the fourth space. The friction sound (see the zigzag lines, the systolic lines being thick, the diastolic thin) is scarcely audible anywhere without pressure, but with pressure it is heard, double, over the whole region of the pericardial dulness except over the apex and front of the left ventricle, where there are probably adhesions, and where a loud mitral murmur prevails. The rub- 554 PERICARDITIS. bing sounds are louder over the two lower thirds of the sternum and to each side of it, than higher up. Figure 89, from the same patient as figures 86, 87, 88. Period of complete adhesion of the pericardium to the heart. For pericardial dulness-fifty-two days after admission, thirty-nine to forty-three days after the second acme. For the impulse-eighty-eight days after admission, when the dulness, tested by post- mortem examination, was about the same as on the fifty-third day after admission. The region of pericardial dulness (see the black space) is very extensive, measuring about Seven inches from left to right, with a slight downward inclination, and nearly five inches from above downwards. Its upper boundary was behind the lower border of the manu- brium ; its lower boundary, behind the lower end of the ensiform cartilage, the sixth left space and the seventh left rib; its right boundary was situated midway between the right nipple and the edge of the sternum ; and its left boundary extended to the sixth and seventh ribs at the outer side of the chest. The impulse on the fifty-third day was present in the fourth, fifth, and sixth spaces from two inches within, to two inches without, the nipple line, and was quite absent from the sternum and the spaces between the cartilages ; since that time the patient has been getting gradually worse; and the impulse has been becoming gradually stronger and more exten- sive, and is now, on the eighty-ninth day, felt over the whole sternum, the epigastrium, and the cartilages to each side, and on the left side down to the seventh left rib, where it beats against the outer side of the chest (see the curved lines occupying all that region). The impulse heaves up rather slowly during the systole, and immediately after it, falls suddenly backward. The impulse in the first and second spaces, over the pulmonary artery, is double, protruding slightly during the systole, and going back with a flapping rapid move- ment during the diastole, conveying the impression of a sharp impulse or shock, synchro- nously with the second sound. Ninety-first day. The impulse is still felt over the sternum, but feebler than two days ago, similar in character, but not felt. comes again healthy after the attack, the size, position and customary beat of the organ are restored : but in those in whom valvular disease is established, the nature and extent of the disease are made appa- rent by the force, extent, and position of the impulse. When the resulting mitral disease is severe, the impulse of both the right and left ventricles is extended, and is felt beating from the lower half of the sternum to the left nipple. When, how- ever, the mitral affection is slight, and such as scarcely or not at all to interfere with the function of the organ, then the impulse resumes its natural boundary and strength; and thus the impulse becomes a true measure of the extent of the valvu- lar disease. When both the aortic' and mitral valves are affected, the apex-beat and the impulse generally of the left ven- tricle become more markedly developed, the action of the right ventricle being still unduly strong. In those comparatively rare cases in which the aortic valve is alone affected, the right ventricle is un- touched ; but the size and force of the left ventricle are increased inexact proportion to the increased labor thrown upon that cavity by the degree of the crippling of the valve. The apex-beat and general shock of the left ventricle become ex- tended outwards beyond the left nipple, and downwards into the sixth space, when the valvular affection is great; but they are held almost within the natural limits when it is slight. When the heart be- comes adherent and there is disease of one or more of its valves, the impulse of the organ becomes extended in every direc- tion-to the right, over and beyond the sternum ; to the left beyond the line of the nipple ; downwards, over the ensiform cartilage, and even below it in the epigas- trium ; and especially upwards, to the second space and to the adjoining portion of the sternum. In some cases the whole impulse bears at first forwards during the systole, and then drags the walls of the chest in a characteristic manner back- wards ; while in other cases, in which there is complete fibrous attachment of the adherent pericardium to the sternum, that bone and the adjoining costal car- tilages are steadily drawn inwards during the systole, and spring forwards with a shock during the diastole. An essential difference is also established between the influence of respiration on the area of the impulse of the adherent and the non-ad- herent heart. When the heart is not ad- herent, a deep inspiration, by drawing down the heart and covering it with the expanded lungs, causes a complete transfer of the impulse from the fourth and fifth spaces to the epigastrium and the sixth and seventh cartilages; but when the heart is adherent, the outspread dragging impulse almost retains its position during a deep inspiration, neither materially less- ening its area over its upper borders, nor materially increasing it below. There is, in short, no transfer, such as occurs when there are no adhesions, of the impulse during a deep breath from the intercostal spaces to the ensiform cartilage and epi- gastrium and the adjoining left costal cartilages. Thus in a patient who has recovered from rheumatic endo-pencar- vibration or thrill of the heart. 555 ditis we are enabled to judge by the position and force of the impulse, whether the valves, if affected, are seriously or only slightly affected; and, by the extent to which the play of the impulse is influ- enced by respiration, whether the valvular affection is combined or not with exten- sive and binding adhesions of the heart. "Vibration or Thrill felt by the Hand over the Region of Peri- cardial Friction. A sense of vibration or thrill was felt over the seat of the friction sound at the region of its greatest intensity in fully one-fifth of the patients with rheumatic pericarditis (13 in 63). In seven of the cases, or more than one- half of them, the thrill was felt over the whole region of the impulse, extending in two instances over the second and third left spaces, in one, over the spaces from the second to the fifth, in three, over those from the third to the fifth, and in one, from the fourth to the sixth spaces. In two other instances the thrill was confined to the second space, apparently over the pulmonary artery, in three to the region of the apex, and in the remaining case it was present both over the second space and the apex. In all these patients the friction sound was harsh and grating, vibrating, or creaking in character. In those cases in which the vibration was felt over the whole region of the im- pulse, the thrill was present at the time of the acme of the effusion, or in one in- stance two days after it; and the same may be said, with one exception, of those in which the vibration was felt in the second space. The duration of the thrill was short. It was observed for only one day in seven cases, for two days in three, for three days in two cases, and for four consecutive days in the remaining one. In two cases, the thrill, after being absent from its pre- vious seat over the body of the heart for several days, returned over a limited space when the surfaces were comparatively dry, the effusion having disappeared. The character of the friction thrill or vibration is peculiar, and differs from the thrill due to altered blood-currents, chiefly in the following points. The blood-thrill presents a succession of equal vibrations, often like those made by the vibrating musical cord ; is diffused ; has a focus of greatest intensity, from which it lessens and fades away all round ; gives the im- pression to the hand of being deeply seated as well as superficial; begins, when dias- tolic after the impulse ends, and often continues, when systolic, for a short period after the cessation of the beat of the ven- tricle ; retains its character, position, focus of intensity, and general outspread, unchanged or with only slight modifica- tions from day to day : and finally, has a long previous history pointing to an affec- tion of the heart, and probably dating from an attack of acute rheumatism. The friction thrill or vibration, on the other hand, is shallow, giving a sensation as if it were made just under the hand by the rubbing together of two rough surfaces ; has often a grating, rasping, or irregu- larly vibrating character; presents no focus of intensity, but is spread, with varying force, over the region of the im- pulse ; begins and ends rather abruptly, being limited to the period of the impulse and not passing beyond or preceding it; does not end with an abrupt shock ; is short-lived and transient, and, if felt on one or two following days, it always changes in extent, and perhaps in posi- tion, and alters in character ; and finally has a short previous history of local pain, extended dulness on percussion, increased prominence over the region of the peri- cardium, and elevated impulse. Some- times, however, the blood-thrill and the friction-thrill are so much alike that they cannot be distinguished by the hand. The character of the thrill is, however, at once cleared up by the ear ; the friction- thrill being accompanied by a friction sound which is in all cases increased by pressure, and is most vibrating, grating, or creaking and harsh at the very seat of the vibration; while the blood-thrill is accompanied by the murmur, usually musical, that distinguishes the valvular affection. The thrill of presystolic murmur is dis- tinguished by the position of the thrill over and to the left of the interventricular septum, the peculiar large vibrating char- acter of the murmur ; the abrupt shock with which the thrill and murmur ter- minate ; the persistency of the thrill, murmur, and shock from day to day ; and the long previous history. The character of the friction sound pre- sented in the various cases a close approx- imation to the character of the thrill or vibration. The sensation conveyer! to the hand when applied over the seat of thrill in the thirteen cases under examination was not always of the same character. Thus, under these circumstances the hand felt a sense of grating or rasping in two, of vibration in four, and of thrill in seven of the cases. On listening over the region of the thrill or vibration in these cases a loud harsh friction sound was heard in seven patients, in five of whom the sound was described as being "to and froin five others of them there was a noise resem- bling the creaking of leather; in three the sound was grating, in one rasping, in two 556 PERICARDITIS vibrating, in one grazing, and in one "churning." In several of these cases the friction sound presented, as we have already seen, different phases at different periods of their progress. In all of them the friction sound became less harsh and extensive when the vibration or thrill over the region of the pericardium ceased to be perceptible. It is to be remarked that when the thrill was perceptible in these cases, espe- cially if it extended over the ventricles, and was not limited to the region of the apex or that of the pulmonary artery, the area of the friction sound was increased as well as the intensity. In one of the cases the rubbing sound was audible over the whole front of the chest, and in sev- eral of the patients it spread downwards to the ensiform cartilage and to the left and right seventh and eighth costal car- tilage. The character of the friction sound, associated with the presence of a thrill over the heart and great vessels, whether creaking or grating, vibrating or rustling, or to and fro, will be considered in the next section. Auscultation. Position and Character of the Sounds heard over the Heart and Pericardium dur- ing the Early Stages of Pericarditis.- In more than one-half of my cases of rheu- matic pericarditis (33 in 63), I observed the character of the sounds of the heart at or soon after the commencement of the attack, and before the effusion into the pericardium had arrived at its height. I was frequently surprised by the rapidity with which the affection attained to its acme. In twenty-three of these patients friction sound was heard for the first time before the fluid in the pericardium had reached its greatest amount; and in fif- teen of these the rubbing sound was de- tected only one day, and in four two days before the time of the acme. Modification of the Sounds of the Heart at the Commencement of Pericarditis, before the Occurrence of Friction Murmur or Fric- tion Sound.- There were five cases in which the sounds of the heart were modi- fied before the occurrence of a friction sound, or the period of the acme. In one of them the heart sounds were muffled two days before the occurrence of the friction sound and the acme ; in three oi them those sounds were ringing in char- acter from three to four days before the acme ; and in one of these the systolic sound was rough and unduly prolonged four days before that period. All the cases of this group but one presented on pressure either a single or double murmur or a rubbing sound subsequently to this modification of the heart sounds, and before the occurrence of the acme. Position and Character of the Friction Murmur, influenced by Pressure, heard at the Beginning of Pericarditis.-A murmur, which was excited or rendered more in- tense by pressure, was heard over the region of the heart before the period of the acme of effusion into the pericardium in eight cases. Pain was felt directly over the seat of the pericardial inflammation in seven of the cases, being excited by pressure on the surface of the chest in three of them. In five of the cases the pain was present at the same time as the appearance of a murmur on pressure, and in two the pain preceded the murmur by a day or two. In four cases the friction murmur was single and systolic. In four cases a double murmur, excited or intensified by pres- sure, preceded the friction sound and the acme of pericardial effusion. In the last case of this group, a youth aged 17, a fatal case, the friction murmur prevailed more or less through the whole of the ill- ness until the heart became adherent. The double friction murmur, heard dur- ing the early period of pericarditis, is thus distinguished from the double mur- mur caused by aortic incompetence, com- bined as it usually is with mitral regurgi- tation. It is accompanied, and often preceded, by pain over the heart, usually increased by pressure ; it comes into play suddenly ; its area is limited to the mid- dle, or lower half of the sternum, and the adjoining left, and, on rare occasions, right cartilages ; it is accompanied by the natural heart sounds, but is not rhythmi- cal with them, the heart sounds and mur- mur being heard as it were side by side ; it does not begin with a double accent, or shock, the double accent or shock of the natural heart sounds, but is of equal in- tensity throughout; it is invariably ren- dered more intense by pressure, which often converts it into a true to and fro frottement, and which always obscures or silences the natural heart sounds. It is not accompanied by marked visible pulsa- tion of the great arteries in the neck, or by the sudden pulse at the wrist of aortic regurgitation, audible when the arm is raised ; it is accompanied by extended dulness on percussion over the region of the pericardium ; and as a rule it speedily gives place to a friction sound, with which, however, it may coexist, being audible beyond the circumference of the friction sound especially below, and on either side. In all these respects the double friction murmur contrasts notably with the double aortic murmur; which is not usually ac- companied by pain over the heart; does not come into play suddenly ; is not lim- ited in its area to the middle or lower AUSCULTATION. 557 half of the sternum and the adjoining cartilages-but extends also to the upper portion of the sternum and to its right; is rhythmical with the natural heart sounds ; commences with a double accent or shock; is not rendered to a material degree more intense by pressure, which never converts it into a friction sound, and which never abolishes the double accent with which the double murmur begins ; is accompanied by marked visible pulsation of the carotid and radial arte- ries, the pulse of the latter becoming audible as a shock when the arm is raised ; is not accompanied by extension of dul- ness over the region of the pericardium ; and does not give place suddenly to fric- tion sound, but is persistent. The single systolic friction murmur is not so easily distinguished from the tri- cuspid murmur as from other systolic blood murmurs, but their differences are sufficiently marked. The systolic friction murmur is accompanied or preceded by pain over the heart, usually increased by pressure ; comes into existence suddenly ; is limited usually to the base of the right ventricle, being heard over the middle or lower sternum, or over the fourth left space; is accompanied by the natural first sound, but is not rhythmical with it, the heart sound and the murmur being distinctly heard side by side ; does not begin with an accent or shock, the accent or shock of the natural first sound, but begins and ends with a single note of equal intensity throughout; extends rarely beyond the period of the systole into that of the diastole; is usually produced, and invariably rendered more intense by pres- sure, so that it obscures or masks the natural first sounds; is accompanied by extended dulness on percussion over the region of the pericardium; and speedily gives place to a double friction murmur or a friction sound. The several systolic blood murmurs may be thus distinguished from the single or systolic friction murmur. The tricuspid murmur is more likely to be taken for a friction murmur than any other systolic murmur, for it is situated over the front of the right ventricle-over and to the left of the lower half of the sternum-and, like the friction murmur, it is a shallow sound, and it may appear and vanish quickly. It differs, however, in these respects ; it is rarely accompa- nied by pain and. tenderness over the heart; is never accompanied by the natu- ral first sound over the right ventricle, for that sound is converted into the murmur ; always commences with an accent, the accent or shock of the first sound of the right ventricle ; may be intensified, but is not changed in character by pressure, which, however, brings the ear more close to the murmur ; is not accompanied by extended dulness on percussion over the pericardium ; and does not give place to a double friction murmur or a friction sound. The systolic mitral murmur is readily distinguished from the friction murmur by the intensity with which it is heard to the left of and below the apex; and its great relative feebleness, or silence over the right ventricle-to the left of the lower portion of the sternum ; and by its persistence. When the mitral murmur is audible in the situation just spoken of it is feeble, and is accompanied by the natural sounds of the right ventricle. The heart sounds and the murmur are rhythmical and go well together; and pressure, though it makes the mitral murmur somewhat more clear, does not mask or obliterate the healthy sounds of the right side of the heart. The direct aortic, and pulmonic systolic murmurs are distinguished at once from the systolic friction murmur by their situ- ation above the level of the third cartilage ; the pulmonic murmur, which is often scratching in character, and is therefore apt to be mistaken, when first heard, for a friction sound, being limited to the second left space ; and the direct aortic murmur being heard over the upper sternum, and to the right of it, and in the neck over the carotid. The essential features of difference be- tween the friction murmurs and the blood murmurs are these : The friction murmurs do not begin with an accent, but usually maintain the same tone and pitch through- out ; while the blood murmurs begin with an accent or shock : the friction murmurs are intensified and altered by pressure, becoming sometimes rubbing in character; while the valve murmurs are only intensi- fied by pressure : the friction murmur and the natural heart sounds are heard at the same time, but they do not play together or in unison, being audible as it were side by side, each having its own rhythm ; and on pressure the friction murmur becomes so loud and even rubbing in character as to mask and extinguish the heart sounds ; while the blood murmurs are in perfect accord with the heart sounds : the friction murmurs come suddenly, with pain and increased pericardial dulness, and are transient; the blood murmurs come grad- ually, without pain or increased dulness, and are permanent. Friction Sound in Pericarditis 'before the Occurrence of the Acme of the Effusion into the Pericardium. - Friction sound was heard during the early stage of Pericardi- tis, in every gradation from a sound scarcely to be distinguished from a mur- mur up to a grating, vibrating, or creak- ing noise. In a few of the cases, the early friction 558 PERICARDITIS sound was not audible until pressure was made over the heart. In nearly all the cases, the friction sound was double from the first, but in two, and perhaps three patients the sound was single and systolic when first heard. In a small group of four patients, a smooth or feeble double friction sound, intensified by pressure, came into play from one to four days be- fore the occurrence of the acme of the affection, when the friction sound became louder and more harsh. In the last great division of cases of pericarditis with friction sound before the acme, the double friction sound, as a rule, was loud and harsh, was intensified by pressure, and set in suddenly ; and the effusion into the pericardium speedily at- tained to its acme after the first observa- tion of the friction. This set of cases divides itself into three groups; in the first group (1), the friction sound became inaudible during the acme ; in the second (2), the friction sound became less loud and harsh during the acme; and in the third group (3), the friction sound re- mained during the acme with little or no change. (1) In two cases, the friction sound, harsh at the onset, disappeared during the acme. It is difficult to explain the disappearance of the friction sound at the time of the acme of the effusion in these two remarkable cases on physical grounds, but the following circumstances show that it was mainly due to lowering of the power of the heart. It is natural to ex- pect that when the fluid increases, it should interpose itself between a portion of the right ventricle and the anterior wall of the chest, and so limit the area of the friction sound, and lessen its inten- sity. This will not, however, account for the disappearance of the rubbing sound at the period of the acme, since the impulse was then still perceptible, though higher in position and less forcible. (2) The second group of this division, in which a loud double friction sound ap- peared suddenly before the acme of the effusion, and became less loud during the acme, consists of five patients. The case of this group that I shall re- late, is illustrated by the accompanying figures (90, 91, p. 559); during its later stages, by figures 92, 93, 94, pp. 575, 576. A housemaid, aged 20, came in on the fifth day of her illness, the heart sounds being natural. On the third day there was increased dulness on percussion over the region of the heart; and a to-and-fro friction sound over the whole of the re- gion of cardiac dulness, to which it was exactly limited. The impulse was pre- sent, as before, in the fifth space, but was higher in position. The dulness and the friction sound extended from the sternum almost to the nipple, and from the third left cartilage to the sixth, but did not pass beyond the sternum to the right, so that the rubbing sound was limited to the right ventricle. It was stronger over the sternum than the cartilages, and became everywhere much harsher on pressure. On the fourth, the double friction sound was heard over the greater part of the sternum, and was audible over the manu- brium during the expiration only. The friction sound had somewhat the charac- ter of a bellows murmur over the fourth space. It was not quite rhythmical with the sounds of the heart, which were also audible. It was harsher and louder dur- ing the systole than the diastole, and was rendered more intense by pressure. On the fifth day, the effusion into the peri- cardium was at its acme-reaching up to the second space and the manubrium. The impulse was raised from the fifth to the third space. The area of the friction sound was more extensive upwards, but more limited below. It was heard over the whole sternum, being louder over the manubrium on expiration, over the lower portion of that bone on inspiration, and was most harsh and strong over the mid- dle third of the sternum. The rubbing sound was heard from the second to the fourth cartilage, but not apparently below it, and was harsh in the third space. A bellows murmur was audible over the fourth cartilage on the light application of the stethoscope; but when pressure was made, a creaking noise was heard there during the systole, and a rubbing sound during the diastole. I believe that this group and this case represent the natural progress of the fric- tion sound from the commencement of pericarditis to its acme when the effusion is at its height. During the first blush of inflammation, the surfaces of the heart and the sac are crowded with vessels, but are as yet scarcely coated with lymph. A single or double friction murmur, in- duced or intensified by pressure, may then be the only sound excited by the rubbing of the heart against the pericardium. Speedily their surfaces become coated with a finely honey-combed rugose cover- ing ; and the amount of fluid in the sac increases so as to enlarge the area of dul- ness over the pericardium, and to expose the whole of the right ventricle and the apex, but neither the right auricle nor the great vessels. The heart is slightly raised and the apex beat ascends from the lower to the higher part of the fifth space. A double friction sound is audible over the whole region of pericardial dulness, to which it is exactly limited, louder and more continuous during the systole than the diastole, and rendered more intense by pressure, which brings into full play both sounds, exciting a to-and-fro rustle or frou-frou. AUSCULTATION 559 Fig. 90. Fig. 91. Figure 90, from a housemaid aged 20, affected with rheumatic pericarditis. Early period of the increase of the pericardial effusion. First day of the friction sound ; third day after admission. The sounds of the heart were natural when she was admitted. The pericardial effusion probably already occupies to some extent the space between the under surface of the heart and the floor of the pericardium, and elevates the heart to a slight degree, and, to a moderate extent, displaces the lungs upwards and to each side; and the centre of the diaphragm, where it forms the base of the pericardium, and the subjacent portions of the liver and stomach downwards. Owing to the displacement of the lungs upwards and to each side from before the heart, the whole of the right ventricle except the upper portion of the conus arteriosus, the inner or left border of the right auricle, and the apex and a portion of the front of the left ventricle are exposed. Probable region of pericardial dulness on percussion (see the black space). The outlines of the region of pericardial dulness, which is increased in extent, are not described on this occa- sion, but the extent of the friction sound and the position of the impulse are given ; and I have assigned to the region of dulness an outline corresponding to the region of friction sound and the position of the impulse. The region of pericardial dulness has not yet acquired the pyramidal or pear-shaped form that it presents during the acme of the pericar- dial effusion, but still retains the general form of the healthy region of cardiac dulness, but its outline is considerably enlarged in all directions, and is higher behind the sternum than over the cartilages. It extends across from the right edge of the sternum to the left nipple ; its upper boundary probably crosses the sternum on a level with the upper edges of the third costal cartilages, and occupies the third space; and its lower boundary is probably situated a little above the middle of the ensiform cartilage, and the upper edge of the sixth cartilage. Third day. The impulse of the heart is felt at the fifth space below the nipple. (See the circle in that space.) Fourth day. The impulse is feeble, being slightly perceptible below the nipple. Friction sound (see the zigzag lines, systolic thick, diastolic thin). Third day. A loud but soft to-and-fro friction sound is heard over the sternum from below the manubrium to its lower end, and up to but not beyond its right border; and over the fourth and fifth car- tilages and intermediate spaces, where it extends almost, but not quite to the nipple, where it is feebler than it is over the sternum. The friction sound is rendered much harsher by pressure. Fourth day. The friction sound is nearly the same in extent, character, and area as it was yesterday, but it is now audible over the manubrium during expiration ; it is lower and louder below during inspiration than expiration ; and it is louder generally during the systole than the diastole. Figure 91 from the same patient as figure 92, affected with rheumatic pericarditis. Period of the first acme of pericardial effusion. Third day of the friction sound and of the increase of pericardial dulness, fifth day after admission. The explanations of pericardial effusion and dulness given with figure 82, page 544, apply also to this figure. The pericardial effusion completely distends the sac, which is pyramidal or pear-shaped, as in figures 80, p. 540; 82, 83, p. 544; 86, p. 551; 88, p. 553. The extent of the effusion, 560 PERICARDITIS. and of the displacement upwards and to each side of the lungs, and downwards of the dia- phragm, liver, and stomach may be inferred from the description given below of the extent of the region of pericardial dulness on percussion. The whole front of the heart is exposed, including the right auricle and ventricle, the apex and front of the left ventricle, the pul- monary artery, and the ascending aorta within the pericardium, owing to the extensive dis- placement of the lungs from before those parts. The region of pericardial dulness (see the black space) on percussion is pyramidal or pear- shaped, like the distended pericardium. The upper and narrower region of dulness over the great vessels (1, 1) is situated behind and below the lower half of the manubrium and extends a little way into the adjoining first and second spaces ; the larger portion of pericar- dial dulness, which includes the heart itself and the volume of fluid effused into the space between its under surface and the floor of the pericardium (2, 2; 3, 3), extends from the second space down to the lower border of the sixth cartilage, and almost to the end of the ensiform cartilage, and from an inch to the right of the sternum to about half an inch to the left of the nipple. The lower boundary of the heart (2, 2) is probably situated behind the lower border of the fifth cartilage; and the heart (2, 2) extends from this boundary up to the third cartilages : and the volume of effused fluid between the under surface of the heart and the floor of the epicardium extends from the lower boundary of the heart down into the epigastric space, almost to the end of the ensiform cartilage, and the lower edge of the sixth left cartilage. The impulse has been elevated from the fifth to the third space, and extends outwards to the nipple line. (See the concentric curves in that space.) The friction sound (see the zigzag lines-systolic thick, diastolic thin) is double, and extends from the nipple to the lower end of the sternum. It is most harsh about the middle of the sternum, and is louder at the upper end of that bone during expiration, and at its lower end during inspiration ; and is more intense during the systole than the diastole. The frottement is also audible over the left second, third, and fourth cartilages; and is soft without pressure, but with pressure it is creaking over the fourth cartilage. A mitral murmur is audible at the apex. For the later views of this case see figures 92, 93, 94, pp. 575, 576. When the effusion lias increased to its utmost limits, the heart is elevated, its impulse being raised from the fifth to the fourth or third space ; the increased effu- sion displaces the lungs and so exposes the whole surface of the heart and great vessels ; and depresses the central tendon of the diaphragm downwards towards the abdomen, fluid being alone present below the fourth Space. The whole region of actual friction is shifted upwards, and with it the whole region of the friction sound ; which is no longer audible below the fourth or fifth cartilage, but spreads over the right auricle and the left ven- tricle, as well as the right ventricle ; and upwards over the great vessels and to the top of the sternum. The friction sound silenced below is intensified and extended above ; so that there is a transfer upwards of the friction sound ; while the dulness on percussion increases in all directions, upwards as well as downwards. Four cases differed from the rest in this, that while the friction sound spread up- wards at the time of the acme, it also either increased downwards, or, retaining its hold below, increased extensively to the left side. The comparative relative Area and In- tensity of the Friction Sound just before^ and during the Acme of the Effusion into the Pericardium.-In twenty-nine cases the comparative area and intensity of the friction sound were observed both before, and at the time when, the effusicn into the pericardium was at its height. Area.-When the effusion into the peri- cardium increases, the heart is raised, and the lungs are displaced upwards, and to the left and right by the increased ful- ness of the sac and the greater elevation of the heart itself; for the organ is then pushed upwards from a wider into a nar- rower space. It is natural to expect that, under these circumstances, the area of the friction sound should steadily increase up- wards and to each side with the increase of the area of pericardial dulness. This was found to be so in the great majority of instances. Thus the area of friction sound was greater at the time of the acme than before it in twenty out of the twenty- nine cases ; while it was less under the same circumstances in only two of them. In six patients, the area of the friction sound was equal before and during the acme ; and in one case the friction sound was absent before, but present at the time of the height of the disease. These clinical facts show that when the curtain of lung in front of the heart and great vessels is displaced by the distended pericardium and the elevated heart, the friction sound spreads upwards, and to the right and left ; so as to be audible over the whole front of the right ventricle, the great vessels, the right auricle, and the apex. The lower boundary of the friction sound, while it retains its place, at the time of the height of the effusion, be- comes softened in character. The focus of intensity of the rubbing sound is shifted 1 At the time of the last observation, made before the effusion had reached its height. AUSCULTATION. 561 upwards, with the upward shifting of the heart and its impulse ; and the intensity of the sound is toned and graduated down- wards, from the seat of its focus to that of its inferior limit. Intensity.-In nearly three-fifths (16 in 29) of the cases, the friction sound was more intense ; and in fully one-third of them (10 in 29), it was less intense, when the effusion into the pericardium was at its height, than just before that time. The tendency, then, is for the friction sound to increase both in intensity and area, during the acme. The exceptions to this rule are, however, much more fre- quent as regards intensity than area ; for the area lessened at the time of the acme, in only two instances*, while the intensity did so at that time, in ten instances out of twenty-nine. The area of the friction sound, then, is, as a rule, larger, and its intensity greater at the time of the acme of the pericardial effusion, than at that of the last previous observation, made from one to two days before the acme. The exceptions to this rule are rare as regards the area, but rather frequent as regards the intensity of the friction sound, which is greater in one-third of the cases on the day before, than at the time of the acme. The change, both in area and intensity, is often notably rapid and great; the character of the friction sound being sometimes altogether altered, and its area remarkably enlarged in the course of one or two days. The Character and Area of the Friction Sound at the Time of the Acme of the Effu- sion into the Pericardium.-The friction sound, audible over the region of the heart and arteries and the pericardium dur- ing the acme of the pericardial effusion, presented great variety of character, inten- sity, and area in the forty-four cases under examination. I. In nine of those cases the friction sound was accompanied during the acme by a thrill over the region of the heart and great vessels; and II. in thirty-five of them the presence of a thrill was not observed. I. Of the nine cases with a thrill, (1) in five a sound resembling the creaking of new leather; (2) in one a grating sound ; and (3) in three a harsh friction sound was respectively audible over the region of the pericardium. II. Of the thirty-five cases in which a thrill was not observed, (1) in seven a creaking sound was heard ; (2) in two the sound was grating in character ; (3) in fifteen a definite friction sound, intensified by pressure, which in two instances excited a creaking noise, usually harsh, but some- times not so, was audible ; (4) in five the friction sound was soft in character, but was rendered harsh or more intense by pressure, except in one instance, in which pressure was not employed ; (5) in four a friction sound, previously absent, came into play when pressure was made over the region of the heart; (6) in one friction sound, present during one, was absent during two of the three days dur- ing which the acme lasted ; and finally (7) in the remaining case a double friction murmur, intensified by pressure, was audible over the region of the pericardium during the acme. I.-Cases with Thrill and (1) a Creak- ing, (2) Grating, or (3) Harsh Friction Sound over the Heart.-In nine of the forty-three cases under review, a systolic thrill was felt over the heart, and (1) in five of those cases a creaking; (2) in one of them a grating; and (3) in three of them a harsh friction sound was audible at the seat of thrill at the time of the height or acme of the disease. In six of these cases the thrill was present over the right ventricle, and, in some of those, but not in all, it was probably situated over the left ventricle also ; in another of them it was present over the apex and the second space, but not over the right ven- tricle ; in one of the two remaining cases it was felt over the apex ; and in the other one over the second space alone. (1) Creaking Friction Sound.--In three of the cases with a thrill over the right ventricle, and in one of those with a thrill over the apex alone, a creaking sound was audible over the seat of thrill. One of these patients, a man aged 27, came in with extensive pericardial dul- ness ; a thrill over the right ventricle extending from the fourth left cartilage to the sixth ; a loud systolic creaking friction sound consisting of five vibra- tions, the diastolic sound being much smoother than the systolic, over the seat of the thrill; and a double frottement ex- tending widely over the front of the chest from the second cartilage down to the ninth on both sides, and audible at the epigastric space. The pericardial dulness on that day extended upwards to the third space, and on the following day to the third cartilage, when it reached its greatest height. The region of thrill had increased upwards, and extended from the third cartilage to the sixth. A creak- ing sound was audible apparently over the whole seat of the thrill, but over the fifth cartilage there was a vibrating, grat- ing, systolic friction sound of a churning character, which was creaking towards the end of the systole, the diastolic sound being short and smooth. (2) Grating Friction Sound.-A grating friction sound without a creak was present on the presumed day of the acme in one case. (3) Harsh Friction Sound.-A harsh friction sound was present with a thrill in three cases. One of these cases, a girl, aged 17, came in with an extensive im- pulse, a double thrill, and a loud, double VOL. IL- 36 562 PERICARDITIS scraping sound over, but not below, the heart. On the second day, there was less dulness, and no note of thrill, and the friction sound was less harsh and exten- sive : but, on the third day, there was less effusion, the impulse was lower and more diffused, and the friction sound was much more intense and extensive. We may, I think say, on reviewing these cases, that at the time of the acme of the disease, when a thrill is present over the right ventricle, a creaking noise is audible over the seat of the thrill; and that from this noise, as from a focus, a to-and-fro sound radiates in all directions over the front of the chest, reaching far beyond the limits of the region of actual friction, becoming more feeble towards its outlying margins, and spreading almost up to the clavicles, out to or beyond the nipples, and down to the eighth or ninth cartilages ; and that when the effusion lessens and the thrill disappears, the creak vanishes, and the friction sound softens, and limits its area to the region of actual friction, being bounded below by the sixth cartilage. The reason for the great ex- tension during the acme of the friction sound upwards, outwards, and down- wards beyond the region of actual friction in these cases is obvious. The heart, surrounded by the distended pericardial sac, is displaced upwards into the higher and narrower portion of the cone of the chest. It works in a confined space, and rubs with its roughened surface against the roughened surface of the pericardium ; and the lungs being pushed aside, it presses against the sternum and carti- lages, and excites vibrations and a creak- ing or grating friction sound over the walls of the chest in front of the heart. The play of the two roughened surfaces of the pericardium upon each other induces vibrations, sensible to the hand, that ex- cite consonant vibrations in the superim- posed sternum and cartilages ; and these parts, acting as a sounding-board, trans- mit the sound to a distance over the front of the cage of the chest in all directions, and especially downwards. When the thrill is limited during the acme to the second space, over the pulmonary artery, or to the apex of the heart, or is felt both over the apex and the second space, the creaking or grating noise is limited to the seat of the thrill; and the friction sound does not extend beyond the region of actual friction, excepting perhaps to a small extent over the circuit of the apex. When in such a case the effusion lessens, the heart descends, and the thrill disap- pears, the friction sound may spread down- wards, so as to reach the eighth carti- lage. II.-Cases in which a Thrill was not ob- served over the Region of the Heart or Great Vessels. (1) Cases in which a Sound like the Creaking of New Leather was audible at the time of the Acme of the Effusion, no Thrill being present.-In seven of the forty-four cases under examination, a creaking noise, usually systolic, was heard without a thrill at the seat of the impulse of the heart at the time of the acme. In all of these cases, and in several of those in which a thrill over the heart was accompanied by a creaking or grating noise, as soon as the fluid in the pericar- dium lessened and the heart descended, the creaking noise was replaced by a comparatively smooth friction-sound. This occurred on the day after the acme of the effusion in four of the seven cases. This sudden disappearance of the creak- ing noise with the diminution of the fluid and the descent of the heart, appears to me to show that the presence or absence of the creaking noise depended more on the position of the heart and on the de- gree and kind of pressure exerted by it during its contraction ; than on the char- acter of the roughened coat of lymph covering the heart and lining the peri- cardial sac, since that lining cannot have changed materially in one day when the disease was at its height. At the time of the acme of the effusion into the pericar- dium, the heart is elevated so as to occupy the upper and narrower part of the cone of the chest; and beats with force in its contracted space against the cartilages and sternum which confine its move- ments. When the heart pulsates thus against the walls of the chest, the move- ments of the former are resisted by the pressure of the latter. The accumulated force of the heart overcomes the resistance of the walls of the chest, and the accumu- lated resistance of those walls then over- comes the force of the heart; these two opposite forces by turns arrest and over- come each other and give rise to a series of fine jerks or vibrations that may give birth to a thrill, and a yibrating creaking noise. In one case, this creaking noise consisted of five distinct vibrations ; and such a succession of vibrations forms, in- deed, the essential nature of the thrill and its attendant creaking sound. The creaking sound, and the main va- rieties of friction sound, may be imitated by rubbing the forefinger on the thumb with varying degrees of force when the back of the thumb rests upon the ear. When the finger and thumb rub gently or with moderate force upon each other, to and fro, the rubbing sound is smooth or harsh in proportion to the gentleness or force employed. When, however, the pressure exerted by the finger on the thumb is great, the resistance to their onward movement on each other causes them to stop in a succession of jerks, which produce a creaking noise. AUSCULTATION. 563 When the fluid decreases, the heart de- scends into the ampler space of the chest; the organ moves with freedom ; and, as it no longer presses with a resisted force against the walls of the chest, the thrill, vibrations, and creak give place to a mode- rated friction sound ; which may be so harsh as to sound like the rubbing of sand- paper ; or so soft as to resemble a murmur. (2) Vibrating, Grating Friction Sound. -The grating, vibrating friction sound ranks next to the creaking noise in inten- sity. It is, in fact, a sister-sound to the creaking noise, with which it is closely allied. Thus, it may be audible when there is a thrill, when it may be heard alone, or associated with a creak; or it may by pressure be converted into a creak; or it may precede or follow, dis- place or be displaced, by that sound; or it may, like it, be produced by pressure. The grating sound, like the creaking sound, is the combined effect of pressure and friction, but the pressure is usually less, while the rubbing surfaces are, I be- lieve, more invariably rough, when the sound is grating than when it is creaking. A grating sound was audible during the acme of effusion in two or three cases in which there was a thrill, and in two in which there was no thrill; and it was ex- cited by pressure in two. It was, there- fore, observed in one-seventh of the cases (6 or 7 in 44). We have already seen that the creaking sound is usually single, but it is the re- verse with the grating sound, which is usually double. The grating friction sound is a jarring, grating, vibrating noise, rough and to-and-fro in character, made in a succession of jerks, each jerk being sepa- rately audible, and varying slightly, and the whole series not combining to form one note like the creaking sound, but, as I have just said, a jarring, grating, vi- brating noise. I made out, as I have already stated, that in one case the creak was composed of five vibrations, or at the rate of twenty-two vibrations in a second ; but, as I took no special note of it, I do not know what number of vibrations were made in a second by the grating noise. I believe, as I have already hinted, that the grating noise is always associated with the rubbing of the two harsh and rough- ened surfaces of the heart and pericardium upon each other, but I have no direct proof of this at present. (3) Harsh To-and-Fro Friction Sound, intensified by Pressure, at the Time of the Acme of the Pericardial Effusion. - Re- sume, including the whole of the preceding cases, whether with or without a thrill.- We have just seen that a creaking noise, usually systolic, was present over the heart at the time of the acme of the dis- ease in one-fourth of the cases in which the dulness was observed at or about the period when the effusion was at its height (12 in 44); while in four other cases it was then excited by pressure, and in two it was heard just before the acme of the effusion. Creaking, therefore, was pres- ent as a primary sound in twelve cases ; as a secondary sound, or from pressure, in four cases; and in two others it was audible just before the acme. We have also seen that a grating friction sound, usually double, was present over the heart when the effusion was at or about its height, as a primary sound in three cases in which there was no creaking, and in one or more in which there was creaking; and as a secondary sound in two in which it was excited by pressure ; while in four others it was present just before or after the period of the acme of the disease. If we combine the two sounds, we find that during the acme the creaking and grating sounds were primary in fifteen cases, and secondary, or excited by pres- sure, in six; while they were associated with each other in one or more. Besides these fifteen cases, in which creaking or grating sounds were primary, there were nineteen cases in which there was a defi- nite friction sound, which was usually harsh ; in all of these it was double, or to-and-fro in character, being audible both during the systole and the diastole of the ventricle, and in all but two it was inten- sified by pressure. Three-fourths, there- fore, of the patients (34 in 44) in whom the pericardial dulness was observed when at or near its height presented either a systolic creaking noise, or a double grat- ing, or a definite to-and-fro friction sound, usually harsh in character. Besides the nineteen cases in which there was a double frottement, usually harsh, at the time of the acme; there were seven cases in which that sound was associated with a creaking noise ; and in one it accompanied a grating noise. In these cases the creaking or grating noise was limited to that part of the right ven- tricle, or the apex, that was pressing with the greatest force upon the costal cartil- ages or sternum, while the double frotte- ment pervaded and often overstepped the rest of the heart and the great vessels. If we group together the eight cases with harsh double frottement, in seven of which the frottement was associated with a creaking sound and in one with a grat- ing noise, and the nineteen cases not so associated, we find that in one-half of those twenty-seven cases the character of the sound is definitely specified <13 in 27) ; while in twelve it is described as a harsh double friction sound ; and in two as a to-and-fro sound. Of the thirteen cases in which the char- acter of the double sound was specified, in four it was described as being like that made by rubbing with sand-paper; in 564 PERICARDITIS. seven as being either rasping, or musical planing, scraping, scratching, grazing or rustling, the latter sound being a genuine frou-frou; while in the remaining two the sound resembled that made by sharpening a scythe. In the whole of the twenty-seven cases except two, pressure with the stethoscope intensified the double froltement; it some- times altered or modified the character of the sound ; and in five instances it trans- formed the double frottement into a creak- ing sound. When the creaking sound was thus brought into birth by pressure, or secondary, it was usually double ; but when the creak was always present, or primary, it was, as I have already shown, usually and essentially single or systolic. In all these cases the double frottement was essentially a to-and-fro sound. The character and volume of the sound, and the relative intensity of the to-and-fro, or the systolic and diastolic friction sounds, varied over the different parts of the heart. As a leading principle, the greater the pressure exerted by the heart, or any portion of it, during its action upon the cartilages or sternum against which it beat, the more intense was the friction sound. The friction sound in the remaining cases of this group was limited to a com- paratively small area. In two of the nineteen cases, in both of which there was a thrill over the right ventricle, the rubbing noise, as I have al- ready stated, extended over the front of the chest, far beyond the region of actual friction. These two cases, however, stand apart, for in the remaining seventeen the area of the friction sound was limited to the region of actual friction ; with, how- ever, this slight exception, that in six of the patients the to-and-fro sound spread upwards to the top of the sternum, and in one of them it was diffused outwards as far as the left armpit. The upper limit of the distended pericardial sac and of actual friction is rarely higher than the transverse centre of the manubrium, which is about an inch below the top of the ster- num ; therefore in the six patients just spoken of, the friction sound extended itself upwards for from an inch to fully two inches above the actual seat of fric- tion over the great vessels, which, at their higher portion, are partly covered by lung. The explanation of this extension of the friction sound upwards beyond the imme- diate seat of friction is the same as that of the diffusion of the friction sound over the front of the chest far beyond the re- gion of the distended pericardium and of actual friction, when a thrill and a corre- sponding creaking noise are present over the heart. The to-and-fro movements of the heart upon the pericardial sac, both being covered with lymph, excite a to- and-fro sound which is audible over the region of those movements. The vibra- tions that produce the sound are commu- nicated to the sternum, which is played upon by the rubbing surfaces; and the sternum, which acts as a sounding-board, propagates the sound to its own upper end, which is at some distance from the seat of the parent vibrations. The extension of the friction sound beyond the region of actual friction depends on the loudness and intensity of the rubbing noise, and the force with which the heart when it is rubbing to-and-fro, presses against the sternum and cartilages. Of the six cases in which the to-and-fro sound mounted to the top of the sternum, in three there was a creaking sound over the heart, with a thrill also in two of those ; in two others a creaking sound was excited by pressure ; and in the remaining one a loud, harsh, double friction sound was present over the region of the pericardium. Although a creaking friction sound was audible over the apex in four instances, in only one of them did the to-and-fro sound spread to the left beyond the apex, but in that one the rubbing sound extended outwards into the left armpit. In that case there was dulness over the left lower lobe, and bron- chial breathing between the left axilla and the spine. It is, therefore, evident that the heart and pericardium were dis- placed towards the left side owing to the condensation of the left lung, and that this circumstance facilitated the extension of the friction sound to the left axilla. With these few exceptions, the region of friction sound coincided in these cases with the actual region of friction at the time when the effusion into the pericar- dium was at its height. (4) Cases in which a Soft Friction Sound, audible over the Heart at the Time of the Acme of the Effusion into the Pericardium, was converted by Pressure into a Harsh Rubbing Noise.-Four cases with a soft friction sound, in which pressure rendered the sound harsh, come under this head- ing, and in one of these the friction sound elicited by pressure resembled the noise made by sharpening a scythe. In a fifth case, with a similar friction sound, the pressure test was not employed. In these four cases a comparatively soft double friction sound was intensified and altered by pressure, becoming converted in one instance into a sound like that made by sharpening a scythe, and in one into a rasping, grating noise. Here pressure expelled any interposed fluid ; brought the opposite roughened surfaces of the pericardium more closely into con- tact ; and aroused counter-pressure on the part of the heart against the car- tilages and sternum during its to-and-fro rubbing movements. These effects spoke AUSCULTATION. 565 out not only in a louder and more diffused, but also in an altogether altered sound; so that the soft sounds, sometimes so murmur-like as to be almost doubtful in quality, became instantly transformed into a loud double and broken noise, like that made by sharpening a scythe, or into a rasping, grating, almost creaking sound. (5) Cases in which a Double Friction Sound, not otherwise audible, came into play when Pressure was made over the Heart during the time of the Acme of Pericardial Effusion.-In four cases during the acme, on listening without making pressure, the healthy sounds of the heart were alone audible ; but on making pressure those sounds were either replaced or accom- panied by a double rubbing noise. In three of these cases, at the time the effusion into the pericardium was at its height, when the stethoscope was applied lightly over the heart, the natural heart sounds were alone heard, friction sounds being everywhere inaudible. When, how- ever, pressure was made with the stetho- scope, a double friction sound was imme- diately brought into play, which could be suspended or renewed at will by with- drawing or replacing the pressure. In one case the friction sound thus generated was limited to the region of the right ventricle, and in another to the base of that ventricle ; but in a third case it was diffused over the whole space occupied by the heart and great vessels. The impulse was feeble in one of these patients, and was felt over the right ventricle in an- other. It is difficult to say why friction sound was absent without pressure over the seat of the impulse ; but it is self-evi- dent that if we press the cartilages or sternum inwards upon the walls of the heart moving to and fro, those walls will work with increased counter pressure against the resisting walls of the chest; and may thus elicit a friction sound when previously absent, or intensify a friction sound already existing, owing to the in- creased friction of the two roughened surfaces. In two of the cases a to-and- fro sound was audible without pressure over the apex, and in one of them over the lower border of the right ventricle also; but it was brought into play by pressure over the whole region of the heart and great vessels. The subsequent history of these cases illustrates with great clearness the cause of the absence of friction sound without pressure, and its presence with pressure during the acme of the disease. In three of them, as soon as the effusion into the pericardium lessened,the heart descended, and its impulse became stronger and lower; the fluid interposed between the front of the heart at its lower border and the peri- cardial sac disappeared ; and the friction sound came into spontaneous play where it was before absent without pressure. That sound, indeed, gradually augmented in loudness and intensity, and increased in area upwards, sideways, and especially downwards. (6) Case in which Friction Sound was Absent for Two of the Three Days during which the Acme of Pericardial Effusion lasted.-This patient, a woman aged 21, came in with great pain and a double friction sound all over the region of the heart. The pain was relieved by leeches. Next morning the effusion was at its height, but the friction sound had van- ished and could not be brought back even by pressure. That evening there was a return of pain, and a renewal of the fric- tion sound which lasted until next day, but again vanished on the fourth day, when the effusion was still at its acme. She was in great distress from pain over the heart, but the impulse was faint in the third and fourth spaces. Next day there was less effusion, a lowered impulse, and no distress, and friction sound was rendered audible by moderate pressure over the right ventricle. Why was the friction sound absent in this case of peri- carditis ? When we consider that the impulse was perceptible, it must be al- lowed that the answer is difficult. The loss of blood on the second day and the great distress on the fourth day may in some measure, however, account for the exit of the friction sound. (7) Case in which a Friction Murmur was audible over the Heart at the Time of the Acme of the Disease. - This case of a youth jet. 17, presented a long history, and proved fatal on the forty-eighth day. On examination after death, the heart was found to be universally adherent by means of recent lymph. Throughout the whole period, with rare and doubtful ex- ceptions, the inflammation of the peri- cardium was made evident, not by the ordinary friction sound, but by a true fric- tion murmur. The Area of the Friction Sound, during the Acme of the Effusion,-1The area of the friction sound when the effusion into the pericardium is at its height may, on the one hand, be so extensive as to cover the whole front of the chest, extending from the clavicles down to the ninth right and left costal cartilages; or, on the other, be so limited as to be confined to the middle or lower portion of the sternum. This great diffusion, or narrow limitation of the friction sound at the period of the acme of the disease, is, however, com- paratively rare; and, as a rule, the area of the friction sound corresponds either with the area of actual friction, or with that of dulness on percussion over the pericardium. The friction sound was audible over a great extent in all those cases, amounting 566 PERICARDITIS to nine, in which a thrill was felt over the heart or great vessels, and especially in those in which it was perceptible over the front of the right ventricle. In all the cases with thrill the friction sound was audible over the right auricle and ventricle, the outlying portion and apex of the left ventricle, and the great vessels; in all but one of them, also, it extended to the top of the sternum, be- yond the region of the distended pericar- dium over the great vessels. In these cases, as I have already explained, the friction sound was most intense over the region of the thrill, and it radiated thence over a wide area, becoming gradually less intense from its focus to its extreme limits, being conducted by the sternum and car- tilages acting as a sounding-board. In six of the twelve cases in which a creaking sound was heard over the heart, the area of the friction sound extended down to the seventh, eighth, or ninth cos- tal cartilages; but in five of these the creak accompanied a thrill. In the re- maining six cases the frottement extended to the sixth cartilage, or occupied an un- specified space to the right and left of the sternum. It is evident, therefore, that the great diffusion of the sound in these cases was due more to the thrill, than to the creaking sound that was audible at the seat of the parent thrill. I need not here specify the exact limits of the friction sound in the remaining cases. These clinical facts show that, when the effusion into the pericardium is at its height, if we put out of view those cases in which a thrill is felt over the right ven- tricle, the friction sound is, with a slight exception, practically limited to the re- gion of pericardial dulness, or rather of the heart and great arteries. This excep- tion applies to the presence of the friction sound over the upper end of the sternum, which is fully an inch higher than the uppermost limit of that region. This was observed in nineteen cases, and in ten of these no thrill was noticed over the region of the heart or great vessels. In all these cases the friction sound was conducted to the top of the manubrium, from the actual seat of friction by the sternum itself, act- ing as a sounding-board. When the lower boundary of the fric- tion sound reaches to the lower end of the sternum and the sixth cartilage, that limit is still within the lower boundary of the region of pericardial dulness, which is situated, when the pericardium is com- pletely distended, behind the ensiform cartilage and along the lower margin of the sixth cartilage. As I have already shown, however, the lower boundary of the heart, and consequently of the region of actual friction, is, in the great majority of cases, above the lower end of the ster- num and the sixth cartilage ; for the fluid in the pericardium presses the heart up- wards, and interposes itself between the lower border of the heart and the walls of the chest in front of that border. The position of the impulse is a good practical test of the position of the actual seat of friction. In three of the seven cases in which the friction sound was audible as low as from the seventh to the ninth car- tilages, the impulse was felt in the fifth space, and in one of them, a case of estab- lished valvular disease with enlarged heart, in the sixth space. But with one single exception, in which the beat of the heart was felt in the fifth space, in all the rest of the cases the impulse was not pre- sent below the fourth space, and in nine instances its lowest position was in the third space. In the nature of things, the seat of the actual friction behind the ster- num, except at its upper portion, cor- responded, as a rule, pretty closely with its seat at the intercostal spaces. In all the cases save one the friction sound was audible down to the lower end of the sternum at the time of the height of the effusion, and in twelve of them it was heard over the sixth cartilage. In all these cases, therefore, it is evident that the friction sound was audible below the actual seat of friction. The sternum is an excellent sounding-boa? d, and the conduction of the friction sound to the lower end of that bone, by its own reso- nant vibrations, at once explains the pre- sence of the sound at its lower end. The presence of the frottement over the sixth cartilage, an inch below the actual seat of friction, appears to me to call for a dif- ferent explanation. The observed facts are, indeed, different in these two cases. The sound heard at the lower end of the sternum is, like that at its upper end, usually of the same harsh to-and-fro quality, and of about the same intensity as that audible over the two rubbing sur- faces at the middle of the bone. But this, as a rule, is not so with regard to the fric- tion sound audible over the sixth carti- lage, for that is softer, smoother, and less loud than the sound over the seat of the impulse, from one to two spaces higher up. The presence of the soft muscular space cuts off the direct connection be- tween the fifth cartilage and the sixth. The sixth cartilage is, however, directly attached to the sternum, and that bone, acting as a sounding-board, doubtless conveys some of its own resonant vibra- tions to the cartilage. But it is to be noted that the sound over the fifth space, though softer and feebler than that over the fourth space, is harsher and louder than that over the sixth cartilage. It is self-evident that the sound over the space can scarcely be conducted from the ster- num ; and I think, therefore, that we AUSCULTATION 567 must look to the fluid within the pericar- dium, and to the inner surface and struc- ture of the roughened and thickened peri- cardium itself, as the principal media by which the sound is conducted in these cases to the sixth cartilage. If we except those cases in which a thrill is felt over the right ventricle or at the apex, we find that when the sac is filled with fluid the friction sound stops quite suddenly along the left and right margins of the region of dulness over the pericardium. This sudden arrest of the rubbing sound at its outer border is less marked along the right than the left mar- gin. This is, I consider, explained, firstly, by the softer, smoother, and more equal character of the to-and-fro sound over the right auricle than over the right and left ventricles; and, secondly, by the presence of fluid between the compressed right auricle and the walls of the chest in front of it, along its outer border. If, on the other hand, we look at the left border of the distended pericardium, we find that there the solid ventricles by their own pressure and action against the ribs and spaces, displace the fluid and completely occupy the ground. Here we pass sud- denly from the loud double frottement made by the two rubbing solid surfaces of the ventricle and the rib lined with roughened pericardium, to the silent, soft, non-con- ducting surface of the lung. We may, I think, conclude, with the qualifications just stated, that 'when the effusion is at its height, as well as when it is increasing in quantity, the friction sound is limited to the region of pericar- dial dulness ; and, though with less rigor, to the region of actual friction ; and that the law originally stated by Dr. Stokes, that the area of the friction sound is usu- ally limited to the region of the heart, is correct in the great majority of cases, during the period of the acme of the effu- sion. Before concluding what I have to state with regard to the area of the friction sound, I would here estimate, as nearly as I can, the extent to which the sound was heard over the various chambers of the heart and the great vessels during the acme of the pericardial effusion in the forty-four cases now under examination. In one-half of the cases (21 in 44) the friction sound was audible over the whole front of the heart, including the right auricle and ventricle, the apex and a por- tion of the left ventricle, and the great vessels. In seven or eight other cases it was heard over the right auricle and ven- tricle, in four or five of which it was also present over the apex, and in one over the great vessels. In fifteen other cases the frottement was audible over the right ven- tricle, in nine of which it was also heard over the apex, and in four or five over the great vessels. In six of these cases the friction sound was limited to the right ventricle. If, upon this estimate, we take each portion of the heart separately, we find that the friction sound was present during the acme over the right ventricle in the whole of the forty-four cases under notice ; over the apex of the left ventricle in thirty-four or perhaps thirty-five of those cases; over the right auricle in twenty-eight or twenty-nine of them ; and over the great vessels in twenty-six or twenty-seven of them. Intensity and Character of the Friction Sound over the different parts of the Heart and Great Vessels during the Acme of the Effusion.-When inquiring into the rela- tive intensity and character of the friction sound over the different cavities of the heart, except the right ventricle, and the great vessels at the time of the acme of the effusion, I shall take into account the forty-four cases now under examination ; but as regards the right ventricle I shall limit myself to the twelve cases with pri- mary creaking sound, the two with grating friction sound, and the nineteen cases in which there was a harsh friction sound intensified by pressure, which form a total of thirty-three cases. Although the left ventricle forms the pivot of the heart's action, and does its work with threefold more power than the right ventricle, I shall first examine the friction sound as it presented itself over the right ventricle, because it forms the front of the heart; covers the left ventricle except at its left border and apex ; and is the main seat of actual friction. Hight Ventricle.-As the right ventricle forms the front of the heart, it is always in contact to a greater or less degree with the anterior walls of the chest. Owing to the distension of the pericardium during the acme, and the elevation of the heart into the contracted space at the upper part of the chest, the heart and great ves- sels are stripped of the lung that covered them, and press directly forward upon the middle and upper part of the sternum and the higher costal cartilages and intercostal spaces, from the second to the fifth. The to-and-fro movements of the right ventricle, by rubbing against the opposed surface of the sac, give birth to the to-and- fro friction sound audible in front of the ventricle. Those movements play from right to left during the contraction of the ventricle, and from left to right during its dilatation (see Figs. 62, 63, p. 401). The sweep of the walls is very extensive be- hind the sternum, at the junction of the auricle to the ventricle ; thence it gradu- ally lessens; and comes to a stand-still near the septum. The friction movements are therefore greater, and the friction sounds are louder, at the sternal than the costal halves of the cartilages. As the 568 PERICARDITIS position of the ventricle is raised from the fourth and fifth spaces to the third and fourth spaces, the frottement is usually louder over the sternal portions of those spaces, and the adjoining portion of the sternum, than elsewhere. As the movements made during the emptying of the ventricles are active, and those made during the filling of the ven- tricle are passive, the increased pressure made by it upon the cartilage and sternum during the systole often intensifies the frottement, and, as I have already shown, may even transform it into a creaking noise. Thus, of the thirty-three cases under examination, in six there was a systolic creak over the right ventricle ; in thirteen the systolic friction sound was louder than the diastolic ; in two the sys- tolic and diastolic sounds were equal; and in twelve it is not stated whether there was any difference between the two sounds. From these clinical facts it is evident that the active friction sound made during the contraction of the ventricle is, as a rule, louder than the passive friction sound made during its dilatation. In a small minority of cases, however, the two sounds are equal, and a true to-and-fro sound is produced, the diastolic portion of which speaks with the same intensity, length, and continuousness as the systolic portion. In these cases I believe that the impulse is feeble, and that the systolic friction sound, like the diastolic, is, so to speak, passive, and is not intensified by the greater pressure from within of the anterior wall of the ventricle upon the walls of the chest. The conus arteriosus of the right ventri- cle calls for special notice. It is situated behind the third space and the two ad- joining cartilages, and as it enjoys exten- sive play during the systole, when its movements are twofold, from above down- wards, and from left to right, the friction sound is often notably harsh, loud, and to-and-fro in that situation. Sometimes it is there creaking or grating, when it may be accompanied by a thrill. It some- times resembles the sound made by rub- bing together two opposite surfaces of ■emery paper, of stuff or of silk; or it is rasping, or scratching, or rustling when it may present a true, frou-frou; or it may, though less frequently, be soft in charac- ter. A friction murmur is, however, rarely or never present in this situation. Pressure readily intensifies and alters the friction sound over the conus arteriosus, and sometimes converts it into a creaking sound. As the conus arteriosus is covered in health by a thin layer of lung, it is not usually the early seat of friction sound ; but as the lung, when once displaced from before it, does not readily replace itself, •the rubbing sound is often heard in this position up to a late period in the history of the case. The friction sound is notably double or to-and-fro over the conus arte- riosus, and this may be accounted for by the ready completeness with which the right ventricle spontaneously fills itself during the ventricular diastole. The Apex and Outlying Portion of the Left Ventricle.-The apex and outlying portion of the left ventricle are in health covered by the lung. The extent to which the lung thus affords a protection for the apex depends upon the vigor of the indi- vidual, the size of the chest, and the amplitude of the lungs. The portion of left lung immediately covering the apex is a thin tongue, the lowermost protruding angle of its upper lobe, which laps round the apex of the organ, and interposes itself between that part and the ribs. During the diastole, when the ventricle is inac- tive, the covering of lung is complete; but when the ventricle contracts, owing to the combined muscular rigidity of the organ, and the outward pressure of the blood that is compressed by the contract- ing cavity, it pushes aside the tongue of lung in front of it, so that the apex sweeps against the ribsand their interspaces. It is thus in young persons and those who are not robust; but in strong adults, inured to exercise, the average size of the lung is increased, and the apex is so em- bedded in the lung, that its proper beat cannot be felt, except perhaps at the end of a forcible expiration, or when they lie on the left side. In one instance, and in one only, an obscure friction sound was heard over and limited to the apex before it was audible elsewhere. This was on the day of admission, but on the following day it had left the apex, and transferred itself to the whole right ventricle and right auricle. I can offer no explanation of this exceptional sign. As a rule, the friction sound was, as I have said, limited at first to the right ven- tricle ; but as the disease advanced, the increased fluid in the pericardium dis- placed the left lung and laid bare the apex, so that the friction sound spread itself from the right ventricle to the left. When the effusion was at its height the heart was raised, and the apex-beat was felt in the fourth, or even the third space, at or just above and beyond the nipple. Friction sound was probably audible over the apex during the acme in thirty-four of the forty-four cases now under notice ; it was absent from that point in nine; and its presence there was doubtful in one case. The movement of the apex is, in its nature, the reverse of that of the right ventricle at its junction with the right auricle ; for while, during the systole, that part moves from right to left, the apex moves from left to right, and from below AUSCULTATION. 569 upwards. As the active sweep of the apex takes place during the contraction of the ventricles, it is natural to expect that the friction sound at the apex should be mainly systolic, and the examination of my cases shows that this is so. Of the thirty-four cases in which a friction sound was audible over the apex, in six it was heard during the systole only ; in ten the frottement was double, but was more in- tense and prolonged during the systole than the diastole; and in none was it stated that the two sounds were of equal intensity during the two periods. In six cases there was a creaking friction sound, usually systolic, at the apex. When the lower lobe of the left lung shrinks under the double effect of pulmo- nary apoplexy within the lung, and pleu- risy on its exterior, on the one hand; and of compression of that portion of the lung and of the left bronchus, by the great dis- tension of the pericardium, on the other, the apex becomes completely exposed, and extends far to the left. In one such case, a youth, aged 17, a systolic creaking sound was audible over and beyond the apex, and the friction sound extended far to the left, ceasing suddenly in the axilla. Right Auricle.-The right auricle is in health completely screened from the ante- rior wall of the chest by the middle lobe of the right lung, which separates it from the middle of the sternum and the costal cartilages to the right of the lower half of that bone. Friction sound is therefore never audible over the right auricle until the portion of lung that is interposed be- tween it and the right cartilages is pushed aside by the advancing tide of effusion, so as to lay bare the auricle. When the effusion into the pericardium was at its height, a friction sound was audible over the right auricle in three-fifths of the cases (28 or 29 in 44). The expansion of the right auricle is quite passive, and its contraction is made with so little exercise of force, that its movement to the right during its period of filling, and its movement to the left during its period of emptying, are made so quietly, that it exerts no pressure on the cartilages during its to-and-fro move- ments. It is natural to expect that the to-and-fro frottement, the frou-frou pro- duced by the passive double friction of the right auricle, should be made up of two equal sounds, and as a rule those two sounds were equal over that cavity. In twelve of the twenty-nine cases in which friction sound was audible over the right auricle, the systolic and diastolic sounds were equal; in eleven the frotte- ment was double, but the relative inten- sity of the two sounds was not described ; and in one a systolic sound, almost creak- ing in character, was audible over the right auricle. In this last exceptional case a similar almost creaking noise was heard over the base of the right ventricle at the lower portion of the sternum, and that was evidently the source of the rub- bing sound over the auricle. The two sounds made respectively over the right auricle during the two alternate movements of its dilatation, with contrac- tion of the ventricle, and its contraction with dilatation of the ventricle, are not only equal in character, intensity, and continuousness ; but they are also more soft and smooth in tone than they are over the ventricle ; this contrast being most remarkable in some of those cases that present a thrill and a creaking sound over the right ventricle, and the diffusion of a harsh double friction sound over the whole front of the chest extending down- wards even to the eighth or ninth right and left cartilages. The question here arises whether under these circumstances the soft double fric- tion sound audible over the cartilages to the right of the lower sternum is due to the immediate friction of the subjacent right auricle, or to that of the right ven- tricle, transmitted through the fluid and softened in its transmission? I think that we must infer that the latter is the usual source of this sound, when we con- sider that the yielding right auricle is compressed by the fluid in the pericar- dium at the time of the acme. Why under these circumstances, the two sounds are usually equal, I cannot say. The Ascending Aorta and Pulmonary Artery.-In health the two great arteries lie behind the upper half of the sternum and the spaces to the left of it, above the level of the third cartilages. They not only have the bony protection thus af- forded them, but they are additionally sheltered by a thin covering of lung that is interposed between them and the bony shield in front, and is made up of the inner adjoining margins of both lungs. The aorta is guarded by the strongest portion of the sternum, and the pulmonary artery lies behind the second space and cartilage, and the adjoining margin of the sternum. In the early stages, therefore, of pericarditis, friction sound is never audible over the great vessels. When the fluid increases, the distended pericardium and the elevated heart and great vessels push the double curtain of lungs to each side, so as to bring the great arteries into contact with the sternum and the first and second spaces and cartilages. The heart and great vessels then, as I have already said, occupy the narrower space in the upper portion of the cone of the chest, and there is now no longer room both for them and for the portion of lung superficial to them in health, which is therefore displaced. PERICARDITIS. 570 In considering the character of the friction sound over the two great arteries, we must distinguish the aorta from the pulmonary artery. The roots of those arteries, including under that term their apertures, valves, and sinuses, descend and ascend fully half an inch during the successive periods of the systole and dias- tole of the ventricles; the movement of the systole being more active than that of the diastole. The root of the pulmonary artery is situated at the front of the heart, and when the lung is displaced from before it, the artery lies immediately behind the second, and sometimes also the first, left intercostal space, the second costal carti- lage, and the adjoining border of the sternum. The movement of the pulmo- nary artery, like that of the conus arteri- osus from which it springs, is downwards and from left to right during the systole, and the reverse during the diastole. The friction sound over the pulmonary artery, is not, therefore, so far as I know to be distinguished from that over the conus arteriosus. The two-and-fro sound caused by those two adjoining and connected parts must resemble and blend with each other; but while that of the pulmonary artery is situated over and above the second space and the adjoining border of the sternum, that of the conus arteriosus extends downwards from that point to the fourth cartilage, but widening to the right, so as to occupy the whole breadth of the centre of the sternum. A peculiar systolic scratching noise, that somewhat resembles a friction sound, is sometimes audible over the pulmonary artery during the course of acute rheuma- tism, and is generally associated with endocarditis. This sound is evidently caused by the vibration of the blood ad- vancing during the systole along the artery when not in a state of tension ; and is to be distinguished from a friction sound by its limited area, the sound being confined to the second space, and not accompanied by friction sound elsewhere over the heart; its restriction to the period of the systole and its consequent total want of a two-and-fro character ; its free- dom from change when pressure is made over it; its unaltering character on suc- cessive days ; and the absence of pain over the heart or other symptoms or signs of pericarditis. The root of the aorta instead of being exposed in front, like that of the pulmo- nary artery, is buried deeply in the cen- tre of the heart, being covered by that artery, the conus arteriosus, and the left border of the right auricle. The root of the aorta cannot therefore cause a friction sound. The ascending aorta, where it comes into view above the right auricle and behind the lower half of the manu- brium, is in health deep in situation, being covered by the adjoining margins of the opposite lungs. When, however, the heart and great vessels are lifted up- wards by the advancing invasion of the fluid in the pericardium, the lungs are displaced from before the ascending aorta, which may possibly be pressed against the back of the manubrium. Even then, however, it can only excite a partial fric- tion sound, for its movements, which are downwards and upwards, are very slight. Friction sound was audible at the manu- brium over the ascending aorta and the adjoining portion of the pulmonary artery at the time of the acme of the effusion into the pericardium, and especially dur- ing expiration, in twenty-six or perhaps twenty-seven of the forty-four cases un- der review ; but this friction sound was evidently not generated by the double movement of those vessels, but was con- ducted upwards by the sternum, acting as a sounding-board, from the harsh double friction sound over the right ven- tricle. This was shown by that sound reaching with full intensity to the top of the sternum, which is a little above the transverse aorta, in twenty-six or per- haps twenty-seven of the forty-four cases ; and by the close correspondence between the character of the double frottement over and above the great vessels at the upper half of the sternum, and that over the right ventricles, at the lower half of the sternum. At the time of the acme of the effusion into the pericardium the whole heart is raised, and the lungs are separated from each other in front, so that the pulmonary artery, the conus arteriosus and the rest of the right ventricle, the apex and out- lying portion of the left ventricle, and the right auricle are uncovered, and brought into immediate contact with the walls of the chest in front of them. The whole front of the right ventricle bears upon the sternum and left cartilages with varying force. Sometimes it pro- duces a thrill during its contraction, which may extend over its surface from the third to the sixth cartilages, and is often ac- companied by a systolic creaking sound. At other times, sometimes with, but gen- erally without a thrill, a double grating sound or a harsh friction sound of various tones, the systolic sound being usually louder than the diastolic, springs up over the whole right ventricle. In rare in- stances the two sounds are equal. More rarely a soft friction sound, rendered harsh by pressure, or a to-and-fro sound, excited by pressure but absent without it, is present over the right ventricle. A friction sound is heard over the apex during the acme in about three-fourths of the cases. The apex may, like the right AUSCULTATION 571 ventricle, present a thrill and a creaking sound during the systole ; or a loud, pro- longed systolic friction sound, and a short, feeble diastolic one. In no instance are the systolic and diastolic friction sounds equal over the apex. During the acme the right auricle in two-thirds of the cases presents over its surface, to the right of the lower half of the sternum, a double, smooth, to-and- fro murmur or friction sound, equally loud during its dilatation and contrac- tion. This double smooth frottement over the right auricle is probably transmitted, softened in its transit, through the fluid, from the noisy and active right ventricle. The friction sound, if any, that may be made during the acme by the ascending aorta and the adjoining portion of the pulmonary artery behind the manubrium, is almost always masked by the friction sound of the right ventricle, which is con- ducted by the sternum acting as a sound- ing-board, the sound being thus conducted in more than half of the cases to the upper end of the bone. The double frottement proper to the pul- monary artery when covered with lymph is undoubtedly audible during the acme over the second space, where it must re- semble and blend with the double frotte- ment proper to the conus arteriosus. In every instance pressure^ intensifies the two friction sounds ; and it sometimes transforms an ordinary frottement into a creaking or grating sound ; or a soft fric- tion sound into a harsh rubbing noise ; or it excites a friction sound when one was previously absent. pericardium was equal in extent during the first and the second acme ; while in five it was greater, and in one it was less, during the first than the second acme. In six of the cases, from two to five days, and in five of them from six to eight days, elapsed between the end of the first period and the beginning of the second period of the height of the effusion. Position of the Impulse.-In six of the cases, and probably in a seventh, the im- pulse at its inferior boundary occupied a lower position by from one to two inter- costal spaces during the second acme of the effusion than the first (compare Figs. 94, p. 576; and 88, p. 553, respectively with Figs. 91, p. 559; and 86, p. 551; in two cases the impulse occupied the same position during the two periods; in one instance it was imperceptible throughout; and in one it was very feeble. We thus find that in the great majority of the cases the impulse of the heart was lower during the second acme of effusion, or the period of relapse, than during the first acme. The reason is, I think, evi- dent. When the fluid in the pericardium begins to increase during the early period of pericarditis, the heart, which is then yielding in structure and usually of the natural size, is steadily floated upwards by the increasing tide of effusion into the pericardium, which may indeed compress the auricle, and lessen the size of the heart. The heart, under the double in- fluence of the inflammation on its exterior, and the resulting thick coating of lymph, on the one hand ; and the inflammation on its interior, and the resulting crippling of valves, enlargement of cavities, and thickening of walls, on the other, becomes increased in size. The whole organ is, in fact, enlarged, and it is often unyielding in its position owing to its tough new covering, and perhaps to partial adhesions that may have already connected the double surfaces of the thickened pericar- dium and the heart, especially along and near the septum; and although the re- newed increase of fluid elevates the heart to a certain extent, this second elevation of the impulse is not usually so great as the first elevation. Thrill.-A thrill was felt over the heart for the first time during the second acme in three of the cases. In two of them the thrill was present over the apex, and this was the natural effect of the lowered posi- tion, greater prominence, and increased force of that portion of the heart during the second acme than the first. In the other case the thrill was present over the second left space, but in this patient the second acme was the true one, for the effusion was considerably higher during the second than the first acme. A thrill is, in fact, more frequently present over the second space during the first acme Second Acme. - Renewed Increase of Effusion into the Pericardium owing to Re- lapse.-In eleven cases the effusion into the pericardium, after it had reached its height and commenced to decline, again increased in quantity, and attained to a second acme. Another case that had a relapse and a second acme, that was ad- mitted during the period of the first acme, has not been included in the inquiry that is about to follow. In five of those eleven patients under consideration the fluid, after declining for a second time, again increased so as to present a third acme of pericardial effusion, and in one of the five there was a fourth wave of increase. I shall examine in these cases with re- lapse and renewed acme, the comparative height of the pericardial effusion ; the ex- tent of the heart's impulse ; the area and intensity of the friction sound ; the sever- ity of the general illness; and the in- tensity of the accompanying endocarditis, and its permanent effect on the functions of the valves of the heart during the period of the later acme. Extent of Effusion into the Pericardium. -In five of the cases the effusion into the 572 PERICARDITIS than the second, and over the apex during the second acme than the first, for the reasons that I have just stated. Area and Intensity of the Friction Sound during the Second Acme of Increased Effu- sion into the Pericardium.-During the second Acme of the pericardial effusion a creaking friction sound was audible over the heart in four cases, and a grating noise in one; a to-and-fro sound in five patients, and a double friction murmur increased by pressure in one. In five of the cases the area of the fric- tion sound was greater, and in four it was less during the second than the first acme of the effusion into the pericardium, and in two it was of equal extent during both periods. In five of them the friction sound was audible over a lower position during the second acme than the first, and in none of them was the friction sound lower during the first acme than the second. In like manner, the friction sound was more intense in six cases, and less intense in four, during the second acme than the first ; and in one it was of equal intensity during both periods. In four of the pa- tients both the area and the intensity of the frottement were greater, and in three they were both less, during the second than the first acme. The following agencies, on the one hand, tend to increase the area and inten- sity of the friction sound during the second acme as compared with the first: The greater size of the heart; the increased thickness and force of its walls; the lowered position of the organ and its im- pulse ; and the greater roughness and toughness of the lymph covering the heart and lining the pericardium. The following, on the other hand, tend to lessen the area and intensity of the friction sound during the second acme as compared with the first: The greater ex- tent to which the lungs sometimes cover the heart; the restraint placed on the movements of the heart, and especially of the right auricle, by the thickness and toughness of its envelope of lymph ; and the adhesions that have often already taken place between the pericardium and the heart; and especially along the sep- tum, between the ventricles, and at the apex. Vital influences blend with and counteract these physical influences in producing the result. My analysis of the cases does not enable me to assign to each of those causes its proper share in the production of these effects. In the one fatal case the heart was uni- versally adherent, and in that patient the friction sound was less in extent and in- tensity during the second acme than the first, owing, I consider, to adhesions that had already begun to form between the heart and the pericardium. The friction sound, as we have seen, was lower in extent during the second acme than the first in one-half of the cases (5 in 11), owing to the lower position of the heart and its impulse during that period. In five of the cases the friction sound maintained the same character during the second acme as during the first, but in six others it was altered. Thus, one that had a friction sound on pressure, one that had a smooth friction sound harsher on pressure, and one that had a harsh fric- tion sound creaking on pressure during the first acme, presented, all of them, a creaking friction sound during the second acme ; while one with a to-and-fro sound during the first, gave a grating noise during the second acme. From what I have just said, it is evi- dent that the influences tending to in- crease the area and intensity of the friction sound during the second acme were in greater force than the influences tending to lessen them; and that the fric- tion sound was usually more intense and more extensive, especially downwards, during the second acme than the first. Comparative Area and Intensity of the Friction Sound just before, during, and soon after the Second Acme of Effusion into the Pericardium.-The friction sound is, as a rule, louder and more extensive during the second acme of pericardial effusion than either just before or soon after that period. At this stage, therefore, the frottement increases with the advance, and decreases with the decline of the fluid. Degree of the General Dlness during the Second Period of Increased Pericardial Effusion.-In five of the cases the illness was extreme, in three it was severe, and in three it was slight or probably so dur- ing the second acme. Of the five cases in which the illness was extreme, the face was anxious in four ; there were choreal movements and rigidity, chiefly of the left arm, in one; breathing was laborious in one and quick in four, the respirations ranging from 32 to 48 ; pain was present over the heart in one, and in another pain was felt, appa- rently in the side, on a deep breath; swallowing was difficult in two ; one had diphtheria ; and one raised phlegm tinted with blood. The patients who were thus affected with relapse of the inflammation of the pericardium suffered more frequently with symptoms of great severity during the first than the second period of the increase of the effusion into the sac. Thus during the first acme in seven patients the illness was extreme, including the five in which it was so during the second acme, and in three it was severe. In one case the symptoms were not described. Of the seven cases in which the illness AUSCULTATION 573 was extreme during the first acme, per- spiration was very profuse in three ; the face was anxious, pallid, livid, or of a leaden hue, in four; there were slight choreal movements in one ; breathing was quick in five, the respirations ranging from 40 to 48 ; pain was present over the heart in four of those seven patients and in two others in whom the symptoms were less severe; and swallowing was difficult or painful in three. We thus see that pain attacked the re- gion of the heart in six cases during the first acme, and in only one case during the second acme. The breathing also was more urgently affected during the first acme, when they numbered from 40 to 48 in the minute, than during the second acme, when they ranged from 32 to 48. On the other hand, depression and anxiety were more marked during the second acme than the first. The general illness was much more often extremely severe during the first acme in those cases that suffered from a relapse, than during the single acme in those that had no relapse. Thus of those patients in whom there was a renewal of the acme, the illness was extreme during the first acme of the effusion in two-thirds (7 in 10 or 11), and severe in one-third (3 in 10 or 11); while of those who had no renewal of attack, the illness was extreme in only one-third of the cases (10 in 30 or 32), se- vere in one-half (14 in 30 or 32), and not severe in one-fifth (6 in 30 or 32). In one case of the series with a relapse, and in two cases of the series without a relapse, the symptoms were not recorded. Intensity of the Endocarditis accompany- ing the Pericarditis during the Second Acme of the Effusion; and Permanent Effect of the Endocarditis on the Valves. - All the cases that had a relapse of pericarditis were affected with endocarditis in an in- tense degree. One of the patients had old-standing disease of the mitral and aortic valves ; and in seven of them valvu- lar disease was established when they left the hospital, the mitral valve being affected in all of them, and the aortic valve also in three. In three cases the mitral valve, which was incompetent during the attack, owing to inflammation of the valve, com- pletely regained its function. The proportion of cases in which the valves were permanently crippled among those who were affected with relapse of the pericarditis was much greater than among those who were not so affected. Thus the valvular incompetence became permanent in two-thirds of the patients with relapse of the affection (7 in 10), three of them being affected with both aortic and mitral disease ; and in only about one- fourth or one-third of those who had no relapse (11 in 52 and 7 others who left with lessening murmur). These clinical facts tend to make it probable that when there is a relapse of the inflammation of the exterior of the heart, there is a relapse also of the inflam- mation of the interior of the heart and its valves ; and that the inflammation when thus prolonged tends to cripple the valves for life. Second Relapse of Pericarditis with a Third Acme of Pericardial Effusion.-In five of the eleven cases with relapse and a renewed increase of effusion into the peri- cardium, after the fluid began to decline, there was a second relapse, and the fluid increased in quantity for a third time. In one of those cases there was indeed a third relapse followed by a fourth acme of peri- cardial effusion. In one of the cases the effusion into the pericardium was equal in amount during the first acme, the second, and the third, the wave of increase rising on each occa- sion to the same height. In two of them the fluid was equal in quantity during the first acme and the third, but was less dur- ing the intermediate period of renewed increase ; and in the two remaining cases the wave of increased effusion lessened on each repetition, the effusion being less during the third acme than the second, and less during the second acme than the first. In those five cases from three to five days elapsed between the second acme and the third. The impulse, at its inferior boundary, was lower during the third acme than the first in three of the cases ; and it was lower in one case and higher in another during the third acme than the second ; while its position was unchanged during those two periods in a third. In one of the cases the impulse was imperceptible throughout, and in another it became so at the period of the third acme. The presence of a thrill was not ob- served in any of the cases during the third acme. The friction sound is in a declining state during the third acme. The frottement was of a definite rubbing to-and-fro charac- ter, intensified by pressure, in only one of the four cases during the final acme. In one of those patients the friction sound was double and smooth in character ; in another it was single and systolic; in a third it was almost like a bellows mur- mur ; and in the remaining case it was absent with light pressure, but firm pres- sure brought a to-and-fro sound into ex- istence. Four of the five patients belonging to this group were affected with great general illness during the final acme ; their breath- ing was distressed and rapid, numbering respectively from 36 to 60 in the minute ; while two of them had pain in the chest, 574 PERICARDITIS and the remaining two pain in the region of the heart. The. Area and Intensity of the Friction Sound during the Decline of the Pericardial Effusion.-In forty-three cases the com- parative area and intensity of the friction sound were observed both when the effu- sion into the pericardium was at its height, and during the period of its de- cline. (1) The friction sound spread down- wards to a greater extent during the de- cline than the acme of the effusion into the pericardium, in three-fifths of the cases (26 in 43). (2) In less than one- fourth of the cases (10 in 43) the reverse took place, the friction sound being more extensive, and especially downwards, dur- ing the acme of the effusion than when the fluid diminished. (3) The area of the friction sound extended downwards to an equal extent during the acme and the de- cline of the effusion in a still smaller pro- portion of the cases (7 in 43). (1) Cases in which the Friction Sound spread downwards to a greater extent during the Decline than the Height of the Effusion into the Pericardium. - I shall consider (1) the time of occurrence; and (2) the duration of the downward extension of the friction sound in these cases ; (3) the area ; and (4) the character of the sound ; and the position of the heart and its im- pulse and thrill; and (5) the degree of the general illness during the period in question. 1. Time of the Occurrence of the Down- ward Extension of the Friction Sound.- The friction sound spread rapidly down- wards soon after the fluid in the pericar- dium began to decline in all but a very small proportion of these cases. Thus the rubbing sound had already extended downwards to its lowest position in four- fifths of the patients (21 in 26) during the first three days after the acme. During the three following days the descent of the rubbing sound appeared in four more of the cases ; but in the last of these this condition came into play quite suddenly on the twelfth, and still more on the four- teenth day after the fluid began to lessen. 2. Duration of the Extreme Downward Extension of the Friction Sound.-The downward extension of the friction sound lasted in these cases for a very short pe- riod. In two-thirds of them (17 in 26) it was observed during only one day, and in but two cases, or rather one, did it last over three days. This extension down- wards of the friction sound during the decline of the fluid was therefore short and transitory. 3. Area of the Downward Extension of the Friction Sound.-When the fluid in the pericardium, after having reached its height, lessens in quantity, the heart de- scends, its impulse is lowered by from one to two intercostal spaces, and the friction sound extends downwards. The area of the rubbing noise is, as a rule, by no means limited to the area occupied by the heart itself; but spreads downwards to an extent varying from one to four inches below the lower boundary of the heart. The friction sound does not, in these cases, diffuse itself downwards over the whole breadth of the region below the heart; for it is usually silent over the front of the abdomen in the epigastric space ; while it is present along the right and left seventh and even eighth costal cartilages that bound that space to the right and left; and over the ensiform car- tilage that dips downwards from the lower end of the sternum at the centre of that space. The rubbing noise is usually heard with equal intensity over the right and the left seventh and eighth cartilages. Some- times, indeed, the sound was louder and more extensive over the right seventh and eighth cartilages than the left; and it ap- peared as if in those cases the cartilages that rested on the liver conducted the sound better than the cartilages that cov- ered the stomach. The contrast between the harsh rubbing noise heard in some cases over those cartilages, and the com- plete, silence present over the intervening epigastric space was very remarkable. The friction sound, besides travelling downwards, extended also upwards in one-half of these cases (14 in 26) when the fluid in the pericardium lessened, and the heart and its impulse descended. In one-third of the patients (8 in 26) the area of the friction sound was equally high over the front of the chest during the pe- riod of the acme of the effusion into the pericardium, and that of its decline. In four instances the whole area of the friction sound shifted bodily downwards when the pericardial effusion lessened, and the heart and its impulse descended; so that the upper and lower borders of that area were then simultaneously low- ered. In these four cases while the'lower boundary of the region of friction sound descended from the sixth to the seventh cartilages, its upper boundary descended in two of them from the second left carti- lage to the third, and in the other two from the third cartilage to the fifth. In two-thirds of those cases (16 in 26) in which the friction sound extended much downwards after the acme, it was also audible up to the top of the sternum. In three of those cases the friction sound so covered the front of the chest as to be audible up to the clavicles, while in one of them it reached the first cartilage. In the whole of these cases the friction sound extended from two to nearly four inches above the actual seat of friction. The AUSCULTATION. 575 Fig. 92. Fig. 93. For previous views of this case, see Figs. 90, 91, page 559. Fig. 92, from a housemaid aged 20, affected with rheumatic pericarditis. Period of the decline of the pericardial effusion after the first acme. Fifth day after the acme of pericardial effusion, seventh day after the first observation of the friction sound and increased pericardial dulness, and ninth day after admission. The pericardial effusion has lessened much since the period of the acme, its upper boundary (1, 1) having descended from the middle of the manubrium to the middle of the sternum ; and its lower boundary having probably ascended from a little above the end to about the middle of the ensiform cartilage. The heart (2, 2) is lower, and the amount of fluid between the under surface of the heart and the floor of the pericardium (3, 3), though still consider- able, has evidently lessened by at least one half. The right ventricle, the inner or left half of the right auricle, and the apex and front of the left ventricle are exposed ; but the great arteries are covered with lung. The region of pericardial dulness (see the black space) probably extends from the middle of the sternum between the third cartilages, and from the fourth left cartilage, down to the middle of the ensiform cartilage, and the lower third of the sixth cartilage; and from a little to the right of the lower half of the sternum to the nipple line. The lower boundary of the heart is behind the upper edge of the sixth rib, and the top of the ensiform cartilage. The impulse has descended from the third space during the acme, to the fourth and fifth spaces. (See the circular and curved lines in those spaces.) A double friction sound (see the zigzag lines-systolic lines thick, diastolic thin), which is more harsh on making pressure, is heard over the whole length of the sternum ; which is most intense at the middle of the bone, and is louder at its lower end during inspiration, and over the manubrium during expiration; a creaking sound is audible during systole over the third, fourth, and fifth left spaces ; and a friction sound is heard to the right of the lower portion of the sternum. (The nipple is too far to the left in this figure.) Fig. 93, from the same patient as Figs. 90, 91 (page 559), 92, and 94. Period of the decline of the pericardial effusion; second view, taken the day after a slight and transient second acme, when the fluid was again declining. Remarkable extension of the friction sound over the greater part of the front of the chest, and especially downwards. Tenth day after the first acme of pericardial effusion ; twelfth day after the first observa- tion of the friction sound and of pericardial dulness; fourteenth day after admission; and four days before the occurrence of a second acme. The pericardial effusion has diminished. There is therefore less fluid between the under surface of the heart and the floor of the pericardium (3, 3); the roughened front of the heart is more dry, and is closer to the corresponding roughened surface of the pericardial sac ; the heart (2, 2), which is somewhat enlarged, is lower in position; and the upper boundary of pericardial effusion (1, 1) is lower, and its inferior boundary is somewhat higher than when Fig. 92 was taken five days previously. The whole right ventricle, the left border of the right auricle, and the apex and front of the left ventricle are exposed; while the great arteries and part of the conus arteriosus are covered with lung. The region of pericardial dulness (see the black space), which is bounded above by the 576 PERICARDITIS. fourth cartilage, and below by the sixth cartilage, is probably rather less extensive above, below, and to the right, than in Fig. 92, taken on the ninth day after admission. The impulse is lower, stronger, and more extensive than in Fig. 92, and is present from the third to the fifth spaces, and up to or beyond the mammary line (see the circular and curved line in those spaces) ; and gives therefore direct evidence that the heart is lower in position, and that the effusion has lessened. The friction sound (see the zigzag lines-systolic lines thick, diastolic thin) has gained a very great extension, being audible over a great part of the front of the chest, from the first costal cartilage to the seventh left and the eighth right cartilages ; and from the top of the sternum to the bottom of the ensiform cartilage. This extension of the friction sound is especially marked downwards, where it extends for about four inches below the heart, and is lower on the right than on the left side, reaching over the right eighth cartilage in front of the liver, and the seventh left cartilage in front of the sternum. This is the reverse above, when the rubbing sound extends four inches to the left, and only about two inches to the right of the sternum. The friction sound is harsher than it was yesterday; over the midsternum it is louder during the systole than the diastole ; and it is intensified by pressure; over the manubrium, the two-and-fro sounds are equal; over the ensiform cartilage, friction sound is present during inspiration ; it is creaking during systole over the second and first spaces; and it becomes louder below the mamma during inspiration. Fig. 94. For previous views of this case, see Figs. 90, 91, page 559, and 92, 93 on the preceding page. Fig. 94, from a housemaid affected with rheumatic pericarditis. Third acme of pericardial effusion (the second acme was very slight and transitory). Thirteenth day after the first acme; eighteenth day after admission. The pericardial effusion is greatly increased, but its extent and limits are not definitely described. If we compare this third acme with the first acme (Fig. 92, page 575), we find that the distended pericardium, though it contains less fluid, is wider in relation to its length; that the heart is larger ; and that the lower boundary of the heart is lower, in this the later and renewed, than in that the earlier and original acme. In the first acme the heart was not yet enlarged, or, being compressed by the fluid in the distended sac, was pos- sibly lessened in size; and the walls of the pericardium were still unyielding, so that the swollen sac took the form that it would naturally take if artificially distended with fluid (see Figs. 79, 80, page 540). In this, the third acme, the heart has become enlarged both by pericarditis and by mitral endocarditis ; the lower boundary of the heart, although ele- vated by the accumulated fluid, is lower than in the first acme ; and the walls of the peri- cardium have become thicker, softer, and more yielding than in health, so that the distended sac yields to the right and left, where it meets with no resistance, to a greater extent than it does upwards and downwards, where it meets with much resistance ; and is therefore wider in relation to its length than it was during the first acme, when its form was more purely pear-shaped. The whole front of the heart and great vessels is exposed, including the right auricle and ventricle, the apex and front of the left ventricle, the pulmonary artery, and the ascending aorta within the pericardium. The fluid has evidently interposed AUSCULTATION. 577 itself to a greater extent between the surface of the lower portion of the front of the heart and the walls of the chest during this, the third acme, than during the first acme. The region of pericardial dulness (see the black space), the limits of which are not described, corresponds in general form and outline to the pericardial effusion, and evidently extends more to the right and left, and less upwards and downwards than it did during the first acme. The impulse has again been elevated at its lower boundary, and this time from the fifth space, as in Fig. 93, page 575, to the fourth space, where it is feeble; and it is felt over the third space during expiration. (See the concentric circles in those spaces.) The lower boundary of the impulse is therefore lower by one space than it was during the first acme, when it occupied the third space (see Fig. 91, page 559). The friction sound (see the zigzag lines-systolic lines thick, diastolic thin) is softened, and is limited in area, being heard over the middle region of the sternum, where it is double, and although frictional in character is almost like a bellows murmur; and is audible over the second and third spaces during the systole. Later progress of this case.-On the following day, the nineteenth after admission, the fric- tion sound was almost creaking, or like the sound made by rubbing with sand-paper, over the second and third left spaces. On the twenty-first day, or the fourth after the third acme, the extent of dulness over the pericardial region had lessened ; and a double friction murmur, which was not rhythmical with the sounds of the heart, was audible over the base of the right ventricle, and became harsh on pressure. The friction murmur was still heard on the following day, but after this it was scarcely audible. region of pericardial dulness was limited above in all but three of the patients by the third intercostal space or the fourth cartilage; and the space between this limit and the top of the sternum nearly measures the extent to which the frotte- ment extended above the seat of the fric- tion. When the fluid in the sac declines, the roughened heart rubs against the rough- ened pericardium, and in doing so bears directly upon the lower half of the ster- num with which it is almost in contact; owing to the removal of the anterior layer of the fluid, and the descent of the heart and its impulse. The sonorous vibrations excited by the movements of the heart are directly conveyed to the sternum, and that bone and the costal cartilages at- tached to it act as a sounding-board and transmit the rubbing noise in all direc- tions. In three of the cases the sound was audible over the whole front of the chest. Usually, however, it extended only slightly to the right, and over a greater extent to the left of the lower half of that bone. As a rule, therefore, the rubbing noise extended in a straight line from the top to the bottom of the sternum, and there it divided into two diverging lines, one along the right, the other along the left seventh cartilage, where they form the boundaries of the intervening epigas- tric space. The area of friction sound thus extending along the sternum and the right and left seventh cartilages closely resembles in shape the inverted letter A- Since however the friction sound also extends downwards over the ensiform cartilage, its area is somewhat like a trident with a short central prong. In one-fifth of the cases (5 in 26) the area of the friction sound dwindled dur- ing a short period after the time of the acme, and then suddenly expanded, and especially downwards, at a later date dur- ing the decline of the effusion. In one case the friction sound alter- nately lessened and increased in area and intensity during the ten days that inter- vened between the termination of the acme, and the time at which the frotte- ment had a remarkable downward devel- opment. 4. Character and Intensity of the Fric- tion Sound; and Position of the Heart and of its Impulse and Thrill.-At the time that the friction sound spread downwards when the effusion lessened, the sound was intense, loud, and of a marked char- acter in all but three or four of the twenty-six cases that belong to the group under consideration. In nine of those cases the friction sound was creaking (G), or grating (3) ; in thir- teen it was harsh and loud ; and in four its intensity was not specified. The friction sound in the twenty-six cases under review, as a rule, gained in intensity as it gained in area ; and lost in intensity as it lost in area. Thus in all but six of the cases, the rubbing noise became more harsh when it increased in extent; and in all but two of them it be- came softer when it lessened in extent. When the effusion lessened, the im- pulse, while it descended at its lower boundary, was still felt beating in the higher spaces into which it had been forced during the acme in fully one-fourth of the cases (5 in 19): while, curiously, the impulse ascended to a higher space than it had occupied during the acme in six other patients. A thrill was felt over the heart in five of these twenty-six cases during the acme of the effusion. In four of these the thrill disappeared when the effusion less- ened, and in one it remained, though with lessened intensity. In three other pa- tients a fresh thrill came into play during vol. ii.-37 578 PERICARDITIS the decline of the fluid ; in two of them over the apex, and in the other case at the second space. In these twenty-six cases, when the effusion into the pericardium lessened, the heart, relieved from the pressure of the fluid, descended into its natural space, and even below and beyond it. The heart thus relieved, beat with increased force; its right cavities were enlarged, owing to the increased supply of blood from the system, and the continued re- sistance offered to the flow of blood through the compressed lung and the in- competent mitral valves; and, as the general result, its anterior walls played with greater power and noise upon the sternum and cartilages, and ,the friction sound was heard over a largely increased area. 5. Degree of the General Illness.-At the time that the area of the friction sound was most extensive, especially downwards, when the fluid in the peri- cardium lessened, twenty of these twenty- six cases were less ill or in better health, three of them were probably better, and three were worse in health than they were during the acme. In a large proportion of the cases under review, when the fluid in the pericardium lessened, the heart descended and gained freedom of movement and power, and the general health improved ; and as a natu- ral result the friction sound increased in extent, and especially downwards. The comparatively dry roughened surface of the heart rasped two and fro upon the roughened surface of the pericardium. These influences combined to cause the increased harshness and extension of the friction sound ; which, starting from its focus of greatest intensity over the right ventricle, radiated in all directions over and beyond the region of the heart and the great vessels, outwards to the right and left, upwards to the summit of the sternum, and especially downwards over the ensiform cartilage and the diverging right and left seventh and eighth carti- lages. (2) Cases in which the Friction Sound was audible Downwards to a greater extent during than after the Acme of the Effusion. ■-In ten cases the friction sound was audible to a greater extent downwards when the effusion was at its height than during its decline. Two series of influences are at work in these cases, acting at different times, to enlarge the area of friction sound during the acme, and to lessen it during the de- cline of tlie effusion. 1. When, during the acme, the friction sound is creaking or grating, being some- times associated with a thrill, over the right ventricle, and when it radiates thence in all directions, softened in char- acter, beyond the region of actual fric- tion, the heart, raised by the increased effusion into the narrower space at the upper part of the cone of the chest, beats with increased force directly against the sternum, the higher cartilages, and their spaces, and so excites an intense and widely diffused friction sound. When the fluid lessens the heart de- scends and is again partially covered with lung ; and as it beats over a smaller ex- tent, and with less pressure against the sternum and cartilages, the friction sound lessens in intensity and area. 2. When the friction sound is of mode- rate intensity and extent during the acme, it sometimes lessens during the decline of the effusion. In these cases the impulse at its inferior boundary is not notably lowered, while it disappears from the upper spaces. In some of these cases the action of the heart is throughout feeble ; and probably in others of them slight ad- hesions take place at the apex and septum which restrain and lessen the descent of the heart, the rubbing movements of the right ventricle, and the area and intensity of the friction sound over the higher in- tercostal spaces. (3) Cases in which the Friction Sound extended Downwards to an equal extent dur- ing and after the Acme of the Effusion.-In seven cases the friction sound was of equal extent during the two periods, when the fluid in the pericardium was at its height and was declining. Character and Intensity of the Friction Sound during the Decline of the Effusion, and the Helaiion of the Intensity to the Area of the Friction Sound.-I shall examine these conditions during three periods in the order of time of the decline of the effusion, (1) the beginning of the decline of the effusion ; (2) the gradual and the interrupted progress of the decline of the effusion ; and (3) the final dying away of the friction sound ; and (4) shall then in- quire into cases in which the ordinary friction sound gave place to a friction murmur towards the end of the attack. 1. Character and Intensity of the Friction Sound at the Beginning of the Decline of the Effusion.-When the amount of fluid in the pericardium began to lessen, if the friction sound increased or diminished in intensity, it usually increased or dimin- ished also in area. As a rule, the friction sound increased in intensity and area in those cases in which the frottement extended further downwards after than during the acme ; while it lessened in intensity and area in those in which the friction sound spread more dow'nwards during the acme than after it. When the friction sound spread down- wards during the decline of the effusion, AUSCULTATION. 579 the sound gained in area in nearly every case (25 cases in 26), and in intensity in two-thirds of the cases (18 in 26). We thus see that while an increase in the in- tensity of the frottement almost invariably leads to an extension of its area-for I find only one exception to this rule-and while a diminution of its intensity like- wise generally causes a diminution of its area; yet, in certain cases, the friction sound gains in extent, though it lessens (4 cases in 43) or remains unchanged (3 cases in 43) in intensity. This is ex- plained by the lowering of the heart, and the consequent descent of its impulse during the decline of the effusion in all the cases-the surface of the roughened organ being thus brought into more ex- tensive contact with the sternum at its lower half, and with the corresponding costal cartilages : while in the small num- ber of cases in which, although the fric- tion sound gains in area, it is lessened or not increased in intensity, the heart, re- leased from its confinement in the con- tracted space of the chest above, where it rubbed with force and noise against the sternum and cartilages in front of it, finds itself moving with ease in its proper place in the lower and wider part of the chest, and so presses with less force and less noise than before on the sternum and cartilages in front of it. The causes of the increased intensity as well as area during the decline of the effusion, which, as we have just seen, occur in the great majority of the cases under examination, have been already considered at page 578. 2. The Gradual and Interrupted Prog- ress of the Decline of the Effusion.- In thirty-one of the forty-three cases now being examined, the effusion in the peri- cardium steadily and gradually declined, and, as we have already seen, in twelve of them, owing to relapse, the effusion after beginning to decline, again increased in quantity generally once, sometimes twice, and on one occasion even a third time. The progress of the friction sound dur- ing tht decline of the effusion was rarely uniform. It was in several of the cases silenced and suspended for a time (6 in 43); it more frequently, however, when in full play, became feebler during a short period, and then again louder (13 in 43). In a larger number of the cases the frotte- menty after attaining to its greatest inten- sity, more or less steadily lessened in loudness and extent until it finally disap- peared (23 in 43). In one case the friction sound suddenly and permanently disappeared after an at- tack of syncope. In this patient, a girl, the friction sound vanished when the ac- tion of the heart became enfeebled ; and she died in a second attack of syncope a few hours after the first attack. Cases in which the Friction Sound van- ished and reappeared during the Decline of the Effusion.-In six of the forty-three cases under review and in one other pa- tient the friction sound disappeared and reappeared during tlie decline of the effu- sion. In five of these cases the frottement was absent for from two to three days, and in one of them for about j seven days. In three of the patients the friction sound, as in the case just referred to, van- ished for a time after the application of leeches for the relief of pain. If we view these cases as a whole, and take into the survey the case of the fe- male servant who died from a second at- tack of syncope, the fiist attack having permanently quenched a loud and pervad- ing friction sound, we shall, I think, see that when the force of the heart's action and the volume of the blood in circulation are lessened-either by immediate syn- cope, by loss of blood from leeching, by diarrhoea, sickness, or other exhausting influences, by pain in or over the organ, by extreme distress in breathing, or more often by a combination of several of these lowering agencies - then the rubbing sound, when in full play, may gradually or suddenly vanish, and may suddenly rekindle into full volume after a longer or shorter period of silence. Cases in which the Friction Sound lessened and then increased in Area and Intensity during the Decline of the Effusion.-In thir- teen of the forty-three cases under exami- nation, and in three other cases, the fric- tion sound, when in full play, lessened in extent and intensity, and after a longer or shorter interval again resumed more or less nearly its full sway. In one of these sixteen cases the dimi- nution of the frottement was associated with sudden faintness; in two with loss of blood from leeching ; in eight with in- crease of the general illness-in seven of which as the health improved the friction sound resumed its extent and intensity-- in two with an amelioration of the symp- toms ; in two with irregularity and inter- mission of the pulse and the action of the heart; and in tw'O the state of the health is not described. In eight cases the diminution of the friction sound corresponded with an in- crease of the general illness, which showed itself generally by an anxious expression, accelerated and difficult breathing, and pain over the heart; sometimes with cough and rusty phlegm ; and sometimes with abundant' perspiration. With the renewed increase of the rubbing sound there was in all these cases; save perhaps one, a marked improvement in the health; manifested usually by a comparatively cheerful expression, more easy respira- tion, lessening or absent pain over the 580 PERICARDITIS. heart, and assuaging of cough with dimi- nution of phlegm. (1) Duration and (2) Progress of the Fric- tion Sound during the Decline of the Effu- sion.-(1) Duration.-The friction sound lasted for a very variable period during the decline of the disease. In the group of thirty-one cases that had no relapse and no return of the effu- sion into the pericardium, the friction sound lasted from three to nineteen days, its average duration being ten days. In the group of twelve cases that suf- fered from relapse with return of the effu- sion into the pericardium, the friction sound lasted from eleven to twenty-two days, its average duration being fifteen days. (2) Progress.-Cases in which the Maxi- mum Development of the Friction Sound took place during the Decline of the Effusion.- Period between the Maximum Development and the Cessation of the Friction Sound.- In thirteen of the nineteen cases under examination the area of the friction sound steadily lessened from the day of its max- imum extension to that of its final disap- pearance. It contracted gradually from right to left and from left to right, from above downwards and from below up- wards, towards the centre or focus of ac- tual friction. It thus died away from be- yond and over the great vessels, the right auricle, and the apex, and from the region that it had previously occupied below the lower boundary of the heart. Towards and over the region of actual friction it step by step concentrated itself, and after lingering over the right ventricle with softening tones for a shorter or longer period, it quietly died away. In about one-half of the cases (6 in 13) this subdued sound outlived the period of its greatest intensity and extent for from one to two days ; in the remainder, for from three to seven days; and in one only did it exist for nine days. The front of the right ventricle was, as I have just said, the last home of the fric- tion sound, as it had been indeed the seat of its birthplace. As the position of that ventricle varied in different patients ac- cordingly as the heart was larger or smaller in size, higher or lower in situa- tion, the final seat of the softened friction sound varied in different cases, from the left third and fourth cartilages to the fifth or sixth ; and from the middle third of the sternum to the ensiform cartilage. There was a general but by no means invariable correspondence between the area of the friction sound on its last ob- servation, and the position of the impulse. In only three of the nineteen cases now under review did the impulse occupy the same position when the friction sound was heard for the last time, as when it was most extensive. In four cases it had de- scended at its lower boundary from the fourth space to the fifth; and in four cases it had disappeared from the upper space at the time of the last observation of the friction sound, when compared with the time at which it was predominant. There was therefore in these patients a tendency for the heart and its impulse to take up a lower position, and to be cov- ered to a greater extent with lung as the friction sound was about to disappear, and the case advanced towards its termi- nation. On the other hand, in two other cases the impulse gained ground above, and appeared in the second space for the first time when the frottement was heard for the last time. The descent of the impulse both above and below when the case advances to re- covery and the friction sound is dying out, appears to me to be the natural bias in these cases when the heart is not ad- herent, and descends into its natural situ- ation ; when the right ventricle and pul- monary artery are not greatly enlarged ; and when the upper lobe of the left lung expands in front so as to cover the pul- monary artery and the upper portion of the right ventricle. When, however, the heart becomes more or less adherent; when the pulmo- nary artery and right ventricle become enlarged owing to mitral regurgitation; when mitral incompetence is combined with adherent pericardium ; when the walls of the pericardium are thickened ; or when the left lung does not expand in front of the upper border of the heart so as to cover the pulmonary artery and the conus arteriosus ; and notably when two or more of these conditions combine their influence, then the impulse tends to re- main in or attain to the higher intercostal spaces, and especially the second space. In one remarkable case belonging to the group of nineteen now under review, the friction sound was lost on the fifth day after the acme, and reappeared on the twelfth day with greater intensity and over a larger area than at any pre- vious time. In three other cases the fric- tion sound, after gradually diminishing in intensity and area, became suddenly re- inforced ; and in two others a similar diminution and increase of the frottement took place but to a comparatively slight degree. 3. The final dying away of the Friction Sound.-The friction sound offered greater variety in different cases just before the time of its extinction than at any other period of its existence. (1) In a very small number of the cases (4 in 43) the friction sound, when in full play, suddenly disappeared ; (2) in two- fifths of them (16 in 43) the frottement, after being more or less loud up to a cer- tain date, rapidly declined, and vanished AUSCULTATION. 581 in one or two days ; (3) in a fifth of them (8 in 43) the decline of the friction sound was gradual; (4) and in two-fifths of them (16 in 43) the ordinary rubbing sound gave place towards the end of the case to a friction murmur sometimes double, and increased by pressure (8), sometimes double and excited by pres- sure (5), sometimes single and systolic and intensified by pressure (2), and in one case a single friction murmur was excited by pressure. 4. Cases in which the ordinary Friction Sound gave place to a Friction Murmur to- wards the end of the attack. - In fifteen patients, and possibly in a sixteenth, a friction murmur was audible in lieu of the ordinary friction sound towards the end of the attack of pericarditis. We have already seen that in a certain number of cases, at the beginning of the attack, the ordinary friction sound was preceded by a friction murmur : and that in one remarkable case a friction murmur prevailed throughout the whole course of the disease to the exclusion of the usual rubbing sound. I would here refer to what has already been said as to the fric- tion murmur as it was observed during the beginning of the attack, at pages 556-557. In one case a systolic friction murmur audible on making pressure, and in an- other case a systolic friction murmur in- creased by pressure, was respectively the final sign of pericarditis. In six cases a double friction murmur was audible on pressure towards the close of the affection. One of the cases of this group, a servant girl aged twenty, presented on the seventh day, when the effusion was at its height, an exten- sion of the frottement, when there was a double grating friction sound. On the eleventh, when the effusion was declining there was a feeble murmur-like friction sound over the right auricle, to the right of the lower sternum; and later in the day the heart sounds were natural over the lower sternum, but pressure brought out a double friction murmur not quite rhythmical with the sounds of the heart. A systolic friction sound was audible over the left fifth cartilage. On the fourteenth day a faint double murmur was still ex- cited by pressure over the lower sternum. This was the last day of undoubted peri- cardial friction sound, but on the eigh- teenth day a double grating friction sound burst out on pressure at the end of a deep breath, that was probably pleuritic. In several of these cases a friction mur- mur either prevailed over the right ven- tricle during the early stages, or was lim- ited to certain favorite spots, such as the right auricle, when the friction sound was at its height. Later, the friction mur- mur gradually again developed itself as the harsher friction sounds became soft- ened, and at length spread itself over the heart. Soon, however, this disappeared as a constant sound, but for one or two final days of the disease it could be again awakened by making pressure over the right ventricle. Several of these cases ended with a double friction murmur that was intensified by pressure. In addition to these cases in which the friction murmur prevailed exclusively towards the termination of the disease, there were others in which, while the friction sound was harsh, and even creak- ing or grating over the focus of its greatest intensity, it was yet so toned down towards the lower margins of the area of rubbing sound, especially at and below the ensiform cartilage, that a double fric- tion murmur was audible there, when a loud double grating noise was heard over the right ventricle. In some of the cases also, when a creaking, or grating, or rasp- ing sound prevailed with a thrill over the right ventricle, a double friction murmur was audible over the right auricle. Here the stormy noises prevailed over the forci- ble ventricles, and the soft murmuring sounds over the passive auricle. The occurrence of a creaking, grating, or harsh friction sound depends on the force with which the heart contracts and presses against the cartilages and sternum, and on the roughness of the lymph-covered rubbing surfaces; the creaking sound being mainly excited by pressure, the grating noise by th® roughness of the two surfaces when the one rubs actively upon the other. The friction murmur, on the other hand, is due to the gentle or re- strained movements of the heart, and the comparative smoothness of the rubbing surfaces all over the heart, that occur* towards the end of the attack. It may also be present in its softest and most murmur-like tones over the comparatively smooth and feeble right auricle, and be- low the heart over the epigastrium, when the attack is at its height, and is speaking with the greatest harshness and noise over the more vigorous parts of the organ ; and when the harsh friction sound is evidently softened and rendered murmur-like during its transmission through the fluid inter- vening between the seat of active friction, and the comparatively distant surface of the chest over the right auricle or the epi- gastrium. I have already given the distinctions between the friction murmur and the val- vular murmur when inquiring into the occurrence of the former during the first blush of the affection. The rules that apply to the distinction of the friction murmur during the early period of the attack apply also to its distinction during the later period. These rules have been already given at pages 556-557, but the fol- lowing is a resume of the more important 582 PERICARDITIS. distinctions between the friction murmur and the valvular murmur :- The friction murmur is not rhythmical with the natural heart-sounds, but the two sounds are heard side by side ; the valve murmur is rhythmical with the natural heart-sounds, and the two sounds are in perfect unison. The friction mur- mur does not begin with an accent or shock, but is of equal tone throughout; the valvular murmur begins with an ac- cent or shock, the accent or shock of the corresponding first or second sound which serves as the starting-point for the mur- mur. The friction murmur is greatly in- tensified, and is often altered in tone on pressure ; the valvular murmur is brought nearer to the ear by pressure, but is not altered in tone. There are certain differences between the early and the late friction murmur, although their characters in the main cor- respond. In situation the early and late friction murmurs for the most part correspond, being generally seated over the base or body of the right ventricle. The early friction murmur was situated to the left of the sternum in six cases (6 in 8), in four of which it was also heard over the ster- num ; and it was present over the sternum alone in two cases (2 in 8). The late friction murmur was audible over the sternum alone in four cases; over that bone and to the left of it in five ; to the left of the sternum alone in four ; and to the right of the sternum in three cases, including one case in which it was also audible to the left of the sternum. From these figures it would appear that the early friction murmur is always situated over the right ventricle; but that while the late friction murmur is present over the right ventricle in seven-eighths of the cases, it is audible over the right auricle in one-fifth of the cases. The late friction murmur is smoother and more equal in tone ; more prolonged ; less rustling and more murmur-like ; more alike in tone and intensity during the sys- tole and the diastole ; varies less from day to day ; and lasts much longer than the early friction murmur. Pressure intensi- fies both of them and often modifies their tone, but I think that the early friction murmur is more frequently converted by pressure into a true rubbing sound than the late friction murmur. The complication of a coexisting aortic murmur with the friction murmur is more frequent during the late than the early period of the affection. The Character and Tests oe Peri- cardial Friction Sound. I shall, before concluding the subject of pericardial friction sound, briefly con- aider the characteristic nature and tests of that sound, including its character and rhythm ; its position and extent; the in- fluence exercised over it by respiration; its variation from day to day in character, intensity, rhythm, position and extent; and finally, the effect upon it of external pressure over the region of the pericardium during pericarditis, or the pressure-test of friction sound. Character of the Pericardial Friction Sound.-The friction sound when in full play, and of its usual to-and-fro character, speaks for itself. 1 have already illus- trated, in the preceding pages, the clinical history of the forms and variations, the growth, ripening, and decline of the fric- tion sound. When the friction sound is smooth and soft, almost resembling a murmur, or when a friction murmur is present, the sound no longer declares it- self, from its very nature, to be of a rub- bing quality, and requires for its distinc- tion that other points shall be considered besides the tone, nature, and to-and-fro quality of the sound. The clinical history and distinguishing characters of the fric- tion murmur during the early advance and the late decline of the attack of peri- carditis have been given respectively at pages 556 and 581. The Rhythm of the Friction Sound.-In a large proportion of my cases it was no- ticed that when the friction sound was not of its completely developed to-and-fro and rubbing character, that is, during both the advance and the decline of the pericarditis, the healthy sounds of the heart were heard along with the double or single friction sound. The natural sounds of the heart and the friction sounds were never welded or incorporated to- gether, but were each of them heard sepa- rately, and, so to speak, side by side. They did not seem to begin or end to- gether ; and although they were both sounding at the same time, they yet ap- peared to be completely separate and apart. They were not, therefore, rhyth- mical with each other. That the natural heart sounds are in play within the period of the to-and-fro friction sound is evident, for when that sound becomes sufficiently loud and continuous, whether by the natu- ral advance of the disease, or by pressure made from without, the sounds of the heart are overwhelmed, being masked by the predominant rubbing noises. When the to-and-fro friction sound is loud, harsh, and in full play, the systolic and diastolic sounds being equal in dura- tion-though rarely in loudness, the sys- tolic sound being the louder-each sound seems almost to fill up its respective space, leaving two very short intervals of silence between the two sounds. These two fric- tion sounds never begin with an accent or shock, but they commence, continue, and CHARACTER AND TESTS OF PERICARDIAL FRICTION SOUND. 583 end as a rule with the same tone through- out. In these respects they differ from the natural heart sounds. The first sound always ends in a shock, followed by a short but definite space between itself and the second sound ; and the second sound consists in a short shock, followed by a prolonged space between itself and the first sound. The mitral murmur always begins with a shock or accent, the shock of the first sound, and the murmur fills up the space more or less completely between that shock and the second sound. The diastolic aortic murmur also commences with a shock or accent, the shock of the second sound, and it usually fills up the space but not always completely, between that shock and the first sound. The ab- sence of a commencing shock or accent from the friction sound or friction murmur and the presence of a commencing shock or accent with the valve murmurs dis- tinguish those two classes of sounds from each other. The first contraction of the ventricles precedes by an appreciable period the flow of blood from them into the great arteries; and after that flow has ceased, the exterior of the heart is still in motion. The play of the surface of the heart against that of the pericardium therefore precedes, ac- companies, and follows the natural first sound of the heart, and precedes and ac- companies the coinciding valvular mur- mur if present. The closure of the aortic valve precedes the second sound by the tenth of a revolution of the heart's action. The diastolic frottement therefore both precedes and follows the second sound; and accompanies a diastolic murmur, if present, throughout its whole period. The friction sound being made by the moving exterior of the heart, is in relation to the healthy heart sounds and the valvular murmur, which spring from the interior of the heart, as if it were made, so to speak, by an instrument playing outside the room, while they are made as if by an instrument playing inside the room. The friction sound is therefore a surface noise, working apart from, and often over-riding the healthy heart sounds and the valvular murmurs. The healthy heart sounds and the valvular murmurs are, on the other hand, internal noises made simultaneously and by the same parts, and playing to- gether inseparably and in unison. When listening to the two sounds, the frictional and the natural heart sounds, playing together but not in concert or unison, I have found it very difficult to say whether the systolic friction sound commenced before the first sound of the heart or not. For the reasons just given, however, and that a considerable space of time intervenes between the beginning of the systole and its final shock, amounting to about two-fifths of the healthy revolu- tion of the heart's action, it is evident that the commencement of the systolic friction sound must precede the final shock of the first sound. In one case I heard a short brush at the beginning of the systole, and this no doubt represents the natural be- ginning of the prolonged .systolic friction sound. As a rule the systolic friction sound is of equal tone throughout, whether it is creaking, grating, rubbing, or rust- ling ; but in one instance that sound be- came suddenly less loud about the middle of its course, and remained so to the end of the systole, the second half of the sound being weaker than its first half. In one instance a systolic brush, excited by pressure, occupied the latter two-thirds of the systole ; in another a systolic whiff, excited by pressure, extended into the diastolic period ; and in a third, a double brush was excited by pressure, the systolic being the longer, and each brush occupied a part of the systole and a part of the diastole. I state these signs as I heard them, but cannot account fbr them. The diastolic friction sound presents much greater variety in character and rhythm dhan the systolic friction sound. AVhile the systolic sound is usually con- tinuous through the whole of its proper period, the diastolic friction sound is often of short duration; when it is, I believe, usually present about the beginning of the diastole, and when it accompanies but is separate from the natural second sound ; in one instance, however, the natural sec- ond sound was followed by a diastolic graze. Sometimes there was a double graze or rub during the diastole ; when the entire friction sound resembled the noise made by sharpening a scythe, having one forward or systolic, and two back- ward or diastolic strokes. When the fric- tion sound was to-and-fro, the second sound appeared generally to be equal in duration, but not in loudness, to the first. When a creaking sound was present it was mostly limited to the systole; this was not so, however, with the grating noise, which was usually a double sound. The diastolic sound was usually equal in intensity and length to the systolic over the right auricle, both sounds being in all but one instance soft in character. This double soft to-and-fro sound over the right auricle was evidently transmitted, softened during its transit, from the loud speaking right ventricle, through the fluid, to the cartilages in front of the right auricle. The diastolic friction sound was often absent, and, relatively to the systolic friction sound, was always short and feeble over the apex. In more than one instance, in adults, the diastolic friction sound at the apex appeared to have in it a peculiar twist. Respiration exercised in many of my cases a definite and speaking influence 584 PERICARDITIS. upon the area, and in a few of them upon the intensity of the friction sound. The friction sound became more loud or harsh in three cases during expiration, and in four during inspiration ; and in one the frottement disappeared at the end of a deep breath. The area of the friction sound increased below during inspiration in a large number of cases, or thirty-one, while in a much smaller number of instances, or eight, it increased above during expiration. The Friction Sound varied in character, intensity, rhythm, and position from day to day. The clinical history contained in the previous pages of the friction sounds during pericarditis is pervaded through- out with instances of the great daily vari- ability of the friction sound in all its rela- tions. This changing condition of the friction sound during the successive phases of the disease is one of the important characteristic features of that sound. This feature has been already abundantly illustrated. Position and Extent of the Pericardial Friction Sound. - Dr. Stokes' in 1834 stated that the friction sounds in pericar- ditis are audible generally only over- the region of the heart. I stated indepen- dently, in 1843, that I had never heard the friction sounds beyond the region of the heart.2 We have seen in the previous pages that during the advance of the effu- sion, and usually during its acme, the friction sound is limited to the region of the heart, but that in certain cases with a thrill, the friction sounds spread during the acme from the seat of the thrill as from a focus, in all directions, over the front of the chest, and especially down- wards. During the period of the decline of the effusion, the friction sound, as we have seen, also often extends beyond the region of the heart, over the front of the chest, and especially downwards to the seventh and eighth, and even the ninth cartilages (see pp. 574, 577). The various changes in the area of the friction sound are given in the previous pages, and to those I refer for the more extended study of this subject. The position, limitation, and extension of the pericardial friction sound supply characteristic differences between pericar- dial friction sounds and endocardial mur- murs. The Effect of Pressure with the Stetho- scope over the region of the Pericardium during Pericarditis on the Friction Sound; or the Pressure Test of Pericarditis.-I called attention in 1843, in my paper on the situation of the internal organs,' to the effect of pressure made with the stethoscope over the region of the pericar- dium in rheumatic pericarditis, in inten- sifying or even bringing into play a peri- cardial friction sound. Since then Dr. Walshe-who, in the British and Foreign Medical Tieview, very kindly reviewed my paper just referred to, soon after its pub- lication, and Dr. Stokes, independently observed this sign. This effect of pres- sure is thus spoken of by Friedrich. " Sehr brauchbar is das von Sibson, Walshe, und Stokes, angegebene Zeichen, das namlich Reibungs gerausche bei Druck mit dem stethoskop starker werden, was allerdings Endocardiale Gerausche nicht thun."* The pressure test shows itself in two ways, (I.), when pressure over the region of the heart elicits a friction sound that was previously absent; and the other, (II.), when pressure made over the seat of a friction sound intensifies, changes, or modifies that sound. I. Influence of Pressure over the region of the Heart in exciting a Friction Sound not previously audible.-Pressure made with the stethoscope over the region of the heart elicited a friction sound not other- wise audible in twenty-nine of the forty- four cases that are included in the tables of cases of pericarditis given, in all of which cases the acme of the pericardial effusion was observed. As might be ex- pected, it was usually (1) during the period of the commencement of the at- tack or (2) that of its decline that this sign was observed ; and a friction sound otherwise latent was also thus brought into play by pressure (3) at the time of the acme of the effusion in four patients whose cases have already been touched upon at page 564, and in one case during a second acme of the effusion. 1. Friction Sound excited by Pressure during the onset and early period of the at- tack of Pericarditis.-In eight cases, as has just been stated, the attack of peri- carditis first declared itself by a friction sound induced by pressure over the region of the heart. As a rule this sound, so awakened, was smooth in character. In three instances it appeared as a single or double friction murmur, in one as a whiff, and in one as a soft to-and-fro sound. In the other three cases, however, the rub- bing sound was more marked, being harsh ami systolic in one, of a winnowing cha- racter in another, and creaking, in the third of those cases. In three of these eight cases, pressure was required to bring out the friction sound over the right ventricle during the advance of the effu- 1 Dublin Journal, iv. 60. 2 Situation of the Internal Organs. Prov. Med. Times., xii. 52. 1 Prov. Med. Trans., xii. 540. 2 Friedrich, Die Krankheiten des Herzens, page 229. CHARACTER AND TESTS OF PERICARDIAL FRICTION SOUND. 585 sion. The friction sound was excited by pressure made, in six cases over the ster- num, in one over the fourth cartilage, and in one over the heart. As a rule the spontaneous friction sound partook some- what of the character of the friction sound previously generated by pressure. Thus it was creaking in the case in which it was originally creaking ; harsh in one of those in which it was harsh ; to-and- fro in that in which it was to-and-fro ; rather smooth in the patient with a sys- tolic friction murmur ; and a double fric- tion murmur prevailed through the long history of the fatal case, in which a double friction murmur was originally aroused by pressure. The acme of the pericardial effusion usually occurred in these cases very soon after the first appearance of the excited friction sound, or from the first to the third day, in six of the eight cases. 2. The four cases in which a friction sound, otherwise absent, was elicited by pressure during the acme of the disease have been already considered under their proper heading at page 564. 3. Friction sound excited by Pressure dur- ing the decline of the effusion into the peri- cardium; and during the dying away of the attack.-In the great majority of the cases in which pressure was required to elicit the friction sound during the period of the decline of the pericardial effusion, this sign was a prelude to the dying away of the friction sound. Thus in nineteen of the twenty-four cases that belong to this class the frottement never again appeared as an independent sound ; and the attack of pericarditis was coming to an end. In three of the cases the friction sound, after being for a time only audible when ex- cited by pressure, reappeared for from five to ten days as an independent to-and-fro sound. There was a complete suspension of the friction sound in connection with ex- treme general illness in two of these cases, and the return of the spontaneous friction sound was in both of them associated with improvement of health, and was preceded by the appearance of a pressure friction sound. The friction sound became inaudible except on pressure in nearly one-half of the cases under examination during the first four days after the acme of pericar- dial effusion (11 in 24) ; and in more than one-half of them this sign came into play from five to twenty-one days after the occurrence of the acme (13 in 24). The character of the spontaneous fric- tion sound last observed before the pres- sure friction sound was called forth was, with few exceptions, decidedly of a sub- dued tone. The lower two-thirds of the sternum was the favorite seat of the pressure fric- tion sound which was heard in eleven of the cases over that bone, including two in which it was heard over the ensiform cartilage. In seven of the cases the rub- bing sound was excited by pressure over the cartilages from the third to the fifth, in one other instance over the second space, and in one over the fourth space. Besides these cases the pressure friction sound was heard over the heart in one case, the right ventricle in three, and the apex in three. II. Influence of Pressure over the Region of the Heart in intensifying a Friction Hound already present.-Pressure exercised a marked influence on the friction sound in all but one of the forty-four cases under inquiry, and in that single exception there is no mention of the employment of pres- sure over the region of the heart during the attack of pericarditis. Pressure, therefore, as a means of diagnosis, and of illustrating the clinical conditions of the friction sound in pericarditis, is essen- tially interwoven into every part of what has gone before in relation to friction sound in that affection : and one part has been devoted to the study of cases in which a soft friction sound audible over the heart at the time of the acme of the effu- sion into the pericardium, was converted by pressure into a harsh rubbing noise (see page 564). It is not, therefore, need- ful to give here again in a detached form what has already appeared distributed naturally through the preceding pages. In four instances or observations, an endocardial murmur was masked on pres- sure by the occurrence of a friction mur- mur or friction sound. A friction murmur was modified by pressure in fifteen in- stances ; a systolic murmur being intensi- fied (in 3), rendered double (in 1), or transformed into a double friction sound (in 1), by the employment of pressure; and by the same means a double friction murmur was intensified in five and con- verted into a double friction sound in four instances. In a few instances (3) a fric- tion sound resembling a murmur acquired its complete frictional character by pres- sure ; and in a greater number a systolic friction sound was thus intensified (in 4), or rendered double (in 5). An ordinary friction sound usually double, sometimes soft or grazing (in 18), sometimes of the usual to-and-fro character (in 38), some- times harsh (in 18), was intensified, or altered in tone, or rendered more harsh in seventy-four instances or observations. As a rule a succession of observations was made upon each case, and the same patient often reappears again and again under the varying phases of the friction sound, and of the influence of pressure upon that sound. I have not, as a rule, illustrated in this summary the various transformations that the friction sound may undergo 586 PERICARDITIS. under the touch of pressure ; but those two remarkable noises, the grating and the creaking friction noises, have been separately analyzed, and all the instances in which either of those sounds replaced another character of friction sound, or was strengthened by pressure, are given in the previous summary. A friction sound of indefinite quality was rendered grating by pressure in six instances, and in two a grating friction sound was intensified or rendered more harsh by pressure. A creaking friction sound was in an especial manner the off- spring of pressure when applied over the seat of an ordinary friction sound, since in six instances a friction sound, double in all but one, was rendered almost creaking by pressure, and in twelve instances, va- rious kinds of friction noise, grating, harsh, smooth, and murmuring, were transformed by pressure into a creaking sound ; while in two others, pressure con- verted a systolic creaking sound into a double creaking sound. These eighteen instances occurred in fourteen different cases. In each of two of these patients a creaking sound was excited by pressure four different times in the course of the clinical history of the case ; showing a strong tendency to the repeated recur- rence of this sign when it has been once excited. In six cases a creaking friction sound was rendered more intense by pres- sure, and only one of these cases appears also among those just spoken of in which an ordinary friction sound was converted by pressure into a creaking sound. Although I have only noticed in the summary those two more striking noises, the grating and the creaking, as being ex- cited by pressure, yet there are many other friction sounds of a definitely indi- vidual character that are thus brought into existence. These sounds differ in no essential respect from those that are spon- taneously excited from within by the sim- ple rubbing of the heart against the peri- cardium, when their opposing surfaces are covered with roughened lymph. Pressure over the heart affected with pericarditis excited-either originally or by transfor- mation, among my various cases-a sin- gle and a double friction murmur; a whiff; a single, and more often a double brush; rustling, grazing, scraping, scratch- ing, and sawing friction sounds ; a double sound like that made by rubbing with sand-paper ; and a peculiar double sound, broken during the diastole, that brings to my ear a noise like that made by sharp- ening a scythe. A to-and-fro sound was not unfrequently excited by pressure. I again and again noticed that under the influence of pressure the two friction sounds, and especially the diastolic one, became more continuous. Owing to the increased intensity and continuousness of the friction sound causd by pressure over the heart in peri- carditis, the natural sounds of the heart which were previously audible side by side with the friction sound, but were not strictly rhythmical with it, were fre- quently silenced under the influence of pressure. The Movements of Respiration in Pericarditis. In the Cases included in the following Table the movements of respiration were observed with the aid of the chest meas- urer. TABLE SHOWING THE MOVEMENTS OF RESPIRATION IN PERICARDITIS. I.-Cases in which the Respiratory Movements of both the Chest and Abdomen were observed. * Explanation.-These figures indicate the movements of respiration in hundredths of an inch. Female, set. 1G. Mitral murmur. 1st day. Friction whiff on pressure, pain left side. r7?f6. Rt. Lft. | 2d 15* 8* 5th 5 2 9th 9 7 abdom. 5 9 Rib. Rt. Lft. 2d 25* 15* 6th 6 5 9th 14 6 abdom. 6 5 [Rib. Rt. Lft. 2d 9* 12* 6th 3 3 9th 5 5 abdom. 3 3 4th day. Acme of pericardial effusion. 5th day. Pain in epigastrium. abd. below Lens, cartil. -10 abd. below ens. cartil. [ -s abd. below j _ens. cartil. j * -8 7th day. Better3, effnsfn"!^1 effusion less. 'Rib. Rt. Lft. 2d 15 12 5th 6 5 9th 9 7 abdom. 10 3 19 th day. No friction sound; better. ' Rib. Rt. Lft. 2d 9 7 6th 3 2 ' abd.below ensi- form cartil. 10 ' abd. at navel 15 abd. below ens. cartil -3 abd. below ens. cartil. abdomen at navel ! -4 7 26th day. ' Rib. Rt. Lft. 2d 5 4 5th 2 2 6th 3 3 9th 7 5 abdm. 6' 0 Female, set. 20. Mitral murmur, disappear on recovery. Rib. Rt. Lft. 2d 8 4 6th 1 1 7th 7 3 9th 7 4 abdm. 4 4 bel. ens. car. -6 abd. at navel 7 fRib. Rt. Lft. I 2d 18 12 I 6th 5 3 j abdm. 3 2 9th day. Acme of pericardial effusion, less pain heart, respirat'n 52. 10th day. Resp. 48. 12th day. Feels better. Resp. 50. abd below j ens. cartil. । ! -3 i abd. below ens. cartil. ,abd. at navel 0 0 THE MOVEMENTS OF RESPIRATION IN PERICARDITIS 587 [Rib. Rt. Lft. 2d 15 15 I 6th 4 3 9th 12 8 18th day. Lying on right side, friction sound on pressure. Rib. Rt. Lft. 2d 12 9th 10 7 abdm. 3 5 'Rib. Rt. Lft. 2d 12-20 10-15 6th 5 ? 9th 10 " abdm. 8 10 15th day. Friction sound more limited ; feels better. 21st day. Better, aspect good, resp. 30. no friction Bound. abd. below ens. cartil. I. abd. at navel 5 0 abd. below ens. cartil. 0 abd. below ens. cartil. do. deep br'th 20 .abd. at navel 5 4 "below ens. cartil. ditto, deep breath ? 5 ! 25 abd. at navel 4 Below ensi- form carti- lage, deep breath -50 Below ensi-" form carti- lage, deep breath 22d day. Weak. 33d day. 37th day. >90 Female, set. 15. Mitral valve disease. 1st day. Pain left side,, ill a week. Iio friction sound. [Rib. Rt. Lft. 2d 20- 15-20 6th 6- 3 9th 4 7 .abdm. 6 6 Sth day. Acme, resp. 54, pain side. Rib. Rt. Lft. 6th 3 3 9th 9 4 12th day. Better, but resp. 55, no friction sound. Rib. Rt. Lft. 2d 18 15 6th 6 2 9th 9 2 abd. 1 -3 abd. b. ens. c.-2 abd. below ) ens. cartil. j -1 Male, set. 27. Mitral murmur.- [Rib. Rt. Lft. 2d 7-9 7-10 6th 4 4 ,9 th 9 5 abdm. 7 12 Rib. Rt.. Lft. 2d 6 7 6th 6 3 9th 6 9 [Rib. Rt. Lft. 2d 6 7 6ch 4 2 9th 4 7 .abd. at naveli 20 2d day. Acme, very ill, resp. 36. 3d' day. Better. 7th day. abd. below ens. cartil. ! 12 Rib. Rt- Lft. 2d 30' 20 6th 7- 6 9th 10 10 Female, set. 18 Rib. Rt Lft. 2d 30 20 6th 6 5 9th 15 7 abdm. -3 -2 abd. below ) , ens. cartil. 5 abd. at navel 0 Mitral murmur. [Rib. Rt. Lft. 2d 30 20 6th 6 3 9th 10 7 abdm; 6 3 abd. below ) , ens. cartil. $ Labd. at navel 0 5th day. Acme, pain over heart. Sth day. Pain in chest, friction sound. 11th day. Acme. abd. below ens. cartil. ! -2 24th day. Slight friction, sound, Male, set. 23. Mitral murmur, established on- recovery. ' Rib. Rt. Lft. 2d 25 20 6th 9 10 9th 13 10 abdm. 12 5 rRib. Rt. Lft. .2d 15 12 6th 6 4 9th 13 12 abdm. 6 10 , ab„b. ens. car. 2 uabd. at navel 6 7th day. 3 days after acme, very extensive friction sound. Rib.- Rt. Lft. 2d 20 20 'Cth 6 5 9 th 5' 10th day. Improving, less friction sound; left pleurisy. 13th day. Better, very slight friction sound. abd. below . ens. cartil. I -1 Male, tet. 25. Mitral murmur. 'Rib. Rt. Lft. 2d 20 20 4 th 10 10* 7th 9 10- 9 th 9 10 10th day, Resp. 22, better friction sound. Rib. Rt. Lft. 2d 8 7 6th 16 8 10th 9 9 abdm. 25 20 abd. below ) ens. cartil. J abd. at navel 40 13th day". Better, sits up in bed, friction sound on pressure; Rib. Rt. Lft. 2d 15 15 6th 10 10 abdm. 30 35 6tli day, abd. below ens. cartil. abd.at-navel 40 30 Male, set- 17. Mitral murmur, established, on recovery. 8th day. Before acme pain in heart. Rib. Rt. Lft. 7th 10 4 abdm. 12 7 12th day. Acme.-abdomen below ensiform cartilage;-7. II.-Cases in which, the-Respiratory Movements of the Centre of the Abdomen were observed. A.- Cases observed (1), below the Ensiform Cartilage, and (2) at the Navel. Male, at. 17. Aortic mitral murmur 12th day, second acme. Below ensiform cartilage, -3, at navel, 4 21st day, no friction sound " " " 0 '' 12 85th day, .... .... " " « is,' « 20 Male, at. 15. Mitral aortic murmur 4th day, acme, pain epigast. " " " 6, " 10 5th day, after acme .... " " " 5, 6ih day, " .... " •• " 4. M Female, set. 17. Mitral murmur 2d day, acme? .... " " " 0' " 10 1st day, acme .... " " •• 1 7th day, after acme .... " " <• 5, " loth day, friction sound "■ " " 3 « .2 Male, aet. 17. Mitral murmur 588 PERICARDITIS. B.-Cases observed below Ensiform Cartilage. Male, set. 22. Mitral murmur 4th day, acme .. .. Movement below ens. cartil. -2 7th day, decline of fid " " " 6 9th day, second acn e .... " " " 9 29th day, well. Deep breath .. " " " 110-170 5th day, after acme .. .. " " " 2 11 th day, improving .... •' " " 3 32d day, clothes on. Deep breath " " " 50 Female, set. 21. Mitral murmur 1st day, before acme .... " " " 16 3d day, acme .... " " " 6 11th day, well .... " " " 20 Male, set. 15. Mitral aortic murmur Female, set. 22. Mitral murmur 13th day, second acme .... * " *• -2 22d day, third acme .... " " " 0 Female, set. 19. Mitral murmur 9th day, after acme .... " " " 1 11th day, .... " " " -7 Female, set. 24. Mitral murmur Male, set. 14. Mitral murmur 6th day, after first acme .. .. " " " 3 Female, set. 25. Mitral murmur 4th day, acme, or after .. .. Mvt. bel. ens. cart, or lower, 4 Male, at. 26. Mitral murmur Sth day, before friction sound.. Movement below ens. cartil. 5 Male, at. 35. Mitral murmur 8th day, no friction sound .. " " " 20 17th day. acme .... " " " -3 25th day, .... " " " 17 The movements of respiration were af- fected in pericarditis in three different relations: (1) those of the ribs ; (2) those of the abdomen on each side, just below the eighth cartilage ; and (3) those of the centre of the abdomen. (1) The respiratory play of the upper ribs was more than doubled in extent in three-fourths of the cases observed (5 in 7), so that respiration was as a rule high. This was due to the arrest or restraint of the action of the diaphragm caused by the extensive inflammation of the central tendon of the diaphragm, where it forms the floor of the pericardium. In one of the two exceptional cases, the movements of the second ribs were not at all or only slightly augmented throughout the whole period of the ill- ness ; but in the other case, in which the respiration was greatly accelerated, the action of those ribs, which was slight during the acme of the affection, was much increased during the decline of the effusion. The respiratory movement of the ribs on the left side of the chest was less than that of those on its right side, as might naturally be expected, in more than one- half of the cases (5 in 8) ; but in the re- maining three patients the action of the two sides was nearly equal both during the acme and the decline of the pericar- ditis. The difference in the movement of the two sides of the chest was not, as a rule, limited to the ribs adjoining the pericardium, but extended along their whole range, from the second to the ninth. The study of the Table will show, how- ever, that there were some exceptions to the rule that the play of the ribs was re- strained throughout on the left side ; since in two of the three cases in which the two sides of the chest moved with equal free- dom, the ninth left rib was greatly re- strained in its movements. (2) The lateral movements of the abdo- men below the eighth cartilages were greatly restrained in three-fourths of the cases (6 in 8); and the respiratory play of the left side of the abdomen was much less than that of its right side in the same proportion of cases (6 in 8). (3) The inspiratory movement of the abdomen below the ensiform cartilage was either reversed (in 12), arrested (in 1), or restrained (in 6) in every case of pericar- ditis in which that sign was observed. This is at once accounted for by the in- flammation, in that disease, of the central tendon of the diaphragm where it forms the floor of the pericardium, which leads to the virtual paralysis of the central por- tion of the diaphragm. This fact, that the anterior wall of the epigastric space, instead of advancing, recedes during in- spiration, gives us a physical side of great value in the diagnosis of pericarditis, and of the advance and decline of that disease. Thus in the first case in the Table a girl, aged 16, the anterior wall of the abdo- men below the ensiform cartilage fell backwards during inspiration for the tenth of an inch during the three early days, when the disease was at its acme ; then, as the tide turned and the effusion dimin- ished, the abdomen receded less and less up to the seventh day, when it did so for only the fiftieth of an inch ; after this it regained its natural forward movement, and on the twenty-sixth day the abdo- men at the epigastric space advanced (the tenth of an inch) as it had receded on the day of admission. In the other case the front of the abdomen advanced the sixth of an inch on the day of admis- sion, when the pericarditis had scarcely pronounced itself; the sixteenth of an inch on the third day, when it had reached its acme ; and the fifth of an inch on the eleventh day, when it had declined and disappeared. In my paper on the move- ments of respiration I showed that in health the abdomen at the navel advanced during inspiration a quarter of an inch or a little more, but I did not ascertain the respiratory movement at the epigastric space. A short time ago I observed, with Mr. Rossiter, the respiratory movements of the abdomen in eleven patients in St. Thomas's Hospital, several of whom were convalescent, and one had pericarditis; PERICARDITIS IN BRIGHT'S DISEASE OF THE KIDNEYS. 589 when we found that the inspiratory ad- vance at the epigastric space varied from the sixth to the fifth of an inch. The latter was also the extent of the advance in two healthy men. I consider that this forward movement fairly represents the healthy respiratory play of the part in question ; that in pericarditis, as a rule, the whole of this advance is lost; and that in addition the play is reversed to the extent of from the fiftieth to the tenth of an inch. It is worth noting, in conclu- sion, that in the case of pericarditis ob- served by Mr. Rossiter and myself in St. Thomas's Hospital, a boy, aged 12, in whom the disease was at its height, the wall of the abdomen receded during in- spiration at the epigastric space from the sixteenth to the twentieth of an inch, and at the navel from the thirty-fifth to the fiftieth of an inch. Pericarditis in Bright's Disease of the Kidneys. Dr. Bright, in the first volume of Guy's Hospital Reports, gives 100 cases of albu- minuria, seven of which, according to the tables, and eight according to his descrip- tion, had pericarditis. Subsequently Dr. Gregory and Sir James Christison, in Edinburgh; Martin Solon, Becquerel, and Rayer, in France; and Mahnsten, in Germany, gave each of them a series or summary of cases of Bright's disease, in all of which cases, except those communi- cated by Mahnsten, pericarditis was either infrequent or absent. Dr. Taylor called attention, in 1845, to the large proportion in which cases of pericarditis are affected with Bright's dis- ease, and to the frequency with which pericarditis occurs in cases of Bright's disease. He found that out of thirty-one patients with pericarditis, nine, if not eleven, had Bright's disease ; and that of fifty post-mortem inspections of cases with Bright's disease, five, or one in ten, had pericarditis. Several years later, or in 1851, Frerichs published his important work on Bright's disease, which contains a valuable table showing various conditions that existed in 292 cases collected by him from various sources, and including 21 observed by himself. He states that in 13 of those collected cases there was pericarditis; that is in only 4| per cent., or 1 in 22 of the cases. This return, which has been, and still is, much quoted, gives a lower proportion of attacks of pericarditis in Bright's disease than in the cases given or enumerated by Dr. Bright (7 or 8 per cent., or 1 in 14 or 12), Dr. Taylor (10 per cent., or 1 in 10), M. Rayer (5'4 per cent., or 1 in 18), and Dr. Gregory (5 per cent., or 1 in 20) ; and a higher proper- tion than in the cases observed by Bec- querel (4*6 per cent., or 1 in 62). Fre- richs appears to have overlooked some of the cases of pericarditis in his analysis. Te test his figures, I examined as nearly as I could the same cases or tables given by the observers quoted by him, and I find that in a total of 326 cases, 17 or 19 had pericarditis, or about 5'5 percent., or 1 in 18.1 During the nineteen years, ending in 1869, 285 cases of Bright's disease were examined after death in St. Mary's Hos- pital, and of these 25 or 1 in 11-3 or 8'8 per cent, were affected with pericarditis ; which was present therefore somewhat more frequently in those cases than in 1691 collected cases of Bright's disease, 136 of which, or 1 in 12'3 or 8'17 per cent, had pericarditis. Besides the twenty-five cases of pericar- ditis noted in the records of St. Mary's Hospital, there were fifteen of partial or doubtful pericarditis; but these cases ought not, I think, to be taken into the general account. If we separate the various forms of Bright's disease occurring in St. Mary's Hospital from each other we shall see the proportion in which each form was af- fected with pericarditis. SUMMARY. Acute Bright's disease, from scarlet fever, total number, 6 ; affected with pericar- ditis, 0 ; with partial pericarditis, 1. Acute Bright's disease, not from scarlet fever, total number, 15; affected with pericarditis, 2, or 1 in 7'5, or 13'3 per cent. ; with partial pericarditis, 0. Fatty or large white Kidney, total num- ber, 62; affected with pericarditis, 1, or 1 in 62, or D6 per cent.; with par- tial pericarditis, 5. Contracted Granular Kidney, total num- ber, 128 ; affected with pericarditis, 13, or 1 in 10, or 10 per cent.; with partial pericarditis, 7. Granular Kidney of natural or large size, total number, 34 ; affected with pericar- ditis, 3, or 1 in 11*3, or 8'8 per cent. Granular Kidney, grand total number, 162 ; affected with pericarditis, 16, or 1 in 10, or 10 per cent. ; with partial peri- carditis, 7. Lardaceous disease of Kidney, actual and 1 Frerichs. Dr. Bright, 100 cases; Sir James Christison, 14; Dr. Gregory, 37; Mar- tin Solon, 8; Rayer, 48; Becquerel, 45; Bright and Barlow, 10; Malmsten, 9; Frerichs, 21; Total, 292. Author. The same authori- ties respectively; 100, 14, 39, 10, 55, 45, 9, 33, 21; Total, 326. Cases of pericarditis in the above, Frerichs, 13 ; Author, 17 or 19. 590 PERICARDITIS probable, total number, 22; affected with pericarditis, 2, or 1 in 11, or 9 per cent. Nature of Kidney disease doubtful, 11; affected with pericarditis, 4, or 1 in 2'7, at 36 per cent. ; partial pericarditis, 2. Total number of cases of Bright's disease, 285 ; affected with pericarditis, 25, or 1 in 11'3 or 8'8 per cent. ; with partial pericarditis, 15.' Calculus in kidney, pelvis, or ureter, or dilated pelvis (hydronephrosis), total number, 12; affected with pericar- ditis, 0. Suppurative Nephritis from stricture, &c., total number, 13 ; affected with pericar- ditis, 1, or 1 in 13, or 7*7 per cent. That I might enlarge the area of ob- servation, I have brought together from various sources, including the returns from St. Mary's Hospital, the number of attacks of pericarditis in 1681 cases of Bright's disease; and the number of at- tacks of pleurisy, peritonitis, and pneu- monia, in 1228 cases. I have also given the number of cases with pericarditis, pleurisy, and perito- nitis, pneumonia, pulmonary apoplexy, and purulent deposit or abscess of the lung ; and certain conditions of the heart and aorta in the various forms of Bright's disease among the 285 cases examined at St. Mary's Hospital; distinguishing also those cases in which the heart was small, of natural size, rather large, and large or very large, giving separately those vari- ous conditions as they appeared in the cases affected with pericarditis. Among the cases of Bright's disease collected from various sources, 8'1 per cent, or 1 in 12*3 were attacked with peri- carditis. These cases are arranged in three sec- tions devoted respectively to England, Germany, and France; and the occur- rence of pericarditis in Bright's disease is here shown to be most frequent in Ger- many (1 in 9*5, or 10*4 per cent.), and least frequent in France (1 in 33, or 3 per cent.), while it is of medium or average frequency in England (1 in 11*9, or 8'4 per cent.). Comparative frequency of Pericarditis in the various Forms of ^Bright's disease.-I shall here inquire into the frequency of pericarditis in the different forms of that disease. Pericarditis is not frequent in cases of acute Bright's disease from scarlet fever in the young, since it only occurred in 1 in 14, or 7 per cent, of the patients under 16 years of age. The tendency to peri- carditis in children in such cases is slight, as was pointed out to me by Dr. Dickin- son, who kindly supplied me with the valuable tables of his cases of that class, amounting to 21. Pericarditis is on the other hand frequent in acute Bright's dis- ease in the adult, since it was present in 1 in 6| or 15-4 per cent, of those cases. The value of these returns has been greatly added to by the cases of acute Bright's disease kindly communicated to me by Dr. Greenfield. During the transitional period, when acute Bright's disease slowly gives place to the fatty or large white kidney, peri- carditis is probably frequent, since it oc- curred in one of Dr. Dickinson's four transitional cases. When, however, acute Bright's disease instead of recovering passes into the sec- ond or chronic stage, in the form of large white kidney, the tendency to general peri- carditis disappears, since it only occurred in 1 in 27 or 3'7 per cent, of the collected cases, and one in 62, or 1*6 per cent, of the St. Mary's Hospital cases, and the kidney in that single case was in the third or contracted stage of fatty disease. Five, however, of the St. Mary's Hospital cases with fatty kidney had partial pericarditis, showing that this affection, although still inherent, does not tend to develop itself in that form of the disease. The two great and opposite forms of Bright's disease, the fatty kidney, or the chronic stage of acute Bright's disease, and the contracted granular kidney, show a marked difference in the proportion with which they were respectively affected with pericarditis ; which attacked those with contracted granular kidney from six to four times as often (1 in 101 and 1 in 62) as those with fatty kidney (1 in 621 and L in 26 *62). Cases of lardaceous disease of the kid- ney have pericarditis with a moderate or average frequency (1 in 11, or 9 per cent.,2 and 1 in 13*3, or 7'5 per cent.2). Inquiry into the influence respectively of the fatty kidney, and the contracted granular kidney, in the production of pericarditis.- When inquiring into the influence of these two forms of Bright's disease in the pro- duction of pericarditis it may be well to consider two points which appear to be associated with the production of pericar- ditis, though for different reasons ; (1) the proportion in which cases with fatty and contracted granular kidney were affected respectively with pleurisy, peritonitis, and pneumonia : and (2) the relative propor- tion in which the heart was enlarged and its left ventricle was hypertrophied in those two forms of disease ; and the im- 1 In 285 cases examined after death in St. Mary's Hospital. 8 In the collected cases. 1 For details of the cases of partial pericar- ditis, see pages 592, 593. PERICARDITIS IN BRIGHT'S DISEASE OF THE KIDNEYS. 591 mediate relation, if any, that the enlarged heart may have had to the production of pericarditis. 1. Pleurisy attacked 60 of the 285 cases with Bright's disease occurring in St. Mary's Hospital (1 in 4'8 or 21 per cent.1 and 1 in 6 or 16'4 per cent.2). It will thus be seen that in these cases of Bright's disease pleurisy was twice as frequent as pericarditis (1 in 1P31 and one in 12'32). We have here a marked difference be- tween the pericarditis of acute rheumatism and the pericarditis of Bright's disease, since while in the former disease, or acute rheumatism, the inflammation of the peri- cardium is much more common than that of the pleura ; the pleurisy when present, being usually either due (1) to the spread- ing of the inflammation of the pericar- dium to the pleura, or (2) to pulmonary apoplexy which is the consecutive effect of the double inflammation of the heart, inside and out; in the latter affection, or Bright's disease, the pleurisy is an inde- pendent affection, and is, as we have just seen, twice as frequent as pericarditis in the cases under inquiry. The same in principle may be said of peritonitis, which is practically unknown in acute rheumatism; while it occurs nearly as often as pericarditis in Bright's disease; the numbers being 93, or 1 in 13,2 and 19, or 1 in 15* of peritonitis against 100 or 1 in 12'32 and 25 or 1 in 11'3* of pericarditis. Two-fifths of the cases of pericarditis were also affected with pleurisy (10 in 25) and three-fifths were free from that affec- tion (15 in 25); while only 2 in 25 of those cases had peritonitis. The relative frequency of pleurisy and peritonitis on the one hand, and pericar- ditis on the other, varied much in the different forms of Bright's disease. In acute Bright's disease from scarlet fever in the young, pleurisy occurs three times (1 in 5) and peritonitis twice (1 in 7) as often as pericarditis (1 in 14 ; but it is otherwise in acute Bright's dis- ease in the adult, not from scarlet fever, since in such cases pericarditis is as fre- quent as pleurisy (each 1 in 6'5), while it is twice as frequent as peritonitis (1 in 1T5). Pleurisy attacks many more cases (1 in 4' and 1 in 4*52) with fatty kidney than pericarditis (1 in 621 and 1 in 272); while in those with contracted granular kidney, pericarditis (1 in 10* and 1 in 62) occurs, judging by the collected cases, nearly as often as pleurisy (1 in 4-31 and 1 in 4'82). Although pleurisy is rather more frequent, pericarditis, as we have seen, is much less so in cases with fatty than in those with contracted granular kidney; and it is therefore evident that the causes produc- ing the two inflammations have but little in common, and that the one rarely ex- cites the other. Peritonitis occurred twice as often (1 in 31' and 1 in 152) as pericarditis in cases with fatty kidney, while pericarditis attacked three times as many as peritonitis (1 in 21) in those with contracted granular kidney. Pleurisy and peritonitis (each 1 in 10'82) were both of them more frequent than pericarditis (1 in 13*32) incases of lardace- ous disease of the kidney. Pneumonia, which when it occurs by itself is an occasional cause of pericarditis, while it is less common (1 in 6*4' and 1 in 7'62) than pleurisy (1 in 4'8' and 1 in C2) is more common than pericarditis in cases of Bright's disease. Those two secondary affections, pneumonia and pleurisy, were of exactly equal frequency in cases of acute Bright's disease, whether from scarlet fever or not; so that what has been said with regard to the latter of those affections applies to the former. Pneumonia was common (1 in 41 and 1 in 62) and pericarditis was rare (1 in 621 and 1 in 272) in cases with fatty kidney. It was almost the reverse in those with contracted granular kidney, in which pneumonia (1 in 10' and 1 in 92) scarcely equalled pericarditis in number (1 in 16' and 1 in 62). The proportion of pneumo- nia was, therefore, about twice as great in cases with fatty, as in those with con- tracted granular kidney, while pericardi- tis, rare in the former, was frequent in the latter form of the disease, making it evident that there was little in common between the production of pneumonia and that of pericarditis in these cases. Pneu- monia was present in only one-third of the cases of Bright's disease that were affected with pericarditis (8 in 25). 2. Enlargement of the heart, usually with hypertrophy of the left ventricle, was present in one-half of the cases of Bright's disease under review (129 in 259) in which the size of the heart was de- scribed. The heart was large in more than half of the cases of pericarditis in which the size of the heart was defined (10 in 193); or 10 in 129 of the total num- ber of cases of Bright's disease with en- largement of the heart. Pericarditis occurred in six cases in which the heart was of natural size (or 6 in 61). It would thus appear that 1 in 10T of the latter in which the heart was natural in size, and 1 in 12'9 of the former, with hypertrophy of the heart, had pericarditis. This would seem to say that hypertrophy of the heart had no apparent influence in the production of pericarditis in these 1 In 285 cases examined after death in St. Mary's Hospital. 2 In the collected cases. 3 The size of the heart was doubtful in six cases with Pericarditis. 1 In 285 cases examined after death in St. Mary's Hospital. 2 In the collected cases. 592 PERICARDITIS. cases. If, however, we add the cases in which the heart was small (23), none of which had general pericarditis, to those in which it was natural in size (61), we find that 6 in 84, or 1 in 14 of those com- bined cases, had that affection. If to these we join the cases in which the heart was rather large (45) 3 of which had pericarditis, the result is that 9 in 129, or 1 in 14'3, were thus attacked. From this analysis it would appear that enlargement of the heart exercised a definite but not a predominant influence over the production of pericarditis in cases of Bright's disease. Although hypertrophy of the heart is absent in almost one-half of the cases of Bright's disease with pericarditis, we know that in every form and case of that disease, whether acute or chronic, fatty or granular, the action of the left ventricle is unduly strong ; for it has to send the poi- soned blood through vessels of great ten- sion that oppose resistance to the onflow of the blood. The result is that in every case of Bright's disease, the left ventricle, whether hypertrophied or not, is beating with undue force ; and thus tends, by the pressure of its walls with undue force against the pericardium, to induce peri- carditis. The heart is prevented from becoming enlarged in many cases of Bright's disease by the exhausting loss of albumen, the general waste, and the low- ering character of the disease. This espe- cially applies to cases of fatty, lardaceous, and suppurative kidney. The left ventri- cle, notwithstanding the great waste of tissue that goes on in those cases, is act- ually hypertrophied in a certain propor- tion of them; and it is so in the greater number of those with acute Bright's dis- ease, in spite of the waste of tissue en- tailed by the great loss of albumen and blood in such cases. We have already seen that in acute rheumatism, over-action of the heart tends to induce pericarditis. It is, therefore, consistent with analogy, reason, and the clinical facts, that"in Bright's disease over-action of the heart should increase the tendency to pericar- ditis, that tendency being already resident in the disease. May it not be that on the one hand, the lessened force of the heart, induced by the weeping of albumen, dropsy, and other secondary wasting dis- eases in cases with fatty disease of the kidneys, explains to some extent the rarity of general pericarditis (1 in 621 and 1 in 272), and the comparative frequency of partial and undeveloped pericarditis (1 in 12'4), in that disease ? and that on the other hand, the increased size and action of the heart in cases with granular kidney, which usually lose little albumen, are not dropsical, and are free from ex- hausting secondary disease, tend to in- crease the frequency of general pericar- ditis in that affection (1 in IO1 and 1 in 62) ? Although the cases of partial pericar- ditis, which amounted to fifteen, cannot be classed rightly with those of general pericarditis ; for the partial variety ap- pears to have a tendency to remain par- tial, and those cases are not usually in- cluded among those with pericarditis, yet those cases ought to be studied. One of the fifteen cases of partial pericarditis had acute Bright's disease from scarlet fever (1 in 6, or 16'6 per cent.) ; five of them had fatty kidney (5 in 62, or 1 in 12-4, or 8 per cent.); seven of them had contracted granular kidney (7 in 129, or 1 in 18'3. or 5-5 per cent.) ; and in two the state of the kidney was not specified. The proportion in which partial and general pericarditis respectively attacked the different forms of Bright's disease somewhat correspond. In four of the cases of partial pericar- ditis the heart was very large (1 in 32'2), and in three it was rather large (1 in 15) ; while in five of them the heart was of natural size or small (1 in 16'8), and in three the size of the heart was not de- scribed, It thus seems that great enlargement of the heart does not favor the persistence of partial pericarditis, but rather tends to develop it into general pericarditis. Amount of Fluid in the Pericardial Sac in Pericarditis from BriejhVs Disease.-The amount of fluid in the pericardial sac va- ried considerably in the twenty-five cases of pericarditis from Bright's disease, the smallest quantity being two drams, and the largest about a pint, in which case the contents of the sac were purulent. In one-fifth of the cases (5) the contents of the pericardium are not described ; and in one-fifth of them (5) there were recent adhesions. The sac contained only a small quantity of serum, or not more than one ounce in one-third (5) of the remain- ing cases (15); a moderate amount, or a few ounces, in another third of them (6) ; and much fluid, eight ounces in one in- stance, a pint in another, in the remain- ing third (4) of those cases. It is evident that the presence of adhesions, or of a small, a moderate, or an abundant amount of fluid in the pericardium, depends on the stage of the pericarditis at the time of death ; and that in the several cases the fluid had either been removed, or was lessening, increasing, or at its height, when the final observation was made. It may, I think, be admitted that in the pericarditis of Bright's disease there is 1 The cases of Bright's disease examined after death in St. Mary's Hospital. 2 The collected cases. 1 The cases of Bright's disease examined after death in St. Mary's Hospital. 2 The collected cases. PERICARDITIS IN BRIGHT'S DISEASE OF THE KIDNEYS. 593 less effusion in the pericardium than in rheumatic pericarditis ; but from the evi- dence here given it would appear that there is no very material difference in the amount of fluid in the sac at the time of death in the two classes of cases. Character of the Exudation on the Sur- faces of the Heart and Pericardial Sac in Pericarditis from Bright's Disease.-In a small proportion of cases the lymph cover- ing the heart and lining the pericardium in case of pericarditis from Bright's dis- ease presents the same pale and rough1 surface, firm to the finger, with "cat's- tongue"-like projections, so usual in peri- carditis from acute rheumatism. It was thus in two of the twenty-five cases that were examined after death at St. Mary's Hospital. In two other cases also, both of acute Bright's disease, a rather firm layer of fibrin easily peeled off from the heart, leaving a finely-injected red surface underneath. In the majority of cases of pericarditis from Bright's disease the exudation differs from that usual in rheumatic pericarditis. Universal adhesions of the heart, rare in the latter, are common in the former affec- tion; the heart having been completely adherent in three instances, extensively so in one, and doubtfully so in another of those cases. There was pus in the sac in two cases. The lymph-was soft, granu- lar, imperfectly organized, or in patches in six, in two of which the presence of pericarditis was perhaps doubtful; or was bloody or very red on the surface, or mixed with blood in three of the twenty- five cases of pericarditis from Bright's disease. These conditions, which affected nearly two-thirds of those cases, are rare or unknown in rheumatic pericarditis. The remaining cases were less definite in character, the heart in four of them having been covered by recent lymph, while in two the pericardium was affected with "recent pericarditis." Appearances in Partial Pericarditis.- The cases of partial or doubtful pericar- ditis varied much in their features. In four of them flakes of lymph floated in the serum contained in the pericardial sac, the surfaces of the heart not being named. Pericarditis was limited, slight, or in traces or patches in seven other cases, and in two more it was highly vas- cular or congested. One case presented rough lymph easily detached, leaving an apparently healthy surface; and in the last instance there was a red fluid con- taining flakes of lymph in the sac, and lymph on the heart, the surface of which was healthy. These two cases, and the four in which flakes of lymph floated in the serum, were probably free from actual pericarditis. Physical Signs of Pericarditis Occurring in Bright's Disease.-Dr. Taylor gives careful reports of nine cases of Bright's disease with pericarditis, in three of which there was a friction sound, while in six of them there was no definite sign of the affection. In three of these six cases there were complete recent adhe- sions, rendering friction sound impossible. In one of the three cases in which peri- carditis was not discovered during life, a layer of soft lymph coated the heart, but there was no lymph on any part of the loose pericardium, and this appears to account for the want of friction sound. In one of the three cases that presented a friction sound, a double creaking noise was heard between the apex of the heart and the sternum ; and the heart and sac were covered with soft, slightly rough lymph. In two of the three cases without fric- tion sound, excluding the three with com- plete adhesions, and in two of the three with friction sound, there was no ade- quate explanation, after death, of the ab- sence of that sound in the two former cases, in which the opposed surfaces of the heart and sac were rough and scab- rous ; nor of its presence in the two latter cases in one of which there were exten- sive adhesions of the heart; while in the other the surface of the heart was simply red from fine injection, and there were but a few spots of lymph on the anterior coronary artery. I possess notes of the symptoms during life, and the appearance after death of nine fatal cases of Bright's disease with pericarditis. I cannot find the notes of a tenth case with regard to which I find two lines of an abstract of symptoms. In seven of the cases immediate signs of pericarditis were observed, and in three of them the signs of pericarditis were not observed. Cases in which the Signs of Pericarditis were not Observed.-In one patient, a man, aged 61, with granular kidneys, the heart, which was very fat, was covered and the sac was lined with recent lymph. On the third day after his admission, on which day he died, the heart's action to the left of the ensiform cartilage was loud ; and loud mucous rattles were audible all over his chest. In the second case, a man, aged 47, the opposite surfaces of the peri- cardium, and the heart, at its base, and along the great vessels were rough with a deposit of fibrin. This patient was in the hospital fifty-two days, but there is only one note of the state of his heart, which was on the fifth day after his ad- mission, when the sounds were rather loud. I cannot find the notes of the remain- ing case with Bright's disease and peri- carditis ; but the following is the brief abstract preceding the notes of the ex- amination after death. "At first, dou- vol. ii.-38 594 PERICARDITIS bling of the first sound, afterwards systolic murmur after epistaxis " so that friction sound was evidently not observed in this case. Cases in which the Signs of Pericarditis were Observed.-(1) A creaking noise with a thrill was present in three of the seven cases of pericarditis with friction sound ; (2) a creaking sound without a thrill in two of them, and (3) in the remaining two there was a "friction sound." (1) Cases with Thrill and a Creaking Friction Sound over the Seat of the Impulse, and Frottement extending far beyond and especially below the Region of the Pericar- dium.-There were three cases of this class. One of them a woman, aged 32, who was in the hospital for a week, pre- sented after death some fluid in the peri- cardium, and a rough deposit of recent lymph of a bright red color, which covered the heart and lined the sac. On the day after her admission a systolic murmur was audible over the cardiac region. Two days later, when she complained of pain going across the chest, the upper border of cardiac dulness was situated at the third space ; and a rasping, creaking fric- tion sound, chiefly systolic, was heard all over the front of the chest, and down to the eighth and ninth costal cartilages, its maximum intensity being at the centre of the sternum, and during the middle of the systole. Next day a strong thrill ex- tended over the heart from the right of the sternum to the nipple, and as high as the third cartilage: and the creaking sound was triple, being exactly like that made by the rise and fall and rise in the saddle. On the following day, the fifth, the thrill was less intense, and there was a triple creak at the apex, the friction sound being still audible over the lower cartilage ; and two days later she died. The second patient, a woman, aged 27, with contracted granular kidney, and pericarditis, had several patches of recent lymph on the surfaces of the heart and the free pericardium, and presented a double thrill, a double creak, and an ex- tensive friction sound, which were all ab- solutely suspended for one day, under the influence of flooding. The third case, "a man, aged 33, had mitral-aortic incompetence, and highly albuminous urine. The heart and peri- cardium were greatly increased in size, and the right ventricle was covered with a white fibrinous structure, rough to the finger, like a cat's tongue. On admission he had pain over the heart; and for two days, mitral and double aortic murmurs were audible. He became worse, and on the fourth day the diastolic murmur dis- appeared. On the ninth day he was drowsy, a strong thrill was felt with each impulse from the third cartilage to the fifth ; a loud grating double friction sound was present over the seat of the thrill, the rubbing noise radiating thence up to the top of the sternum, down to the eighth cartilages, and to the left and right; a leather creak was audible at the apex ; and a sound of a friction character was heard behind, over the dorsal spine. On the next day, when he died, the vi- bration had increased, and extended from the third to the seventh cartilages ; it lessened in extent above, on inspiration, below, on expiration ; and was accom- panied by a loud creak during systole, and a fainter creak during diastole, the sound spreading from the seat of the vi- bration over the front of the chest, and the upper third of the belly. (2) Cases with a Creaking Friction Sound, no Thrill being Observed, over the Seat of the Impulse, and a Frottement extending beyond, and especially below the Region of Pericardial Fulness.-One of the two cases of this class was a young married woman, with granular disease of the kidney. A firm coating partly in ridges and partly like a cat's tongue covered the heart and lined the sac. On her admission a creak- ing systolic friction sound was audible at the apex, in the fifth space. Four days later, when the pericardial dulness was at its acme, reaching up to the third carti- lage, her respirations being fifty, the friction sound was no longer creaking but presented itself as an occasional brush ; but three days after this, or on the eighth day, there was a loud leather creak over the whole region of the pericardium. After this the friction sound almost disap- peared ; but on the twelfth and preceding days it had again burst into full play as an extensive leather creaking noise, cover- ing the whole pericardium, and extending down to the seventh cartilage ; and eight days later she died. In the second case, a man, aged 30, with small, probably granular, kidneys, recent, bloody, honeycombed lymph lined the pericardium and covered the heart. On the day of his admission the two sounds of the heart were indistinct. Next day the impulse was extensive, and a loud double creaking sound, more intense, during systole, occupied the whole region of the heart, extending downwards to the seventh and eighth cartilages, and into the epigastrium. During the next few days the frottement wras much smoother and more restricted in area. On the eighth day he was weak and in distress ; the friction sound was audible over the whole pericardium, and beyond it, from the top of the sternum to the lower carti- lage ; and he could scarcely swallow or speak : and in the evening he died. (3) Cases with "Friction Sound."- One of the two cases of this class, a man aged 38, with granular kidney of full size, had recent lymph over the whole surface PERICARDITIS IN BRIGHT'S DISEASE OF THE KIDNEYS. 595 of the heart, and in some places the heart and pericardium were adherent by cord- like prolongations of lymph. On the fifty- seventh day there were doubling of the second sound, and a murmur over the third cartilage. On the seventy-fifth day, which was eight days before his death, "double friction sound over the pericar- dium," was noted for the first time. Three days later the pericardial friction sounds, which were scarcely audible with- out making pressure, were mingled with pleuritic friction sounds ; but after this he was too ill for examination. The other patient, an old woman, with contracted granular kidney and pericardi- tis, the whole surfaces of the heart and sac being covered by recent soft granular lymph, complained, on the twenty-first day after her admission, of great pain at the region of the heart. Next day there was pericardial dulness, and friction sound was present between the sternum and the left nipple ; and three days later she died. Several of these seven cases of Bright's disease and pericarditis presented certain broad features in common. In three of them a thrill or tactile vibration could be felt over the region of the heart's impulse, extending from the third to the fifth, the sixth, and in one instance the seventh cartilages. In one of those cases the thrill extended from the right border of the sternum across the chest to the nipple. In these three cases, and in two others in which a thrill was not observed, a loud sound like the creaking of new leather, usually double, but more intense and pro- longed with the systole, was audible over the whole seat of the thrill, or when that was absent, over the region of the heart's impulse. The friction sound was, how- ever, in none of the five instances re- stricted to the area of the thrill or impulse, or even of the distended pericardium ; but extended upwards to the top of the ster- num, downwards to the right and left along the seventh and eighth costal car- tilages, and over and even below the en- siform cartilage. In these cases the widespread friction sound became softer in tone, and especially downwards, as it widened away from the focus of its great- est intensity. In two of these five cases with creaking and extended friction sound, the deposit of fibrin or lymph on the sur- face of the heart was firm and like a cat's tongue, in one of them it was rough, in one it was bloody and honeycombed, and in the fifth, patches of recent lymph were present on the heart. In three of these cases there was a period of complete or partial suspension of the creaking and extensive friction sound ; which after spreading with great intensity and over a large area, became silent or feeble and contracted in area for a time, and then suddenly burst forth again with full intensity, and over a wide space. It was evident that under these circumstances, some influences were at work exciting the heart at the time of the creaking and widespread friction sound, and depressing the heart when that sound, ceased or became feeble. In one instance, the suspension of the thrill and creak was traced to the influence of flooding. In the two other patients the surface of the heart is describee! as being covered with recent, and in one of them with soft, lymph. In neither of them is it noted that the coating of lymph was rough. In both of these cases it is simply stated that a "friction sound" was present over the region of the heart. In all of these patients pressure inten- sified the friction sound. Cases with a Friction Sound that were not Fatal, or not Examined after Death.- Besides these seven fatal cases of Bright's disease with pericarditis in which friction sound was observed during life, I find three other cases in which the signs of pericarditis were observed when the pa- tients were in the wards. One of these cases, probably fatal, ad- mitted during the recess, very imperfectly recorded, presented a pericardial friction sound, which was chiefly present at and below the left nipple. Another patient, a carpenter, aged 35, had Bright's disease and aortic regurgi- tation of some standing. On the eighty- second day he had great pain in the heart, and four days later a rough double noise resembling a friction sound was audible over the cardiac region. Four days after this there was dulness over the pericar- dium from the third space downwards, and pain over the heart, relieved by leeches; and next day a to-and-fro fric- tion sound was audible over the heart, which continued for six days; after which, when he was in distress from aching over the heart, and sickness, the rubbing noise vanished, being replaced by the lost diastolic murmur of aortic regurgita- tion. This case left the hospital in im- proved health. The last case of Bright's disease with friction sound, was one of great interest, a cab-driver, aged 45. His urine was loaded with albumen, and contained coarse granular and fatty casts. There was, on the fourth day, an extensive im- pulse, and a remarkable doubling of the first sound heard all over the region of the impulse, which was heard along with, but apart from, a peculiar pericardial fric- tion sound chiefly systolic, which was au- dible for two inches below the nipple. This sound which was rasping at first, became creaking two days later, and five days after that, was only audible when pressure was made over the same spot, the sound being like that caused by rub- 596 PERICARDITIS. bing together two pieces of emery paper. Next day there was great extension of the friction sound, which required no pressure for its production, over the whole region of the pericardium; and four days later, the seventeenth after admission, the friction sound was soft, double, and mur- mur-like, chiefly heard on pressure, and was accompanied by the natural heart sounds, with which it was not rhythmical. I could not make out which sound had the start of the other. For a few days a systolic friction murmur was audible on passing beyond the nipple line, and a double rustle was heard on pressure down to the twenty-eighth day. The extensive doubling of the first sound held its ground throughout, and on the forty-fourth and fifty-third days a little frottement was again present, produced by pressure. On the sixty-fifth day he felt lighter over the heart, and a tremor or thrill was per- ceived, extending over the cardiac region from the right to the left nipple. A loud double new-leather creak extended over the whole of this region, but the rubbing noise spread far and wide, being heard from axilla to axilla, and down the ensi- form and seventh and eighth cartilages. The thrill and creak retained their inten- sity and area for five days, but on the 6th day the thrill was feeble, and the creak was replaced by a to-and-fro sound ex- tending from the third to the sixth carti- lage. Doubling of the first sound was mixed up with the friction sound, but pressure intensified the latter and extin- guished the former. On the seventy-third day there was no thrill, and a systolic friction sound, double on pressure, was present between the fourth and sixth car- tilages. Two days later the rubbing sound was no longer audible without pressure, and was quite lost on the seventy-ninth day. In this remarkable case the friction sound was present over a limited region near the apex, from the fourth to the twenty-eighth day; came into play slightly on the forty-fourth and fifty-third days; and on the sixty-fifth day burst out, with a thrill, with great intensity over the region of the impulse, and radiated thence as from a focus, all over the front of the chest, and down to the eighth costal car- tilages, being audible with a lessening area and diminishing intensity to the seventy-fifth day. This long and inter- mittent duration of pericardial friction sound appears to me to be peculiar to the pericarditis of Bright's disease, and is certainly never found in rheumatic peri- carditis. These ten cases-which I have given with some detail, as, with the exception of Dr. Taylor's cases and two related, in this respect briefly, by Traube, I have found no cases of pericarditis from Bright's disease in which the signs are related-presented features that are com- mon in them, but are comparatively rare in rheumatic pericarditis. A thrill was present, as we have just seen, in four of these cases or almost one-half (4 in 10); and a sound like the creaking of new leather was heard in six of those cases, or more than one-half (6 in 10), over the seat of the thrill or impulse ; and that radiated thence as a softening sound over the front of the chest, beyond the region of the pe- ricardium, and downwards over the ensi- form cartilage and the seventh and eighth costal cartilages. These signs were much less frequent in rheumatic pericarditis, since a thrill was present in only one-fifth of those cases, or 13 in 63, and was dis- tributed over the region of the impulse in only seven, was limited to the second space in two, to the apex in three pa- tients, and to both those regions in one ; and a creaking friction sound was present at or near the time of the acme of the pericardial effusion in about one-fourth of those cases, or about 18 in 63. The long duration of the friction sound, and its frequent suspension, observed in several of those cases of pericarditis from Bright's disease, likewise distinguish them from those with rheumatic pericarditis. Calculus in Kidney, Pelvis, or Ureter; or Dilated Pelvis:-and Suppurative Nephritis from Stricture, &c.-I have added, in the Table of Pericarditis in Bright's disease, two sections of cases that, without rank- ing under that affection, float upon its borders ; and substantially belong to the same disease in this respect, that the blood is poisoned, owing to the retention within it of the debris of the broken-up tissues of the body, owing to the imperfect action of the diseased kidney. In the first series, the secreting structure of the kidney is often atrophied by the back- ward compression of the organ, owing to the distension of the pelvis from the presence of calculus in the ureter, pelvis, or kidney. None of these cases, amount- ing to twelve, had pericarditis. In the second series of cases, numbering thir- teen, there was suppurative disease of the pelvis or kidney, owing mainly to stric- ture, or disease of the prostate, or bladder (in 11 cases) ; in one case, to calculus in the ureter, and in another to pyaemia. One of these cases had pericarditis. I refer to the table for the general con- dition of these two sets of cases. Pericarditis, neither Rheumatic nor from Bright's Disease. Rheumatic pericarditis, so common in the wards, is rare in the post-mortem room ; and pericarditis, as we have seen, occurs in as many as eight or nine per cent, of all fatal cases of Bright's disease. UNCOMPLICATED PERICARDITIS. 597 Although uncomplicated pericarditis is a very rare affection, yet its association with other diseases when fatal, and gene- rally as an effect of those diseases, is by no means rare. There is no single malady that is associated with pericarditis nearly so often as the two just mentioned ; yet if we combine all the other fatal cases with that affection, except those with Bright's disease and acute rheumatism, we shall find that pericarditis is found on exami- nation after death nearly twice as often in those combined affections as in Bright's disease, and three or four times as often as in fatal cases of acute rheumatism. The records of the examinations made after death at St. Mary's Hospital during the nineteen years ending 1869-70 contain forty cases of pericarditis that were neither rheumatic nor from Bright's dis- ease. The accompanying summary shows that thirty-nine of these cases of pericar- ditis were associated with some other dis- ease, general or local, and that in only one case was the affection uncompli- cated. Besides these forty cases of pericarditis, there were sixteen with partial or slight pericarditis. In addition to these cases I have analyzed in one view (1) Dr. Chambers' complete and valuable table of the causes of peri- carditis in 136 cases observed after death in St. George's Hospital during ten years ; (2) thirty-seven cases with pericarditis published in the Pathological Trans- actions; and (3) seventy-nine cases col- lected from various sources.1 A. Three cases of pericarditis and three of slight pericarditis had pyaemia, one had scarlet fever, and in one the affection was associated with tubercular disease of the suprarenal capsule ; B. twelve cases of pericarditis were asso- ciated with affections of the heart or aorta; C. fifteen with affections of the lungs or pleura ; D. one with ulcer, and one with cancer of the oesophagus ; E. five with affections of the abdomen ; F. and besides these cases of secondary or associated pericarditis, there was, as I have just said, one in which the affection appeared to be primary, or uncomplicated. A. General Diseases.-One of the three cases of pyaemia was a school-boy whose leg was doubled up under him five days before his admission. He came in with hurried breathing, blue lips, and tender- ness over the chest and abdomen; on placing the hand over the heart a sense of friction was felt, and a loud pericardial friction sound was heard all over the car- diac region. He had delirium, and died during the night. The surfaces of the heart and sac were covered with recent lymph in ridges, and connected by threads; and the muscular substance of the heart was firm, and contained numerous minute purulent dots scattered through the fibres of the left ventricle. Dr. Trotter observed this patient. This case is typical of a frequent method in which pyaemia induces pericarditis. In such cases the inflammation does not at once attack the surface of the heart, but spreads to it from the points of suppu- rative inflammation minutely scattered through the muscular walls of the organ, just as pleurisy is caused by the masses of suppurative inflammation spread through the lungs. Dr. Moxon1 has seen several cases of pyaemic abscesses of the heart, mostly in youths with suppurative perios- titis, or acute necrosis of the long bones, in which pericarditis was often caused by the bursting of small abscesses into the pericardium. This is not however the invariable mode in which pericarditis is caused by pyaemic abscesses of the heart, since in my case, just given, and in Mr. Stanley's,2 there was evidently no rupture of the minute collections of pus in the walls of the heart. Dr. Moxon finds that in cases with pyaemic inflammation of the lung near its surface the pleura becomes involved, and thus every diseased portion of tissue is covered with a layer of lymph; and that when general pleurisy takes place, the abscess has generally burst into the pleura, and so caused the serous in- flammation. This well represents the parallel conditions in cases of pericarditis caused by pyaemic abscesses in the heart. Another case may be named, a man, who had rigors on the day after being operated upon for perineal fistula, and was seized on the following day with vio- lent pain in the region of the heart, the sounds of which were natural. Next day there was a distinct pericardial friction sound, which was feeble in the evening, and was not again distinctly audible. lie died on the twelfth day after the operation, and the pericardium was found to be ad- herent to the heart by a thick layer of re- cent lymph. In this case, unlike that re- lated above, the pyaemic inflammation evidently struck directly at the pericar- dium, since violent pain seized the heart the day after the operation, and next day there was a pericardial friction sound. These two cases show the rapidity with which the processes of inflammation pass through their stages in pyaemia. Pyaemia, including with it erysipelas, 1 Corvisart (6) ; Bertin (5) ; Andral (9) ; Bouillaud (16) ; Dr. Stokes (13, including 4 from Testa) ; Dr. Law (2) ; Sir Thomas Wat- son (3) ; Tringel (13) ; Dr. Graves (5) ; Dr. Mayne (3) ; Dr. Green (1) • Dr. Beattie (2) ; and Dr. Thwaites (1) ; Total, 79 cases. i Lectures on Pathological Anatomy, by Dr. Wilks and Dr. Moxon, p. 122. 2 Medico-Chirurgical Transactions, vii. 323-. 598 PERICARDITIS. Pericarditis in its Association with other Diseases. Cases collected from all sources. Cases. Dr. Chambers' (Decen- nium Pathologium). Pericarditis. B. Post mor- tem Rec., St. Mary's Hospital. Pericar- ditis. 0. Patho- logical Trans- actions. Pericar- ditis. Various Authors. $ Pericarditis. 5s General. Partial. General. Partial. Pericarditis associated with acute rheumatism 19 ? 8 1 13 With Bright's disease 36 25 15 3 1 Dropsy ......... ... 1 A-With general or Constitutional Diseases :- Pyaemia, secondary inflammation .... 18 or 17 3 3 5 1 3 Erysipelas (included with pyaemia St. Mary's Hosp.) 4 ... 1 Smallpox......... 1 Fever ......... 4 1 Scarlet fever ........ 1 Cutaneous eruption ....... i Tubercular disease, supra-renal capsule . 1 Tubercle ......... • ••... 1 Cancer 1? 1 Syphilis 1 A-Total .... 26 or 27 5 4 7 1 8 B-With Affections of the Heart and Aorta :- Wound of the heart. ...... 1 ... ... Blow over the heart (1), fracture of the sternum (1) 1 i Tubercular pericarditis ...... 2 1 i Cancer of heart, pericardium or neighborhood. 3 or 4 1 1 i Neighboring abscess (2 in heart) .... 2 2 Fibroid disease of walls of heart .... 2 ... Aneurism of heart ... ./. 1 Aneurism of ascending aorta ..... 2 1 3 2 Enlargement of heart, without assigned complications • 1 ... " Diseased heart" and " dropsy" .... 18 ... ... Valvular disease of heart 6 4 3 1 8 Cyanosis, malformation ...... 1 B-Total .... 26 12 5 11 1 15 C-With Affections of the Lungs and Pleura:- Pneumonia (generally with pleurisy) 10 8 3 11 Pleurisy (including empyema) .... 5 5 2 1 12 Phthisis ......... 8 2 1 3 Communication bet. pericardium and abscess of lung 1 ... ... 1 Indefinite affection of the chest .... 1 C-Total .... 23 15 6 1 28 D-With wound (1); slough (1); ulcer (1); and cancer (1) of oesophagus ....... 1 2 1 ... E-With Affections of the Abdomen, including the Dia- phragm :- Diaphragmatic hernia (1) ; tumor connected with stomach (1) ........ ...... 2 ... Abscess of liver (3) ; one communicated with peri- cardium ........ 2 1 Peritonitis ........ 3 1 1 E-Total .... 3 5 1 1 Pericarditis, not associated with other affections 2? 1 1 1 13 Grand total .... 136 40* 16* 32 5 79 * Not including those from Bright's disease. UNCOMPLICATED PERICARDITIS. 599 was a much more frequent cause of peri- carditis in Dr. Chambers' cases observed in St. George's Hospital (22 or 23 in 81 or 1 in 3'8 of the cases of pericarditis that had neither acute rheumatism nor Bright's disease) than in those recorded in St. Mary's Hospital (3 in 46 or 1 in 13'6 ; or including partial pericarditis 6 in 56 or 1 in 9'5). Fever, in which the serous inflamma- tions are rare, was only associated with pericarditis in six instances among those from every source. This does not include one of smallpox, properly pysemic, nor one of scarlet fever. Those constitutional diseases, tubercle, cancer, and syphilis, were very rarely complicated with pericarditis, or in only one each among the whole of the com- bined cases, not including however tuber- cular pericarditis or cancer of the heart, in which the action of the disease was strictly local. One single instance of chorea, which is so closely connected with acute rheuma- tism, had pericarditis. This occurred among the collected cases. The case of pericarditis associated with disease of the suprarenal capsules is figured at page 541. This man could not lie down, his chest was universally dull on percussion in front and at the left side, and the sounds and impulse of his heart were absent. Upon these grounds Sir James Alderson, under whose care he was, correctly inferred that he had peri- carditis. B. Affections of the Heart and Aorta.- In one case, a man, pericarditis was caused by a wound of the heart. The right ventricle was penetrated by a wound about half an inch long, and the surface of the heart, and that of the pericardial sac were covered with recent lymph, stained red in many places. He survived the injury nearly five days. The left ven- tricle was penetrated by a wound half an inch long. In another patient who sur- vived nearly two days, fibrinous coagula were found on either side of the wound, but there was no definite note of pericar- ditis. Pericarditis was caused by an in- jury inflicted over the region of the heart in two of the collected cases. Local affections of the pericardium itself, and of the immediately adjoining structures, whether bearing upon it from within, and occupying the walls of the heart or ascending aorta ; or from with- out, and seated in the neighboring tissues, all tend to produce pericarditis. Tuber- cular pericarditis occurred in two in- stances ; and as tubercular disease of the pericardium is rare, it is evident that this affection has a strong tendency to inflame the surface of the heart. Among the affections of the structure of the heart that excited pericarditis by bear- ing outwards upon the pericardial surface of the heart, there were four cases with cancer of the heart; two with fibroid dis- ease of the heart, in which the disease ex- tended to the surface of the organ; and two of abscess of the heart, in one at least of which, described by Dr. Graves, there was no pyaemia, and in which instance the abscess contained two ounces of pus, and did not therefore cause pericarditis by bursting into the sac. These cases are derived from all sources. Aneurism of the heart was the cause of pericarditis in another patient, a well- formed woman, aged 53. The pericar- dium was distended with about eight ounces of fluid, and was adherent in front to the right ventricle, and behind to the left ventricle by quite recent attachments. The mitral valve was thickened and in- competent. An aneurism was discovered, on examination, in front of the left ven- tricle about the size of a small orange. The walls of the left ventricle were thick- ened, but in the position of the sac there was not a trace left of muscular tissue, and the wall was only formed by the pari- etal layer. In all these cases, whether of cancer, fibroid disease, abscess, or aneurism of the heart with pericarditis, the inflamma- tion of the surface of the heart is excited in the same manner. The new mass, projecting into the pericardium, and bear- ing upon it during the active contraction of the organ with a rude and unaccus- tomed force, excites inflammation in the opposite surfaces of the heart and the pericardial sac, and so establishes peri- carditis. Aneurism of the ascending aorta ex- cited pericarditis in eight of the cases de- rived from all sources; and three of the twenty-six cases of that affection observed in St. Mary's Hospital, presented evi- dence of previous pericarditis in the form of pericardial adhesion. In these cases the pericarditis is excited by the con- stantly enlarging aneurism bearing upon the pericardium, in the same manner that it is excited by cancer, abscess, fibroid disease, and aneurism of the heart. Cases with valvular disease of the heart, including all its varieties, without Bright's disease, were attacked with pericarditis in definite, but by no means frequent numbers, since that affection appeared in only 6 of the 117 fatal cases in which the valves of the heart wore incompetent (1 in 20). These proportions are increased if we strike out the thirty cases of the class under examination in which there were complete adhesions of the heart, and in which pericarditis was therefore for- bidden. Thus corrected, the attacks of pericarditis number 6 in 87 (or 1 in 14'5). It will be interesting to ascertain whether valvular incompetence with Bright's dis- 600 PERICARDITIS. ease was more frequently visited with pericarditis, than when it existed free from that affection. In 78 cases of Bright's disease with imperfection of the valves, 5 had pericarditis (1 in 15'6), or, deducting nine in which the heart was completely adherent, the numbers stand 5 in 69 or 1 in 14. From these comparative results it would seem that Bright's disease scarcely increases the tendency to pericarditis in valvular disease of the heart, for the pro- portion is almost identical in the two sets of cases. Partial pericarditis was present in 4 of the 117 cases with valvular insuf- ficiency that were free from Bright's dis- ease ; and in three of the 78 cases of that class in which the kidneys were affected. The six cases of pericarditis have been just distributed over the whole series of cases with valvular disease, the varieties of the affection being merged under one common title. If, however, we distin- guish the different affections of the valves from each other, we find a remarkable dif- ference in the proportion in which they were respectively attacked with pericar- ditis. The cases of mitral incompetence included all but one of those attacks of pericarditis, or 5 in 32 ; or, deducting 12 with complete adhesions of the heart, 5 in 20 or 1 in 4 of those cases were thus affected. The remaining instance of peri- carditis appeared in one of the thirty-one cases of mitral-aortic insufficiency, or de- ducting fourteen with complete pericar- dial adhesions, 1 in 17 of those cases. Not one of 32 cases with aortic valve-dis- ease, or of 20 cases with mitral obstruc- tion, had pericarditis. Pericarditis in cases of valvular disease had a strong but not exclusive preference for mitral incompetence among the col- lected cases, including those in the Patho- logical Transactions, for among eleven cases in which the affection of the valve was specified, eight had mitral insuffi- ciency, while two had mitral-aortic, and one had aortic valve-disease. May not the comparative frequency of pericarditis in mitral valve-disease be due to the re- sistance to the flow of blood through the lungs, and the consequent distension of the right ventricle with blood ; the pow- erful action of that ventricle, which presses so strongly upon the walls of the chest in front; and the fulness of the coronary veins-which occur in the final stage of that affection ? The cases of pericarditis in Bright's disease, with valvular insufficiency, were equally distributed over the whole series , two with mitral incompetence, one with mitral contraction, one with aortic, and one with mitral aortic valve-disease being thus affected, Pericarditis attacked one case in which there was hypertrophy of the heart with- out valvular disease, or any other compli- cation except pericardial adhesion. There were altogether eleven cases of hyper- trophy of the heart thus circumstanced, and so in six of them the heart was adhe- rent, rendering pericarditis impossible, that affection attacked one in five cases of this class. It will be well to inquire as to the pro- portion in which pericarditis attacked cases with and without hypertrophy of the heart. The heart was enlarged in 130 out of 655 cases of all the kinds that were free from Bright's disease,and among these 130 cases, 12, or 1 in 11, had pericar- ditis. The heart was diseased in 86 of those cases in which the organ was enlarged, ex- cluding eleven without other complications except adhesion; and including those cases with adherent pericardium, the heart was not diseased in 45 instances. Of the cases just leferred to, 26 of the 86, and 9 of the 45, had pericardial adhesions, and could not therefore have pericarditis. After deducting the cases with adhesions, 7 in 60 (or 1 in 8'6), with disease of the heart, and 5 of the 36 (or 1 in 7), without other affection than hypertrophy of that organ, had pericarditis. Without going into de- tail it may be briefly stated that of the rest of the cases, after deducting those with adherent pericardium, 6 in 104 (or 1 in 17) of those in which the heart was rather large, 4 in 267 (or 1 in 66) of those in which that organ was natural in size, and 1 of the 26, in which it was small, had pericarditis. These returns make it evident that en- largement, or hypertrophy of the heart exercises a powerful influence on the pro- duction of pericarditis. Besides the cases enumerated, there were 107 (or 1 in 6) in which the size of the heart was not de- scribed, and of these sixteen (or 1 in 6'7) had pericardial adhesions, and nineteen (or 1 in 4, excluding those with adhesions) had pericarditis. It thus appears that the size of the heart was not described in nearly one-half of the cases with pericar- ditis, owing evidently to the mind of the reporter being preoccupied by the morbid anatomy of the inflamed organ. One of the cases in which the size of the heart is not noted had mitral incompetence, and may therefore be ranked with those in which the organ was enlarged ; and ten of them had pneumonia (in 6), pleurisy (in 3), or empyema (in 1). In these ten cases the labor of the right ventricle must have been increased and prolonged, with the effect of enlarging the right side of the heart. This would tell more on the cases with pleuro-pneumonia than in those with simple pleurisy or empyema, but in such cases, with much effusion into one side of the chest, the obstacle to the stream of blood through the lungs is often UNCOMPLICATED PERICARDITIS. 601 great. This was well evidenced in a case, already alluded to at page 446, of exten- sive effusion into the right side of the chest which I saw through the kindness of Dr. Wane. Mr. James Lane drew off' a large quantity of fluid from the affected side. Before its removal there was a mitral murmur and doubling of the sec- ond sound. The doubling disappeared when the fluid was being extracted, and after a time the murmur vanished. In these cases, therefore, the prime effect of the spreading of inflammation from the pleura to the pericardium was heightened by the added secondary influence of the increased size and labor of the right ven- tricle. C. Eight patients with pneumonia (8 in 46), three with pleurisy (3 in 26), and two with empyema (2 in 17) had pericarditis. In all these cases (13 in 89), whether the primary affection was pneumonia or pleu- risy, it was the pleurisy affecting the outer surface of the pericardium, and spreading thence to its inner surface, that imme- diately kindled the pericarditis. Three of the eight cases with pneumo- nia and pericarditis were under my care, but in none of them did I detect a friction sound. Two of the three cases with pleurisy and pericarditis were my patients, and in both of them friction sound was heard. One of these was a little girl, who had been attacked a fortnight before with pain in the left side and over the heart, and was brought to the hospital in the mother's arms, in distress, pale, and breathing hurriedly. There was extensive pleurisy of the left side, and next day there was dulness on percussion, and a double, rather smooth friction sound over the whole peri- cardium. Chorea soon appeared, and on the seventh day, when there was a mitral murmur, the effusion had reached its acme. Two days later, when the friction sound was limited to the lower sternum, she died. The other case was a man who had been ill six months with pleurisy of the left side. On the eleventh day after admission double pericardial friction sound came into play, and continued to the nine- teenth day. After two days it vanished from over the heart, and was only audi- ble at the apex; it was thus ten days later, and on the following day he died. The heart was almost universally adher- ent by yellow lymph. Although in these thirteen cases the pleurisy excited inflammation of the ex- terior of the pericardial sac, which trav- elled through its fibrous structure to its interior, and then attacked the surface of the heart; yet in many of the seventy- six other cases with pleuro-pneumonia or pleurisy the exterior of the pericardium was inflamed, and yet the sac proved to be a barrier to the inflammation, which did not extend inwards so as to excite pericarditis. We have seen that in rheu- matic pericarditis the inflammation hab- itually travels through the fibrous walls of the sac, and attacks its exterior, or pleural surface, exciting pleurisy ; so that pericarditis tends to pass from within outwards much more than pleurisy of the pericardium does so from without in- wards. A case of pleurisy with pericarditis, under my care, that recovered presented a peculiar pericardial friction sound on pressure, to the left of the lower sternum, that lasted about three weeks. I have just alluded to the important secondary influence which the increased size and force of the right ventricle exer- cises in reinforcing the primary influence of the extension of the inflammation from the pleura to the pericardium in cases of pneumonia and pleurisy. Pericarditis attacked two cases of phthisis out of a total number affected with that disease amounting to 12. This does not include the two cases of tuber- cular pericarditis with phthisis already spoken of. Dr. Stokes gives an import- ant case communicated to him by Dr. McDowell in which pneumo-pericarditis was caused by a fistulous communication between the pericardium and a small cav- ity at the summit of the right lung; the apices of both lungs were healthy, but the bases of both lungs were solidified from a deposit of miliary tubercle and from pneumonia.1 D. Two cases were attacked with peri- carditis owing to disease of the cesopha- gus where it passes behind the pericar- dium. In one of these patients, who was under the care of Dr. Chambers, the oesophagus was ulcerated from the bifur- cation of the trachea to half an inch above the diaphragm. The ulcer gave way into the pericardium, which was filled with fluid from the stomach, and the interior of the sac was lined, and the heart was covered with recent fibrin. The other patient, with cancer of the oesophagus behind the pericardium, a woman, aged 47, a cook, under my care, complained of slight difficulty in swallow- ing, referred to the fauces. A to-and-fro friction sound, louder with the diastole than the systole, was audible over the cardiac region, being most intense over the sixth cartilage, and heard from thence to the ninth cartilage. Pleural friction was also present. This patient died on the fifth day after admission. E. There was a small and remarkable group of cases, in which pericarditis was 1 Dr. Stokes, on Diseases of the Heart and Aorta, p. 25. 602 PERICARDITIS caused by affections involving the dia- phragm. One of them had diaphragmatic hernia; two others had abscess of the liver involving the diaphragm; and an- other had a tumor connected with the pericardium, and communicating with the stomach. Ln the case of diaphragmatic hernia which was under the care of Sir James Alderson, the stomach, omentum, spleen, and transverse colon were forced through an opening into the left side of the chest, which contained six pints of liquid, partly digested blood, partly food. The heart was displaced to the right of the sternum, and there was pericarditis. In one of two other cases an abscess, with thickened walls, containing several ounces of greenish pus, was situated be- tween the pericardium and the liver, in- volving the diaphragm, and communicat- ing with a small abscess in the liver. The pericardium contained many ounces of puriform fluid, and its lining membrane and the surface of the heart were "hyper- semic," the latter being very red and vel- vety. In the other case, the diaphragm was pushed up by the liver in a conical projection, which was formed by an ab- scess occupying the interior portion of the left lobe of the liver, and the contiguous part of its right lobe. The pericardium contained two or three ounces of turbid fluid, and the surface of the heart was roughened by a recent deposit of lymph. Dr. Graves gives an important case in which pneumo-pericarditis was caused by a hepatic abscess which communicated with the pericardium and the stomach. In the fourth case the pericardium was full of thick yellow fluid, and there were some nodules on the aorta ; a dense white tumor which was interposed between the pericardium and the diaphragm was soft- ened in the middle, and formed a cavity which communicated with the stomach and spleen, and resembled an ulcer. One case of peritonitis out of a total of 64 had general, and another had partial pericarditis. F. There remains one fatal case of peri- carditis in which there was no evidence that the affection was secondary to, or associated with, any other disease. In this patient, a woman, aged 44, the pericardium was nearly the eighth of an inch thick, and its sac contained a large quantity of sero-purulent fluid. The sur- faces of the heart and the sac were covered with recent layers of plastic deposit, which was arranged at the base in a honeycomb shape, and was lengthened out at the apex into bands. The heart was small, hard, and contracted ; the lungs were congested behind; and there was a quarter of a pint of brown fluid in each lateral cavity of the chest. Two cases of pericarditis, under my care in St. Mary's Hospital, presented no other definite affection. One of these, a schoolboy, aged 12, was attacked, eighteen days before his admission, with pain in both sides of the chest, worse in the left. On admission the impulse of the heart was in the fifth space, there was fulness over the pericardium, duhicss from the second cartilage to the sixth, and a loud to-and- fro sound, which was intensified by pres- sure, over the same region and up to the top of the sternum. Next day the dulness had lessened, but the friction sound was strong and grating, and extended beyond the region of dulness. For several days it was more feeble and limited ; on the fourteenth, and two days later, it was again louder, but on the nineteenth day it had vanished. The other patient, a preg- nant woman, took cold six weeks before admission. The heart's action was tu- multuous, and on the third day the im- pulse extended from the sternum to two inches and a half beyond the left nipple, a to-and-fro sound appeared over and be- low the region of the heart, and a mitral murmur at the apex. Next day an im- pulse of a grating character, almost a thrill, extended over the region of the friction sound. These signs continued with variations, but lessening, and on the fourteenth day the impulse had shrunk inwards for two inches and a half, being bounded by the nipple line. Three days later a systolic murmur was converted by pressure into a friction sound, which dis- appeared on the eighteenth day. The Treatment of Pericarditis. Pericarditis, as we have just seen, is so rarely met with except as a combination of, or associated with, some other disease, that in the treatment of such cases we have to consider mainly the primary affec- tion, and along with this the local man- agement of the secondary inflammation of the pericardium. I shall of course here practically limit myself to this latter and local point. It will be important, how- ever, to touch upon the measures, in the treatment of the main disease, that may tend to prevent the occurrence of pericar- ditis. I shall briefly consider (1) the pre- ventive treatment of acute rheumatism, in relation to the possible occurrence of pericarditis, and (2) the local treatment that the presence of pericarditis may ren- der desirable in those diseases which are more or less frequently complicated with that affection. (1) The chief objects to be kept in view in the treatment of acute rheumatism are (1) the mitigation of the endocarditis that is the usual and natural effect of that dis- THE TREATMENT OF PERICARDITIS. 603 ease, and (2) the prevention of pericar- ditis, which, though the frequent, is not the customary complication of that dis- ease. Fortunately the measures that tend to palliate the inflammation of the inte- rior of the heart, tend also to prevent the inflammation of the exterior of that organ. The absolute rest of every limb and joint; and the soothing application of the bella- donna and chloroform liniment, sprinkled on cotton wool, to the affected joints, sup- ported by flannel, applied over the seat of pain with uniform and comfortable pres- sure, are the most important measures in the treatment of acute rheumatism for the prevention of pericarditis. The rest and support of the affected joints should be strictly maintained for several days after the disappearance of the local inflamma- tion ; for the too early use of an affected joint or limb, after the relief of pain and swelling, often leads to a relapse, first attacking the joints of the over-used limb, extending to other joints, and often pro- ducing endocarditis and pericarditis. I have given, at pages 492, 493, brief notes of six cases, in which a relapse of the joint affection, usually thus occasioned, induced endocarditis and pericarditis. (2) The employment of a few leeches, and the application of cotton-wool or a poultice, sprinkled with the belladonna and chloroform liniment, over the region of the heart during the early and painful period of an attack of pericarditis, are the means that I have for a long time em- ployed in the treatment of that affection. I have before me the collected notes of 36 cases of pericarditis, in which several leeches were applied over the region of the heart. In 29 of these cases there was pain over the region of the inflamed peri- cardium, and in 7 of them there was no note of the presence of pain. In 24 of the cases suffering from pain, marked relief, sometimes complete, followed upon the application of the leeches ; and this relief in a fair proportion of the cases so speed- ily followed the local bleeding that the relief must be attributed to the leeching. Brief notes of cases in which the applica- tion of leeches relieved the pain over the region of the inflamed pericardium will be found in the preceding pages (493, 498, 503, 507). The local bleeding, besides assuaging the local pain, lessened the op- pression in the chest and the difficulty of respiration in many cases. In one instance leeches were applied over the seat of pain five times ; although on each occasion relief seemed to follow, yet the pain soon again increased. In five cases leeches gave little or no relief. Although in these cases pain was not materially lessened by the local bleed- ing, yet in every instance but one, its action on the patient's state seemed to be favorable. In that patient, whose case has been already referred to at pages 497, 504, 506, and 507, there was pain over the heart, the action of which was very tumultuous at the time of admission. Leeches were applied with great relief, but unfortunately the' bleeding from one of them could not be stopped, and she lost much blood. After this the action of the heart was irregular and intermittent, and she was evidently weakened by the hemorrhage. She finally died after a long and severe illness, which was closed by an attack of smallpox. The employment of leeches produced a definite but very variable effect on the friction sound, and tended to lessen the force and extent of the impulse. Some- times the friction sound was lessened in intensity (in 8), but as often it became more intense (in 8) after the local bleed- ing. In one patient (p. 565) its effect was to suspend the rubbing sound, which had been previously extensive and rough, for one day ; but in the evening pain returned, and with it the frottement over the re- gion of the heart. Another patient on admission had excessive pain across the heart, where there was a double thrill, and a double harsh scraping friction sound ; four leeches were applied ; and next morning there was scarcely any pain, no friction sound, and no note of thrill. The friction sound returned on pressure that afternoon, and was again present on the following day. In one in- stance-I speak from memory-I exam- ined a patient with pericarditis immedi- ately after the withdrawal of leeches,*and found that the friction sound that had been previously audible was entirely abol- ished. This disappearance of the friction sound in such a case is evidently not due to any change in the character of the lymph on the surfaces of the heart and sac, although their vascularity may be lessened, but to the diminished force of the action of the organ. In direct con- firmation of this, we have already seen that in several cases friction sound was abolished, suspended, or softened, by the weakening of the action of the heart (see pages 506, 565). The effect of leeching the region of the heart on the amount of effusion in the pericardium in cases of pericarditis was not very marked. The leeches were ap- plied at the time of the acme of the effu- sion in ten cases, and in all of them but two the amount of effusion had lessened on the following day, and in the remain- ing two on the third day after the local bleeding, which lessened local pain in eight of these cases. To balance these instances, in eight others the effusion in- creased after the application of the leeches, and attained its acme in a day or two ; at 604 PERICARDITIS the same time, however, the pain over the region of the heart was relieved in six of those cases, but was not so in two of them. Blisters applied over the heart are fre- quently employed in the treatment of pericarditis. 1 resorted to them occasion- ally up to the year 1856. I cannot, how- ever, find any instance in which they ap- peared to be of service, and they were certainly, in some cases, a source of dis- comfort. It is evident that a blister over the region of the heart adds a second and outward inflammation to the primary and inward inflammation, and it therefore, unless there is a counterbalancing gain, increases the evil. Blisters were the definite cause of mischief in a case that I shall have occasion to quote when I speak of the removal of the fluid from the dis- tended pericardium. In that instance they wrere applied seven times in succes- sion over the prsecordial region. A blister cannot alter the lymph covering the heart and lining the sac ; and cannot directly lessen the amount of fluid in the pericar- dium, which, as we have again and again seen, tends of itself to diminish rapidly when it has reached its acme. It appears to me that a blister over the distended pericardium would rather increase than lessen the morbid supply of blood to those inflamed parts to which it is so contigu- ous. Blisters, besides inflicting local in- jury, taint the blood by increasing its fibrin, and are apt to lead to a secondary and low kind of inflammation in distant part§, and perhaps even to degrade the character of the pericardial inflammation itself, and to prolong its existence. It may be said that exciting pain at the surface of the chest in these cases lessens the severity of the internal pain. This is true, but this effect may be induced in- nocuously, by the application of chloro- form over the seat of suffering, com- bined with belladonna liniment, sprinkled on cotton-wool, and covered with oiled silk. Paracentesis of the Pericardium.-We have seen again and again that when the fluid in the pericardium has reached its acme, it very soon begins to diminish. It is therefore evident that puncture of the pericardium is very seldom called for. In some rare instances, however, the quan- tity of serum in the sac is so great as to interfere seriously with the action of the heart, breathing, swallowing, and speech ; owing to the compression of the auricles and vense cavse, the trachea and left bron- chus, the oesophagus and the descending aorta; and the inflammation of the re- current nerve. Generally the fluid of it- self lessens so quickly that these threaten- ing symptoms pass by without real danger to life. In some rare instances, however, life is in danger owing to the distension of the pericardium, and then paracentesis of the pericardium may become urgently called for. Riolan,1 in 1649, proposed that in dropsy of the pericardium, the sac might be opened by trephining the sternum an inch from the ensiform cartilage. Senac,2 and Laennec,3 at long intervals, both gave the same advice, the point selected by Laennec being immediately above the ensiform cartilage. Desault4 attempted to open the pericardium between the sixth and seventh ribs, and Larrey5 between the fifth and sixth ribs; but they both evidently failed to enter the pericardium. Romero® opened the pericardial sac in three cases of "hydro-pericardium," twice with success, through an incision made in the fifth space, near the junction of the cartilages to the ribs, this wound being made, partly to explore, partly to open the pericardium or the pleura. The first circumstantial account of tapping the pericardium was in a patient of Skoda's, with pericarditis from cancer of the heart, operated upon by Schuh in 1840,4 who first inserted a trocar by a perpendicular punc- ture through the third space close to the sternum over the great arteries, and fail- ing to get fluid, penetrated the sac through the fourth space and obtained a certain amount of reddish serum. This patient lived for nearly six months, and died with extensive cancer of the chest.6 In 1841 Heger performed paracentesis of the pericardium in another patient of Skoda's with pericarditis. He entered the pericardium through the fifth space, two inches from the left border of the sternum. Altogether 1500 grammes (about 48 ounces) of a brownish serum, finely flocculent, escaped, and nineteen days later, the fluid having reaccumu- lated, he again punctured the pericar- dium at the same place, and 500 grammes (about 16 ounces) of a reddish troubled fluid escaped in the course of four hours. This patient died 51 days after the second 1 Encheiridium Anatomicum et pathologi- cnm, p. 213. 2 Senac, de la Structure du Coeur, ii. 369. 3 Laennec, Traits de l'Auscultation Medi- ate. * Trousseau et Lasagne, Arch. Gen. de Med. Nov. 1854. 6 Diet, des Sc. Medicales, v. xl. p. 370. These cases are given imperfectly. 6 Trousseau and Lasagne publish this case at length in the Archives, but in his Clinique MMicale Trousseau states that Schuh pene- trated in his first puncture a mass of cancer, altogether of a thickness of six inches, which had invaded the sternum. It was not, how- ever, until more than a month after the op- eration that this tumor showed itself. Arch. G. de MM. 1854, p. 520. THE TREATMENT OF PERICARDITIS. 605 operation. The pericardium was in great part adherent, and there were nineCand five pints respectively in the two sides of the chest, and a tubercular cavity of the left lung. These two patients died from the primary diseases, cancer, and tuber- cle ; but both operations were successful. Behier thought that he punctured the pericardium through the sixth left space in a case related by him in 1854 ; the pa- tient died twenty-six days afterwards, but there was no pericarditis, and no mark of puncture in the walls of the sac. Jobert,1 in 1854, after cutting the skin punctured the pericardium with a trocar, in a case of pericarditis, a patient of M. Trousseau's, through the fifth left space, 1*2 inch from the edge of the sternum. The canula was agitated by the beating of the heart-the fluid came at first in drops and then very slowly, and altogether 400 grammes (about 13 ounces) of liquid flowed in the course of an hour and a half. The patient left the hospital eleven weeks after the operation, suffering from phthisis. Trousseau,2 in 1856, operated on another case, and opened the chest with a bistoury below the nipple through the nearest intercostal space, and pene- trated into the pericardium, from which flowed nearly 100 grammes (about three ounces) of a red serosity; and twice as much yellow serum came from the pleura. The patient died five days after the ope- ration. The last of the French operators that I shall name was M. Aran,3 who in 1855, after cutting through the skin, pene- trated the pericardium with a trocar through the fifth space, about an inch from the extreme limit of pericardial dul- ness, and withdrew about 350 grammes (fully 11 ounces) of reddish transparent fluid, and then injected a solution of iodine. Twelve days later he tapped a second time and withdrew 1350 grammes (about forty ounces) of albuminous liquid. This patient recovered from the opera- tion, but three months later presented signs of phthisis. I have now to speak of two important cases of pericarditis with symptoms threatening life, in which Dr. Clifford Allbutt resolved with his colleagues on the performance of paracentesis of the pericardium. One of these cases was ope- rated upon by Mr. Wheelhouse, who vividly describes the condition of the pa- tient and the steps of the operation. He found the patient sitting up in bed, his head resting on his hands, his elbows on his knees, struggling for breath. I quote the following from his description, and refer to his paper for the full details of the operation; and the precautions adopted during its performance : "I choose for my purpose a small trocar. This I placed on the upper margin of the fifth rib, half an inch to the left of the ster- num ; and inclining it upwards and in- wards, thrust it steadily forwards through the intercostal space towards what I be- lieved to be the centre of the ventricle. I pushed it onwards until I could distinctly feel the movements of the heart with the instrument; and then, sheathing the point, I advanced the canula well up to the heart, until I could feel and see, and demonstrate to those around, the impulse of the heart as communicated to the in- strument. The trocar was then with- drawn, and the fluid allowed to escape. This it did at first in a steady stream, which soon subsided into a saltatory flow coincident with the heart's contractions. The fluid consisted of a pale pink coagu- lable serum, and upon the whole, about three ounces escaped. During the ope- ration the patient gradually obtained re- lief ; and after the canula was withdrawn, the bed-rest was removed, and he was able to lie down."1 This patient com- pletely recovered, and was in perfect health the other day wflien Mr. Wheel- house, in reply to my inquiries, kindly informed me as to the state of the patient. In the second of Dr. Clifford Allbutt's patients Mr. Teale drew off, as Mr. Wheelhouse had done, through a fine canula five ounces of fluid which gave the patient great relief. The reaccumula- tion of the fluid called for a second opera- tion, which was performed with con- siderable relief. Finally, however, this patient, a girl, died of bronchitis.2 The operation has been performed within the last three years on three occa- sions, and I owe the references to these cases to the kindness of Mr. Holmes. M. Villeneuve, in 1873, operated by means of the aspirator, on a child with arching and fluctuation over the prtecordial region. He punctured the tumor at its most promi- nent part, and removed two syringefuls of serum. On withdrawing the canula a jet of liquid spirted out of the wound, which remained open owing to the inter- nal wall of the cavity having been very much thinned by the repeated application of blisters, seven of them having been placed one after another, without any im- provement, on the same place. A peri- cardial fistula, yielding pus, was estab- 1 Trousseau et Lasagne, Arch. G. de Med. 1854. 2 Trousseau, Clinical Medicine. New Syd. Soc. iii. 365. 3 Bulletin de l'Academie Royale de Mede- cine, xxi. 142. 1 See British Medical Journal, Oct. 10, 1808, p. 385. 2 See Dr. Clifford Allbutt's important pa- per, Lancet, 1869, i. 807. 606 PERICARDITIS. lished and did not heal up until the sixth month after the operation.1 In the other case, a man in whom paracentesis of the chest and abdomen had already been per- formed, Dr. Valtosta, in 1874, opened the pericardium by making an incision over the fifth space, commencing about half an inch from the sternum. The layers of muscles were then carefully divided and an elastic dilatation was felt. A punc- ture was made in this, the point of a small trocar was introduced, and about ten ounces of fluid was removed with imme- diate relief. This patient died four weeks after the performance of the operation.2 M. Chairon contributed a third case in 1875, in which more than 1000 grammes (about 33 ounces) of liquid were removed from the pericardium. The result is not given. With reference to the method of operation, he says the spot to be preferred is the fifth intercostal space, at an inter- mediate point between the nipple and the sternum, rather nearer to the former, al- ways being guided by the apex of the heart. The aspiratory method should, he considers, be preferred.3 [Dr. W. Pepper,4 of Philadelphia, per- formed this operation successfully in 1877. The patient was a girl, seventeen years of age, apparently moribund from cardiac embarrassment and dyspnoea. These symptoms were at once relieved, and at the end of a month the patient could walk about. Fifteen months afterwards, she died from a complicated attack of pleurisy with ascites. Dr. J. B. Roberts5 states that, to the year 1879, paracentesis pericardii had been performed seven times in America. Al- together, he has found authentic records of forty-nine instances of the operation ; of these, twenty-three were followed by recovery, and twenty-six by death. Dr. Pepper mentions6 one case in which large pleuritic and pericardial effusions being both present, he removed the fluid from the pleural cavity by aspiration; de- signing to follow this, if needful, with peri- cardial paracentesis. The fluid in the pericardial sac, however, was absorbed without farther interference, under medi- cal treatment.-II.] Proposed Operation for Paracentesis of the Pericardium.-This operation cannot well be called for unless the amount of effusion into the pericardium be so great as to compress the vena? cavte and the auricles, the oesophagus, trachea, and left bronchus, and the descending aorta, so as to inter- fere with the action of the heart, swallow- ing, breathing, and the supply of blood to the abdomen and lower limbs. Under these circumstances the pericardial sac is greatly distended downwards towards the abdomen, and the heart itself is elevated. The result is that the mass of the fluid occupies a large space below the heart, measuring between one and two inches from above downwards, between the lower surface of the ventricles and the floor of the pericardium, where it is formed by the central tendon of the diaphragm ; which is depressed downwards almost or quite to the level of the upper border of the sixth space, in the manner represented in the figures at pages 544, 551, 553, and 576, and also, in principle, in Pirogoff's important work. When it is considered that in these serious cases the lower border of the heart is above, while the mass of the fluid is be- low the level of the lower edge of the fifth cartilage, I advise that the fine trocar, such as that used by M. Aran, Mr. Wheel- house, Mr. Teale, and M. Chairon, should be inserted into the distended pericardium at a point just above the upper edge of the sixth cartilage at the lowest part of its curve, more than an inch within the mam- mary line; and that the instrument should penetrate gently inwards with a direction slightly downwards, so that it may ad- vance into the collection of fluid below the level of the heart; and that the liquid should be slowly and gently extracted by the use of a syringe or the aspirator. By this proceeding the collected fluid will be alone penetrated and the heart will be quite untouched. Extensive incisions, and the injection of irritating fluids should be of course avoided. In every case in which the heart has been previously healthy, and is of the natural size, its lower border is elevated above the level of the fifth space when the effusion into the pericardium is at its height, so that in such cases the procedure I have advised, which has the sanction of Aran's and Chairon's operations, can be performed with ease and safety. When, however, the heart is enlarged owing to the existence of valvular disease of some standing, the heart is sometimes, as in the cases spoken of at page 549, to be felt beating in the fifth or even the sixth space at the time of the acme of the effusion, when the urgent distress and danger of the patient may demand para- centesis of the pericardium. Under such circumstances, which can be readily dis- covered by ascertaining the position of the impulse - which should always be some distance above the point of penetra- tion, for a thin layer of fluid interposes itself between the surface of the heart 1 London Medical Record, iii. p. 532. 2 Ibid., iii. p. 275, 532. 3 Ibid, p. 694. [4 Am. Journal of Med. Sciences, April, 1879, p. 430.] [s Phila. Med. Times, Aug. 16,1879, p. 546.] [8 Ibid., p. 560.] ADHERENT PERICARDIUM. 607 above its lower border, and the front of the chest-another point than that just indicated in the fifth space must be chosen for the operation. This point should then be selected at the space between the left edge of the ensiform cartilage and the right border of the seventh cartilage in the epigastric region ; or, if needful, owing to its margin being covered by the seventh costal cartilage, the ensiform car- tilage, at its left border, may itself be perforated, first with the point of a bis- toury, and then with the fine trocar. Trousseau states that Larrey advised that the puncture of the pericardium should be made through this space ; but in the operation which he performed with a view-erroneous in this instance-to enter the pericardial sac, that great sur- geon, as we have seen, entered the cavity of the chest between the fifth and sixth ribs. The lower border of the fully-dis- tended pericardium is usually a little above, and sometimes even below, the lower end of the ensiform cartilage, as in Fig. 88, page 558 ; which is from a case, exactly in point, with mitral regurgita- tion and enlargement of the heart; and the pericardium may therefore be safely punctured through a point corresponding to the middle or the lower portion of that cartilage. The presence or absence of the impulse of the right ventricle in the epi- gastric space, and the position of the lower border of the pericardial dulness in that space, must be previously ascer- tained. Those two important points of diagnosis, which can be readily made, will prove a safe guide to the surgeon as to the place which he should select for the operation, which he will rightly fix sufficiently below the seat of the impulse, so as to avoid the heart; and sufficiently above the lower border of the pericardial dulness, so as to prevent the canula being tilted upwards when the floor of the peri- cardium elevates itself as the sac is being emptied. When he pushes the trocar onwards he must use all the precautions so clearly described by Mr. Wheelhouse, so that if the point of the instrument comes upon the front of the heart, he may withdraw the trocar at tire same time that he gently presses the canula forwards and downwards. In the great majority of cases the fluid, after it has reached its acme, soon begins to lessen, and continues to do so steadily from day to day. Under these circum- stances I do not advise the use either of aperients, which tend to disturb and lower the patient, or of diuretics. If, however, the quantity of the fluid is stationary, or lessens very slowly, then diuretics may sometimes be of use. ADHERENT PERICARDIUM. Br Fkancis Sibsox, M.D., F.R.S. The discovery of adherent pericardium during life is in some cases impossible, and in some, doubtful or difficult; but in others, and these are amongst the most important cases, its existence may be ascertained during life on reasonable and well-ascertained grounds. When the adhesions are partial, or when the heart, though completely adhe- rent, is small, is not bound by external adhesions to the anterior walls of the chest, and is covered to the natural ex- tent by the lungs, their expansion being free and unconstrained, then the varying relation of the heart and lungs to the chest is quite natural, and the diagnosis of the adhesions is impossible. If the ad- herent heart be enlarged, and is not at- tached to the lower half of the sternum and the cardiac cartilages by combined pericardial and pleural adhesions, so that the active or automatic and the passive or respiratory movements of the heart are scarcely or but little interfered with, the inspiratory expansion of the lungs is freely permitted, and the diagnosis of the adherent pericardium may be difficult, obscure, or even impossible. When, however, the heart is, as usual, enlarged, being often affected with valvu- lar disease, the adhesions may be short, fibrous, and binding ; and the front of the organ may be fixed to the two lower thirds of the sternum and the adjoining cartilages by pleuro-pericardial adhesions, so that the automatic and respiratory movements of the heart, and the inspira- tory expansion of the lungs are restrained: thus the discovery of the adhesions dur- ing life may generally in such cases be made by a careful study of the physical signs ; its diagnosis being the more cer- 608 ADHERENT PERICARDIUM. tain and easy in proportion as the heart is more enlarged, and more firmly fixed to the anterior walls of the chest. Anatomical Description of Adher- ent Pericardium. Partial Adhesions.-Pericardial adhe- sions vary greatly in firmness of tissue and length of fibre, and when they are partial they are usually longer than when they are general. Four conditions seem to regulate the position, extent, and firmness of partial adhesions of the heart. (1) Tlte amount of movement of the various parts of the heart and arteries ; for it is evid-ent that the more limited the movement of any part, the greater must be its tendency to adhesion : the relation of the surrounding sac (2) to the heart ; and (3) to the outer borders of the pericardium, which are close to the heart, and are therefore more often adherent; (4) the gravitation of the heart in the fluid, since the posterior or depending parts of the heart, when the patient lies on the back, attach them- selves readily to the parts on which they rest. Partial adhesions take place most fre- quently near the apex and along the line of the ventricular septum ; at the outer border of the left ventricle and the outer side of the right auricle, where the move- ments of those cavities are most limited, and to which parts the outer borders of the sac cling; the posterior surfaces of the left auricle and of the ventricles which rest upon the sac ; and the great arteries at their higher parts, where the extent of their movement is least, and where they are most contiguous to the pericardium. The visible commencement of the ascend- ing aorta is often free from adhesions, owing to the hollow, containing liquid, formed in front of that part of the vessel, between the appendix of the right auricle and the origin of the pulmonary artery. In several instances a patch of the right ventricle, to the right of the septum, and midway between the pulmonary artery and the lower border of the ventricle, was adherent when the rest of the ven- tricle was free ; and it is to be remarked that this patch is the part of least move- ment, or stable equilibrium, of the walls of the right ventricle (see fig. 62, page 401). A frequent seat of partial adhesions is a point a little above and to the left of the apex of the heart. These adhesions near the apex frequently become stretched and attenuated, and at length give way. Several pendulous, filamentous, fibrous bands often hang from this point, near the apex, on the surface of hearts that are free from internal disease ; but which display white fibrous patches on their surface ; the filaments and the patches being evidently alike the result of a pre- vious attack of pericarditis. The parts of the surface of the heart and arteries that are usually not adherent when other parts are so, are the front of the right ventricle, especially in the neigh- borhood of the right auricle and pulmo- nary artery, and above its own lower bor- der ; the appendix and ventricular border of the right auricle ; and the parts of the aorta and pulmonary artery nearest to the heart, those being the parts that have respectively the greatest extent of move- ment during the action of the heart, as may be seen in the figures at page 401. General Adhesions.-The adhesions are formed of fibrous threads of variable and often of considerable length, and they usually allow of a fair amount of move- ment of the heart. Long and loose ad- hesions interfere but little with the free play of the heart; but short, close, and firm attachments embarrass the action of the organ. The length of the fibres of adhesion varies over the different parts of the heart; their length usually correspond- ing to the amount of movement, and the power exercised by the respective parts during the action of the organ. The ad- hesions are generally longer at the apex than elsewhere: those over the left ven- tricle are longer than those over the right ventricle ; those over the auricular por- tion of the right ventricle are longer than those over its body and near the septum, and I believe that the same applies to the left ventricle also. The adhesions over the right auricle are much shorter than those over the right ventricle ; and the auricular appendix is contracted in size by the fibrous covering. The attachments of the left auricle, the aorta, and the pulmo- nary artery are generally closer than those of the right auricle. When the adhesions are long and loose, and the heart is free from valvular dis- ease, and from any other influence tend- ing to cause enlargement of the organ, the size of the heart is usually natural. It was thus in two of the cases examined after death at St. Mary's Hospital, in four cases that I observed at Notting- ham, in many of those referred to by Dr. Stokes, in ten briefly described by Dr. Gairdner, and in 34 out of 90 cases col- lected by Dr. Kennedy. When pericardial adhesions are asso- ciated with valvular disease, the heart is always enlarged. It was so in 25 out of 2G cases, and in the remaining instance, a case with mitral contraction, the heart was rather large. I have compared a double series of cases of valvular disease side by side, in one series with, and the other without adherent pericardium, and, not going here into details, I may say that the cases with adhesions were on an PHYSICAL SIGNS OF ADHERENT PERICARDIUM. 609 average five and a half ounces heavier than those in which there were no ad- hesions, an increase that was to a consid- erable extent accounted for, in many in- stances, by the augmented thickness and weight of the pericardial sac. The in- creased size of the heart would seem, I therefore, in such cases, judging by this i analysis, to be traceable more to the affec- tion of the valves, than to the adherent pericardium. We find, however, that in two-thirds of the cases without valvular disease in which the pericardium was ad- herent, the heart was enlarged (12 in 19) ; and in one-fifth of them it was rather large (5 in 19); while in only one-tenth of them the organ was of natural size (2 in 19). These proportions are borne out by Dr. Kennedy's important analysis of col- lected cases of adherent pericardium, who found that in fifty instances the heart was enlarged, in thirty-four it was of natural size, while in five it was atrophied. We may therefore conclude that in cases with the double affection of valvular disease and adherent pericardium, the valvular disease is the essential cause of the en- largement of the heart; yet that the ad- hesions, by giving an additional spur to the action of the organ, add to the more important enlarging effect of the valvular disease of the organ. It is the natural effect of pericarditis for the inflammation to spread from the pericardial to the pleural surface of the fibrous sac. When, therefore, the peri- cardium becomes adherent to the heart in those cases, it becomes adherent also to the walls of the chest in front of the peri- cardium. These pleural adhesions often occupy an extensive space in front of the chest, and may extend from the' second left cartilage to the sixth ; from the manu- brium to the upper half of the ensiform cartilage ; and from the right border of the sternum to the apex of the heart, to the left of the nipple line, as in the cases referred to in former pages, and there described. Though these are extreme instances, yet they are typical of many cases with pleuro-pericardial adhesions. When the adhesions are short and pow- erful, and when, being pleuro-pericardial, they bind the walls of the heart exten- sively to the walls of the chest in front of them, a great and constant strain is put upon the ventricles ; for they cannot con- tract upon themselves to expel their con- tents until they have dragged the sternum and cartilages powerfully inwards. The ventricles thus expend their force in two directions, one towards the interior to ex- pel their contents, resisted in doing so by valvular incompetence; the other from the exterior, to compel the front of the chest, which is united to them like a solid buckler, to share in their contraction. Under these influences the ventricles j tend to undergo a change in form, and to become flattened out, the one in front of the other. Two cases observed by me in Nottingham were thus influenced. The enlarged and thickened right ventricle, instead of sweeping half round the left ventricle, usually cone-shaped, lay directly in front of it; and the septum between the ventricles, instead of bulging forwards into the right cavity, became flattened. When the adhesions, being extensive and pleuro-pericardial, are not short and close, but of moderate length, and do not, therefore, bind the sternum and carti- lages to the heart like a buckler, they do not seriously embarrass the commencing action of the ventricles ; but during their contraction, the ventricles at length begin to draw upon the walls of the chest; and in the course of the systole they drag those walls inwards. When the adhesions are, as usual, longer and less solid, the ventricles con- tract more after their wont, and retain more or less perfectly their power. The right ventricle is usually enlarged as well as the left, but not always, for the size of the ventricles is necessarily influenced by the valvular affection. When that affec- tion is mitral or mitral aortic, the right ventricle shares the labor and the enlarge- ment with the left ventricle; when the aortic valve is alone affected, the left ven- tricle is often alone enlarged; and when there is mitral obstruction, the enlarge- ment may mainly affect the two auricles, that of the ventricles being somewhat moderate. The ventricles, when the pericardium is adherent, tend to enlarge outwards in every direction, and especially upwards to the manubrium, as well as downwards, into the epigastric space, to the right, and to the left. The great arteries are lifted up on the top of the ventricles into an unusually high position, and are crowded into the narrowed space at the top of the chest, almost as high as the root of the neck. When the adhesions are dense, strong, and contracted, they sheathe the whole heart in a tight, tough envelope, which grasps the auricles and ventricle, prevents their free expansion, and forcibly lessens the organ. Physical Signs of Adherent Pericardium. Clinical History. (A) From a succession of Observers.-Dr. Burns, in 1809, gave cases to show that when the pericardium is adherent, pulsation is felt in the epi- gastrium-a sign that had been previously observed by Korner-caused, he says, by the repercussions of the heart affecting the liver, which is the immediate seat of vol. ii.-39 610 ADHERENT PERICARDIUM. the pulsation.1 He gives a case of adhe- rent pericardium in which Dr. Rutherford found a strong pulsation of the heart, ac- companied by a jarring motion, most re- markable at the contraction of the ven- tricles. Heim, according to Kreysig,2 observed that a hollow appeared under the ribs during each systole when the pericardium was adherent. Sander3 found, in a case of adherent pericardium with great enlargement of the heart, deepening of the space on the left side of the ensiform cartilage, followed quickly suddenly arrested. In the recital of four of his cases, to which his general account does little justice, he states that they pre- sented a second or diastolic shock or back- stroke. Dr. Williams,' in 1840, remarked that when the pericardium adheres both to the heart when enlarged, and to the walls of the chest, the heart pulsates in close con- tact with those walls; so that the pulsa- tions are felt very widely, extending up- wards as well as downwards, drawing in the intercostal spaces at each systole; and that respiration does not lessen the region of cardiac dulness on per- cussion, and of impulse. Dr. Law, in a communication that I have not been able to find, states that change of posture does not alter the position of the impulse. In my paper on the situation of the internal organs, I, in 1844,2 de- scribed four cases of adherent peri- cardium, and gave figures showing the position of the internal organs after death, two of which figures I reproduce here (see Figs. 95, 96). In one of these cases, a young wo- man, the heart was small in size, and presented during life no phy- sical sign of disease of the heart, but the pulse was very feeble ; she had palpitation, dyspnoea, and ana- sarca ; and her lips were blue. The heart was very large in the three remaining cases, two of which had mitral regurgitation, and the third had narrowing of the mitral, aortic, and tricuspid orifices. One of the two cases with mitral disease has been already described, and is figured at page 559. In the other case of the same class, the impulse was very strong and jogging ; shaking and heaving the whole chest. The apex protruded strongly ; the lowrer half of the sternum advanced firmly at the beginning of the systole, and fell back gradually and firmly during its continuance. The lower end of the ensiform cartilage receded during the systole ; the impulse was irregular, 140 to 160 (see figure 95). The remaining case with adherent peri- cardium presented physical signs that differed materially from those observed in the two other cases. The obstructed, mitral, and aortic apertures tested by the cone, each measured half an inch, and the tricuspid orifice three-quarters of an inch. The heart was very large, weighing thirty-two ounces ; and ah its cavities, and especially the ventricles, shared in the enlargement. The following were the Fig. 95. by a shock, perceptible to the hand ; ful- ness over the cardiac cartilages ; and ex- tensive impulse over the front of the chest. Corvisart4 noticed that in these cases respiration is high, and this he connects with the trouble of the whole heart caused by the laborious action of the diaphragm, to which it is attached by the adhesions. Dr. Hope,5 in 1839, observed that peri- cardial adhesions sometimes caused a prominence of the cardiac cartilages, sometimes an abrupt jogging motion of the heart, corresponding with the systole and the diastole, that with the diastole having the character of a receding motion 1 Burns, on the Diseases of the Heart, p. 62. 2 Kreysig, Die Krankheiten des Herzens, ii. 625. 3 Hufelunand Bibliothek d. p. Heilkunde, Bd. 51, 120. 4 Corvisart, Sur les Maladies du Coeur, p. 35. 5 Dr. Hope, on the Diseases of the Heart, p. 194. 1 Dr. Williams, on the Diseases of the Chest, p. 24. 2 Prov. Med. Trans. PHYSICAL SIGNS OF ADHERENT PERICARDIUM. 611 physical signs: "Strong protruding im- pulse at the apex between the sixth and seventh ribs. During the systole, the sternum and the left and right costal car- analyzed, and reports of three cases ob- served by himself. In the first case, a youth, there was dulness on percussion, equal in extent during inspiration and expiration, from the second left space to the ensiform cartilage, and from the middle of the sternum to the left nipple ; and fulness over the second space, which advanced during the systole and sank in during the diastole ; the third, fourth, and fifth spaces deepened with the systole and filled out with the diastole; the heart's impulse was feeble, and the apex-beat was imperceptible. The heart sounds were natural, but the second sound was split over the pul- monary artery. The pericardium was tied to the walls of the chest by filamentous bands, and was univer- sally adherent to the heart, which was natural in position; the right ventricle was enlarged, the right auricle was changed into a stiff crumbling tuberculous mass, and the conus arteriosus was widened, its walls being only a line in thickness. The second case, which passed through all its stages under Skoda's eye, a youth, was admitted with pericarditis. The friction sound, then loud and extensive, became feeble and limited to the apex on the 15th, and was lost on the 19th day. On the 37th day there was a systolic deep- ening of the third, fourth, and fifth spaces, and the apex-beat was imperceptible. A month later, when he left the hospital, during each systole, besides the indraw- ing of the spaces, there was indrawing of the lower half of the sternum, which sprang forward after the systole with a perceptible shock. He was admitted ten weeks later with pneumonia, when the heart-signs were unchanged, and he died fully six months after his first admission. The right ventricle was enlarged; the valves were healthy; the heart, which lay in the middle of the chest, was firmly adherent to the pericardium, which was, in turn, strongly glued to the walls of the chest by a tuberculous exudation. Skoda's third case was a man, with nar- rowing of the mitral orifice, ascites, and oedema. The region of cardiac dulness re- mained unchanged during inspiration and expiration. There was a considerable deepening of the fifth space during the systole, after which the hollow quickly disappeared, and a shock was perceived there at the beginning of the diastole. After his death, five months later, the pericardium and pleura were found to be universally adherent, and the right side of the heart was considerably enlarged. These cases, published by Skoda, form a valuable addition to the clinical history of adherent pericardium, for the true Fig. 96. tilages over the right ventricle became steadily depressed ; immediately after the systole they advanced with a shock."1 (See Fig. 96.) In the general description I thus defined the character of the impulse in the two classes of cases just given: "The ster- num, costal cartilages, and xiphoid carti- lage are heaved forward firmly and stead- ily at the beginning of the systole ; and during its continuance those parts fall back steadily and quickly, coinciding with the mode of systolic contraction of the right ventricle. In some cases the sternum and costal cartilages spring forward with a jerk during the diastole." M. Bouillaud,2 in 1846, described a sign by which he had been able to announce the existence of adherent pericardium in six or seven cases. It consisted in evi- dent retraction of the pericardial region ; the movements of the heart not being free, but embarrassed or curbed. He does not state during what period in the revolu- tion of the heart's action the depression of the pericardial region took place. Skoda,3 in 1852, published an important paper on the diagnosis of adherent peri- cardium, in which he gives a critical ac- count of most of the communications just 1 Loc. cit. p. 562. 2 Traits de Nosographie Medicate, i. 3 Zeitschrift der Gesellschaft der Aerzte zu Wien, 152, i. 306. 612 ADHERENT PERICARDIUM. points of diagnosis have here been clearly observed, stated, and confirmed ; and are given with force, and as the effects of the central cause, the doubly adherent peri- cardium. They do not, however, present any new points of diagnosis, for it will have been seen, in the previous narrative, that he has been anticipated by one or more authors in the observation of each diagnostic sign. Thus the systolic deep- ening of the intercostal spaces had been observed by Heim and Dr. Williams, the return shock over the previously retracted space by Sander, and the great extent of the cardiac space upwards, and the non- diminution of that space, by Dr. Williams and myself; while the retraction during the systole of the lower half of the ster- num, and its advance with a shock imme- diately after the systole, was observed by myself in the case already given. Great diagnostic value is to be attached to the principal points specially illustrated by Skoda's paper, namely: the systolic indrawing of the lower sternum or inter- costal spaces by the contraction of the adherent heart; and the diastolic shock or back-stroke that immediately follows, given bv the return elasticity of the chest- walls. Cejka,' in 1855, published four cases of adherent pericardium, three of which con- firm, with more or less precision, the points illustrated in Skoda's paper. In one of them, with contraction of the aortic orifice, there was systolic indrawing of the third, fourth, and fifth spaces, and so strong a blow was given by the return elasticity of the chest walls that it was like the impulse of the heart. In another instance, an old man with adherent peri- cardium, a chronic affection of the lungs, dilatation of the aorta, and thickening of the mitral valve, the fifth and sixth spaces were drawn inwards with each systole, and became quickly even with each dias- tole. The impulse was not perceptible, and there is no note of diastolic back- stroke. In the third patient, with aortic aneurism, the vaulting of the sixth left space, caused by the systole, gave place towards the end of th# case to a slight drawing inwards of the corresponding re- gion. Cejka's fourth case of adherent pericardium, also with aneurism of the aorta, presented no impulse and no appa- rent drawing inwards during the systole. Clinical History. (B) Cases observed in St. Mary's Hospital and at Nottingham.- 1. Cases examined after Death.-The peri- cardium was completely adherent in fifty- one, and partially so in nine of the cases free from Bright's disease, recorded after death in St. Mary's Hospital up to the year 1870. Besides these, seventeen of the cases with Bright's disease had uni- versally, and three of them had partially, adherent pericardium. Rheumatic pericarditis had evidently been the cause of the adhesions in more than one-half of the cases, since of those with complete adhesions, 29 in 51 that were free from Bright's disease, and 9 in 17 with Bright's disease, had valvular disease of the heart; while the valves were affected in 7 out of 8 of those with partial adhesions that were free from Bright's disease, and the three cases of that class with that affection. General adhesion of the pericardium was rarely associated with disease of the aortic valve (2 in 32), and with mitral ob- struction (1 in 21), in cases free from Bright's disease, while that affection was very frequent in such cases with mitral and mitral-aortic valve disease (13 in 33 of the former and 11 in 31 of the latter affection). Adherent pericardium was present in one case with disease of the tri- cuspid valve. Partial adhesions of the pericardium were noted in one case with aortic regurgitation, in two with mitral obstruction, in none with mitral, and in two with mitral-aortic regurgitation, with- out Bright's disease; since the aortic valve was affected in 1 in 4 of the cases, while only two had mitral and two had mitral-aortic disease. Among the cases of complete (17) and partial (3) adhesions with Bright's disease, 4 (in 21) had aortic valve-disease, 5 (in 29) had mitral and 2 (in 20) had mitral-aortic valvular disease, and 1 (in 9) had mitral contraction. Aneurism of the ascending aorta was the evident cause of adherent pericardium in three instances (3 in 25), and cancer of the heart in one (1 in 10). * There was no other affection of the heart or aorta, excepting enlargement of the organ itself, in more than one-third of the cases with complete adhesions (19 in 52). The adhesions were not accompanied by any other affection in less than one- half of these cases (7 in 19), and they were complicated in more than one-half of them with pyaemia (in 2), apoplexy (in 1), pneu- monia (in 3), empyema (in 2), phthisis (in 3), or peritonitis (in 1). All those affections, excepting the last two, were acute ; and they could not, therefore, have given rise to the adhesions. Phthisis, and especially empyema, which is so often associated with phthisis, may, owing to the duration of those diseases, have in- duced first pericarditis and then adhe- sions. Notwithstanding this, the whole of those cases may be taken into account when considering the effect of pericardial adhesions on the size of the heart, for none of them by themselves cause enlarge- ment of that organ, excepting pneumonia, and, less often, phthisis, both of which 1 Vierteljahrschriftfurdiepraktische Heil- kund, 1855, 128. PHYSICAL SIGNS OF ADHERENT PERICARDIUM. 613 affections tend to increase the right ven- tricle in size. The heart was enlarged, its valves being thickened but competent in one instance, in fully two-thirds of the cases with ad- herent pericardium that were free from any other cardiac disease, and in which the size of the heart is mentioned (11 in 16); it was rather large in three of them ; and in only two instances was the heart of its natural size. We may however, I think, estimate that in one-third of these cases the adhesions did not cause an in- crease in the size of the heart. These results do not differ materially from those arrived at by Dr. Kennedy,1 who found that in 90 cases of adherent pericardium in which valvular disease was not present, the heart was of natural size-" healthy" -in 34, or fully one-third, hypertrophied in 51, or three-fifths-being dilated also in 26-and atrophied in 5. It is proved that pericardial adhesions do not necessarily cause enlargement of the heart. I saw four cases in Notting- ham in which the heart was of natural size and one in which it was lessened; Dr. Gairdner2 gives brief notes of ten cases in which the heart was not morbid, and by inference was not affected in size ; and Dr. Stokes' informs us that Professor Smith found that general adhesions of the pericardium correspond with atrophy or with hypertrophy of the heart in nearly equal proportions. We may, I think, safely conclude from what has gone before that adherent peri- cardium may, and often does, exist with- out influencing the size or healthy func- tion of the heart; that in a few rare instances it may induce atrophy of that organ; and that in nearly two-thirds of the cases it tends to cause an increase in the size of the heart, both as regards the thickness of its walls and the capacity of its cavities. We have just seen that the heart was enlarged in the majority of the cases of adherent pericardium that were free from any other affection of the heart itself. When we take this into account it is natu- ral to expect that the heart should be more enlarged in cases with valvular dis- ease when they are affected with adherent pericardium than when they are not so ; and the analysis of the cases of this class that were recorded at St. Mary's Hospital by taking a simple average of the weights of the hearts with valvular disease, with or without pericardial adhesions, gives some support to this anticipation, as will be seen by the examination of the follow- ing summary of the average weight of the heart in those cases. Average weight of the heart in cases of valvular disease with and without adherent pericardium. The cases were not affected with Bright's disease except where speci- fied. Mitral regurgitation, pericardium adherent (4) . average weight, 21 ounces. Ditto, pericardium not adherent (14) . . " " 16'6 " Ditto, with Bright's disease, pericardium adherent (3) . " " 25 " Ditto, pericardium not adherent (19) . . . *' " I()'4 " Mitral obstruction, pericardium adherent (1) . . " " 21 " Ditto, pericardium not adherent (14) . . " " 14 " Aortic regurgitation, pericardium adherent (2) . " " 26'7 " Ditto, pericardium not adherent (23) . . " " 22 " Mitral-aortic regurgitation, pericardium adherent (6) " " 26*3 " Ditto, pericardium not adherent (12) . . " " 22 " Total of combined valvular diseases, without Bright's disease, pericardium adherent (13) . . . " " 23*3 " Total of combined valvular diseases, without Bright's disease, pericardium not adherent (63) . . " " 19 " This method is far from doing scientific justice to the question before us ; for cases of all ages, both sexes, and various de- grees of disease, are brought together under one common heading, although in reality many of these cases differ mate- rially from each other. Notwithstanding this, a rough and ready answer is given to us that is probably not far from the scientific truth. We find, then, that the average weight of the heart in the thirteen cases of valvular disease, with adherent pericardium, was 24$ ounces, while its weight in sixty-three cases of a like kind, in which the pericardium was not ad- herent, was 19 ounces, or 5| ounces less than the first series. It is to be kept in view that the pericardium was included with the heart in the first set of cases, and what its average weight may be under the varying circumstances I do not know. It may, however,! think, be concluded that in the cases of valvular disease of the heart the existence of adherent pericardium ten- ded to increase the size and weight of the heart, but not to a great extent. 1 Edinburgh Medical Journal, iii. 986. 2 Ibid. Feb. 1851. 3 Dr. Stokes, Diseases of the Heart. 614 ADHERENT PERICARDIUM. The size of the heart, as we have seen, has been usually described ; its weight being often given, in the cases with ad- herent pericardium observed in St. Mary's Hospital. The relative size of the differ- ent cavities of the heart has, however, only been described in 11 of these cases. I have, therefore, with a view to discover the influence that the presence of adherent pericardium may have on the size of the various cavities of the heart and the thick- ness of their walls, brought together 18 additional cases from various sources-or 29 in the whole-in which the general condition of the various cavities of the heart was described, and which are given in the following summary :- Cases with adherent pericardium in which the size of the different cavities of the heart was described :- 1.-Cases in which both ventricles were enlarged (hypertrophy and dilatation) 16 Of these, 6 were free from valvular or other heart disease (1 had Bright's disease); 10 had valvular disease (3 aortic, 2 mitral, 3 mitral-aortic, regurgitation, 2 mitral contraction). 2.-Cases in which the right ventricle was enlarged, the left being not so (in 1), or small (in 1), or not described (in 3) ...... 5 Of these, 3 were from valvular disease, 1 had mitral regurgitation, and 1 aneurism of the aortic sinuses. 3.-Cases in which the left ventricle was enlarged, the right being small (in 1), or not described (in 7) ......... 8 Of these, 3 had no valvular disease, 1 had aortic, and 3 mitral regurgitation, and 1 had aneurism of the apex of the left ventricle. Total .......... 29 There was valvular disease of the heart (15), or aneurism of the heart (1) or aorta (1) in 17 of these cases, and as those affec- tions exercise a definite influence of their own on the size of the cavities of the heart, they must be left out of view in considering the direct effect of adherent pericardium on those cavities. The same must be said of one instance with Bright's disease among the remaining 12 cases in which there was no valvular or other affection of the heart or aorta. Hyper- trophy and dilatation of both ventricles existed in 5 ; of the right ventricle in 3 ; and of the left ventricle in the remaining 3, of these 11 cases. From this it would appear that adherent pericardium, when it produces enlargement of the heart, tends to affect both ventricles to an equal but varying degree. 2. Physical signs observed during life in cases with adherent pericardium admitted into St. Mary's and the Nottingham Hos- pitals.-I have observed nine cases with adherent pericardium in St. Mary's Hos- pital, and have added one recorded there by Dr. Markham ; and have examined seven such cases at Nottingham, four of which I published in 1844, and have given briefly above. There was no valvular disease of the heart in three of these seventeen cases, while in the remaining fourteen, one or more of the valves was affected,mitral regurgitation being present in nine of them, mitral-aortic regurgita- tion in three, and mitral obstruction in two, of those cases. In one of the three cases in which the valves were healthy, in which case Bright's disease was present, the sounds of the heart were natural but weak, and the presence of impulse was not noted. In another of them, a man, with empyema and lardaceous disease of the kidney, the heart being only slightly enlarged, the impulse was at one time imperceptible, but afterwards, when it could scarcely be felt over the ribs, it was perceived over the ensiform cartilage. In these two cases, and in that of the same class al- ready alluded to at page 608, in which the heart was small, the presence of ad- herent pericardium could not, I think, have been discovered during life. The signs of the heart were not noticed in one of the cases in which adherent pericardium was associated with mitral regurgitation, an old man who presented various sonorous noises over the lungs. In one of two cases, both men, with mitral disease, observed at Nottingham, in which the heart was very greatly enlarged, the left ventricle was greatly hypertro- phied and dilated, the right being so to a minor degree ; and the impulse was feeble, the second sound, distinct over the ster- num, was scarcely audible at the apex, and the lungs were oedematous. In the other case, with hypertrophy of both ven- tricles, the impulse was inconsiderable, but was diffused over the whole left mam- mary region. The next case is an important one, re- ported by that careful and accurate ob- server, Dr. Markham, for it shows that the apex-beat may be strong, and far to the left, in some unusual cases of adher- ent pericardium. In this patient, a girl, the impulse was heaving and extensive, and was violent far to the left of the nip- PHYSICAL SIGNS OF ADHERENT PERICARDIUM. 615 pie line, and beneath the sixth rib. The second sound was very loud over the pul- monary artery, but was absent at the apex. M. Aran likewise describes a case of adherent pericardium, in which the apex-beat was present in the sixth space, three and a half inches from the sternum, and the systolic impulse was strong and progressive, and was not followed by a diastole impulse. Skoda takes exception to my observation that the apex protruded extensively to the left in two of my cases published in 1844, given briefly above at pp. 608, 609. We shall see that the apex- beat is usually feeble, and does not often extend far to the left in cases of adherent pericardium; but it was certainly other- wise in this case of Dr. Markham, in that of M. Aran, and, I would say, also in my two published cases. It appears to me that in this patient, and in the other cases just given, there was no sign character- istic of adherent pericardium. The next instance was too ill for care- ful physical examination, and presented a feature unusual in cases with pericardial adhesions. The healthy impulse was much more diffused than natural, being present in the epigastric space and four or five intercostal spaces, and the lower ribs retracted during the diastole, which is a rare occurrence. The apex-beat, which was felt in the fifth and sixth spaces, did not extend outwards so far as the nipple line. The two following instances present features that were sufficient to character- ize them during life as being affected with adherent pericardium. In the first of these cases, the left ventricle was hyper- trophied, the right ventricle was small, and both the auricles were very large. The apex-beat was seated in the sixth space, an inch to the left of the nipple line, and 5| inches from the sternum, and in spite of the great and extensive hyper- trophy of the left ventricle, was feeble. The second sound, which was heard over the right ventricle, was faint at the apex. There was, on the 54th day after admis- sion, a diffused impulse chiefly over the cardiac cartilages, extending down to the seventh costal cartilage, and to the ensi- form cartilage. The impulse advanced quickly and fell back suddenly during the systole, and was followed with a sharp sudden shock or jerk over the whole re- gion of the impulse. There was slight pulsation of the liver below the ensiform cartilage. Breathing was rather high, the movement being chiefly at the upper part of the chest, with retraction at its lower part. The other case, equally re- markable, and the last of the series with mitral incompetence, had points of close resemblance to the last, with points of marked difference. In this case the front of the heart adhered strongly to the inner surface of the sternum through the me- dium of the pericardium. The walls of the right ventricle and auricle were much hypertrophied, while the left ventricle was only somewhat thickened ; thus re- versing the conditions that were present in the former case. There was some ful- ness over the region of the heart. The impulse over the heart, and especially over the right ventricle, was very exten- sive, spreading from the third to the seventh cartilage; and from the right cartilages, across the sternum and ensi- form cartilage, to the sixth left space, an inch and a half beyond the nipple line. The impulse was peculiar, and told re- markably on the sternum, first heaving that bone forwards with sudden force, and then drawing it backwards with great strength. "The heart" (or rather the front of the chest) ' ' seemed to be dragged backwards during each systole. The apex-beat was feeble, low down, and far to the left, in the sixth space, an inch and a half beyond the nipple line. There was some pulsation of the liver in the epigas- tric region. The second sound was loud and plunging over the right ventricle, and feeble at the apex, where a mitral mur- mur was loud and extensive. After- wards the fulness over the heart, and the extent and force of the impulse lessened, but the beat of the heart retained its re- markable character, first advancing, and then fbrcibly retracting, during the sys- tole. Later still the apex-beat, which was very weak, extended only a very little beyond the nipple line. Notwith- standing this contraction of the region of the impulse, it extended from right to left over a width of six inches. A deep in- spiration caused a marked lowering of the upper and lower borders of the region of the impulse, in spite of its great extent. After a few days he became drowsy, felt tight in the chest, and died three weeks after his admission." It is to be re- marked that while in the previous case a diastolic shock or back-stroke followed the systolic retraction, which was pre- ceded by a systolic advance ; in this ease there is no note of back-stroke, though I cannot vouch for its absence ; but the sud- den systolic heave followed by a forcible systolic retraction of the sternum and car- tilages, as if those parts were dragged backwards by the heart clinging, as it were, to its buckler, pointed definitely to adherent pericardium as the cause of the chain of signs. The two cases of adherent pericadium with mitral-aortic incompetence present, like the last two cases, physical features that denote the presence of the adhesions, though not perhaps with the same em- phasis as the two first related. In the first case, a youth, the heart was of very great size, so as completely to cover the left lung. On his admission, three months 616 ADHERENT PERICARDIUM. before his death, the impulse was gradual, but ended abruptly with a shock; and extended from the third cartilage to the sixth, but scarcely beyond the nipple line ; there was also a marked general pulsation over the whole liver, both in front and at the right side. A month later the impulse had extended itself to the left, being diffused, and shaking the whole of that side of the chest, the apex- beat being an inch and a half to the left of the nipple line. Afterwards the im- pulse extended more to the right and was felt in the epigastrium, but its character- istic features are not again described. The other instance was a boy, and in him the heart, which was considerably enlarged, clung so close to the sternum and cartilages that it was found best to remove the viscera en masse from behind. There was fulness over the cardiac re- gion, and the beat of the heart, which was extensive, reaching down to an inch and a half below the sternum, and ex- tending thence to the seventh cartilage, was of a peculiar character, beginning with a diffused heaving impulse, which gave way to a sudden and sharp retrac- tion. He always said, after this exami- nation, that he felt better, though he really was not so, and eight days later he died. The two remaining cases with adherent pericardium had mitral contraction. In one of them, a young woman, the heart was very large; the impulse extended from the second space to the seventh cos- tal cartilage and the ensiform cartilage, and, even when she lay on the left side, the apex beat was feeble. As in the last case, there was strong pulsation over the whole liver, extending from the front to the back. The remaining case with ad- herent pericardium and mitral contrac- tion was observed by me in Nottingham in 1835, and although it presents no signs characteristic of the adhesions, is perhaps of interest, as being, so far as I know, the earliest case in which the so-called pre- systolic murmur was described. The size of the heart is not given, but there was no hypertrophy of either ventricle. The mitral opening was half an inch in di- ameter. A thrill, extending over a large space, was communicated to the hand when applied over the apex, which was terminated by a jerk. A peculiar pur- ring sound was heard at the apex, the vibrations being longer and louder as the time progressed, the sound ending in a strong, loud, clear jerk, synchronous with the pulsation. The sound occupied two- fourths of the time, no other being audi- ble at the apex. Resume of the Physical Signs observed in Cases of Adherent Pericardium.- The steady retraction of the lower half of the sternum during the whole of the systole of the ventricles, and the sudden starting forwards of the lower half of the sternum at the beginning of the diastole with a return shock or blow, was observed in iny own case, published in 1844, and in one of Skoda's given in 1852. The drawing inwards of the cardiac intercostal spaces during the systole was first observed by Heim, and afterwards by Dr. Williams, by Skoda in three cases, and by Cejka in three more. This sign, which is sometimes present in other cases renders the existence of adherent pericardium probable, and espe- cially if this sign is still present when the patient draws a deep breath ; but if it is followed by a diastolic shock the diagno- sis of that affection is certain. The ex- istence indeed of a diastolic back-stroke taken by itself pronounces that the heart is adherent. This sign, which generally gives the impression of a double impulse, was first noticed by Sander; afterwards by Dr. Hope in four cases of adherent pericardium ; in the two typical instances just given and described respectively by myself and by Skoda, who observed it in another instance ; by Cejka in one, and by myself in two others given above. A double movement of the systolic im- pulse, first forwards with a heaving motion, then backwards with a forcible retraction, was observed by myself in a case in the Nottingham Hospital, to the description of which Skoda takes excep- tion, and afterwards in three other cases in St. Mary's Hospital. The outward pressure, equal in every direction, of the blood contained in the ventricle during its contraction naturally forces forwards the walls of the chest in front of it at the beginning of the systole. During the continuance of the systole, the adherent sternum resists the contraction of the heart, but in the struggle the bone yields, and is drawn forcibly inwards by the active ventricle. The non-diminution of the region of pericardial dulness and of the impulse was observed by Dr. Williams ; and the absence of change in the position of these signs when the patient lay on the left side was noticed by Dr. Law. The non-diminution of the area of peri- cardial dulness and impulse is undoubt- edly a valuable sign of adherent pericar- dium ; in one of my cases, however, the impulse below was unusually strong at the end of expiration, and in another of them the upper and lower borders of the im- pulse palpably descended during a deep inspiration. This is indeed different from the diminution of the extent of dulness and impulse, and, what is still more im- portant, from the bodily transfer during a deep breath of the seat of the dulness and impulse from the cardiac cartilages and the first space near the nipple, to the epi- PHYSICAL SIGNS OF ADHERENT PERICARDIUM. 617 gastric region, including the ensiform cartilage and the adjoining seventh costal cartilage. One of my cases illustrates in its own manner the other point just referred to-the non-shifting of the seat of the impulse when the patient turns on the left side. In that case, when the patient lay on the left side, the apex-beat, which was an inch and a half to the left of the nipple line, and in the sixth space, was very feeble. This is very different from the great transfer of the position of the apex-beat from the fifth space, a little lower than the nipple, and within the mammary line, to the sixth or seventh space, two inches to the left of that line, which was observed to be the case in several patients, in whom the chest was healthy, by Dr. Humphreys, Dr. Coup- land, and myself, in the Middlesex Hos- pital. These, so far as I know, are the only signs that are characteristic of adherent pericardium ; but there are certain other signs that, without ranking in precision with those just named, have their signi- ficance. The drawing inwards during the sys- tole of the space between the ensiform cartilage and the seventh costal cartilage, was noticed by Sander in a case of adhe- rent pericardium; and in another case, I observed that the tip of the ensiform car- tilage was retracted during the contrac- tion of the ventricle. There was pulsation of the liver in four of my cases, which was limited to the epi- gastric space in two of them, but in the two others extended over the whole organ, in front, at the side, and in one even be- hind. Burns considered that the impulse so often present in the epigastric space in cases of adherent pericardium is due not immediately to the heart itself, but to the pulsation of the liver. It is evident, from the brief recital of the cases that has just been given, that a great variation in the extent, force, char- acter, and position of the impulse exists in cases of adherent pericardium. The impulse was imperceptible in one of Cejka's, and at an early period in one of my own cases of adherent pericardium ; and it was feeble in one of Skoda's and two of my own cases; it was heaving during the systole and very extensive in one of Dr. Markham's cases, and in one of my own ; it was tumultuous and very irregular in one of my cases ; it was strong and very greatly extended, both upwards to the second space, and downwards to the epigastric space and the seventh car- tilage, and to the right and left, across the chest, from a full inch to the right of the lower half of the sternum, to a full inch to the left of the nipple line in the sixth space, in cases observed by Dr. Hope, Dr. Markham, and myself; and in two of Dr. Hope's cases the violent action of the heart was observed over the whole front of the chest. The apex-beat is, as a rule, feeble, even when it extends from an inch to an inch and a half to the left of the nipple line, being felt in the sixth space. Sometimes indeed, as in one of Skoda's cases, it is imperceptible ; and at others it is situated, even when there is general enlargement with hypertrophy of the ventricles, to the right of the nipple line, as occurred in one of M. Aran's cases in which the apex- beat was in the fifth space, two and a half inches from the sternum; and in two of the cases given by Dr. Gairdner, who points to this restraint of the apex as a probable element in the diagnosis of adhe- rent pericardium.. There are, however, important excep- tions to the rule that the apex-beat is usually restrained in its action and some- times in its position by adherent pericar- dium, for in two cases published by me in 1844, the apex-beat was far to the left and low down, strong, gradual, and pro- truding ; and as we have seen, the apex- beat presented the same condition in Dr. Markham's, and to a less degree in M. Aran's important cases. The impulse was found in the epigas- trium in Mr. Burn's cases, in two of Dr. Hope's, and in four of my own. M. Aran, in 1844, gave the extinction of the second sound as the unique sign of adherent pericardium, on the strength of the absence or great feebleness of that sound in those cases reported by him. He does not distinguish between the sec- ond sound over the pulmonary artery and right ventricle, and that over the left ven- tricle. Dr. Markham describes the sec- ond sound as being, in his case with mitral incompetence, very loud, heard like a beat, over the pulmonary artery, while there was no second sound over the apex. In one at least of my cases ob- served at Nottingham the second sound was loud or natural over the right ven- tricle, while it was indistinct and dull at the apex, and in two of the cases given above the second sound, loud over the pulmonary artery and right ventricle, was feeble at the apex of the heart. The last physical sign that I shall con- sider is the movement of respiration in relation to adherent pericardium. In two cases of adherent pericardium ob- served by myself in Nottingham, the in- spiratory movement of the abdomen at its centre was equal to that at its sides: although in health, the central move- ments are from two to three times as great as the lateral movements of the abdomen. At the same time in both 618 ENDOCARDITIS. those cases the lower half of the sternum fell inwards, or was drawn backwards, and the left ribs, from the fourth to the sixth, either retracted or were stationary, or had much less movement during inspi- ration, than the corresponding right ribs. The retraction of the sternum was caused by the forcible displacement downwards of the central tendon of the diaphragm, where it forms the floor of the pericar- dium ; and as under these circumstances the lungs could not interpose themselves between the heart and the sternum, that bone was partly forced backwards by atmospheric pressure and partly dragged backwards by the adherent heart, when drawn somewhat downwards by the dia- phragm. ENDOCARDITIS. By Francis Sibson, M.D., F.R.S. Endocarditis, to a greater extent even than pericarditis, is chiefly associ- ated witli acute rheumatism. The extent to which this is the case will be seen by the study of the accompanying table at page 621, from which it may be seen that endocarditis without pericarditis was es- tablished in one-third of the cases, or in 107 out of a total number of 325. If to these we add those cases with pericarditis that were also affected with endocarditis, amounting to 54, we find that endocarditis attacked one-half of the cases of acute rheumatism, or 161 in 325. In addition to these cases, in which the presence of endocarditis was rendered certain by the character of the signs and symptoms ob- served during the attack, there was a con- siderable proportion of the cases, amount- ing to one-fourth of the whole (76 in 325), in which endocarditis was either threat- ened (in 63) or very probable (in 13). Endocarditis is not, however, limited to acute rheumatism, being also present in a considerable proportion of cases affected with chorea, and in a small but uncertain number of those with pyaemia and Bright's disease. Cases, also, of estab- lished valvular disease of the heart are subject to intermitting attacks of endocar- ditis affecting the diseased valves. I shall, in this article, (1) first give a brief account of the anatomical appear- ances that present themselves after death in endocarditis, and then (2) a clinical history of rheumatic endocarditis, as it presented itself in the cases with acute rheumatism under my care in St. Mary's Hospital, during the years 1851 to 1869-70; those cases being divided into two series, an earlier series from 1851 to 1866, and a later series, treated by means of rest, from 1867 to 1869-70. I.-The Anatomical Appearances Observed in Cases of Endocar- ditis. The anatomical appearances found af- ter death in cases of endocarditis have been well described from actual observa- tion in the excellent and readily available works of Rokitansky,1 Hasse,2 and Rind- fleisch,3 which have been well translated ; and in the original and interesting lec- tures of Dr. Moxon4 and manual of Dr. Payne.5 The inflammation of the interior of the heart is as a rule limited to the left ven- tricle, this being evidently due to the great labor to which that ventricle is sub- jected when it drives the blood into the arteries of the system, and to the com- paratively slight effort with which the right ventricle sends its blood through the vessels of the lungs. In the foetal state, the right side of the heart, which is then the most powerful side, and has the greatest amount of work to do, is subject to endocarditis, judging by the frequency with which the pulmonary valves are ad- herent, so as to contract the orifice of the pulmonary artery. Dr. Norman Cheevers finds that sixty such cases have been ob- served by various authors. The mitral 1 Rokitansky, Pathological Anatomy, Syd. Soc. iv. 175. 2 Hasse, Pathological Anatomy, Syd. Soc. 124. 3 Rindfleisch, Pathological Histology, New Syd. Soc. i. 279. 4 Dr. Wilks and Dr. Moxon, Pathological Anatomy, 125. 5 Dr. Jones, Dr. Sieveking, and Dr. Payne, Pathological Anatomy, 384. ANATOMICAL APPEARANCES IN ENDOCARDITIS. 619 and aortic valves are the chosen seat of endocarditis, and especially the mitral valve. It is not, however, the whole of either valve that is the immediate seat of the inflammation; which, as a rule, is limited to the lines and surfaces of con- tact of the valves, close to the edges of their flaps where they come together and press against each other so as to close their respective apertures. The aortic valve is shut by the blood quietly filling the sinuses towards and at the end of the systole and during the diastole. The blood, when the sinuses are filled, presses the sides of the flaps against each other with a diffused and equal but firm pres- sure. This pressure is made on the first closure of the valve at the end of the sys- tole, by the blood filling the sinuses ; but this pressure is suddenly reinforced by the back-stroke or return wave of blood, caused by the recoil of the distended aorta and arteries, which propels the blood equally in every direction, forwards and sideways, as well as backwards with a return stroke, which beats on the aortic valve sinuses, and the ascending aorta, and which causes the second sound, which follows the closure of the valve by the tenth of a revolution of the heart's action. Afterwards the pressure of the aortic flaps upon each other is kept up during the diastole by the pressure of the blood, due to the steady contraction of the coats of the aorta and its branches. The pres- sure upon the aortic flaps bears, not upon their exact margins, but upon their sur- faces of contact, a little within those margins, and upon the sesamoid bodies ; and the endocarditis affects, not the exact margins of the flaps, but their surfaces of contact. The mitral valve is shut on exactly the same principle as the aortic valve, by the pressure of the blood driven during the systole into the small open cells on the under or ventricular surface of the valve, in the manner described and figured at page 392. The force with which the blood presses upon the closed mitral valve, owing to the contraction of the ventricle, is much greater than the force with which the blood presses upon the aortic valve, owing to the recoil of the previously dis- tended walls of the aorta. The flaps of that valve are pressed together by the backward portion only of the effect of the recoil of the aorta walls, which expands itself in every direction ; and that force of recoil is itself but a portion of the original propulsive force of the left ventricle, which presses with its full power upon the closed mitral valve. The surfaces or lines of contact and closure of the mitral valve ex- tend along and just within the borders of its two flaps. This border of contact is not a mere edge, but a surface or line of adaptation, made up of the small bead- shaped cells, that dove-tail into each other along the margins of the flaps; those flaps being held in their place by the simultaneous contraction of the papillary muscles, acting on their tendinous cords ; the result is that the margins of contact of the mitral flaps press against each other when the valve is shut with much greater tension, force, and concentration, than the margins of contact of the aortic valve; under the triple agency of a finer margin of contact, greater pressure of blood, and the muscular force and tendinous traction proper to the valve. The mitral valve, which is situated in the muscular centre of the ventricle and in the focus of its in- ternal inflammation, is more immediately and frequently subjected to endocarditis than the aortic valve, which has broader surfaces of contact, less pressure of blood, and no muscular and tendinous traction. Endocarditis, as I have said, does not therefore attack the very rim of the flaps of the mitral valve at the attachment of their outspreading tendinous cords, but the line or margin of contact just within the edges of the valves. When the mitral valve is inflamed, a frill of small bead-like granulations lines the whole proper bor- der of contact and closure of the valve ; and tends to prevent their perfect adapta- tion, and to cause regurgitation through the valvular aperture when the ventricle contracts. These prominences consist of a swelling and granular disintegration of the connective tissue, with softening of the intercellular structure. Each of these prominences is covered by a cap of fibrin deposited from the blood" in the manner well represented by Rindfleisch.' Endo- carditis affects the surfaces of contact of the aortic valve in the same way that it alfects those of the mitral valve. This is the usual manner in which endocarditis affects the mitral and aortic valves, whether the parent affection, ren- dering those parts prone to inflammation, be acute rheumatism, chorea, or pyaemia. Sometimes, however, the inflammation deepens at its original seat on the surfaces of contact of the mitral valve, and extends beyond those surfaces, so as to affect a large portion of the flaps of the valve on their ventricular surface. Under these circumstances, the inflamed, softened, and thickened structures may undergo granular degeneration, and its ventricular layer may become broken or ulcerated. The auricular layer of the valve thus tends to yield before the pressure of the blood, which forces its way through the breach in the ventricular layer, and to form pouches or aneurisms protruding into the left auricle. The auricular byer may then be involved in the inflam- mation, and become in turn subjected to 1 Loe. cit. p. 281, fig. 87. 620 ENDOCARDITIS. granular disintegration and breaking up of tissue, so that the llap of the valve may become perforated. The fibrin of the blood deposits itself everywhere on the inflamed surfaces, often in the form of vegetations, which may become exten- sive ; and thus the fibrin often lines, closes, and conceals the perforation. We have already seen how many points in its favor, as regards its tendency to endocarditis, the aortic valve presents over the mitral; and it presents another in this respect-that while the pressure of the blood bears directly upon the in- flamed surface of contact of the mitral valve during its closure at the time of the systole, the pressure of the blood does not bear upon the inflamed ventricular sur- face of contact of the aortic valve when it is closed at the time of the ventricular diastole, but upon the uninflamed upper or aortic surface of the valve. Although this condition, favorable to the aortic valve, exists, I have seen preparations in which a small aneurism, or aneurisms, of one or more of the flaps of the aortic valve protruded downwards into the ventricle. The advantages are not, however, en- tirely on the side of the aortic valve when it is affected with endocarditis; for a serious counterbalancing disadvantage exists under such circumstances, as I shall now mention. The sesamoid body, and the margin or surface of contact of the valve on each side of the sesamoid body, which are the seat of endocarditis when it affects the aortic valve, receive the di- rect pressure of the column of blood in the aorta ; and those parts, which are softened by the inflammation, tend therefore to be pushed downwards towards the ventricle during the ventricular diastole ; with the effect of sometimes producing retrover- sion of the sesamoid body, and to a greater or less extent of the softened flap, of which it is the centre. We here see the great disadvantage in which the inflamed aortic valve is placed from the want of tendinous cords and papillary muscles to support its flaps when rendered soft and yielding by endocarditis. Another special evil accruing to the aortic valve from a similar class of cause, is the tendency of the sesamoid body, and the adjoining portion of the flap affected with endocarditis, to lay hold of deposits of fibrin from the regurgitating stream of blood, with the effect of establishing a chain of fibrinous vegetations, which form one upon another, and which hang pend- ant into the left ventricle, being forced in that direction by the return current of blood. When this chain of fibrinous con- cretions forms upon either the right or the left posterior flap of the valve, it is driven downwards and backwards by the stream of regurgitation, so as to beat against and rest upon the anterior flap of the mitral valve, with the effect of causing ulcerative endocarditis of that flap. As the blood regurgitating from the aorta into the ventricle beats upon that flap, it parts with its fibrin which clings to the inflamed surfaces of the mitral valve, and forms on these a second chain of fibrinous concretions. The flaps of the mitral valve are, as we have seen, the principal seat of endocar- ditis, but inflammation may also attack the papillary muscles, and especially where they are brought into contact with each other towards the end of the systole, and cause fibroid degeneration of those muscles. The tendinous cords may also sometimes become inflamed, softened, and disintegrated, when the grave result of rupture of the cord may ensue. I have just given a series of notable in- stances of the occurrence of endocarditis, locally excited by the contact with each other of the two opposing surfaces of the valve ; of two adjoining papillary mus- cles ; and of a pendant chain of fibrinous concretion beating against the anterior flap of the mitral valve. These are not the only parts of the interior of the heart that may be inflamed from this cause, for wherever two surfaces of the endocar- dium come into contact with and rub against each other, endocarditis may be excited in both of those surfaces. The influence of the labor of the left ventricle and the mutual contact of its internal surface in tending to produce endocar- ditis is illustrated in an original and able manner by Dr. Moxon. I would refer to his work and to the others already named for the study of the various effects of endo- carditis. Among the effects of endocarditis, I would here simply name the formation of vegetations on the inflamed valves, already in part illustrated ; the produc- tion of embolism by the washing away from the vegetations of fibrin into the current of the blood ; the ulceration of the surface of the endocardium; the establishment of valvular disease from the thickening and enlargement of the valves; the contraction, adhesion, or re- troversion, and perforation of their flaps ; the rupture of the tendinous cords ; the formation of aneurisms of the valves; the fibroid and atheromatous degenera- tion of the fibrous and muscular struc- tures of the ventricle ; the production of aneurisms of the heart; ami other effects that will be found described in the works to which I have referred. II.-CLINICAL HISTORY OR RHEU- MATIC ENDOCARDITIS. The accompanying analytical tables of 325 cases of acute rheumatism under my TABLE SHOWING CONDITION OF CASES OF ACUTE RHEUMATISM. 621 care in St. Mary's Hospital during the years 1851-66, show the proportion in which those cases were free from endocar- ditis, and were threatened with or at- tacked by that affection ; and the number that were attacked by pericarditis, dis- tinguishing those with established endo- carditis ; also those in which endocarditis was doubtful, and those in which it was absent. The analyses contained in the tables sufficiently indicate the reasons for ar- ranging the cases in the manner adopted. TABLE SHOWING THE CONDITION OF THE CASES OF ACUTE RHEUMATISM, WITH ESPECIAL RELATION TO THE ABSENCE OR PRESENCE OF ENDOCARDITIS. I.-Cases of Acute Rheumatism in which there was no Endocarditis. Affection of joints somewhat severe or moderate, no general illness, no palpitation, signs over heart not named . . .......... 2 Joint affection slight, some general illness, heart not named ...... 13 Joint affection not, or scarcely severe, some or little general illness, heart sounds healthy 10 Joint affection not, or somewhat severe, some or considerable general illness, heart not named ............... 5 Joint affection not severe, some or considerable general illness, heart sounds healthy . 10 Joint affection severe, some general illness, heart not named . . . . . .6 Joint affection somewhat severe, considerable general illness, heart sounds healthy, or loud and ringing ............. 7 Joint affection severe, some general illness, heart sounds healthy . . . . .11 No description of state of joints, or general illness, heart sounds feeble . . . . 1 Joint affection not, or rather severe, slight or no general illness, slight prolongation of first sound .............. 7 Joint affection rather severe, slight or no general illness, doubtful occasional obscure murmur . . ............. 1 Previous valve-disease, mitral regurgitation ......... 2 Death, delirium .............. 4 I.-Total 79 II.-Cases of Acute Rheumatism in which Endocarditis was threatened. Some general illness, pain over the cardiac region, heart not named .... 1 Great general illness, pain left side, or region of heart, signs of heart not named . . 2 Great general illness, pain left side, heart sounds healthy ...... 3 Great general illness, pleurisy, heart sounds healthy ....... 1 Great or considerable general illness, pain left side, or region of heart, heart sounds healthy ............... 8 Great general illness, delirium, pain left side ......... 1 Considerable general illness, first sound very loud ........ 3 Considerable general illness, doubling of first sound ....... 1 Considerable general illness, first sound or heart sounds feeble or indistinct ... 3 General illness, pain over region of heart or left side, first sound indistinct or muffled . 2 Blight general illness, prolonged first sound ......... 13 Great general illness, prolonged first sound ......... 3 Great general illness, lung affection, prolonged first sound ...... 4 General illness, pain in region of heart or chest, prolonged first sound . . . .10 Little general illness, faint or obscure murmur early or late in the attack . . . 5 Considerable general illness, obscure murmur after cessation of attack (endocarditis probable) . . . ........... 1 Previous valve disease, considerable general illness 2 II.-Total ......... G3 III.- Cases of Acute Rheumatism in which Endocarditis was probable. Great general illness, pulmonary apoplexy in 1, prolonged first sound (situation un- known), almost a murmur in 1, a pulmonic murmur in 1 . . . . .2 Great general illness, severe cough in 2, prolonged first sound at apex, almost a mitral murmur in 2, almost a tricuspid murmur in 1, a pulmonic murmur in 3 . . . 4 Great general illness, prolonged first sound at right ventricle, almost a tricuspid mur- mur, and a pulmonic murmur ........... 1 Slight general illness, tricuspid murmur, ending in prolonged first sound in 1 . .2 Slight general illness, previous or established mitral regurgitation murmur did not vary materially in 1, murmur became louder in 1 . . . . • • • • 2 Considerable general illness, previous or established mitral-aortic regurgitation, aortic murmur absent at first in 1, mitral murmur became musical in 1 . . . . 2 III.-Total 13 ENDOCARDITIS. 622 IV.-Cases of Acute Rheumatism in which Endocarditis was present without Pericarditis. Prolongation of first sound, almost a murmur, pain in heart 1, in chest 1, extreme general illness ............. 2 Tricuspid murmur, murmur absent on recovery ....... 7 Tricuspid murmur, murmur lessening on recovery ....... 6 Tricuspid murmur-Total . . . . . . . . . . - 13 Mitral murmur, murmur disappearing on recovery ....... 25 Mitral murmur, murmur lessening on recovery ....... 10 Mitral murmur, murmur established on recovery ....... 14 Inflammation of mitral valve, died, murmur in 1, no note of murmur in 1 . .2 Mitral endocarditis total, mitral murmur in 50, no note of murmur in 1 . - 51 Aortic murmur, murmur disappearing on recovery ....... 5 Aortic murmur, aortic regurgitation established on recovery ..... 5 Aortic murmur-Total ........... - 10 Mitral-aortic murmur, murmur disappearing on recovery ..... 3 Mitral-aortic murmur, mitral murmur established, aortic murmur disappearing . 2 Mitral-aortic murmur, mitral-aortic regurgitation established ..... 4 Mitral-aortic murmur-Total ......... - 9 Previous valvular disease, mitral regurgitation ....... 6 Previous valvular disease, mitral and tricuspid regurgitation ..... 3 Previous valvular disease, mitral regurgitation, adherent pericardium aortic regurgi- tation .............. 1 Previous valvular disease, aortic regurgitation ....... 3 Previous valvular disease, mitral-aortic regurgitation (tricuspid murmur 2) . .9 Previous valvular disease-Total . . . . . . . . . - 22 IV.-Total cases of Endocarditis ......... *107 F.-Cases of Acute Rheumatism with Endopericarditis. Heart Previously healthy, 46. Tricuspid murmur, 3 Mitral murmur, 36 Aortic murmur, 1 < Mitral-aortic murmur, 6 Murmur disappearing on recovery, 1 Murmur established on recovery, 2 ■ 3 Murmur disappearing on recovery, mitral 17, aortic 1, mitral aortic 1 H9 43 Murmur lessening on recovery, mitral, 8 Murmur established on recovery, mit- ral 11, mitral-aortic, 5 J 16 Total cases of endocarditis in which the heart was previously healthy . . 46 Cases of endocarditis with previous valvular disease, mitral 5, mitral-aortic 3. . 8 Total cases with endopericarditis .... .... 54 IV., V.-Total with endocarditis .... .... 161 VI.-Cases of Acute Rheumatism with Pericarditis; Enodcarditis being doubtful . . 3 VII.-Cases of Acute Rheumatism with Pericarditis in which there was no Endocarditis . 6 V., VI., VII. Cases of acute rheumatism with pericarditis.-Total . . 63 Grand total of cases of acute rheumatism ....... 325 * 108 cases of endocarditis appear in the tables at pages 475-476. I find that one of those cases has been accidentally enumerated twice over, a woman, aged 23. I have considered the cases of endocar- ditis according to the character of the valvular affection of the heart due to the inflammation of the interior of the ven- tricle, and have arranged these cases into those (I.) with an uncomplicated tricuspid murmur; (II.) with mitral regurgitation ; (III.) with aortic regurgitation, (1) not accompanied by a mitral murmur, and (2) accompanied by a mitral murmur ; (IV.) with prolongation of the first sound with- out a murmur; (V.) with endocarditis supervening upon previous valvular dis- ease. I.-Cases of Rheumatic Endocar- ditis with an Uncomplicated Tri- cuspid Murmur. In a moderate proportion of the cases ef rheumatic endocarditis under my care in St. Mary's Hospital during the fifteen years ending 18GG-amounting to 13 out of a total number of 107, or one in eight -there was a murmur over the right ven- tricle from regurgitation through the tri- cuspid valve, without a mitral murmur. In nearly all of these cases there was a greater or less amount of general illness, and in one-third of them (4) there was pain in the region of the heart. A tri- cuspid murmur was present also in 2 cases, in which endocarditis was probable, and in 2 that have been included, with a little doubt, among the cases of pericar- ditis. In the majority of these cases the mur- mur had disappeared when recovery was established ; and in the remainder the murmur was then diminishing in loud- ness, extent, and clearness. This tricuspid murmur is usually pres- RHEUMATIC ENDOCARDITIS WITH TRICUSPID MURMUR. 623 ent over the body of the heart, or, in other terms, over the right ventricle ; and ex- tends from the lower half of the sternum to a line a little within the left nipple, which line corresponds with the ventricular septum, and from the third to the sixth cardiac cartilage. The presence of this murmur in these cases over the right ven- tricle in the early stage of endocarditis, and that, too, when no other murmur pre- vails, naturally suggests to the mind at first sight that it is due to endocarditis affecting the right ventricle and the tri- cuspid valve. This inference is, however, forbidden by the following considerations (1) Endocarditis and disease the result of endocarditis of the tricuspid valve, are very rarely discovered on dissection in those who have died from rheumatic in- flammation of the interior of the heart, or from valvular disease, the effect of such inflammation. (2) The tricuspid murmur, when un- complicated with disease of the mitral valve: was not established in any of my cases, but had either ceased altogether, or was steadily declining on the recovery of the patient. (3) The tricuspid murmur was fre- quently associated with a mitral murmur, and less often with a mitral-aortic or an aortic murmur of recent origin. A tricuspid murmur was present over the right ventricle in one-half, or 27 in 50, of the cases with recent mitral murmur. In 7 of those 27 cases the presence of a tricuspid murmur was somewhat doubtful. In eight of those cases the mitral was pre- ceded by the tricuspid murmur, and in six of these the tricuspid murmur had ceased to be audible when the mitral came into play. In thirteen other cases both murmurs were present when they were first noticed, which was at the time of ad- mission, in fully one-half of those patients. The mitral murmur appeared before the tricuspid in five cases. The tricuspid murmur disappeared when the mitral murmur was still audible in two-thirds of the cases (16 in 27); both murmurs ceased at the same time in seven instances ; and in four the tricuspid murmur outlived the mitral. A tricuspid murmur was also present in one-third (3 in 10), of the cases of endocarditis with mitral disease of old standing. A tricuspid murmur was present in two or three of the eight cases of mitral-aortic, and in about four of the ten cases of aortic, regurgitation of recent origin ; and in two of the five cases with aortic, and none of the seven instances with mitral aortic valvular disease of old standing affected with endocarditis. (4) I have observed tricuspid regurgita- tion as a marked and lasting feature in a case of button-hole contraction of the mitral valve; in several instances in which the tissue of the lung was permanently condensed, owing to repeated attacks of bronchitis ; in patients affected with con- tracted granular kidney, in whom obstruc- tion of the pulmonary circulation, with enlargement of the right ventricle, had followed upon obstruction of the systemic circulation, with its attendant tension, dilatation, and thickening of the systemic arteries, and hypertrophy of the left ven- tricle. These circumstances point irresistibly to the conclusion that the tricuspid regur- gitation is usually due to the so-called " safety-valve" function of that valve, and not to endocarditis of the right side of the heart. In all these cases resistance to the flow of blood through the lungs has in- duced tension of the pulmonary artery, and distension of the right ventricle and auricle, with, as a result, incomplete closure of the tricuspid valve. The pent- up blood flows back through that aper- ture, and upon the veins of the system; with the effect of distending those veins, and of giving proportionate relief to the blood gathered up in excess in the pul- monary vessels. At each contraction of the right ventricle, indeed, instead of the whole of the blood flowing forwards into the over-charged pulmonary artery, a por- tion of it flows backwards into the right auricle, and veme cavse. Inflammation of the left side of the heart, even when there is no regurgitation through the mitral orifice, impedes the flow of blood from the lungs into that side of the heart; and the accumulation of the blood in the pulmonary vessels, thus caused, induces and is relieved by the tri- cuspid regurgitation. The tricuspid murmur was present on admission in two of the thirteen cases of endocarditis in which that murmur existed without mitral regurgitation. In nine of the remaining cases, the tricuspid mur- mur was not observed until from two to seven days after admission, and generally on the fourth or fifth day. In one case the murmur did not appear until the 26th day after admission. In nine of these instances the duration of the illness before their admission is stated. In one of them the murmur ap- peared on the 7th day ; in five, from the 10th to the 12th; and in two, from the 14th to the 16th day after the beginning of the attack of acute rheumatism; and we may therefore infer that the tricuspid murmur generally comes into play about the 10th or 12th' day of the primary at- tack. In four instances the murmur was pre- ceded by a prolonged first sound over the right ventricle, and in one by a very loud, and in another by a peculiar booming first sound. ENDOCARDITIS. 624 In five of the cases there was direct evidence of endocarditis at the time of admission, in the shape of pain in the heart, and a prolonged first sound ; al- though the murmur did not pronounce itself fully until several days had elapsed. In two of them, indeed, the murmur did not appear until there was a marked im- provement in the general symptoms. The duration of the tricuspid murmur in these cases was very variable. In two instances it was only observed once, and in eleven it disappeared in from two to nineteen days ; in eight the murmur when last noticed had become much more fee- ble, and in three of these the first sound became prolonged at the apex, at the time that the tricuspid murmur was di- minishing. In three cases a pulmonic murmur, which indicates lessened tension of the pulmonary artery, appeared when the tricuspid murmur was lessening. From these observations we are enti- tled, I consider, to infer : 1. That the appearance of a tricuspid murmur over the body of the heart, extending from the sternum to the nipple, and limited to that region, which corresponds to the right ventricle, is usually the effect and the evidence of endocarditis affecting the left side of the heart. 2. That when this murmur is neither coupled with nor re- placed by a mitral murmur, we may safely foretell that when the inflammation leaves the heart, the valves will be per- fect and the organ free from disease. A tricuspid murmur, as I have already remarked, is often the prelude, and for a time the accompaniment, of mitral mur- mur in cases of rheumatic endocarditis. The latter murmur, however, in two- thirds of the cases (16 in 27) outlives the former, which is essentially a transient murmur. I have already given the pro- portion in which mitral regurgitation is accompanied, preceded, or followed by a tricuspid murmur (see p. 622). The duration of the tricuspid murmur in these cases, in which it was associated with a mitral murmur, though variable, was usually short. In ten instances it was only heard once, and that generally on the day of admission, but in one-half of these the existence of the murmur was doubtful; in six cases it was audible for from two to seven days, and in seven from nine to sixteen days ; while in three, after a short duration, it vanished and reap- peared after about twenty days, and in another case after a much longer period. The tricuspid murmur appeared much earlier in a large proportion of those cases in which it was associated with mitral re- gurgitation than in those in which it was the only murmur audible. The murmur was present at the time of admission, or on the second day-in two-thirds of the cases (19 in 27), in which there was both a tricuspid and a mitral murmur, and in only one-sixth (2 in 13) of those in which the tricuspid murmur was alone audible. This contrast between the two sets of cases is more striking if we date the murmur from the beginning of the attack. The tricuspid murmur appeared on or before the eighth day in at least nine cases in which there was both tricuspid and mitral regurgitation ; and in one only in nine of the cases in which the tricuspid murmur was alone audible. In one of the cases in which both murmurs were in full play on the day of admission, the patient had been ill only two days, in two others four days, and in three others a week. These cases of combined mitral and tricuspid regurgitation, in respect to the more rapid development of the murmur, and not in that respect only, present greater inten- sity, energy, and rapidity of inflammation in the left cavities of the heart, than in the cases in which the tricuspid murmur was alone audible. In almost all the cases of tricuspid incompetence there was at the time of admission great general ill- ness ; but this and other points of clinical interest must be reserved until mitral re- gurgitation is specially considered. In four of these cases the tricuspid murmur was replaced on its disappearance by a transient prolonged first sound over the right ventricle. The tricuspid regurgita- tion reappeared after being absent for a longer or shorter period in five of the pa- tients. In four of these the renewed tri- cuspid murmur was conjoined with mitral murmur, but in the remaining one it cropped up alone 47 days after it had dis- appeared, and 34 days after the cessation of the mitral murmur. The tricuspid murmur is easily recog- nized by its position and character. It is distributed over the right ventricle from the sternum to the nipple and from the 3d cartilage to the 6th. it usually stops at the septum, occasionally extends over the right auricle, to the right of the lower sternum, and is sometimes audible over the epigastrium below the lower boundary of the heart. The tricuspid murmur is usually grave or even vibrating in tone, and superficial, and it begins with an ac- cent or shock, and ends with the second sound. In cases of extensive mitral regurgita- tion without tricuspid murmur, the first sound is feeble while the second is inten- sified over the pulmonary artery, owing to the tension of that artery, the second sound being usually loud over the right ventricle, and sometimes even at the apex. When, however, mitral is coupled with tricuspid regurgitation, the blood is thrown back upon the right auricle and the venfe cavse, the tension of the pulmo- nary artery is relieved, and the first sound RHEUMATIC ENDOCARDITIS WITH TRICUSPID MURMUR. 625 over that artery is moderately loud, or prolonged, or even murmuring; and the second sound, though perhaps rather loud, ceases to be intensified. The mitral murmur is usually softer and less grave in tone than the tricuspid, being more like a bellows-sound ; it ap- pears also to be deeper ; and its point of greatest intensity is situated to the left of the nipple, and, in endocarditis, towards the axilla. When the mitral murmur is loud and vibrating, and especially if ac- companied by a thrill over the apex, per- ceptible to the finger, it is heard very ex- tensively, radiating in every direction. It then becomes audible over the right ventricle. This transmitted mitral mur- mur over that ventricle is readily distin- guished from the tricuspid murmur origin- ating within the right ventricle itself; for the transmitted or mitral murmur is accompanied and more or less masked by the normal first sound of the right ven- tricle ; while the immediate or tricuspid murmur, besides being grave and shal- low, begins with an accent, and is insep- arably incorporated with the first sound of the right ventricle. When the mitral and tricuspid mur- murs coexist, it is usually easy to distin- guish them from each other upon the principles just stated ; for the tricuspid murmur over the right ventricle is then palpably more superficial than the apex murmur, instead of being less so, as it is when the mitral is alone audible ; the first sound of the right ventricle does not mask or mu file the murmur ; and the difference in tone of the two murmurs is perceptible, the mitral being soft and smooth, the tri- cuspid grave or vibrating. Two cases were typical instances of this difference in tone of the two murmurs when thus coex- isting ; in one of them the mitral murmur was a soft bellows-sound. while the tri- cuspid murmur was grave ; and in the other the tricuspid murmur was harsh and grating, while the mitral was soft. When the mitral murmur is rasping and vibrating in character, the difficulty of distinguishing the presence of a conjoint tricuspid murmur is increased. An in- stance of this was presented by a patient in whom the apex murmur was short and rasping, while there was a bellows sound over the right ventricle. Here the rasp- ing mitral murmur might have become softened by its transmission through the ventricle. It is sometimes difficult to distinguish between a tricuspid murmur and a fric- tion sound, especially when the latter is murmur-like in character, as it frequently is at the beginning and towards the end of an attack of pericarditis. The chief points of distinction are-that the friction sound is usually double or to-and-fro in character ; the tricuspid murmur being single : the friction sound is not exactly rhythmical with the heart sounds, those sounds being readily heard distinct from the friction sound when that sound is not loud and grating, so as to extinguish every other noise ; the tricuspid murmur is incorporated with the heart sounds; the friction sounds starts off without a shock, and retains the same tone through- out ; the tricuspid murmur begins with an accent or shock. The pressure test usually clears up every doubt. When the stethoscope is applied over the right ven- tricle with increased force, the tricuspid murmur may be intensified, but is not materially changed in character; while the friction sound is usually both intensi- fied and changed in tone, it ceases to be murmuring, and becomes grazing, rub- bing, grating, or creaking in character. When pericarditis supervenes upon a tricuspid murmur, the pressure test is sometimes in the early stage almost essen- tial to the discovery of the friction sound; sometimes, however, the patient under these circumstances is so ill that you can- not make pressure. Local pain will then usually guide the treatment, and time will clear up the obscurity. In five of my cases, aortic regurgitation was accompanied by a tricuspid murmur; and in two of these by a mitral murmur also. Cases of endocarditis with aortic regur- gitation present obstruction to the flow of blood through the lungs, and so may cause tension of the pulmonary artery and tri- cuspid regurgitation; more, however, owing to tlie inflammation of the interior of the left cavities and the mitral valve itself, than to the aortic regurgitation, which is rarely sufficient in volume to in- duce congestion in the lungs. This is shown by the clinical fact that there were four instances with tricuspid murmur in the sixteen cases of endocarditis in which there was recent aortic regurgitation, in seven of which there was mitral regurgi- tation also; while there was no instance of tricuspid murmur in the fourteen cases of endocarditis in which there was aortic regurgitation owing to the previous dis- ease of the valve, in one-half of which cases there was mitral regurgitation also. A tricuspid murmur was present in three cases of endo-pericarditis; and in two of those cases the murmur was per- sistent ; while in one of them it disap- peared, after the recovery from acute rheumatism. I will give here the proportion in which a tricuspid murmur was present in cases of acute rheumatism with endocarditis under my care from October, 1866, to 1869, treated by means of rest. There were altogether 31 cases of endo- carditis in a total of 74 of acute rheuma- tism, and in none of those thirty-one cases VOL. II.-40 626 ENDOCARDITIS was one tricuspid murmur present with- out a mitral or other murmur. While the tricuspid murmur unaccom- panied by another murmur was absent in those cases ; although it was present in the proportion of one in eight of such pa- tients treated during the previous fifteen years; the proportion in which the con- joint tricuspid and mitral murmurs were present was fully maintained in the cases treated by rest. Mitral regurgitation was present without aortic regurgitation in twenty of those cases, and of these, tri- cuspid murmur was present in nine, or if we add two doubtful cases, in eleven in- stances. In none of these instances did the tri- cuspid murmur precede the mitral; in four the two murmurs appeared at the same time ; in four the mitral preceded the tricuspid murmur by from one to three days, and in one (45) by nine days. In three of these cases the mitral mur- mur outlived the tricuspid ; in two it was the reverse ; in three they were combined to the last, and in the remaining case the mitral murmur probably lasted beyond the tricuspid. The relation of prolongation of the first sound over the right ventricle to tricuspid murmur will be considered at pages 628, 639. IL-Cases of Rheumatic Endocar- ditis with a Mitral Murmur. The mitral and the tricuspid valves, while they correspond in general struc- ture and function, differ essentially in the construction and arrangement of their flaps and in the whole setting of the valve. The tricuspid valve, as I have already stated, is composed of three great flaps and several intervening small ones, which meet somewhere about the centre of the valve; and the aponeurotic ring which forms the base of those flaps is surrounded on all sides by muscular walls. (See figs. 47, 48, p. 385; and figs. 59, 60, 61, pp. 395, 396.) In health, when the ventricle is not over-distended, the flaps of the valves adapt themselves to each other perfectly, and close the tricuspid aperture com- pletely during the contraction of the ventricle. I When, however, the cavity is over- distended, as it is under the various cir- cumstances which I have already de- scribed, the flaps of the valve adapt themselves only partially to each other, especially, so far as I have observed, at the meeting-point of the three great flaps, and regurgitation ensues. The so-called "safety-valve" function of the valve is thus brought into play, with the effect of relieving the tension of the vessels of the lungs, and throwing the blood backwards upon the veins of the system. The result is that the tricuspid murmur is, with rare exceptions, not a sign of in- flammation of that valve, but of the over- distension of the right ventricle, caused by obstruction to the flow of blood through the lungs. The mitral valve is formed of one great semilunar or convex flap, the base of which is incorporated with the powerful aponeurotic structure that is continuous with the two posterior sinuses of the aorta ; and of a crescentic or horse-shoe flap, complex in structure, being formed of three segments, set in the muscular walls at the base of the left ventricle. The set- ting of the base of the valve is therefore two-thirds muscular and one-third apo- neurotic. There is no tendency in the aperture to widen outwards at the base of the valve equally in all directions, for the aponeurotic structure, when healthy, though elastic, is practically unyielding. The single anterior semilunar flap, held in check by its proper cords and fleshy columns, fills up the posterior crescentic flap with perfect adaptation. The edges of the opposed flaps press against each other with increasing force in proportion to the increasing pressure of the blood on their under surfaces ; and the over-disten- sion of the left cavity does not, owing to the structure to which I have alluded, readily tend to widen the orifice and open up the valve. The healthy mitral valve, therefore, when the left ventricle is not greatly enlarged, possesses only under circumstances of extreme backward pres- sure or forward resistance a function like the "safety-valve" function of regurgita- tion with which the tricuspid valve is endowed. Such a function of the mitral valve would indeed be the opposite of a " safety" valve function, for it would im- mediately endanger the lungs by throwing the blood backwards upon their vessels. (See figs. 47, 48, page 385 ; and figs. 52-58, pp. 391-393.) The result is that when the right ven- tricle is over-distended, it relieves itself backwards through the tricuspid aperture upon the veins of the system; and that when the left ventricle is over-distended, it, with rare exceptions, relieves itself directly forwards upon the arteries of the system, and so the lungs are spared in both instances. I derive the more important evidence of the correctness of this view from the well- understood pathological history of aortic regurgitation from widening of the orifice of the aorta, owing to atheroma of its walls. In those cases the cavity of the left ventricle becomes greatly, sometimes enormously, enlarged, and yet I know of RHEUMATIC ENDOCARDITIS WITH A MITRAL MURMUR. 627 comparatively few instances of this kind in which the mitral valve was therefore incompetent. Mitral regurgitation, without disease of the structure of the valves, occurs most frequently among cases in which there is great arterial tension owing to Bright's disease, and great consequent distension of the left ventricle ; in which cases there is often also an atheromatous, or thick- ened state of the mitral valve, with, as an effect, widening of the fibrous portion of that aperture, and possible regurgitation. Mitral murmur is, as a rule, neither a sign of over-distension of the left ven- tricle, nor of a supply of blood to that cavity too small in amount, or too thin in quality. The existence then of a mitral murmur in a first attack of acute rheumatism is a direct sign of inflammation affecting the left side of the heart. Mitral regurgitation, not connected with previous disease of the valve, and without aortic regurgitation, was present in 50 out of 107 cases of rheumatic endocarditis under my care in St. Mary's Hospital, from 1851 to 1866, and in 20 of 31 such cases treated by rest from 1866 to 1869. In twenty-five of the earlier series of cases the murmur had disappeared, and in ten others it was lessening at the time of the patient's recovery, while in fourteen of them the murmur seemed to be estab- lished ; and it was absent in one and present in the other of two fatal cases of mitral endocarditis at the time of death. In the cases of the later series the cor- responding numbers were thirteen, four, and three, the latter being the only cases in which the murmur was established at the time of the patient's recovery. In one-half of the cases of both sets the mitral murmur was heard on the day of admission or the next day ; the numbers being 28 in 50 of the first set, and 9 in 20 of the second set. The murmur pre- sented itself within six days of admission in three-fourths of the remainder, or seventeen of the earlier and nine of the later series, and from 8 to 17 days after admission in the remaining cases, amount- ing to one-seventh of the whole. Among the thirty-seven cases of endo- carditis, combining the two series, admit- ted with mitral murmur, one-third, or eleven, had been ill from 2 to 7 days, nearly one-half, or fifteen, from 8 to 14 days, six from 2 to 4 weeks, two for a longer time, and three for an unknown period. The mitral murmur became audible after admission in thirty-six cases, and of these the murmur appeared in six during the first 7 days, in eleven from 8 to 14 days, and in eight from 15 to 28 days after the beginning of the attack of acute rheu- matism ; in six at a later period ; and in three at a time unknown. The mitral murmur may be present in full force on the third day of the attack, or its appearance may be delayed until the fortieth day. In a fair proportion of the cases, amounting to one-fourth, it is developed during the first week, and in the larger number, or two-thirds, before the end of the second week. General illness. - In nearly every case of endocarditis the patient presents great or considerable general illness. Thus in sixty-two of the seventy-one cases of mitral endocarditis the illness was great or considerable, in two it was definite, and in five it was slight; while in two there is no description of the general state of the patient. In most of the few exceptions to this rule of the presence of great general ill- ness in these cases, the murmur was established at the time of their admission, and the severity of the attack was already mitigated or passing away. Those cases in which there was no endocarditis, present a very different as- pect, since in scarcely one-third of them was there considerable general illness. As might be expected, constitutional illness was more severe and frequent in those instances in which there was a threat of endocarditis, though its exist- ence was not actually demonstrated by valvular incompetence, since in nearly two-thirds of them the general illness was either great or considerable. The illness in cases of endocarditis is peculiar. It differs from and is super- added to that due to simple rheumatic inflammation of the joints, and is such as to call the attention of the physician to the state of the heart. The face may be flushed all over, the forehead, nose, lips and chin being of as high a color as the cheeks, a state that is usually associated with profuse perspira- tion, drops of sweat standing in beads on the surface-a condition, however, that may be present in cases with severe affec- tion of the joints without endocarditis. Thus when endocarditis exists the face loses the brightness, glow, and smooth- ness, and the variety of hue and tone of health, and becomes clouded, being dusky, dull, or ashy in hue, or glazed, or unduly white, or even of a bluish tint. The countenance, no longer expressive of interest in tilings and persons around, or even of pain in the limbs, is marked by internal trouble. The aspect of the pa- tient is altered, often profoundly so, being anxious, depressed, or indifferent. The eye loses its lustre and expression, and becomes heavy and dull. Sleep is often absent, the nights being restless; but this is perhaps more often due to the inflammation of the joints than to that of the interior of the heart. The nervous system is often gravely 628 ENDOCARDITIS. affected. Delirium at night, the patient wandering, muttering, and complaining, is occasional, but rare; it occurred in two instances, in which the affection of the heart was evidently the primary ex- citing cause of the mental trouble. In another patient the head was confused on the third day. Choreal movements, as we have seen, an1, in some instances a definite effect of endocarditis, especially of the non-rheu- matic kind, traceable frequently to cere- bral embolism; but choreal movements, and indeed embolism, were of very rare occurrence in my cases of rheumatic endo- carditis uncomplicated with pericarditis. In one instance the patient, previously anxious, and with sordes on his teeth, was nervous and fidgetty ; and in another, starting appeared on the 6th day, having been preceded on the 4th day by pain in the heart. Sickness is occasionally present. It was so in four of my cases. These cases, however, point not to the stomach as the cause of sickness, but rather and usually to the state of the nervous system, and more immediately to that of the brain it- self ; as in a case in which giddiness and sickness appeared together, and in an- other in which sickness was preceded by restlessness. Failure in the power of the heart is an occasional occurrence in cases of endo- carditis. Thus, two of my patients were attacked with fainting. One of these fainted on the day of admission, and again on the thirteenth, and on the fol- lowing day was sick, so that failure of the heart may be a cause of sickness. In the other case pain in the heart and fainting appeared on the seventeenth day after admission. We may fairly attribute the fainting in these cases to the actual fail- ure of the heart itself, caused by the in- ternal inflammation of that organ. The pulse is often quick, feeble, and fluctuating. I believe that it is dichrot- ous, but I have not employed the sphyg- mograph in any case of endocarditis, being perhaps deterred by the state of the wrist. Perspiration is often especially profuse and of long continuance ; sudamina being also present in some of the more severe cases. The breathing is usually affected, being more or less quickened. In rare instances pulmonary apoplexy or extravasation is the result of the difficulty to the flow of blood through the lungs, which is the general effect, varying in degree, of endo- carditis. The chain of symptoms here described points mainly to the affection of two great functions. The nervous power is lowered; and the circulation of the blood through the fine vessels of the lungs and the body is enfeebled. Pain in the Pegion of the Heart.-Pain in the region of the heart, sometimes severe and lasting, sometimes slight or transient, amounting perhaps only to uneasiness, was present in about one- fourth of the cases of tricuspid and of mitral murmur belonging to the earlier series, and in one-half of the later series, treated by rest. If to these we add other cases having mitral or tricuspid murmur in which there was pain in the left side, or in the chest; the proportion thus affected reaches to nearly one-half in the first se- ries, and to fully one-half in the second. The pain in the heart was sometimes, but not generally, severe. In a few in- stances the pain was increased or excited by pressure. We may fairly infer that in those cases pericarditis was imminent or was actually present, though not, except in rare instances, with such intensity as to cause even a transient friction sound. Palpitation was very rarely complained of, but fainting, as I have already stated, occurred in two instances. Prolongation of the First Sound occur- ring during the Early Period of Mitral Endocarditis.-In one-half of my patients affected with mitral regurgitation, as we have just seen, a murmur was established at the time of admission. In one-half of the cases in which the murmur was not thus established, prolongation of the first sound preceded, and was merged into, the murmur. In all but one of those cases the first sound was prolonged at the time of ad- mission, and in that case and twro others a tricuspid murmur was then in full play. The tricuspid murmur was likewise her- alded by prolongation of the first sound in one-half of the cases in which that murmur was not already present at the time of admission. In a number of the cases, the exact position of the prolongation of the first sound -was not defined; but wherever it was so, the mitral murmur was preceded by prolongation of the first sound at the apex ; and the tricuspid murmur by pro- longation of the first sound over the front of the heart, or the right ventricle. I think that no cardiac sign is more readily recognized than prolongation of the first sound, and yet there is none so difficult to define. That this is so, how- ever, is natural, for it is a transition sound. It forms, as we have just seen, the transition from a clear healthy first sound to a murmur ; and as we shall see, at a later period, in a large proportion of the cases, it forms a transition between a mitral or tricuspid murmur when dying out, and the restoration of the healthy first sound. In one-half of the cases in which the prolongation preceded the mur- mur, there was a double transition, the murmur being both preceded and followed by prolongation of the first sound. This RHEUMATIC ENDOCARDITIS WITH A MITRAL MURMUR. 629 prolongation is sometimes so like a mur- 1 mur that it is difficult to make the dis- tinction, and this is especially the case I just before the time of transition, when the prolongation precedes the murmur ; and just after that time, when it follows the murmur. Prolongation of the first sound is the absence of silence and the presence of a wavering, grave, feeble sound during the interval between the first and second sounds. It is not the prolongation of the shock of the first sound which is itself significant, being sometimes a precursor of the more telling signs of endocarditis. The prolongation of the first sound is not the same as the natural loud vibrating character of that sound over the super- ficial cardiac region which is almost always present in cases of anaemia, when the muscular force of the ventricles is maintained, and even in excess, but when the blood is scanty and thin, being de- ficient in red corpuscles. Prolongation of the first sound is, I re- peat, a feeble, indeterminate, wavering sound, that fills up the space between the first and second sounds, which space is silent in health. It presents every grada- tion, from a sound so feeble that it is with difficulty discovered, to a sound so mur- murlike that it can scarcely be distin- guished from the murmur into which it so often ripens. Prolongation of the first sound was noticed on the first day of ob- servation in fourteen cases ; the prolonga- tion developed into a murmur in two- thirds or nine of those cases before the seventh day after admission ; and in the remaining third, or five, between the seventh and fourteenth days. In two other instances the prolongation, absent on the day of admission, appeared on the following day, and in the other after a lapse of four days. It is evident that in all these cases the endocarditis was present before the ap- pearance of the murmur for a period of time at least as long as the previous period of duration of the prolongation of the first sound. There are other modifications of the first sound, besides its prolongation, that point to endocarditis, if they do not indi- cate it, which have been, in a few in- stances, the precursors of murmur. It will be sufficient if I simply name them. 1 They are-1. Loud heart sounds, the first being sharp, the second ringing ; or both sounds may be ringing. 2. Healthy sounds with powerful action of the heart. 3. ! Roughness of the first sound. 4. A hum- ming noise over the right ventricle, and in one case at the apex, where it was as- sociated with murmur. 5. Doubling of the first sound (over the ventricle), which occurred in two cases associated with a prolonged first sound, which was not fol- lowed by a murmur in one of those cases. 6. Feeble first, loud second sound, fol- lowed by tumultuous action of the heart and mitral and aortic murmurs. 7. Ex- tensive presystolic murmur (rrrp) present in one case for five days, followed in suc- cession by loud heart sounds (6th day), doubling of the second sound (15th day), and a faint mitral murmur, not limited to the apex. 8. Loud "plunging" first sound over both ventricles, present on the 4th day, followed by prolongation of the first sound on the 6th, and mitral murmur on the 8th; and 9, muffling of the first sound, which in one case suc- ceeded the murmur, which was extin- guished by an attack of pain in the heart, followed by fainting. All the above varieties in character of the first sound were, in the instances re- ferred to, followed within a very few days by a mitral murmur. The only one of these varieties of the first sound that I would speak of is the last: the peculiar "plunging" sound. I call it so for want of a better name. The sound is something like what I have heard in the working of a steam-engine. It was as if the piston made a peculiar plunging sound when it dipped down and reached the bottom of its play. I have heard this sound in at least three cases. One of them was attacked afterwards with delirium, long torpor, almost coma, extreme depression, and pericarditis, but no murmur. In all the cases, the con- stitutional symptoms more or less threat- ened endocarditis. Besides these peculiarities of the first sound preceding mitral murmur, there is one other affection of the sounds of the heart that I would name; and that is a complete silence of both sounds; which occurred in one case threatened with en- docarditis, in which a mitral murmur did not appear. In that case there was ten- derness over the heart, fighting for breath, a piercing pain between the chest and back, and great depression, lasting for some days. On the 8th day she looked more bright, on the 9th the sounds of the heart were audible, on the 14th its impulse had returned and was gaining power, and on the 26th day the sounds were of natu- ral loudness, and there was no murmur. In most of the cases of endocarditis with mitral murmur there is undue, but not great, strength of the impulse of the right ventricle, which may be seen and felt between the cardiac cartilages to the left of the lower sternum. This is found even in the earlier stages, and before the appearance of the mitral murmur. It is evident from what has just been stated, that while in some cases that mur- mur bursts into full play at the commence- ment of the attack, being audible on ad- mission, and on the 3d, 4th, 5th, 6th, or 630 ENDOCARDITIS. 7th days after the seizure; in others it is not audible until a period varying from the 8th to the 30th day, although there is unequivocal evidence that the inflamma- tion in the left side of the heart was pre- sent before and at the time of admission. This evidence consists in the existence of a tricuspid murmur, or a prolonged first sound, or pain in the region of the heart or in the chest, with great or considerable general illness. The inflammation of the valve cannot cause regurgitation until perfect adapta- tion is prevented by the formation of small prominences, covered with a deposit of fibrin upon the surfaces or lines of con- tact of the margins of the valve, or by the softening and yielding of its flaps. In three of the cases tricuspid or mitral murmur became audible after admission, when the patient's illness increased. In ten other cases, however, it was the re- verse, for in all of them the murmur came into play when the patient's health began to improve. We are therefore, I conceive, warranted in assuming that in a considerable num- ber of the cases, the active stage of the endocarditis is passing away at the time of the appearance of the murmur. Progress of Cases of Endocarditis with a Mitral Murmur.-Cases with a mitral mur- mur from endocarditis affecting a valve previously healthy, may usually be readily distinguished from those in which the murmur is due to established disease of the mitral valve by the character, seat, and area of the murmur, its changes, du- ration, and transition, its cessation or establishment; by the size of the heart and the force, extent, and position of its impulse; and by the nature of the first and second sounds over the right ventri- cle, the pulmonary artery, the aorta and great arteries in the neck. The mitral murmur is always situated over the apex and body of the left ventricle, and the ventricular septum. The centre of the murmur and its point of greatest intensity and purity is usually just below the left nipple. Sometimes it is limited to this point, but in general it covers a larger area, spreading inwards towards the right ventricle, outwards and upwards towards the axilla and over the lung, and down- wards over the stomach. This area is rarely extensive, being usually limited by a diameter of from two to three inches. When the heart is high, owing to the elevation of the diaphragm, and when the left ventricle is exposed in consequence of the shrinking of the overlapping portion of the left lung, the murmur extends up- wards towards the axilla, and even above the mamma, and a little outwards rather than downwards. The direction of the tnurmur upwards towards the axilla is peculiar to the mitral murmur of endocar- ditis, for when disease of the valve is estab- lished, the lungs expand downwards to an unusual extent, and so muffle or arrest the murmur in its course towards the axilla. The extent of the area of the murmur depends much upon its character. A smooth, soft, bellows murmur, especially if it is rather feeble, is in general limited to the apex and left ventricle; so also is a weak, grave murmur. But when it is vibrating, loud and almost musical, and especially if a thrill is felt by the finger over the apex-then the area of the mur- mur is extensive. Sometimes, indeed, it is so all-pervading that it may be heard over the whole cage of the chest, front and back, and even upwards into the neck and downwards over the abdomen. It is only in established mitral disease, or in very rare cases of endocarditis with extensive mischief to the valve, that we find this pervading vibrating murmur with perceptible thrill. In cases of established mitral disease the murmur is usually audible to a great- er or less extent over the region of the stomach, often comihg quite down to its lower boundary. The vibration in the left ventricle, which rests immediately upon the stomach, the diaphragm alone interposing, awakens a corresponding vi- bration in the stomach, and as this takes place in a hollow sac, its tone is often me- tallic, and it thus sometimes imparts a musical character to the murmur at the apex. In cases of endocarditis with mitral re- gurgitation, the murmur is often so feeble that it is limited to its birthplace, and is unable to generate corresponding vibra- tions in the adjoining organs. In these patients the murmur is inaudible over the stomach; but in other cases of endocar- ditis, according to the loudness and pene- trating quality of the tone, the murmur makes itself heard over a greater or less portion of the stomach, at that part of it nearest to the apex of the heart. The murmur was heard over the lower part of the back of the chest in only two of the fifty cases of endocarditis with mi- tral murmur of the first series, and in one of the twenty cases of the second series. In one of these cases the murmur was audible over the lower part of the back, the lungs being condensed, on the 4th day, but it was not again heard in that position. In another such case the mur- mur was heard over the back of the chest from the 27th to the 34th days after ad- mission, but ceased to be so on the 36th; and in the third case the murmur was heard below7 the shoulder blades for the first time on the 18th, and for the last time on the 42d day. After that date the murmur was less loud, and its area was correspondingly lessened. RHEUMATIC ENDOCARDITIS WITH A MITRAL MURMUR. 631 I have to add to these, one case of death with inflammation of the mitral valve ; the anterior flap was softened and en- larged, its edge and that of the posterior flap were covered with lymph or fibrine, and the valve permitted extensive regur- gitation through the mitral aperture. The patient, a young man previously in good health, had been ill a fortnight with acute rheumatism; when admitted, he had an anxious expression, hurried and difficult breathing, and sickness. A loud mitral murmur, beginning with a sharp shock and followed by the second sound, ex- tended forwards almost to the sternum, where the heart sounds were healthy, and backwards to below both shoulder blades. From the 9th day to the 11th he raised phlegm tinted with blood, he was propped up in bed, and there was dulness and fine crepitation over the left lower lobe. On the 14th he sat forward in bed in great distress, breathing with difficulty. In the course of that day he died, and on dissec- tion he presented the inflammation of the mitral valve and the extensive pulmonary apoplexy that were evidenced during life. The patients usually lay flat in bed, their pain being increased by movement, and as the back was not examined, some of these might have presented a murmur over the lower lobes of the lungs behind ; but when we regard the limited area over which the murmur was usually heard in front and at the side, it is evident that it could scarcely have been audible behind. I think it probable that three cases, in addition to those just named, may have been exceptions to this rule, and perhaps two others, for in them the murmur was loud, while in the first three it was vibra- ting in tone. The mitral murmur at the time of its first appearance, or of its transition from prolongation of the first sound, is as a rule either weak and grave; or it is a soft, feeble, bellows murmur, and is there- fore limited in area. The mitral murmur invariably begins with an accent or shock, which corre- sponds with the shock of the impulse, and it generally ends with the second sound. It fills up, in fact, the space between the first and second sounds, that space being often lengthened, so as to admit of greater prolongation of the murmur, with the ef- fect of altering the rhythm of the heart. Sometimes the murmur does not quite fill up this space, so that there is a dis- tinct silent pause between the end of the murmur and the second sound. The presence of the accent or shock at the be- ginning of the first sound distinguishes an endocardial murmur from an exocardial or friction murmur. The pressure test comes in to settle the difficulty of distinguishing one condition from the other. If the noise be endocar- dial, the sound may become louder from the closer application of the stethoscope, when pressed upon the walls of the chest; but the quality of the noise is unaltered, it is rhythmical with the heart sounds, it retains its accent or shock, it fills up the space between the first and second sounds, and it ends exactly with the second sound. But if the noise be frictional, it usually loses its murmur-like tone when the pres- sure is made-and becomes rustling or grazing, grating or creaking in character ; it extinguishes the first and second sounds of the heart, which were previously heard side by side, but not incorporated with the murmur; it brings out a double sound where there was but a single one before, a sound to-and-fro in character, or a noise not unlike that made by the sharp- ening of a scythe, with a single down- stroke during the beat of the heart, and a double up-stroke during its pause. Some- times the mitral murmur is masked or confused at the apex by the coexistence of a vibrating systolic noise. The inter- position of a piece of paper or cloth be- tween the stethoscope and the surface of the chest annihilates this vibrating noise, and the mitral murmur is then heard with perfect purity and clearness. The inter- position of the lung effects the same end -for this vibratory noise is heard only where the heart is in direct contact with the walls of the chest; and hence, when using the naked stethoscope, we meet with cases in which the murmur is more smooth and bellows-like just to the left of the apex or towards the axilla, than it is over the apex itself. For this effect, how- ever, the layer of lung must be thin and the tone of the murmur must be pene- trating. In cases of endocarditis, with mitral regurgitation, the murmur is often muffled by a rumble, or a comparatively feeble vibration. The interposed paper or the intervening lung extinguishes this vibrating noise, and brings a pure, soft, bellows murmur into play. The changes that the mitral murmur of endocarditis undergoes during the prog- ress of the case are remarkable, and they vary in almost every instance. These changes consist in alterations of its tone, loudness, and area ; in its transition from a true murmur to prolongation of the first sound ; in the substitution of a tricuspid for a mitral murmur, or the reverse, or the companionship of the two murmurs ; in the suppression and reawakening of the murmur; and frequently in its final extinction, either directly or by passing again into prolongation of the first sound, which precedes the restoration of the healthy sounds of the heart. In one-fourth of the cases (18 in 70) the mitral murmur was only heard on one occasion. 632 ENDOCARDITIS Of 50 cases, in all of which the mitral murmur was heard more than once, that murmur was of equal loudness during the successive observations in one-fifth (11); became gradually weaker in one- third (17), but in six of these it passed through a double oscillation and increased and lessened a second time ; became grad- ually stronger in one-fifth of the cases (11), in one-half of which it again grad- ually declined; was suspended and then renewed for a time in one-fourth of the cases (12), when the murmur again faded away ; and it sometimes yielded to the healthy sounds of the heart, and some- times to prolongation of the first sound. In two instances, already included in the abstract just given, there was a double disappearance and reawakening of the mitral murmur, which in one of them met with final extinction, while in the other it became established. The changes in the area of the murmur corresponded in a considerable degree to the changes in its loudness, the former widening as the latter increased, and nar- rowing as it diminished. In the great majority of the cases, and especially in those in which the murmur disappeared, the tone of the murmur un- derwent but little change. It became progressively louder and feebler, more clear and more obscure in almost every instance, but it usually retained its origin- al character. The murmur was observed to be soft and smooth, approaching to the character of a bellows sound, in less than one-half of the first series of the cases of endocar- ditis with mitral regurgitation, and in less than one-third of the second series ; the cases in each series in which the mur- mur was not characterized amounting to fully one-third of the whole. In a small proportion of the first series and a large proportion of the second se- ries of cases, the murmur was grave in character, being in some of them feeble, and in a few loud and almost vibrating. Musical, sawing, and rasping murmurs formed but a small proportion of the total number of cases, and these were they that passed through a series of changes in tone and character. One case, a youth, was a notable and rare instance of the variety of changes in tone through which the mitral murmur may pass. He had been ill a fortnight, and had suffered from pain in the heart. On admission he presented a tricuspid murmur. To this a loud mitral murmur was added on the 3d day, when he was very ill. On the 8th he was better, and from that day to the 15th the murmur was weak, soft, and smooth. On the 21st it was louder, and on the 29th it alto- gether changed its tone and became mu- sical. After this, without apparent cause, it underwent two variations, having first the character of a sawing and then of a bellows sound. The tone of the murmur then again altered, and it became grave, and finally on the 52d day it had regained its lost musical character. We must now answer the important practical questions suggested by these ob- servations, what are the character and progress of the murmur when the attack tends to end in perfect restoration of the efficiency of the valve ? and what, when it tends to become permanently incompe- tent, owing to the establishment of mitral disease ? The answer may be already almost gathered from what has gone before. When the murmur is permanently feeble, soft, and smooth, with an approach to, or even the formation of, a gentle bellows sound, or when it is feeble and grave, the complete restoration of the efficiency of the valve may be anticipated. In illus- tration of this statement we find that the murmur was feeble, soft, and approaching to a bellows sound in 14 of the 25 cases of the first series that ended in recovery of the valve; and in 4 of the 10 that left with a lessening murmur, the correspond- ing number in the two like classes of cases of the second series being 5 in 17, while of the 17 cases that ended in established valve disease out of a total of 71, the murmur was feeble in none, and was smooth or soft in 6, most of which pre- sented a definite bellows murmur. The feeble grave murmur was more fre- quently developed in the later than in the earlier series of cases, but in both its presence was almost always followed by the restoration of the function of the valve. When the loudness of the murmur steadily diminished, or when it first rose and then fell, or when after disappearing it reappeared and again faded away, the integrity of the valve was generally re- gained. When the murmur was loud, its area being extensive; when it presented a sharply-defined loud, bellows, musical, sawing, or rasping sound ; when it was vibrating in tone; when it steadily in- creased in loudness, or only slightly rose and fell to rise and fall again, without a temporary disappearance; then valvular disease was, as a rule, though not inva- riably, permanently established. One patient, a nurse in the hospital, left with a loud mitral murmur, but after a time, when she resumed her work, the murmur had given place to healthy heart sounds. Condition of the Heart and the Great Vessels in Cases of Endocarditis affecting the Mitral Valve.-In these cases there are, as I have already illustrated, many affections of the heart besides imperfec- tion of the mitral valve with its attendant RHEUMATIC ENDOCARDITIS WITH A MITRAL MURMUR. 633 murmur. When inflammation affects the great central cavity of the heart, the pivot of its action, the whole organ is in- volved, and every part of it becomes, in succession, modified in its action ; and in the force, movement, and sounds by which it makes that action known. Inflammation of the fibrous structure of the left side of the heart is as essen- tially a part of acute rheumatism, as is inflammation of the fibrous structure of the joints. The inflammation may com- mence in the heart at the same time that it commences in the limbs. It attacks that part of the heart that is working | with the greatest force, just as it attacks those parts of the limbs that are subjected to the greatest labor. The increasing in- [ flammation of the joints calls forth in- creasing force in the action of the left ventricle, and so stirs up and adds to the inflammation that may have already ex- isted in that cavity from the commence- ment of the attack. This inflammation of the ventricle, like the inflammation of every other organ, lessens the power of the muscular cavity to expel its contents, and to propel the blood round the vessels of the system. This imperfect transmission of blood to the system, the demand for which is increased by the inflammation in the limbs, causes distension of the left au- ricle, and impedes the transmission of the blood through the lungs. This induces distension of the pulmonary artery and its branches, with, as its effects, accentu- ation-or loudness and sharpness, or shock -of the second sound, with relative fee- bleness, or even absence, of the first sound over that artery; and distension of the right ventricle, with increase in the action of its walls and in the force and extent of its impulse. We have, thus, two ventricles beat- ing side by side, the left one, the seat of the inflammation, beating with lessened power; the right one, with increased force. The increased fulness and force of the right ventricle tend, when they pass cer- tain limits, to reverse the flow of a portion of the blood, and to send it from the right ventricle back into the right auricle; with the effect of relieving the distension of the arteries of the lungs, increasing the ful- ness of the veins of the system, and pro- ducing a tricuspid murmur. After a time, the whole volume of the blood is diminished, and the proportion of its red corpuscles is lessened ; and then appear as later and secondary effects, a murmur over the pulmonary artery, and sometimes a murmur over the aorta and its great branches-murmurs that are due to the lessening of the contents, and re- laxation of the walls of those vessels. Such murmurs in the great arteries ap- pear, however, also in the early stages of i the affection, in the aorta more frequently, owing evidently to the lessened power of the inflamed left ventricle, and the dimin- ished supply of blood that is therefore sent into the aorta, the walls of which are thus relaxed; and in the pulmonary artery occasionally, for reasons that have yet to be ascertained. The close study of the condition of the heart and great vessels generally throws more light upon the degree of the inflam- mation of the heart, and its effect on the vital powers of the organ, than does the simple observation of the mitral murmur. I shall now rapidly review the condi- tions of the heart and great vessels as they presented themselves in the cases of endo- carditis with incompetence of the mitral valve-that valve being previously in the virgin state and uninjured. The Impulse of the Heart.-I find that I have taken notes of the state of the im- pulse in one half of the cases with mitral incompetence, or in 25 out of 50 of the first series, and 9 out of 20 of the second. The beat of the heart was, as a rule, not extensive or strong. It showed itself rather in the higher than the lower car- diac intercostal spaces, being present in only one instance below the fifth space, less frequently in that space than in the fourth, and sometimes even in the third space. While the impulse at the apex was in general feeble or absent; that of the right ventricle, though rarely power- ful, was usually somewhat increased in strength, being present in the third and fourth, and even the fifth spaces between the cartilages. This impulse of the right ventricle was not as a rule marked or strong, but it could be felt diffused over those spaces when the ball of the palm of the hand was applied over them, or when the fingers were pressed gently into the spaces. In a few instances the action of the heart, and especially the impulse of the right ventricle, was strong and diffused or powerful, or even tumultuous and violent, soon after admission; and then the size of the heart, which was not in general notably affected, became enlarged, the chest over the cardiac region being more prominent than over the corresponding space on the right side. In one or two patients the impulse pre- sented a peculiar shock. But the distinctive feature with regard to the impulse in a fair proportion of the cases was its variation during the succes- sive periods of the disease. Thus, in one instance, it was feeble on the first day in the fourth space, very strong on the 3d day, moderate in strength in the fifth space on the 8th day, and in the third and fourth spaces on the 12th day. In another patient the impulse was felt in the second and third spaces on the 2d day, when 634 ENDOCARDITIS. there was pain in the heart; on the 5th, the pain still continuing, the heart beat violently; from the Gth to the 18th the pulsation was strong in the second space, and from the 28th to the 34th it was dif- fused from the third to the fifth spaces. In this case mitral disease was established, and the gradual extension of the impulse of the right ventricle told with precision the story of the increasing valvular disease in the left ventricle. The study of the impulse conveys the most important lesson in all cases of endo- carditis. Its absence may tell of the want of vital power; and its excess in the right ventricle, while it is wanting in the left, shows lessened power from inflammation in the latter cavity, and consequent in- creased labor in the former. Its gradual increase in force, and enlargement in area, with persistence of mitral murmur to- wards the period of the termination of the attack of endocarditis, and after its cessa- tion, mark advancing and established val- vular disease ; and its extent and force point out the amount of the back-flow of blood from the left ventricle into its auri- cle, and the obstacle to the onflow of blood through the lungs induced thereby. The impulse of the right ventricle is, in short, a measure of the extent of the in- jury to the mitral valve, and of the con- sequent resistance to the circulation through the lungs. The impulse of the right ventricle was diffused and strong, extending out to the nipple, in a considerable proportion of the cases in which there was a tricuspid mur- mur. In a few instances the impulse of the right ventricle was so high as to be pres- ent in the second space ; but generally the pulsation felt in that space was due to the presence there of the distended pul- monary artery, when that pulsation was double, the second impulse being more smart and shock-like than the first. In these cases the pulmonary artery was dis- tended, the first sound was feeble or ab- sent, -while the second was unusually loud and strong, penetrating the ear with a shock. The apex beat is, in cases of endocar- ditis with mitral regurgitation, usually slight, sometimes absent-during the early period, before the mitral murmur is de- veloped, owing to the weakened muscular power of the inflamed left ventricle ; and •-after the appearance of the murmur, owing to the relief afforded to the organ by the greater ease with which its sur- charge of blood is sent backwards into the auricle than forwards into the aorta. There are, however, certain exceptional cases of great interest, several of which have come under my observation, in which the left ventricle beats with great force, and unduly to the left. In three of these cases there was exten- sive pulmonary apoplexy, or pneumonia of that type, in the lower portion of the left lung. One was a youth, with hurried and dif- ficult breathing, tinted phlegm, and dul- ness over the lower portion of the left lung, which was solid and lessened in size, owing to pulmonary apoplexy. The con- densed and solidified lung shrank away from its natural position between the walls of the chest and the apex of the heart; and the apex was therefore com- pletely exposed, beating with all its force upon the fifth space more than an inch beyond the left nipple. At that time there was no mitral murmur, but as soon as the lung began to recover itself, the murmur came into full play. When the lung again expanded, it covered the apex of the heart, and its beat was no longer perceptible. The whole heart in this case was displaced to the left; and its dis- placement was still greater in the sister case, in which the apex beat was situated three inches beyond the nipple line ; the impulse of the right ventricle was placed to the left of the costal cartilages; and the double pulsation of the pulmonary artery, with a strong second shock, was present in the second space above the mamma. A fourth case, when admitted, had pain in the region of the heart, and the apex beat was situated an inch and a half to the left of the nipple. Five days later the extreme limit of the impulse had shrunk one inch, being seated half an inch to the left of the nipple. Accent nation of the Second Sound, with Silence, Feebleness, or Prolongation of the First Sound over the Pulmonary Artery.-• Accentuation of the second sound over the pulmonary artery, in the left second space, is a well-established sign attendant upon mitral regurgitation, and it may be present in every degree. The second sound may be more or less loud and sharp or ringing-or it may pen- etrate and strike the ear with a loud shock ; when a double impulse is to be felt over the pulmonary artery, the first being gentle and gradual, while the second gives to the hand a smart shock. This increase in loudness and sharpness of the second sound is due to distension of the pulmonary artery, owing to the diffi- culty with which the blood travels through the vessels of the lungs. Whenever the blood thus accumulates in the lungs, whatever be the cause, the same effect is induced. In cases of phthisis, and notably when there is hemor- rhage from the lung and shrinking of its tissue, the pulmonary artery, enlarged and tense, displaces the lung superficial to it, and presses against the second space; where there is a double impulse RHEUMATIC ENDOCARDITIS WITH A MITRAL MURMUR. 635 the first gentle, the second felt and heard as a shock. In bronchitis, emphysema and pneumonia, there is the same disten- sion of the pulmonary artery, but greater in degree. The interposition of the lung, enlarged owing to the disease, screens the pulmonary artery from the hand and the ear, so that over it the second sound is often not unduly loud ; but it is so in some instances over the right ventricle. Whenever the tension of the pulmonary artery is thus so great as to cause a strong and loud shock with the second sound, the first sound is either almost silent, or feeble, or faintly prolonged. When the blood is sent into a tight and full artery, it makes but little, often no sound, either in the shape of shock or murmur ; but the second sound caused by the smart and strong reflux of the blood upon the walls and closed valves of the artery, makes a loud, sometimes a ringing or metallic sound. The same occurs in the aorta when it is enlarged and ren- dered tense, owing to the difficulty with which the blood leaves the arterial sys- tem in advanced cases of contracted gran- ular kidney. When you listen over the aorta a single sound is often heard, a loud ringing metallic second sound, the first being almost or absolutely silent. Some- times in these cases the artery is so large and tense that it presses against the second right intercostal space, producing there a double pulsation, the first gentle and gradual, the second smart and with a shock. I find that I have described the second sound as being loud or sharp or ringing in about one-half of the 50 cases of the first series and 9 of the 20 of the second series of cases of endocarditis with mitral mur- mur, and in 5 of 13 of those of the first series with an uncomplicated tricuspid murmur. This does not of course include all of this class. It was noticed that the second sound was sharp or loud in the early period in a large proportion of the cases in which that sign was observed, or in 13 out of 25 of the first series, and 7 out of 9 of the second series. In all but six of the patients in whom it was noticed that the second sound was intensified, it continued to be loud down to a late period, to the time in fact of approaching recovery. Loudness of the second sound may be associated with each of the signs, singly or in combination, that are habitually found in cases of endocarditis with inflam- mation of the mitral valve. It accompa- nied a mitral murmur, either alone or in combination with a tricuspid murmur in 22 of the cases ; in about 15 cases it was allied with prolongation of the first sound over the left and sometimes the right ven- tricle ; and in 8 cases it was joined to tri- cuspid regurgitation, which was, however, combined with other important signs in every instance but one. The first sound of the pulmonary artery was affected, when the second sound over that artery was loud or sharp, on ten occasions, in different patients : in 4 of these there was a pulmonic murmur, in 4 the first sound was prolonged, being generally free from shock, and in 2 it was silent or scarcely audible. These numbers, however, taken by themselves give a very inadequate idea of the relation of the first to the second sound of the pulmonary artery in cases when that second sound is intensified. Thus, as we have just seen, pulmonic murmur was followed by a sharp second sound in four instances, but there were altogether 32 cases in which a pulmonic murmur was heard, and in only four of them was it stated that the second sound was thus affected at the time when the pulmonic murmur was audible. In one of the cases in which there was a pulmonic murmur on admission, the second sound was free from accent; while on the 3d when the pulmonic murmur had disap- peared, that sound was slightly accentu- ated over the pulmonary artery. Again, in only two of the cases is it noted that the first sound of the pulmonary artery was silent or scarcely audible when the second sound was loud. Since, however, my attention has been drawn to the rela- tion of the first to the second sound of the pulmonary artery, in every instance that I have observed accentuation of the sec- ond sound, especially with, but even with- out shock, the first sound has been either very feeble, being occasionally prolonged, or almost or even quite silent. This con- dition was signally marked in a case of chorea under my care in the hospital, a boy, who on admission, presented no mitral or other murmur over the heart. After gaining ground steadily he became rather worse, his temperature rose, he had pain in his chest, and the second sound was loud, the first feeble over the pulmonary artery ; and six days later a mitral murmur came into play. At the same time the right ventricle, previously quiet, beat with great force, and a strong shock was felt over the pulmonary artery with the second sound. On listening over that vessel, a loud second sound pene- trated the ear and struck it as it were with a shock, and the first sound was silent, the second sound being alone audi- ble to all who listened. After a short time he became very ill, and for two days he passed his evacuations involuntarily in bed. He kept both hands flexed on his wrists, and his fingers on his hands. He soon began to improve, and gradually as this boy gained strength, speech, power to move, and freedom from irregular 636 ENDOCARDITIS. movements; and as his lungs enlarged, the mitral murmur being still audible, the second sound though still loud lost its shock, the second impulse ceased to be felt over the pulmonary artery, and the first sound, though feeble, became more and more audible. In a fair proportion of the cases in which the second sound was sharp and loud at the early period of the disease, that sound retained its character unal- tered through all the surrounding changes in the sounds of the heart. Let us take one case. At first there was a tricuspid murmur, the second sound being sharp; on the 6th day there was a mitral mur- mur, and the second sound was loud ; next day the murmur was less marked, but the second sound was still loud ; and on the 11th the murmur had given place to prolongation of the first sound over the right ventricle, and yet the second sound still remained loud. In another instance on the 9th day there was an obscure mitral murmur, on the 16th there was mitral, tricuspid and direct aortic mur- murs, on the 19th these had all vanished, and on the 23d the tricuspid and direct aortic murmur had returned ; and yet on each occasion there was the same sharp second sound over the pulmonary artery. I could give several instances of this kind and would refer to four cases. In these instances the sharp second sound went on drumming, like the tomtom in the streets, whatever was the variety of the surrounding noise, or even when there was freedom from murmur or prolonga- tion of the first sound. The intensified second sound is, how- ever, by no means always so unvarying in its note. Thus, in one very interesting case on the 11th day the second sound was very loud over the pulmonary artery, the first being scarcely audible ; on the 34th both sounds were loud over the ventricles, the second being very loud ; and next day all the sounds were natural. I must refer to one other case, in which on admission the first sound was faint, the second loud over the pulmonary artery, the first sound being prolonged over the ventricles ; on the 13th day the two sounds were equal over the artery and there was a feeble murmur at the apex ; on the 27th the second sound was again louder than the first; and on the 40th a singular change took place, the first sound being louder than the second over the pulmo- nary artery-while over the aorta it was the reverse, and on the 50th day the na- tural standard was regained, the second sound being louder than the first. The close study of the second sound and of its relation to the first over the pulmonary artery, is of practical import- ance in cases of endocarditis affecting the mitral valve. It may foretell the coming murmur in the early, and betray the re- cently extinct murmur in the later, period of the disease ; and during its progress, it points by the degree and force of its ac- cent to the amount of the resistance to the pulmonary circulation, the intensity of the internal inflammation of the ven- tricle, and the extent to which the func- tion of the ventricle is impaired. It is, in short, a tell-tale sound pointing to the agency in the central cavity of the heart w hich gives it birth. The intensified sec- ond sound of the pulmonary artery, or that of the aorta, is associated as we have seen with a corresponding feebleness, or even silence, of the first sound of each of the vessels respectively. The observation of the one sound demands a correspond- ing observation of the other sound. When the artery is distended, it enlarges, length- ens, and advances, and comes gradually into contact with the second intercostal space, displacing the intervening lung from before it. You can then feel the double pulsation of the great artery ; the first movement is gentle, gradual, barely perceptible to the touch; the second strikes the walls of the chest and the applied hand with a sudden smart shock or tap. When you listen to it the ear takes in the same effect through another sense ; the first sound is in extreme cases silent, or is soft and gentle, feeble and perhaps soine- what prolonged ; while the second pene- trates and strikes the ear with a loud shock, often ringing and metallic. Over the pulmonary artery, as I have just said, that subdued sound or even silence, and this shock, betoken tension of the artery, and obstacle to the flow of blood through the vessels of the lungs ; w hether that obstacle be caused by a back flow, due to inflammation or disease, with incompe- tence, of the mitral valve ; or directly to disease of the lung itself, whether from phthisis, contracted lung, pneumonic bronchitis, or emphysema; the shock being in these last cases shielded from the hand and muffled to the ear by the interposition of a couch of lung, thick- ened by the undue expansion of the air cells induced by the disease. When the aorta is thus distended, push- ing aside the lungs, beating with a double pulsation upon the second right intercostal space, over the ascending aorta, the first gentle and gradual, the second, a smart shock, the first feeble or even silent, the second, a loud ringing, metallic shock, you know that the blood forces its way with difficulty through the fine vessels of the system, and that the cause of this is the contamination of the blood, induced by advanced granular contraction of the kidney. Two conditions are needed for the pro- duction of this double effect, one, that just spoken of, the obstacle to the onflow RHEUMATIC ENDOCARDITIS WITH A MITRAL MURMUR. 637 of the blood ; the other, the force with which the pulsating ventricle sends its blood into the artery. Lessen that force, and the supply of blood is lessened, the proportion of blood in the vessels and the power to pass it on is brought more into equipoise ; the tension of the blood being relieved, the first sound becomes again audible, and the shock of the second sound is subdued, so that it becomes merely un- duly sharp or loud. Additional observations are wanted on this important practical point of the rela- tive loudness of the first and second sounds over the pulmonary artery and aorta; combined with information as to the poisoning and accumulation of the blood, structural change in the walls of the ar- teries, and vital power. The two sounds must be listened to, and their relative in- tensity noted, which I do by the ready method of figures of varying size written on a diagram of the body on which the outline of the ribs is traced. The size of each figure denotes the relative intensity and actual loudness, judged of by the ear, of the two sounds. When the first sound is silent, and the second is loud and with a shock, I mark it thus, °/2 ; when two sounds are equal, thus, 1/2; when the first is louder than the second, thus, l/2; and when the second is louder than the first, thus, */2. Every shade can be thus rendered. Combined sphygmographic and cardiographic tracings, some of which I have made, in these cases, will give posi- tive and scientific accuracy to our know- ledge. Doubling of the Second Sound.-In two of the cases of endocarditis with mitral murmur, there was doubling of the second sound. One of these came in with doub- ling of the first sound, or almost a murmur at the apex, on the 4th day a peculiar plunging first sound, with scarcely any second sound, appeared over the ventri- cles. On the 6th day there was doubling of the second sound. On the 8th day mitral and pulmonic murmur appeared, followed by a tricuspid murmur, and on the 10th these murmurs had all vanished. In the other case the doubling of the sec- ond sound appeared late and was very tenacious. There was a mitral murmur up to and on the 23d day, when the sec- ond sound was prolonged over the pul- monary artery. On the next day there was doubling of the second sound over that artery. The second second sound was louder than the first-and this proved that the later sound was the pulmonic, the earlier the aortic sound. In this in- stance the doubling of the second sound, which lasted to the 60th day, disappearing on the 69th, was due, I consider, to the longer time occupied by the right ventricle than the left in emptying itself, owing to the resistance to the flow of blood through the lungs. Pulmonic Murmur.-A systolic murmur over the pulmonary artery, at the second left space, was heard in a considerable number of the cases of endocarditis with mitral murmur. This number amounted to one-third of the first series, or seven- teen in fifty-two, and to one-half of the second series, or ten in twenty. This murmur was present also in one-third of those cases of endocarditis affecting the left side of the heart, in which there was tricuspid, but not mitral, murmur. In more than one-half of those cases the pulmonic murmur appeared towards the close of the attack, when all the acute symptoms had gone by, when the period of convalescence was approaching or es- tablished, when the patient was pale and thin, having lost a large proportion of the red corpuscles from the blood, and was weak from the exhausting nature of the disease. In nearly one-half of the re- maining cases this murmur appeared at the middle period, and in one in four of the whole number it was audible soon after the admission of the patient. The murmur almost always occupied a well-defined limited area at the edge of the sternum in the second space, just over the pulmonary artery. It never extended as far as the right edge of the sternum, but it could be heard very feebly in the first space, and occasionally in the third. When the position of the pulmonary artery was unusually low, the murmur moved downwards, being then heard strongly over the third space, and feebly over the second and fourth spaces. The pulmonic murmur rarely presents a smooth soft bellows sound, but is usu- ally grave and superficial, without how- ever being large in character or very loud. The murmur appeared as a peculiar scratching noise in one-half of the cases, or 4 out of 8, in which the sign appeared soon after admission, and besides these in one on the 8th and in another on the 21st day. The scratching nature of the sound when I first observed it (I found it noticed in one case as early as the year 1852) was very puzzling. It strongly suggested friction sound. But it differed in these respects: it was always systolic, being never to-and-fro ; pressure sometimes highly intensified, but never altered it in tone ; it clung to one spot ; and it gradu- ally disappeared without passing into a wide-spread double friction sound. Its noise was exactly like that made by scratching slowly and gently with a pin on a deal table. The cause of the pulmonic murmur is exactly the same as that of the aortic "anaemic" murmur, which is audible only during the systole. It is due to the 638 ENDOCARDITIS. blood being very thin and lessened in quantity, and propelled into the vessel when its walls are relaxed, with undue force, by the ventricle. When the pulmonary artery is flaccid, its contents have free room to vibrate as they move onwards in the current of the circulation, and therefore pulmonic mur- mur is engendered. The pulmonic mur- mur thus indicates that there is relaxation of the pulmonary artery, or a condition the opposite to that of tension of the ar- tery. The second sound following the murmur may be loud, but it is usually fee- ble. It is loud if, during and towards the end of the contraction of the right ventri- cle, the pulmonary artery becomes tense ; its walls then recoil with force upon their contents and propel them with equal pressure in two directions, forwards into the vessels, and backwards upon the as- cending pulmonary artery, its sinuses, and valve, where the back-stream strikes with a sudden shock, the shock of the loud second sound. The second sound is, on the other hand, feeble if the flaccid artery does not become distended during the systole ; when the recoil of the walls is therefore weak, and when the back- wave breaks with only moderate force upon the roots of the artery. Silence or feebleness of the first sound is the opposite in character and cause to pulmonic murmur. If the artery is dis- tended when the ventricle begins to con- tract, the column of blood moves steadily forwards, the walls of the vessel and its contents are not thrown into vibration, and the first sound is either absent or feeble. The extreme tension of the pul- monary artery thus induced, leads, when the blood has ceased to enter it, to the re- coil of its walls with excessive force upon their contents, which are driven with a strong back-stroke or shock upon the walls, sinuses, and valve of the artery. When the lung is displaced from before the pulmonary artery, thus distended, this shock is felt by the hand and heard striking against the ear with a loud me- tallic sound. Pulmonic murmur, as we have just seen, came into play most frequently when the disease was passing away. It was therefore rarely, or only once or twice, associated with a mitral murmur when at its zenith, and uncomplicated with other murmurs. In fully one-half of the cases (13 in 24) it accompanied prolongation of the first sound, or a feeble mitral murmur; in nearly one-half of them (9) it appeared with a conjoint mitral and tricuspid murmur; and in one-fourth with a simple tricuspid murmur, a companion sign that was therefore present in three- fourths of the cases. In one-fourth of the cases (6) it was traced side by side with an anemic murmur over the aorta or carotid artery ; and thrice it was unac- companied by any murmur. Nearly all these instances point to a state in which the tension of the pulmonary vessels was either not yet established or was passing away. A pulmonic murmur was audible in a large proportion (or 5 in 13) of those cases that I have classed as being probably affected with endocarditis. In all of these cases there was prolongation of the first sound. In three of them it was noticed soon after admission, and in the two others at a late period of the illness. A pulmonic murmur was heard in a small proportion of the cases in which en- docarditis was either threatened or only transient, amounting to 7 in 63 of the first series, and 2 in 22 of the second, or one-tenth of the cases. In all of these but one it appeared at alate period, when the intensity of the disease was passing away. Pulmonic murmur is not then a direct sign of endocarditis. Its presence, how- ever, in the early period of acute rheuma- tism usually points to endocarditis, and to the actual or approaching presence of a mitral or tricuspid murmur. Its existence at a late period in a case of endocarditis generally points to relief in the severity of the disease, to the cessa- tion of the inflammation of the heart, to a definite removal of the tension of the pulmonary artery, due to congestion in the lungs, and to the establishment, for a time, of the opposite state of that vessel, its walls being relaxed and the quantity of its blood diminished. The pulmonic murmur, then, while it is a sign threatening inflammation of the interior of the left side of the heart in the early stage of acute rheumatism, is a sign of the passing away of endocarditis when it appears at a time when that affection has been established. Pulmonic murmur never becomes permanent. It generally diminishes rapidly when the patient leaves the bed, and gains color and strength, and in the convalescent patient it is often inaudible when standing or after walking, when it may be still heard if the patient is lying down. I have heard the pulmonic murmur in several cases of enteric fever, when it in- dicates the condition of which I have just spoken, or relaxation of the pulmonary artery. The pulmonic murmur usually, I be- lieve, tends to become less vibrating and more feeble during the progress of the systole, when the artery is becoming less relaxed, and to die out at the end of the systole when the vessel is becoming tense, and the stream of blood is being gradually brought to a stand-still. RHEUMATIC ENDOCARDITIS WITH A MITRAL MURMUR. 639 Tricuspid Murmur in Cases of Endocar- ditis with a Mitral Murmur.-I have al- ready illustrated this sign when I de- scribed tricuspid murmur in cases of endocarditis of the left side of the heart without mitral murmur. I refer to that part at pages 622-625, and shall here therefore only state generally the condi- tions under which this murmur is found. A tricuspid murmur is not, as we have already seen, a sign of inflammation of the right side of the heart, and of the tri- cuspid valve ; but of inflammation of the left side of the organ and of the mitral valve. When the left ventricle is weak- ened by that inflammation, it sends less blood into the vessels of the system, and an undue amount of blood therefore accu- mulates in the vessels of the lungs. The pulmonary artery is over-filled, and the left ventricle is distended. The "safety- valve" function of the tricuspid valve is then brought into play, regurgitation takes place, and by throwing a portion of the blood backwards upon the veins of the system, it lessens the pressure of the blood forwards upon the arteries of the lungs. Tricuspid regurgitation, then, while it declares the presence of inflammation of the left ventricle and the mitral valve, relieves the congestion in the lungs, which is one of the worst effects of that inflam- mation. A tricuspid murmur is present in nearly one-half of the cases of endocarditis with mitral murmur. A tricuspid murmur may precede a mitral murmur, accom- pany it, alternate with it, or waken up after it has disappeared. A tricuspid murmur, then, is a friendly sign-it warns you of inflammation elsewhere, and re- lieves the ill effects of that inflammation. It is a danger signal, and a break, lessen- ing the mischief. Aortic Systolic Murmur (Anaemic).-A direct aortic murmur was noticed in twelve of the seventy cases of endocarditis with mitral murmur, and there were others in which its presence was doubtful. This murmur appeared in the early period of the disease in eight of the cases, and in the later period in four. In three of the patients in whom the murmur appeared early, it lived through the whole of the attack; and in one other of them, after vanishing for a time, it again appeared when the patient was recovering. In all the cases but one, the aortic murmur was associated with conjoint mitral and tricuspid murmurs, and in fully one-half of them, seven, the aortic was coupled with a pulmonic murmur, usually at a late period of the disease. These twin murmurs, the aortic and pul- monic, are due to the same cause, a defi- cient supply of blood in the great arteries, which are therefore imperfectly filled. Their walls are consequently flaccid, and their contents have free room to vibrate as they move onwards in the current of the circulation. The direct aortic murmur is much less frequent than the pulmonic murmur in cases of mitral endocarditis. But the aortic murmur appears early in the attack much more frequently in proportion than the pulmonic murmur. The reason of this would appear to be that in the early stage the inflamed left ventricle sends its blood with insufficient force and volume into the aorta, and vibrations with their consequent murmur therefore ensue. At a later period, the lessened volume of the blood circulating through the body, and the diminution of its red particles, lead to the formation of the murmur. The question is an interesting one, and is not easy to answer, why the pulmonic murmur is so much more frequent than the aortic at the later period of the affec- tion ? May it not arise from two influ- ences ? (1) The increased size to which the pulmonary artery has attained during the period of its tension, when the disease was approaching to and at its acme ; and (2) the greater relative influence that the diminished supply of blood has upon the comparatively restricted area of the arte- ries of the lungs, when compared with the much larger area of those of the body ? Prolongation of the First Sound occurring at a late Period in Cases of Endocarditis with Mitral Regurgitation.-We have al- ready seen that in a considerable propor- tion of those cases of endocarditis that are admitted before the appearance of a mitral murmur, that murmur is preceded by prolongation of the first sound. Prolongation of the first sound (as we have seen at page 628) may develop into a tricuspid or mitral murmur, and when the murmur fades away, it may give place to a renewal of the prolongation of the first sound. This was precisely what occurred in one case, a patient in whom, when admitted, the first sound was pro- longed ; on the 10th day a tricuspid mur- mur was audible, which was replaced on the 19th by prolongation of the first sound. In another case the sounds were at first healthy, but the first sound was prolonged at the apex on the 4th day, a tricuspid murmur appeared on the 6th, which yielded on the 9th to prolongation of the first sound over the right ventricle, and on the 48th day the sounds were again healthy. In five cases with mitral murmur a similar chain of transforma- tions took place. In one of these a mitral murmur, which appeared on the 5th day, superseded prolongation of the first sound at the apex ; that murmur became weaker on the 10th, and was joined on the 12th by three other grave feeble murmurs, a 640 ENDOCARDITIS. tricuspid, a pulmonic and an aortic. On that day the murmurs were audible when the patient lay down-but they passed into prolongation of the first sound when he stood up-and on the 20th day that prolongation was only audible when he lay down, the sounds being healthy when he stood up ; owing evidently to the greater amount of blood that was then demanded by the body and the lungs, and was consequently supplied to the aorta and pulmonary artery. In a few of the patients the murmur during the illness yielded for a time to prolongation of the first sound, and then reappeared. One case, a female patient, was a notable instance of the variety of transformation sounds that may occur in this disease. When admitted, she pre- sented a mitral or tricuspid murmur ; on the 3d day the first sound was prolonged, and on the 6th the sounds were natural. But on the evening of that day a mitral murmur set in which remained for several days, being joined by other murmurs. On the 14th those had vanished, the first sound being prolonged. On the 16th a tricuspid murmur appeared, which was exchanged for a mitral murmur on the 27th, which from that date became per- manently established. In many instances the position of the prolongation of the first sound is not spe- cified, but when it is, the situation of the murmur as a rule corresponded with that of the prolongation of the first sound out of which it grew and into which it faded -both being present at the apex when the murmur was mitral, and over the right ventricle when it was tricuspid. The passage from murmur to prolonga- tion and the reverse was often very grad- ual; they often each glided insensibly into the other. The prolongation was often murmur-like in character, and the mur- mur was often so obscure as to be quite as fitly ranked with prolongation. In several of the patients, prolongation of the first sound over one ventricle was accompanied by a murmur over the other. Thus in three cases a tricuspid murmur was associated with prolongation of the first sound at the apex; and in another instance a mitral murmur was coupled with prolongation over the right ventricle. One case is an example of both kinds in succession. At the time of admission, when the patient was very ill, the sounds were loud, the first being sharp. From the 2d day to the 7th there was a tricus- pid murmur with prolongation of the first sound at the apex ; and on the 21st there was a double exchange, a mitral murmur being joined by prolongation of the first sound over the right ventricle. Some- times there was a double prolongation of the first sound, at the apex, and over the right ventricle, as occurred in four cases. I have noticed this coupling of the sign only in cases observed at a later period, and I am certain that it occurs much more frequently than my earlier notes would indicate. In a large proportion of the cases the murmur passed into pro- longation of the first sound towards the period of convalescence. This was no- ticed in six of the thirteen cases of endo- carditis with tricuspid murmur; in six- teen of the forty-one cases of endocarditis with mitral murmur of the first series, in one of which that sign gave place finally to a permanent mitral murmur; and in twelve of the twenty of the same class of the second series. Prolongation of the first sound is the first whisper of an approaching murmur, the last of a departing one. It is a sign of coming danger, and it usually betokens, towards the conclusion, a favorable issue. Prolongation of the first sound, or an obscure murmur, was heard in seven of the seventy-nine cases of the first series, and in none of the fourteen cases of the second series that were classed as having had no endocarditis. Of those patients in whom endocarditis was threatened or probable, the first sound was prolonged, or there was a doubtful murmur, in forty-three of the seventy-six cases of the first series, and eighteen of the twenty-six of the second series. In more than one-half of the cases thus affected there was great general ill- ness (35 in 61), and of these in fifteen there was pain in the region of the heart. We must look then upon prolongation of the first sound as a sign of actual, or probable, or threatened, inflammation of the heart; whether we regard its pres- ence in those cases of pronounced endo- carditis with a mitral or a tricuspid mur- mur, or in those of probable or threatened endocarditis, in which the murmur was not declared. The duration, the degree, and the pro- gress of endocarditis is not to be esti- mated by the presence of a mitral murmur alone, but by the effects also of the in- flammation upon the body, the lungs, and the heart. The face is anxious and dusky; there is sometimes pain in the heart; the breathing is quickened and oppressed; the impulse of the left ventricle is weak, while that of the right is unduly strong ; the circulation through the lungs is im- peded ; the pulmonary artery is distended, its first sound is silent or feeble, and its second is accentuated; a tricuspid mur- mur is often present, sometimes alone, sometimes conjointly with a mitral mur- mur ; prolongation of the first sound pre- cedes and follows the mitral and tricuspid murmurs; and amemic murmurs are often heard both over the pulmonary artery and the aorta, during the early and also RHEUMATIC ENDOCARDITIS WITH AORTIC REGURGITATION. 641 the late period of the disease, but rarely during its acme; the pulmonic murmur being more frequent at the period of con- valescence, the aortic murmur during the early stage of the disease. III.-Cases of Rheumatic Endocar- ditis with Aortic Regurgitation. (1) Not Accompanied by Mitral Murmur. (2) Accompanied by Mi- tral Regurgitation. (1) Aortic Regurgitation, not accompa- nied by Mitral Regurgitation.-Incompe- tence of the aortic valve is much less fre- quent in rheumatic endocarditis than incompetence of the mitral valve. There was a diastolic aortic murmur not accom- panied by a mitral murmur in ten ; and there was a mitral murmur without a diastolic murmur in fifty of the first series of cases-while there was mitral regurgi- tation in twenty, and aortic regurgitation in none of the later series of cases. This brings up the cases of mitral in relation to aortic regurgitation to the proportion of seventy of the former to ten of the lat- ter. Besides these, eight of the first series and one of the second presented both mitral and aortic incompetence. This makes the total number of cases in which there was aortic regurgitation eighteen, and the total number in which there was mitral regurgitation seventy-nine. In more than one-half of the cases of endocarditis with aortic regurgitation, there was no mitral murmur (10 in 18). The mind naturally infers that in these patients the inflammation was limited to the aortic valve, and did not extend to the mitral. The close examination of the cases, however, leads, I consider, to the conclusion that in all of them there was inflammation of both the mitral and the aortic valves. A mitral murmur appeared in one of the ten cases for a single day, and was not again beard. That was the only case in which this, the central and immediate sign of mitral endocarditis, was noticed. In the others, however, the more impor- tant secondary signs of inflammation of the interior of the left ventricle were present. In five of the cases a tricuspid murmur was audible over the right ventricle. In three of these that murmur was heard before the murmur of aortic regurgitation came into play; in one, the two murmurs were, present on the day of admission; and in the fifth case, the tricuspid mur- mur appeared a week later than the aortic, but the aortic murmur was pre- ceded by prolongation of the first sound, which was present on the day of admission. The first sound was prolonged over one or both of the ventricles in six of the cases ; in three of which there was, and in three there was not a tricuspid murmur. In two of the three in which there was no tricuspid murmur, prolongation of the first sound preceded the aortic murmur. Thus eight of the ten cases of endocar- ditis with aortic incompetence, without mitral murmur, presented either a tricus- pid murmur, or prolongation of the first sound over the ventricles, or both signs. In six of them, one or other of those signs preceded the appearance of the aortic in- competence ; in one other the patient came in with both aortic and tricuspid regurgitation murmurs; and in the re- maining one only did the aortic murmur precede by three days the prolongation of the first sound. The ninth case was ad- mitted with aortic regurgitation, and he suffered from pain in the region of the heart. The tenth case, a female patient, was an anomalous and doubtful one. She was very ill when admitted, when she had pain in the left side, and the sounds of her heart were rough. On the twelfth day a soft double murmur was audible in the second left space which was probably due to aortic incompetence. (2) Cases of Rherimatic Endocarditis with Aortic Regurgitation, accompanied by Mi- tral Regurgitation.-In eight cases mitral and aortic incompetence were combined, and in six of these the mitral murmur preceded the aortic. Both murmurs were present on admission in one of the two remaining cases, and they appeared to- gether in the other one on the seventh day after admission. These illustrations, and the considera- tions that I have just advanced, appear to me th render it conclusive, that the inflammation always commences in the interior of the left cavities, affecting pri- marily the mitral valve; and that it ex- tends at a later period, and in a limited number of cases to the aortic valve. These facts lead us to expect that in cases of endocarditis the aortic diastolic murmur appears at a later period than the mitral murmur. In two only of the cases was the aortic murmur heard on the day of admission. One of these had been ill a week, and that was the earliest date of the appearance of the murmur. In three of the patients the aortic murmur appeared from the 7th to the 10th days, in one-fourth of them (5) from the 10th to the 15th days, and in more than one-half (10) from the 22d to the 88th days, after the beginning of the attack of acute rheumatism. We have seen that aortic regurgitation is preceded with rare exceptions by a mitral or tricuspid murmur, or a pro- longed first sound over the ventricle, or in other words by evidence, immediate or VOL. II.-41 642 ENDOCARDITIS. secondary, of inflammation of the left cavities of the heart and the mitral valve. In a small proportion of the cases, amounting to three in eighteen, the mur- mur of aortic regurgitation was preceded by prolongation of the second sound over the aorta or the carotid artery. This pro- /ongation of the second sound over the aorta before the appearance of the aortic diastolic murmur, has evidently the same relation to that murmur that prolonga- tion of the first sound has to a mitral or tricuspid murmur. It is a transition sound, and is the immediate herald of the coming complete murmur of regurgitation. An anaemic systolic aortic murmur sometimes precedes the appearance of the diastolic murmur made by aortic regurgi- tation ; but it more often comes at the same time or later, when the two sounds combine to form a true double murmur. This double murmur was present in eleven of the eighteen cases of endocarditis with aortic regurgitation, in four of which the systolic murmur was audible before the diastolic murmur, in five they appeared together, and in two the latter murmur came first into play. The situation of the aortic diastolic murmur of endocarditis is ruled by the position of the aperture of the aorta, and the direction of the back current flowing through it into the left ventricle. The murmur is more loud and intense .to the left of the middle of the sternum, just over the root of the aorta, than else- where. It takes there a direction down- wards and to the left, and is audible to the left of the lower three-fifths of the sternum, becoming feebler as it descends, and is lost usually before it reaches the limit of the lower end of the sternum. The murmur was heard also in five cases as high as the lower end of the manu- brium, and indeed over that portion of the sternum. In rare cases it is audible at the apex. In my cases of endocarditis with aortic regurgitation, the most frequent position of the murmur was to the left of the lower portion of the sternum, a space that ex- tended from the middle of the sternum to its lower end, and from the third left costal cartilage to the sixth ; a space that is immediately in front of the right ven- tricle, w'here it is denuded of lung. The murmur was audible over this space in thirteen of the eighteen cases. In four others it was heard at or to the left of the mid-sternum, a position that is included in the space noted as being to the left of the lower sternum, and which is, there- fore, the position at which the aortic diastolic murmur of endocarditis is heard most frequently and with the greatest in- tensity. In two of the cases the murmur was audible just below, and in one of these over the manubrium. In none of them is it stated that the murmur was heard to the right of the upper portion of the ster- num, a position in which the direct aortic murmur was audible in five of the cases. In the exceptional and doubtful case, the double murmur was restricted to the left second space. There was certainly no regurgitation in that case from the pulmo- nary artery into the right ventricle, and we are therefore, I think, entitled to con- sider that it was, like the others, a case of aortic endocarditis, with regurgitation. In a patient under my care in St. Mary's Hospital an exquisite musical plaintive diastolic murmur sprang up at a late period just over and below the lower por- tion of the manubrium, and over the pul- monary artery in the second space, and was limited to that region. In this case the position of the heart was high and the murmur was heard over a correspondingly high and limited area. In four, and in four only, of the cases the diastolic murmur was heard at the apex. When we consider that the current of blood flows from the aorta back into the left ventricle, it seems natural to expect that the murmur of aortic regurgitation should be heard over the left ventricle, into which the stream of blood falls ; and not over the right ventricle, which, with its double wall and its full contents, is in- terposed between the stream of return- blood and the ear. But the fact is the reverse of this. The murmur is always heard in front of the heart, over the right ventricle, and rarely over the left ventri- cle, to the left of the septum. After a little reflection, the reason of this curious deviation of the direction of the sound becomes apparent. When the aortic valve is incompetent, two streams pour side by side into the left ventricle. One of these comes down, in a large volume of blood, from the left auricle, through the mitral orifice, into the left ventricle ; and this large living stream of blood occupies and completely fills the whole of the outer portion of that cavity, which is the part that is in con- tact with the walls of the chest at and beyond the septum, and at the apex. The other stream is that of regurgitation from the aorta. It is a small and an active stream which plays downwards into the innermost portion of the cavity, or that portion of it which lies immediately be- hind the right ventricle. The large liv- ing stream of blood that pours down from the left auricle into the outer part of the left ventricle, through the mitral orifice, cuts off the inner, deeper, and finer cur- rent flowing back from the aorta into the left cavity, and so silences it. This an- swers the question, why do you not hear the murmur of aortic regurgitation at the RHEUMATIC ENDOCARDITIS WITH ACUTE REGURGITATION. 643 apex and over the left ventricle ? The answer, however, to the second question is still to seek, why do we hear that mur- mur through the right ventricle, with its double walls and its large volume of blood entering freely through the tricuspid ori- fice? When thinking out the answer to this question, we must steadily come back upon the facts as to the position of the aortic orifice, the nature of that part of the ven- tricle immediately in front of the aortic aperture, the direction of the return-cur- rent of blood into the right ventricle, the point of the greatest intensity of the mur- mur, and the bearing of the fading away of the murmur. The aortic valve lies behind the middle of the sternum, at its left edge; in front of it is the conus arteriosus, which is the shallowest part of the right ventricle, its cavity being there wider than it is deep, and its posterior wall being there pushed forwards by the left ventricle and the root of the aorta and the aortic orifice through which this back-current flows ; the walls of the conus arteriosus are here thin, especially the front wall; the blood con- tained in this part of the right ventricle is not in lively motion during the dias- tole, for it is above the current of blood from the right auricle into the right ven- tricle ; and that current pours across from right to left, low down into the larger, deeper, and lower portion of the ventricle behind the lower part of the sternum and upper part of the ensiform cartilage. The murmur rapidly loses loudness and inten- sity as it approaches the lower part of the sternum in front of the tricuspid current, and it is lost before we reach the top of the ensiform cartilage. We now see that the murmur of aortic regurgitation has a shorter way to travel, and passes through a less troubled blood, by passing straight through the arterial cone of the right ventricle, immediately in front of the aortic aperture, than it would if it were to force its way through the large and deep living current of blood that flows from the left auricle, through the mitral orifice, into the left ventricle, and that completely occupies the body and outer or left side of that cavity, where it presents itself at and beyond the septum and at the apex. When active endocarditis passes away and leaves the aortic valve permanently incompetent, the murmur becomes more intense, and its area more extensive. The diastolic murmur may then be pres- ent over the whole length of the sternum, extending to the right of that bone at its upper portion ; and slightly to the right, and to a great extent to the left of that bone at its lower portion ; the area of the murmur sometimes extending as far out- wards as the region of the apex of the heart. The murmur of aortic regurgitation in cases of endocarditis is usually soft, smooth, and like a bellows sound. Some- times it is musical, the note being fine and plaintive, limited in area to the mid- dle of the sternum, or a little above that point, not penetrating, and easily ob- scured by the other sounds of the heart, and by respiration. It was thus in one case-a very pale woman aged 49. On her admission she presented tricuspid, carotid, and loud mitral systolic murmurs, and a musical diastolic murmur over the middle of the sternum. On the fourth day she was better, and all the murmurs were less marked ; and on the sixth they were gone. Next day there was an ob- scure musical diastolic murmur, which also disappeared in a few days. In one case, on the 101st day after admission there was a double musical murmur to the left of the lower sternum. In another case, already alluded to, an exquisite musical murmur appeared just below the manubrium, extended to the left during the time of convalescence, was limited in area, and disappeared in about a week. In another patient, a man, who came in with a mitral murmur, which estab- lished itself, a distinct double murmur appeared for the first time on the 69th day. Six days later the diastolic murmur appeared as a long whistle, but it resumed its usual character on the following day. One other patient that presented a pecu- liar musical diastolic murmur was a woman, aged 40, ill with acute rheuma- tism for four days, who came in with a faint blowing tricuspid murmur, which went on the third day, when she had pain in the heart. On the tenth she was bet- ter in every respect, but a peculiar dias- tolic murmur appeared to the left of the lower sternum, like the twang of a harp- string, which was still audible next day; but this was soon replaced by an ordinary short diastolic murmur to the left of the mid-sternum, which ceased after a few days, when both sounds were a little pro- longed. Dr. Broadbent observed this case with me. In another patient, a man affected with acute rheumatism and endo-pericarditis, a loud, grave musical murmur sprang up in the course of the illness, a vibrating murmur, with a perceptible thrill over the aorta, in the second right space, where the murmur was most intense ; but the sound was heard to a great extent over and even below the chest. This murmur became established. Of the remaining cases (14), in nearly one-half (6) the murmur was soft, or like a bellows sound, and this was undoubtedly its predominant character in the rest, al- though in them the precise nature of the murmur is not stated. In about one-half of the cases of rheu- 644 ENDOCARDITIS. matic endocarditis with aortic regurgita- tion, the murmur disappeared when the patients were under observation ; while in the greater proportion of the remain- ing half, the murmur became fixed, being associated with established mitral regur- gitation in two-thirds of those cases. It was interesting and a source of anxiety to watch the progress of the mur- mur, dwindling and disappearing in the former set of cases, and ripening into per- manent valvular disease in the latter set. We have already seen that the fine musical diastolic murmurs with a limited area disappeared, while the louder ones of that class became established. The character of the early murmur of aortic regurgitation gave little ground for foreseeing whether the incompetence would be permanent or transient. Thus in three, if not four, instances, a diastolic murmur, obscure, faint, feeble or con- fused at first, ripened later into an estab- lished aortic valve disease. The history of the murmur, its develop- ment or decay, the widening out or con- traction of its area, and the presence or absence, the increase or diminution of the characteristic signs of aortic regurgita- tion attendant upon the murmur; give more information as to the actual state, progress, and probable, future of the pa- tient than the exact character of the murmur on any particular day. A statement of the duration of the murmur, and of the attendant secondary signs in the cases in which the valve com- pletely regained its function ; and a brief recital of the leading points in one or two of the cases that ended by producing aortic valve disease, will illustrate prac- tically the probable future prospect of the affection in these important cases. The diastolic murmur was short-lived in all but three of those cases that ended in restoration of the function of the valve, its duration being from one to eight days. In the three others the murmur, which diminished steadily in loudness, or some- times remitted, lasted from fifteen to fifty days. We shall be the better able to under- stand the extent to which these cases de- part from health, and approach to disease, of the aortic valve with regurgitation, by rapidly reviewing the characteristic signs of the established disease, so as to obtain a standard of comparison. The characteristic signs of permanent aortic regurgitation are-enlargement of the left ventricle, fulness over that ven- tricle, and undue force of the apex-beat, which extends beyond and below the left nipple; strong visible pulsation of the carotid arteries; sudden hammering stroke and collapse of the pulse, especially when the arm is raised, when the pulse is visi- ble, and is audible with a loud shock that gradually lessens and disappears when the arm is lowered beneath the level of the heart; diastolic bellows murmur over the whole sternum, its maximum in- tensity being to the left of the middle of the bone; the murmur extending to its left at the lower portion of the sternum, becoming more feeble downwards, and to its right at the upper portion becoming more feeble upwards ; a direct aortic mur- mur, generally audible over the manu- brium, and to its right, where there is a true double aortic murmur; and a grave vibrating systolic murmur in the neck, over the visibly pulsating carotid arterv, which is not followed either by a second sound or a diastolic murmur. When the patient sits up, the extent of regurgitation and the collapse of the artery increases; and as a consequence, the diastolic murmur often becomes louder and more intense and extensive over its proper region; and the systolic murmur becomes more grave over the aorta and carotid artery, or is replaced there by a local and sudden shock when the regurgi- tation is very great so as to empty the ascending aorta during the diastole, the shock being occasioned by the blow with which the advancing column of blood is impelled by the stroke of the left ven- tricle upon the walls of the empty aorta and carotid artery. If the incompetence of the aortic valve is caused by great enlargement of the aperture of the aorta, owing to dilatation of the vessel from atheroma, the artery extends to the right of the upper sternum, displacing the lung, and may present there a thrill and a loud vibrating musi- cal murmur, heard, perhaps, at some dis- tance from the surface, and extending over the whole chest, front and back, the neck, and even the abdomen. My cases of endocarditis with aortic regurgitation ending in complete restora- tion of the valve, presented, with the ex- ception of the double murmur, to a very slight degree the characteristic signs of disease with incompetence of the aortic valves. The diastolic murmur was pres- ent at the mid-sternum, and a little higher, and extended downwards, and to the left, becoming gradually feeble; but it was never heard upwards, over and to the right of the upper sternum, unless it was joined to a mitral murmur. The area of the diastolic murmur was thus limited and it was feeble, very soft, and like a bellows sound, or plaintively musical. A systolic murmur was present over the aorta, or the carotid artery, or both, in two-thirds of the cases, this being an ansemic murmur, and not one caused by obstruction. It was due, in fact, to the flaccid state of the aorta, caused primarily RHEUMATIC ENDOCARDITIS WITH ACUTE REGURGITATION. 645 by the comparatively small amount of blood sent into it by the inflamed and weakened left ventricle, and increased by the reflux of a portion of that blood sent back again into the left ventricle through the inflamed and insufficient aortic valve. This flaccid state of the aorta avowed the blood contained in it to play freely to and fro in a series of noisy vibrations, with the effect of inducing a grave systolic aortic murmur. The impulse was rarely notably strong. It was observed in four of the nine cases of this class. The apex-beat was felt close to the nipple in one of these patients; and in another, in whom the murmur lasted long, it was present on admission in the fifth space, outside the mammary line, and was stronger than usual on the 7th day ; but it retreated within the nipple line from the 12th day, varying in position from the fourth to the fifth space. The second sound, which is usually lost over the carotid artery in disease of the aortic valve, was audible in the neck in seven out of the nine cases of endocarditis in which the incompetence of the aortic valve was only temporary. In several of these cases the second sound was at one time or other less clear than natural over the neck, being feeble in two, grave in a third, and in a fourth, first prolonged, then silent, and afterwards natural, but feeble. Although, then, in these cases, the sec- ond sound is still audible, perhaps, over the aorta, and certainly over its branches, the innominate and carotid arteries, it is often palpably modified in character. The presence of a second sound over the great arteries at the root of the neck, and over the ascending aorta, where it is, however, rendered doubtful by being blended with the transmitted presence of the pulmonic second sound, is due to the slight degree of the imperfection of the aortic valve. The shock of the second sound is therefore caused over those parts by the recoil of the walls of the distended arteries after the end of the systole, which sends the blood not only forwards into the arteries, but with a pressure equal in every direc- tion, also backwards with a return-stroke upon the inner walls of the ascending aorta, including its sinuses, and slightly imperfect valve. The aortic second sound, although present, is often modified in tone and blunted, owing to the force of the back-stroke of the blood being impaired ; (1) by the reflux of a small portion of the blood into the left ventricle through the inflamed and slightly insufficient valve ; and (2) by the lessened supply of blood to the aorta and arteries from the left ven- tricle, the action of which is weakened by the inflammation of its inner surface. The degree to which the second sound over the neck is rendered feeble, blunted, pro- longed, or almost or quite silenced, is a key to the knowledge of the amount of regurgitation, and of the defective supply of blood from the left ventricle. This im- portant element of diagnosis is farther illustrated by what is found in cases of Bright's disease with contracted granular kidney, when the aortic valve is rendered slightly insufficient by the great distension and enlargement of the aorta. Here the blood is sent by the powerful left ventricle into the aorta and the arteries, already rendered tense by the difficult onflow of the poisoned blood through the small ves- sels ; and the relief afforded to the tension by the reflux through the insufficient valves is so slight, that the back-stroke of the blood-caused by the recoil of the arte- rial valves is still made with so much force that the second sound usually re- tains the metallic ring, and the first sound the feeble note, so characteristic of aortic tension from Bright's disease. Some of the cases of endocarditis with aortic regurgitation, ending in disease of the aortic valve, acquired step by step the characteristic signs of the permanent affection. One case of this class, a man, ill a week, came in with quick breathing, a slightly prolonged second sound, and a rather ex- tensive impulse. On the 5th day a soft mitral murmur appeared, which was loud on the 7th, when a diastolic murmur was also audible over the sternum, which ex- tended next day slightly both to the apex and the neck. A week later there was a combination of mitral, tricuspid, and double aortic murmurs, and an obscure second sound was heard in the neck. At the end of the third week the disease was setting into its permanent form, the im- pulse being extensive, the carotid pulsa- tion visible, and the second sound absent from the neck. The diastolic murmur, feeble on the 24th day, was loud on the 34th, when it was combined with a mitral murmur, and the apex-beat was strong. Another patient, a laborer, ill eight weeks, was admitted with profuse per- spiration, tremulous hands, rather quick breathing, and a double murmur to the right of the upper half of the sternum. On the 4th day the murmur was louder, and was audible over the right ventricle ; but on the Gth he was faint, and the murmur was again limited to the aorta. On the 8th day he felt better, and the aortic mur- mur was again audible to the left of the lower portion of the sternum, as well as to the right of its upper portion. Varia- tions followed, renewed diminution of the aortic murmur over the right ventricle being joined to renewed illness ; but after this the systolic murmur became rasping, especially over the third right cartilage, 646 ENDOCARDITIS. and the diastolic bellows sound became again widened in area. The third case of this class, a woman, ill a week, came in with prolongation of the first sound, but no murmur. On the 3d day an obscure diastolic murmur was audible at the left nipple, and on the 7th this murmur was present along the whole sternum, especially from below the manu- brium, and to the right of its upper por- tion. The second sound was heard in the neck, and the pulse was not distinctly audible at the wrist. On the 15th the diastolic murmur, smooth and prolonged, was more extensive downwards ; the sec- ond sound, feeble at the apex, was audible in the neck; and a mitral murmur was present for the only time. On the 29th day the pulse was visible at the wrist, and on the 52d, when she was almost well, there was some fulness over the region of the heart, its impulse being stronger over both ventricles, and especially at the apex. The diastolic murmur was most intense at the fourth cartilage, but was audible along the whole sternum, except its sum- mit. The second sound was still present in the neck, and the pulse was not audi- ble. In these three cases of endocarditis, the affection of the aortic valve advanced steadily, but with variations, under my notice, and during the evolution of the disease its characteristic signs came into play one by one. The next case, a man, stands alone; the aortic regurgitation, after being sus- pended for a time, returned, and again lessened, without disappearing. In the last group of four cases of endo- carditis with aortic regurgitation, ending in disease of the aortic valve, the murmur appeared at a late period of the disease. In one of these patients, a man, the murmur appeared suddenly without warn- ing and in full force on the 88th day, being heard loud along the lower sternum. He had previously presented a variable mitral and an occasional tricuspid mur- mur. This mitral murmur was suspended during a period when the patient was ill with enteric fever, and when prolongation of the first sound was its temporary sub- stitute. A second case of this class, a boy, ill a week, came in with pain in the heart, a friction sound, and a mitral murmur, which was still present on the 5th day. After this there is a gap in the narrative until the 49th day, when there was still a mitral murmur. On the 69th day a double aortic murmur suddenly appeared for the first time, and already the pulse at the wrist was audible when the arm was raised. This diastolic murmur varied, increased, and extended to below the en- siform cartilage, but not to the top of the sternum , was once a long whistle, but generally a bellows sound ; was accompa- nied by a mitral murmur at the apex, probably by a tricuspid, and certainly by a direct aortic murmur, there being no aortic second sound. The impulse of both ventricles became extensive, strong, and peculiar, pointing to adherent peri- cardium ; it presented a double shock, one during the systole, and the other at the commencement of the diastole. In the third case, a woman, one of re- markable interest, a faint diastolic mur- mur appeared to the left of the lower sternum on the 47th day, having been preceded and accompanied by varying mitral and tricuspid murmurs. In this case the thyroid gland became very large on the 64th day ; was a good deal smaller on the 74th, and finally resumed its natu- ral size. There was a distinct double murmur on the 101st day. The last case presented healthy heart- sounds on the 17th day after admission, and on the 22d a soft diastolic murmur came into play to the left of the lower sternum, and a double aortic murmur just below the manubrium. The pulse was audible when the arm was raised, and the impulse was normal in extent. These interesting cases of aortic regurgi- tation, coming on by surprise at a late period in cases of endocarditis, usually with a persistent mitral murmur and ex- tensive and deep-seated inflammation of the interior of the left cavities, show that the aortic valve, though it suffers rarely and slightly when compared with the mitral valve, may silently and without warning, and when the patient appears to be well, break down in its functions by the steady and long advance of a latent in- flammation. When we consider how remote the aortic valve is from the focus of the in- flammation, how passive and rigid the structures at the outlet of the left ventri- cle are in which that valve is imbedded, how gently the flaps of the valve come together, how comparatively slight is the force exerted upon the valve by the back- flow of the blood in the artery, due to the recoil of the walls of the aorta-that ves- sel being imperfectly supplied with blood by the inflamed and weakened left ventri- cle-a force that spends itself mainly in driving the blood forwards, and second- arily in impelling it backwards on the valve, it is only natural that the aortic valve should be rarely incompetent during the attack of endocarditis, and more rarely permanently crippled. These cases per- haps point to a gradual extension of the inflammation on the ventricular surface of the valve, and to the gradual yielding of the inflamed and softened valve ; which at length gives way suddenly at its mar- gin, and so admits of regurgitation from the aorta into the left ventricle. PROLONGATION of the first sound. 647 IV.-Cases of Rheumatic Endocar- ditis with Prolongation of the First Sound. The examination of the cases of endo- carditis in which there was tricuspid, mitral, or aortic murmur, alone or in combination, show, 1 think conclusively, that prolongation of the first sound at the apex or over the right ventricle points to actual or imminent endocarditis. Thus prolongation of the first sound both preceded and followed a temporary tricuspid murmur in three cases, preceded the appearance of that murmur in two other cases, and followed its disappearance in two additional ones. The first sound was therefore prolonged in one-half of the cases (7 in 13) in which a tricuspid murmur was present without a mitral murmur. Again, a mitral murmur when present without aortic regurgitation was pre- ceded and followed by prolongation of the first sound in seven cases ; and was pre- ceded by it in nine, and was followed by it in twenty other instances. The first sound therefore was prolonged in fully two-thirds (36 in 50) of the cases of endo- carditis with mitral murmur in which there was no aortic regurgitation. Finally, the first sound was prolonged in six of the ten cases of endocarditis with aortic regurgitation in which there was no mitral murmur ; and in four of the nine in which there was both aortic and mitral regurgitation or in more than one-half (10 in 19) of the cases of endocarditis with aortic diastolic murmur. If we combine the three series of cases with tricuspid, mitral, and aortic regurgi- tation, we find that in a little more than three-fifths of the whole number (53 in 82' the first sound was prolonged over one or other or both of the ventricles, and that this proportion held its ground in each of the three classes of valvular mur- mur from endocarditis. If we deduct from the 29 patients in whom there was no pro- longation of the first sound, those who both came in and went out with tricuspid or mitral murmur, amounting to fully twelve cases, and who could not therefore present prolongation of the first sound preceding or following a murmur, we naturally increase the proportion in which the first sound was prolonged ; and this proportion would necessarily be still fur- ther increased if we could deduct the unknown quantity of cases in which the prolongation of the first sound escaped observation. It is evident then that prolongation of the first sound is a sign of transition ; that it tends to expand into a mitral murmur when situated over the apex, into a tri- cuspid murmur when over the right ven- tricle, and occasionally into a systolic aortic murmur when situated over the aorta ; and that when either of these mur- murs passes away, it naturally glides into prolongation of the first sound over the region of the lost murmur. Prolongation of the first sound over one or both of the ventricles in a case of acute rheumatism is in itself then a sign, actual, probable, or threatening, of endocarditis affecting the left cavities of the heart. If it is present when the face is covered with a diffused flush, or is dusky and anxious, when the breathing is quickened or op- pressed, or when pain is seated in the region of the heart, and the second sound is intensified over the pulmonary artery, we may at once conclude that the patient is affected with endocarditis. I have included among the cases of endocarditis two of the patients affected with acute rheumatism, who had prolon- gation of the first sound without murmur, but in both of whom that sound was murmur-like; and who had also several important symptoms pointing to internal inflammation of the heart, including pain over the heart in one, pain in the chest in the other, and very great general ill- ness. I have ranked seven of these cases with prolongation of the first sound apart, among a class in which endocarditis was probable and I may say almost certain. In more than one-half, or five, of these nine cases, including both those in which endocarditis was present, and those in which it was probable, the prolongation of the first sound was murmur-like in character. In six of these cases there was a pulmonic murmur ; in four the face was dusky ; in three there was restlessness or delirium ; in two others the sleep was bad ; in three there was pulmonary apo- plexy, or cough, with phlegm ; in one there was pain in the heart; and in two there was pain in the chest. It is more difficult to settle the exact position of those cases with prolongation of the first sound that I have ranked among those threatened with endocardi- tis. Among the cases of this class be- longing to the first series, amounting in the whole to 63, almost one-half (30) pre- sented prolongation of the first sound : and in five more there was a donble mur- mur ; while in nine others the sounds of the heart were affected, the first sound being very loud in three, and doubled in one ; while both sounds were feeble or indistinct in five. Of the 30 patients in whom there was prolongation of the first sound, in one- half (14) there was great or considerable, and in 16 there was slight general illness. I think that we may consider that the fourteen patients with great or consider- able general illness, nine of whom had pain in the region of the heart, were probably, or almost certainly, affected 648 ENDOCARDITIS. with endocarditis. To these perhaps may be added the four patients who presented an obscure murmur. Three of these, how- ever, had but slight general illness. If we add to the fourteen with great general illness and prolongation of the first sound, the case with an obscure murmur and also with great general illness, we may conclude that fifteen of those who were threatened with endocarditis were almost certainly attacked with that affection. Among the 79 cases that are ranked among those who had no endocarditis, seven had prolongation of the first sound, and one had an obscure murmur. All of these had but slight general illness, and I think that they have been properly assigned to their present place. If we examine the cases of the second series, or those treated by means of rest, we find that out of twenty-two cases threatened with endocarditis fourteen pre- sented prolongation of the first sound. Of these nine had pain in the region of the heart, or great general illness, or both, while in one of them the general illness was slight. Eight of these cases may therefore, I think, be almost ranked with the cases of endocarditis. In two of the remaining cases threatened with endocarditis there was a transient murmur. V.-Cases of Rheumatic Endocardi- tis with previous Valvular Dis- ease of the Heart. Previous valvular disease of the heart was present in 22 of the 107 cases of endo- carditis of the first series, and in 7 of the 28 of the second series of cases admitted into St Mary's Hospital under my care during the years 1851-1869-70. Among the cases of the first series, ten had mitral, five had aortic, and seven had mitral- aortic regurgitation, and the seven of the second series had mitral incompetence. Sixteen additional cases with previous valvular disease appear among my 325 cases with acute rheumatism of the first series; and of these eight had endocar- ditis combined with pericarditis, four had "probable" endocarditis, two were "threatened" with that affection, and only two presented no sign or symptom of endocarditis. We thus see that of the total number of cases of acute rheuma- tism with established valvular disease (amounting to 38), 30 (or 79 per cent.) had endocarditis ; in 6 (or 16 per cent.) endocarditis was probable or threatened ; and 2 (or 5 per cent.) had no endocardi- tis. Compare these cases broadly with the rest of the cases of acute rheumatism in which there was no previous valvular disease. Of the total number amounting to 287, 161 (or 56 per cent.), had endocar- ditis, of which 54 had pericarditis also ; in 73 (or 25 per cent.) endocarditis was probable or threatened, including 3 with pericarditis : and in 83 (or 29 per cent.) there was no endocarditis, including 6 with pericarditis. We thus see that pre- vious valvular disease of the heart, in cases of acute rheumatism, exercised an all-powerful influence in exciting endo- carditis. Nor can we wonder at this im- portant result. It has been the key-note, underlying the whole of this long clinical history of pericarditis and endocarditis, that whatever part liable to be affected by the disease, was exposed to the burden of labor, was exposed, in exact proportion to that labor, to the attack of inflamma- tion, the severity and extent of the in- flammation being proportioned to the amount of labor. The presence, then, of established val- vular disease, which adds very seriously to the labor of the heart in cases of acute rheumatism, adds very seriously to the probability, the almost certainty, of endo- carditis in such cases. We have just seen that the influence of valvular disease, which tells with such force in the produc- tion of endocarditis, has but little effect in exciting pericarditis. The reason is, I think, obvious. The great extra work is thrown upon the interior, and not upon the exterior, of the left ventricle, and es- pecially upon its mitral valve. A second local influence, in the altered apertures and roughened surfaces of the mitral and aortic valves, and especially at their mar- gins, comes in to heighten the effect of the local labor in the production of endocar- ditis. The two conditions that prevailed through the whole series of cases of estab- lished valvular disease -with endocarditis are-the variability of the murmur from day to day ; and great general illness. That chain of signs distinguished every case, and that chain of symptoms affected all but two of the whole series of instances of endocarditis with disease of one or more of the valves of the heart. The variability of the murmurs showed itself not only in their greater or less loudness during the successive phases of the disease, but also in their transforma- tion from one tone to another quite dif- ferent ; their extinction, suspension, and reappearance; and their extended, con- tracted, and shifted areas. This varia- tion in the nature, character, and field of the murmur, is governed mainly by three leading influences :-(1) the changes to ■which the valves themselves and the in- terior of the heart are subjected by the inflammation ; (2) the varying power of the heart under the influence of increas- ing general weakness, and returning strength ; and (3) the tumultuous action of the heart owing to local pain, or the struggle to pass the blood onwards through RHEUMATIC ENDOCARDITIS WITH VALVULAR DISEASE OF HEART. 649 the obstructed orifices; or its intermis- sion and failure from the exhaustion of previous overwork. I shall illustrate the variable character of the murmur in these cases of endocar- ditis with previous valvular disease by the brief notes of a few cases, first select- ing from among those with mitral regur- gitation, then those with aortic, and finally those with mitral-aortic valvular disease. The first instance with mitral disease that I shall quote was a young woman who had left the hospital four days pre- viously with a mitral murmur, due to a primary attack of acute rheumatism. She came in suffering from a fresh attack, with a distressed, anxious look, a dusky face, rather livid lips, and accelerated breathing. She had pain over the heart, its action being rapid and tumultuous, and an indistinct murmur. On the 3d day there was a loud systolic murmur at the apex, and the second sound was sharp over the pulmonary artery : and on the 4th she had agonizing pain in the heart, its action was tumultuous, and its sound could not be defined ; she struggled vio- lently and perspired profusely. Next day a loud systolic murmur, tricuspid as well as mitral, was audible over the whole region of the heart. On the 10th day the tricuspid murmur was audible along the sternum, and a second impulse, with a loud second sound, were present over the pulmonary artery in the second left space. On the 18th she was bright and cheerful, but a cough was still present, and the murmur was softer. On the 23d day she walked about the ward, but on the 29th there was a return of pain on movement, and the murmur was louder. After this she did well, there was a thrill over the heart, the murmur was loud over the apex, and was heard over the left scapula. Here the mitral murmur was obscured when the heart was tumultuous ; and was loud and smooth, and joined by a tricus- pid murmur, when the health improved and the heart was steady in its action. Another case, with previous mitral regur- gitation, had, when admitted, tightness of the chest, pain over the heart, and a loud systolic murmur. Three days later, with less pain, the murmur was almost musical at the apex, and quite so below it over the stomach; two days later she looked better, and the murmur presented a third change, being not nearly so loud ; but next day, with returning tightness of the chest, there was a fourth transforma- tion of the murmur, which was rasping or almost musical over the heart; the 10th day, however, with renewed improve- ment, showed a fifth variation in the mur- mur, which was no longer rasping; but on the following day there was a sixth change, and the murmur was musical around the apex; after this, on the 13th day, the murmur was grave, this being its seventh variation ; its eighth occur- ring on the 18th day, when it was again musical over the stomach, and when it was joined by a systolic murmur over the aorta. After this, with steady im- provement, the murmur was no longer variable. A third case illustrates the variations of the murmur during the con- valescent period. These two cases are typical, but their successive snatches of ever-varying mur- mur, contrast with the murmur, now swelling, now dwindling, that is found in other and more simple cases. I will just quote one of these. A youth, a carpen- ter, came in with pain in the chest and a prolonged musical systolic murmur at the apex. This murmur was persistent, but it varied in tone, being grave on the 8th day, when pain was present. The heart's beat was strong. Each of the remaining seven cases pre- sented features of its own ; the variations of the murmur being great and compli- cated in four of them, and in three of them comparatively simple. In four cases, if not five, the mitral murmur was associated with a tricuspid murmur, in one with a pulmonic, and in one with a direct aortic murmur; while in one the first sound was prolonged over the right ventricle. In one of the cases just enu- merated, a diastolic aortic murmur ap- peared and disappeared, reappeared, and was finally extinguished, the mitral mur- mur being permanent throughout. The aortic murmurs of established val- vular disease scarcely vie with the mitral murmurs in variety of tone, loudness and area, and alternate extinction and re- turn, in cases of rheumatic endocarditis ; but I may state that the study of the five cases that I can cite shows that in all these points the diastolic-aortic murmur presents frequent variation ; though the systolic murmur of aortic contraction is much less subject to change. In one case with aortic regurgitation, probably of some standing, tricuspid and mitral murmurs were added temporarily to the diastolic murmur, which varied much and was not always audible during the attack of endocarditis. At the cessa- tion of the illness a double aortic murmur was alone audible. In the other case a double aortic murmur, which went and came again during the illness, was appa- rently joined on the 28th day by a tricus- pid murmur, which had departed on the 34th, leaving a double aortic murmur. The remaining seven instances had pre- vious mitral-aortic valvular disease. Two of the cases belonging to this last group were admitted twice with mitral aortic endocarditis, so that the actual number of patients belonging to it is reduced to five. One of those two patients that 650 ENDOCARDITIS. were thus admitted twice with endocar- ditis, had left the hospital six months previously, after an attack of rheumatic endocarditis, and came in with double aortic, and mitral murmurs ; which varied somewhat in loudness and extent, but were substantially unchanged during this illness. Four years later she returned with severe acute rheumatism and endo- carditis, and died after a very long ill- ness, albuminuria having been finally added to her ailments. The murmurs underwent several oscillations, sometimes the mitral, sometimes the aortic diastolic murmur, being very loud, while at other times one or other of those murmurs was almost or quite extinguished at the heart; the mitral murmur being however gener- ally distinctly though feebly audible over the back of the chest. In the three remaining cases the varia- tions in the murmurs were rather in loud- ness and extent of area, than in the tone and character of the sounds. The extent and strength of the impulse, and their variation during the attack, are among the most decisive tests of the pre- vious presence of valvular disease in cases of rheumatic endocarditis. As a rule, the impulse in such cases is unduly diffused, strong, and propulsive ; and this applies more in degree to cases with mi- tral-aortic, than to those with simple mitral regurgitation. The extent of the impulse in a case of valvular disease with- out endocarditis, is a test of the undue amount of labor to which the heart has been put to overcome the obstacle to the circulation of the blood caused by the affection of the valves. The supervention of endocarditis sometimes, by rendering the heart's action tumultuous, increases the impulse ; but sometimes its effect is the reverse, and by lowering the power of the heart, it lessens the impulse. Among the ten cases of endocarditis with previous mitral incompetence, in- cluding one in which aortic incompetence sprung up temporarily during the attack, in five the impulse was strong, in one it was diffused, in two it was moderate, in one it was feeble, and in one it was not described. In three of those cases the impulse was stronger during the attack of endocarditis than after it, and in two it was the reverse. The impulse of the left ventricle was usually increased in the cases of established mitral incompetence, but that of the right ventricle was, in proportion, more affected in those cases. Among the five cases of previous aortic incompetence with endocarditis, includ- ing the two that were joined during the attack, one by mitral, the other by tricus- pid incompetence, in three the impulse was strong and extensive, especially to- wards the apex ; in one it was diffused but rather feeble ; and in one it was of moderate force and extent. The impulse was more extensive during the attack of endocarditis than after it in one case. The impulse was strong, extensive, and unduly far to the left, in live of the seven cases of previous mitral-aortic incompe- tence with endocarditis ; it was diffused but rather feeble in one ; and in one it was feeble. The impulse appeared to be strengthened during the period of the en- docarditis in four instances, while in one case it was the reverse. Pain was present over the region of the heart in four of the ten cases of endocar- ditis with previous mitral incompetence, in four of the five with aortic incompetence, and in four of the seven with mitral-aortic incompetence. There was pain in the side or chest, or tightness of the chest, not in- cluding those with pain in the heart-in four of the ten with mitral; in one of the four with aortic; and in three of the seven with mitral-aortic valvular disease. There was no pain either in the heart, chest, or side, in two of the ten cases with mitral; in none of the five with aortic ; and in one of the seven with mi- tral-aortic valvular disease, or in only three of the twenty-two cases under con- sideration. We have seen that pain in the heart, side, or chest, occurs in by far the largest proportion of such cases ; and that pain in the parts named is much more frequent in cases of endocarditis in which the heart was previously affected with valvular disease, than in those cases of endocarditis in which the heart was previously healthy. The respiration was seriously affected in a very large proportion of the cases of valvular disease with endocarditis. This condition in such cases is inevitable, for the effect of all the diseases of the valves is to interfere with the efficient onflow of the blood towards the system, and there- fore to throw the blood backwards upon the lungs. This applies of course with primary and immediate force to incompe- tence of the mitral valve, which throws a portion of the blood just received back again upon the lungs, with the effect of overcharging the pulmonary vessels. The return of the blood back again from the aorta, owing to aortic incompetence, into the left ventricle from which it has just been sent, is, however, only one short stage forward from the seat of mitral incompe- tence ; and the almost immediate effect of the aortic incompetence is to produce a back-flow of blood upon the pulmonary vessels, and to delay the blood in those vessels and congest them. The presence of this surplus amount of blood in the lungs, which upsets the healthy balance of the circulation through the lungs and the body, compels the respiratory organs to exert themselves to the top of their power, so that they may, if possible, ex- pel forwards into the body the weight of blood that oppresses them. Hence result CLINICAL HISTORY OF ENDOCARDITIS IN CASES OF CHOREA. 651 laborious, difficult, and rapid breathing, pulmonary apoplexy, pleurisy, catarrh, and bronchitis. The respiration was rapid in four, the chest was painful or tight in two, and cough with pulmonary apoplexy occurred in another of the cases with mitral valve- disease ; while in two of those cases there is no note of the state of the lungs, and in one they were healthy in function. The breathing was quick, or there was cough, or pain in the chest, in four of the five cases with aortic, and in six of the seven with mitral-aortic valvular disease. More than three-fourths, therefore, of the cases of valvular disease with endocar- ditis had serious disturbance of the respi- ratory functions. CLINICAL HISTORY OF ENDOCAR- DITIS IN CASES OF CHOREA. The association of chorea with endo- carditis has long been known, both clinic- ally and from examination after death ; and it has already received illustration in this volume, at pages 531, 532, where two important cases of chorea are alluded to that have been published by Dr. Broad- bent and Dr. Tuckwell, in both of which there was endocarditis, and minute cere- bral embolism ; and in one of which there was acute rheumatism as well as chorea. I had also occasion, in this article on en- docarditis, to give at page 635 a case which illustrates the association of chorea with endocarditis. I shall now give a brief account of the cases of chorea treat- ed by me in St. Mary's Hospital, with especial relation to their association with endocarditis. Clinical History of the Cases of Chorea, in relation to the presence of Endocarditis, observed by the Author in St. Mary's Hos- pital.-I find notes of 40 cases of chorea that were under my care in St. Mary's Hospital, and in 34 of them the signs of the heart are noted, while in 6 of them they are not so. CASES OF CHOREA IN RELATION TO THE PRESENCE OR ABSENCE OF ENDOCARDITIS. 1.-Cases in which there was no endocarditis, heart sounds healthy . 10 2.-Cases in which there was probably no endocarditis :- a. Slight prolongation of the first sound ..... 5 b. Ansemic murmur over the pulmonary artery .... 1 - 6 3.-Cases in which there probably was endocarditis : - a. Prolongation of the first sound ....... 3 b. Murmur, tricuspid or pulmonic ...... 2 - 5 4.-Cases in which there was endocarditis :- a. With mitral regurgitation Ending in restoration of valve ...... 2 Lessening of murmur on recovery . . . . .2 Mitral regurgitation established on recovery . . .8 12 b. With aortic regurgitation........ 1 - 13 34 Cases in which the heart was not observed ...... 6 Total 40 Association of the Cases of Chorea with Rheumatism.-The well-established as- sociation of chorea with articular rheu- matism, renders the study of the connec- tion of rheumatism with these cases of chorea necessary before we consider the occurrence of endocarditis in chorea. Acute rheumatism, as we have just seen, is so very frequently accompanied by en- docarditis that we must be careful, when ascertaining the frequency of endocarditis in chorea, not to attribute the internal in- flammation of the heart too readily to chorea, when it may be caused by the rheumatism associated in certain cases with that affection. Articular rheumatism, in a subacute form, was definitely present during the attack in six of the forty cases of chorea. In five of these cases the rheumatic affec- tion immediately preceded the occurrence, and continued for a short time after the supervision of the attack of chorea. In one of the cases, in which there had been no previous rheumatic attack, the joints became inflamed in the course of the choreal affection. In addition to these six cases of chorea with pronounced articular rheumatism, there were five cases of chorea in which there was pain in all the limbs (in 1), or in the shoulder and hips (in 1), or in the legs 652 ENDOCARDITIS. (in 1), or in the hands (in 1), or there was stiffness of the arms and legs, and of the left ring-finger (in 1). In none of these cases, however, was there swelling or red- ness over the joints; but this does not apply to the redness which affected the wrists, elbows, and face in one patient from violent friction. There were also five cases of chorea that were free from rheumatism during the attack, that gave a history of antecedent acute rheumatism, occurring from two years to two or three months, and in one instance for an uncer- tain period, before the occurrence of the chorea. The proportion in which endocarditis appeared in those cases will be given presently. Proportion of Cases of Chorea in which Endocarditis was present.-In nearly one- third (10 in 34) of the cases of chorea in which the sounds of the heart were ob- served, those sounds were healthy; in one-sixth of them (5) there was slight prolongation of the first sound, and in one case there was a pulmonic murmur. I have classed the six latter cases among those in which there "was probably no endocarditis, and I think we may infer that those sixteen cases, amounting almost to one-half of the whole, were free from inflammation of the interior of the heart. In three cases in which there was marked, almost murmur-like, prolonga- tion of the first sound, and in two with a tricuspid or pulmonic murmur, amount- ing to almost one-sixth of the whole (5 in 34), the presence of endocarditis was probable. The remaining cases, amounting to fully one-third of the whole (13 in 34), gave complete evidence of the existence of endocarditis, in the presence of a mi- tral murmur in twelve instances, and of a diastolic-aortic murmur in one. I think it probable that the majority of the six cases of chorea in which the heart was not observed, ought to be added to those in which there was no endocarditis. Cases of Endocarditis with a Mitral Murmur.-The cases of choreal endocar- ditis with mitral regurgitation, consider- ing the comparatively small number of those cases, offered as great variety in character, mode of commencement, course, and result, as the cases of rheu- matic endocarditis with mitral regurgi- tation. Endocarditis with mitral regurgitation ended more than twice as often in estab- lished mitral disease in chorea, than in acute rheumatism. Mitral regurgitation became permanently established in two- thirds of the cases of chorea with mitral murmur (8 in 12); and in less than one- third of the cases of acute rheumatism with mitral murmur of the first series (14 in 49), and in only one-sixth of those of the second series treated by rest (3 in 20). The integrity of the valve was re- stored in one-sixth of the cases of chorea with a mitral murmur (2 in 12), and in another sixth of them the murmur was becoming feebler when the patient left the hospital (2 in 12). The mitral murmur in fully one-half of the cases (7 in 12) was situated in the re- gion of the apex, and was not described as extending beyond that region; but was simply entered as a systolic mitral murmur, or a systolic murmur at the apex. The five remaining cases, compared with those just dismissed, presented greater breadth of area ; variety in into- nation and volume of sound; and indi- vidual life. In two of these cases the mitral mur- mur was very extensive, being audible over the back of the chest, above and be- low the scapulae, and the greater part of the left side. One of them, when admit- ted, had been ill with chorea in a severe form for some weeks, but the affection was now but slight. A loud systolic murmur centred itself at the apex ; and was audible along the sternum, and far to the right of its lower portion, though feeble at its upper part; from the third to the seventh left costal cartilages ; in front of the epigastrium and the liver; and all over the dorsum, especially on the left side. The impulse of both ventricles was immoderately strong and extensive, the apex-beat being present an inch to the left of the nipple-line. These signs under- went little change after the admission of the patient, and it was evident that the endocarditis had ceased. The other case came in with acute en- docarditis, a mitral murmur being audi- ble at the apex and over the right ventri- cle. A few days later it could be heard towards the axilla, and over the back, as high as the upper part of the scapula. At the end of the seventh week the murmur was grave and musical, and a fortnight later it appeared as a prolonged bellows sound. After this it was hardly so loud, but towards the end of the fourth month after admission it was grave and vi- brating. This case had an interest much broader than the simple relation of chorea to en- docarditis ; for it had interwoven with it from its commencement, and throughout an important part of the early period of its course, the relation of acute rheuma- tism to chorea, and of acute rheumatism to endocarditis also. It began with in- flammation of the ankle, conjoined with chorea. Six weeks later, when admitted, the knee was inflamed, chorea being the most pronounced disease, and the two af- fections being accompanied by endocar- CLINICAL HISTORY OF ENDOCARDITIS IN CASES OF CHOREA. 653 ditis. Was this endocarditis the direct offspring of the subdued attack of acute rheumatism, or of chorea, or of the two conjoined affections, each taking its part in giving a combined birth to endocar- ditis ? During the third week the arms were slightly rheumatic, as well as the lower limbs, and the patient lay motionless in bed, apparently stilled by the affections of the limbs and joints, the chorea being almost or quite latent. After this the rheumatism insensibly disappeared, the chorea insensibly reasserted itself, and for the remainder of the patient's long his- tory, the chorea, modified in form and severity, was the only apparent affection ; accompanied throughout, however, by endocarditis. The other three instances of which I have to speak were cases of chorea, unal- loyed, during the attack, by rheumatic arthritis ; but two of them had suffered some time before from acute rheumatism. One of them, a girl, had been long ill with chorea, and had gone through a rheumatic attack two years before. She came in with a loud, smooth, systolic murmur at the apex, which was audible over the right ventricle. After this the murmur underwent minor transforma- tions, being like a bellows sound on the 4th day, and almost musical on the 8th, when the apex-beat extended further out- wards, the murmur being faintly, if at all, audible below the angle of the left scapula. The apex-beat extended a little beyond the nipple. This case came in with endocarditis, which was evidenced by the varying character of the murmur ; but there is nothing to show whether or not this patient had acquired mitral dis- ease from the old attack of acute rheuma- tism. This last question does not complicate the next case, for though this patient, a girl, had twice been affected with acute rheumatism, yet she had no murmur, but a prolonged first sound, on admission. A murmur, however, appeared at the apex on the 4th day, which was grave on the 6th and the 8th, and was loud on the 14th day, when it extended towards the axilla. The apex-beat was strong on the 6th day, three and a half inches from the sternum ; but on the 8th it could scarcely be felt. The last case, a boy, was free from rheumatic taint, and presented no mur- mur during the first six weeks; but at the end of that time he had pain in the chest, and a week later a smooth bellows murmur appeared at the apex, which three weeks later spread upwards towards the axilla, and downwards over the sto- mach. After this, during a long period, extending from first to last over five months, the murmur underwent various changes, being a very smooth bellows murmur on the 62d day, audible upwards towards the axilla, and downwards over the stomach. Ou the 76th the murmur was very loud and superficial, being heard towards the axilla, but for a very short way below the heart. The first sound was very feeble, while the second was very loud over the pulmonary artery, in the manner already related at page 623. After this the mitral murmur underwent various modulations, being moderately loud on the 102d day, very loud at the apex on the 105th, but scarce- ly audible over the lung to the left, or to- wards the axilla; much weaker on the 126th; but on the 135th day it was loud below, especially on expiration, and was not heard outwards during inspiration. On the 146th day, and the last report, there was very slight fulness over the heart, the impulse of the right ventricle, which seven weeks previously was strong, extending from the third cartilage to the sixth, and from the sternum to the nipple, was on the last observation less strong to the right of the lower sternum, and ex- tended from the second to the fourth car- tilages. The mitral bellows murmur was not so smooth as before, and was again heard up to the axilla. The double im- pulse of the pulmonary artery, previously marked, was no longer perceptible. There was no murmur over the back. He went out comparatively well, being free from choreal movements. In this case, as in that just related, during the attack of endocarditis, when the patient lay speechless in bed, the heart became enlarged, and the lung shrank away from before the heart, ex- posing its increased impulse over a large area ; and the mitral murmur was heard extensively over the region of the con- tracted lung, and that of the stomach. At a later period, however, with return- ing health, strength, and exercise, the lung expanded freely, and interposed it- self between the greater part of the heart and the walls of the chest, so as to cut off the extended border of the area of im- pulse, and to lessen that of the murmur by damping and silencing its sound. Case, of Endocarditis with a Eiastolic- Aortic Murmur.-This patient, a boy, came in with a second attack of chorea, which began three weeks previously with pain in the legs of a rheumatic character, followed, a week later, by choreal symp- toms, which became gradually more se- vere. On his ad mission the heart sounds, so far as they could be made out, were healthy, but on the 3d day a diastolic murmur was audible over the centre of the sternum. Ten days later this mur- mur was heard, very prolonged and loud, over the whole length of the sternum; being audible to the right of the upper ENDOCARDITIS. 654 part of the bone, and to the left of its lower portion, but becoming weaker to- wards the apex of the heart. On the 86th day the diastolic murmur was still loud, and maintained its ground every- where ; and it was joined by a systolic murmur, loudest at the sternum and not mitral. Three weeks later the diastolic murmur was inaudible at the middle of the sternum, and was feeble at its upper and lower portions ; but on the 79th day, the last observation, it had apparently resumed much of its loudness ami extent, and the systolic murmur was silent. In this case, as in one of those just told, the question must be put, Was the endo- carditis caused by the primary articular rheumatism, or by the resulting chorea, or by the combined influence of the two affections ? ENDOCARDITIS IN PYAEMIA. There was only one instance among the 71 cases of pyaemia or secondary inflam- mation examined after death in St. Mary's Hospital in which the appearance of endo- carditis was observed and reported. That case, a man, who was under my care, presented a spot in the right lung, an inch long, consisting of pus, and appar- ently broken down lung-tissue, and super- ficial to this a patch of dry fibrinous de- posit on the pleura ; and numerous spots, similar but smaller, through the back of the middle and lower lobes of that lung. There was also a large globular and fluc- tuating tumor on the upper and inner part of the left kidney three inches in diameter. On cutting into it highly offen- sive blood-like fluid escaped, and on laying it freely open there was a clot of blood and a little pus. The sac was lined with a delicate, highly organized, chorion-like membrane, with . numerous prominent bloodvessels ramifying on its surface. There was a large black spot of apoplectic effusion in the substance of the kidney near the membrane. The structure of the kidney was healthy. The heart was of natural size, and there was a patch of recent roughness on the surface of the left auricle. Several no- dules, from the size of a split pea to that of a millet-seed, were situated on the free margin of the mitral valve. The corpora Arantii of the aortic valve were enlarged. The patient was admitted in a state of great depression, his mind wan- dered, and mucous and sonorous noises were audible over the chest. The state of the heart was not observed. The attack of endocarditis was in this case the marked secondary effect of the pyaemia, but the solitary occurrence of this instance with endocarditis in 71 cases of pyaemia shows that the inflammation of the interior of the heart, so common, as we have seen, in acute rheumatism and chorea, is rare in pyaemia, though less so, as we shall see, than in the fatal stage of Bright's disease. The signs of the heart affection were not observed in this case of pyaemic endo- carditis. I have had, however, frequent opportunities of examining a patient af- fected with pyaemia, in the course of whose very serious illness the signs of endocarditis appeared and held their ground. Pleurisy first showed itself, and the evidence of inflammation in both lungs ; and after a time a systolic murmur became audible at the apex. This mur- mur was constant, but it varied in loud- ness, tone, and area during the course of the illness. After this patient's recov- ery a mitral murmur was established. ENDOCARDITIS IN BRIGHT'S DISEASE. I have only been able to find one in- stance with evidence after death of endo- carditis in the whole of the cases of Bright's disease described in the post- mortem records of St. Mary's Hospital, amounting to 207, excluding those in which there was regurgitation through the mitral or the aortic valve, or through both valves, or obstruction of the mitral orifice. That case was one of fatty dis- ease of the kidney in a man, aged 41, who was under my care. His heart was rather large, weighing 124 ounces, and was dilated and flabby. The structure of the valves was healthy, with the excep- tion of a patch of white deposit on the anterior flap of the mitral valve, which did not appear, after death, to interfere with the function of the valve. This man, when admitted, presented a yellowish pallor and puffiness of face. He had been a healthy man until he took cold, nine months previously, after which he became gradually weak and pale, and had palpitation and frequent vomiting, symptoms with which he was still troubled. There was some albumen in his urine. The right veins of his neck were rather swollen and pulsating, and there was pul- sation of the temporal artery. The heart's impulse was very feeble, and diffused over the cardiac space during expiration only, but it could be felt between the en- siform cartilage and the left seventh cos- tal cartilage. The liver was firm and low, and presented a diffused pulsation in the epigastric space. A soft systolic bellows murmur was audible at the apex, and a peculiar short double murmur between the nipple and the sternum, which was obscured by the natural heart sounds. These murmurs varied considerably from day to day, but CLINICAL HISTORY IN VALVULAR DISEASE OF HEART. 655 they were generally audible, though the ' diastolic noise was more or less obscure. About a week after his admission a pecu- liar humming venous murmur was heard to the right of the sternum when he sat up, but not when he lay down, which, sometimes, disappeared without apparent cause, when it could be brought back by pressure over the jugular vein. On the 42d day he presented consider- able general dropsy, and for the first time the murmurs were very faint and obscure, and two days later they were lost. After this the mitral murmur was sometimes audible, but was generally not so, and the diastolic murmur was only heard once, corresponding with a thrill near the apex. The last observation was made on the 77th day, when a faint systolic mur- mur was heard over the seventh carti- lage, and feeble doubling of the first sound over the sixth cartilage. The urine was then scarcely albuminous, and it had been so during a considerable period of the his- tory of this patient, who died on the 98th day. I have ranked this case as one of endo- carditis, because of the presence of a white deposit on the mitral valve, which was otherwise healthy, and of the history of varying murmurs, pointing to changing affection of the mitral and aortic valves. The long duration of the case, and the small amount of change to which the valve had been subjected, make it doubt- ful whether the endocarditis was present in more than its effect, the white deposit on the mitral valve, at and before the time of death ; but if we take that appear- ance, and the varying signs of double regurgitation into account, I think we may infer that this case was one of endo- carditis. It is true that both mitral and aortic regurgitation may be present in Bright's disease when there is very great tension of the arteries, and great hyper- trophy, with dilatation of the left ventri- cle ; that in such cases those murmurs usually vary in character, according to the varying intensity of the causes that gave them birth; that they may be sus- pended, restored, and again lost, even permanently ; but this case did not present those conditions, for the heart, though dilated, was not greatly enlarged, and was not hypertrophied, since it only weighed 12| ounces. Admitting, then, that this was a case of endocarditis occurring in a patient affected with Bright's disease, it is evi- dent. that as this was the solitary instance of that kind that was noticed among so many cases of Bright's disease without disease of the valves, that although endo- carditis may occur in that disease, yet that it is rare. This becomes more marked when we compare the cases of acute rheumatism, and of chorea, with those of Bright's disease ; for in the two former affections, from one-half to one-third of the cases were affected with inflammation of the interior of the heart. The frequent presence of thickening of the mitral valve, and occasionally of the aortic valve ; and the large proportion of cases of valvular disease without a pre- vious history of acute rheumatism ; per- haps point to the occurrence of endocar- ditis in those cases during the earlier period of their history. If so, endocardi- tis, and pericarditis, behave very differ- ently from each other in Bright's disease, for while pericarditis is common towards the fatal period of this disease, especially when the kidney is granular, and is rare during its earlier history, endocarditis is very rare towards its fatal period, but is not very infrequent during its earlier his- tory ; that is-if the thickening of the valves, and especially of the mitral valve, and complete valvular disease, have their origin in the Bright's disease itself. CLINICAL HISTORY OF ENDO- CARDITIS OCCURRING IN CASES OF VALVULAR DISEASE OF THE HEART. The influence of previous valvular dis- ease in rendering endocarditis more fre- quent and severe in cases of acute rheu- matism has been already seen at page 648. We then observed that the presence in that affection of disease in the valves of the heart, by adding to the labor of that organ, and by rendering its internal apertures more rough and irregular, in- creased the danger of the occurrence of internal inflammation of the heart, and intensified that inflammation when estab- lished. So great, indeed, is the influence of val- vular disease in exciting and intensifying inflammation of the diseased valve, that we find that endocarditis is apt to occur in such cases, even when free from acute rheumatism, chorea, or any other general disease. I would refer here to some interesting remarks by Dr. Moxon on this important subject. The accompanying table (p. 656) will show at a glance the proportion in which endocarditis was present at the time of death in the cases of valvular disease of the heart treated in St. Mary's Hospital. Pathological Evidence of Endo- carditis in cases of Valvular Disease of the Heart. It is difficult, even impossible, in every case to say, from the appearances pre- sented after death, whether or not endo- 656 ENDOCARDITIS. carditis is present on the affected valves, and the adjoining surfaces of the ven- tricle and auricle. This is due to the' readiness with which, in certain cases, a deposit of fibrin from the blood as it streams backwards and forwards through the mitral and aortic apertures, attaches itself to the surfaces of the imperfect valves, roughened by disease. This is equally the result, whether those surfaces be roughened by the slow degeneration of the diseased fibrous tissues, which, al- though they may have been generally in- flamed at the starting point of the disease, yet they may have long ceased to be so ; or whether the surfaces of the valve be inflamed by a recent and renewed attack of local endocarditis. In many instances, however, it is self-evident that inflamma- tion actually affects the valve, for the ap- pearances presented are precisely those that are found in cases of recent endocar- ditis, owing to acute rheumatism, chorea, or pyaemia. Those appearances in these cases are to be confided in, for the dis- eased valves have been described, without, however, as a rule being defined as being inflamed, by a succession of able and careful pathologists, including the dis- tinguished names of Dr. Markham, Dr. Burdon Sanderson, Dr. Murchison, Mr. Gascoyne, Dr. Charlton Bastian, and Dr. Payne. Table showing the number of cases with established valvular disease, among those not affected with acute rheumatism, in which endocarditis wras present at the time of death. Affected W th Bright's disease I.-Cases with established mitral regurgitation :- a. Cases with endocarditis, not affected with Bright's disease 9 5 b. Cases with fibrinous concretions on the valve, probably not affected with endocarditis ......... 2 3 c. Cases in which no description of the valve was found 1 2 d. Cases without endocarditis or concretions ..... 22 19 I.-Total 34* 29' II.-Cases with aortic regurgitation : (A)-from disease of the aortic valve :- a. Cases with endocarditis, not affected with Bright's disease 5 1 b. Cases with fibrinous concretions, endocarditis doubtful or absent . c. Cases in whieh there was no description of the valve 5 5 2 2 d. Cases without endocarditis or concretions 13 12 Total ........ 25 20 (B)-From great dilatation of the aorta, the flaps of the valve being healthy bnt insufficient 5 1 IL-Total with aortic regurgitation . 30 21 III.-Cases with mitral-aortic regurgitation :- a. Cases with endocarditis, not affected with Bright's disease 5 3 b. Cases with fibrinous concretions, endocarditis doubtful or absent . c. Cases in which there was no description of the valve 4 0 3 0 d. Cases without endocarditis or concretions ..... 16 16 III.-Total 28 19 IV.-Cases with obstruction of the mitral orifice - a. Cases with endocarditis affected with Bright's disease 1 1 b. Case with roughness and ulcer at edge of valve .... 0 1 c. Cases with vegetations or concretions on valve, endocarditis doubt- ful or absent .......... 2 1 d. Cases without endocarditis or concretions ..... 18 6 IV.-Total 212 9« 1 I am not certain that these numbers in- clude the whole of the cases with mitral re- gurgitation, since most of the original copies of those cases have been lost or misplaced, and I have taken them from a detached tabu- lated abstract of those cases. This note applies also to the cases of mitral regurgitation given in the Table at page 651. 2 In 5 of these cases the size of the mitral aperture is not described; in 5 it was con- tracted to a moderate extent, and in 19 to a great extent; and in 1 it was almost closed by a ball of organized fibrin. CLINICAL HISTORY IN VALVULAR DISEASE OF HEART. 657 Among the cases of mitral regurgitation, five presented "fringes" and one a ring of small papillary elevations or granula- tions around the free edges of the valve, and two others had warty or rough ex- crescences, and another had nodules of lymph on those free edges ; and in one of these, the auricular surface of the valve was roughened. One of those instances described, I think, by Dr. Payne, pre- sented also yellow succulent elevations, almost resembling a false membrane, but seated under the epithelium. I have also included among the cases of endocarditis four instances with vegetations on the auricular surface of both flaps of the mi- tral valve, and one with extensive ulcera- tion of its anterior flap, in which case the adjoining surface of the ventricle was in- flamed ; five other cases presented large excrescences, or concretions and smaller vegetations, but these I have not included among those with endocarditis, although some of them may have had that affection. This may be said also of a doubtful case in which the posterior flap of the valve was attached to the wall of the ventricle by adhesions readily separated. Five of the fourteen cases that I have classed among those with endocarditis were affected with Bright's disease, and nine of them were not so. Forty-one cases with mitral regurgita- tion were free from vegetations, and of these, nineteen had Bright's disease, and twenty-two were free from that affection. The cases with aortic regurgitation pre- sented comparatively few instances or se- vere, with endocarditis, but these pre- sented great variety in their features. One of them showed deposits of red vege- tations towards the edge and centre of each flap of the aortic valve. In another, the flaps of the valves were cemented to- gether, and then free margins were rough- ened, by fibrinous deposit. In a third the aortic aperture was converted into a mere chink by adhesions; and there was an irregular deposit of lymph, forming vege- tations, about the basis of the conjoined flaps, some being hard, some cheesy, and others apparently quite recent. The uni- ted flaps projected like a funnel into the aorta in the fourth instance, and a little above the valve, and therefore on the inner surface of the aorta, was an oval patch, half an inch long, with a red highly vascular flocculent surface. The aortic valve, in the fifth case, was enlarged but soft. One of the flaps had ulcerated away at the sides, and a large nodular mass was appended to its sesamoid body. The sixth case was one of great interest, with contraction of the descending aorta below the subclavian artery so as scarcely to admit a probe, and embolism, blocking up the left brachial artery. The valve was universally red, soft, pulpy, and form- less, and the aperture was contracted. I had originally only ranked five of these cases as being affected with endocarditis, but I think that the whole six may safely be so classed. Only one of these six cases with endocarditis had Bright's disease, the remaining five being not so affected. Ten other cases presented concretions of various size, some being large, one like an alpine strawberry, attached to the aor- tic valve ; these cases being affected, and unaffected, by Bright's disease in equal numbers. Twenty-five of the cases with aortic regurgitation were free from con- traction, and of these, thirteen had Bright's disease, and twelve were free from that affection. In six cases, aortic regurgitation was due to great enlarge- ment or dilatation of the ascending aorta, the flaps of the aortic valve being healthy in structure, but of insufficient size to close the widened orifice of the aorta. It will I think be sufficient if I state the proportions in which the cases with mitral aortic regurgitation were affected with en- docarditis, presented concretions, without distinct evidence of endocarditis, and were free from concretions, without en- tering into details. I consider that eight of those cases had endocarditis, five being free from, and three being affected with, Bright's disease; four of them had con- cretions on the valves, none of which had Bright's disease ; and in thirty-two there was no concretion on the valves, one-half of these being free from, and the other half affected with Bright's disease. I shall deal with the cases with ob- structed mitral orifice in the manner that I have just dealt with those having mitral- aortic regurgitation. Two of them had endocarditis, one being free from, and one affected with, Bright's disease, and an- other case having that disease presented roughness and ulceration of the edge of the contracted mitral valve; three had vegetations, one of those only having Bright's disease, and twenty-five of them had neither endocarditis nor concretions in any form on the obstructed mitral ori- fice, only seven of which cases had Bright's disease. It is evident that while cases with mi- tral regurgitation are affected in a rather large proportion, or nearly one-fourth (14 in 63), with endocarditis, only one, or at most two, in twenty-nine of the cases with obstruction of the mitral orifice gave evi- dence after death of that affection. Cases with aortic regurgitation occupy a mid- dle position between the two classes just considered, 6 in 51 (or 1 in fl) of these cases being affected with endocarditis. The cases of aortic regurgitation that were free from Bright's disease were much more frequently affected with endocardi- tis (5 in 30 or 1 in 6) than in those that were affected with that disease (1 in 21). vol. n.-42 658 ENDOCARDITIS. Cases with mitral-aortic regurgitation have endocarditis rather more frequently (8 in 47 or 1 in 6) than those with aortic regurgitation (6 in 51 or 1 in 9), and less frequently than those with mitral regur- gitation (14 in 63 or 1 in 4|). Valvular disease was less frequently at- tacked with endocarditis in those cases that were affected with Bright's disease (11 in 78 or 1 in 7) than those that were free from that affection (20 in 105 or 1 in 5'2); and, as we have seen, this tendency in Bright's disease to lessen the frequency of the occurrence of endocarditis in cases affected with valvular disease, prevailed through the whole of the varieties of dis- ease of the valves that we have been in- vestigating, excepting iu cases with mi- tral obstruction. The Signs and Symptoms of Endo- carditis AFFECTING CASES WITH Valvular Disease. The signs and symptoms of endocarditis when it occurs in cases of valvular dis- ease of the heart, not affected with acute rheumatism, do not differ essentially from the signs and symptoms of endocarditis, when it attacks cases of acute rheumatism affected with valvular disease of some standing. 1 have already given a brief clinical history of a series of cases of that class at pages 648-651, and it will, I think, be sufficient if I here refer to the narrative and resume of those cases. As in those cases so in these, the two great distin- guishing features of the supervention of endocarditis upon valves already affected with regurgitant or obstructive disease are (1) the great variability of the valvular murmurs, and of the size of the heart, as indicated by the alternate extension and contraction of the area of the impulse, and the alternate increase and diminution of its force ; and (2) the great general ill- ness with which the patient is affected, an illness not marked by dropsy, but by ele- vation of temperature, over-action or fail- ing power of the heart, and pain in the cardiac region, side, or chest, hurried, difficult, and labored respiration, con- nected often with a congestive affection of the lungs, showing itself sometimes in the form of bronchitis or of pulmonary apo- plexy with its attendant pleurisy. 1 would again refer to the illustrations I have given with regard to those vital symptoms in a previous part of this article. I would here remark that the occur- rence of a special fever, such as enteric fever, may, as we have already seen, sus- pend a mitral or an aortic regurgitant murmur for a time ; but this occurrence proclaims itself by its own distinctive symptoms. I have not given any account of the temperatures of the body in the above clinical histories of pericarditis and endo- carditis ; for the thermometer was only employed in the later cases, and therefore in an insufficient number to enable us to arrive at general results. Endocarditis affecting the Tricuspid Valve. Endocarditis and structural disease of the tricuspid valve are admitted to be so rare in the adult, that there are few clini- cal or pathological records describing affections of that valve. I have examined the whole of the cases of valvular and other diseases of the heart, and of Bright's disease, contained in the post-mortem records of St. Mary's Hos- pital, from 1851 to 1869-70, with" the spe- cial object of ascertaining the frequency, extent, and character of any affection of the tricuspid valve that might occur iu those cases, and the result is given in the accompanying Table. Cases with Affection of the Structure of the Tricuspid Valve, not including instances in which the valve was incompetent owing to the great size of the tricuspid aperture; but including all those in which the edges of the valve were thickened, but the function of the valve was unaffected. Affected with Bright s disease. a. Cases with endocarditis, not affected with Bright's disease 1 1 b. Case with fibrinous concretion on valve ..... 0 1 e. Case with contraction of mitral valve ..... 0 1 d. Cases with thickening and corrugation, or roughness of valve (1 with mitral-aortic reg., 1 with mitral obstr.) . 2 0 c. Cases with thickening of valve, valve not incompetent 11* 7« 14 10 The tricuspid valve was affected with endocarditis in two instances; one of these patients was a woman, aged 40, who had been subject to acute rheumatism when a child, and had palpitation on 1 Of the 11 without Bright's disease, 2 had mitral, 2 aortic, 3 mitral-aortic regurgitation, 2 mitral obstruction, and 1 had no valvular disease. 2 Of the 7 with Bright's disease, 2 had aortic regurgitation, and 5 had no valvular disease. TREATMENT OF ENDOCARDITIS. 659 slight exertion. She had been a patient in the hospital ten months previously with dropsy, ascites, albuminuria, and a mitral murmur. The ascites and dropsy disappeared, but they were greater than before when she was readmitted, when the lips and nose were blue ; and the urine was scanty and very albuminous. The mitral murmur was louder than before, and dyspnoea appeared in paroxysms. The heart was rather large (12 inches), and presented patches of lymph on its surface; the walls of the right ventricle were half an inch thick, being thicker than those of the left ventricle. Warty, rough, irregular fibrous excrescences were pres- ent around the margin of the mitral ori- fice ; looking towards, and being entirely in, the left auricle ; the ventricular sur- face being free from deposit: and there was a smooth fibrinous deposit on the (auricular) surface of the tricuspid valve. The other case with endocarditis of the tricuspid valve, was a woman aged 42, who had contraction of the mitral orifice, which allowed of the passage of but one finger. The heart was of very great size, and its cavities contained twenty ounces of blood, although it only weighed 13| ounces. The tricuspid valve had all its flaps thickened with excrescences along their margins, but the valve itself was competent. She became subject to palpi- tation twelve months previously after a shock or fright. Three days before ad- mission, she raised half a pint of bright blood. The legs and feet were swollen, she had pain in the chest, the heart's action was violent, and there was a con- fused rumbling sound at the apex. There was no albumen in the urine. She be- came gradually worse, and finally palpi- tation and dyspnoea were superseded by drowsiness. In both of these cases, the right side of the heart was excited to excessive and continuous labor by the diseased condition of the mitral valve, which in one instance was affected with regurgitation, and in the other with great obstruction. In one remarkable case a large concre- tion was attached to the tricuspid valve. This patient was a man, aged 69. The heart was large, weighing 16 ounces, the tricuspid valve was universally thickened, and a fibrinous deposit, the size of a nut, was present on the anterior surface of one of the flaps. The tendinous cords were hypertrophied and atheromatous. One of the valves of the pulmonary artery was converted into a hard concrete mass. There is no account of the left side of the heart. These were all the instances that I can find in which there was endocarditis of the tricuspid valve, or the presence of concretions on its flaps ; but the inquiry into the number of other cases in which the tricuspid valve was affected may throw some light on the probable frequency of antecedent endocarditis of the tricuspid valve, as a probable cause of disease of the valve. I may briefly state that in one case there was a contraction of the tricuspid orifice, so as barely to admit two fingers ; and thickening round the margins of the valve; and although the other valves were stated to be healthy, a mitral mur- mur was audible during life. In another case, with mitral obstruction, the edges of the tricuspid valve were thick and corru- gative; and in a third patient, who had been affected with acute rheumatism six months previously, which was followed by mitral-aortic regurgitation, the tricuspid valve, which was not seen, felt rough and thick. These are the only cases that per- mit definite evidence that in them the tri- cuspid valve had been previously affected with endocarditis. There were however eighteen other cases, as may be seen in the Table, in which there was some thick- ening of the tricuspid valve, in two of which it was stated to be atheromatous ; but in none of these cases did it appear that the tricuspid valve was incompetent. Twelve of those cases had mitral, aortic, or mitral-aortic regurgitation or mitral obstruction; and of the remaining six cases that were free from valvular disease, five had Bright's disease. It does not appear to me that any of these cases present definite evidence of the previous existence of endocarditis of the tricuspid valve as the cause of the thickening of its flaps, although it is prob- able that in some of them the valve had been originally inflamed, and especially in those cases that presented aortic, mitral, or mitral-aortic regurgitation, or mitral obstruction. TREATMENT OF ENDOCARDITIS. Endocarditis is so completely an affec- tion associated with those important dis- eases, acute rheumatism and chorea, in which it is rare, with pyremia and Bright's disease, in which it is common, and with established valvular disease, that the pro- per treatment of the parent affection must in all such cases be the proper treatment of the associated inflammation of the val- vular structure of the heart. The treat- ment of those diseases, however, should be modified in the form of additional pre- cautions when endocarditis appears ; and the general treatment of acute rheumatism and chorea must, from the first, be mainly governed by the consideration that in both of them endocarditis is the most se- 660 ENDOCARDITIS. rious natural complication of the general disease. What I have said with regard to the treatment of acute rheumatism in relation to the prevention of pericarditis, applies also to the treatment of acute rheumatism in relation to the prevention, if possible, and the alleviation of endocar- ditis. We have already seen that one- half of the first series of cases of acute rheumatism are affected with endocardi- tis (165 in 325) ; and that in one-half of the remainder (79 in 164) the occurrence of endocarditis is either threatened (in 63) or probable (in 13). This treatment may be summarized in the brief but effectual rules of (1) the absolute rest of every limb and joint, and of the whole body, during the attack of acute rheumatism ; and the maintenance of this absolute rest, espe- cially in the limbs and joints that have been most recently affected, for a period of several days after the complete disap- pearance of the local inflammation ; and (2) the application of the belladonna and chloroform liniment, sprinkled on cotton- wool, over the affected joints, and the support of those joints by the application of flannel over the affected parts so equally adjusted as to give relief and comfort to the patient. We have already seen that the great cause of the inflammation af- fecting the interior of the left ventricle is the powerful exercise and overwork of that ventricle in maintaining the circula- tion through the vessels of the inflamed parts, which at the same time call for a greater supply of blood. The fibrous structures of the heart, in common with the fibrous structures of the joints, are prone to inflammation in acute rheuma- tism; and in the struggle to which the left ventricle is subjected, the valves of that ventricle readily become inflamed at their surfaces and lines of contact. When endocarditis threatens, or first discloses itself, and especially if there be pain in the region of the heart, the application of three or four leeches over that region may be of essential service in lessening the in- flammation, and so perhaps permanently saving the valve. It will be well also to cover the region of the heart with cotton- wool, sprinkled with the belladonna and chloroform liniment. The influence of the treatment of acute rheumatism by means of rest, and the em- ployment of soothing applications and comfortable support to the joints, on the occurrence, severity, and permanent ill effects of endocarditis, will be best illus- trated by comparing the clinical history of the 74 cases treated by rest, with that of the 325 cases not so treated. There was endocarditis alone, or com- bined with pericarditis, in one-half (161 In 325) of the first series of cases that were not treated upon a system of abso- lute rest; and in two-fifths (34 in 74) of the series that were so treated. Valvular disease became established in 43 of the 127 cases (or 1 in 31, or 34 per cent.) of endocarditis with a cardiac mur- mur, including those with pericarditis also (18 in 46), but excluding all those that had previous valvular disease, of the series not treated by rest; and in 3 of the 24 (or 1 in 8, or 12'5 per cent.) of the same kind of cases, of the series that were treated by rest. If we extend the com- parison to the whole of both series of cases, excluding those that had previous valvular disease, we find that 43 in 281, or 1 in 6'6, of the series that were not treated by rest, and 3 in 61, or 1 in 20, of the series that were treated by rest, had established valvular disease, indicated by a permanent murmur after their recovery from acute rheumatism, and at the time of their last examination. There was no murmur, and therefore no valvular disease, when the patient re- covered from the attack of acute rheu- matism, in 60 of the 127 cases with endo- carditis, and without previous valvular disease (or 1 in 21, or 44'4 per cent.), that were not treated by rest; and in 17 of the 24 (or 1 in 1'4, or 71 per cent.) of the cases of the like kind that were so treated. The murmur w'as lessening in intensity at the time of the last observation, when the patient had recovered from acute rheumatism, in 24 of the 127 cases just spoken of (or 1 in 5'4) that were not treated by rest; and in 4 of the 24 (or 1 in 6) of the analogous cases that were treated by rest. We here find that, in the series of cases of acute rheumatism that were treated by a system of absolute rest, the propor- tion of those that were attacked with endocarditis was slightly less than that of those that were not so treated. Thus far the comparison is but slightly in favor of the treatment of acute rheumatism by a rigid system of rest; and this would seem to suggest that a certain, and a very large proportion of cases of acute rheu- matism are habitually and intrinsically attacked by endocarditis. When, how- ever, we extend the comparison, and as- certain the proportion in which those cases of endocarditis, not previously so affected, acquired permanent valvular disease, so as to injure health during the remainder of life, and to shorten life it- self, we discover that the series of cases not treated by a system of absolute rest were thus permanently injured in a far larger proportion of cases, amounting to more than twice as many, or in the ratio of 8 to 3, than in those that were treated by rest. If we pursue the inquiry further, so as carditis: synonyms-definition. 661 to discover the relative extent to which the interior of the heart was inflamed in the two series of cases, we discover that there was but one instance, or 1 in 24, of those with endocarditis and without pre- vious valvular disease, of the series treated by a rigid system of rest, that gave definite evidence of inflammation of both the aortic and mitral valves; while in 19 instances in 127, or 1 in 6'7, of the same kind of cases that were not treated by a rigid system of rest, there was direct evidence of aortic regurgitation. In nine, or rather ten, of those cases that were not treated by rest, there was a mitral mur- mur, and therefore direct evidence of in- flammation of the mitral valve ; but in the remaining nine cases there was also evidence of mitral endocarditis in the shape of a tricuspid murmur, or prolonga- tion of the first sound, with intensifica- tion of the pulmonic sound, and obstacles to the flow of blood through the lungs. The whole chain of evidence points then, I think, irresistibly to the conclusion that the extent, severity, and permanent ill effects of the endocarditis were much greater in the series of cases that were not rigidly treated by rest than in the series that were so treated. Pericarditis, also, attacked a much larger proportion of the cases not treated by a system of rest, or 63 in 325, or 1 in 5'2, than of those that were treated by rest, or 6 in 74, or 1 in 12'2. Thus more than twice as many of the former series of cases, that were not treated by a rigid system of rest, were attacked with peri- carditis, than of the latter series of cases that were treated by a rigid system of rest. I am of opinion, however, from a care- ful revision of the clinical history of those cases, that the treatment by opium, which was pursued in a considerable proportion of the first series of cases that were not treated by rest, had some influence in in- creasing the frequency and severity of inflammation of the heart, and especially of its exterior. Taking this into account, however, I consider that the clinical evi- dence here afforded shows, that the se- verity and permanent ill effects of endo- carditis, and the frequency and severity of pericarditis, are greatly lessened by a system of treatment by rest absolutely maintained; and combined with the use of local means in the shape of the appli- cation of the belladonna and chloroform liniment, and of equal and comfortable support to the affected joints, and the employment of leeches applied over the region of .the heart, when that organ was attacked by inflammation, and especially on its exterior, and when accompanied by pain. The clinical evidence in favor of the treatment of acute rheumatism by rest is conclusively supported on the pathologi- cal grounds stated at the commencement of this article (see page 618), and in Dr. Moxon's very striking, important, and convincing lecture on endocarditis, to which I have there referred. We have there seen that the surfaces or lines of contact, pressure, and friction of the valves, and chiefly of the mitral valve, are especially affected with endocarditis. Thus the overwork of the left ventricle of the heart, and the resulting friction, pres- sure, and tension of its valves, in cases of acute rheumatism and chorea, tend to augment the primary influence of the pa- rent disease, and to excite and intensify the inflammation of the interior of the heart, and especially of the mitral valve. CARDITIS. By W. R. Gowers, M.D. Synonyms.-Myocarditis ; Interstitial Myocarditis. Definition.-An acute affection of the walls of the heart, consisting in intersti- tial serous exudation or cell-infiltration, and degeneration of the muscular fibres. The latter may occur without any change in the interstitial tissue. This has been regarded as a " parenchymatous myocar- ditis." But this change, when general throughout the heart, occurs as the result of some general blood state, and is unas- sociated with other evidence of inflamma- tion in the heart or remaining organs. Without denying the possibility of the occurrence of a general parenchymatous inflammation of the heart, it seems more consistent with the relations of the process to consider these cases as examples of acute degeneration. (See Art. "'Fatty Degeneration.") CARDITIS. 662 Varieties.-The inflammation may be general, affecting all parts of the heart; or it may be partial, being limited to a small area. When general it may be diffused uniformly through the heart; it may affect the superficial layers only(when secondary to pericarditis); or it may re- sult in scattered foci of suppuration. Circumscribed inflammations may result in the formation of an abscess in the wall of the heart. Lastly, the varieties have been distinguished of primary and second- ary inflammation ; the former occurring apart from, the latter in consequence of, preexisting disease, general or local. Etiology.-In the consideration of the causes of the disease, the variety which is due to the extension of inflammation from the pericardium may be excluded from consideration, since it owns the same causes as the pericarditis to which it is due, and is commonly the consequence of acute rheumatism. Other forms of cardi- tis occur in the male much more fre- quently than in the female sex ; and at all ages, but rather more frequently be- fore than after thirty years of age. As a primary affection, carditis is extremely rare: a few of the recorded cases have been ascribed to exposure to cold after severe exertion, or to blows on the pre- cordial region. In other cases no excit- ing cause could be discovered. As a secondary affection it has occurred in a few cases of acute rheumatism, apart, it is said, from endo- or pericarditis, and also in various septictemic affections. Its chief local causes are pericarditis, endo- carditis in rare cases, embolism, and growths in the heart. Pathological Anatomy.-The in- flamed muscular substance is at first in- jected, and then swollen and softened. Points of extravasation are scattered through it; the tissue becomes paler, of a reddish-gray tint, and may break down into a pulpy mass, partly from the acute degeneration and destruction of the mus- cular fibres, and partly owing to their separation by an interstitial infiltration of serum, blood-corpuscles, and corpuscular inflammatory products, derived from the interstitial connective tissue-elements or from the blood. These may be in the form of pus cells, which may be dissemi- nated through the heart in the tracts of connective tissue, or may be aggregated in minute abscesses, in the localized form of inflammation, softening and breaking down of tissue may occur with- out actual pus formation, and a pseudo- abscess may result. If pus cells are formed, a true abscess of the heart is the consequence, and the destruction of the muscular fibres may be so complete that only pus may be found in the cavity. The adjacent tissue is, however, softened and degenerated. Such an abscess may attain the size of a hazel-nut. This local inflammation is much more common in the wall of the left than in that of the right ventricle, and is very rare in the auricles. It is most common in the left ventricle near the apex, in the posterior wall, or in the septum. When softening, purulent or non-purulent, has occurred., the wall is bulged at the spot, and second- ary pericarditis may be produced. When the inflammation is adjacent to the inner surface, it may invade the endocardium, and spread to an adjacent valve. Ulti- mately, in most cases, the outer or inner wall of the abscess or pseudo-abscess gives way, and the contents escape into the pericardial cavity or into the ventri- cle ; causing, in the former case, purulent pericarditis, in the latter, an "acute aneurism of the heart," and septicaemia, usually fatal in a few hours. Both walls have given way at the same time, and "rupture of the heart" has occurred. An abscess in the septum has burst into both ventricles; from the upper part of the septum it has burst into the aorta be- hind the aortic valves, or into the right auricle. In this way a fistulous commu- nication has been established between the two ventricles, between either or both ventricles and the aorta, or between the left ventricle and the right auricle. If the inflammation subsides without the formation of pus, the cellular products may develop into fibrous tissue. This often occurs in the superficial layers of the heart after pericarditis, and it may occur in the localized form of carditis, a circumscribed patch of fibrous tissue re- sulting. Less commonly caseation takes place, even after pus has been formed, and the caseated mass may shrink and calcify. Symptoms.-The symptoms of acute inflammation of the heart are sometimes distinct enough, but are in other cases obscure or misleading. The local signs are those of cardiac weakness, suddenly developed, after, it is said, a transient stage of excitement. The impulse is weakened or imperceptible; the first sound toneless. A systolic murmur has been heard in some cases, due, perhaps, to incapacity of the papillary muscles. The cardiac dulness is normal, or some- times widened, from acute dilatation. The pulse is feeble, frequent, and may be irregular. Uneasiness about the sternal or cardiac region has been an early symp- tom in several cases, increasing in some •to acute pain. The general symptoms are those of heart failure, and those which depend on cerebral anaemia may be so pronounced as entirely to obscure the real nature of the case. Dyspnoea is the most HYDROPERICARDIUM. 663 constant symptom, continuous or felt on the slightest exertion. Nausea and vom- iting, collapse, with coldness of extremi- ties, and clammy perspiration occur. Convulsions, delirium, and coma have been prominent symptoms in several cases. The central temperature is raised; in one recorded case it reached 107°. The symptoms of collapse rapidly increase, and death occurs usually in a few days. Friedreich found the average duration to be four days, the minimum being a few hours, the maximum a week. Localized inflammation of the heart may be attended by similar but less ur- gent symptoms, or may run an entirely latent course until the occurrence of the grave symptoms which proclaim the rup- ture of an abscess, such as, on the one hand, those of acute pericarditis, or on other, those of systemic or pulmonary embolism. In one case a pustular rash occurred, it is conjectured from embolism of the cutaneous arteries. Diagnosis.-The diagnosis is a ques- tion rather of theory than of practice, for the disease is extremely rare, and its symptoms are produced by many other causes. The sudden onset of symptoms of cardiac weakness and failure, less sud- den than in cases of rupture, more sud- den than in cases of acute degeneration, if coupled with considerable elevation of temperature, and especially if occurring in the course of a disease such as pyae- mia, may give rise to a suspicion of the existence of carditis. Abscess of the heart is even more equivocal in its symp- toms. The rupture of an abscess may be suspected if sudden symptoms of systemic or pulmonary embolism or of pericarditis, supervene on less urgent symptoms of cardiac failure. Prognosis. - General carditis has hitherto only been diagnosed after death, and it is doubtful whether recovery has ever taken place. In the circumscribed form it is probable that subsidence of the inflammation has, in a few cases, per- mitted the continuance of the heart's ac- tion and the disappearance of the symp- toms. The prognosis in the form which is secondary to pericarditis is much less grave, since a large proportion of the muscular tissue is not damaged, and, with the subsidence of the adjacent in- flammation, recovers good functional power. Treatment.-The treatment of car- ditis is necessarily symptomatic. Its ex- istence can rarely be ascertained, and, if known, no means of direct treatment ex- ists. Rest to the heart is the first point to be secured. Cold to the precordial re- gion has been recommended ; warm poul- tices would perhaps give more relief. Warmth should be applied to the extremi- ties, to equalize the circulation and lessen the tendency to correlated congestion of internal organs. The heart's action must of necessity be sustained by stimulants which, with the recumbent posture, con- stitute the best treatment for the cerebral symptoms. For the cardiac failure in septicaemia, full doses of the perchloride of iron have seemed to the writer to be of distinct service. IIYDROPERICARDTUM.-HYDROPS PERICARDII. By J. Warburton Begeie, M.D. The occupation of the pericardial sac to a greater or less extent by serous fluid, a condition known under both of the terms mentioned above, or simply as Dropsy of the Pericardium, is not of un- frequent occurrence. Laennec indeed speaks of this condition as being very common. " L'hydro-peri carde," he says, "ou l'accumulation d'une quantite plus ou moins grande de serosite dans le peri- carde, est un cas extremement commun but he qualifies this statement by the re- mark, that idiopathic effusion into the pericardium is very rare, that ordinarily but a few ounces of serum are found in the sac, and that this quantity is effused shortly before death, sometimes at the very moment of dying, or even imme- diately thereafter. The causes of dropsy of the pericardium are various, and some of them most obscure. Dr. Walshe recog- nizes an AcHTe and Passive Hydroperi- cardium ; also, a third form dependent on mechanical obstruction.1 The first of these three varieties is very rare. Dr. Walshe, 1 Trait6 de 1'Auscultation. Des Maladies Au Coeur, chap. xxii.: De 1'Hydro-pericard. 1 Diseases of the Heart, p. 266. 664 HYDROPERICARDIUM however, refers to certain instances of Bright's disease, in which he has known the pericardium fill with fluid, the symp- toms indicating an irritative state, while the signs of pericarditis were wanting. Examples of a precisely similar kind are familiar to the writer, in connection with the dropsy of scarlet fever. He has seen a sudden and copious effusion into the pericardium occur at the same time that dropsical swelling manifested itself in the more ordinary situations, and in such cases, found no evidence whatever of plas- tic formations either upon or within the heart. Passive Hydropericardium is seen in connection with other dropsies, with ana- sarca and ascites, but especially with hy- drothorax. The relation of the latter, however intimate, as in some cases it is, to pleural dropsy, is by no means con- stant. On two occasions we have found a very large Hydropericardium in cases of primary cardiac disease with great anasarca, but with little, if any, hydro- thorax. Mechanical Hydropericardium. - An effusion of serous fluid into the cavity of the pericardium has been fonnd in con- nection with aneurism of the aorta, with cancerous disease seated in the anterior mediastinum, exerting injurious pressure on the great venous trunk, and thus pre- venting the due return of blood through the coronary and pericardial veins, and certain morbid states of the heart itself, in which the venous circulation is greatly embarrassed. In such instances the dropsy, evidently due to direct obstruc- tion near its seat, may with great pro- priety be called mechanical. The serous fluid which occupies the pericardial sac is sometimes colorless ; at other times, although quite limpid, and without any admixture of albuminous floculi, it presents a lemon yellow, or even rose-colored tints ; rarely is it sanguino- lent. The quantity of fluid varies greatly. Usually it is not excessive, but, on the contrary, moderate. In Passive Hydro- pericardium, Dr. Walshe has stated the amount to be from eight to twelve ounces; more than the latter quantity he has never seen. Instances, however, are on record in which a very large accumulation of serous fluid has been found in the pericar- dium. Benisart has related one, in which there existed four pints, or eight pounds (huit livres). From twelve to eighteen ounces of fluid can be injected into the healthy pericardium of an adult, but there can be no doubt that the pericardium, contrary to what is stated in certain anatomical treatises,' is extensible ; the fibrous, as well as serous nature of the membrane may impair, but does not pre- vent its extensibility. In all probability, those cases of enormous distension of the sac by fluid, which are described by Cor- visart, Avenbrugger, and others, were examples of pericarditis. It is apparently when altered by inflammation that the pericardium becomes most capable of dis- tension. Dr. Stokes refers to a case published by Sir Dominic Corrigan, in which the heart was covered with a pulpy lymph, and there was a vast effusion of liquid into the sac,1 and Dr. Graves, in describing a most interesting case of Hydropericar- dium, connected with malformation of, and recent deposition of lymph upon the pulmonary valves, makes the remark, " the pericardium was distended with straw-colored fluid, so abundant that we expected to find pericarditis;"2 implying that this distinguished physician regarded pericarditis as the usual determining cause of large pericardial effusions. The most important and reliable indi- cations of the existence of Hydropericar- dium are furnished by percussion and auscultation, but independently of these, there are other particulars, the value of which is by no means small. A sensa- tion of discomfort in the region of the heart is frequently complained of, and even a sense of weight-a symptom of pericardial effusion to which Lancisi at- tached great significance. Senac describes the undulatory movement of the fluid as visible between the third, fourth, and fifth ribs ; and Corvisart, the sense of fluctua- tion in the same situations, as distin- guished by touch. Dyspnoea, more or less urgent, is usually present in cases of Hy- dropericardium. It must, however, be admitted that there exists no small amount of difficulty in assigning the true share in the production of this symptom to the effusion within the pericardium, seeing that it may in most cases be in part likewise attributed to the visceral disease, on which this form of dropsy depended, or possibly to the hydrothorax, by which it is so likely to be accompanied. A feeble- ness of the pulse, and, not unusually, an intermittent or irregular condition of the pulse exists. By auscultation, the heart- sounds are feebly audible, and appear to be distant or remote. On percussion there is extended pericardial dulness, for the most part not rising so high, nor passing to the same limits laterally, as is the case in chronic, and even in some instances of acute inflammatory effusion within the pericardium. The dilatation of the pre- cordial region, or even of the left lateral region, as noticed by Louis, the epigastric tumor described by Corvisart, and the ex^ 1 E. g., Holden's Illustrated Manual of Anatomy, p. 98. 1 Diseases of the Heart, p. 20. 2 Clinical Lectures : Pericarditis, p. 578. ANGINA PECTORIS AND SUDDEN DEATH. 665 tension of the left lung upwards, of which Dr. Graves and Dr. Stokes have written, are rare but striking phenomena connected with large pericardial effusions, depend- ent, however, on inflammatory action. Besides the general symptoms to which reference has been made, it must be held in view' that others of the same nature wflll be likely to show themselves, the latter, however, having a more distinct relationship with the visceral disease on which the dropsy depends. The Hydro- pericardium, moreover, will in all prob- ability be connected with some other dropsical effusion, hydrothorax or ana- sarca, or it may be ascites. The remedies most useful in the treat- ment of dropsies are seldom effectual in relieving the dropsy of the pericardium. The writer has known the repeated appli- cation of blisters over the region of the heart to produce a decided impression in one case. The stronger diuretics and hydrogogue cathartics, "will," as Dr. Walshe observes, "be tried, were it only for the removal of the usually concomitant dropsies. ' ' Paracentesis pericardii, which has been repeatedly performed in the treatment of pericarditis attended by large effusion, and in some instances success- fully performed, is of course an available means for affording temporary relief in the truly dropsical affection, temporary because, although the heart be freed by the operation from the surrounding fluid, unless the disease giving rise to the dropsy be removed, the fluid must necessarily re- accumulate. ANGINA PECTORIS AND ALLIED STATES; INCLUDING CERTAIN KINDS OF SUDDEN DEATH. By Professor Gairdner, M.D. The phenomena of the disease, or group of symptoms, termed Angina Pec- toris by Heberden, are perhaps the most interesting in themselves, and the most deserving of study in relation to other forms of cardiac disorder, of any which we shall have to consider in this section. In treating of this difficult subject, we must separate with great care the essen- tial facts of the disease from the various speculations, or associated ideas, that almost inevitably force themselves into the mind in considering the facts. And this separation is by no means easy ; for in this instance the facts themselves are apt to be more or less withdrawn from exact observation ; the phenomena char- acteristic of the disease being mostly sub- jective^ i. e., present to the consciousness of the patient only, and only through his description of them made known to the physician. It may even be said with truth, that no one fact in a typical case of angina pectoris is necessarily other than subjective, with the exception of the awful terminal fact of sudden death. And when this is wanting, or when it is de- layed, there is hardly any combination of the remaining symptoms that may not vary in individual cases, or be differently presented by the sufferer, according to the exactness and concentration of his habits of thought, the vividness and power of his imagination, or the degree and kind of his individual sensitiveness to morbid impressions. Still, the fact of sudden death, super- added to the evidence of certain sensa- tions preceding death, may be considered to afford the nearest approach we have to an accurate definition of this disease. What these sensations are we shall en- deavor to indicate, in so far as the inade- quacy of language will allow, from the consideration of such individual instances as have been minutely and carefully re- corded either by the sufferers themselves, or by physicians simply giving expression to the spontaneous testimony of their patients. By following the ideal descrip- tions of those who have allowed them- selves to be guided by theories of the dis- ease rather than by the facts, we might easily add to the fulness without increas- ing the value of our description. First on the list of symptoms, accord- ing to Heberden and the majority of authors who have followed him, is pain.1 1 In his Commentaries (1796), Heberden treats of this disease under the general title "De dolore pectoris" (Sec. Ixx.). In his first communication on the subject to the College of Physicians in 1768 (Medical Trans- actions, vol. ii. p. 59), he merely terms it "A Disorder of the Breast." The two descrip- tions do not differ in essentials, but a few de- tails of difference which seem to be of more or 666 ANGINA PECTORIS AND SUDDEN DEATH. How far pain, in the ordinary sense of the word, is essential to the idea of angina pectoris, we shall afterwards consider ; for the present it may be sufficient to observe that pain, or at least a sensation of local distress amounting in certain cases to pain of a peculiarly overwhelming char- acter, is in this disease closely associated with the symptoms immediately preced- ing death. This peculiar anguish, or, as it might justly be called, agony of suffering, is paroxysmal; it frequently reaches its climax within a few minutes, and is re- lieved or disappears entirely within a like period of time, or at most within an hour or two; it recurs at uncertain intervals, sometimes without any obvious exciting cause, at others manifestly determined by exertion, and especially by too rapid walk- ing up-hill, in which case it often ceases, especially in the earlier attacks, almost immediately on standing still: it is in- stinctively associated in the mind of the patient with the idea of a particularly severe form of oppression or suffocation ; or rather to be more exact, with some indefinable sense of impending danger, to which he is unable to give expression, and which he endeavors to convey to others by similitudes that do not satisfy his own mind. A frequent expression is that recorded by Dr. Latham in the case of a very eminent man of the highest in- tellectual power ; after an attack he said he "could scarcely bear it if it were as severe as it had been and shortly after- wards, "One can bear outward pain ; but it is not so easy to bear inward pain."1 This essential unbearableness of the suffer- ing is most characteristic of angina pec- toris, and it is quite independent of the degree of severity of the pain in other respects. And further it is to be observed that the intolerance here alluded to is not the mere impatience of the nerves, which can be mastered by a strong will and a calm heroic self-restraint; it is the sense that the very springs of life are implicated, and that under a prolongation or increase of the pain the whole machine must sud- denly give way.2 It is from this sense of impending death (rarely thus expressed in words by the patient), and from the fact that sudden death actually occurs during the paroxysm in a certain number of cases, that the pain, or special sensation, of angina pectoris derives almost all that it has of a distinctive character; and therefore Dr. Latham has justly elevated this most important but almost indescrib- able symptom to a co-ordinate rank with the pain itself, in his description of the disease as a whole. Angina pectoris, according to his admirably succinct defi- nition, " consists essentially of pain in the chest and a sense of approaching dis- solution." " The subjects of angina pec- toris report that it is a suffering as sharp as anything that can be conceived in the nature of pain, and that it includes, moreover, something which is beyond the nature of pain, a sense of dying."1 Such, then, are the most important or essential facts which clinical observation teaches in reference to angina pectoris. Let us now consider them separately, and more in detail. The pain of angina is usually felt at the lower sternum, but sometimes also under the middle or upper sternum, in- clining, however, towards the left side.2 Sometimes the pain extends to both sides of the chest in front, and perhaps more frequently into both shoulders, and into the back. Very specially characteristic is a "pain about the middle of the left arm,"3 sometimes present in the right, or in both arms, which, according to Dr. Heberden, occasionally precedes,4 but more commonly follows the pain in the chest. This, together with a degree of numbness of the left arm, may be de- scribed as present in the majority of cases in which the pain extends beyond the thorax.5 The pain and numbness to- 1 Op. cit. pp. 366, 364. 2 11 Always inclining more to the left side." (Heberden, Med. Trans.) " Non raro inclina- tior ad sinistrum latus."-Comment. 3 Heberden, Med. Trans, uti supra. "Dolor sfepissime pertinet a pectore usque ad cubi- tum loevum. . . In nonnullis vero . . . ad dextrum pariter ac laevum cubitum per- tigit, atque etiam' usque ad man us; sed hoc rarius evenit; rarissimum autem est, ut bra- chium simul torpeat ac tumeat."-Comm. loc. cit. 4 Med. Trans, vol. iii. p. 3. 5 The group of symptoms here alluded to, though first clearly indicated by Heberden as characteristic, was described long before by Morgagni in the case of a woman, forty-two years of age who died suddenly during a paroxysm, and was found to have a dilated and ossified aorta. The description is worth quoting, from the fact that it is probably one of the first clinically exact records existing in medical literature of a case of this kind. The patient had been "diu valetudinaria, diuque obnoxia paroxysmo cuidam ad hunc modum se habenti. A concitatis corporis motibus less importance will be noticed below. The eminently careful and exact use of language by Heberden in his singularly condensed clinical studies, whether in Latin or in Eng- lish, tends to invite attention to even the minutest discrepancies between his earlier and later statements. 1 Latham, " Diseases of the Heart," vol. ii. pp. 375-76. It is no secret, that the case was that of the late Dr. Arnold, of Rugby. 2 "Qui hoc morbo tenentur, occupari solent . . . ingratissimo pectoris angore, vitfe extinctionem intentante, siquidem augeretur, vel perseveraret."-Hebekden, Comm. loc. cit. ANGINA PECTORIS AND SUDDEN DEATH. 667 gether, or the pain alone, may extend down to the lingers, or may stop short at the elbow, usually at the inner side of the arm; and painful sensations, more or less definite in character, may be felt also in the neck, or in one or both lower ex- tremities ; but these are exceptional, and there is reason to think that in some cases the local symptoms connected with aueu- rismal tumors implicating the nerves may have been confounded with those more specially characteristic of angina pectoris.1 At all events, these local varieties of pain are not to be regarded as essential ele- ments of the disease, although from their occurrence and their distribution they may lead to more defined conceptions of the nervous plexuses involved,.and thus occasionally to the detection of an organic cause, or of something tending to throw light upon the peculiarities, or to guide the treatment of an individual case.2 Local tenderness on pressure is an oc- casional but by no means a constant symp- tom of angina pectoris. Sometimes, on the other hand, the pain is decidedly re- lieved by pressure, or by rubbing, as well as by counter-irritation of the parts affect- ed. The pains are aggravated by move- ment of the whole body, and especially by severe or even moderate exertion in walk- ing, which indeed becomes impossible during a severe paroxysm. Very marked relief is often afforded by the eructation of wind from the stomach, whether spon- taneously or under the influence of car- minatives. Rest of body, and warmth to the extremities, are among the more ob- vious of the physiological conditions which have been observed to have a well-marked effect in relieving the pains of angina, in their less extreme varieties. The peculiar sensation which culminates in the sense of impending death, has been very variously described,1 and indeed seems from its very nature to be almost indescribable. Among the uninstructed, or in the case of persons unaccustomed to observe and analyze their own sensations, nothing is more common than to find the term "breathlessness," or "want of breath," applied to every kind of thoracic oppression, and the sense experienced in angina pectoris of constriction, or in other cases of repletion in the chest, accom- panied as it usually is by gasping or irregu- lar respiration, is undoubtedly often called a want of " breath," or " suffocation," by persons who are simply feeling about, as it were, for an expression whereby to repre- sent an uncommon and intensely oppres- sive sensation. A similar confusion lies latent even under the more technical lan- guage of Heberden, in his use of the Greek 1 It is difficult to judge from Heberden's descriptions how far the "angor pectoris, in- tentans vitae extinctionem," was regarded by him as a simple pain. In his first memoir he speaks of the "sense of strangling, and anxiety with which it (the disorder of the breast) is attended," and applies the name Angina Pectoris on account of these charac- ters rather than on the ground of pain. The anonymous patient who described his own case in the third volume of the "Medical Transactions," apparently discriminates very sharply, on the one hand between the pain in the left arm and chest, coming on "when walking, always after dinner, or in the even- ing and on the other, the "sensations which seem to indicate a sudden death which he describes as being like " a univer- sal pause within me of the operations of na- ture for perhaps three or four seconds," and afterwards "a shock at the heart, like that which one would feel from a small weight fastened to a string to some part of the body, and falling from the table to within a few inches of the floor." This distinction of the sensation of impending death from the pain was unfamiliar to Heberden, who says he does not remember to have heard it mentioned by any other patient; and thinks that the sudden death of this patient, which came to his knowledge afterwards, was connected more with the pain than with this peculiar sensation. Dr. Parry speaks of the first symptom in angina pectoris as "an uneasy sensation, which has been variously denomi- nated a stricture, an anxiety, and a pain." Dr. Latham was probably among the first to define the sense of impending death as being distinct from the pain. ingruebat molestus quidam angor intra su- periorem thoracis sinistram partem, cum spirandi difficultate, et sinistri brachii stu- pore: quae omnia, ubi motus illi cessarent, facile remittebant. Ea igitur mulier, cum circa medium Octobrem a. 1707 Venetiis in continentem trajecta, rheda veheretur, Ise- toque esset animo, ecce tibi ille idem parox- ysmus; quo correpta, et mori se, aiens, ibi repente mortua est." The examination after death showed disease of the aortic orifice and aorta, and Morgagni regards the sudden death as due to the sudden excitement of car- riage exercise ("insolitum in Veneta fcemina rhed?e motum") operating upon a circulation weakened and obstructed by chronic disease, as to lead to ultimate failure in the power of the heart to propel the blood ("ut sanguis restitans promoveri amplius non poterat").- De Sedibus et Causis Morborum, ii. Epist. xxvi. 31 et seq. 1 As, for instance, in several of the cases recorded by M. Trousseau in his interesting chapter on the subject. (Clinique de 1'Hdtel- Dieu, vol. ii. p. 434 et seq. deuxieme Edition; Paris, 1865.) English Translation, 1868, vol. i. p. 596 et seq. 2 In one very exceptional case, recorded by Heberden in the "Commentaries," there was po pain complained of in the chest, but only in the left arm, having, however, in other respects the characters of angina. After fif- teen years of occasional and increasing suffer- ing, the patient died at seventy-five years of age. 668 ANGINA PECTORIS AND SUDDEN DEATH. term Angina,1 which, according to its ety- mology, signifies a strangling, and accord- ing to its actual and primitive use was ap- plied chiefly to certain affections of the throat, occasionally leading to sudden death by laryngeal suffocation, and giv- ing rise to a sense of choking, or of con- striction in the fauces. Yet Heberden, in using this term, had thoroughly real- ized the fact that angina pectoris is not really a suffocation or a breathlessness, in the ordinary acceptation of these terms. At most it is a sensation which by its urgency and oppressiveness recalls the impression of suffocation, and which may in certain cases be associated with true dyspnoea, or still more frequently with orthopnoea. In many instances, however, careful examination shows, and the pa- tients themselves may be easily convinced, that respiration is really not impeded ; that inspiration and expiration are alike free and noiseless ; that the air is taken into the chest in full measure, and (in so far as the evidence of stethoscopic ex- amination goes to prove the fact) that the mechanical renewal of the air in the vesi- cles of the lungs is perfectly accomplished. In this sense, the observation of Heber- den is profoundly exact, that in the be- ginning of this distemper the patients "nulla tenentur spirandi difficultate, a qua hie pectoris angor prorsus est di- versus."2 And yet it might possibly be maintained that in a more transcendental sense respiration, i. e., the chemistry of respiration, is usually impeded ; that the transit of the blood through the pulmonic capillaries is for the time suspended or impaired, that the right heart is perhaps unduly loaded, and that the sensation of " breathlessness" is therefore not without a physical equivalent in the state of the blood, for the time restricted in its supply of oxygen. In the more advanced stages of angina pectoris, indeed, especially when in connection with organic disease, it rarely happens that some positive evi- dence of real dyspnoea does not exist, at least as a complication, if not as a part of the disease. Even in such compli- cated cases, however, it is usually easy for the experienced clinical observer to de- tect a difference of habit and aspect from cases in which the breathing is primarily impaired, e. g. as in aggravated cases of emphysema with bronchitis, or of double pneumonia, or extensive pleuritic effusion unconnected with a cardiac cause. We are obliged, therefore, under these circumstances, to accept the necessary limitations of ordinary language in con- veying extraordinary or almost indescrib- able impressions. It is certain that the patient in angina pectoris has a sense of obstruction in the thorax so overwhelm- ing and so full of apparently imminent danger that he instinctively likens it to a suffocation yet it is equally certain that in many cases impeded respiration, in the ordinary sense of the term, is not present. This remarkable sensation, which is some- times represented as a tightness or con- striction, sometimes, on the other hand, as a fulness or over-distension of the chest, contributes even more than the pain to the indescribable anguish of an- gina pectoris; and it is this sensation especially which gives to the pain its peculiar character of "unbearableness" already noticed ; this also, which carries with it in its graver forms that impress of immediately impending death, by which the real danger, and the ultimate proba- ble event, are rendered so vividly present to the consciousness of the patient.2 1 "A sense of dissolution, not a fear of it," said one of the most gifted men I ever knew, and one most competent to analyze sensa- tions.-J. R. R. Editor. 2 A recent medical observer, himself a suf- ferer from angina, whose case will be referred to again in the section on treatment, has contributed what is perhaps the only really exact description in medical literature of one form of the constrictive sensation: ' ' The front of the chest seemed to be bulged out in a convex prominence, which suddenly termi- nated at the lower end of the sternum in a sharp and deep depression towards the spine. This was a purely subjective phenomenon. There was no contraction of the diaphragm, and no retraction of the abdominal walls. But though the hand laid upon the parts convinced my mind of their normal condition, it in no way modified the sensation." (Dr. W. Herries Madden, in the Practitioner, vol. ix. 1872, p. 334.) In the case of John Hun- ter, to be cited below (a case of instruction in detail as to many phases of disease in- cluded in the present article), the sense of thoracic constriction in one attack was pre- ceded for a fortnight by symptoms of "ner- vous irritation" in the left side of the face and head, as well as down the left arm. The special sensation in the chest in this case was a "feeling of the sternum being drawn backwards towards the spine, as well as of oppression in breathing ; although the action of breathing was attended with no real difficulty." (See infra, p. 683.) The special Character of the breathing in Hunter's case, elsewhere alluded to, will be found to be a most exact anticipation of what has since been called "ascending and descending," or by some, "suspirious" respiration; a form of disturb- ance frequent in cases of angina, though it seems to have escaped Heberden's observa- 1 From strangulo, whence also the compound words Cynanche and Synanche, and the Latin verb angere, which acquired the secondary sense of undefinable distress conveyed also by anxietas, and still more by our English word anguish. 2 Heberden, Comment, loc cit. "Have no shortness of breath." (Med. Trans, uti supra.) ANGINA PECTORIS AND SUDDEN DEATH. 669 The other symptoms of angina pectoris have been variously described ; so vari- ously, indeed, as to lead to a suspicion of inaccuracies of detail on the part of individual observers of the paroxysm. On all hands it is agreed that in the in- tervals the patient may have all the ap- pearances of perfect health; his color may be good, his appetite unimpaired, his breathing apparently natural, the action and sounds of the heart perfectly normal. It is equally certain that the paroxysm itself is unattended by fever, and that in uncomplicated cases it has none of the characters, as it has none of the consequences, of an inflammatory seizure.1 But it is difficult to accept without hesitation the statement of some authorities, that throughout the attack the pulse may be entirely undisturbed either as to its rate of frequency, or as to its characters.2 In most of the cases in which details have been carefully given, the pulse, at the height of the seizure, has been found small, often imperceptible or irregular in rhythm, but not necessa- rily accelerated, and sometimes morbidly slow; the countenance has been pale as death, the features pinched and anxious, the extremities cold ; there has been often a cold sweat on the brow, sighing or in- terrupted respiration, and other signs of approaching syncope. On the other hand, it must be admitted that in a few in- stances the heart has been heard beating in the very midst of a paroxysm without appreciable alteration in the character of the sounds and impulse, and the pulse has been also said to be regular, and neither rapid nor weak. The senses and the consciousness have also been observed to be frequently quite entire in the midst ot' the paroxysm, though this fact also, like some of the others above mentioned, must be held as subject to numerous excep- tions. On the whole, the strict analogy between the phenomena of angina pec- toris and ordinary syncope cannot be un- reservedly maintained, notwithstanding the arguments of Dr. Parry,1 who, how- ever, has undoubtedly marshalled a strong array of facts and reasonings in favor of this view of the case. The paroxysm of angina pectoris remains, after all, a mode of morbid function sui generis, although in some instances the manner of death in the paroxysm is more or less allied to syncope. The condition of the nervous system, and especially of the brain and spinal cord, in angina pectoris, opens up many very difficult, and at present even insol- uble problems connected with its ultimate pathology. For practical purposes it is sufficient to state the facts established by clinical observation. While it is quite certain, as stated above, that integrity (in a practical sense) of the nervous functions may be maintained up to the very instant of death in certain cases of angina, it is equally well ascertained that in other in- stances giddiness, vertigo, disorders of the special senses, spasms, tonic and clonic, and almost every kind of disorder of the general sensibility and conscious- ness may occur, and may also be the dis- tinguishing features of particular parox- ysms in persons in whom at other times paroxysms may occur devoid of all such phenomena. It is probable that in some of these forms of the disease the cerebro- spinal complications may be determined by special derangements of the circulation within the cranium, or even by disease of tion. See also the remarks on the case of Seneca, below; and at page 683, note. 1 Dr. Latham has admirably modernized Heberden's arguments on this point. (Op. cit. vol. ii. p. 383.) 2 "The pulse is, at least sometimes, not dis- turbed by this pain." (Heberden, Med. Trans.) "Arterise eorum, qui in hoc dolore sunt, naturaliter prorsus moventur. . . . In ipsa accessione pulsus non concitatur." (Comment, loc. cit.) Several authors have followed Heberden here without observing that his real meaning is not that there is no alteration of the pulse, but that there is no excitement of it, i. e. that the pulse is not quickened (" non concitatur") as in inflamma- tion. Dr. Parry, regarding the disease as a syncope, speaks from another point of view, and has no difficulty in showing that the pulse, though not always greatly disturbed, " becomes more or less feeble according to the violence of the paroxysm." Such personal experience as I have on this point leads me to agree with Dr. Parry. The recent experi- ments and sphygmographic tracings of Dr. Lauder Brunton will be discussed in connec- tion with the pathology of the disease further on. 1 His expressions are as follows: "From the preceding observations, I think it evi- dently appears that the Angina Pectoris is a mere case of syncope or fainting, differing from the common syncope only in being pre- ceded by an unusual degree of anxiety, or pain in the region of the heart, and in being readily excited during a state of apparent health, by any general exertion of the mus- cles, more especially that of walking." (In- quiry into the Symptoms and Causes of the Syncope Anginosa, commonly called Angina Pectoris, &c., p. 67.) To the points of differ- ence here noted must be added the persist- ence of the sensibility up to the very instant of death in many cases of angina pectoris, and the incomplete extinction of the pulse; while in ordinary syncope (as for example from emotion, or from hot rooms) the most absolute temporary insensibility, with a radial pulse which cannot be felt, and respiration just sufficient to maintain life, may occur as symptoms and be maintained for some min- utes, with almost no danger to life. 670 ANGINA PECTORIS AND SUDDEN DEATH. the arterial system extending to the brain ; but there are very rarely any per- manent changes, either of structure or of function, tending to throw light on these attacks. On the other hand, it seems premature to infer, with Trousseau, the existence of any distinct relation between epilepsy as a predisposing cause, and angina pectoris ; still more premature to affirm that "in certain cases, and per- haps in a considerable number, the angor pectoris is one expression of this formidable and cruel disease, a phase of its vertigin- ous form, or in two words an epileptiform neuralgia. ''1 The extreme rarity, on the one hand, of true angina pectoris among the countless multitudes of confirmed epi- leptics, on the other of genuine and well- formed epileptic attacks among the sub- jects of angina pectoris, seems to oppose a considerable difficulty in the way of accepting M. Trousseau's hypothesis. That the relation, however, between the occasional cerebro-spinal symptoms in these cases, and the cardiac disorder, is more than a coincidence, is shown by the fact that a very similar series of symptoms is observed in some cases of fatty heart; and the author of this article has in more than one instance observed like phenomena in connection with large aneurisms within the thorax. In certain cases of angina pectoris, more especially when perfect rest cannot be obtained during the attacks, they are apt to be attended by more or less of sickness, and even of vomiting; but these symp- toms are rarely obstinate. Flatulence has been already noticed as a frequent accom- paniment of the paroxysm, the discharge of the imprisoned air by the mouth usually giving marked relief. In some instances the close of the paroxysm is accompanied or followed by a copious discharge of watery urine, as in hysteria. In one case Dr. Walshe has observed tetanic spasms, with complete opisthotonos, followed by local tonic spasms continuing for some hours after the paroxysm. The diagnosis of angina pectoris is not very difficult in severe cases, except in so far as difficulties may arise from the inability of the patient to express his sufferings in -words, or on the other hand from the too fluent and misleading de- scriptions of comparatively insignificant pains referred to the heart, by persons either unduly frightened or unduly sensi- tive. Persons who have lost near rela- tives or even intimate friends, by sudden death of cardiac origin, are extremly apt to be terrified by nervous symptoms of this kind ; gouty and rheumatic sufferers are frequently a prey to flying pains which now and then occupy the habitual seats of angina pectoris, and which sometimes give rise to alarms not justified by the event, all the more when suspicion has been once aroused, and when, as happens not unfrequently, the physician as well as the patient may be for some time in doubt as to the cause of the symptoms. Dis- orders of the stomach, and still more notably of the uterus, frequently lead to pains in the left side, which may pass for cardiac angina. Intercostal neuralgia may have many causes, and not unfre- quently radiates towards the left arm. In hysterical and romantic girls, pains about the heart are often associated with palpi- tation and irregular sighing respiration, sometimes also with well-marked irregu- larities of cardiac rhythm, or with mur- murs requiring care in their discrimina- tion, though not, on the whole, very apt to lead into serious error. Each of these cases requires its own special diagnosis, with reference to the cause of the symp- toms ; and it should always be remem- bered that the number of persons pre- senting themselves on account of such symptoms immensely exceeds that of the sufferers from genuine and dangerous angina pectoris. Moreover, the urgency of the symptoms is usually far less in these affections than in the true angina. The pains, in the milder disorders, are usually much less defined in character, and are never, or hardly ever, accom- panied by so grave a sense of impending dissolution. The diagnosis requires tact and judgment rather than any elaborate rules of investigation, to save the phy- sician from error. A much more difficult diagnosis, and one in which in many cases it is impossi- ble to arrive at more than a proximate conclusion, is the determination of how far any organic disease, and what kind of organic disease, may have had to do with the symptoms present in any particular instance of angina pectoris. Clinically speaking, it may be said that, as a ques- tion of pure experience in the living patient, the formidable prognosis of true angina is not necessarily relieved by the knowledge that after careful examination no organic disease can be discovered ; for, In the first place, organic disease may exist ■without the possibility of discovery ; and, secondly, they are precisely the forms of organic disease most difficult of discovery that have been shown to be most frequently associated with death from angina pectoris. Given, therefore, a very perfectly characterized instance of angina in repeated paroxysms nearly fatal, and tending to increase in severity, it cannot be said that the special diagnosis of organic associated lesions has any very immediate practical significance. The * Clinique M6d. de l'II6tel-Dieu, t. ii. p. 444. Paris, 1865 ; and in the English trans- lation, vol. i. p. 602. ANGINA PECTORIS AND SUDDEN DEATH. 671 prognosis in such cases is emphatically grave in the highest degree, and remains so even after the most careful examina- tion of the organs of circulation has given only a negative result. In cases of minor urgency, however, and in cases where the diagnosis of the angina paroxysm is not perfectly clear and well defined, or where one or two such paroxysms only have oc- curred at long intervals, it becomes a very important question for the physician, and still more for the patient, whether or not there is any organic lesion of the chest forming a barrier to ultimate re- covery, and in case any such lesion exists, whether it is of a kind likely to be rapidly and inevitably fatal, or the contrary. These considerations give an importance to the details of diagnosis in angina pec- toris which at first sight they might not seem to possess, as bearing on prognosis and treatment. Dr. Latham has very truly said that in this respect at least the paroxysm of an- gina bears a certain resemblance to the paroxysm of epilepsy. In the attack it- self we are obliged to act by routine, and are unable to discriminate. It is in the intervals that the physician tries to ad- vance beyond the mere name that has guided him in dealing with the most urgent symptoms, and by careful examina- tion of every organ and every function to discover how the whole organization can be most effectually strengthened against the enemy that is at the gates-nay, that is threatening the very stronghold of life itself. Such a complete investigation, and no other, constitutes diagnosis. It needs scarcely be said that in the first instance the attention of the physi- cian must be concentrated upon the heart, arteries, and great veins. He will inquire with the utmost care into the whole de- tails connected with the circulation, both during the paroxysm and during the in- tervals. He will carefully look for evi- dences of hypertrophy, dilatation, valvular disease. But above all, and even in the absence of these, he will endeavor to esti- mate the probabilities of structural disease in the fibre of the heart itself, or of dis- ease in the coats of the arteries leading, it may be, to induration and obstruction, or to aneurism. Dr. Jenner, the discoverer of vaccina- tion, was the first to make a decided advance in the pathology of angina pectoris. He did not himself publish anything on the subject, but communicated his informa- tion to Dr. Parry,1 by whom his views were substantially adopted and brought before the public. A very remarkable series of facts appeared to these observers to show conclusively that angina pectoris was dependent in many, if not in most cases, on "ossification," or some other form of obstruction by disease, of the cor- onary arteries of the heart. Subsequent researches have proved that this view cannot be exclusively maintained, al- though according to Lussana1 this condi- tion has been found present in twenty- one out of thirty-six fatal cases. The statistics adduced by Sir John Forbes3 show that in twenty-four out of forty-five cases examined after death there were found diseases and degenerations of the aorta ; in sixteen cases the coronary arte- ries were diseased, and in a like number the valves of the heart; while in ten cases there was positive disease, and in twelve cases preternatural softness, of the heart itself. Many authors, from Morgagni downwards, have recorded cases of tho- racic aneurism having in a more or less perfectly developed form the character- istic symptoms of angina pectoris; and we have already alluded to M. Trousseau as confirming by his large and carefully- watched experience the view that such cases may very closely resemble, and may, in fact, for a lengthened period, and after careful observation, be undistinguishable from what he regards as the truly idio- pathic forms of angina. The author of this article is able from personal experi- ence to say that no organic disease has appeared to him more frequently to as- sume the symptomatic characters of angina than aneurism ; and he is also prepared to state as the general result of inquiries pursued over many years, and particu- larly directed to this* subject, that even small aneurisms, arising very near the heart, and especially such as project into the pericardium, or compress in any de- gree the base of the heart itself, are much more apt to give rise to angina-like symp- toms than much larger tumors in more remote positions. The attention of the physician in cases of supposed angina pec- toris should therefore always be very minutely directed to the state of the arterial system as a whole, and more especially to any evidences that may ex- ist of irregularities in the sounds or impulse of the arteries near the heart, or of the aorta in its ascending portion. The care- ful examination by percussion of the sub- sternal region, and especially of the upper sternum ; the comparison of the sounds of the heart with the arterial sounds, as heard at different points of this region; the detection of even slight traces of ab- normal impulse, or of evidences of arterial obstruction at the root of the neck; the comparison of the radial pulses, and the 1 Gazzetta Med. Lombard. 1858-9 (ref. by Friedreich in Virchow's Handbuch, vol. ii. p. 422). 2 Cyclop, of Pract. Med. ; art. Angina Pectoris. 1 Op. cit. p. 3. 672 ANGINA PECTORIS AND SUDDEN DEATH. thorough investigation even of remote parts of the arterial system, may lead to inferences favorable, or the contrary, to the idea of an organic cause for the symp- toms of angina pectoris. Not less important, could it be obtained with reasonable precision, would be the evidence, in any case of angina, of a per- manently weakened or disorganized state of the muscular fibre in the heart itself. We have seen that in twelve of the forty- five dissections collected by Sir John Forbes, there was found preternatural softness, and in ten positive disease of the heart, apart from valvular lesions. That many of these must have been cases of fatty degeneration of the ultimate texture of the organ is rendered extremely proba- ble, if not absolutely certain, by the re- sults of later inquiries,1 which show that in a large proportion of cases of sudden death such changes in the tissue of the heart have been revealed by the micro- scope. On the other hand, it must be admitted that fatty heart has been often observed to be present to a very great de- gree when no symptoms at all resembling angina pectoris have been recorded during life, and when death, too, has not been sudden, but has occurred in the course of ordinary and sometimes of acute disease, having no apparent connection with the state of the heart. This subject will come under consideration hereafter, but in the mean time it may be stated in general terms that while a degenerated state of the cardiac muscular fibre is with great probability to be inferred in angina pec- toris, there are few positive criteria which can be applied so as to ascertain the fact of the degeneration, much less its patho- logical character, or the extent of fibre involved in any particular case. Only after careful and repeated examination of the heart under various conditions of ac- tivity and comparative repose, will a care- ful physician venture an opinion as to the soundness of the organ in this respect, and even then it will be prudent to express his opinion with some degree of reserve. The practical inferences, moreover, which can be safely founded on such an opinion, either in relation to prognosis or treat- ment, are far from being clearly estab- lished. Having as far as possible investigated the condition of the heart and arteries, it will be the duty of the physician to com- plete his diagnosis by a survey of the con- dition of the other organs and functions. Although in many of the most extreme cases of angina pectoris the lungs seem to be perfectly healthy, yet a certain amount of pulmonary congestion or obstruction may attend the disease in particular cases, especially in those complicated with dila- tation of the heart, or with valvular dis- ease. Such cases usually present more or less alteration of the complexion in the direction of lividity, and are also attended by cough, or by true dyspnoea. And it must not always be concluded that the effect of a pulmonary or bronchial compli- cation is to give a more dangerous or hopeless character to the symptoms of angina. On the contrary, the pulmonary disease being frequently of a manageable kind, the application of the proper treat- ment will sometimes extricate the patient from a state of the greatest apparent dan- ger, and allow of the return of the heart to a state either apparently normal, or nearly so. The author has a most vivid recollection of one case in particular, where, on numerous occasions during five or six years, he had to attend a patient manifestly suffering under complex dis- eases of the heart and lungs, with distinct paroxysms of angina, and physical signs of dilatation of the heart. In the worst attacks there was always a nearly or ab- solutely complete disappearance of the pulse at the wrist; the complexion was livid, and the expectoration was of the character usual in hemorrhagic condensa- tion of the lungs, which was also indicated by dull percussion at both bases ; yet from this formidable state the patient again and again rallied under careful treatment of the pulmonary disease, and although the state was evidently one of hopeless char- acter as regards the ultimate termination, he was able in the intervals to pursue a rather laborious occupation. In other instances, the symptoms of angina pecto- ris are associated with enlargement or disease of the liver, and it is not easy to say whether the hepatic disorder is of primary or of secondary origin ; but here also the cautious use of remedies is often very effective in removing the obstruction to the portal circulation, and thereby in restoring the heart to a comparatively sound condition, in which the threatening symptoms of angina may disappear.1 Re- 1 It occasionally happens that the very in- tense and sickening pain of biliary calculus presents a degree of resemblance to angina in its accessories ; and the author has even ob- served cases in which the diagnosis remained doubtful until the yellow tinge of the con- junctiva, appearing after an interval of hours, relieved the apprehensions of the physician. The remarks in the text, of course, apply not to this condition of pseudo-angina, but to the combination of true angina with hepatic con- gestion. But the admission of the existence of such a combination is not to be taken as a confirmation of the view of Brera, and of the elder Latham, that angina pectoris may be 1 Dr. Quain lias stated the argument with reference to the older observations of soft flabby heart, with great force and conciseness in his paper on "Fatty Diseases of the Heart;" Medico-Chir. Trans, vol. xxxiii. p. 129. ANGINA PECTORIS AND SUDDEN DEATH. 673 nal disease forms a very serious and often unmanageable complication, attended by most distressing sickness, or by violent dyspnoea or orthopnoea, and requiring great caution in the use of internal reme- dies, but perhaps not altogether beyond the scope of treatment. Dyspeptic com- plications are usually of secondary import- ance, and cannot be said to be characteris- tic. They are most frequently associated with gouty angina. Among constitutional states, gout is unquestionably the one which is most frequently related to angina pectoris ; in- deed, it would scarcely be too much to say that a large proportion of the sud- denly fatal endings of gout in its irregu- lar and atonic forms, more especially in the forms popularly termed "gout in the stomach," or "gout in the heart," are of this character.1 No doubt the pathology of the states indicated by these terms is very uncertain, and the terms themselves vague and unsatisfactory to the last de- gree ; but enough remains after every de- duction to show-1. That gouty persons, and especially those who have had regu- lar gout, degenerating after repeated at- tacks into the irregular and atonic forms, are subject, in an unusual degree, to the causes of sudden death; 2. That not only is death in such persons apt to be extremely sudden, but, further, the course of the disease is apt to be disturbed by violent paroxysms of internal pain ; 3. That in certain cases the pain has dis- tinctly the character of angina, while in other instances it seems to be associated with dyspeptic suffering, and with dis- orders of the liver and kidneys-the lat- ter, at least, distinctly represented by a special form of disorganization which can be discovered and recognized after death ; 4. That in gouty subjects the heart and arteries are very prone to become disor- ganized, and that the disorganization is specially apt to assume the form which other observations show to give a predis- position to angina, viz., calcareous de- generation of the aorta, especially of its commencement, and of the coronary ar- teries ; 5. That cerebral disorders of va- rious kinds in the gouty have often a like orgin in disease of the arteries of the brain. From these various observations, which will be found amply supported by the experience of physicians, and illus- trated in the treatises of best authority upon gout, it may be inferred that the so- called metastasis of gout to the heart is the result of gradual degenerative changes operating more or less throughout the or- ganism, which, if not so distinctly re- lated as has sometimes been supposed to the gouty paroxysm in its ordinary form, are at all events closely associated with the causes of gout, and therefore form part of its history as a disease of the con- stitution. So much may be fairly asserted here, without involving us in this article in a discussion of the complicated ques- tions of pathology and diagnosis, as well as of treatment, which arise out of the general question of gouty metastasis. As regards other constitutional states associated with, or tending to produce, angina pectoris, nothing is known of suffi- cient importance to find place here. But the careful physician will always endeavor in each case to discover all the causes of deranged general health which may be interfering with the normal state of the functions ; and thus, with each new ob- servation thoroughly and scientifically re- corded, the diagnosis of the disease, and with this many questions bearing on its pathology and treatment, will probably be rescued from the obscurity that at present surrounds the whole subject. What has to be said here about the causes of angina has been to a consider- able extent anticipated in the preceding sketch of the diagnosis. All the asso- ciated diseases maybe regarded as causes, or on the other hand, and sometimes with greater probable truth, as conjoined effects of one or more common causes. Thus, to take the last-mentioned instance, gout may be more or less directly a cause of the angina paroxysm ; or gout and angina pectoris, each of them separately considered in relation to previously exist- ing states of the constitution, may have grown out of like proclivities in respect of age, sex, inheritance, habits of life, &c. In following out this obscure subject, there is great danger of running into over-refinements, which may mislead, and at all events may not be supported by sound practical observation. A few facts, however, remain to be stated as to the predisposing causes. In his classification of cases according to age, Sir John Forbes found that only one-seventh of the cases recorded (12 out of 84) were below the fiftieth year of age; and in respect of sex, only one-eleventh (8 out of 88) were in women. It is just possible, indeed, that these apparent facts may be greatly biased by the mode of col- lection of the instances.1 In a disease the simply a disorder of the liver and nothing more. 1 On this subject see Dr. Brinton's thought- ful dissertation on "Gout in the Stomach," in the second edition of his work on Diseases of the Stomach, p. 354, 1864. vol. n.-43 1 Sir John Forbes, in giving the numbers in the text, expressly states that it is neces- sary to "make some allowance for circum- stances connected, with these recorded cases, before they can be received as grounds for fixing the statistics of the disease, taken 674 ANGINA PECTORIS AND SUDDEN DEATH. symptoms of which are so purely subjec- tive, the deaths of men of eminence, or men of a certain force and decision of character, leading to clear and precise statements as to their symptoms and morbid history, will culminate, as it were, in the minds of physicians, and will be recorded prominently when others would pass unobserved, or at least unrecorded ; and in this point of view it is worth while to remark that the Registrar-General's returns, bearing on sudden death, do not show anything approaching to this re- markable disparity of males and females, nor even the marked if not exclusive pro- clivity of the advanced ages to this form of death. On the other hand, the Regis- trar's returns no doubt include under the term "sudden death" a great mass of utterly heterogeneous cases, some of which have no natural alliance with the disease now under consideration ; and the convictions of individual physicians of large experience tend more or less in the direction of Sir John Forbes's averages.1 Another fact, of importance if correct, ! and so far corroborated by Dr. Walshe, is to be found in certain tables by Sir Gil- bert Blane,2 showing the rarity of Angina Pectoris in hospital practice. Both in hospital and private practice, however, perfectly typical instances of the angina of Heberden are rather rare ; and Sir G. Blane's figures, supported as they seem to be by an appeal to so large a number of miscellaneous cases (3835 hospital, 3813 private), probably mean only that Sir G. Blane was too busy to know much about the internal sensations of his hospital pa- tients, and knew only a little about a very few of his more distinguished private pa- tients. Medical statistics are altogether perverted from their legitimate use when statements of this kind are put forward without qualification, as if numerically exact. It is certain that conditions at least closely allied to angina pectoris are not very rare in hospital practice, and the author of this article has seen enough even of typical instances in hospitals to neutralize the force of Sir G. Blane's re- mark. Still, it may be conceded as at least probable, that in the higher ranks of society cases of extremely sudden death, associated with the symptoms de- scribed by Heberden, and not of aneuris- mal origin, or connected with valvular disease of the heart, bear numerically a higher proportion to the whole field of disease than among the classes usually treated in hospital. The subject, how- ever, is one still open to investigation, and one on which a really adequate con- tribution of carefully and impartially ob- served facts would be of great advantage to science. The facts above recorded, so far as they may be trusted in leading to- wards a conclusion, tend to support the theory of the gouty origin of true angina pectoris. It cannot fail to be remarked that the disease seems to be dominated by the same proclivities of age, sex, and condition in life as gout. And there is further a very general impression among physicians and among the public, not sup- ported by exact statistical evidence, but not on that account to be disregarded, that sudden death from heart disease is frequently hereditary, or at least is found to cling as a tolerably well-marked charac- teristic to certain families, sometimes for several generations. On the other hand, it should be stated, in qualification of this impression, that there are numerous in- stances of eminently gouty families in which no such tendency has been ob- served. The general result of the inquiry into predisposing causes has been stated by Sir John Forbes in terms which may well receive the assent of physicians, at least as a provisional conclusion, till further and more exact analysis of the facts be- comes possible. " Like many other dis- eases," he writes, "angina is the attend- ant rather of ease and luxury than of temperance ; on which account, though occurring among the poor, it is more fre- quently met with among the rich, or in persons of easy circumstances. "* To this it must be added, that the influence of sedentary occupations is remarkably ap- parent in Dr. Quain's collection of cases of fatty heart, in many of which the death was sudden, and with symptoms more or less allied to angina. Thus, in twenty- four of the cases in Dr. Quain's memoir,2 in which the habits of life were noted, they were found to be "sedentary" in twenty-two, "active" only in two cases; and in several cases the sedentary habits were obviously determined by injuries which had restricted the power of exer- cise, or by accumulations of external fat without reference to its degree of severity." His idea is that the "more severe cases, par- ticularly such as depend on organic disease of the heart and great vessels," occur chiefly in males ; the milder in females. "The very severe cases naturally attract more attention, more particularly if they have been termi- nated by a sudden death, and followed by a dissection; and these are the cases that are usually recorded and published." (Art. An- gina Pectoris, Cyclop, of Medicine, vol. i. p. 83.) 1 Among authorities of the first class, Trous- seau is almost singular in disputing this po- sition. " I do not think it proved," he says, " that males are more subject than females to this singular affection." Op. cit., Eng. Transl. p. 603. 2 Med.-Chir. Trans, iv. 133. 1 Loc. cit., vol. i. p. 83. • Med.-Chir. Trans., vol. xxxiii. p. 194. ANGINA PECTORIS AND SUDDEN DEATH. 675 amounting to excessive corpulency. In some cases also, the disease itself has pro- duced an aggravation of the tendency, by still further limiting the capacity for phys- ical exertion, and thus allowing of fatty accumulation. Thus, in the well-known case of John Hunter, who certainly was not chargeable with any original sins of laziness, and who died of angina, it is re- corded that after the tendency had been clearly declared, "the want of exercise made him grow unusually fat." Thus far we have treated of Angina Pectoris as a distinct morbid form or group of phenomena, in which disorders of the circulation tending to sudden death are associated with local pain and other symptoms in the chest of a more or less definable character. But it must be added that many cases of sudden death, in which there is reason to attribute the ultimate result to disease of the heart, have oc- curred apparently without pain, some- times without any, even the slightest, previous evidence of cardiac uneasiness, and certainly without any of the more characteristic and special symptoms of angina pectoris. It remains to consider these cases before proceeding to discuss the pathology of the whole subject. Dr. Latham has justly remarked, in reference to the present subject, that "cases of sudden death often present themselves as mere fragments to our ob- servation. Individuals are found dead. The mode of their dissolution and the circumstances preceding it are unknown." It can only be inferred remotely, as it were, and that only in some instances, from some casual and often very imper- fect observation, that in these individuals the symptoms might possibly have been shown, had they been fully ascertained, to "hold a pathological kindred" with angina pectoris. But again : cases not infrequently occur in which the symptoms observed during life resemble angina pectoris, but where certain of the characters attributed to that disease are either entirely wanting or imperfectly developed. It may be the pain that is wanting to the completion of the picture; it may be the sense of im- pending death, or it may be that sudden death does not actually occur, although most of the other symptoms of angina are present. Can we, with any degree of security, bring out of these nosological "fragments" such new combinations as may tend still further to throw light on the pathology of angina ? In this difficult inquiry, in which we are reduced to the study of "broken lights" and " fragments" of truth, we feel more strongly than ever the inade- quacy of language, as between man and man, in treating of the mysteries of life. We are engaged upon what ought to be a strictly inductive clinical investigation; but the very elements of the induction are in great part withheld. Many pa- tients, when threatened with death, refuse to speak about it, and remain, up to the very last, silent as to what is passing within. Many other patients throw out hints and indications, but are either un- able or unwilling to enter into a detailed analysis of their sensations. A few describe their sensations with great minuteness, but in terms which are almost sure to mislead. From these various causes it happens that sudden death may appear to occur absolutely without previous warning, or with very imperfect previous warning, and yet there may have been in reality a very decidedly abnormal state, fully pre- sent to the consciousness of the patient, but not spoken out by him ; either because the symptoms were unspeakable, or be- cause from one cause or other he was indisposed to speak. On the other hand, sudden death may not occur, and yet a patient may have lived days, or months, or even years, in the apprehension of sud- den death, being warned by such internal sensations as have been described in refer- ence to the paroxysm of angina. When, indeed, pain is the culminating symptom, the patient rarely omits, or refuses to speak out; he is then sufficiently explicit as regards the pain, but in many cases he leaves the other and less definable sensa- sations to be inferred. But where pain is not the culminating symptom, we are often reduced to inference altogether; and it is only in the case of persons whose outward lives and inner thoughts are much before the public, that an inferential diagnosis can be arrived at. Two cases of this kind, occurring in different ages of the world, and under very different cir- cumstances, appear to afford in some degree the means of access to some of the information we are in quest of. One of these is the case of the Roman philosopher Seneca; the other that of the Christian divine Dr. Chalmers. The former case has been often referred to (though with some hesitation, the source of which will be immediately apparent) as one of an- gina pectoris ; the latter has been recorded expressly as a case of sudden death from fatty heart. The case of the philosopher Seneca wras as follows:- In early life he was apparently of deli- cate constitution. It is recorded of him by Dio, that but for the apparent proba- bility of his early death spontaneously, Caligula would have had him destroyed. The supposed disease at this time was a tabes. He himself records that he was nursed with difficulty through a long ill- ness by his aunt (Consolatio ad Helviam, 676 ANGINA PECTORIS AND SUDDEN DEATH. 16). He further speaks in one of his epistles of having been extremely subject to catarrhal duxes (destillationes), anil in another he says that almost every form of bodily disturbance had affected him at one time or other.1 It seems, therefore, extremely probable that Seneca was one of those martyrs to tubercular disease in early life, who, after a more or less pro- tracted period of ill-health became some- what more robust in constitution towards the middle term of life. He was, how- ever, to the last more or less delicate, and at the time of his violent death at the instigation of Nero, he is said by Tacitus to have been "emaciated in body from scanty nourishment."2 The peculiar symptoms, however, which have specially attracted the attention of writers as in- dicating angina pectoris, seem to have been confined to the last two years of his life, according to the opinion of Lipsius, who considers the epistles to Lucilius as having been written when he was sixty- one or sixty-two years of age. What gives a peculiar interest to the descrip- tion, and at the same time may possibly make necessary a qualification of some of its expressions, is the somewhat affected and pretentious tone in which in these letters Seneca, a disciple of the Stoic philosophy, congratulates himself on the ease and freedom with which he could look death in the face, and maintain under severe illness, and in the prospect of sudden death, the calm, self-possessed, and cheerful spirit of the sage. His philo- sophy, under these circumstances, has in its details no important relation to the present inquiry ; but the fact that his mental condition was such as is here described is important. After a long truce from suffering, he says,3 his bad health has returned upon him suddenly. He is as if given over to one disease, as regards which he adds: " I know not why I should give it a Greek name, for it may fitly enough be called Suspirium-a sighing, or want of breath." The attack is very brief and like a hurri- cane-it is over almost within an hour. As compared with any other disease it is like the difference between being sick merely, and giving up the ghost-so that the physicians themselves call this disease meditatio mortis; and sometimes death, which is always threatening in it, actually occurs. Knowing these things Seneca adds that he is by no means confident of recovery, even when relieved from severe symptoms. lie considers only that he has got a respite ; he is perfectly prepared for death ; he does not at any time count even upon seeing out the day. He is, however, buoyant and cheerful, enter- tains himself with gladsome and strong thoughts, even in the midst of the stifling (in ipsa suffocatione). Death is, after all, not to be dreaded by the wise man ; death may take him unawares, but he is never- theless always ready to go. Even at the best, he adds, reverting to his own pre- carious condition, his state is not one of entire comfort; the breathing' is not quite natural; he feels always a degree of im- pediment (hcesitationem quandam ejus et moram'). "Be that as it may be," he adds, "provided my sighing is not in sad earnest" (dummodo nisi ex animo suspirem). He holds himself as in the condition of one likely to be soon ejected, but yet not to be ejected, inasmuch as he is -willing to go. Nihil invitus facit sapiens; neces- sitate™, effugit quia vult quod ipsa coactura est."2 In this case of Seneca wre have, in a highly developed form, the sense of im- pendingdeath, associated with something which he himself crflls a "suffocation," occurring in paroxysms, and causing daily and hourly uncertainty as to his tenure of life. But we have not the severe and peculiar pain of the angina of Heberden, nor have we the actual fact of sudden death, at least in the usual sense of the word ; for, as is well known, Seneca was put to death by Nero, or rather was in- vited to put himself to death ; and what we are able to gather from contemporary history as to his last moments would lead us to infer that death came by no means easily, but after a rather long and tedious struggle. Much doubt has been expressed accordingly, since this narrative "was sug- gested to Dr. Parry by "a learned physi- cian" as a case of angina pectoris, whether the symptoms will bear that construction. Dr. Parry himself inclines to consider it "rather a disorder of respiration than angina pectoris."3 Sir John Porbes, on the other hand, says that "the case of Seneca, as described by himself, has been generally considered a case of angina, and we think most justly."4 It is evi- 1 Omnia corporis aut incommoda aut pericula per me transierunt. Epist. ad. Lucilium, 54. 2 The scanty nourishment here spoken of was not starvation, but probably deficient power of assimilation; for Seneca, as is well known, was enormously rich, and there is no reason whatever to suppose that his stoi- cism ever took the form of asceticism, or of voluntary fasting such as to injure bodily health. 3 Epist. ad Lucilium, 54. 1 "Non ex natura fluit spiritus." The double sense of spiritus in Latin, as of the Greek irvsvfAa, must be kept in view in inter- preting this expression. 2 Loo. cit. Compare also Epist. 61. 8 Op. cit. p. 36. 4 Loc. cit. p. 81. The opinion of Dr. Stokes, published in 1854, and founded mainly on the character of the respiration as implied in the word "suspirium" (which, as we shall hereafter see, he had himself occasion to de- ANGINA PECTORIS AND SUDDEN DEATH. 677 dent that materials fail us in attempting to decide the question ; and they fail pre- cisely at the very point where materials always must fail, unless the fact of actual death, and of sudden death with symp- toms and signs referable to the heart, comes in to decide the point in favor of angina. True, the absence of recorded pain on the one hand, and the presence of something like a record of dyspnoea on the other, have been regarded as additional circumstances in favor of the view that Seneca's disease was spasmodic asthma. But in spasmodic asthma, however severe, there is rarely that vividly present sense of impending death so much dwelt upon by Seneca. Moreover, the noisy paroxysms of asthma would probably have pro- voked some more distinct allusion to the wheezing as a feature of the attack. Hav- ing regard to the idiom of the Latin lan- guage, indeed, the question as between some form of cardiac suffering and asth- matic dyspnoea must remain doubtful; but while the allusions to the breathing are of a very indefinite character, it must be remarked that the sense of impending death is the one obvious fact in the de- scription. 1 Turning now to the case of Dr. Chal- mers, we find in almost every point the converse of that of Seneca. We have here the awful fact of sudden death in all its solemnity and mystery-not only without any adequate clinical history of chronic disease, but without any evidence of angina, or any - other form of acute attack preceding the fatal event. And what adds to the mysteriousness of the result is, that the death took place, not amid any exciting crisis of passion, or of physical exertion, but in the darkness and stillness of the night, when body and mind alike had been undisturbed for hours. One indeed, who knew him,2 has said of his conversation and manner the evening before his death: "I had seen him frequently in his most happy moods, but I never saw him happier." But this is not all. The narrative of Dr. Chal- mer's death, and of the last weeks of his life, has reached us from two particularly well-informed sources. Dr. Hanna, who was his son-in-law and perhaps his most intimate friend, has given us the facts as known to his domestic circle. Dr. Beg- bie, who was his medical attendant, has recorded them with special reference to the observation, made after death, that the heart was in an advanced state of fatty degeneration, soft and friable, the muscular fasciculi barely traceable, with- out visible stria), and everywhere con- taining fatty granules ; the ventricles un- usually thin, the " coronary artery loaded with calcareous deposit, much contracted, and in one place obliterated, presenting considerable resistance to the knife."3 It scribe as characteristic of fatty degeneration of the heart), is too important for its details to be omitted here. We therefore give it en- tire, as it occurs in "The Diseases of the Heart and Aorta," p. 530. "We must agree with Dr. Parry in the opinion that the symp- toms here detailed are not those of angina pectoris. It is remarkable that the occur- rence of pain is not alluded to. But their similarity to that abnormal respiration, al- ready described as the attendant on the fatty heart, is too obvious to be overlooked. For in this affection we see that special form of dyspnoea which may be described as a parox- ysm of sighing. Seneca's words, ' Satis enim aptedicisuspiriumpotest,' and again 'Brevis autem valde, et procellae similis, impetus est,' are singularly expressive of a severe case of the cardiac sighing observed in persons la- boring under fatty heart, for which, when the highest point of suspirious breathing has been reached, we can have no better compari- son than that of a storm. And the words ' Deinde paullatim suspirium illud quod esse jam anhelitus coeperat, intervalla majora fecit et retardatum est et remansit,' well ex- presses the gradual ascent from what we may term the apnoeal period to the extreme point of the paroxysm, and its subsequent decline." It is important to observe, that Dr. Stokes, in the chapter on Deranged Action of the Heart, expresses himself as follows with re- gard to angina pectoris in general: ' ' The respiratory phenomenon which belongs to angina is some form of the sighing respira- tion so important a symptom in the fatty or weakened heart. . . . Upon the whole we may conclude that the special group of symptoms described as angina pectoris by Heberden, Parry, Percival, and Latham, is but the occurrence, in a defined manner, of some of the symptoms connected with a weak- ened heart." Op. cit., p. 487. These re- marks of one of the greatest masters of mod- ern medical observation will be found to have a very special importance in connection with what we have ventured to call, in a subse- quent paragraph, Angina sine Dolore. 1 Seneca, particularly notes that the physi- cians called, his disease meditatio mortis; a very unlikely and unusual form of medical expression for a disease so well known as or- dinary spasmodic asthma. On the other hand, it must be admitted that suspirium was sometimes used as synonymous with asthma. Compare Gael. Aurel. Morb. Chronic. L. iii. 1; and Plin. Nat. Hist, xxiii. 7, 63, § 121. Celsus makes use of difficultas spirandi, and spiritus difficultas, but not of suspirium. The noise of the breathing is specially noticed by Celsus-' ' spirare aeger sine sono et anhela- tione non possit" (L. iv. 8); and also by Cael. Aurel, "stridor, atquesibilatiopectoris." Loc. cit. 2 The Rev. Mr. Gemmel, who was living in his house at the time. See Hanna's Life of Chalmers, edition of 1854, vol. ii. p. 775. 3 Edinburgh Monthly Journal of Medical Science, vol. xii. 1851, p. 205. There were 678 ANGINA PECTORIS AND SUDDEN DEATH. is in the presence of these pathological data (given on the authority of Dr. Ben- nett) that we have to explain, if we can, the known facts of Dr. Chalmers's later life, and of its sudden and mysterious close. And the peculiar interest and value of the case in relation to our pres- ent inquiry consists in the following statements, which are carefully condensed from the two narratives above referred to. Dr. Chalmers was a man not only of great genius and devotion, but of' the most incessant and absorbing occupa- tions. During a life extending nearly to the term of "threescore years and ten," he was scarcely ever withdrawn from public observation. He was eminently, in the highest and best sense, ara| chSpwr- a leader and ruler of men; the "care of all the churches" was upon him, as on St. Paul, and the earnest and ceaseless labors of a life devoted to noble ends, were continued up to the very day before his death, in 1847, in his sixty-eighth year. In 1834, it is true, on the 23d of January, he had suffered a rather alarm- ing attack of hemiplegia, from which, however, he soon recovered ; and in June of the same year there was again a threat- ening ; but with these exceptions his health appeared to have been always good, and equal to every ordinary exer- tion whether of mind or body. " lie was hardly ever incapacitated by infirmity or loss of health from prosecuting his enter- prise ; and from early manhood to green old age, even up to his latest hour, he toiled, and spent his energies and strength." Probably no man in Scotland in the present century, with the doubtful exception of Sir Walter Scott, had led a life of such persistent literary activity, combined with so much and so various intercourse with men of all ranks in so- ciety. In his later years he retired more than previously from public business, but, as Dr. Begbie writes, "he was firm and robust. With accumulating years came a disposition to obesity; and with the silver-gray on the massive forehead came also the pallid and somewhat sickly look of fading health. Yet he seldom com- plained ; or, if indisposed, it was only by some trivial ailment arising from indiges- tion. He was sometimes sick at stomach, but he was never faint, nor ever swooned away. . . . He had no p rmcordial pain or distress in breathing; no palpitation of the heart, or intermission of the pulse. He ascended heights with wonderful fa- cility; he slept on either side, and his rest was calm and refreshing." Such was his state apparently, according to his physi- cian, up to a period indefinitely near the fatal close. It so happens that of the last month of Dr. Chalmers's life we have very exact records, including many memoranda, let- ters, &c., from his own hand. It was a month fraught with unusual excitement and exertion for a man in his sixty-eighth year. On Thursday the 6th of May, 1847, he set out for London to attend a com- mittee of the House of Commons on a subject in which he was very deeply in- terested. lie preached1 in Marylebone Church on the 9th, and on the 12th sub- mitted to a long, searching, and fatiguing examination, wherein Sir James Graham tried to " heckle" him (as he expresses it) for an hour together; but, he writes at the close of a lengthened description of the day's proceedings, "we concluded in a state of great exhaustion, but with an erect demeanor and visage unabashed." Such was his own humorous account of an event which obviously gave him much anxiety. In London, also, he made many visits and saw many sights, not sparing himself at all, or complaining in any way. On the 15th he went to Brighton, where he preached on the 16th, returning to London on Monday. On Tuesday he went to Oxford, seeing the sights of the place, and then going on to Bristol; the remainder of the week he spent there in excursions with great enjoyment, and among friends. He preached on Sunday 1 It may be worth while to remark here that preaching, with Dr. Chalmers, was something very different from the mere delivery of writ- ten words in an audible tone of voice. It was, in truth, a work into which he threw all his great energy of mind and body, and in its effect fully justified the remark of the old Scotchwoman who found it necessary to apologize for her favorite preacher reading his sermon, "Ay, but its/e/f reading Mon." That Dr. Chalmers preached on every Sunday during this excursion is therefore a notewor- thy fact, and the more so as he appears at this time to have been little in the habit of preaching when at home. In a more recent case, where death from heart disease was not sudden, but on the contrary very lingering, and where the very earliest symptoms, twen- ty-seven years before, had been such as to give warning of an impending danger, preach- ing had to be abandoned almost from the first; and although afterwards resumed, it became, in a second attack of ill health, the first duty that had to give way, from its manifest tendency to overstrain the weakened organ. (See the Autobiography and Memoir of the Rev. Dr. Guthrie, recently published; especially vol. ii. pp. 201-41, 215, 16, 18, 406-11.) It is to be observed that a very active use of the pen, and a great deal of work and enjoyment of life, continued possi- ble to Dr. Guthrie for eight or nine years after the formal closure of his career as a preacher. He died in 1873, in his seventieth year. also traces of very chronic disease of the membranes of the brain, but probably not of such amount and character as to have much clinical importance as regards the fatal event. ANGINA PECTORIS AND SUDDEN DEATH. 679 at Bristol, and on Tuesday the 25th was at Darlington. In this interval he wrote a long and carefully considered note on the Education Question for Mr. Fox- Maule, and took a most affectionate leave of his sister, Mrs. Morton, with many effusions of pious feeling, but apparently without any despondency or personal mis- giving as to the future ; on Friday the 28th he returned home, as Dr. Hanna re- cords, "bearing no peculiar marks of fa- tigue or exhaustion." The next day (Saturday) was fully oc- cupied in preparing a Report for the Gen- eral Assembly, which he was to read on the following Monday. On Sunday morn- ing (30th of May) he did not rise to break- fast, but, in answer to inquiries, said- " I do not by any means feel unwell; I only require a little rest." He conversed " with the greatest clearness and vigor;" attended church, and walked some dis- tance afterwards with a friend on his way homewards; spent the evening in appa- rent good health and spirits, and among other occupations wrote to his sister at Bristol a hopeful and affectionate letter, expressive of perfect contentment and satisfaction. He retired to rest at the usual time, and the next morning was discovered dead and cold. The separate accounts given by Dr. Hanna and Dr. Begbie leave no doubt that death took place long before the morning light, but at what exact period it was impossible to say. The body had an attitude of calm repose. "The bed- clothes were scarcely disordered; on them rested a basin which had received the contents of the stomach." 1 This was the only evidence of anything like a death- struggle. Had it not been for this, it might have been supposed that Dr. Chal- mers died in his sleep. Cases like that of Dr. Chalmers (in re- spect to the suddenness of the fatal close) have often been recorded; but in very few of those in which the fatal result has been most sudden and startling have there been any such records of the incidents preceding death as are given above. In not a few of the cases observed personally by, or more or less intimately known to, the author of this article, there has been reason to believe that considerable suffer- ing, or sense of disability, though not always of one and the same character, has been present; and in some of these it might easily, perhaps, have escaped at- tention had the individual been extremely reticent, or not surrounded by anxious friends, intent upon everything that ap- peared to affect the comfort of one dear to them, or the well-being of a family. In several instances, the first note of real alarm has been sounded on the discovery of an irregularity in the pulse ; in one such case, sudden death took place within a fortnight, or at most three weeks, after this discovery.1 In other cases there has been an indefinite distress felt on exertion, or on going up a hill; in a few, the more regular form of angina pectoris. One pa- tient who had more or less of angina-like pain (so-called) breathlessness on exertion for at least some years, died at the last in bed, in the night, and at the side of his wife, who was not even awakened, or in any way made aware of his being at all uneasy, but found her husband motion- less and half-cold, probably some hours after the event.2 It therefore becomes ex- ceedingly probable that the actual death was either painless, or at least that the duration of the suffering was so brief, as not to have given an opportunity for any expression of it. Thus a person may have been affected with angina pectoris once or oftener, and he may die suddenly, and yet it may not be at all clear that he has died in a paroxysm of angina. On the other hand, symptoms of a different order from the genuine, painful, angina pectoris, may become associated with angina-like paroxysms at a subsequent period ; and yet, even then, the death may not be strictly sudden (in the sense above described), or even unexpected as to its occurrence, but rather the gradual culmination of days or weeks of sleepless agony. It is notorious among physicians that in valvular diseases of the heart, and even in aneurisms, in which the popular impression, derived from a few startling instances, is to the effect that sudden death is always to be expected, this mode of termination is in fact exceptional. One 1 In the case of Dr. Guthrie, above men- tioned, a similar irregularity, with symptoms not very dissimilar in other respects, appeared to threaten sudden death in 1846, while death did not actually take place till 1873. 2 This case was recorded with additional details, in Gout: Its History, Causes, and Cure, by William Gairdner (first edit. 1849, pp. 38-42), as a case of fatty degeneration of the heart, liver, and kidneys. The narrative there given of the symptoms is by my father, but I have a most distinct personal recollec- tion, even at this distance of time, of all the essential facts, which both from intimate friendship, and from early professional stud- ies, had more than usual interest for one who was just then engaged for the first time in minute pathological research; especially as occurring only a few months after the death of Dr. Chalmers. The patient became sub- ject to the first symptoms of cardiac disease in 1841; had a smart attack of regular gout in 1846, followed by giddiness and cardiac pains, which were rarely altogether absent afterwards. He died suddenly, as described, in September, 1847, in the 63d year of his age.-W. T. G. 1 Monthly Journal, ubi supra, p. 205. 680 ANGINA PECTORIS AND SUDDEN DEATH. or two cases, widely reported, and taking possession of the imagination by their peculiar and mysterious close, become the types of a whole series, in which the inci- dents are only slightly or not at all re- moved from the ordinary course of fatal disease, as to the fact of the end being to a certain extent expected and foreseen. But even here we are beset by anomalies of experience arising from the extreme difficulty of realizing facts depending so much upon subjective impressions. For example, a young man intimately known to the author of this article went to Edin- burgh many years ago to study medicine, it being known to himself and some of his friends that there was some internal flaw or weakness, in regard to the precise na- ture of which he always maintained a strict reserve. It was reputed (as in the case of Seneca) to be more or less of the character of "asthma;" but no regular asthmatic paroxysm was ever brought under notice. This young man pursued all his medical studies and took his degree without apparent difficulty ; living in the main carefully, but often visiting the hos- pital at night and doing all the miscella- neous work of a hardworking student. He afterwards •went to the Crimea and served through the whole campaign, up to the taking of the Redan fort, as an assist- ant-surgeon attached to a regiment; his letters at this time giving most minute descriptions of all his personal impressions of the scenes and great events around him, but being almost entirely silent as to his own physical sensations, if he had any, of chronic disease. He was afterwards af- fected with some of the current diseases of the service, and had also an attack of rheumatic fever, after which he was sent home, but continued with his regiment on its return, and finally died at Chichester in a time apparently of profound tranquillity, and with such startling suddenness that he had barely time to use some of the most familiar remedies and common external appliances before he was called away, his fellow-officers having had no previous note of warning whatever. A subsequent inquiry led to the discovery that the local applications which he had himself directed in the moment preceding his death were precisely those which he had learned in the Edinburgh Royal Infirmary to apply in several cases of angina pectoris, in the study of which he had interested himself. He had also, it appeared, confided to his mother the idea that he might possibly die suddenly, owing to some imperfection of which he was sensible at the heart. He died in his twenty-seventh year. The pericardium was found to be firmly adhe- rent, and the heart rather small, its mus- cular fibres pale, and apparently altered in texture. In this instance it would seem probable that symptoms of an ap- preciable, but still of a tolerable kind, may have existed for many years, unreported, undescribed, and perhaps not even dis- tinctly realized by the patient himself, though he was one carefully instructed in all that relates to this subject, and known to have taken a special interest in it from the point of view of medical observation.1 The cases adverted to above have been, with one or two exceptions, cases of sud- den death in which the symptomatic his- tory of the facts leading up to the fatal result is either imperfect, or altogether mysterious ; and in which also the pic- ture of angina pectoris as drawn by Heb- erden fails at some point or other to apply to the facts. But in cases of true angina of the most typical kind, and especially in those associated with a distinct organic lesion, such as calcification or other dis- ease of the coronary arteries or fibre of the heart, it might easily be argued that the fact of a sudden, as opposed to a more ordinary mode of death, is not less mys- terious than in any of those cases in which it has been preceded by no such typical symptoms. For, after all, what we know in cases of true Angina is simply the fact that pain of a certain order and of a cer- tain degree of severity often brings death in its train ; how the death occurs, and what precise conjunction of phenomena or pathological causes determines its oc- currence at a particular moment, we know as little apparently in the painful as in the comparatively painless cases. It is plainly out of the question to suppose that a chronic, and in its very nature gradually advancing lesion, like fatty de- generation or disease of the coronary ves- sels in the direct and immediate deter- 1 For additional details see the Edinburgh Medical Journal, vol. v. 1859, p. 95. Heber- den's remarks in his first paper (1768) as to the association of angina with sudden death are important. He had at that time seen about twenty cases (four years later he notes fifty, and in his Commentaries about a hun- dred cases); of the twenty cases first observed he had known six to have died suddenly; and perhaps more may have so perished, without the fact being known. "But," he argues, "though the natural tendency be to kill suddenly, yet some of those afflicted may die in another manner" (unless such persons could be considered as exempt from all the other diseases proper to advancing age) "since this disorder will last, as I have known it more than once, near twenty years." Heber- den had first become aware of the tendency to sudden death in angina, on mentioning the peculiar symptoms to a physician of great experience, who had told him that most of these cases had in his experience been sud- denly fatal. The careful manner in which Heberden's own experience had been matured (so to speak) for publication appears very clearly in these incidental remarks. ANGINA PECTORIS AND SUDDEN DEATH. 681 mining cause of a death which occurs in a moment, or of spasmodic seizures which come on in the midst of comparative health, and pass away in many instances in a few minutes, or at most in an hour or two, leaving the patient with a quiet pulse, free from serious complaint, and (apart from certain forms of exertion) able for many of the ordinary duties of life. The cardiac fibre which carried Dr. Chalmers safely over the last three weeks of his life, with its harassing duties and ac- tive exertions in various places, cannot be reasonably supposed to have become sud- denly so much more diseased (physically speaking) that it must needs be disabled to the extent of ceasing to act altogether, in the absolute quiet of an undisturbed night, after a day peacefully and happily spent in his own home, and an evening closed in a state of radiant satisfaction and joy, without any apparent trace of morbid misgivings. A like argument would probably apply to many or most of Dr. Heberden's cases of angina pec- toris ; to all cases, indeed, in which the element of spasm (so called) is a promi- nent feature ; and in the elaborate argu- ment, so well rendered and modernized by Dr. Latham, in which Heberden vindi- cates for his "dolor pectoris" a place among the spasms, as opposed to inflam- mation or organic disease, we are only seeking, with him, for a mode of reasoned description or of generalization for facts which are confessedly mysterious. The whole of the argument that has been raised since Heberden's time as to whether death in these cases is caused by spasm or by paralysis of the heart, and the small amount of actual information or real sci- ence which has emerged from the some- what fruitless controversy, shows strongly how much we may deceive ourselves with the idea that in describing a mere associa- tion of symptoms with certain pathologi- cal lesions, we have fully explained the nature of the connection of the one group of facts with the other. From this point of view one more instance of sudden death, with all its preceding life-history, may be regarded as having a sufficient interest for us to be cited here with some detail. The great comparative anatomist and profound physiologist John Hunter died, as is well known, with startling sudden- ness in the year 1793 ; and from all that has been transmitted to us of the circum- stances of his fatal illness, and of the symptoms from which he suffered for twenty years before his death, it is evi- dent that the opinion of one, at least, of his most intimate and confidential friends, as well as probably the secret convictions, in the end, of the distinguished sufferer himself, pointed in the direction of the angina pectoris of Heberden as the true nosological interpretation of his morbid state. The detailed posthumous narra- tive of the symptoms, coming, as it does, almost from the very lips of Hunter,1 and characterized by all his restless activity of mind in the search after truth, forms unquestionably one of the most instructive chapters in the whole history of medicine. There is hardly a sentence in this wonder- ful narrative which will not repay the careful study of the physician ; and al- though the substance of the whole is here faithfully preserved, the need for conden- sation will compel the sacrifice of many of the vivid touches which reveal the mind of genius intent, even amidst physical suffering, upon the mysteries of his own being. How far these descriptive touches had been reasoned out into clear conceptions in the mind of Hunter himself does not appear from the narrative ; it is certain, however, that his most intimate and con- genial friend, Edward Jenner, postponed for many years the publication of certain highly original observations on angina pectoris (afterwards adopted and in part published by Dr. Parry), from the fear of compromising the feelings of John Hunter by a too obvious reference to his case.2 1 "Each symptom," writes Sir Everard. Home, "was described at the time it occurred, and either noted by himself, or dictated to me when Mr. Hunter was too ill to write. . . As the statement is made up from detached notes which were not written with a view to publication, it will appear in point of lan- guage extremely deficient; it was thought, however, best to leave it in its present form, lest by altering the language the effect of some of the expressions might be diminished, or misunderstood."-Life of Hunter, prefixed to the Treatise on Inflammation, 1794, p. xlv. 2 The circumstances as delivered in writing by Jenner to Dr. Parry, are curious, and spe- cially interesting as bearing on the early symptoms in John Hunter's case. "The first case I ever saw," writes Jenner, "of angina pectoris was that in the year 1772, published by Dr. Heberden, with Mr. Hunter's dissec- tion. There, I can almost positively say, the coronary arteries were not examined. An- other case of a Mr. Carter, at Dursley, fell under my care" (date not given); but in this case "the coronary arteries were become bony canals. " " Soon afterwards Mr. Pay- therus met with a case" . . . "At this very time, my valued friend Mr. John Hun- ter began to have the symptoms of angina pectoris too strongly marked upon him ; and this circumstance prevented any publication of my ideas upon the subject, as it must have brought on an unpleasant conference between Mr. Hunter and me. I mentioned both to Mr. Cline and Mr. Home my notions of the matter ; but they did not seem to think much of them. When, however, Mr. Hunter died, Mr. Home very candidly wrote to me, imme- diately after the'dissection, to tell me I was right." In 1778, Jenner wrote a distinot 682 ANGINA PECTORIS AND SUDDEN DEATH. It is well established, also, that the case did, in fact, fulfil the anticipations of Jen- ner, both as to the fatal event, and as to the appearances observed after death. It has rarely happened, surely, that two minds so keenly alive to theoretic truth, and yet so observant of detail, have been applied to any even the most indifferent obscure case in medicine; for in this in- stance it is the author of the "Treatise on the Blood, Inflammation," &c., who is both sufferer and narrator, while it is the clear-sighted and eminently truth-loving discoverer of vaccination who forms and announces to us the diagnosis. John Hunter "was a very healthy man for the first forty years of his life, if we except an inflammation of iiis lungs in the year 1759. In the spring of 1769, in his forty-first year, he had a regular fit of the gout, which returned in the three fol- lowing springs, but not in the fourth." In the spring of 1773 (rather more than twenty years before his death) he had the first appalling attack of what may, from our present point of view, be fairly re- garded as angina pectoris, though the pain (perhaps from some association of ideas with "gout in the stomach," the regular attack having, as stated above, not appeared at the expected time) was in this instance referred to the region of the pylorus. "While he was walking about the room, he cast his eyes on the looking- glass, and observed his countenance to be pale, his lips white, giving the appearance of a dead man ; this alarmed him, and led him to feel for his pulse, but he found none in either arm ; the pain continued, and he found himself at times not breathing. Being afraid of death soon taking place if he did not breathe, he produced the voluntary act of breathing by working his lungs by the power of the will."1 The " sensitive principle" was not affected ; for three-quarters of an hour he continued in this state, when the pain gradually lessened, and in two hours he was com- pletely recovered. The next attack was in 1776 ;2 it was distinguished, however, by a very decided amount of vertigo, which was not present, apparently, in the first attack; he felt as if he had drunk too much, and was a little sick ; on lying down it seemed as if he was suspended in the air; motion in a car- riage gave the uneasy " sensation of going down, or sinking ;3 motion, either of the head or foot, was insufferable, from the idea it gave of ranging through vast dis- tances. "The idea he had of his own size was that of being only two feet long." The special senses were extremely acute; the appetite indifferent; the pulse about sixty, and weak. In this state he con- 1 In this and other passages the mind of Hunter is very apparent. The speculations which follow may possibly be those of Sir Everard Home, and at all events they are not of much value as regards the present nar- rative. 2 This date is probably a mistake, either of Hunter or the copyist; the true date was 1777, as appears from a letter to Jenner on May 11th, in which Hunter writes: "Not two hours after I saw your brother, I was taken ill with a swimming in the head, and could not raise it off the pillow for ten days; it is not yet perfectly recovered." During his convalescence Hunter went to Bath for three months, on the advice of his friends, who took a much more serious view of his case than he himself appeared to do. It was during his residence at Bath, apparently, that Dr. Jenner saw Hunter personally, and formed the strong views as to the character and probable issue of the case which he ever afterwards retained, and which he wrote out, as above mentioned, for Dr. Heberden in 1778. 3 There is a characteristically Hunterian note here given in Home's narrative, which is valuable as showing how much these de- tails of subjective phenomena interested John Hunter as a physiologist, while as mere per- sonal matters he gave all his own sufferings extremely little consideration. "It is very curious that the sensation of sinking is very uneasy to most animals. When a person is tossed in a blanket, the uncomfortable part is falling down ; take any animal in the hand and raise it up, it is very quiet, but bring it down, and it will exert all its powers of re- sistance, every muscle in its body is in ac- tion ; this is the case even with a child as early as its birth." statement of his fears about Hunter's case, and of his views on the pathology of angina pectoris, intending it as a communication in private to Dr. Heberden; but, probably from the fear that it might lead to publica tion, the letter never was sent (see Life, of Edward Jenner, by Dr. Baron, vol. i. p. 39). It is, moreover, certain that Hunter, in a fa- tal case recorded by Dr. Fothergill ("Medical Observations and Inquiries," vol. v. p. 254), had actually observed disease of the coronary arteries in connection with sudden death from angina pectoris as early as March, 1775; so that the presumption is exceedingly strong that Hunter not only was intimately ac- quainted with Jenner's views on the subject, but also had in part suggested them. There is thus a chain of evidence of no ordinary consistency tending to show that Hunter, who never formally identified his own symp- toms with those of the angina pectoris of He- berden, was nevertheless cognizant of their real nature and probable termination, at least as early as Jenner's suspicions took ori- gin, which, as we shall afterwards see reason to believe, was in 1777. The death of Hun- ter, in 1793, was in fact almost an exact reproduction of the very circumstances of Fothergill's case, viz., "in a sudden and vio lent transport of anger;" and the appear- ances on dissection were also strikingly simi- lar. ANGINA PECTORIS AND SUDDEN DEATH. 683 tinued for about ten days ; bleeding was of no service, purging and vomiting (by medicine) "distressed him greatly;" nothing appeared to be of the least use. From this severe illness he gradually re- covered, but only after a long convales- cence ; and he does not seem to have been ever again perfectly well, having, it is said, grown much older looking in the in- terval between this and his next severe attack, which was in 1785. The illness of April, 1785, may be said to have commenced with an ordinary at- tack of gout, followed by a great variety of anomalous nervous sensations which are minutely described, but over which it is not necessary to detain the reader.1 Suffice it to say, that from this time on- wards Hunter became increasingly subject to paroxysmal attacks, which assumed more and more the characters of typical angina pectoris. The nervous disturb- ance appears to have been at first periph- eral, e. (/., "a sensation of the muscles of the nose being in action," an unpleasant sensation in the left side of the face, jaw, and throat, which seemed to extend into the head on that side, and down the left arm as low as the ball of the thumb, where it terminated all at once." After a fortnight these symptoms of nervous irritation "extended to the sternum, pro- ducing the same disagreeable sensations there, and giving the feeling of the ster- num being drawn backwards towards the spine, as well as that of oppression in breathing, although the action of breath- ing was attended with no real difficulty ; at these times the heart seemed to miss a stroke, and upon feeling the pulse, the artery was very much contracted, often hardly to be felt, and every now and then the pulse was entirely stopt." He had also pains in the heart itself, as well as the diaphragm and stomach, attended with considerable eructations of wind, "a kind of mixture of hiccough and eructa- tion." In the most severe attacks "he sunk into a swoon or doze, which lasted about ten minutes, after which he started up, without the least recollection of what had passed, or of his preceding illness." The agonies he suffered were dreadful,1 and when he fainted away he was thought to be dead. As in other instances of angina, these attacks were at first brought on chiefly by motion, " especially on an ascent, either of stairs or of rising ground." The affec- tions of the mind that were chiefly injuri- ous were anxiety and anger ; "it was not the cause of the anxiety, but the quantity of it, that affected him ; the anxiety about the hiving of a swarm of bees, the anxiety lest an animal should escape before he could get a gun to shoot it," brought on an attack ; ' ' anger brought on the same complaint, and he could conceive it possi- ble for that passion to be carried so far as to deprive him of life; but what was very extraordinary, the more tender pas- sions of the mind did not produce it;" compassion, admiration, &c., might be carried to the extent of tears, "yet the spasm was not excited." "He ate and slept as well as ever, and his mind was in no degree depressed ; the want of exercise made him grow unusually fat." Mrs. Hunter, in writing to Jenner, called the disease, even at this stage, "flying gout."2 We have already seen what Jenner thought of it several years before. Hunter himself was probably familiar with Heberden's description, and at all events had assisted in Heberden's inquiry by performing the examination of the very remarkable case recorded in the " Medical Transactions" in 1772. He himself began to suffer in 1773. That he had realized in some degree the danger of his position, therefore, can scarcely be doubted. He had indeed no unmanly fear of death, and was far too busy to occupy himself with what he would have regarded as weak sentimentalisms about himself. He probably avoided the subject deliberately,3 and felt himself able to pur- sue all his various occupations with the same ardor as ever, in the intervals of suffering. But he was deeply sensible of the risk to which he was sometimes ex- posed by over-exertion, and still more by his uncontrollable temper ; he was accus- tomed to say, that "his life was in the hands of any rascal who chose to annoy and tease him;"4 a remarkable expres- 1 Dr. Pitcairn elicited on this occasion, by special inquiries, that Hunter's mind had been much harassed, in consequence of his having opened the body of a person who had died of the bite of a mad dog, about six weeks before ; in doing which he had wounded his hand. For a fortnight, it is added, his mind had been in continued suspense, from the idea that he might be seized with symptoms of hydrophobia ; and it certainly seems very probable, as it was supposed, that the ner- vous symptoms alluded to may have been in some measure, at least, determined or pro- duced by this accident. 1 This is the personal testimony of Sir Everard Home, who witnessed this attack, having become Hunter's regular assistant in his practice, and acted for him during his ill- ness. It is probable, but not expressly stated, that Home also was a witness to the first at- tack of illness in 1773, as he was then a young man living in Hunter's house. 2 Palmer's Life of John Hunter, p. 96. 3 In all his published correspondence there is only one brief allusion to his own illnesses, the one given above from a note to Jenner, 4 Palmer, ut supra, p. 119. 684 ANGINA PECTORIS AND SUDDEN DEATH. sion, and a sad anticipation of the actual ending. The close of 1789 brought with it a new set of complications, which may be briefly summarized as loss of memory, and vari- ous kinds of visual disturbance, especially the apparent deflection of objects from their true direction; some of the former subjective sensations, mentioned in the attack of 177G, returned upon him. " Dreams had the strength of reality, so much so as to awaken him; the disposi- tion to sleep was a good deal gone, an hour or two in the twenty-four being as much as could be obtained. Neither the mind, nor the reasoning faculty, however, were affected; indeed he reasoned most acutely in regard to his own visual de- rangements, and pursued the questions suggested by them in physiology with a keenness which was quite characteristic. At last the busy, ever-active mind was to cease from its labors, and the strong, much-enduring bodily frame, wearied out and spent in the service, was to give way. His recovery from this indisposition was less perfect than from any of the others ; he never lost entirely the oblique vision ; his memory was in some respects evidently impaired, and the spasms became more constant; he never went to bed without their being brought on by the act of un- dressing himself; they came on in the middle of the night; the least exertion in conversation after dinner was attended by them. Even operations in surgery if at- tended with any nicety, now produced the same effects. The end is well known. There is rea- son to think it was almost foreseen by himself. A dispute of a painful, but not, after all, of a very serious or overwhelm- ing character, had embittered his relations with the governors of St. George's Hos- pital. On the lfith of October, 1793, he determined to be present at a meeting, where, however, he apprehended a per- sonal dispute. He expressed to a friend the feeling that such a dispute might be fatal to him, but went nevertheless. Something that he said in the Board- room was noticed, and flatly contradicted. He stopped, left the room in a silent rage, and had just time to gain the next room, when " he gave a deep groan, and fell down dead." The appearances in the dead body were complex. The pericardium was very un- usually thickened ; the heart very small, Its muscular substance pale ; the coronary arteries were converted into open bony tubes ; the valves of the left side of the heart also were involved in a similar de- generation ; the aorta was dilated, in its ascending part, to the extent of one- third. The carotid and vertebral arteries within the cranium were also bony, and the basilar artery " had opaque white spots very generally along its coats. ' ' The structure of the brain itself was normal. To these observations of what may be almost called historical cases, bearing upon the fact of sudden death and its associated symptoms, I will add only a few details gathered from a long and close observation of cardiac diseases in general. Apart from what has been variously termed cardiac asthma, dyspnoea, or orthopnoea, which in many cases receives its clear explanation from the associated states either of the pulmonary circula- tion, or of the lungs, bronchi, and pleurse, as disclosed by physical signs, there is often an element of subjective abnormal sensation present in cardiac diseases which, when it is not localized through the coincidence of pain, is a specially indefinable and indescribable sensation, almost always felt to be such by the pa- tient himself. I make this remark de- liberately, as the result of experience, and well knowing that it is liable to be brought into question in particular instances; that, in fact, a large part of what has been described under the titles given at the commencement of this paragraph, has been inextricably confounded by syste- matic writers with the sensation, or group of sensations, to which I refer.1 To this group of sensations, when not distinctly accompanied by local pain, I have, in various instances, given the name of Angina sine dolor e, recognizing, thereby, what I believe to be its true diagnostic and pathological significance, and its alliance with the painful angina of Heber- den ; the pain in which, however, as we have already seen, is an exceedingly vari- able element, both in degree and in kind. This painless, or at least not definitely and locally painful, angina, is found in connection with every kind of cardiac lesion which ends in death (whether sud- den or not) in varying proportions ; often associated with the other phenomena which make up the picture of a confirmed case of organic heart disease tending to death, but not rarely also under circum- stances which admit of its being sepa- rately described. Among the valvular le- sions of the heart, incompetency of the aor- 1 "In considering this subject, we must not forget," writes Dr. Stokes, "that under the name angina pectoris, physicians have in- cluded, and still include, many examples of diseases which vary in their nature and com- binations. Well-marked instances of the af- fection as described by Dr. Latham, are rarely met with; and the same may be said of the purely nervous cases noticed by Laennec. 1 have never seen either of these forms. The dis- ease which in this country" (Ireland?) "most often gets the name of anginapectoris, might be more properly designated as cardiac asthma." Op. cit. p. 488. ANGINA PECTORIS AND SUDDEN DEATH. 685 tic valves is the one which most frequently gives rise characteristically to this pecu- liar form of suffering; and in the majority of the cases in which it arises early in the course of aortic valvular disease there is neither dropsy, or lividity, nor hsemopty- sis ; very often there is no disease of the lungs ascertainable by physical signs, and in particular no wheezing, even in very severe paroxysms of this truly cardiac anguish or indefinable distress. But there is, in variable degrees, a sensation which can only be called anxiety or cardiac op- pression ; the patient acquires a haggard, almost a frightened look, and from his habitual attitude and manner, as much as from anything he distinctly declares in words, it becomes evident that he is suf- fering from a sense of insecurity which he cannot possibly express. In the more aggravated cases the loss of sleep is a serious part of the suffering, and patients will sometimes declare that they are afraid to sleep, lest some other and greater evil than the loss of sleep should come upon them; obviously an experience actually acquired, that sleep is, in this state, sometimes the precursor, and appa- rently the cause, of a formidable increase in the symptoms. An intelligent patient in this condition recently put the ques- tion to his medical attendant, with respect to a very moderate dose of hydrate of chloral, proposed to be given after many sleepless nights, whether it would not be "dangerous," i. e. (as he afterwards ex- plained to me), whether the sleep artifi- cially induced might not be the means of determining an attack which might prove fatal. When sleep is obtained, it is brief and easily disturbed, often by frightful dreams; and when these occur they are mixed up with the sensations of ah ap- proaching paroxysm, so that the dream may appear to be the actual cause of the paroxysm. • An assertion of the patient just alluded to was that he "woke up with the peculiar sensation on him, and it was too late to check it." In very extreme cases, which are often, however, complicated with true orthopnoea, dropsy, and other more recognized cardiac and respiratory symptoms of secondary ori- gin, the patient may for weeks together be unable to lie down or to take ordinary rest, and on the other hand may be almost continually half-asleep; in such cases accidents are apt to occur, from the pa- tient falling forwards in a fit of sheer exhaustion, or getting burned or other- wise injured while in' a state of insensi- bility. Nor are more distinctly cerebral symptoms wanting. In some of these cases I have seen attacks closely resem- bling epilepsy, without any subsequent paralysis ; when, however, hemiplegia or aphasic symptoms occur, it is most prob- able that they are due to more distinctly organic changes in the nervous centres ; and usually to cerebral embolism. It would be vain to indicate the verbal ex- pedients by which patients endeavor to describe their sensations, when found in an attack of this paroxysmal suffering. Palpitation, and breathlessness are often alluded to, separately or together; but still more often it is a sense of "oppres- sion," or of "pressure," which is some- times described as if the chest were actually being compressed from before backwards ; one patient described it as a "kind of surging up," which came, as he thought, from the bowels, and was at- tended with the feeling of wind, and also, I suspect, with a degree of hysteric globus, rising, as he described it, to his throat, and causing him to pant for breath. The respiration is by no means necessarily or invariably disturbed in these cases, though it is frequently more or less quickened, and sometimes the oppo- site ; in certain cases the respiration is alternately frequent and unfrequent ; several rapid panting or gasping respira- tions are continued over half a minute to- gether, and are gradually succeeded by a corresponding period of comparative qui- escence, which at times culminates in a positive arrest or suspension, for a time, of a respiratory act (see the narrative of John Hunter's case above cited).1 1 It is very remarkable that Dr. Stokes, who is undoubtedly entitled to the credit of having first distinctly realized, and clearly stated, the importance of this type of respira- tion as indicating cardiac disease (especially weakened action, or fatty degeneration, of the fibre of the heart) should have so com- pletely overlooked the case of John Hunter, while fixing upon the symptoms described in Seneca's case as characteristic (see note, p. 676). The same remark applies to all the now numerous dissertations, in Germany as well as in this country, on the "Cheyne- Stokes respiration," as it has been called on the continent. " It consists," says Dr. Stokes (op. cit. p. 324), "in the occurrence of a series of inspirations, increasing to a maximum, and then declining in force and length, until a state of apparent apnoea is established. In this condition the patient may remain for such a length of time as to make his attend- ants believe that he is dead, when a low in- spiration, followed by one more decided, marks the commencement of a new ascending and then descending series of inspirations." Probably the first really exact description of this phenomenon was by Dr. Cheyne, in 1818 (Dublin Hospital Reports, vol. ii. p. 216). The peculiar interest and value of Hunter's case, however, for us consists in its giving the personal impressions, or subjective sensa- tions, of that great physiologist in a way that no merely objective description could effect, and wholly apart from hypothesis. It is curious to observe how completely Hunter's description of his own sensations corresponds 686 ANGINA PECTORIS AND SUDDEN DEATH. This peculiar type of "suspirious," or irregularly sighing, respiration (as it has been termed), is so far characteristic of the "angina sine dolore," that 1 cannot but regard it as being in some way re- lated to lesions involving the respiration through the cardiac nerves. Whether dependent necessarily on cardiac causes or not, however, it is certainly not neces- sarily associated with any organic lesion of the lungs or air-passages ; it occurs, as Dr. Stokes has recorded, " without any rale or sign of mechanical obstruction." Frequently the irregularities of respira- tion do not go beyond a few quick gasps, or deep sighing inspirations, at a time, and the period of apnoea, or of rare and slow respiration, is correspondingly short- ened ; but when this condition of the res- piration, even in its minor degrees, is associated with the peculiar look of inde- scrible anguish, the head thrown back, the arms extended or tossed about, and the whole frame showing by sheer muscular restlessness the terrible character of the agony (indicated often by cries, even when without local or positive pain), it scarcely requires the aid of a verbal description to make the diagnosis of angina clear to the observer. It is, however, important to remark that the character and peculiarly altered rhythm of the breathing are essen- tially distinct from the laborious but more regular and at the same time noisy respi- ration of true spasmodic asthma and of asthmatic bronchitis. I have also ob- served that organic and valvular deform- ities of the right side of the heart, even when complicated with great cyanosis, are only slightly characterized by the symptoms I have now endeavored to in- dicate ; and, on the whole, the diseases of the mitral valve are less apt to be ac- companied by this form of angina than those of the aortic, and the obstructive lesions less than the regurgitations. Di- latation of the heart in its more aggra- vated forms, however caused, and aneu- risms (as already indicated) arising very near the heart, or projecting into the peri- cardium, are apt to be accompanied by considerable degrees of angina, as above described. And some of the worst cases I have seen have been those, in which the only lesion that could be fairly presumed to exist was fatty or other degeneration of the fibre of the heart, sometimes with, sometimes without, direct evidence of moderate or slight dilatation of the left ventricle.1 As in the case of the locally painful, or neuralgic angina, the relation of the symptoms to the organic legion is by no means constant, even when the lat- ter can be shown to be present, and to be presumably, in a certain sense, the cause of the symptoms. And it may further be affirmed, that the essentially paroxysmal character of this angina is such as to lead us inevitably to look for an explanation of it beyond the positive and permanent organic lesion of the heart or aorta, what- ever that may be in the particular case. We are now in a position to discuss, with such assistance as can be had both from clinical observation and from physi- ological pathology, the extremely obscure subject of the mode in which the innerva- 1 In one case of this kind, a much valued friend and a distinguished clergyman of the Church of Scotland, who died at the age of forty-one, after a gradually progressive illness watched with the greatest anxiety, and with full fore-knowledge of its character and proba- ble termination, the beats of the heart fre- quently numbered as low as 22-24 in the minute; and I have counted them as low as 18, without any marked irregularity. The radial pulse was at these times exceedingly soft and small, but although the suffering was at times intense, it was not usually ac- companied by positive definable pain, at least until the last few days or weeks of the dis- ease, when (the patient not being at the time under my own immediate observation) I had the testimony of a well-informed medical friend as to the really angina-like character of the paroxysms. The suspirious respiration was always present in the more considerable paroxysms of suffering, and was usually not altogether absent. There were on several occasions very alarming pseudo-apoplectic or slight epileptic attacks, without permanent disorder either of the intellectual functions or of voluntary movement. Although this truly noble-minded and self-denying man pursued the work of his life up to the very verge of sudden fainting or death in the pulpit, yet his death in the end was by no means sud- den, but rather a lingering agony. The en- tire duration of his fatal illness was under two years, and he continued at his post, with some interruptions, until about eight months before his death, which happened in January, 1865. Up to a few days before his death he maintained his pastoral connection with his congregation by means of letters, some of which have been published, and show all the power of a robust mind under the guidance of Christian principle and hope. Dr. Walsh e, who saw this case with me in consultation, agreed with me in considering it one probably of fatty degeneration of the heart; but there was no post-mortem examination. with Galen's commentary on a notable pass- age in Hippocrates, where a certain kind of "rare and large" respiration is described as "like a person who forgot for a time the need of breathing, and then suddenly remem- bered." See the very interesting account of the most ancient observations on this subject by Dr. Warburton Begbie, in his recent Ad- dress in Medicine (British Medical Journal, August 7, 1875, p. 166) in which there will also be found a brief but exact account of the more modern theories as to this kind of re- spiratory disorder. ANGINA PECTORIS AND SUDDEN DEATH. 687 tion of the heart is affected in Cardiac Angina-in other words, the ultimate pathology or pathogeny of the affection. We have seen that the dolor pectoris, or an- gina pectoris, of Heberden was specially distinguished by him from all those pains in the chest which were regarded as due to inflammation, accompanied or followed by organic changes corresponding with the extent and severity of the inflamma- tory process. In other words, the essen- tial pathology of angina, according to Heberden, was that of a neurosis. This we believe to be the only just rendering of the argument of this great physician, when he assigned to angina pectoris a place among the distensiones, or spasms. Later observers and pathologists have been much exercised in the attempt to resolve the question, whether sudden death, occurring under such circum- stances, is from spasm, or from paralysis, of the heart; but we may safely conclude that no such question was, otherwise than remotely, involved in Heberden's argu- ment. That argument was directed to- wards a very practical and real conclu- sion, and was not at all, we may well suppose, intended to foreclose questions of physiological pathology, which, accord- ing to all the evidence before us, were not before his mind, or, at least, not matured for discussion at the time at which he wrote. Angina pectoris had to be placed carefully apart from the pyrexiae and the phlegmasice ; had any doubt been left open on this subject, the dolor pectoris would have been considered as demanding the treatment of all so-called inflammatory pains in that day-large and repeated bleedings, vomitings, purgings, &c.' Hence the anxious care with which He- berden insisted on the paroxysmal and non-febrile character of the pain, and on the collateral circumstances which led him to bring it into the great group of the spasms; e. g. "subito accedit, etrecediV''- " in ipsa accessione pulsus non concitaturff' &c. It is needless to pursue the argu- ment in detail ; possibly, indeed, the de- tails might be open to question in some instances. But on endeavoring, as Dr. Latham has done, to grasp the essential principles of the argument, as seen through a somewhat obsolete phraseology, we may readily assent to them, even if we should suppose that Heberden, in his desire to prove angina pectoris a neurosis, may have somewhat neglected the evidence of its being often associated with organic disease.2 He found in the suddenness of the paroxysms, in the apparent good health of the intervals, in the relief often afforded by stimulants and by opium, the basis of his pathology of angina; and we may easily admit that some cases, at least, of the typical angina of Heberden must have been fairly open to tin* con- struction of being cases of spasm, and nothing more. But we now know that this typical angina is only the culminating form of a group of symptoms, which, in their less pronounced, less definitely pain- ful, and more complicated forms, are found to permeate the whole field of car- diac pathology and diagnosis. The an- gina which consists purely of a paroxysm of pain, and of a paroxysm which kills suddenly and instantaneously, is rare ; but the angina which consists of a ten- dency to paroxysmal aggravations (not always purely of pain), superinduced upon, and complicating, the other symp- toms and sequelae of cardiac organic dis- eases, is matter of every-day experience. In both forms there occurs occasionally a paroxysm which ends in death ; but in the second form death is less frequently instantaneous and unexpected, both be- cause the paroxysms are individually less intense, and because the fatal result, seemed to him to imply the existence of or- ganic change ; and to one only, in which " a very skilful anatomist could discover no fault in the heart, in the valves, in the arteries, or in the neighboring veins, excepting some small rudiments of ossification in the aorta. Nor were any indications of disease found in the brain." There is no doubt that Heber- den's personal experience of angina was al- most purely clinical, not pathological; but it has the advantage, for us, of being stated in language singularly terse, exact, and free from the suspicion of prejudice. Heberden claims, in his Commentaries, to have seen nearly a hundred cases of angina pectoris, of which three were in women. One was a boy twelve years old, "who had something re- sembling this affection." All the rest were in men near or past the fiftieth year of their age. At the time of his first paper, in 17G8, Heberden had " never seen one opened, who had died of it. Most of those," he adds, "with whose cases I had been acquainted were buried before I heard that they were dead." The case specially alluded to above was almost certainly that of the "Unknown," who, in April, 1772, wrote to Heberden a minute account of his symptoms, and dying suddenly about three weeks thereafter, was found to have left in his will express instruc- tions that Heberden should be informed of his death, with the view of having his body examined. This was accordingly done by John Hunter, and it is this case to which Dr. Jenner alludes, when he says that he can almost certainly affirm that the coronary ar- teries were not examined. The case was recorded in the third volume of the Medical Transactions. 1 Angina pectoris, quantum adhuc illius naturam intellexi, ad distensionem, non autem ad inflammationem, videtur pertinere. . . . Sanguinis missio, vomitus, et purgantia mihi visa sunt aliena.-Comm, uti supra. 2 He refers, however, to several cases which 688 ANGINA PECTORIS AND SUDDEN DEATH. when it arrives, is brought about in part by other causes than the immediate causes of the paroxysm. And even if we should maintain that fatal angina is always more or less dependent upon organic changes,1 there would still remain to be explained these unquestionable facts, viz. : 1. Pain, suddenly coming and going; 2. The paroxysmal character of the symptoms, other than pain; 3. Absolutely sudden death in a few cases. On these grounds, now as in the time of Heberden, we may assuredly claim for angina pectoris a place among the neuroses, even while the admission is freely made that the element of neurosis is often superinduced upon organic, too often indeed incurable, dis- ease in the heart itself, or in its nutrient vessels, or in the first part of the aorta. Certain authorities have treated of an- gina pectoris as a form of visceral neural- gia, or " hypersesthesia"2 (Romberg) of the cardiac plexus. The latter term (as Dr. Anstie has well pointed out) is essen- tially a bad one ; the former, in the case of typical angina, is perhaps admissible, viewing the disease from the side of the pain alone ; but it errs both by excess and by defect, inasmuch as, on the one hand, pain of the severe form implied in the term neuralgia is not always the central or exclusive phenomenon, even of the cases ending in sudden death ; while, on the other hand, a form of cardiac pain, or pseudo-angina3 (as it has been termed) is not infrequent, which has most of the attributes of a neuralgia in the highest possible degree, and which, though emi- nently paroxysmal, is by no means apt to lead to sudden death or to any grave consequences whatever. This admission, which is very candidly and fully made by the late Dr. Anstie1 in his interesting dissertation upon the subject, appears to me a very cogent reason for maintaining, rather than consenting to forego, the now well-known term angina pectoris, for which he entertains so strong an aversion, but which is, nevertheless, quite indis- pensable to us, as carrying the impress of a long line of personal observations, ex- tending back to that" molestus quidam an- gor," which Morgagni has described as having suddenly terminated the life of a Venetian woman in 1707. And if it must he admitted that the name " angina pec- toris" has sometimes been used in ignor- ance, or rather (from disregard of purely clinical experience) in a way really ob- jectionable and tending to confusion, it is equally certain that the term " neuralgia" is beset with theoretical interpretations which tend to bias both clinical and pa- thological research. We have endeavored in the preceding pages to give an impar- tial statement of a wide range of phe- nomena, into which a neuralgic element enters in various proportions. A consist- ent theory must take account of that ele- ment, but will not allow it to take pos- session of the entire field. Another question that requires con- sideration is, the nature of the disorders in connection with motor nerves which unquestionably occur in angina pectoris. Here, again, we find ourselves in the presence of vague and often quite fruitless discussions, indicated by the general terms spasm, paralysis, hyperkinesis, &c., and, among the older authors, asthma convulsivum, stenocardia, syncope angi- nosa, &c. A third department of the inquiry, less generally entertained, inasmuch as the phenomena to which it refers are less constant, is the nature of the connection between the cardiac symptoms in angina 1 Eulenburg refers to Desportes, in Lartigue -"De l'Angine de Poitrine," p. 78, Paris, 1846 ; Surmay, L'Union Medicale, xxxi., No. 80, p. 34; for evidence of angina without disease of the heart. Anstie, in his Treatise on Neuralgia, pp. 69, 70, details, briefly, a fatal case, in which ' 'not the slightest organic heart mischief could be detected, either dur- ing life or after death." Latham has also recorded cases where the appearances after death were, at least, of very questionable and doubtful character. But it is difficult to prove a negative by isolated instances which are opposed to the general results of patho- logical research. [I met with a marked case, in 1879, in which autopsy showed no disease of the heart, except a comparatively slight fatty degeneration in some portions.-H.] 2 "Pain has been described by some of the most distinguished writers on nervous diseases as a hypercesthesia. Yet there is really very little difficulty in convincing our- selves, if we institute a thorough inquiry into the matter, that pain is certainly not a hypersesthesia, or excess of ordinary sensory function, but something which, if not the exact opposite of this, is very nearly so."- Anstie on Neuralgia, p. 2 et seq. 3 ' ' Genuine angina pectoris is undoubtedly a very rare affection. On the other hand, I almost daily meet with a form of complaint combining in a minor degree many of the characters of angina; and to this imitation of the true disease I propose to give the name of pseudo-angina. I believe that herein lies the explanation of Laennec's notion (so dis- cordant with the experience of English ob- servers) that angina pectoris is of very fre- quent occurrence."-Walshe, Diseases of the Heart and Great Vessels, 4th edit., 1873, p. 208. Compare the observations on Diagnosis in p. 670, of present chapter. 1 On Neuralgia, and the Diseases that re- semble it, by F. E. Anstie, M.D., 1871; pp. 63, 64. The first sketch of this most valuable treatise, contributed by the much-lamented author to the present work in 1868, contains no detailed reference to angina pectoris. ANGINA PECTORIS AND SUDDEN DEATH. 689 pectoris, and those cerebro-spinal mani- festations which sometimes occur, and which we saw well illustrated in the case of John Hunter. Is it possible to give any account of these three orders of phenomena which shall be consistent and intelligible, which shall be founded on positive facts and well-ordered experients, and shall thus fulfil the purposes, even provisionally, of a reasonable theory of angina pectoris ? In endeavoring to answer this question, it will be necessary to refer to physiologi- cal researches which are still very incom- plete, and even to clinical facts which have not as yet been tested by a sufficient number of independent observers. But it certainly seems as though some large and fruitful lines of research had recently been opened up amid much darkness and confusion. We owe to Dr. Lauder Brunton1 the clini- cal observation of a fact which, besides its therapeutic consequences (to be after- wards considered), may be regarded as shedding a new light upon the pathology of angina pectoris. In investigating a case of rheumatic disease of the aortic valves (obstruction and regurgitation), with dilatation of the aorta, and consider- able hypertrophy of the heart, he found that during the angina-like paroxysms of pain to which the patient was subject, the sphygmograph invariably showed a great diminution in the amplitude of the pulse- wave, with blunting of the apex, slow or greatly postponed recoil, and obliteration of the dicrotic wave ; the ordinary pulse of the individual (at least in the right radial artery) being characterized by a very ample and instantaneous upstroke, a pointed apex, a rapid recoil, and a dis- tinct though not exaggerated dicrotic wave. Repeated experiments convinced Dr. Brunton that these altered characters of the pulse were due to an increased ten- sion in the systemic arteries during the paroxysm, and that this increased tension was chiefly, if not solely, owing to " con- traction of the small systemic vessels, so sudden and so great as to deserve the name of spasmodic."1 Following up this line of observation, and being aware that Dr. B. W. Richardson2 and Dr. Arthur Gamgee3 had performed numerous experi- ments which showed that nitrite of amyl, when inhaled in small quantities, had the effect of remarkably lessening arterial tension by diminishing the contraction of the arterioles, Dr. Brunton was led to employ this substance for the purpose of relieving the symptoms in this case, and had the great satisfaction not only of find- ing that almost immediate ease was given in the severer paroxysms, but that the observations previously made on the rela- tion of the paroxysm to increased vascu- lar tension, were enphasized (so to speak) by the action of the nitrite of amyl. For ■when in the severest paroxysms the pulse was almost annihilated to the finger (though still regular and somewhat ac- celerated), thirteen drops of the nitrite of amyl inhaled from a cloth produced, in one minute and twenty seconds, a de- cided effect at once on the sphygmo- graphic tracing and on the pain ; while one or two smaller doses, repeated over sixteen minutes, restored the amplitude of the pulse-wave, and entirely removed the pain. It is, perhaps, unnecessary to multiply details, especially as regards doubtful points.4 The experiment was 1 Clin. Soc. Trans., ubi supra, p. 199. A lithograph, with eleven tracings in different states of the patient, is given, on which the description in the text is founded. 2 Dr. Richardson's numerous and valuable reports of experiments on anaesthetic vapors, and on nitrite of amyl, from 1863 onwards (brought in successive years before the Brit. Association of Science), determined the power of this substance as an anti-spasmodic and paralyzing agent, and made numerous sug- gestions as to its probable curative value in tetanus, asthma, and other spasmodic dis- eases. Dr. Richardson also repeated, and investigated scientifically, Guthrie's acci- dental observation in 1859, as to its effect in dilating the capillaries ; and he inferred that this effect was due to its paralyzing the ar- terioles through the vaso-motor nerves. 3 Dr. Gamgee's (unpublished) experiments were made with the sphygmograph and haemo- dynamometer, and led directly to Dr. Brun- ton's trials of the nitrite of amyl in angina, by demonstrating in animals and in man its action in lessening arterial tension. 4 There is an ingenious attempt to show that a partial restoration of the original form of the pulse-tracing, which was shown to correspond to a remission, but not cessation, of the paroxysm under nitrite of amyl, was due to the persistence of abnormal tension in the pulmonary circulation, after the systemic had been relieved. The pain, under such circumstances, "disappeared from the greater part of the cardiac region, the neck, and the arm, but remained persistent at a point about two inches to the inside of the right nipple 1 Lancet, July 27, 1867, p. 97; Journal of Anatomy and Physiology, vol. v. p. 92; Trans, of the Clinical Society of London, vol. iii. p. 191. The case, which is fully recorded in the Clinical Society's Transactions, was that of a man aged twenty-six, admitted into the Royal Infirmary of Edinburgh under Pro- fessor Maclagan, on Dec. 7, 1866; and sphyg- mographic observations, begun at his in- stance, were continued under Prof. Bennett, to whom the case was transferred on Feb. 1, 1867. There were palpitation of the heart, and violent throbbing of the carotids, besides the angina-pain. The aconite and digitalis were ordered by Professor Maclagan; the small bleedings by Professor Bennett. vol. ii.-44 690 ANGINA PECTORIS AND SUDDEN DEATH. repeated sufficiently often to show that in this patient at least, increased arterial tension and angina-spasm were constantly associated, and that agents which pro- duced diminution of the arterial tension always relieved the paroxysms. Among these agents, it is to be noted (though none was nearly so powerful as nitrite of amyl), small blood-lettings (of four ounces) were found to exercise a noted influence. Digitalis, on the other hand, appeared rather to aggravate the pain, and both digitalis and aconite made the pulse in- termit, which was never the case with the nitrite. On the whole, it must be ad- mitted, that notwithstanding certain un- avoidable deficiencies, the experiment is as complete as can reasonably be expected in the evidence it affords of a correlation of some kind between angina-paroxysms and increased arterial tension, in at least one clearly-defined case of organic car- diac disease.1 Many other experiments, both on man and on animals, have been performed, which amply confirm the action attributed to the nitrite of amyl in this case. The therapeutical part of the subject will re- ceive consideration afterwards; in the mean time it is sufficient to say that the relaxing effect of the vapor on the arte- rioles, and its efficacy, in some cases at least, in greatly and instantly relieving the breast-pang, have been placed beyond reasonable doubt. The points still open to further investi- gation seem to be these: It is as yet not proved that all the forms, and all cases of angina, are characterized by increased ar- terial tension during the paroxysm. If, indeed, there be cases corresponding ex- actly with the original description of Heberden, cases in which (the heart being to stethoscopic and physical examination normal) "the pulse is not disturbed by the pain," it would be extremely desirable to have sphygmographic observations of such apparently uncomplicated angina- paroxysms. But we have already ex- pressed doubts of the existence of such cases; at all events, the one recorded by Dr. Brunton is not such a case, but rather one in which the phenomena of the arte- rial tension must be regarded as wholly abnormal, being influenced by the fact of aortic regurgitation, a strictly mechanical cause of permanently and morbidly lowered blood-pressure in the arteries. But again : Supposing it proved that a suddenly-developed and decided increase in the arterial tension is a characteristic, or even an essential feature of the true angina-paroxysm, we may still regard it as an open question whether the change in the blood-pressure is to be attributed entirely in such cases to contraction of the arterioles, or partly also to changes in the innervation of the heart itself, which would account at once for the pain and for the sudden death which sometimes occurs during the attack ? Dr. Brunton has himself pointed out a fact which tells in this direction, notwithstanding the elaborate reasonings by which he supports the theory of vaso-motor derangement ending in spasm of the arterioles as the starting-point of the paroxysm. The ex- periments of Marey and others have shown that the effect of high blood-pressure in the arteries, per se, is to retard the pulse; while diminished arterial tension arising from relaxation of the artbrioles (as in fever, or in capillary congestion from the effect of external warmth) increases the frequency of the heart's contractions. N ow in the case alluded to, what actually took place was exactly the reverse of what might have been expected on the theory above mentioned. During the se- verest paroxysms, when arterial tension was at its height, the pulse was small and rapid, and when the pain and spasm had been subdued by the inhalation of the nitrite, the pulse diminished in frequency while regaining strength and volume. Dr. Brunton considers these phenomena as indicating " a derangement of the car- diac regulating apparatus, producing quickened instead of slowed pulsation." Further observations, therefore, seem to be required before it can be safely as- sumed that either vaso-motor derange- ment on the one hand, or disorder of the cardiac innervation on the other, is the primary or essential phenomenon of true angina pectoris ; although we may proba- bly take it as provisionally established that some law of intimate relation exists between increased blood-pressure in the arteries and certain forms, at least, of the angina paroxysm. The peculiar interest of Dr. Brunton's observations, for us, consists not in his having finally settled the nature of this relation, but in his having shown that a remedy which has the remarkable power of instantly diminishing arterial tension . . . So long as this condition remained the pain was almost certain to return."- Clin. Trans, iii. p. 199. 1 It is to be observed, that although the diagnosis actually made was that of aortic obstruction and regurgitation without aneurism, and although this was quite in accordance with the physical signs, and particularly the murmurs, described in the report, the re- markable difference in the sphygmographic tracings of the two radial pulses cannot but be regarded as leaving a doubt open as to the negative part of the diagnosis. On the other hand, aneurism, if present, may have been responsible in part for the definite character of the pain, which is usually not so well marked in cases of aortic regurgitation sim- ply. ANGINA PECTORIS AND SUDDEN DEATH. 691 has also a corresponding and almost equally instantaneous control over those paroxysms of angina in which increased arterial tension is known to occur. We shall recur to this subject when speaking of treatment. Meantime it seems necessary to observe that Dr. Brunton had been anticipated, in several quarters, in the merely specu- lative attempt to connect the symptoms of angina pectoris with vaso-motor changes. Thus Traube1 had argued that the dimin- ished volume and increased tension shown in the arteries in many attacks of steno- cardia are to be viewed, in connection with the increased rate of the pulse and the feeling of anxiety (angstgefiihl), as related to an increased stimulation of the nerve-centre of the vaso-motor system. Cahen2 had treated at length of various neuralgic affections (including trifacial neuralgia, and various painful affections of the pelvic organs) as affections of the vaso-motor system of nerves attended by congestion; and he referred angina pec- toris to the same category, and indicated arsenic as a valuable remedy for such cases, without, however, adding anything important to the symptomatology of an- gina. Landois3 had made a somewhat similar generalization as to some cases of excessive nervous palpitation, which he regarded as being a vaso-motor angina pectoris. Finally, Nothnagel, in a very ingenious and interesting contribution to the clinical study of the " vaso-motor neuroses," devotes an entire article4 to the special consideration of "Angina Pectoris vaso-motoria," upon the basis of five detailed cases (without special sphyg- mographic observations). But the de- tails of Nothnagel's cases will show that, however closely some of the subjective symptoms of angina pectoris may be sim- ulated by a purely vaso-motor lesion, there are some very striking differences between the disease so induced and the true angina pectoris of Heberden. For- 1st, in the greater number of Nothnagel's cases the disease yielded easily to very simple treatment, and in none was there a fatal issue, or even, apparently, much real apprehension of immediate or urgent danger; 2dly, the sensations in the ex- tremities (deadness, coldness, formica- tion, not pain) were usually present in all the extremities indifferently, and preceded the palpitations and the cardiac uneasi- ness by some minutes ; 3dly, the specially cardiac or other internal sensations were, a very distressing sense of palpitation, attended by anxiety, and sometimes by vertigo, or incipient faintness ; 4thly, in one of these cases only was the pulse-rate decidedly altered, and in that case it was diminished from 84 to 64-60 during the attack; 5thly, pain was either absent, or assumed little prominence among the symptoms; 6thly, the sensation of im- pending death was evidently connected with, and probably caused by, the palpita- tion (in Heberden's most characteristic case above quoted,1 as also probably in John Hunter's case, the very opposite of this was the fact; the feeling was of "a pause in the operations of nature for per- haps three or four seconds"). 7tlily, several of the cases recorded were below the typical age (30, 38, 39, 46), and one only above it (63); that one being a wo- man. The lesson, therefore, taught by Nothnagel's cases is not, properly speak- ing, that typical, still less that fatal, an- gina pectoris is always to be regarded as due to vaso-motor spasm, but rather that, under certain peculiar conditions of the system, a sudden check to the circulation in the extremities, determined by vaso- motor spasm, may become cause of an increased action of the heart, palpitation, and pseudo-angina; the disease so in- duced, however, being devoid of the char- acteristic pains and the more aggravated phenomena of fatal angina ; and that in such cases heat, aud mild counter-irrita- tion of the surface, have almost complete power to control both the external and internal manifestations; the prognosis being (according to N.) entirely favor- able. At the same time, although we cannot admit that Nothnagel's cases were genuine cases of Heberden's angina, they are very instructive, and may, no doubt, afford some insight into the pathology of the true disease. Leaving, for the moment, the line of inquiry suggested by these observations, ■we may revert to the pain of angina, which has been commonly regarded as a neuralgia of the cardiac plexus; the im- pressions of pain in the severer cases being radiated outwards through the nu- merous connections which are known to exist between the special ganglionic sys- tem of the heart, and the spinal nerves entering into the cervical and brachial plexuses through the cervical ganglia. It is difficult, from the very nature of the case, to prove this proposition; but there is no inherent improbability in it, unless, indeed, we should assume that the cardiac nerves of the ganglionic system are inca- pable of giving rise to acute pain ; an as- 1 Die Symptome der Krankheiten des Res- pirations- und Circulations-apparatus, p. 41. (Ref. in Rothnagel's article, infra.) 2 Archives G^n^rales de MMecine, 1863, vol. ii. p. 564. 3 Correspondenz-Blatt fur Psychiatric, 1866 (quoted by Nothnagel). 4 Deutsches Archiv. fur Klinische Medizin, vol. 3, xiv. p.309. Compare also vol. 2, p. 190, Case VII. 1 See page 667, note. 692 ANGINA PECTORIS AND SUDDEN DEATH. sumption not in accordance with the facts of medical experience in the cases of gall- stone, colic, &c. Holding in view, more- over, the proved association of angina pectoris in many cases with disease of the coronary arteries of the heart, and with other lesions exclusively within the range of the ganglionic system of the heart and aorta, it is difficult to resist a bias in favor of the view that the nervous system of the heart itself is the origin or the chief seat of pain, in the great majority of the cases. To these arguments it may be added that in most cases the internal sen- sations (whether distinctly referred to the heart or not by the patient) are obviously first in the order of time and of degree ; the brachial, intercostal, or cervical pains being sometimes altogether absent, and usually present only in the more severe and protracted attacks. It has, however, been plausibly maintained, notwithstand- ing these facts, that the spinal nerves are the true seats of the apparently cardiac pains of angina, and that all the appa- rently reflected sensations in the limbs, &c., are transmitted, like the external neuralgise, through a spinal centre. Dr. Anstie, who holds this view, adduces the unilateral character of the brachial pain in at least four cases out of five (?), as an al- most irresistible argument against the rad- iation of pain outwards from the cardiac ganglia, through the peripheral nerves of communication. "It appears greatly more probable," he writes, "that angina is essentially a mainly unilateral morbid condition of the lower cervical and upper dorsal portion of the cord; liable, of course, to be seriously aggravated by such peri- pheral sources of irritation as would be furnished by diseases of the heart, and especially bv diseases of the coronary arteries." 'This question is one which can scarcely be made less obscure by any arguments falling within the scope of this article. We have already indicated some of the difficulties that have to be encountered in extending the group, or order, of the neuralgice so as to include angina pectoris; meaning by that term, of course, the formidable and fatal disease we have been chiefly describing, and not the very numerous, or rather innumerable, in- stances of pains referred to the heart, by hysterical women and others, which have no such significance. Referring chiefly to fatal cases of angina pectoris, Sir John Forbes and all the more considerable au- thorities from Heberden downwards con- cur in giving an immense preponderance to the male sex. Without insisting too much on the numerical details, which for reasons formerly indicated may perhaps be considered as somewhat biased by the mode of collection, it may be well to com- pare this overwhelming proportion of males who fall victims to cardiac angina (an excess on the male side greatly ex- ceeding the greater proclivity of males to organic disease of the heart in general) with the numerical statements given in- cidentally in Dr. Anstie's work as regards the liability of the two sexes to neuralgise in general. "Eulenburg saw a hundred and six cases of neuralgia of all kinds, of which seventy-six were in women, and only thirty in men : my own experience is very similar; viz., sixty-eight women and thirty-two men out of a hundred hospital and private patients."1 A difference so extreme as this is not to be accounted for " by supposing that as men take a much larger amount of strong physical exercise than women, they will furnish a much larger proportion of subjects in whom an ill-nourished heart will break down under its work, and be seized either with paral- ysis or cramp;"2 and it seems scarcely necessary to do more than place these facts before the reader, in order to make it apparent that many of the arguments by which analogies drawn from the study of neuralgia in its more familiar forms are 'applied to angina pectoris, are question- able, if not altogether unsound. And yet I wound by no means be understood to deny that persons hereditarily predisposed to neurotic diseases, and especially to those of advanced life, may be specially liable, cceteris paribus, to angina in its more painful forms. Much care, how- ever, is necessary in sifting facts and de- tails of symptoms when recorded with a view to make good a general theory of this kind ; and when we are called upon to accept a narrative of epidemic angina pectoris in a ship's crew, in which " num- bers of men were simultaneously affected, ' ' while others were seized with "other forms of neuralgia, and severe colics,"3 I cannot but infer that the limits of a safe induction have been considerably ex- ceeded. In like manner, "remarkable" cases of "hysteria, the paroxysms of which were always accompanied by steno- cardiac attacks," can only serve to give a doubtful character to the theoretic inter- pretations which Eichwald has obtained 1 Op. cit. p. 156. 2 Ibid. p. 72. This might be a valid hy- pothesis were it possible to affirm that the subjects of fatal angina are chiefly drawn from the class of men that take the greatest amount of strong physical exercise. The op- posite, however, is notoriously the fact. We have already alluded to the generally re- ceived statement of Sir John Forbes, that angina pectoris is "the attendant rather of ease and luxury than of temperance;" and that it is comparatively rare (in its simple and typical form), among the laborious classes. 3 Ibid. p. 74. The authority given is Gu61i- neau, Gaz. des Hopitaux, 1862. ANGINA PECTORIS AND SUDDEN DEATH. 693 from such a field of experience.1 And even Eulenburg, notwithstanding the sobriety of his tone in general, and the great importance of his work as a maga- zine of valuable information and research, has shown how much a sound clinical ob- servation has been subordinated to theo- retical ideas, when he pronounces dog- matically that the disorders of respiration in angina are merely " consequences of the pain ; the patient is afraid to inspire deeply, but if induced to do so, can gene- rally accomplish it. "2 It may be doubted, I think, on the whole, whether much real knowledge has been gained by the classi- fication of angina pectoris among the neuralgue ; to which, nevertheless, the character of its pain shows a remarkable affinity. Proceeding now to consider the motor derangements which form a part of the angina-paroxysm, and especially those which, affecting the heart itself, deter- mine the fatal termination, it is impossi- ble to overlook the facts brought to light by physiology as regards the influence of certain nerves on the movements of the heart. In particular, the remarkable in- hibitory influence of the efferent nerves proceeding to the heart through the pneu- mogastrics, demonstrated by the brothers Weber3 in 1846, and in 1856 shown by Waller4 to be due to filaments from the spinal accessory nerves joining the pneu- mogastrics near their origin, has a pecu- liar interest for us in connection with this subject. It has been conclusively shown that by a galvanic current transmitted outwards through these filaments, or by galvanization of the centre in the medulla from which they are derived, the heart's action may be controlled, or even stopped, so that a true cardiac paralysis is the re- sult of a strong current, while weaker galvanic action produces an indefinite re- tardation in the rate of the cardiac pulsa- tions. Whatever theory be adopted as regards the so-called inhibitory influence, its results are toe closely allied to the phe- nomena of syncope, pure and simple, to escape attention in treating of sudden death from angina. But it has been fur- ther shown by Cyon and Ludwig,1 that a reflex influence may be so transmitted through nerves arising from the pneumo- gastrics (viz., the so-called depression- nerves), as at once to control the cardiac pulsations through the inhibitory efferent nerves, and to diminish tension through the vaso-motor system. As we have al- ready seen reason to believe that in an- gina pectoris the vascular tension is usu- ally increased rather than diminished, it may be inferred with great probability that if the pneumogastric nerve be impli- cated at all in the angina-paroxysm, it is probably more as an inhibitory or efferent, than as a reflex or efferent nerve. It must not be forgotten, however, that paralysis of the sympathetic nerve has the effect also of enfeebling and retarding, though not, apparently, of stopping, the heart's action ; which, in a certain sense, may be regarded as not essentially dependent upon influence transmitted from any nerve-centre, though subject, as we have just seen, to control through the inhibi- tory or efferent cardiac filaments of the pneumogastric. If we endeavor now to determine, in the light of these facts, what is the par- ticular mode in which the heart's action is suddenly arrested in a paroxysm of an- gina, it must be confessed that no ultimate decision seems possible. Almost all the vague and unsatisfactory speculations for- merly alluded to, as to whether spasm or paralysis is the prevailing condition in the fatal paroxysm, have proceeded on the assumption that these two conditions are essentially contrasted, or rather oppo- site to, and inconsistent with, one an- other ; the former representing undue strength, the latter undue weakness, or absolute annihilation of contractile en- ergy. Now this assumption can by no means be regarded as a legitimate, or even a probably correct one. At least it may be fairly affirmed, as a probable re- sult both of physiological and pathologi- cal inquiries, that spasm (i. e., irregular or abnormal contraction, whether painful or not) in a voluntary muscle is much more allied to weakness, or to deficient innervation, than to absolute excess of normal energy. And the frequency of the association of rigid or tonic spasm with paralysis, in the voluntary muscles, would tend to show that there is no absolute in- consistency, at least, in the supposition 1 See Eulenburg, infra, p. 433. Perhaps the same remark applies to the presumed re- lationship between angina pectoris and spas- modic asthma, as indicated by Kneeland, Amer. Journal of Med. Science, Jan. 1850, and Anstie, op. cit., p. 68. It is to be re- marked that Trousseau, in his vast and varied experience, has not recorded anything tend- ing to confirm the relationship of these two neuroses, except in a case where both of them were dependent on aneurism of the aorta. See his Clin. Med., English transla- tion, vol. i. p. 634. 2 Med. Times and Gazette, March 26, 1870, p. 329. We have seen how emphatically this idea is contradicted by the specific state- ments in John Hunter's case, as well as by all the most exact clinical observations from Heberden downwards. 3 Wagner, Handworterbuch der Physiolo- gie, Bd. iii., 2te Abtheilung, S. 42. 4 Gazette Medicale, Paris, 1856, t. xi. n. 420. 1 Journal de 1'Anatomie, Paris, 1867, t. iv. p. 472. 694 ANGINA PECTORIS AND SUDDEN DEATH. that both spasm and paralysis may, in varying degrees, be present in the heart's arrested action which leads up to sudden death in the angina-paroxysm. As far as observation goes, in the case of spasm of the involuntary muscles (other than the heart), it seems as though abnormal, or painful, disturbance of rhythmic action were almost always an indication of weak- ened innervation, rather than of superflu- ous energy in the contractile apparatus as a whole. The spasm of colic, for instance, is associated with constipation, or deficient peristaltic action of the intestines; the false pains, or painful spasms, of the ute- rine muscles retard, instead of expediting, the process of delivery. We might, there- fore, not unfairly argue from these analo- gies, that a painful spasm of the heart might be expected to interfere with its rhythmic or normal action quite after the manner of a paralysis, the abnormal being substituted for the normal action, and the whole sum of disordered effort being less than the sum of normal energy expended in healthy cardiac action. So that it might very well be presumed that painful spasm is by no means unlikely to be as- sociated with a tendency to sudden stop- page of the heart's action, or virtual pa- ralysis, whether from inhibitory nervous irritation through the pneumogastrics, or from disorders originating in the cardiac ganglia themselves, and allied in charac- ter to true paralysis of muscular energy. It must, however, be conceded to the ad- vocates of the theory of paralysis, pure and simple, that nothing but the presence of severe pain in the angina-paroxysm, and the absence of this symptom, as a rule, in purely paralytic affections, tends to support the spasm-theory of angina. Post-mortem examinations have generally shown that the heart is found flaccid, rather than rigidly contracted ; and the lesions found in the muscular substance of the heart itself are usually such as would confirm the idea of decidedly and permanently weakened energy, rather than a disposition to abnormal contrac- tion. Rupture of the muscular bundles, so commonly observed in tetanus and other severe spasms of voluntary muscles, has never been recorded in sudden deaths from angina pectoris; while anaemia, fatty degeneration, and fibro-tendinous substitution, have been the predominat- ing lesions of the muscular fibres itself. The question as between spasm and pa- ralysis, therefore, is one of great diffi- culty, if not indeed practically insoluble in the present state of our knowledge. While dealing with hypotheses of which no absolute or experimental proof can be obtained, we may remark that vaso-motor spasm, operating indirectly through the smaller arteries upon the muscular fibre of the heart itself, may possibly give a clue to some of the pathological changes which attend the paroxysm, and especially those which precede dissolution. Both Erichsen1 and V. Bezold2 have shown that as a result of deligation or occlusion of the coronary arteries, the heart's contractions become feeble or irregular, and ultimately cease ; the normal action being restored again on removal of the ligature or of the compression. Now apart from the ob- vious bearing of these facts upon the case of organic obstruction or constriction of the coronary vessels (perhaps the most clearly established of all the permanent organic changes in connection with fatal angina pectoris), is it not extremely prob- able that a similar effect, or an aggrava- tion of a pre-existing tendency to inter- rupted cardiac action, might occur, if in a case of disease of the aorta or coronary arteries, cardiac anaemia were aggravated for the moment by vaso-motor spasm of the smaller arteries within the heart it- self? Even without such preceding or- ganic disease it is conceivable that extreme vaso-motor spasm might affect the cardiac circulation directly through its smaller arteries, and so produce changes more or less similar to those observed in the ex- periments above mentioned. What has been already stated, however, in regard to Nothnagel's observations would seem to show that really fatal angina does not occur in this way; and that the first effects of general vaso-motor spasm upon the heart are more of the nature of palpi- tation, or excited action, than of inter- rupted or suspended pulsation. On the whole, it must be admitted that the ultimate pathology of the angina par- oxysm does not admit of being reduced to any very precise expression or definition ; but various more or less probable conjec- tures may be made, in accordance with known facts and experimental researches, as well as with clinical and pathological observation, to account for the facts. Viewing the paroxysm as a neurosis, we might attribute its phenomena partly to vaso-motor spasm, and partly to inhibi- tory influence transmitted through the vagus nerve from the medulla oblongata. This latter influence would account more reasonably and probably than any other for those cases of angina in which mental causes and sudden shocks of any kind are known to influence the production of the paroxysm, without the intervention of peripheral changes such as can be attri- buted to vaso-motor spasm. In cases, again, resembling in their symptoms those described by Nothnagel, whether accom- panied by organic disease or not-cases in which coldness of the surface, deadness 1 London Medical Gazette, July 8, 1842. 2 Centralblatt fur die Med. Wissenschaften, 1867, No. 23. ANGINA PECTORIS AND SUDDEN DEATH. 695 of the extremities, and perhaps palpita- tion or increased rate of the pulse can be ascertained to precede the cardiac pain, there would be reasonable ground for pre- suming that the vaso-motor nerves were the earliest involved in the morbid circle, though it is still probable that, if such cases ever end in sudden death, it is through some more direct impression on the cardiac nerves, or on the coronary cir- culation. It is very doubtful, however, whether under any circumstances fatal angina pectoris can be viewed as a pure neurosis. Much more probably, the par- oxysm is the expression in symptoms of sudden changes arising, indeed, from neurotic accidents, but only assuming grave importance in respect of their co- incidence with a permanent cause of det- riment to the circulation. Either the heart's fibre is permanently weakened, or its arteries are obstructed and diseased, or the general arterial circulation is dis- turbed through disease in the first part of the aorta, aneurismal or other. In cer- tain cases it may be that the innervation of the heart is directly implicated in or- ganic disease ; at least in two cases of this kind1 the cardiac plexus and cardiac branches of the vagus were found to be compressed in connection with angina- paroxysms which proved fatal; though probably the inferences which have been drawn from these rare instances may not be applicable to the general pathology of the subject. But whatever be the nature of the permanent change underlying the disease, its effect in the most characteris- tic cases is not much felt when the circula- tion is in a moderately tranquil state. In some of the very worst cases, indeed, it has been clearly ascertained that very shortly before a fatal paroxysm the pa- tient has been in a state of entire comfort and tranquillity, with a regular and nor- mally acting heart, and all the functions apparently so well-adjusted as to involve no appearance of any disease tending to shorten life. Usually there is an incapa- city for sudden or severe exertion, and a liability to grave disturbance under strong emotion; but, on the other hand, a pa- tient has been known to say, ivithin three days of his death in a paroxysm, "I can walk with ease ten or fifteen miles, after I have been stopped three or four times at intervals of a hundred yards."1 In such cases the paroxysms are plainly neurotic ; but the disease is nevertheless not a pure neurosis. It is, on the contrary, obviously of a complex character, involving a per- manent nucleus, so to speak, of organic change, together with a neuralgic element, more or less pronounced, and, connected with this, perhaps as a reflected neurosis in some cases, an element of motor dis- turbance in the heart's action, which may in some cases be of vaso-motor origin, while in others it may be more directly determined through the inhibitory fila- ments of the vagus. It is probably in the former class of cases that the action of nitrite of amyl is most immediately and surely productive of benefit. There remains for remark only one ob- scure, and apparently non-essential, part of the pathology of angina pectoris, viz., the nature of the cerebral accidents we have indicated in the description of the disease as sometimes coinciding, some- times alternating, with the more decid- edly cardiac attacks. It is to be observed that among these accidents spasms, giddi- ness, temporary attacks of coma, associ- ated with, or followed by, various dis- orders of the special and general sensi- bility, are common ; while on the other hand, paralysis, either spinal or cerebral, is rare. These facts point strongly in the direction of a neurosis, and very probably a vaso-motor neurosis, of the cerebral circulation ; and we know that in animals most of the symptoms above referred to may be induced artificially, by cutting off the arterial vascular supply of the brain and medulla oblongata, as in the well- known experiments of Sir Astley Cooper. The Prognosis of angina pectoris is diffi- cult to realize in individual cases, in pro- portion to the absence of clear lines of distinction between this and the various affections resembling Heberden's angina, which we have discussed in various parts of this article. Probably a critically ex- act, or absolute, prognosis, could only be founded on a knowledge of the nature and extent of the organic changes underlying the paroxysmal neurosis; and although we have already indicated a doubt as to whether the latter ever terminates fatally in the absence of such organic changes, yet it is beyond all question that the amount of organic disease which can be detected in any given case during life is a most insecure guide in estimating the 1 Heine, in Muller's Archiv, 1841, p. 236; and Lancereaux, in Gazette Medicale, 1867, p. 432. In the former case the heart was at times observed to cease beating for several seconds, and at these times there was a feel- ing of indescribable anxiety, like that of an- gina pectoris; in the intervals of the parox- ysms the patient felt perfectly well. The right phrenic nerve, the nervus cardiacns magnus, and the pulmonary branches of the left vagus were all involved in, or compressed by, calcareous deposits. In Lancereaux's case, the cardiac plexus was found vascular, and compressed by exudation ; but the coro- nary arteries were also obstructed, and the aorta was diseased. The patient died of angina pectoris, in a paroxysm. 1 Walshe, Diseases of Heart and Aorta, 4th edit., p. 199, note. 696 ANGINA PECTORIS AND SUDDEN DEATH. probabilities of death during a paroxysm, in that particular case. " It is accordant with my experience," says Dr. Walshe, " that fatal angina is more to be dreaded in association with organic defects, either difficult or impossible to diagnose (such as slight fatty metamorphosis and calcified coronary arteries), than with those grave forms of structural mischief that are readily discoverable by physical examina- tion. " 1 Add to this that the mere infer- ence from symptoms as to the gravity of the prognosis is likewise extremely open to fallacy; inasmuch as a series of com- paratively mild or lessening attacks may sometimes (under apparently unchanged conditions) be succeeded by the most vio- lent or dangerous, even fatal, paroxysms; while on the other hand, one or more at- tacks, very nearly fatal, may be followed by a long interval of comparative, or nearly complete, freedom. From this dilemma there is, in the present state of our knowledge, no escape; and all that we can do, therefore, towards the estab- lishment of a guarded and limited prog- nosis in any case, is to study carefully its individual features, and particularly the relation of the symptoms to particular causes of aggravation, or of relief. Gen- erally speaking, a form of disease which yields, gradually, to carefully pursued hygienic treatment, and in which the paroxysms are obviously under the con- trol of the remedies about to be discussed, is relatively favorable ; while the opposite indications justify the gravest prognosis. An absolutely favorable prognosis could only be justified by circumstances tending to place the disease in the category of pseudo-angina, as above indicated; and indeed it may be generally observed that the gravity of cases of angina in the ex- perience of individual observers is often found to be in an inverse proportion to their estimated frequency, cases of hys- teria, intercostal neuralgia, spasmodic dyspnoea, &c., being admitted by some more freely than others into the category of angina. There seems no reason to doubt, however, that a person affected with absolutely typical angina pectoris may survive for years, even after repeated paroxysms; and in some cases, apparently of the most threatening kind at one stage of their progress, the disease has been so far reduced in its frequency and severity that we may even, perhaps, speak of such cases as cured, in a practical sense. But cures of this kind are rarely, if ever, re- corded with such minute attention to de- tails as to inspire confidence, apart from the credit due to the reporters ; and per- haps even the statements of Heberden as to the long survival of some of the cases mentioned in his first paper (see p. G80, note) may require qualification on the ground that clear evidence is wanting as to the absolutely typical character of the symptoms referred to.1 Among cases actually ending by a fatal paroxysm, it has not occurred to me personally to have been informed of a longer duration than six or seven years, counting from the first well-defined seizure ; but I have known more than one instance of survival for much longer periods, after attacks bear- ing so much resemblance to true angina as only to have required death to have occurred in a paroxysm, as a conclusive argument for considering them to be typi- cal instances of the disease. In John Hunter's case, as we have seen (assuming the first attack of supposed gout in the stomach to have been really identical in character with succeeding seizures) a du- ration of rather more than twenty years, with numerous intervals of tolerable health and great mental activity, may be regarded as well established. Dr. Walshe has " met with an instance in which there was the strongest evidence that the first paroxysm had occurred twenty-four years prior to my interview with the patient."2 And, in the general experience of physi- cians who have had occasion to see much of cardiac disease, it is by no means un- common to find cases of valvular or other very positive and well-defined organic disease, in which symptoms of a danger- ous or proximately fatal kind, probably more or less allied to angina, have pre- ceded the fatal issue by an interval of very many years ; sometimes, indeed (as in the case of the Rev. Dr. Guthrie, already referred to3) for more than a quarter of a century. Such cases, however, are rarely quite typical instances of Heberden's an- gina, and accordingly only a small pro- portion of them are characterized by the very sudden ending proper to the disease as described in the "Commentaries." It is difficult to obtain exact clinical histories of cases extending over so many years, but in one, in which I was consulted in 1872, and which terminated fatally some months ago, there was reason to suppose 1 It is at least worth noting (though xhe omission may be accidental) that in the Com- mentaries these statements are not repeated; and perhaps the language, though carefully guarded, admits of the inference that thirty years of additional experience had rather in- creased than diminished Heberden's sense of the gravity of the prognosis. " Exitus hujus affectus est perquam memorabilis. Qui enim eo tenentur, siquidem, nullo casu interveniente, angina pectoris ad ax/aw pervenerit, omnes repente cor- ruunt, et fere momenta per eunt." . . . ^Uni- cum vidi (mgrum), in quo hoc malum sponte sub fnitum est." 2 Op. cit. p. 200. 3 See ante, p. 686, note. 1 Op. cit. p. 201. ANGINA PECTORIS AND SUDDEN DEATH. 697 that the foundations of the aortic valvular lesion of which the physical signs were apparent, and of which the obvious symp- toms had certainly existed many years before 1872, had been laid as early as 1852, when the patient had sutfered from pulmonary hemorrhage. The threatening symptoms present on that occasion had been popularly attributed to a consump- tive tendency, but Dr. Christison, who was consulted, had evidently detected some valvular lesion of the heart, and had carefully questioned the patient as to its possible rheumatic origin. It is not, in- deed, certain, or even perhaps very proba- ble, that well-marked and considerable aortic regurgitation existed at this period, nor is it possible now to ascertain at what precise interval after the first commence- ment of the disease the angina-like symp- toms, which were notably present when I saw the patient, first became apparent. What I can personally affirm is, that in 1872 the symptoms and physical signs were those of old-established aortic regur- gitation, with very considerable hyper- trophy of the left ventricle, and all the usual concomitants ; and notwithstanding this, the patient assured me that so late as 1870 he had explored the Aletsch gla- cier, and on other occasions, from about 1865 onwards, had been able to carry out walking tours in Switzerland, the Tyrol, and the Dolomite country, the character of which may be inferred from his having walked over the Monte Moro pass and the Gemmi, visited the Mer de Glace, and gone nearly to the Jardin, in addi- tion to all the usual excursions about Chainounix. Moreover, this gentleman was in 1872 performing the duties of a parish clergyman in a populous place, sparing himself somewhat, indeed, in visiting, but preaching often more than once a day, and, as he affirmed, without any apparent injury or physical exhaus- tion ; and the question most urgently and repeatedly pressed upon his medical ad- visers was as to his carrying out an engagement of marriage, entered into several years before, and maintained with full knowledge on both sides of the pre- carious condition of his bodily health. I need not say that no medical encourage- ment to this step could be obtained ; but the marriage, nevertheless, took place in about a year after I was first consulted, and the death of this patient not long ago shows how real was his danger, and at the same time what a terrible burden of posi- tive organic disease may be borne without apparently "giving in," by one whose objects in life are of sufficient importance to induce him to disregard the silent warnings of internal suffering. In yet another case known to me, in which, however, the symptoms were far more decidedly and typically those of angina pectoris, while the physical signs were much less manifest than in the preceding case, the patient was able to make numer- ous Ion" journeys to the Holy Land, Egypt, &c., and always felt himself the better for them. This patient in the end perished suddenly. The Treatment of angina pectoris resolves itself naturally into two depart- ments, viz., that of the paroxysm, and that of the intervals. The former treat- ment is essentially palliative, and di- rected exclusively to the urgent symp- toms then existing; the latter aims at being founded, in a wider sense, upon the diagnosis and prognosis of the individual case, after a complete examination into the state of all the bodily functions. Heberden's views of treatment were limited to the first indication-the control of the paroxysm. "Wine and cordials taken at going to bed will prevent, or weaken the night fits ; but nothing docs this so effectually as opiates. Ten, fif- teen, or twenty drops of the tinctura Thebaica taken at lying down will enable those to keep their beds till morning who had been forced to rise, and sit up, two or three hours every night for many months."1 We have already seen that Heberden altogether repudiated the (so- called) antiphlogistic treatment as inap- plicable to this disease, which he con- sidered as belonging to the order of spasms, not of inflammations. In his later work he repeats in general terms the above recommendations, and adds to them a single phrase in favor of rest and warmth. He has seen an approach to a cure in one case, where the patient pre- scribed to himself the labor of sawing wood for half an hour every day. Be- yond this, he has little or nothing to tell, and does not profess to have greatly ad- vanced the cure of a disease, " qui vix ad hue locum, aut nomen in medicorum libris invenit." It may be fairly inferred from these expressions, that Heberden's view's of the treatment of angina remained almost stationary for at least thirty years ; and that here, as in the matter of prog- nosis, he does not appear to have gained confidence with his advancing experience. The treatment of the paroxysm by opiates and stimulants of various kinds has in fact been repeated by almost all the lead- ing authorities, and is even now the only medical treatment which can be said to have received general assent. Latham, Stokes, and Walshe, among our more modern authors, concur in recommending from forty to sixty drops of laudanum, together with wine, brandy, or aromatic spirits of ammonia, repeated according to the violence of the paroxysm. Hoff- * Med. Trans., vol. ii., ut supra. 698 ANGINA PECTORIS AND SUDDEN DEATH. mann's anodyne, or sulphuric ether in half-drachm doses, has been a favorite remedy with many ; and musk, camphor, and other anti-spasmodics, have also been employed, though confessedly of less value than ether, which has also been fol- lowed by good results when administered by inhalation. Of late years, opium has been given hypodermically, and, it is stated, with more immediate as well as more successful results than when ad- ministered by the mouth. In so far as the principle of the treatment can be in- ferred from the success that has attended those remedies in some cases, it would appear that a rapidly induced narcotism, benumbing the sensory nerves and extend- ing, perhaps, to the centre through which painful sensory impressions are reflected in the form of a paralyzing or inhibitory influence on the heart, by the motor fibres of the pneumogastric, is the first object to be accomplished in the presence of over- whelming pain, while the second and not less important object is to stimulate the heart's action by all the known excitants of the circulation. Warmth to the ex- tremities and to the epigastrium, sina- pisms to the thorax, and sometimes be- tween the shoulders or at the back of the neck, may be regarded also as additional means of fulfilling the latter indication, and of assisting the cardiac contractions by their influence on the vaso-motor nerves. In my own experience, no reme- dial agencies have appeared more power- ful than warm pediluvia with mustard, and fomentations applied at the same time to the arms and thorax, as hot as they can well be borne. With these, and with ether and other diffusible stimulants, I have often been able to dispense with the use of large opiates, in doubtful cases, or in cases where they seemed to be in some respects contra-indicated. It is well, if possible, to be informed of the condition of the kidneys, and of the lungs before prescribing opiates. Dr. Stokes1 evidently looks upon large opiates as un- safe where fatty degeneration of the heart's fibre is suspected : and Niemeyer2 discountenances narcotics altogether. The use of opium, however, is too valua- ble in typical cases of Heberden's angina, when apparently uncomplicated, to be readily given up. It should be given with discretion, its effects being carefully watched ; and it should probably be with- held, or given in extremely moderate doses, wherever there is risk of urremia, or of bronchial and pulmonary sudden congestion or oedema, or of the cerebral accidents that accompany angina in cer- tain cases, especially those in which the cardiac fibre is the seat of degeneration. In these cases, too, it is not usual for the mere pain of angina to be so threatening, per se as to suggest opium in the same high doses as in the more typical instances where the paroxysm occurs in the midst of apparent good health. Hydrate of chloral, from its well-marked sedative and anodyne powers, has been suggested as a substitute for opium in cases of painful angina but on the other hand, the depressing action of chloral- hydrate in large doses has been supposed to be a fatal objection to its employment in cases of weakened cardiac action. My experience of this remedy in severe cases resembling angina pectoris is limited to one case, but it is so remarkable as to de- serve notice here. John McN., set. 35, was subject to paroxysms of intense car- diac suffering, of a rather obscurely pain- ful character, but with considerable orthopnoea, palpitation, sleeplessness, and frightful dreams. Uis symptoms are more particularly referred to in an earlier part of this article, and from a very care- ful consideration of them I arrived at the conclusion that they were essentially of the character there described as angina sine dolore, with slight bronchitic compli- cation, and slightly albuminous urine-• sp. gr. 1013-20. The heart's action was irregular, and the physical signs pointed unmistakably to hypertrophy of the heart and liver, with valvular and (probably) arterial disease. The details are too com- plicated to be introduced here, but my diagnosis was-Aortic insufficiency, with aneurism. The case was certainly not one in which extreme doses of any nar- cotic would have been regarded as expe- dient ; but, guided by experience ac- quired before he applied to me, I allowed this patient to have thirty grains of hy- drate of chloral to obviate the sleepless- ness, and if possible to ward off the at- tacks. It answered well the first night, and on a succeeding occasion the same dose was ordered, and was to be given a little before midnight. By a misunder- standing of the directions three drachms of hydrate of chloral were sent instead of a like quantity of the usual syrup, and this being in one dose, apparently to be given as a draught, the patient took 180 grains at once of chloral-hydrate, from the hands of a night-nurse, after a restless and disturbed evening, at 11.30 P. M. Next morning I found him very drowsy, but not quite comatose, as he could be roused to give rational answers as to his own condition ; the breathing was quiet, and only slightly stertorous. The pupils were, on the whole, contracted, but vari- ably so ; the pulse, which had been irreg- 1 Diseases of the Heart and Aorta, p. 489. 2 Text-book of Practical Medicine, Ameri- can translation, vol. i. p. 371. 1 Strange, Medical Times and Gazette, Sept. 4, 1870. ANGINA PECTORIS AND SUDDEN DEATH. 699 ular m rhythm, was decidedly more natu- ral than before ; the face was a little con- gested, and the eyelids puffy, but the surface generally warm, and the whole appearances not such as to justify any very great alarm, especially as at the time it was supposed that only thirty grains of chloral-hydrate had been given, the mis- take being found out afterwards. The patient gradually recovered from the effects of the overdose, and it is very re- markable that he always continued to at- tribute to this happy accident (as it might be called, speaking of the result only) a comparative immunity afterwards from the angina-like symptoms. The irregu- larity of the pulse recurred after the effects of the overdose of chloral had passed off, but under repeated doses of from thirty to sixty grains he became much better in all respects, and a course of iodide of potassium, with careful hy- gienic management, accomplished what, so far as the more immediately urgent symptoms are concerned, may almost be called a temporary cure of a very perilous condition. This man is now performing regulated duties as a railway servant, and is still occasionally taking hydrate of chloral, though warned not to allow it to become a regular habit. It is clear, there- fore, that in some cases, at least, of angina pectoris chloral-hydrate might probably with advantage replace opium in the treatment, and that irregularity of the heart's action does not always prove a contra-indication to its use. Inhalations of chloroform have been proposed, and in some cases employed, for the relief of painful angina ; but, from the supposed tendency of deep chloroform- ansesthesia to paralyze the heart, this remedy has never been warmly supported or largely employed by physicians in such cases. The inhalation of ether seems preferable as attended with less risk; and chloroform, if given at all, should be in doses short of complete amesthesia, whether by inhalation or by the mouth. Of all the more modern additions, how- ever, to the resources of the physician in the angina-paroxysm, the most important by far appears to be the employment by inhalation of nitrite of amyl, as first rec- ommended by Dr. B. W. Richardson, and successfully carried out on a basis of careful clinical and experimental observa- tion in angina by Dr. Lauder Brunton. We have already indicated in this article the nature of the scientific evidence on which this therapeutic suggestion rests, and have now only to consider the details of purely clinical experience in relation to this remedy, and the qualifications and cautions required in its employment. On this subject our knowledge is still very incomplete, but it is nonethe less neces- sary to place on record here whatever can be said to be well established as a guide to the practitioner. My own experience, I may remark in passing, is certainly favorable to the use of this remedy, not only in positive an- gina pectoris, but also in many cases of cardiac asthma, and even of true spas- modic asthma without cardiac complica- tion. In the very few cases of typical angina in which I have prescribed it, I have had distinct testimony as to the re- lief afforded, although my opportunities of close observation of the actual parox- ysms have not been such as to enable me to add anything of real value to the state- ments of other observers. Looking to the practical aspects of the question, there is probably no single observation hitherto made which, as a simply clinical narra- tive, can rank beside the history of his own case by Dr. W. Ilcrries Madden of Torquay.1 We shall therefore give here some details of this remarkable personal experience. Dr. Madden seems to have suffered from a temporary break-down in health at 24 years of age, "with obscure heart-symp- toms, and threatened lung, mischief." Uis father had died shortly before from angina pectoris-"the organic cause in his case being atheromatous obstruction of the coronary arteries." In the winter of 1859, at about 44 years of age, Dr. Williams detected slight mitral incompe- tency. In the spring of 1871, Dr. Mad- den records that he suffered from an attack of bronchitis, with great nervous prostration, but recovered in autumn, and was able to perform all his usual duties during the next winter and spring, in the midst of "a good deal of professional anxiety and much painful worry of a dif- ferent nature." On July the 8th, 1872 (at 57 years of age), he had his first at- tack of angina, which occurred "sud- denly, without the slightest warning," and was characterized by "pain extend- ing across the front of the chest, along the inside of the left arm, and across the chin." In about ten days the frequent recurrence and increased severity of the attacks compelled him to desist from all professional duty. Notwithstanding the repose so obtained, the attacks, after a few days' interval, continued to increase in violence, lasting, for the most part, for a quarter of an hour or twenty minutes, and recurring frequently at intervals of about three hours. "Various remedies were tried, but with little or no benefit. Hypodermic morphia was the most use- ful, but it was impossible to employ it often enough without producing danger- ous narcosis." At this period Dr. Mad- den was led, after considerable hesitation, to give a trial to the nitrite of amyl, 1 The Practitioner, vol. ix. 1872, p. 331. 700 ANGINA PECTORIS AND SUDDEN DEATH. which he had previously supposed to be suitable only for those cases in which the face was pallid during the paroxysm. "As mine was flushed," he writes, "I dismissed from my mind all thoughts of trying it, and paid the penalty of hasty conclusions in the shape of a large amount of acute suffering." The result of the first trial of five drops, inhaled during a severe attack in the night, "was truly wonderful. The spasm was, as it were, strangled at its birth. It certainly did not last two minutes, instead of the old weary twenty. And so it continued. The frequency of the paroxysms was not di- minished for some time; but then they were mere bagatelles as compared with their predecessors. Under these improved circumstances, strength gradually return- ed ; the attacks became less and less fre- quent, and finally ceased. At the time of writing these lines (October 11, 1872) I have not had an attack for five weeks, and have resumed my ordinary duties, of course with care." It is most satisfac- tory to be able to add, from a private letter with which the author has been favored, from Dr. Madden, that his con- fidence in the remedy continues unabated, but that at this date (August, 1875) he has not required to use it for a consider- able time. As regards the more obvious effects of the inhalation of nitrite of amyl, Dr. Madden records that "the first effect was often bronchial irritation, causing cough ; then quickened circulation ; then a sense of great fulness in the temples, and burn- ing of the ears; then a violent commo- tion in the chest, tumultuous action of the heart, and quick respiration. The angina pain died out first in the chest, next in the left upper arm, and last of all in the wrist, where it was usually ex- tremely severe. . . . When the pain had ceased there was generally for some time a strong involuntary tendency to suspen- sion of breathing, each prolonged pause being followed by a very deep inspiration. There was not at any time the slightest confusion of thought, or disturbance of vision, but occasionally slight and tran- sient headache." The physical signs in Dr. Madden's case seem to have varied somewhat, and latterly had more the characters of aortic than of mitral dis- ease. The description of the peculiar subjective sensations connected with the heart-pang in this case has been already quoted at p. 668, note 2. It can be but rarely that, in a disease so paroxysmal and uncertain in its char- acters as angina pectoris, the conditions of a therapeutical experiment can be so perfectly attained as in this case. The hereditary predisposition, the age and sex of the patient, the proved existence of positive cardiac disease, and the vivid and personal narrative of the symptoms, com- bine in assuring us that the angina was of the most formidable kind, and all but typical, if not indeed absolutely so, in character. On the other hand, the relief was so marked, so strikingly instantane- ous, and so frequently observed in re- peated paroxysms, as to leave no doubt of the control exercised by the remedy. And further, the ultimate relief amounts to something more than a palliative reme- dial action; something, indeed, closely approaching the character of a cure. Further, as Dr. Madden has remarked, the relief is shown not to have been con- tingent upon the external evidences of vaso-motor disturbance during the parox- ysm, although closely associated (as in Dr. Brunton's case) with the physiological action of the remedy in relaxing arterial tension. It is to be remarked, however, that beyond the more obvious facts, no very exact observations were made in Dr. Madden's case as to the connection be- tween the attacks of angina and vaso- motor changes. " The. presence of in- tense pain," he says, "is not favorable to the exercise of calm, philosophic analysis, and I can only tell what I felt." But although this case, and others more or less resembling it which have been published, give the utmost assurance of the beneficial action of nitrite of amyl in the angina paroxysm as a fact ascertained by experience, yet the moment we pro- ceed beyond the mere fact, we find the question of the modus operandi, indica- tions, and contra-indications of the remedy surrounded with difficulties which have not as yet been resolved by scientific ob- servation. It has been commonly sup- posed that the action of the amyl-nitrite is purely peripheral, i. e., on the vaso- motor nerves of the vessels only, apart from the vaso-motor nervous centre ; and that the relief caused in angina is in direct relation with the previously in- creased vascular tension, as suggested by Dr. Lauder Brunton in his first experi- ment. We had occasion to point out, however, when speaking of that remark- able case in its relation to the theory of the angina paroxysm, that the state of the heart's action corresponding with the period of increased vascular tension on the one hand, and with the relief through amyl-nitrite on the other, was different from what could be attributed to vaso- motor spasm and paralysis alone; and that there remain phenomena of the par- oxysm which can be explained, in all probability, only through the innervation of the heart itself. A like difficulty still surrounds the explanation of the physi- ological and therapeutic action of the nitrite of amyl. Though unquestionably producing some of its well-known effects through vaso-motor paralysis, we are not ANGINA PECTORIS AND SUDDEN DEATH. 701 quite able to affirm with confidence that its action is purely peripheral, or even that it is quite uniform in all cases of an- gina. Thus in Dr. Madden's case it seems to have produced, as a primary result, " quickened circulation, tumult- uous action of the heart, and quick re- spiration." This is, in fact, the usual effect of amyl-nitrite on healthy persons, in whom the pulse-rate may be raised in a few seconds from a normal state of about 70 to 120 or 140 pulsations in the minute ; the flushing of the face, and the other distinctly vaso-motor effects follow- ing the rise in the pulse-rate. In Dr. Brunton's case, on the other hand, the pulse became slower when the spasm was being relieved. In a case published by Dr. Haddon, which, though rather im- perfectly reported, appears to have been one of aortic incompetency with angina- like pain, the pulse was jerking, and 80 per minute at the commencement of the inhalation, and after only three drops were inhaled, "the pulse lost its jerking character and became gradually slower," but the face did not become flushed, and the pain was not relieved. In the course of a minute, " the pulse beat so slowly that I thought the heart would stop alto- gether ; while the patient raised himself on his elbow, and with a pale face moved his head about, as if for breath. At the same time he seemed confused, and did not answer questions."1 Under brandy and free ventilation the pulse recovered its former character and frequency, and the patient fell asleep in half an hour. In another case, which proved on post- mortem examination to be one of an -mr- ism of the first part of the aorta, pressmg on the right ventricle and pulmonary artery, and with universal adhesion of the pericardium, besides a degree of com- pression of the left phrenic nerve by a diseased bronchial gland, the paroxysms of coughing, which were among the most apparently dangerous symptoms in the case, were greatly aggravated on one occasion by the inhalation of five drops of amyl-nitrite, and a critical state of apncea was induced. It is obvious that neither of these cases was one of typical angina, and it is quite possible that the phenomena may have been only accidentally con- nected with the inhalation; but Sander has recorded two cases, and Samelsohn one case,2 in which alarming symptoms of collapse followed closely on the inhalation of amyl-nitrite. In the latter case there was not even a suspicion of internal dis- ease, the inhalation being done experi- mentally, with a view to test its effects upon spasmodic closure of the eyelids in an anjemic young woman. The usual flushing occurred, but was in an instant "replaced by a deadly pallor; the pulse became thread-like and slow, the skin cold and clammy, respiration difficult, and gasping ; consciousness was retained. " These symptoms recurred again and again at intervals for an hour, and even up to next day the patient complained of feeling very cold. It is stated that she was men- struating at the time, and that on subse- quent occasions she inhaled the nitrite without any such alarming incidents. It is quite possible that the eflects of fright, or agitation, or some other accidental dis- turbing cause, may in these cases have complicated the action of the amyl-nitrite; but still they form a warning, not only that dangerous results may in certain circumstances follow its inhalation, but that the theory which regards its action as purely vaso-motor, and still more that which considers the vaso-motor nervous centres, and the brain and spinal cord generally, as not within the range of its direct influence, must be held in the mean time as subject to reservations to be afterwards ascertained by experience. Generally speaking, the administration of nitrite of amyl in angina has been found to be free from danger, when used in doses of from two or three up to ten minims on a cloth or handkerchief, abun- dant access of air being allowed at the same time. The first effects of the remedy in healthy persons are, as stated above, increased frequency of the cardiac pulsa- tions, with a feeling of palpitation, and throbbing of the carotids, followed in the course of thirty to forty seconds after the commencement of the inhalation by Hush- ing of the face, warmth of the head, face, and neck, with perspiration ; the latter symptoms being often general. Breath- lessness and disposition to cough, giddi- ness, headache, slight indistinctness of vision, lassitude, and a feeling of intoxi- cation, are among the variable after- effects. The actual thermometric tem- perature of the body does not appear to be much, if at all, affected ; and conscious- ness is always preserved.1 When given in angina the effects are similar, with the 1 Compare Goodhart, Practitioner, vol. vi. 1871, p. 12; and Talfourd Jones, ibid. vol. viii. 1872, p. 213. Dr. Wood (Amer. Journal of the Med. Sciences, new series, vol. Ixi. 1871, p. 422) found that by poisonous doses in animals temperature was lowered "to a degree which is almost unheard of in the his- tory of drugs." He also found that this sub- stance has "the curious chemical property of checking oxidation." It prevents the change of venous into arterial blood, produces gradual paresis, depresses the action of the heart, and yet fails to affect consciousness and sensibility almost to the very last. Some of these re- sults appear to require confirmation. 1 Edin. Med. Journal, July, 1870, p. 46. 2 London Medical Record, March 17, 1875, p. 168 ; and Aug. 16, 1875, p. 479. 702 ANGINA PECTORIS AND SUDDEN DEATH. exception of the discrepancy formerly al- luded to as regards the cardiac pulsations. The flushing of the face must be fully de- veloped, in severe attacks of angina, be- fore any relief is to be obtained ; but in minor attacks the pain and sense of con- striction give way before a very few drops; almost immediately on the first inhala- tions, or even after merely applying a bottle containing a little of the remedy to one nostril. Three to five drops on a small piece of lint, or on a handkerchief, may be said to be an ordinary, or experi- mental dose, as a commencement. When the patient has become thoroughly fa- miliar with the effects of the remedy he may, if intelligent and conscientious, be entrusted with a quantity suflicient for ordinary use at his own discretion. One patient mentioned by Dr. Jones' had used about thirty ounces in six months; but the large quantity was accounted for by his belief that the remedy when kept in the pocket in a small stoppered bottle, became "flat," and required to be re- newed. Dr. Jones believes that he was right in this impression. This patient discarded the lint, and always inhaled directly from the bottle, which he always carried about with him, containing about half a teaspoonful of the remedy. "One night his father found him sound asleep, with his hand hanging over the bed, and the bottle held firmly in its grasp." He declared that "he would not be without ' his bottle of drops ' for a hundred pounds." This was a most remarkable case of relief, in what seems to have been aortic regurgitation, in a man of twenty- one years of age. It shows, however, that this remedy, like all others of the same class, is liable to abuse. The remaining remedies of the angina- paroxysm are probably of small account in comparison with those already men- tioned ; but it is desirable to add a few words with respect to some of them. Notwithstanding the opinion of Heber- den, blood-letting has been recommended, and in some cases, perhaps, successfully practised ; the cases being probably those in which evident signs of cardiac venous congestion existed, In Dr. Brunton's case small blood-letting, of a few ounces only, appeared to give relief. Dry cup- ping between the shoulders is a more rea- sonable, or, at all events, less spoliative method of unloading the heart, and might in some cases co-operate advantageously with the use of warm stimulation of the surface as above recommended. Laennec first suggested the transmission of a mag- netic current through the chest; but this suggestion may be said to have had no practical result, and the first apparently effective use of electrical or galvanic cur- rents in angina pectoris is due to Du- chenne, of Boulogne,1 who professes not only to have relieved, but to have cured a typical case of severe angina of five months' duration, in a currier, aged fifty, " of a stout build and sanguine tempera- ment, rather fat, and with a short neck," by treatment for a fortnight only with a strong faradic current passed through the skin of the nipple and upper region of the sternum. The description of the case is extremely striking, but its phenomena being purely subjective, there is not any absolute guarantee for its being more than a severe case of intercostal neural- gia, in which the extremely violent action of the " induction-apparatus graduated to maximum intensity, and working with very rapid intermissions," produced the effect of a strong and sudden counter-irri- tation. On any other supposition, in- deed, the results are almost too wonder- ful for belief. The first shock produced excruciating pain, so that the patient uttered a loud shriek, and the current had to be arrested. This artificial pain, however, completely and immediately removed the angina pain, as well as the sensations of numbness and formication which accompanied it; and "the patient felt at once in his normal condition. " Suc- ceeding paroxysms were similarly ar- rested, and in a fortnight the patient was able to resume his employment. Another case, communicated by Aran to Duchenne, is especially cited by Trousseau (who re- cords both cases in great detail) as "giv- ing more value to the preceding consider- ations but this will probably not be the judgment of the reader of the preced- ing pages, when he learns that the subject of Aran's therapeutical experiment wras a woman of thirty-two, who had been ex- tremely hysterical, if not cataleptic, from intense grief, and had been for a long time a prey to a multitude of nervous dis- orders, the result of violently disturbing emotions.2 Eulenburg has employed the 1 De 1'electrisation localis6e et de son ap- plication & la pathologic et a la th^rapeutique. 3ieme edit. Paris, 1872, p. 808. See also note Sur 1'influence thSrapeutique de 1'excita- tion Slectro-cutanee dans l'angine de poitrine, Bulletin de Therapeutique, 1853; and com- pare note below. 2 It is, perhaps, worthy of remark, that the experience of twelve years after his first acquaintance with the facts of Duchenne's and Aran's cases had not enabled Trousseau to add anything of a more personal kind to his long citation from Duchenne's narrative, first published in 1853. See the 2d edition of Trousseau's "Clinique de 1'Hotel Dieu" (vol. ii. pp. 453-57), published in 1865, not long before his death. Duchenne himself, in the 3d edition of his well-known work (re- ferred to above) published in 1872, and called in the preface ' ' presque un nouveau livre, ' ' 1 The Practitioner, vol. viii. p. 219. ANGINA PECTORIS AND SUDDEN DEATH. 703 constant current, up to a strength repre- sented by thirty elements of Siemen's bat- tery, applying the positive pole with a large surface for contact to the sternum, and the negative to the lower cervical vertebrae ; the successes which he claims, however, are rather equivocal, and it may be inferred from the method of his reasoning that he only employed the remedy in cases regarded as of vaso-motor origin.1 I am not aware of any case in which angina pectoris of obviously organic origin has been, even temporarily, re- lieved by any form of electrical or galvanic application ; but possibly further trials may still be desirable. Digitalis, aconite, and veratrum, have all proved either use- less or injurious. The treatment of the inter-paroxysmal state in angina pectoris depends essentially on the careful application to the individ- ual case of all the practical suggestions arising from a very complete diagnosis, and from a consideration of the causes which have been observed or supposed to be chiefly at work in predisposing to, or in actually bringing on, the paroxysms. Generally speaking, tranquillity, both of body and mind ; especially the suspension of all occupations, or even amusements, that tend to overstrain the heart, or hurry the breathing ; very moderate daily exer- cise on level ground, and only to such an extent as is requisite for preserving the bodily tone, or for good digestion; the avoidance of all manner of food tending to flatulence, and the regular, but strictly moderate evacuation of the bowels, either spontaneously or by the mildest laxatives, are measures of hygiene so obviously sug- gested by simple prudence as hardly to require more than a passing allusion. It is not by any means certainly ascertained whether the subjects of angina ought to use alcoholic stimulants in any measure habitually^ or to reserve them for the criti- cal period of the attack. I incline to the latter opinion. Venereal excitement is probably in all cases an unfavorable influ- ence. The use of tobacco in great excess has been specially investigated as a cause of angina by M. Beau ;* but although I have frequently observed palpitation and intermission of the heart's action in smokers, it has not occurred to me to ob- serve true angina pectoris thus produced. It will be obviously right, however, to discountenance any indulgence of this kind which is even doubtful as to its ef- fects upon the heart's action. Beyond these simple measures of precaution, the treatment must vary according to the cir- cumstances observed in each case, and it may even be said that there are cases in which no clear indication exists for any treatment beyond that of the paroxysm. But if it be discovered that gout, or con- gestion of the liver or lungs, or well-marked dyspeptic symptoms, or renal derange- ment, has concurred with, or alternated with, the paroxysms, or even that any of these disorders has been a marked feature of the case, without any obvious relation to the angina, it may be found that in undertaking the treatment of these appa- rently intercurrent disorders the cure or alleviation of the paroxysms may follow in due course. It is said, indeed, by some that gouty angina is peculiarly amenable to treatment, and therefore less formida- ble in its prognosis than other kinds ; and although this is probably only an imper- fect statement of the fact that cures of angina-like symptoms are sometimes ob- tained by remedies in the gouty habit,2 yet as a practical question of duty there can be no doubt that we are bound to treat the constitutional disease, as the best means known of influencing the lo- cal symptoms. It will therefore be expe- dient to use all possible means for eradi- cating, or at least diminishing, the gouty predisposition, in cases of angina so char- acterized, by careful regulation of the diet and the use of anti-arthritic remedies, such as the carbonates of potash and lithia, or even in some cases small doses of colchicum ; though it is very doubtful how far a well-marked attack of gout in the foot ought to be checked, either by colchicum or any other' disturbing remedy, in those who have had angina and other internal manifestations of the disease. _ A holiday at Carlsbad, Vichy, or Tbplitz, or, according to the fashion of last cen- gives only one new case, with scanty and unsatisfactory details, in which, moreover, after "partial amelioration" under the method of electro-cutaneous excitation previously de- scribed, the patient died suddenly when en- tering M. Duchenne's consulting-room. He refers, however, to a case of cure by M. Boul- let, and to " several cases of cure" communi- cated to the Academy of Sciences, in Febru- ary, 1869, by M. Ed. Becquerel. These last I have not been able to discover. M. Bec- querel simply reports M. Boullet's case with- out commentary, and with such brevity and want of essential details as to deprive it of all real clinical value. Evidently there is great inexactitude here, as well as a "plenti- ful lack" of trustworthy facts. 1 Med. Times and Gazette, May 7, 1870, to. 490. 1 De 1'influence du tabac a fumer sur la production de 1'angine de poitrine.-Gazette des Hopitaux, 1862. 2 On the other hand, a large proportion of the fatal cases of angina pectoris has been, as already shown, connected with gout, and between these two opposite sides of the ques- tion it is not easy to find a secure basis for the alleged relatively favorable prognosis of gouty angina. 704 ANGINA PECTORIS AND SUDDEN DEATH. tury, at Bath, may help to dispose of the remains of gout when its regular form threatens to pass into irregular manifes- tations. Fothergill and others have af- firmed the cure of angina pectoris in this way.1 If the urine shows persistently, or even frequently, a tendency to deposit lithic acid crystals, the treatment will, of course, be guided by this indication : and if acid dyspepsia is present, it will be necessary to use remedies at once ant- acid and tonic. If, on the other hand, the neuralgic element is highly pro- nounced, more especially if it is heredi- tary, or has been manifested in the indi- vidual patient in other forms, the angina pectoris being presumably a mere form of a more extended constitutional neurosis ; we may probably look in such cases for relief to nervine tonics, but especially to iron, strychnine, and arsenic. I have seen in one or two cases very decided good results from the last of these reme- dies, given in the form of the ordinary Fowler's solution, nt v. for a dose, two or three times a day over a considerable pe- riod ; and I can to this extent support the statements of Dr. Anstie, who in this country has chiefly advocated the use of arsenic in angina pectoris, and who refers to a case published by Philipp,1 as having first strongly directed his attention to the subject. Anstie begins with three min- ims, and increases the dose gradually, if well tolerated, up to eight or ten minims three times a day; he has found, how- ever, that some neurotic patients cannot tolerate arsenic from the irritability of their alimentary canal, and in such cases it must be discontinued, or perhaps some other form of administration might be devised. Anstie gives several striking cases, in one of which, at least, there had been a few slight attacks of gout, and a few small calculi; another was that of a woman, aged forty-six, who was still men- struating, though irregularly, and who certainly seems to have had extremely severe symptoms of the order of angina; she was cured by a six months' course of arsenic in doses gradually mounting to 21 minims daily; after eight weeks the pa- tient abandoned the remedy, supposing herself cured, but had to recur to it from experiencing a renewal of her sufferings, which again yielded to a precisely similar treatment.2 Arsenic is specially adapted for anaemic cases, and often exercises a favorable influence over the function of haematosis; but in cases where anaemia is well-marked it may be combined with iron, or the latter may be given with strychnine (ten minims of the sesquichlo- ride tincture with gr. strychnine three times a day). Phosphorus has lately been recommended by Dr. Broadbent, in doses of from fi'5 to ?'o gr. twice daily, but has not as yet been adequately tested. Zinc, silver, and most of the older reme- dies of this class, have been, on the whole, found wanting in true angina pectoris, though sometimes useful in pseudo-angina. A remarkable experience was that of Bre- tonneau (detailed by Trousseau),3 who, following out a very crude chemical theory of the calculous origin of angina, professed nevertheless to have stumbled upon the practical result of treating cases of angina successfully by large doses of bicarbonate of soda, combined in certain cases with belladonna. The directions given are very complicated, but the essential part of the treatment seems to be as follows : The alkaline treatment is begun with two * The case here specially referred to was mentioned by Fothergill in 1773, incidentally, in a paper on angina pectoris, as "the first case apparently of this nature that occurred to me, above twenty years ago." He adds, " the person is now, or lately was, living, and in good health . . . He was at that time about thirty years of age, and the young- est subject I have ever seen affected with this disorder." The symptoms are fairly de- scribed, considering the early date, and long interval between their occurrence and the publication, but can scarcely be looked upon as thoroughly characteristic. He "went to Bath several successive seasons, and acquired his usual health. This is the only instance that has occurred tome," writes Fothergill, "of a perfect recovery from this obscure, and too often fatal malady." We have seen that Heberden's experience also yielded only one case of apparently perfect recovery. In one other case, with distinct gouty complications, Fothergill prescribed Bath waters, with good results as regards the gout, but with no favorable effect on the angina. In another case the Buxton water appeared to be of tem- porary service. Fothergill seems to have been strongly impressed with the necessity of reducing exuberant fatty deposition in an- gina pectoris, and for this purpose recom- mended vegetable diet; though he did not anticipate in any respect later observations as to the connection of sudden death with fatty degeneration of the fibre of the heart itself. See Medical Observations and In- quiries, vol. v., 1776, p. 223, "Case of an Angina Pectoris, with Remarks and p. 252 of " Farther Account of the Angina Pectoris, by J. Fothergill, M.D., F.R.S." 1 Berliner Klin. Wochenschrift, 1865. See, however, Cahen (ut supra) Archives GenSrales, 1863 ; and a much older case by Alexander, of Halifax, 1790 (History of a case of Angina Pectoris cured by the Solutio arsenici), Medi- cal Commentaries, vol. xv. p. 373. This last case has, apparently, had very little effect on English practice, but is referred to by Des- granges, Trousseau, and other continental authorities. 2 Anstie, op. cit. Compare pp. 78, 182-84, 226-27. 3 Op. cit., Eng. transl., vol. i. p. 610. ANGINA PECTORIS AND SUDDEN DEATH. 705 scruples of the bicarbonate of soda, daily, in divided doses, rising gradually to eight or ten scruples, increasing and diminish- ing the dose alternately over intervals of ten days, and then suspending the treat- ment for fifteen or twenty days together; these various processes are repeated up to the end of a year or more, after which a pause of several months is allowed. At all stages of this lengthened treatment, belladonna may be given in gradually in- creasing doses, up to the point of relief to the spasms, or until symptoms of incipient poisoning occur, viz., "unpleasant dry- ness of the mouth, marked disturbance of vision, accompanied by a very striking dilatation of the pupils." Notwithstand- ing the great therapeutic reputation of Bretonneau, I have not been able to learn that any one else in France has personally succeeded with this treatment, and even M. Trousseau, his most distinguished pu- pil and follower, does not profess to do more than record his master's opinions. The facts as stated may therefore proba- bly remain among the curiosities of medi- cal experience; but as they have been generally referred to, it is necessary to make brief allusion to them here. In cases of angina connected with posi- tive organic disease, the treatment must follow the lines of that of the cardiac or vascular lesion which is discovered to be the cause of the symptoms. It is very doubtful,, however, whether in cases of fatty heart, or of calcareous and other degenerations of the vessels, there is any positive special treatment which can be recommended with confidence. In cases of aneurism, on the other hand, the iodide of potassium, in large doses of 20 to 30 grains and upwards, will be found of great value in checking all the painful sensa- tions, and even, in some cases, arresting or suspending the disease ; and the bro- mide of potassium, or of ammonium, may be given in some cases along with the iodide, as a palliative. A late American writer* specially commends the bromide of ammonium, and gives two cases in which, in doses of 15 to 20 grains, it seems to have averted the paroxysms. Note on the Literature of Angina Pec- toris.-The leading authorities have been mostly referred to in the preceding pages, and will be found quoted much more numerously and in chronological order in the two great French dictionaries men- tioned below,2 under the head " Anginc de poitrine." I have not in the text of this article referred to the letter of M. Rougnon to M. Lorry, in 1768,1 which has been set forth by M. Jaccoud and others as constituting a claim on the part of France to priority, or at least to a simultaneous discovery of angina pectoris with that of Heberden. From the ac- counts given of this letter, as I have been Practical Medicine, vol. iv.; the essay of Wichmann, Ueber angina pectoris und poly- pus cordis (Ideen zur Diagnostic, vol. ii. 1801); Brera (Della stenocardia; saggio pato- logicoclinico, Modena, 1810); Desportes (Traits de 1'angine de poitrine, Paris, 1811); Zechi- nelli (Sull' angina del petto e sulle morte repentine, Padova, 1814) ; Jurine (M&noir® sur 1'angine de poitrine, Paris et Geneve, 1815) ; Lartigue (De 1'angine de poitrine, Paris, 1846) ; Lussana (Intorno all' angina pectoris, Gazetta Medica Lombarda, 1858-59), besides the great and well-known works of Senac, Corvisart, Laennec, Testa, Kreysig, Bouillaud, Hope, Latham, Stokes, Walshe, Friedreich (in Virchow's Handbuch), Bam- berger, and others on Diseases of the Heart, the most recent being that of Dr. Hayden, Dublin (1875), which reached me after the first part of this article was written, but to which I have been indebted for several sug- gestions in the latter part of it, and some valuable references. The works of Romberg and Eulenburg, on Diseases of the Nerves, should also be consulted ; and the articles in all the older systematic treatises and diction- aries, whether British or continental. With the exception of Rougnon, all the authorities quoted in any of these sources up to 1778 are English. In that year Elsner published at Konigsberg a monograph, entitled, "Abhand- lung uber die Brustbraune," which was fol- lowed in 1782 by Gruner (Spicilegium ad an- ginse pectoris . . . ), and Schaffer (Dis- sertatio de angina pectoris, 1787). Several articles or treatises soon followed in Germany, Denmark, and Holland; but I do not know if angina pectoris is even mentioned by name in French medical literature prior to the pa- per of Baumes in 1808, " Recherches sur cette maladie a laquelle on a donne les noms d'an- gine de poitrine et de syncope angineuse" (Annales de la Soci£t6 de Medecine pratique de Montpellier, 1808). The first Italian monograph was that of Brera in 1810, cited above. After this, the literature becomes much more copious ; but the well-known ar- ticle of Dr. Forbes, in the first volume of the Cyclopaedia of Practical Medicine, 1833, will always remain, especially for the English reader, the chief source of exact information down to a comparatively recent date. 1 Lettre a M. Lorry touchant les causes de la mort de M. Charles, ancien capitaine de cavalerie, arrivSe a Besan?on le 23 fevrier, 1768 (Besamjon, 1768, 8vo.) Rougnon de- scribed the paroxysms of pain, and ascribed these and the sudden death to ossification of the costal cartilages. He did not give any name to the disease, or indicate otherwise its pathological and clinical relations. 1 Dr. Rufus K. Hinton, Philadelphia Medi- cal and Surgical Reporter, March 6, 1875. 2 Nouveau Dictionnaire De Medecine et de Chirurgie pratiques, tome 2ieme. 1865, p. 509 (Art. by Jaccoud). Dictionnaire Ency- clop^dique des Sciences Medicates, tome 5ieme. 1866, p. 65 (Art. by Parrot). Consult also the Bibliography in Forbes, Cyclopaedia of VOL. IL-45 706 DISEASES OF THE VALVES OF THE HEART. able to read them, it is manifest that M. Rougnon is in no just sense of the words a rival or competitor of Heberden ; he is, however, probably entitled to the credit of having independently described a single case of sudden death, with symp- toms more or less resembling Heberden's angina, as we have seen that Morgagni had done a century before. Without in the least degree desiring to detract from what is due on this account to Rougnon, it must be here pointed out that Heber- den's position is entirely different. In- stead of describing only one case, and reasoning inaccurately as to its pathology, Heberden founded a minute and exact clinical description upon the observation of not less than twenty cases, of which, he informs us, six had been known to him as having perished suddenly. Heberden's account of the " Disorder of the Breast," accordingly, soon became known to medi- cal men in various countries as an accu- rate and comprehensive sketch of a new disease, while Rougnon's case passed into oblivion, without even in France exciting the attention that was perhaps due to it as an isolated observation. The claim advanced on behalf of Rougnon is evi- dently an after-thought, and cannot now be admitted. If sudden death from an- gina is to be recognized in any sense at all as a discovery on the strength of an individual case, the credit undoubtedly belongs to Morgagni rather than to Roug- non. It is right, however, to add that I make these remarks without having per- sonally read Rougnon's letter, which I have inquired for in vain in the medical libraries of this country. DISEASES OF THE VALVES OF THE HEART. C. Hilton Fagge, M.D., F.R.C.P. The literature of diseases of the valves of the heart, as of all other thoracic dis- eases, is necessarily divided into two periods ; that before, and that after, the discovery of auscultation. The earlier period, however, contains very few obser- vations. Burns' quotes two cases of aortic obstruction, briefly related by Riverius and Willis respectively, towards the end of the seventeenth century. Dr. Gee2 points out that Vieussens in 1715 recorded a case of disease of the aortic valves, in which the pulse was "fort vite, dur, inegal, et si fort que Vartere de Vun et de V autre bras frappait le bout de mes doigts autant que Vauroit fait un corde fort tendue et violem- pnent ^branlee.'''' Friedreich3 is therefore not quite accu- rate in heading his list of papers and works on affections of the endocardium with Meckel's essay in the Mem. de l'Acad. Roy. des Sciences, published in Berlin in 1756. But it is in the second half of the eighteenth century that we find the first detailed observations of diseased cardiac valves. Arnone the most striking of these is one recorded by John Hunter, in his "Treatise on the Blood, &c.," which originally appeared in 1794. It is that of a Mr. Bulstrope,' who had "almost throughout his life had an irregular pulse and upon the least increase of exercise a palpitation at his heart, which was often so strong as to be heard by those who were near him . . . He of late years (about the age of thirty), took to violent exercise such as hunting; and often in the chase he would be taken ill with pal- pitations and almost a total suffocation. Some of these fits continued several days : at such times he became black in the face. Sometimes an universal yellowness took place ; and then he could not lie down in his bed, but was obliged to sit up for breath. He consulted Dr. Heberden and Sir George Baker ; the palpitation I sup- pose they thought either arose from spasm or was nervous, for they ordered cordials. I was sent for on the same day to give a name to the disease. My opinion was that there was something very wrong 1 "Observations on some of the most fre- quent and important Diseases of the Heart." Edinburgh, 1809, pp. 175, 176. 2 "Auscultation and Percussion," 1870, p. 260. 3 " Krankheiten des Herzens," Virchow's Handbuch der speciellen Pathologie und The- rapie, 1867, p. 198. 1 The preparation from this case is still in the Hunterian Museum of the Royal College of Surgeons, which also contains several other specimens of diseased cardiac valves, pre- served hy Hunter himself. The passages cited in the text are from the ' ' Catalogue of Path. Specimens," vol. iii. p. 197. DESCRIPTION AND ANATOMY. 707 about the heart, that the blood did not flow freely through the lungs. . . . That the means to be practised were rest, bleed gently, eat moderately, keep the body open and the mind easy. . . . Eight ounces of blood were taken from him that day, which relieved him. . . . At last he became yellow, and his legs began to swell with water . . . and he died. The heart was very large . . . the valves of the aorta shrivelled up, thicker and harder than common. The diseased structure of the valves accounts for every one of what may be called his original symptoms ; the blood must have flowed back into the cavity of the ventricle again at every systole of the artery. . . . We can easily trace the effects of this ret- rograde motion, which would only be a stagnation of the blood beyond the left ventricle, first in the left auricle, then the pulmonary veins, then the pulmonary arteries, next the right auricle, and in all the veins of the body ; producing that darkness in the face, <fcc." Even earlier than this, Senac, in his Treatise on the Heart (the second edition of which ap- peared in 1783) had related a case in which the auriculo-ventricular valves were ossi- fied, and remarked that the pulse was necessarily small, because the blood did not all pass into the aorta, but some of it flowed back into the auricle. Soon after the commencement of the present century, three works on diseases of the heart were published, in which valvular affections are treated of with considerable detail: that of Corvisart,1 in 1806 ; that of Allan Burns,2 in 1809; and that of Kreysig,3 in The study of these works is of consider- able interest. Corvisart gives an admira- ble account of the anatomical appearances exhibited by diseased valves, which he distinguishes as undergoing calcareous or osseous induration, or as presenting excrescences (vegetations).4 It is remark- able, however, that he seems to have had no conception of these diseases as causing regurgitation, or imperfect closure of the valves.1 The tendency of valvular affec- tions to cause dilatation of the heart (or, as he terms it, "aneurism of the heart") was well known to Corvisart. By Burns and Kreysig considerable advances were made. Both these writers recognize val- vular lesions as producing two distinct effects, "obstruction" and "regurgita- tion," and trace many of the consequences of the latter condition. Kreysig lays special stress on inflammation of the en- docardium as causing the lesions in ques- tion. Burns may even be said to hint at the occurrence of cardiac murmurs, for he speaks of regurgitation from the ventricle into the auricle as producing not only a jarring sensation but also " a hissing noise, as of several currents meeting. In all probability" (he goes on to say) "it is something of this kind which is described as audible palpitation in some diseases of the heart." The history of the subsequent literature of valvular affections is involved in that of the auscultatory phenomena which they produce; and hereafter, when these are under consideration, I must endeavor to deal with the most important parts of it. Description- and Anatomy.-The pathological changes met with in the valves of the heart are naturally divisible into two groups; 1. Those which are acute: 2. Those which are chronic. 1. The acute affections are of an inflam- matory nature, and come under the gen- eral head of endocarditis. Indeed, it has long been known that the membrane forming the valves is more liable to in- flammation than any other part of the endocardium. And, as we shall presently see, recent observations have shown that this is true in a more absolute sense than had been imagined: and that when in- flammation of the linings of the heart's 1 "Essai sur les Maladies et les lesions or- ganiques du Coeur et des Gros Vaisseaux." So far as diseases of the heart are concerned, however, this writer (who will always be re- membered as having popularized Avenbrug- ger's discovery of percussion) is better known by his second edition, which appeared in 1811, and was translated into English by Mr. Hebb in 1813. 2 Op. cit. 3 "Die Krankheiten des Herzens." Ber- lin. 4 The word "vegetation" is now commonly used in this country, but it may be interest- ing to note that Mr. Hebb, the translator of Corvisart, never employs it as an English term, but always incloses it between brack- ets, and uses "wart" or "excrescence" as its equivalent. 1 This must be borne in mind in estimating the claims of different writers to priority in regard to the discovery of the presystolic thrill and bruit. Corvisart first mentioned the sign afterwards known as fr^missement cataire. He speaks of it as " a particular rustling, difficult to describe, perceptible to the hand when it is placed over the praecor- dial region, and which doubtless proceeds from the difficulty which the blood experi- ences in passing through an aperture no longer proportionate to the amount of fluid to which it has to give vent." It might thus appear that Corvisart associated thrill with mitral stenosis. But it must be recollected that he summed up the effects of all valvular diseases in the contractions of the correspond- ing orifices which he supposed them to cause. He had no conception that the presence of thrill was of any value as regards a differen- tial diagnosis of valvular affections. 708 DISEASES OF THE VALVES OF THE HEART. cavities is met with, it has almost always been set up by a similar affection of one of the valves. The microscopical anatomy of inflam- mation of the valves may, therefore, be dismissed in a very few words, as being the same as that of endocarditis in gen- eral. The minute bloodvessels, which recent observers have shown to exist in the valves, become gorged with blood, and the cells of the external tunic of these vessels undergo proliferation.1 But this change is quite subordinate to that which occurs in the proper substance of the valve itself: in the connective tissue of which young cells are formed in large numbers, while the intercellular material becomes softened. The tissue is thus much swollen ; and as the change in ques- tion is not at first general, but is confined to certain spots, the result is the forma- tion of a number of small granulations, projecting from the surface of the valve. These granulations are very commonly limited, in the first instance, to a particu- lar region in each valve, namely, that which lies immediately behind the line of closure. Thus, in a cuspid or auriculo- ventricular valve, the earliest swelling is found on the auricular surface, and a lit- tle above the free edge; in the case of the semilunar valves, it is on the ventricular surface, and along the delicate curved line, limiting the apposition of the valves, that stretches on either side of the corpus Arantii. In these positions the granula- tions are often pretty uniformly arranged, like a row of minute beads. The remem- brance of their scat may be facilitated by imagining the valves to have been coated on their apposed surfaces with a layer of some soft substance (such as butter), which during closure of the valves would be forced into precisely the positions that the granulations occupy. And according to the view formerly entertained, that the granulations were formed of an exudation of plastic lymph, it was easy (with Sir Thomas Watson2) to refer their arrange- ment to this cause. But, as we have seen, the microscope shows that they are swellings of the tissue of the valve itself, and this explanation is, therefore, un- tenable. The granulations vary in ap- pearance ; being sometimes colorless, sometimes red (the latter perhaps from imbibition). Their consistence is differ- ent in different cases: sometimes they are so soft as to be detached from the valve by the slightest touch ; sometimes they are so hard as to resist all attempts to remove them. They are much more often seen on the valves of the left, than on those of the right side of the heart: the former being in fact much more sub- ject to endocarditis than the latter. When acute endocarditis occurs as part of a rapidly fatal general disease, the presence of such a line of minute granu- lations is generally the only sign that in- flammation of the valves had existed: and if (as is often the case) the affection be confined to the auricular surface of the edge of the mitral valve, it may be en- tirely overlooked, unless attention be spe- cially directed to this spot. But in certain cases, the changes are far more considerable. The granulations are very much larger, and become con- fluent, so as to form masses, which fairly deserve the name of vegetations. These bodies, projecting into the stream of the blood, necessarily offer a favorable surface for the reception of coagula; and thus colorless fibrin of firm consistence is de- posited upon them, often in large quan- tity. This so closely resembles in appear- ance the swollen tissue of the valve itself, that it may be impossible to say where the one begins and the other ends. In- deed (as has already been mentioned) the older theorists (who thought that the valves, which wTere then supposed to be non-vascular, were incapable of inflam- mation) believed even the smallest granu- lations to have been thus deposited from the blood. When this opinion was shown to be incorrect, its opposite prevailed; and it is only after repeated and pro- longed discussions that pathologists have come to the conclusion that the larger masses have the double origin just attrib- uted to them. These, again, are often found to be still further increased in size by the deposition of dark red clots upon them, while the patient is in the act of dying, or during the post-mortem coagu- lation of the blood. These vegetations necessarily float to and fro with the valve to which they are attached, and thus they are almost always brought into contact with the surface of another valve opposed to them, or with some part of the endocardial lining of the heart's chambers. For it must be added that they are not always sessile, but are often suspended by a pedicle of some length, allowing them to swing backwards and forwards through a considerable range of movement. The result is that they frequently set up inflammation in the parts against which they rub. This fact was, I believe, first pointed out by Dr. Moxon, who, in 1868 and 1869, ex- hibited to the Pathological Society several illustrative specimens.1 My own obser- 1 Rindfleisch, "Lehrbuchderpathologischen Gewebelehre." Leipzig, 1871, p. 205. 2 "Prine, and Pract. of Physic," 4th edi- tion, vol. ii. p. 294. * Path. Trans, xix. p. 148, xx. p. 156. It will be shown further on that Dr. Hodgkin long ago described the effects of friction in the case of valves affected with chronic disease. DESCRIPTION AND ANATOMY. 709 vations have convinced me that his state- ments are perfectly correct. A vegetation hanging from an aortic valve is often thrown upon the wall of the aorta during the ventricular systole, and sets up there a little ulcer, penetrating into the middle coat, or even down to the adventitia: during the diastole the same vegetation is carried downwards, and touches the an- terior surface of the mitral valve, or the endocardial lining of the ventricle, and the spot touched is found, after death, to be precisely indicated by the presence of a little fresh mass of vegetations. The opposed surfaces of the aortic valves are often seen to be coated with vegetations, in such a way as to suggest that the one was affected secondarily to the other, although it may not be possible to say which was primarily diseased. Or, again, a button-like mass of vegetations project- ing from one aortic valve has been seen to bore a hole right through the substance of the valve opposed to it. A cluster of vegetations growing from the auricular surface of the mitral valve often sets up inflammation in the base of the opposed segment of the valve, where the vegeta- tions meet it during closure of the valve: and from this spot the inflammation spreads into the auricle.' Dr. Moxon has even expressed the opinion that vegeta- tions attached to the lining membrane of the heart's cavities are scarcely met with, except as the result of friction, in the way just described, the valves being first diseased. And I would add my belief that there are few cases of acute inflam- mation of the valves, in which secondary effects of this kind may not be traced. The rapid and extensive movements performed by these floating vegetations have probably much to do with the fre- quency with which portions of them be- come detached and carried with the blood-stream to distant parts, producing effects which we shall hereafter have to consider. But it must be added that they are also very liable to undergo a finely granular metamorphosis (according to Rindfleisch, not fatty), which renders them still softer than they originally were. In this softening process the inflamed tis- sue of the valve itself takes part; so that large portions of it often become disin- tegrated, and an ulcer is produced, which may destroy the whole thickness of the valve and perforate it. Such ulceration, for instance, may separate one or both edges of an aortic valve from attachment to the arterial wall; or eat away a large part of its substance. In the mitral valve, it is not uncommon for a hole to be pierced right through its substance. In this case, however, the edges of the aper- ture are always thick and raised, and covered with large vegetations; and these generally meet across it, so that there is no reason to suppose that by such a per- foration the physiological action of the valve is in any way impaired. Indeed, these vegetations are often so massive, that the existence of a perforation, and even of an ulcer, may escape notice unless it be specially looked for. The records of post-mortem examinations at Guy's Hos- pital contain only one notice of such a perforation in the course of six years; but I have little doubt that it had really occurred more often. It must be added that the ulceration not rarely extends from the valves themselves into the adja- cent parts of the muscular substance of the ventricle. The same process of softening and ul- ceration, occurring in the chord® tendineae of the cuspid valves, leads to their rup- ture. This is by no means infrequent; in six years I find it recorded sixteen times in the reports of post-mortem examina- tions just referred to. Clinically it would appear to be of far greater importance than perforation of the valve : I imagine that it must invariably render the valve incompetent. The changes which pre- cede rupture of the chordae would appear to consist in a swelling and thickening of their substance. Generally they give way in about the middle of their length ; but sometimes they are torn away from the musculus papillaris, which may then ex- hibit no trace of their original insertion into it. The left and the right chordae of the mitral valve appear to be equally lia- ble to rupture. Sometimes the laceration is confined to a single chorda ; sometimes it affects nearly all those that arise from one musculus papillaris. The ruptured chordae float to and fro with the stream of blood, which necessarily regurgitates freely into the auricle at each systole. Once I saw such a loose end tied neatly into a knot, which took some time to undo. In another instance three or four broken chordae were twisted up spirally into a body resembling an uvula, being matted together by a deposit of fibrin. In a third case, recorded by Dr. Moxon, the free extremities of two such chordae seemed to have become adherent to the surface of the mitral valve above, forming loops, beneath which a probe could be passed. Large masses of fibrin are whip- ped out from the blood, and deposited on the sides and extremities of ruptured chordae, and often unite them together, so that it is impossible to say how many of them may have been torn through, until the superjacent mass of coagulum is re- moved. 1 These statements are derived from the detailed reports of the post-mortem examina- tions at Guy's Hospital during the last few years, most of which were made by Dr. Moxon, but some by myself. 710 DISEASES OF THE VALVES OF THE HEART Another effect of this process of ulcera- tion, especially in the mitral valve, is the formation of a so-called "aneurism of the valve." An ulcer having formed on its ventricular surface, the base of this yields before the pressure of the blood, and a pouch is formed, projecting from the au- ricular face of the valve. Such an aneu- rism is generally very small: I lately saw one which was of about the size of a per- cussion cap ; it had on its summit a mass of small vegetations. This form of aneu- rism must be distinguished from that de- scribed by Dr. Thurnam,1 which arises in the gradual yielding of all the coats of the valve, and which may attain a much larger size. 2. In chronic diseases of the valves the appearances vary greatly, not only in in- dividual cases, but also according as one or another valve is affected. But they may generally be summed up as depend- ent on the growth of a firm connective tissue, which thickens the substance of the valve, and by its contraction leads to great alteration in its form, and more or less seriously impairs its functions. Cal- careous matter also is often deposited. This " sclerotic" change - if we may adopt the term sclerotic as equivalent to the chronische sclerosirende Endocarditis of German authors-may either be primarily chronic, or arise out of an acute inflam- mation of the valve. In the latter case, vegetations are sometimes found, showing that endocarditis had once occurred ; and these may even be calcified. But they met with in disease that has from the first been chronic. The difficulty of de- termining the way in which valvular changes arise is further increased by the fact that thickened valves are very liable indeed to the supervention of an acute process, identical with that already de- scribed as belonging to acute endocarditis. It would appear that the elements of the morbid tissue in chronically diseased valves are apt to undergo a fatty change, analogous to that which gives rise to atheroma in chronic arteritis. The result is that the structure of the valves becomes softened and gives way, and thus that a process of ulceration is set up, precisely as in acute endocarditis. A very large pro- portion of the cases in which the autopsy shows the chord® tendine® of the mitral valve to have been freshly ruptured are cases of long-standing valvular disease, in which inflammation has thus supervened. Another common result is that masses of calcareous deposit, evidently of old forma- tion, are found lying loose in the floor of recent ulcers. a. In the cuspid valves the effect of chronic disease is generally to produce a stenosis or narrowing of the aperture. The wall of the valve, especially towards its free edge, becomes greatly thickened, and its segments cohere together. The morbid tissue is exceedinglv dense and hard, so that by the older writers such valves were described as cartilaginous : it often contains masses of calcareous de- posit, and these sometimes attain a very considerable size. The chord® tendine® undergo a similar change and coalesce, so that sometimes each muscuhis papillaris gives origin only to a single massive col- umn, which may be more or less fluted, or pierced with one or two slits, indicating the lines of separation between the chord® of which it was made up ; at the same time the chord® generally become much shortened, so that the edge of the valve is drawn down ; and thus with its small aperture it has very much the appearance of a funnel, projecting far into the cavity of the ventricle. Dr. Douglas Powell,1 has endeavored to distinguish two forms of stenosis of the mitral orifice, in one of which the valve presents this funnel shape, while in the other it is stretched horizon- tally, like a diaphragm, between the auri- cle and the ventricle. But it appears to me that no such distinction can be fairly drawn, and that in all cases a narrowed mitral valve tends more or less to assume the form of a funnel, although this is no doubt much more marked in some in- stances than in others. The orifice at the bottom of the funnel is sometimes circu- lar : but in the case of the mitral valve it more often resembles a slit, of which the [Fig. 97. are not necessarily present. In several cases of valvular disease, that had, in each instance, doubtless arisen in attacks of acute rheumatism which the patient had had some years previously, I have, on post-mortem examination, found that the mitral valve exhibited no trace of vegetations: it was simply thickened, with its chordae ; and its orifice was nar- rowed. Here the affection had been of acute origin: but the appearances were undistinguishable from those which are Fibroid thickening of Mitral Valve.] 1 Med.-Chir. Trans., ser. ii. vol. iii. p. 250. 1 Med. Times and Gaz., 1871, vol. i. p. 395. DESCRIPTION AND ANATOMY. 711 axis corresponds with the line uniting the meeting angles of the original segments of the valve. The latter variety has long been known as the button-hole mitral. In either form the aperture may be so con- tracted as hardly to admit the tip of the little finger ; and cases are often met with in which only two fingers can be intro- duced, instead of the three which can be passed through the healthy valve. But the effect of chronic disease of the mitral valve is not always to produce stenosis. It may be the very reverse. It is said that sometimes one of the flaps of the valve becomes adherent to the ventri- cular wall, and so is rendered incapable of meeting its fellow. But this is a very rare occurrence ; indeed I doubt whether it is ever met with. At any rate I have not been able to find a single instance of it in the recent records of post-mortem examinations at Guy's Hospital. These records, however, contain one case in which Dr. Moxon found the edge of the anterior curtain of the valve turned up on its ventricular surface, and adherent there, so as to form a ridge on this sur- face,1-a change by which the depth of the curtain must of course have been diminished. It might be thought that the same process of contraction which ordi- narily causes stenosis of a thickened valve might (if acting in a direction at right angles to that in which it usually acts) draw up and shorten the valve without narrowing its orifice. Writers have in fact described such an appearance. But it is one which I have never myself seen, nor have I met with any recorded instance of it: and I am not sure that it ever oc- curs. Not uncommonly, however, some of the chordte tendinese become elongated, and do not properly tether the membran- ous part of the valve, which therefore be- comes inverted into the auricle during the ventricular systole; and this result is often favored by the conversion of the corresponding muscularis papillaris into a dense fibrous tissue. Sometimes those chordfe which are inserted nearest the centre of the valve alone undergo this process of lengthening, and this part of the curtain is then found after death to be bent on itself and flaccid, having evi- dently been accustomed to yield before the pressure of the blood. Sometimes, again, the chordse become shortened by disease, instead of being elongated, and thus tether the valve too closely, and pre- vent the apposition of its segments. I believe that the preceding paragraph includes descriptions of all the chronic changes in the cuspid valves, by which regurgitation is produced, without ob- struction to the onward current of blood. Each of these, however, is of infrequent occurrence. In six years, during which period sixty-seven cases of mitral steno- sis presented themselves in the post-mor- tem threatre of Guy's Hospital, I find only twelve recorded instances of what I may term pure regurgitant disease of the same valve ; in six of which the edge of the valve is stated to have been inverted into the auricle, in the manner above de- scribed. The fact just stated will doubtless sur- prise many readers, who are aware of the frequency with which mitral regurgitant disease is clinically spoken of. The ques- tion must be discussed in detail further on ; but it may be well here to state that, in a large proportion of cases, a reflux of blood into the auricle during the ventri- cular systole is probably independent of disease in the valve itself, and due to changes in the walls and cavity of the ventricle, destroying the due proportion between the auriculo-ventricular orifice and the valve by which it should be closed. It must be added that many cases are placed after death under the head of mitral stenosis, which had before been regarded as examples of regurgitant dis- ease. For when moderate obstruction and regurgitation coexist, the latter is often clinically more noticeable, and (as I believe) is often alone discoverable before death ; while at the autopsy the appear- ance of the valve may be exactly similar to that which is found in another case, in which during life obstruction had been the main feature. fl. In the semilunar valves the morbid appearances resulting from chronic disease vary much more than in the cuspid valves. First may be mentioned the adhesion of the valves together. This begins at the point where the corners of adjacent valves are inserted into the aortic wall, and gradually creeps along their free edges, uniting them together. All three valves may thus be fused into a single mass, projecting into the arterial channel in the form of an inverted funnel, with a central aperture, which is often of very irregular form, and may be extremely small, being, in most cases, further narrowed by the presence of rough calcareous nodules of greater or less size, deposited in the sub- stance of the altered valves. While this process is going on, the natural attach- ment of the corners of the valves to the aorta often gradually becomes oblite- rated ; two of the pouches, or even all three of them, become thrown into one ; and three slight projections in the floor of the resulting funnel-shaped mass are often 1 This condition is analogous to one which is commonly seen in cases of perihepatitis, where the anterior thin edge of the liver is neatly folded over on to the convex surface, and bound down beneath the thickened cap- sule, the apparent rounded margin of the liver being thus really derived from the un- der surface of the organ. 712 DISEASES OF THE VALVES OF THE HEART. all that is left to indicate the original lines of separation between the different valves. In other cases the effect of chronic dis- ease of the semilunar valves is, that they become puckered and shrivelled. Instead of forming pouches, they often rather resemble flat, narrow shelves, projecting a little way from the wall of the artery, the mouth of which they are quite unable to close. The corpus Arantii, with the thin curved borders on either side of it, disappears entirely ; and all that is left is a thick, shapeless body, often with its rounded edge retroverted, and perhaps torn away from its aortic attachment on one side, so as to hang down like the lip of a jug, or a dog's ear. Or, again, the valve may contract, and its free border thus become tightly drawn across be- tween its points of attachment, so that the open pouch is converted into a deep pocket with a narrow' entrance, into which the tip of the finger cannot be made to enter. This result, however, is not always due to changes in the valves them- selves. Sometimes it depends on chronic disease in the coats of the base of the aorta, attended with yielding and dilata- tion of its walls, by which the valves, although healthy, are unduly stretched. So considerable may this yielding be, that in one case recorded in the reports of post-mortem examinations at Guy's Hos- pital, the corners of adjacent valves had become distant from one another a quar- ter of an inch at their points of attach- ment. When a valve, thickened, or retro- verted by chronic disease, comes into con- tact with any part of the lining of one of the heart's cavities during the movements of that organ, further morbid changes are produced by the friction, as is the case in acute affections. There is, however, this difference, that the endocardium does not become ulcerated or covered with vegeta- tions, but is thickened, opaque, and slightly roughened. This was pointed out by Dr. Hodgkin as far back as the year 1829.1 In the case of Dr. Cox, one of aortic disease, in which a valve was stretched to upwards of an inch in length, " the coats of the aorta for about an inch and a half above the retroverted and dis- tended valve, and against which it must have been carried during the systole of the heart, were considerably thickened, and presented an uneven surface. On the inner surface of the heart there were some irregular spots of opacity at the part where the diseased valve would have struck during the diastole." Dr. Hodgkin adds that "the partial thickening on the inter- nal surface of the heart and vessels, in consequence of some unusual contact, is a morbid appearance, which has not been particularly pointed out by pathological anatomists, yet it does not appear to be a rare occurrence. " Except Dr. Moxon, I do not find that any writer has since alluded to the appearance in question. But in another respect our knowledge has ad- vanced greatly since the publication of Dr. Hodgkin's paper ; for we find him relying on these effects of contact as prov- ing that the blood had been subjected to two motions-the one progressive, and the other retrograde-a fact with which, of course, every one is now familiar. Ac- cording to Dr. Peacock and Dr. Bristowe,' it is not uncommon in cases of disease of the aortic orifice for the endocardium below the valves to present a fibroid thickening in the form of bands or reticu- lations, due probably to the impact of the regurgitant stream of blood on that part. Of this I have lately seen a striking in- stance. The same thing may also occur in the auricle, as the result of mitral re- gurgitation. [Fig. 98. Calcareous Degeneration of Aortic Valves.] It will be observed that in the semi- Innar, as in the cuspid, valves the effects of chronic disease are twofold. It may either cause obstruction to the onward flow of blood, or give rise to regurgitation and to a backward current. All writers, in fact, insist on this distinction, while admitting that both effects often exist together. Dr. Moxon, therefore, rather surprised me a short time ago by stating that in his experience the occurrence of aortic obstruction, apart from regurgita- tion, has been extremely rare. I at first supposed that he was referring to fatal cases only, among which pure aortic ste- nosis would naturally be infrequent, since this is generally said to affect the prospect of life less than any other form of valvular affection, and since, moreover, it is very apt to become complicated sooner or later by the development of regurgitation. 1 "On Retroversion of the Valves of the Aorta," Lond. Med. Gaz. vol. iii. p. 439. 1 Path. Trans, xxi. p. 105. ETIOLOGY 713 Thus, in looking through the records of post-mortem examinations for the last six years-during which time there have oc- curred sixty-eight fatal cases of aortic regurgitant disease-I find only two, or perhaps three, of pure aortic stenosis; and in at least one of them the patient's death was due not to this affection, but to coexisting mitral stenosis. But I after- wards ascertained that Dr. Moxon be- lieved aortic obstruction, independent of regurgitation, to be rare clinically, as well as in the dead-house ; and this opinion certainly appears to be confirmed by the fact that, during part of the period in which I acted as Medical Registrar at Guy's Hospital (within which period seventy-one cases of aortic regurgitation came under observation) I find only two recorded instances of pure stenosis of the orifice in question ; and in one of these regurgitation became developed before the patient's death. The changes to which the aortic valves are liable are not all included in the thick- enings, and adhesions, and puckerings that have hitherto been described. In some cases the tissue of the valves under- goes atrophy ; and they become so thin, that it is difficult to believe that they were capable of sustaining a column of blood. A striking example of this came lately under my notice. A young man, set. thirty-two, had long suffered from asthma, and becoming anasarcous was admitted into Guy's Hospital under the care of Dr. Wilks. After death the aortic valves were found to be most remarkably thinned; they had no more substance than the most delicate tissue-paper, and no corpora Arantii could be felt in them. One of them was slightly fenestrated near its margin. They were very small, and, when left to themselves, fell back into the Sinuses of Valsalva. The pulmonary valves presented the same change in a minor degree; and the mitral valve was likewise unusually thin. The heart was much enlarged. The lungs were emphy- sematous ; and it appeared to me that the thinning of the heart's valves was due to a process of atrophy, perhaps related pathologically to that which caused the pulmonary emphysema. I have since found, in the records of post-mortem ex- aminations at Guy's Hospital, a similar case, observed by Dr. Moxon. It is that of a man, aged fifty-six, whose lungs are stated to have been senile and a little emphysematous, and to have contained much black matter. The heart was small; the right side was dilated, forming the apex; the pericardium was every- where adherent; the mitral and aortic valves were very delicate in appearance.! This atrophy of the aortic valves is proba- bly rare, and has not yet been shown to have any clinical significance. But there would certainly appear to be danger of the rupture of such thin structures, when strained in an efibrt of coughing or in any other way. I have still to mention another abnor- mal appearance in the aortic valves, formerly supposed (by Corrigan) to ren- der them incompetent, but now known to interfere in no way with their functions. I refer to the small openings which are sometimes found in the thin, crescent- shaped borders which extend on either side of the corpora Arantii. By some writers analogies have been found for such a fenestrated condition of the aortic valves in the normal state of the same valves in some of the lower animals; while others have regarded it as exhibit- ing an identity of structure between the semilunar and the cuspid valves; the filaments which remain above the aper- tures being supposed to answer to the chordae of a mitral or tricuspid segment. It has also been doubted whether this fenestration of the aortic valves is the result of a slow atrophic change, or whether it is simply a defect of original development. And with reference to this point Dr. Wilks1 states that he has seen it in young people, and has therefore al- ways regarded it as congenital. Etiology.-Before passing to the con- sideration of the other causes of disease of the cardiac valves, it may be conveni- ent to discuss the views of certain writers, who have attributed to congenital mal- formation (or to intra-uterine disease) some affections that, as it appears to me, may arise at any period of life. These views are of considerable antiquity. In his account of Mr. Bulstrode's case, already referred to, John Hunter ex- presses a doubt whether the shrivelled appearance of the valves of the aorta was "a natural formation, or a disease." And of another specimen, in which there were two valves only instead of three, one of which had a kind of fraenum or cross-bar attaching its middle to the side of the artery,-the catalogue of the Hun- terian Museum says, " this malformation was in all probability congenital. " Early in the present century, Mr. Burns de- scribed as a " species of mal-conformation of the heart," that condition in which the mitral valve, instead of being formed of two flaps, presents the appearance of a septum, with an aperture in its centre, stretching across the opening. More re- treme thinning of the aortic valves, in another patient, who died of the effects of pulmonary emphysema. 1 Pathological Anatomy, p. 93. 1 Since this was written I have (in Novem- ber, 1874) met with a third instance of ex- 714 DISEASES OF THE VALVES OF THE HEART. ccntly several observers have expressed similar opinions. Dr. Conway Evans,1 in recording a case in which the mitral valve was funnel-shaped, says this condi- tion was "evidently of congenital origin." Dr. Kelly has recently maintained the same view.2 And Dr. Peacock devoted to this question a part of his first Croonian Lecture, delivered before the Royal Col- lege of Physicians in 1865. The arguments for and against the opinion that certain affections of the val- ves are congenital require to be taken separately for the different valves. And, first, with regard to the mitral valve. Great stress has been laid on the fact that mitral stenosis is very frequently associated with tricuspid stenosis. It is generally said that all the valves on the right side of the heart, which are so rarely subject to disease in after life, are much more liable to intra-uterine disease and to malformation than the valves on the left side. And congenital union of the pul- monary valves is really common, being indeed the most important malformation of the heart, and being generally attended with other evident malformations, such as an aperture in the septum, &c. Now, since the relatively higher function of the right side of the heart during foetal life is supposed to be the cause of the greater liability to congenital disease in the pul- monary (as compared with the aortic) valves, writers have assumed that this liability must be shared by the tricuspid valve also. But, as a matter of fact, there is no proof that disease of the tri- cuspid valve before birth is otherwise than an exceptional occurrence, like dis- ease of the aortic valves, or of the mitral yalve at the same period. Friedreich,3 indeed, says that in newly-born infants minute soft granulations are not rarely found on the auricular surface of the tri- cuspid valve ; but, as they do not gener- ally disturb the functions of the valve, he hardly regards them as morbid, consider- ing them rather to stand on the boarder between physiological and pathological appearances. Dr. Peacock, however, has related4 a case in which there was a thick exudation of recent lymph on the auricu- lar surface of the tricuspid valves, in a cyanotic child, who died when about seven months old. It is stated that the cusps were thickened and adherent at their angles, so as to contract the dimen- sions of the orifice : but this still admitted a ball twenty-four lines in circumference, while the mitral aperture had a circum- ference of only eighteen lines. Friedreich has related a similar instance. Now it is certainly possible that tricuspid stenosis may have its origin in the inflammatory process described by these writers, as oc- curring in certain infants at or soon after birth. But in that case it might fairly be expected that the mitral valve, if affected at all, should be so in a slighter degree. Now I believe that it is invariably the case, that when both the valves in ques- tion are stenosed, the mitral is much thicker and much narrower than the tri- cuspid. For instance, it was so in Mr. E. Pye Smith's1 case, which Dr. Peacock cites as of congenital origin. Another argument in favor of the view that.mitral stenosis may be due to mal- formation is based upon the fact that the patient has sometimes been in bad health for many years, or even from birth. Thus, in Mr. Pye Smith's case, the patient had been ailing all his life ; and, although thirty-seven years of age, did not appear more than fifteen or sixteen, and had never presented any signs of puberty.2 In 1870, Dr. Kelly exhibited to the Patho- logical Society3 a heart with a button-hole mitral valve, taken from a woman aged thirty-three, who, even when a child, " could not run about well or indulge in any severe exertion on account of great shortness of breath and palpitation of the heart." But, so far as I can learn, such cases are quite exceptional. Patients affected with mitral stenosis generally state that they have had perfect health until a few months, or at most two or three years, before they first came under medi- cal observation for their heart-disease. Moreover those who are practically con- versant with the routine of morbid ana- tomy will, I think, agree with me, that in the bodies of those who have had rheu- matic fever some years before death, the mitral valve is very frequently found pre- senting appearances which clearly indi- cate the gradual development of stenosis. In such cases the inferior edge of the valve is thickened, and harder than natural; its orifice no longer admits three fingers readily ; its chordae are beginning to cohere. Every stage of transition may be seen between a healthy valve and one presenting the most extreme degree of stenosis. My belief, therefore, is that it is needless to refer this affection of the mitral valve further back than a past at- tack of acute rheumatism, if the patient has had such an attack. And even when shortness of breath and other symptoms of cardiac defect have existed from child- hood, it appears to me more likely that the stenosis is due to morbid changes arising in the years that may have elapsed 1 Path. Trans, xvii. p. 90. 2 Ibid. xxi. p. 91. 3 Op. cit., p. 216. 4 Path. Trans, v. p. 64. 1 Path. Trans, iii. p. 283. 2 Dr. Peacock, ' ' Malformations of tha Heart," 2d ed., 1866, p. 139. 8 Path. Trans, xxi. p. 91. ETIOLOGY. 715 since birth, than to malformation or dis- ease occurring in the short period of intra- uterine life ; especially since in the foetus the left side of the heart is so situated as to be very little susceptible of morbid action. Secondly, as concerns the aortic valves. Adhesion of two or more of these valves sometimes occurs in very young children. Thus Dr. Lloyd1 exhibited to the Patho- logical Society the heart of an infant thir- teen months old, in which there were only two aortic valves, and these were very red, rough, hard, cartilaginous on their surface and puckered : one of them was twice as large as the other, and had an indistinct ridge intersecting its centre. Dr. Workman,2 again, showed to the same Society the heart of a little girl, only four years old at the time of death, in which the aortic orifice was much contracted, and its valves thickened and fused to- gether. Again, adhesion of the aortic valves has sometimes been found in young persons, associated with the simi- lar change in the pulmonary valves which is believed to be invariably of congenital origin. Thus Dr. Wilks3 has recorded the case of a girl, set. eighteen, in whom the pulmonary valves were adherent, and the aortic valves were two in number, the larger of them having in its interior a raised line indicating the point of union of two former valves. Dr. Ogle4 saw an- other instance of the same kind, in a girl fourteen years old, in whom "two con- tiguous aortic valves had their adjoining angles torn away from their attachment to the aorta, and subsequently united to each other at a lower level." It is no doubt probable that in all these cases the union of the aortic valves occurred before birth: but such cases are extremely rare, and surely afford no ground for supposing that the adhesions which are so com- monly found at an advanced age are also congenital. I must next insist on the fact, that the cases last referred to have characters which distinguish them in a very import- ant way from those in which the union of the valves is known to be congenital. In the first place, partial adhesions of the aortic valves are very commonly met with in older subjects, especially when the coats of the aorta are also diseased. The adjacent edges of the valves are found to have grown together for one or two lines, the rest remaining free. There can be no question of any congenital de- fect, since I am not aware that such par- tial adhesions are ever observed at an early period of life :5 yet it is obvious that the continuation of the same process would lead to the complete fusion of the valves, after which the line of union might be expected to gradually waste and disappear. Again, when the aortic valves are adherent, the orifice is generally ir- regular, and the substance of the valves greatly puckered and often deformed by large masses of calcareous deposit. Of this several capital illustrations are given in Dr. Peacock's published Croonian Lec- tures. He supposes that in these cases the union of the valves took place before birth. But the appearance is very differ- ent from that which is seen in the affec- tion of the pulmonary valves which (as has already been stated) is known to be congenital. In that case the united valves form a smooth, dome-shaped body, with a regular orifice in its centre, and three small ridges or frsena on its upper surface, placed at equal distances from one another. An argument in favor of the view that adhesions of the aortic valves are congen- ital has been found in the fact that, when there are only two valves, they are some- times of equal size. It is supposed that the union must have taken place while the valves were in course of development. In reality, however, this fact merely proves that adhesion occurred before they were fully grown. A case in point re- cently came under my notice. A man, set. twenty-three, died in Guy's Hospital of febrile delirium in the course of acute rheumatism. There was no recent val- vular disease ; but two of the aortic valves were adherent, and the resulting valve was scarcely larger than the third valve, which was itself much thickened along its whole edge, and also contracted, so that it lay flat against the aortic wall. The pericardial sac was universally closed by old adhesions. Now this patient was said to have had chorea and rheumatic fever in childhood, and afterwards to have suffered from distinct symptoms of heart- disease, dyspnoea, palpitation, &c. His illness at that time was doubtless the cause of the morbid changes both outside his heart and in its interior. Two points remain to be considered, which afford powerful, and to my mind convincing, arguments against the view that adhesions of the aortic valves are always, or even frequently, of congenital origin. The first is the extreme frequency with which such adhesions are found in the later periods of life. Thus, according to Dr. Peacock,1 "of forty-three cases in which the aortic valves were diseased, either alone or in conjunction with the 1 Path. Trans, i. p. 60. 2 Ibid, xviii. p. 55. 3 Ibid. x. p. 80. 4 Ibid. v. p. 70. 5 Since this was written I have met with an instance, in which a partial adhesion of two of the aortic valves was found in the body of a boy, set. 16, who had been drowned. 1 Croonian Lectures. 716 DISEASES OF THE VALVES OF THE HEART. mitral valve, in eleven (or 25'5 per cent.) there was malformation of the valves, which probably laid the foundations of the subsequent disease." Dr. Peacock goes on to say that this proportion is much larger than would d priori have been ex- pected. I think that it shows clearly how untenable is his position. It is scarcely conceivable that a congenital malforma- tion, which we have seen to be extremely rare in infants, should be so commonly found in adults. Again, the duration of life in the cases under consideration is altogether adverse to the opinion that the valvular disease had existed from the time of birth. Congenital malformation may, of course, be found in the bodies of those who have lived long, provided these mal- formations were not such as to interfere with the functions of any vital organ : and in exceptional cases, even when they did so interfere. But, if we average a considerable number of cases, we may surely assert with confidence that a con- genital adhesion of the aortic valves, greatly narrowing the aperture, must in- evitably tend to shorten life. Yet we find Dr. Peacock deducing from his sta- tistical inquiries that "in cases of aortic valvular disease assigned to malformation, the age of all the patients averaged 42*3 years, and the extremes of ages were eigh- teen and seventy-six : while the mean age of the patients in whom aortic valvular disease originated in other ways was only slightly greater, or 47'4 years, and the extremes of age were twenty-one and sixty-two." The influence of congenital defect in the causation of diseases of the cardiac valves is perhaps not limited to the cases which we have hitherto been considering. According to Virchow,1 who has recently devoted much attention to the defective development of the aorta that is found in patients affected with chlorosis, inflamma- tion of the mitral or aortic valves is found with disproportionate frequency in these cases. He thinks that the congenital nar- rowness of the aorta impedes the outflow of blood from the left ventricle, and so increases the strain to which the valves are exposed. In connection with this subject, the late Dr. Barlow2 must be mentioned. He believed that in certain young subjects the trachea failed to un- dergo due development. This, he thought, led to imperfect expansion of the chest, and consequently the supply of blood to the left side of the heart was impeded ; and not only the aorta, but likewise even the orifices of the heart's chambers, were prevented from attaining their proper size. Dr. Wilks has put up in the mu- seum of Guy's Hospital* a specimen illus- trative of Dr. Barlow's theory. I find, however, that in this, as in both Dr. Bar- low's cases, mitral stenosis existed in a degree quite disproportionate to that of the other changes; and I must confess that I am inclined to think that this was the primary lesion, that it arose in child- hood (as seems often to be the case), and that the smallness of the trachea was but a part of a defective development of the body generally, consequent on the imper- fect state of the circulation caused by the valvular disease. We have now to ask, what are the causes by which diseases of the valves of the heart are generally produced ? And the answer to this question is, that by far the most common cause is an attack of "rheumatic fever," or "articular rheu- matism," as it is termed in Dr. Garrod's article in the first volume of this work. Dr. Garrod has there pointed out that as far back as 1788 Dr. Pitcairn had noticed that persons subject to rheumatism were attacked more frequently than others with symptoms of heart disease; and that other writers at the commencement of the present century mentioned the same fact. But they were exceptions. Few things in medical literature are more curious, than to read the works of Burns and Kreysig and Corvisart on diseases of the heart, and to find that they had not the slightest suspicion of the rheumatic origin of these affections. So late as the year 1835, in- deed, Bouillaud2 was able to claim for himself the discovery that rheumatic peri- carditis (a disease at that time generally recognized), is frequently accompanied by inflammation of the lining membrane of the heart-for which disease he then pro- posed the name of endocarditis. After this I suppose that the occurrence of valvular disease of the heart in the course of rheumatic fever soon became universally known; and several writers have published numerical statements with regard to its frequency. In these there is a fair general agreement. Dr. Pea- cock3 quotes Dr. Fuller as stating that in his cases of acute rheumatism some car- diac complication was present in 49'3 per cent. ; while Dr. Barclay found that in his cases the proportion was 39 per cent. Dr. Peacock gives 42'4 percent, as the cor- responding proportion in the cases -which came under his care from 1846 to 1868. It is to be observed that, in these figures, pericarditis is included as well as endo- carditis ; and also that in many cases 1 "Ueber die Chlorose, und die damit zusammenhangenden Anomalien im Gefass- apparatus," Berlin, 1872, p. 18. 2 Guy's Hospital Reports, 1st series, vol. vi. p. 235. 1 Prep. 1412®. Catalogue, vol. i. p. 31. 2 " TraitS Clinique des Maladies du Coeur," Paris, tom. i. p. 275. 3 Clinical Society's Transactions, ii. p. 222. ETIOLOGY. 717 Uiere was old disease of the heart from former attacks of acute rheumatism. Both Dr. Fuller and Dr. Peacock have attempted to distinguish these cases, and to determine the exact frequency of re- cent endocardial mischief; but I doubt whether much reliance can be placed upon their results, which are based upon stetho- i scopical evidence only. Indeed, it is ques- tionable whether we can trust to auscul- tation for determining the presence or absence of early endocarditis. I believe that at Guy's Hospital it has been found that in fatal cases of acute rheumatism (and still more of chorea) there has been by no means a ''lose correspondence be- tween the observation of a murmur dur- ing life and the detection of vegetations on the valves after death. Sometimes, when a systolic murmur has been present, the valves have been healthy ; and, on the other hand, when no murmur could be detected they have been found to be diseased. On the other hand, objections of at least equal force may be urged against the use of pathological observations to determine the question as to the numeri- cal frequency of endocarditis in acute rheumatism. As far as I know, no series of unselected cases of fatal acute rheu- matism has as yet ever been published. But I find that at Guy's Hospital, in a period of rather more than twenty years, there have been thirty-two such cases, in most of which the disease was a first at- tack. Now in twelve of these cases the valves were perfectly healthy ; in twenty cases one or more of them was diseased. Six times the mitral valve was alone affected; three times the aortic valves alone: in ten cases both the mitral and the aortic valves were diseased ; and in one other case, both these and the tricus- pid also. This would give 62*5 per cent., as the proportion of eases of acute rheu- matism in which acute endocarditis occurs. Now I shall presently show that in all these cases the changes in the valves were slight, and that they were not at all concerned in causing death. The fatal termination was doubtless generally due to hyperpyrexia, which (as is well known) often comes on in cases that had pre- viously appeared to be of a mild char- acter. Still I think it cannot be denied that the thirty-two fatal cases were on an average cases of excessive severity ; for in twenty-one of them there was recent pericarditis. Probably, therefore, we can- not accept these cases as showing that 62*5 per cent, is really the proportion of cases of acute rheumatism in which endo- carditis occurs. Indeed, if the cases could be regarded as average ones, we should have to suppose the proportion to be really higher still, for in many of them death occurred at a very early stage. After all, it may perhaps be said that the exact determination of the frequency of endocarditis in acute rheumatism is of less consequence than has been supposed: for Dr. Peacock's observations render it probable that this may vary considerably at different periods and among different classes of the population. For practical purposes we may perhaps take it at from 40 to 50 per cent. Next to acute rheumatism, chorea is the disease which most frequently gives rise to disease of the cardiac valves. I believe that this fact was first pointed out by Dr. Hughes in a paper in the Guy's Hospital Reports.1 He found that out of 14 fatal cases of chorea, in which the state of the valves of the heart is mentioned, there were only two in which these structures were reported to be healthy. In the last twenty years we have had at Guy's Hos- pital sixteen other fatal cases of chorea, in which post-mortem examinations have been made ; and in only two of these were all the valves perfectly healthy. Nine times there were vegetations on the mitral valve alone ; twice on the aortic valves alone ; three times on both the mitral and the aortic valves. Probably, however, these figures must not be taken as indi- cating the liability to the occurrence of cardiac disease in non-fatal cases of chorea, since severe forms of the disease are at once more likely to destroy life than mild ones, and more likely also to be compli- cated with valvular inflammation.2 Thus it would not be safe to infer (as might at first be supposed) that disease of the car- diac valves is absolutely of more constant occurrence in chorea than in acute rheu- matism itself. Even in protracted fatal cases of chorea, I believe that the cardiac affection is al- ways slight in degree ; not going beyond the presence of a row of minute granula- tions on the edge of one or more of the valves, which might easily escape notice, if not specially looked for. Pericarditis, again, scarcely ever occurs as a result of chorea apart from rheumatism ; having, in fact, been present in only one of the thirteen cases that I have collected. It is, I think, generally supposed that acute rheumatism differs from chorea, not only in the liability to pericarditis, but also in the much greater severity and extent of the endocarditis which attends it. It was, therefore, with some surprise that I found that in each of the fourteen cases of 1 Series ii. vol. iv. p. 360; and Series iii. vol. i. p. 217. 2 I may mention, however, that in one of the fatal cases of chorea under consideration the girl's death was accidental, having been due to diphtheria, which she caught from another patient. In this instance vegetations were found in the aortic valves. DISEASES OF THE VALVES OF THE HEART. 718 fatal acute rheumatism, which I have al- ready mentioned as having presented val- vular disease, the affection consisted merely in the presence of a row of minute granulations, precisely like those seen iff chorea. In no instance were those larger vegetations present that are so commonly found under other conditions, nor was there ever any ulceration. A third disease, which may also lead to changes in the valves, exactly like those which occur in acute rheumatism and in chorea, is pyaemia. In 1865 I exhibited to the Pathological Society two specimens in which there were well-marked vegeta- tions on the mitral valve, in pyaemia after surgical operations. Similar cases have since been recorded by other observers. In six years (from 1866 to 1871 inclusive) I find that the records of post-mortem ex- aminations at Guy's Hospital contain twelve cases of pyaemia in which one or more of the cardiac valves has been found diseased. In two or three of these cases, however, the affected valve has been found ulcerated. This has sometimes been ob- served, when the pyaemia was evidently of external origin. Thus in 1867 I find a case of pyaemia recorded, in which part of the flap of the mitral valve was found ulcerated away from its chordae. The point is of some importance, because (as 1 have shown elsewhere)1 it suggests a doubt as to the interpretation of some of the cases in which ulcerative endocarditis has been believed to have been the cause of blood-poisoning by Dr. Kirkes and others. Another, but an indirect, cause of endo- carditis is, I believe, the existence of chronic spinal deformity. I have recently2 recorded several cases of this kind in which death took place from pulmonary obstruction and dropsy. In one of them the aortic valves were found to be retro- verted and covered with vegetations. This at first seemed to be difficult of ex- planation : but I subsequently found reason to attribute it to the increased ten- sion within the aorta that must have re- sulted from the sharp bend in its descend- ing part where it was tied by its inter- ' costal branches into the very acute angle formed by the diseased vertebrae. Since then I have seen acute endocarditis affect- ing the aortic and the mitral valves in a man who died of bronchitis and dilatation of the bronchial tubes, consequent on an- chylosis of all the vertebrae together, and of the ribs to the vertebrae. But in this case I did not discover any evidence that the aorta had been compressed or inter- fered with. A somewhat analogous case to the first one mentioned in this para- graph has, however, occurred to me, in which the aorta was compressed by large masses of caseous glands, and in which the aortic valves were affected with acute endocarditis. And Dr. Goodhart lately met with a case of congenital stenosis of the descending part of the arch of the aorta in which there was a similar affec- tion of the valves. There are still some other diseases in which similar minute granulations on the cardiac valves have been occasionally found in the post-mortem theatre of Guy's. Thus in six years (1866-71) I find their presence recorded in three cases of cancer (of the uterus, the liver, and the gall- bladder respectively), in one case of phthisis, in one case of lobular pneumonia, in one case of Bright's disease, in one case of puerperal peritonitis, in one case of syphilitic disease of the liver, twice in cases of dilated heart, and once when there was old adhesion of the two surfaces of the pericardium. They were also found in one case of cholera ; but as the disease proved fatal in 12 hours, it must be sup- posed that they existed before the attack commenced. It has been stated that in all the fatal cases of rheumatic fever that have come under observation at Guy's Hospital within the last few years the changes in the valves have been slight, and in fact identical with those which are well known to occur in chorea. But I must not omit to mention that writers have recorded instances in which the valves have been much more severely attacked. Thus Sir Thomas Watson1 relates two cases in which death is stated to have occurred in a first attack of rheumatic fever, compli- cated with acute pleurisy, three weeks and four weeks respectively after admis- sion of the patients into hospital. In neither instance was any trace of pericar- ditis discovered after death. In each, one of the aortic valves was a mass of ragged ulceration ; and the adjacent portions of the two other valves were in a slighter degree implicated. In one of the cases the ulcerating process had penetrated through the valve into the muscular sub- stance beyond, and eaten a hole com- pletely through the septum. In the other case an abscess as large as a hazel-nut was found in the muscular substance of the septum, immediately opposite the disorganized valve. Now the occurrence of such an abscess is so rare in acute rheumatism, that I almost think it is per- missible to express a doubt whether the case was not rather one of pyaemia, or of primary ulcerative endocarditis, with articular pains : for such cases have often been mistaken for cases of rheumatic 1 Path. Trans, xvii. p. 60. 2 Guy's Hospital Reports, series iii. vol. xix. p. 199. ' Lectures on the Principles and. Practice of Physic, 4th edition, 1857, p. 315. ETIOLOGY. 719 fever. Sir Thomas Watson goes on to remark that these were the only instances of the kind which he had seen. In the other fatal cases of acute rheumatism re- lated in his book only slight changes in the cardiac valves were found after death. It may be convenient here to complete all that has to be said in reference to the general etiology of the acute destructive disease of the valves, which has recently attracted so much notice, under the name of Ulcerative Endocarditis-a name first given to it, I believe by Charcot and Vul- pian in 1861. Besides its occasional ori- gin in pyaemia and perhaps in acute rheu- matism (as just mentioned), this affection has often been found to occur in the latter months of pregnancy, or a few weeks after delivery. Virchow' says that in the Cha- rite at Berlin there is never a year in which several instances of this do not occur. It is true that in the majority of these cases inflammation of the uterus is present, so that the endocarditis might be supposed to be simply a manifestation of pyaemia, but occasionally the pelvic organs are quite healthy. Very often, however, ulcerative endocarditis can be traced to none of these conditions, and may be said to arise spontaneously, so far as our knowledge at this time extends. The patient may have previously been a healthy subject, and the disease may arise suddenly with shivering, so that it is often mistaken for enteric fever or some other acute disease. But such cases are exceptional; much more commonly ulcer- ative endocarditis attacks valves which were previously unsound, and its effects overlie and are blended with those of chronic valvular disease. We may now pass to consider the caus- ation of chronic affections of the cardiac valves; and of these a large proportion, probably the majority, arise out of the acute affections already described as occur- ring in the course of acute rheumatism and of chorea (for pyaemia, being itself almost always fatal, can hardly be credited with a share in the production of these more remote changes). With regard to the details of the processes by which these results are brought about, it may be said that at the present time we know scarcely anything. We do not even know whether an acute affection, once developed, ever subsides entirely, and leaves the valve per- fectly healthy. I think that this must not infrequently occur, especially after chorea, for we have seen that the valves are very often affected in this common malady, and yet it has in my experience comparatively seldom happened that pa- tients laboring under valvular disease have stated that they had previously had chorea. Another argument to the same effect may perhaps be found in the com- parative rarity of chronic rheumatic dis- ease of the aortic valves in women. We have seen that the aortic valves were found to be affected in thirteen out of twenty cases of acute rheumatic endocar- ditis. Now of these cases at least seven occurred in females. But in the years 1867-71, for 23 cases of chronic aortic dis- ease with history of previous acute rheu- matism in males, only 6 cases in females came under observation in the post-mor- tem theatre at Guy's. It would seem to follow that in women rheumatic inflam- mation of the aortic valves must often subside entirely without leading to chronic disease. If this be true, it is of very great importance, for it may teach us a most valuable lesson. We shall presently see that the aortic valves are in men lia- ble to strain and pressure, from which in the other sex they are free ; and that in consequence non-rheumatic disease of the aortic valves is in men very common, in women comparatively rare. It appears very probable that the same freedom from strain and pressure may also enable these valves in women to recover from rheuma- tic inflammation more perfectly than in men. And, if so, we may learn how to obviate the ill-effects of such inflamma- tion in both sexes, and in the case of all the valves, by keeping the patients at rest, and making them abstain from work and exertion of every kind, for a long period after an attack of endocarditis. It is at any rate certain that the granu- lations, which appear to be constantly present in acute affections of the valves, have generally but a transitory existence. Sometimes, indeed, they become calcified, and can thus be recognized long after all acute disease has passed away. But more often they disappear, and thus in chronic rheumatic disease the surface of the thickened and calcified valves is often found to be perfectly free from them. When uncalcified granulations or vegeta- tions are found in cases of long standing, I believe that they are always of rather recent formation, and due to the super- vention of an acute inflammation, to which fas we have seen) valves already diseased are particularly liable. In a considerable proportion of cases, however, chronic valvular disease can be traced to none of the conditions that have as yet been mentioned. And its etiology appears then to be different in the case of different valves. Affections of the aortic valves often accompany similar morbid changes in the walls of the base of the aorta itself, changes often spoken of as "atheromatous," but really dependent 1 "Ueber die Chlorose . . . Endocar- ditis Puerperalis," Berlin, 1872, p. 20; see also Trousseau, " Lectures on Clinical Medi- cine," New Sydenham Society's Trans, vol. iv. p. 459. 720 DISEASES OF THE VALVES OF THE HEART. on a chronic inflammation of the arterial coats, or (as it is termed by Virchow and others) an arteritis deformans. This dis- ease occurs especially in men (as, for ex- ample, sawyers, smiths, strikers and riv- eters, bricklayers' laborers, and hodmen) whose occupations involve great muscular efforts, by which the arterial pressure and the strain on the aortic coats are in- creased. Writers have generally stated that persons of rather advanced age are more liable to it, but Dr. Allbutt says that it is very common in Leeds among quite young men.' According to Pea- cock, a similar affection is not infre- quently observed to occur in girls engaged as nursemaids, and in other servants, who are subjected to straining efforts be- fore they have attained their full strength. It is further to be noted that, although the affection of the valves in all these cases appears to be identical in nature with that which occurs in the walls of the aorta, the two are by no means invariably affected in an equal degree. Dr. Allbutt has suggested the opinion that continuous labor, such as hammer-work, is more in- jurious to the aorta itself, and that sud- den strains, like the lifting of weights, tell rather upon the valves. The relative frequency with which valvular disease is thus due respectively to mechanical strain or injury and to the effects of antecedent acute disease, probably differs greatly among different classes of the population, and in different localities, according to the occupations of the lower order in them. Dr. Allbutt tells us that in Leeds, in hospital practice, heart diseases due to acute rheumatism are among young men fewer than those which he has learnt to attribute to over-exertion of the body. In this statement, however, no account is taken of the affections of different valves separately. I believe that in hospital practice in London one fails to obtain a history of a past attack of rheumatic fever in at least half the cases of chronic regurgitant disease of the aortic valves that are met with in adults, and that in almost all these cases the changes in the valves are associated with similar changes in the walls of the aorta, and are the re- sult of habitual or repeated straining ef- forts of one kind or another. It is far otherwise in the case of the mitral valve. In this structure atheroma appears only in the form of slight cream- colored patches, placed near the base of the valve, and therefore incapable of im- peding its closure. Nor can any morbid change in the mitral valve be traced in association with the disease of the aortic valves just described as due to arteritis deformans. Still, there are a large num- ber of cases of mitral stenosis in which no previous attack of acute rheumatism or chorea seems to have occurred, and the subjects are many of them children, in whom no definite illness could have been overlooked or forgotten. Such cases have been by some writers attributed to congenital malformation, a view which I have already endeavored to disprove. Other observers have supposed them to be due to latent rheumatism : that is, to manifestations of the rheumatic state, which has for some reason failed to dis- play itself in the characteristic articular malady. On closer inquiry it may some- times be elicited that such patients have formerly suftered from "growing pains" or "rheumatic pains" of greater or less severity, and certain observers, among whom may be mentioned no less an au- thority than the late Dr. Addison, have pressed these into service as affording evidence of the existence of a constitu- tional state. It must be admitted that rheumatic pericarditis often precedes any affection of the joints, and that in young people already suffering from valvular disease of the heart without any history of previous rheumatism, the joints some- times become swollen and painful, or chorea is developed. I have therefore no doubt that many of these cases of mitral stenosis are really the results of a rheu- matic tendency. But it is still a question whether they are not too frequent for such an explanation to be applicable to all of them in which no history of previous rheumatism can be traced. It would appear, therefore, that the mitral valve is very liable, even in chil- dren and young subjects, to undergo those changes which lead to stenosis, either as the result of a spontaneous chronic morbid process, or else as the consequence of some disease (other than rheumatism or chorea), the tendency of which to produce endocarditis is as yet unknown. Can this disease be scarlatina or diphtheria ? I have read (but I do not know where) that M. Bouchut has recently brought forward diphtheria as often leading to the formation of granula- tions on the mitral valve, but in the few autopsies that I have made these have been absent. As is well known, scarla- tina is often followed by acute rheuma- tism, or an articular disease allied to it: and this may be complicated with endo- carditis, as has been shown by Trousseau and others. Nay, in cases of chronic valvular disease it is not very uncommon for the patient's illness to be referred back to an attack of scarlatina. But I am nevertheless very doubtful whether this disease can be called in to account for the cases that now need explanation, for I fail to find any evidence that scar- 1 " The Effects of Overwork and Strain on the Heart and Great Bloodvessels," St. George's Hospital Reports, v. p. 23. ETIOLOGY. 721 latina in itself is capable of setting up en- docarditis. So far as I am aware, when a child dies of scarlatinal dropsy, or of any one of its other sequelae, the valves are constantly found healthy. Within the last few years it has been a matter of frequent discussion among pa- thologists whether syphilis is ever a cause of disease of the cardiac valves. The idea is indeed no new one ; for Corvisart1 long ago suggested that vegetations of the valves were of venereal nature. No less an authority than Virchow2 has since stated his readiness to admit the possi- bility that this may sometimes be the case : but he has given no case in proof. When Mr. Myers3 and other army sur- geons recently showed the frequency of heart disease in soldiers, and attributed it to the faulty clothing and accoutre- ments which they are made to wear, or to the exercises they are called upon to per- form, it was objected that soldiers are very subject to syphilis, and that this was really the cause of the cardiac affections to which they are liable. But to that argument a rejoinder was made that sailors are equally apt to have venereal disease, while they are not found to suffer in the same proportion from morbus cor- dis. For my own part, I confess that I have met with no facts, either by observa- tion or by reading, that would lead me to believe that syphilis has anything to do with the diseases under consideration. The effects of sudden violence in injur- ing the cardiac valves still remain to be considered. Corvisart appears to have been the first writer who reported a case in which the valves of the heart were clearly shown to have been injured during muscular exertion. Since that time sev- eral instances of the kind have been placed on record: and in 1865 Dr. Pea- cock4 collected seventeen cases, four of which had come under his own observa- tion. It has already been stated that in ad- vanced valvular disease softening and laceration are very apt to occur, whether as a result of slight muscular efforts, or independently of any such cause. But symptoms of heart disease have then gen- erally existed for a long time. The pecu- liarity of the cases now under considera- tion is, that the subjects of them are apparently in perfect health when the in- jury arises, and have never had rheuma- tism, or been suspected of any cardiac disease. It is indeed true that such acci- dents have been observed chiefly in adult men, whose occupations have long been such as are known to carry with them the liability to induce chronic changes in tire heart and great vessels: and some have therefore argued that the lacerated valve might not have been in a healthy state at the time of the injury, but might have previously undergone degeneration. And this supposition is very difficult to nega- tive, since death seldom occurs in such cases until after the lapse of a consider- able interval, when of course the state of the valves before their rupture cannot be determined. But in this, as in so many other instances, the maxim may be ap- plied, "De non apparentibus et de non ex- istentibus^ eadem est ratio. " For practical purposes it is more important to remember that a valve may rupture in a man who has hitherto been active and robust, and free from the slightest symptom of cardiac disease, than to discuss whether the valve has or has not previously undergone slight degenerative changes, which no one could have discovered or suspected. Perhaps the most striking example that could be quoted, in which mechanical in- jury led to the rupture of a previously healthy valve, is recorded by Dr. Wilks in the sixteenth volume of the Pathologi- cal Transactions (p. 77). The patient, a youth aged nineteen, fell from a height, and alighting on a stone struck his left side violently, so as to lacerate a portion of the intestine, as a consequence of which peritonitis arose, and proved fatal on the third day. It had been observed that he had considerable oppression at the chest, and much distress in breathing after the accident; but unfortunately no stetho- scopical examination was made. At the post-mortem examination it was found that the most posterior of the aortic valves was torn through, from its free margin to its base, a little on one side of its attached edge. Only a ragged portion remained attached to the aorta, while the bulk of the valve was free to flap backwards and forwards. A small deposit of fibrin had already commenced to form on the ragged edges. In this case there was no mark of bruis- ing on the chest, nor any sign of injury external to the heart. But I think it can hardly be doubted, from the history of the accident, that the cause of the laceration was the blow on the side, rather than any muscular effort made by the youth at the moment. The case would then be strictly parallel to those which are not unfre- quently met with, in which an accident gives rise to severe laceration of some one of the abdominal viscera, or of the interior of the brain, without there being any bruise on the surface, or visible track by which the vibrations had passed to the deeper structures. In this respect, however, Dr. Wilks's case would appear to be exceptional, if the conclusions of Dr. Peacock are to be 1 Op. cit. p. 194. 2 Arch. f. Path. Anat. xv. 1858, p. 288. 3 Path. Trans, xx. p. 141. 4 Croonian Lectures. vol. ii.-46 722 DISEASES OF THE VALVES OF THE HEART. relied on in reference to the question at issue. The last-named observer collected seventeen cases of rupture of a valve from injury. In three or four of them the pa- tient had sustained direct injuries at the same time ; but Dr. Peacock was never- theless of opinion that in all of them the immediate cause of the rupture was the violent effort made at the same moment. " In one case the patient had made a long and rapid journey on horseback : two men were pulling or loading heavy casks, two were running violently, one was rowing, another was striking with a heavy sledge, a third was endeavoring to force open a door, and others were climbing rapidly, endeavoring to leap over a fence, and carrying heavy deals. In others, violent coughing appears to have been the cause of the rupture." The comparatively small number of cases which Dr. Peacock could collect is in itself a sufficient proof that rupture of a valve in a previously healthy subject is after all a decidedly rare occurrence ; and this conclusion is confirmed by the fact that few cases of the kind are recorded in the Pathological Transactions, which are generally particularly rich in examples of the more striking forms of disease. Among the different valves, those of the aorta are the most liable to injury, having proba- bly been ruptured in ten out of Dr. Pea- cock's seventeen cases. Laceration of the columns of the mitral valve seem to have occurred in four instances, and of the tri- cuspid in the remaining three. In the aortic valves the part torn appears to be usually the attached margin or angle. Effects.-Diseases of the cardiac valves produce serious effects of various kinds, by which the patient's health is disturbed and his life often endangered. In these are to be found the ' ' symptoms" of the diseases in question. But before entering upon their consideration it will be conve- nient to discuss first another class of effects also resulting from such diseases, and in the eyes of the physician no less import- ant, although to the patient himself they are of but little direct concern. I refer to the altered sounds, accompanying the heart's action, that are heard by the ear or stethoscope applied to the patient's chest-the " auscultatory signs" of valvular lesions. In England these altered sounds are termed indifferently 11 murmurs" or " bruits." The latter term is of course a relic of the French influence that pre- dominated in this country for many years after the discovery of auscultation. But it may be worth while to note that French writers themselves apply the word " bruit" indifferently to the natural heart sounds, and to the murmurs heard in disease, adding the epithet " anormal" when a murmur is to be referred to, or else desig- nating it a de souffle" from the blowing character which generally belongs to such morbid sounds. Numerous theories have been formed to explain the production of cardiac mur- murs ; but they have attracted more at- tention abroad than in this country, Eng- lish writers having generally passed them by, as of theoretical rather than of prac- tical importance. One of the earliest of such theories was, however, originally propounded by Sir Dominic (then Dr.) Corrigan, in the year 1829; and, quite recently, the labors of certain French ob- servers have gone far towards establishing the correctness of this view, to the exclu- sion of all others. It must be remarked that murmurs are by no means confined to the heart, but may arise in almost any part of the circu- latory system ; and this fact has to be taken into account by any theory that would explain their production. Laennec had ascribed the bruit de souffle to "a special vital state-a sort of spasm or ten- sion of an artery."1 Corrigan2 easily showed that this opinion was untenable. "Apply, " he says, " the stethoscope under the outermost third of the clavicle, not allowing it to pass ('(press) on the sub- clavian. In a strong healthy man, not agitated, the mere impulse of the diastole of the vessel is felt. Now compress the artery above the clavicle, so as to diminish the current of blood through it: a loud bruit de souffle is heard. Make strong pressure, so as to stop the flow of blood : no sound is heard. If the sound in this experiment arose from the arterial tube being excited into muscular action by the stimulus of the pressure, why does it cease when the stimulus is increased?" And he goes on to give the following explana- tion of the bruit de souffle:-"When an artery is pressed upon, as in the experi- ment above related, the motion of the blood in the artery immediately beyond the constricted part (looking from the heart) is no longer as before. A small stream is now rushing from a narrow orifice into a wider tube, and continuing its way through surrounding fluid. The rushing of the fluid is combined with a trembling of the artery, and the sensation to the sense of hearing is the bruit de souffle." Further on he applies the same theory to the murmurs heard in aneurisms 1 "Traits de l'auscultation mediate," sec- onde Edition, 1826. In his first edition Laen- nec had described the bruit de souffle as occur- ring when the heart was too full of blood, and as caused by contraction of one of the heart's orifices. But afterwards, finding that there was no organic lesion which coincided constantly with the bruit, he expressed the opinion cited in the text. 2 Lancet, 1829, vol. ii. p. 1. ETIOLOGY. 723 and in narrowing of the auriculo-ventricu- lar orifices of the heart, &c.; and he proves that the condition supposed to produce murmur may be imitated by passing a forcible current of water through a portion of small intestine. In this experiment, as soon as constriction was made on any part, a very loud bruit de souffle imme- diately became evident just below the narrowed part, where no sound had been previously heard. The writers who followed Corrigan dealt with the causation of cardiac murmurs from an entirely different point of view. By Gendrin (1841-2) they were placed in the same category with the morbid sounds heard in pericardial inflammations ; and since the latter are due to friction between the two serous surfaces, he naturally attri- buted the former, which he termed " bruits de frottement endocardiaques," to friction between the blood and the surface over which it passes. This friction theory has since been generally adopted.1 But in the year 1858, Chauveau, of Lyons, published an important memoir, in which he endeavored to show that the friction theory was untenable, while he revived Corrigan's views, and placed them on a firmer physical basis.2 In the first place, he proved that roughening the interior of an artery does not cause a bruit. Thus he exposed the carotid artery of a horse, and tore through the internal and middle coats, at four or five points near one another. The tube was, of course, greatly roughened, but no bruit was pro- duced. On the other hand, whenever a dilatation was placed in the course of an artery, the blood entering the dilated part gave rise to a bruit de souffle. This Chau- veau ascribed to the fact that under such circumstances a sonorous jet is formed, such as Savart studied experimentally under the name of the " veine fluids. " He even laid bare the pulmonary artery of a horse (in which artificial respiration was kept up after pithing), and introduced his finger into the artery through a slit in its wall. When the vessel was narrowed by tightening a thread round its base, he could feel the vibrations of the veine fluide which was generated, whereas the flow of the blood had previously been scarcely perceptible. Chauveau therefore sums up the results of his experiments in the statement that "the bruit de souffle is produced by the vibrations of the veine fluide, which is always formed when the blood passes into a part of the circulating apparatus ac- tually or relatively dilated." Very soon after the discovery of auscul- tation, it was found that a bruit de souffle could sometimes be heard even in persons in whom the heart was perfectly healthy, especially in those who were chlorotic or anaemic. Such a bruit has been generally attributed to the thin and watery state of the blood, rendering it liable to be thrown into vibrations while flowing through the vessels. This explanation, however, is far from satisfactory, and has indeed been rendered untenable by the experiments of Chauveau and others, who have shown (in opposition to some earlier experiments of De la Harpe) that the production of murmurs in general is altogether inde- pendent of the nature of the fluid in which they are formed. It would seem, however, that the theory of Chauveau, just stated, is applicable to such ansemic murmurs. As is well known, these are of two kinds-the arterial, and the venous, or "bruit de diable.'1'1 The former is audible chiefly at the base of the heart, along the aorta, or the pulmonary artery. Now, Chauveau has shown that in anaemic horses the arteries generally are one-third smaller than in healthy animals ; the mass of blood is greatly re- duced ; the heart and its orifices become diminished in size, so as to adjust them- selves to the altered volume of the blood ; but the great arteries, being compara- tively inelastic, retract less perfectly. The conditions for the production of a mur- mur are thus satisfied. Moreover, the arterial pressure during the cardiac dias- tole is found to be very much lower than usual; hence, when the artery becomes distended by the heart's contraction, the force with which the blood enters is far greater than in health. In other words, the range of pressure within the arterial system is greatly increased. The venous aneemic murmur, or bruit de diable, receives a very similar explana- tion. As Hamernyk long ago showed, it is met with only at the root of the neck ; and the cause of this lies in the anatomi- cal fact (first pointed out by Berard) that in this region the lower ends of the jugu- lar and subclavian veins on each side are adherent to the deep cervical fascia, and therefore cannot collapse. This venous ampulla, as it has been termed, evidently affords the conditions necessary for the generation of a veine fluids, whenever the blood-stream in the jugular vein above is narrowed, whether by simple adjustment of its calibre to the diminished volume of the blood in ansemia, or by the pressure of the stethoscope, or by both combined. Thus, as might be expected, in some healthy subjects a bruit de diable can be generated by nice compression of the jugular vein with the stethoscope ; and, on the other hand, even in those who are ansemic a certain amount of pressure is required to develop the murmur, unless 1 See Walshe, "A Practical Treatise on Diseases of the Heart and Great Vessels," 1862, p. 86. 2 Gazette Medicale de Paris, 1858, p. 247. 724 DISEASES OF THE VALVES OF THE HEART. the morbid state is present in an extreme degree. Since the publication of Chauveau's essay, this subject has been studied by several French writers, especially by Marey, Luton,1 and Bergeon,2 who have expressed their general adhesion to his views. And for my own part I think that they have proved that a bruit de souffle occurring in an artery or vein at a distance from the heart is invariably caused by the generation of a sonorous veine fluide, and due to the passage of a narrow jet of blood into a wider cavity or part of the vessel. But this explanation is certainly not applicable to all cardiac murmurs. The bruit caused by a sonorous veine fluide is heard only in the dilated part of the chan- nel, and not at all (or very faintly) in the narrowed part behind it. In other words, it is propagated in the direction of the stream of fluid. Now, as we shall see presently, some cardiac murmurs obey this law ; among which are those of mitral and aortic stenosis. But in mitral and in aortic imperfection this is not the case: the murmur is audible, not only in the direction of the regurgitant blood-stream, but also on the other side of the orifice (over the left ventricle in the case of the mitral valve ; along the aorta in the case of the aortic valves). Now' Bergeon has given a complete explanation of this, and has showm that it may be easily imitated in experiments (such as have several times been referred to), in which water is made to traverse tubes narrowred at a cer- tain point. One has only to provide the tube at the seat of constriction w'ith a lip or rim projecting backwards into the stream, and a second murmur is at once generated, which is heard behind the obstruction. A cul de sac is formed, and the fluid which occupies this receives the shock of the onward current, and is thrown into sonorous vibrations. It is evident that this experiment exactly meets the case. The incompetent valves, whether mitral or aortic, project back- wards into the blood-stream, exactly like the lip or rim employed by Bergeon. But I think that the very success of this attempt to enlarge the range of conditions to which Chauveau's narrow theory would limit the production of a cardiac bruit de souffle, shows how cautious we ought to be in assuming that we are now perfectly acquainted with all these conditions. In expressing my belief that vascular mur- murs have always such an origin as Chau- veau supposes, I am mainly influenced by the consideration that the circulation of a stream of fluid through a tube is a very simple physical matter, the phenomena of which have been thoroughly studied ex- perimentally. But it is far otherwise in the case of the heart. In the left ventricle we have a contracting chamber, with pro- jections of various kinds from its inner surface. During its systole, in particular, the mitral valve with its tendons and columns must tend to project into its cavity, with a space between it and the posterior wall of the ventricle. Under normal conditions the chamber empties itself completely during its systole, and this space can hardly be said to exist. No murmur is then generated. But let the ventricle be dilated, and let its con- traction be imperfect and incomplete-as we must necessarily suppose it to be, if the quantity of blood poured into the aorta be not greater than in health, and if there be no mitral regurgitation (of which there is certainly in many cases no evi- dence). Is it not very probable that under such circumstances the blood in the space behind the mitral valve may be thrown into vibrations, and so a bruit de souffle be generated, exactly as in the cul de sac employed in Bergeon's experi- ments ? Such a bruit would be heard at the heart's apex, and nowhere else. We shall hereafter see that precisely such a bruit is very frequently heard, in various diseases, and that its interpretation is still open to very great doubt. Now, cardiac murmurs, instead of being soft and blowing, are sometimes very rough and harsh. The older French aus- cultators laid stress on such varieties, and gave them special names, as " bruit de rdpe" '■'■bruit de scie^ " bruit de etrille^'' devoting great pains to the determination of their precise physical causes. Little success, however, appears to have attend- ed their efforts: as might indeed be ex- pected from the erroneous view's that they entertained concerning the origin of mur- murs in general. The rough and harsh murmurs in question are very generally accompanied with a thrill that can be felt if the hand be placed on the surface of the body at the spot where the murmur is audible: and to this Laennec gave the name of fremissement catair e. Now', ac- cording to Bergeon, murmurs are rough and attended with fremissement, when they are intense, and when the tube (he is speaking of simple physical experi- ments) is thin and elastic. It might, therefore, be thought that such murmurs owe their peculiar quality to the fact that the walls of the orifice take part in their production, and that they are not pro- duced by the vibrations of the fluid alone. Such a view, however, is entirely incon- 1 " Nouveau Dictionnaire de Melerine et de Chirurgie Pratiques," art. Auscultation. 2 ' ' Des Causes et du Mechanisme du Bruit de Souffle," Paris, 1868, p. 103. In this es- say will be found a detailed investigation into the physical cause of cardiac and vascu- lar bruits. ETIOLOGY. 725 sistent with Savart's experiments already referred to. And clinical facts are equally adverse to it. As we shall presently see, no murmur is so generally harsh, and so commonly attended with thrill, as the so- called presystolic murmur of mitral ste- nosis. But in this affection, the margin of the orifice, far from being thin and elastic, is almost always thick and hard, and often contains much calcareous mat- ter. The peculiar quality of the murmur in this case is evidently not due to the fact that the orifice itself, as well as the fluid, vibrates. What, then, is its cause? There can, I think, be hardly any doubt that it depends upon the circumstance that the jet of blood in which the murmur is generated, entering the flaccid empty ventricle, impinges on its inner surface at a point which must be very close indeed to the part of the ventricle which strikes the chest-wall and produces the heart's impulse. The physician may thus almost be said to receive with his finger the full shock of the sonorous jet propelled into the left ventricle through the narrowed mitral orifice. It would be interesting to determine whether similar conditions are traceable in other cases in which similar murmurs occur : for instance, in cases of aneurism. For the present it must, I think, be concluded that the harsh rasp- ing quality of a bruit, and the accompany- ing thrill, are not due to any peculiar state of the orifice at which the bruit is produced, but rather to the intensity of the murmur itself, and to the fact that the jet of blood which generates it is di- rected towards the surface of the patient's body. Another modification of murmurs is that in which they are high-pitched and resemble the note of a musical instrument, or a whistle, the cooing of a dove, the puling of a chicken, or the mewing of a cat. These are generally spoken of as "musical" murmurs; and according to Bergeon, they may arise in either of two ways. Sometimes they are due to the fact that the channel into which the veine fluids passes is not straight but bent, so that the veine impinges on its wall on one side. This is the case, for instance, in the jugular fossa at the base of the skull; where (according to this writer) a musical bruit is often generated, which gives rise to an intolerable singing in the ears. More frequently such a bruit is due to the pres- ence of a thin membranous flap or valve, vibrating in the stream of blood which flows over its surface ; the musical char- acter of some cardiac murmurs appears generally to be due to something of this kind. But the subject is one still admit- ting of further elucidation. In vol. vi. of the Pathological Transactions, Dr. Pea- cock has recorded a case in which a musi- cal murmur, exactly resembling the sound of a cuckoo-clock, was audible at the dis- tance of some feet from the patient: after death no special morbid appearance was discoverable in explanation of it. But the differences in the quality of car- diac murmurs, which we have hitherto been considering, are of trifling conse- quence (so far as the interpretation of their cause is concerned) in comparison with two other points, to which we must now turn our attention. The first of these is their rhythm, or relation to the move- ments and natural sounds of the heart; the second their seat, or capability of being heard at different parts of the surface of the chest. The passage of the blood through the heart and arteries is effected by three suc- cessive movements, each of which may, under certain circumstances, cause a bruit. (1) The most important of these is the ventricular systole: and since the contraction of one or other ventricle is invariably the cause of any murmur that coincides with it in time, such murmurs are very fitly termed systolic (or, some- times, ventricular-systolic). They, of course, take the place of, or follow, the first sound: they coincide with the closure of the auric- ulo-ventricular valves, or at least occur when these ought to close. (2) After the ventricular systole comes the elastic re- coil of the aorta and pulmonary artery. This, again, may generate a bruit, which coincides with (or replaces, or follows) the second sound, and occurs at the moment when the sigmoid valves should fall to- gether. It would have been better that the name given to such a murmur should have indicated its origin: but no conve- nient title suggests itself, and since the ventricle is dilating at the time, the bruit in question has always been termed dias- tolic. This is unfortunate, for the ven- tricular diastole is only very indirectly concerned in its production, and may in- deed have nothing at all to do with it. (3) Moreover there is a third movement, which likewise occurs during the ventric- ular diastole, and generates a third kind of bruit. This is the auricular systole. In health, it produces no sound; but in disease it may give rise to a very loud murmur: the best name for this would undoubtedly be that of auricular-systolic (proposed for it by Dr. Gairdner); but in practice it is generally called presystolic, because it more or less closely precedes the ventricular systole. Thus it is usual to designate the rhythm of a bruit by indicating its relation to the contraction of the ventricles ; a murmur that is synchronous with this contraction is called systolic: one that follows it is called diastolic; one that precedes it is called presystolic. Now, when the heart is beating slowly, it is generally easy to distinguish which of the cardiac sounds 726 DISEASES OF THE VALVES OF THE HEART. or murmurs is systolic, from the fact that the pause before the first sound is very much longer than that which follows it. But when the pulsations are more rapid, this criterion is lost, for the increased pace is gained at the expense of the pe- riod of rest, and the one pause may then be as short as the other. The well-known difference in quality between the first sound and the second may then enable the rhythm to be detected; but this again often fails ; and one is driven to deter- mine the ventricular systole by noting at what period the heart's apex strikes the chest or (which is to me more easy) by feeling the carotid pulse with the linger while one is listening to the heart. A systolic sound or murmur having been thus identified, it remains to con- sider whether any other bruit that may be audible is diastolic or presystolic. And here, again, all depends on the rate of the heart's beats. When these are infrequent, and the diastolic pause is prolonged, the so-called diastolic murmur, occurring at the commencement of this pause, is easily differentiated from the presystolic murmur that occupies its termination, and runs up to the following ventricular systole. But it is quite another case when the heart's action is rapid, and the pause pro- portionately shortened. The distinction between a presystolic and a diastolic mur- mur may then, as I believe, become quite artificial, so far as their mere rhythm is concerned. But there still remain differ- ences of quality and seat, which usually enable the nature of the murmur to be determined without much difficulty. We will now consider the three kinds of bruits in the order of their occurrence : I. the Presystolic; II. the Systolic; III. the Diastolic. And since each of these may be developed on either the right or the left side of the heart, it will be neces- sary to mention two varieties of each. But, as has already been stated, disease of the left valves is greatly more common than of the right. I. A presystolic murmur, due to the auricular systole, is never produced unless the auriculo-ventricular orifice is narrow- ed. And practically it is almost always indicative of that chronic change in the corresponding valve that has been de- scribed under the name of stenosis.1 a. When developed at the mitral orifice, this murmur is much louder at the heart's apex than anywhere else. It is also re- markably local, being sometimes audible only at a single spot, and not being trace- able round the side of the chest towards [Fig. 99. (Gairdner.)] the left scapula, as is the case with the systolic murmur of mitral regurgitation. The quality of a presystolic, or (as it is sometimes called) 11 direct," mitral mur- mur is in most cases peculiarly harsh, and it is often accompanied by a thrill percep- tible to the touch. It is generally spoken of as having a "churning" or " grinding" character; and this may enable a prac- tised ear to distinguish it at once from other bruits. I think I have never yet heard a direct mitral murmur which has been soft or musical. There is, however, an important modification of the presys- tolic murmur, which, I believe, I first de- scribed in a paper on this subject in the Guy's Hospital Reports for 1870-71. Such a murmur is often very short; and it may be so short as to resemble a tone, and thus to be hardly distinguishable from the natural first sound of the heart. Now, it happens that in cases of this kind the real first sound is commonly peculiarly sharp and clear, and so resembles the second sound; while the second sound is itself inaudible at the heart's apex. Thus the sounds heard at this spot may at first ap- pear to be normal; while on closer exami- nation it may be discovered that their rhythm is entirely different from that of the healthy sounds; and that one of them is in fact an abbreviated presystolic bruit. 1 It is indeed possible that a mass of vege- tations, formed upon the surface of the valve during acute disease, might so obstruct the channel as to lead to the development of such a murmur; but (so far as I am aware) no case of the kind has as yet been placed on record. I have always believed hypertrophy of the auricle to play an important part in the development of a presystolic murmur; and this implies the existence of chronic dis- ease. ETIOLOGY. 727 In the paper above referred to, I have de- scribed a case in which this observation led to the confident assertion that mitral stenosis existed in the case of a woman who had no other sign or symptom of car- diac disease, having been admitted into a surgical ward for gangrene of the leg. She died six weeks later ; and the mitral orifice would admit only one finger-point. It is only within the last few years that presystolic murmurs have been rightly interpreted. The name was invented by Gendrin.1 He did not, however, attach any special importance or diagnostic value to such murmurs. But in 1843, Fauvel communicated to the Archives Generales a paper in which he showed by the narration of four cases (three of them fatal) that a presystolic murmur was indicative of mi- tral stenosis. Subsequent French writers, however, have thrown very little light on this subject. For many years the Paris School of Medicine was divided into two camps with regard to the rhythm of the heart's impulse, which Beau would have to be synchronous with the ventricular dias- tole. Agreement on minor points was therefore out of the question; and He- rard,2 Bouillaud,3 and Durosiez,4 may be mentioned as having written on the subject of mitral stenosis, and expressed views opposed to those of Fauvel. Durosiez, in 1862, thought it sufficient to make a pass- ing reference to "ce fameux bruit pre- systolique, dont tout le monde a parle, sur lequel personne ne s'entend, que Hope lui-meme avoue n'avoir jamais entendu, que M. Bouillaud enfin neglige et meme nie." Racle, again, in his "Traite de Diagnostic medical," published in 1859, speaks of it as " une distinction plus sub- tile que reelle." In Great Britain the first writer who alluded to this subject was, I believe, Dr. Gairdner of Glasgow, who expressed views precisely similar to those of Fauvel, except that he preferred to term the mur- mur auricular-systolic, rather than pre- systolic. Subsequently papers on the same subject were published by Dr. Wilks, Dr. Gull, Dr. Hayden (of Dublin), Dr. Peacock, Dr. Sutton, Dr. Simpson (of Manchester), and Dr. Hyde Salter.5 Thus in my communication to the Guy's Hospital Reports I was able to refer to twenty-eight cases (seven contrib- uted by myself), in each of which a post- mortem examination proved the existence of mitral stenosis, and in which this con- dition had been diagnosed from a pre- systolic murmur heard during life. Since then the subject has been taken up by Dr. Douglas Powell and Dr. Silver. Even now, however, there are observers who deny that the rough grinding murmur heard in cases of mitral obstruction is really presystolic in rhythm. In the year 1872 Dr. Barclay contributed to the Lancet1 a series of papers, in which he endeavored to prove that the peculiarity in the rhythm of this murmur really de- pends on the circumstance that the closure of the mitral valve is delayed. Instead of this closure occurring at the commence- ment of the ventricular systole, he be- lieves it to take place only when the sys- tole is nearly completed ; the first sound being of course postponed likewise. Dr. Barclay thus regards the murmur as really regurgitant and not obstructive, although he does not deny its constant association with mitral stenosis. But it ap- pears to me that no one who has studied the relation between the murmur and the heart's beat or the carotid pulse can admit that Dr. Barclay's hypothesis is tenable. Neither beat nor pulse can be felt while the bruit is audible ; they both follow it. It is important here to mention that the presystolic bruit by no means always merges gradually into the heart's first sound, as would appear from the accounts given of it by some writers. Much more often it is separated from the first sound by a distinct interval which seems to me sometimes as long as that which separates the natural first from the second sound. The murmur, too, is often prolonged through a period much exceeding that of the natural auricular systole. This has been explained in two different ways. The late Dr. Salter supposed that the first part of the murmur is generated while blood is flowing passively from the auricle into the ventricle. I have argued that the auricle begins to contract earlier, and goes on contracting longer, than in the healthy heart, and that the whole of the bruit is thus due to the auricular systole. This view has since been established by the cardiographic observations of Mr. Mahomed.2 I append copies of twro of his tracings, taken from the heart's apex in the same patient at an interval of seven months. It will be observed that the slight elevation which Marey proved to be due to the auricular contraction takes 1 Lemons sur les Maladies du Coeur, &c., 1841-42. 2 Arch. genSr. de Med., ser. v. tom. ii. p. 543. 1853. 3 Traite clinique des Maladies du Coeur, 1836. 4 Arch, g^n^r. de Med., ser. v. tom. xx. p. 385. 6 Edinburgh Medical Journal, vol. vii. part 1, p. 438. 1861. 6 In my paper in the Guy's Hospital Re- ports, I have gone into the literature of this question in much greater detail than is pos- sible here. 1 Vol. i. pp. 283 et seq. 1 Med. Times and Gaz., 1872, vol. i. p. 569. 728 DISEASES OF THE VALVES OF THE HEART. place very soon after the preceding ven- tricular systole, and is succeeded by a gradually ascending line, throughout the whole duration of which the auricular systole is sustained. The figures seem to speak for themselves: and unless it can be shown that their peculiarities are capa- ble of some different interpretation, it appears to me that they not only estab- lish the point now under consideration, but also give the coup de grace to Dr. Bar- clay's hypothesis. Fig. 100. Fig. 101. It is the more necessary to insist on the fact that the presystolic murmur is often separated from the following first sound of the heart by a distinct interval, be- cause I believe that this fact has had much to do with the impression that so long prevailed as to the real rhythm of such murmurs. The old view was that the murmur caused by mitral obstruction should be diastolic in rhythm ; and with the single exception of Dr. Markham all writers were agreed that diastolic apex murmurs were very rare. Evidently, therefore, those observers mistook for sys- tolic the murmurs which they heard : and collateral evidence of this is further af- forded by the fact that they described as systolic the fr^missement which wre know to go with the murmur. Nor did the mistake end here. I have shown in my paper that the real first sound of the heart at the apex was mistaken for the second sound, which it resembles so closely in character. It might appear needless to discuss the errors of a bygone period. But a little experience in clinical teaching shows that these very errors are still committed by every student, who has not had his attention specially drawn to them. And it appears to me that some of the most recent German writers have not yet extricated themselves from the same pitfail. Dr. P. Niemeyer, of Mag- deburg, in an elaborate work on " Per- cussion and Auscultation," published in 1870, gives as diagnostic of mitral stenosis "aloud long systolic apex murmur and strong frimissement cataire; in rare cases, also, a short diastolic murmur." But Traube, Felix von Niemeyer (of Tiibin- gen), and Friederich, describe the direct mitral murmur as presystolic. I have already remarked that presys- tolic murmurs are often of long duration, and thus commence very soon after the second sound has completed the previous cardiac movement. It must be added that when the heart-sounds are traced downwards from the base, these murmurs have sometimes an apparent relation to Cardiographic tracings, the second sound, which is very apt to mislead the student, and which I cannot altogether explain. At the base, the second sound is clear and single; lower down, it appears to be reduplicated ; still lower, the presystolic murmur seems to grow out of it. In my paper in the Guy's Hospital Reports I have discussed this subject at some length, and quoted the statements of Hamernyk, Drasche, and Guttmann, in regard to it. Here I must limit myself to a simple statement of the fact. An objection frequently made to the view that these long murmurs are due to a prolonged auricular systole-and indeed to the view that they are due in any way to mitral obstruction-is, that since the pulmonary veins are unprovided with valves, blood would be forced back into them during the whole duration of the auricular systole, and the circulation through the lungs would be brought to a standstill. But it is forgotten that, in cases of mitral stenosis, the tension in the pulmonary vessels is very high-much higher than under normal conditions; whereas the left ventricle is in the condi- tion of an empty flaccid sac, and thus readily receives the blood expelled by the contraction of the auricle. This objec- tion, therefore, appears to have but little weight. &. When developed at the tricuspid ori- fice, and due to stenosis of the correspond- ing valve, a presystolic murmur is heard, according to Dr. Hayden,1 principally over the fifth left costal cartilage, and the fourth intercostal space, close to the ster- num. Dr. Hayden has lately recorded a case of this kind, in which, between the area over which the tricuspid presystolic murmur was audible, and that over which a coexistent mitral presystolic murmur was audible, there was a space in which neither could be distinctly heard. Both lesions, therefore, were diagnosed; and 1 Dublin Journ. of Med. Science, May, 1874. ETIOLOGY. 729 after death the right auriculo-ventricular orifice would admit only the point of the middle finger ; and the left one was smaller still. The tricuspid murmur was even harsher in quality than the mitral one, and began earlier in the ventricular dias- tole. As far back as 1864, Dr. Haldane1 related a similar case, in which the tri- cuspid orifice was found after death to admit only the point of the forefinger. But it must be added that a mitral pre- systolic murmur was at the same time audible ; and the mitral was in fact much the narrower of the two valves. Indeed, although tricuspid stenosis in moderate degree is common enough when mitral stenosis is considerable or extreme, I am not aware that it is ever clinically met with apart from such an association.2 II. A systolic (ventricular-systolic) murmur may have various origins. As we shall presently see, it has not always anything to do with the valves. And when it is due to valvular disease or im- perfection, it may be formed at any one of the orifices into either ventricle; namely, either the mitral, the aortic, the tricus- pid, or the pulmonary. Evidently a ini- tial or tricuspid systolic murmur must be due to regurgitation: an aortic or pul- monary systolic murmur must be obstruc- tive or direct. These four varieties of systolic murmurs may be in part distin- guished by their seat. a. A mitral systolic murmur is loudest at or near the heart's apex ; that is, if the left ventricle be of normal size, about the fifth costal cartilage, and a little internal to the nipple ; if the heart be enlarged, further downwards and outwards. It is not heard over the base of the heart, nor near the ensiform cartilage ; or, if it can be heard there, it is much less loud than at the heart's apex. It can very gener- ally be traced along the left ribs (or, to use a common expression, into the axilla), and is audible at the angle of the left scapula. The question will hereafter be discussed whether it is not invariably heard in these positions when of sufficient intensity. b. An aortic systolic murmur is most plainly heard in the second right inter- space, and is traceable over the ascending [Fig. 102. (Gairdner.)I arch, that is, towards the inner end of the right clavicle; and often also along the arteries of the neck, or even of other parts of the body. c. A tricuspid systolic murmur is heard over the ensiform cartilage, and sometimes to the right of it. It is also (according to Gairdner and Sutton1) heard over the surface of the right ventricle ; that is to say, a little to the left of the sternum ; but it "is little audible above the level of the third rib." I should myself have fixed its upper limit at a much lower point. In some rare cases it is very loud, and may then be heard over a wide area ; but most commonly it is a faintly audible bruit; and I think it is then generally dis- coverable at one spot only. Indeed this appears a principal reason for its presence being often overlooked. d. A pulmonary systolic murmur is loudest about the third left costal car- tilage, and is transmitted upwards and to the left, towards the middle or inner end of the left clavicle. The clinical significance of these four murmurs varies widely in different cases. They must, therefore, be discussed sepa- 1 Ed. Med. Journ., vol. x. 1864, p. 271. 2 An exception must be made for a very remarkable case which occurred to Dr. Gaird- ner, and in which a rounded tumor projected into the interior of the right auricle, in such a way that it formed a kind of ball-valve to the tricuspid orifice. In that case a tricuspid presystolic murmur was heard several years (I think, ten years) before death by Dr. Gairdner, who published his diagnosis in his work on Clinical Medicine. I am not aware that he has yet placed the result of the post- mortem examination formally on record. I saw the preparation of the heart, with the tumor, at the meeting of the British Medical Association in 1873. One remarkable feature about the specimen was that there was no marked hypertrophy of the right auricle. This certainly throws some doubt on the opinion which I have expressed in a note to p. 381. 1 London Hosp. Reports, iv. 1867-68, p. 288. 730 DISEASES OF THE VALVES OF THE HEART. rately ; and it will be convenient to take the two basic murmurs first. As we have seen, the pulmonary valves are scarcely liable to any disease beyond congenital malformation. In practice, therefore, a pulmonary systolic murmur, if due to change in the valves, almost always indicates a congenital defect, and needs no further discussion here. An aortic systolic murmur, on the other hand, is frequently caused by acquired stenosis of the orifice in question. But, as has already been stated, such stenosis is (far more constantly than is generally sup- posed) accompanied by regurgitation ; and the systolic murmur, therefore, is fol- lowed by one which is diastolic. A systolic murmur, however, audible at the base, and traceable along the aorta, is by no means limited to cases in which there is actual stenosis. Formerly it was held that any roughening of the orifice, or of its valves, or even of the lining membrane of the vessel, would suffice to generate it. But even then it was recog- nized that such a murmur was frequently heard under various conditions, when after death no morbid change in any of these parts was discoverable. This led to the theory that the murmur was due to an altered state of blood ; at first, that an anaemic state only could produce it; but afterwards, that various changes in the composition of the blood might gen- erate it. I have already, in discussing the physical theory of murmurs, men- tioned the ingenious explanation given by Chauveau of some of the more striking of these anaemic murmurs, as they have been called. This explanation, indeed, hardly covers the whole range of the bruits that have been regarded as haemic, in the wider sense of the term. And it must be admitted that the precise signifi- cance of many basic murmurs has still to be determined. It is important to note that many undoubtedly anaemic murmurs appear to be seated rather in the pulmo- nary artery than in the aorta; and that they are sometimes of a harsh quality, such as might a priori have been sup- posed to belong rather to murmurs due to some very definite organic cause. It must be added that the so-called haemic murmurs are believed to arise in many acute diseases, including not only fevers, but also those affections in which endocarditis is apt to occur, as, for in- stance, acute rheumatism. In this dis- ease there is a further ground for uncer- tainty as to the cause of a basic murmur, in the fact that a similar sound may prob- ably be caused by the presence of lymph in small quantity outside the heart, round the bases of the great vessels. In this connection I must not omit to mention the fact that in children (even when in good health) a murmur over the pulmonary valves may be generated by the pressure of the stethoscope, as is shown by the fact that it disappears when the instrument is lightly applied. It is said that a similar murmur has some- times been observed even in adults, when the chest-walls are thin and yielding. And consolidation of the anterior edge of the left lung appears sometimes to cause pressure on the trunk of the pulmonary artery, and consequently a systolic mur- mur. Yet another suggestion with re- gard to these basic pulmonary murmurs has recently been made by Quincke; and Dr. Balfour1 has adopted it. It is that they sometimes depend upon the edge of the left lung being retracted, in conse- quence of which the heart, during its sys- tole, compresses the pulmonary artery against the parietes of the thorax, instead of merely pushing aside this edge of the lung. In support of this it is asserted that the murmur disappears when the diminution of the cardiac dulness shows that the lung has recovered its normal dimensions. Dr. Balfour even relates a case in which the murmur ceased when- ever the patient inspired deeply and held his breath. But I must confess that I see little probability in this explanation. This is perhaps the most convenient place for noticing the suggestion of an- other German writer (Naunyn), which is also quoted with approval by Dr. Bal- four ; namely, that the systolic murmur of mitral regurgitation is sometimes heard an inch or two to the left of the sternum, between the second and third ribs. The seat of such a murmur is supposed to be in the appendix of the left auricle. I must confess that when I read Naunyn's paper on the subject I thought there must be some mistake : and this suspicion is not removed by Dr. Balfour's remarks on the subject, for I find him saying that this remarkable modification of the mitral regurgitant murmur is almost invariably present when the insufficiency is depend- ent upon anaemia and chlorosis ! Passing on to consider the clinical sig- nificance of apical systolic murmurs, we may take first that which is audible near the ensiform cartilage, and which is re- ferred to the tricuspid valve ; and of this murmur the interpretation is seldom dif- ficult. According to universal belief, it it always due to regurgitation through the tricuspid orifice. In some cases this is the result of primary disease of the valve itself, which (as we "shall see further on) is occasionally affected with an acute ulcerative change. In such cases a bruit would doubtless be heard by any physi- cian sufficiently acute to search for it. Most commonly, however, there is no actual change in the valve itself; its seg- 1 Med. Times and Gaz., 1874, ii. p. 556. ETIOLOGY. 731 ments are kept apart by the dilatation and distension of the right ventricle, while at the same time its orifice is greatly widened. The distension of the ventricle may re- sult either from disease of the valves on the left side of the heart, or from some chronic affection of the lungs, such as emphysema or fibroid disease. The cases in which I have heard the loudest tricus- pid regurgitant murmurs have been those in which there was cirrhosis of one lung. Two good examples of this are recorded in Dr. Bastian's table in the second vol- ume of this work (cases vi. and xiii.). I well remember the second of these cases, which occurred in the practice of the late Dr. Addison, when I was his clinical clerk. The murmur was so loud that it was heard over the heart's apex, as well as over the ensiform cartilage ; and Dr. Addison, although repeatedly pressed upon the point, would not admit that the case was other than one of primary mitral regurgitation. Indeed, as Dr. Wilks has pointed out, cases of cirrhosis of the lung are often so like those of primary heart disease in their general aspect and symp- toms as to be mistaken for examples of such disease. There might, indeed, well be the same uncertainty about the theoretical signifi- cance of tricuspid, that we shall see to prevail in regard to the corresponding mitral, murmurs. But in practice such doubts have not arisen, since tricuspid systolic murmurs are not very often heard, and they are perhaps never heard unless those conditions of obstructed pulmonary circulation are present which most physi- ologists regard as readily capable of in- ducing regurgitation through the orifice in question. Physicians, therefore, have been more disposed to admit the occur- rence of regurgitation when murmur is absent than to doubt its existence when murmur is present. It is very different with those systolic murmurs which are audible at the apex of the heart, and which (if of valvular origin at all) must be referred to the mitral orifice. They are perhaps the commonest of all murmurs, and their significance is the most uncertain. There are, in the first place, certain sounds which an inexperienced auscultator may easily mistake for endocardial mur- murs, but which really arise not in the heart, but in that little flap or tongue-like process of the lung which commonly pro- jects forwards over the apex of the heart, just below the seat of its visible impulse. The contraction of the ventricle, altering the form of the heart, causes a movement of air into or out1 of this portion of the lung, and thus produces a murmur which, though of respiratory origin, is distinctly systolic in rhythm. " The sound in ques- tion is generally soft and blowing ; but I have several times known it to be of dis- tinctly musical quality. Its most import- ant peculiarity is that it is not constant, but accompanies only those beats of the heart which occur at a particular period of the respiratory act, this period being generally that of inspiration. Thus, when the patient breathes out, the first sound may be quite natural; but when he draws in his breath, a systolic murmur may be audible, which acquires its maximum in- tensity when the cardiac beat happens to coincide with the acme of the inspiratory effort. When the patient is made to hold his breath, the murmur in question is often, but not always, suppressed for the time. A little care, however, excludes this source of fallacy. If the murmur be heard uniformly with every ventricular systole without exception, we may conclude that it arises within the heart itself.1 And the same conclusion may also be arrived at, even when the murmur fails to accompany certain beats, provided that its absenoe depends not upon any relation to the res- piratory rhythm, but upon the circum- stance that the corresponding heart-beats are feeble and imperfect. IIow, then, is such a systolic apex murmur produced ? Now, if after death some of the tendin- ous cords of the mitral valve be found softened and ulcerated through by disease -or if the edge of the valve have become turned inwards towards the auricle-or even if the orifice be so thick and hard that it obviously must have remained patulous : if any one of these conditions should be present, we may be sure that regurgitation occurred during life, and we have good grounds for inferring that any systolic apex murmur that may have been audible was due to regurgitation. The conditions just mentioned are, however, comparatively seldom met with. But it is to be observed, that, if we ex- clude these conditions, we can never with certainty determine, when we are examin- ing the heart after death, whether the mitral valve was or was not competent. We have no means of testing satisfactorily the action of the valve. We may, indeed, Review for July, 1873), a sound within the lung can be generated only by the entrance of air into that portion of lung, and not by its exit. We must therefore suppose that when the heart assumes a globular form dur- ing its systole, air is sucked into the flap of lung in question. > Evidence is, I think, wanting to show that a white patch on the serous surface of the apex, or any like condition, can generate the murmur in question. 1 According to certain modern views on the theory of the respiratory murmur (of which a full account is to be found in the Med.-Chir. 732 DISEASES OF THE VALVES OF THE HEART. tie the base of the aorta ; and having cut open the apex of the left ventricle, may hold the heart upside down, and pour water into the cavity to see whether it runs out. But in such an experiment the conditions are very different from those which obtained during life. Then, the base of the muscular columns was moved towards the orifice by the ventricular con- traction : while those columns at the same time underwent shortening, so as to keep the tendinous cords stretched to the proper degree. Now, ventricular wall and fieshy columns are alike relaxed. Errors may thus arise in either direction. When the muscular columns are converted into non- contractile fibrous tissue, the valve may have been very imperfect in the living body, and yet may close well enough when tested after death. Conversely, when the ventricle is dilated, without the tendinous chordae being increased in length, it may happen that the valve allows reflux to oc- cur after death, although it had before been efficient. This deficiency in the proof of mitral regurgitation, when a case has reached the dead-house, would be of but little con- sequence, if the orifice or its valve were constantly found to be obviously diseased in those cases in which a systolic apex murmur had been heard during life. But all who have worked at the subject know that this is not so. To quote the words of Dr. Bristowe,1 "In a large proportion" of such cases "the mitral valve and the orifice it protects are found to present a perfectly healthy appearance. " Now Dr. Bristowe has proposed a very ingenious solution of the difficulty. lie believes that valvular incompetence exists when- ever a systolic apex murmur is heard; and in the case now under consideration he attributes this incompetence to " dis- proportion between the size of the ven- tricular cavities and the length of the chordae tendinere and musculi papillares. " He has shown in fact that while the for- mer are found after death to be dilated, the latter are often small and seem to be on the stretch. But these observations are exposed to the full force of the objec- tions already made to the post-mortem evidence of mitral regurgitation. The appearance of the mitral cords and col- umns in a dilated ventricle relaxed by death can surely afford no proof that these parts were too short to allow the valve to close, when the ventricle itself was short- ened by its own systole. Dr. Bristowe regards it "as an axiom, that the existence of a systolic murmur at the apex of the heart is a sure indica- tion of incompetence of one or other of the auriculo-ventricular valves." And he deems it unnecessary to offer any evi- dence in support of this position, beyond the fact that in all the cases recorded in his paper the general symptoms and the condition of internal organs (lungs, liver, spleen, &c.) were such as are found in this form of disease. Subsequent writ- ers, however, have dealt with this ques- tion in a different way. Both Dr. Austin Flint1 and Dr. Andrew2 have expressed the opinion that the murmur by no means necessarily indicates such regurgitation : according to the latter observer, indeed, regurgitation is absent in 34 per cent, of the cases in which the murmur is audible. These authorities believe that there are two criteria which may be applied to the determination of the fact, that in a par- ticular case a systolic apex murmur is really due to mitral regurgitation. The criteria are : 1. That the murmur should be audible in the left side of the back, about the inferior angle of the scapula; 2. That the pulmonary second sound should be intensified. 1. A good illustration of the fact that the murmur caused by mitral regurgita- tion is heard in the left side of the back is afforded by cases in which the tendinous cords are ruptured or ulcerated through. It has been so in the cases which I have seen, and I have not met with any re- corded instance to the contrary. But in such cases the murmur is generally loud, and the amount of regurgitation probably large. I am not sure that when the mur- mur is feeble one can fairly expect that it should always be carried backwards : for one must remember that, though the di- rection of the blood-stream is towards the vertebral column, the auricle is not itself in any close relation with the part of the chest-wall at which one looks for the mur- mur. Consequently, although I am pre- pared to admit that whenever a systolic murmur is heard in the back, it is caused by mitral regurgitation, I cannot regard the fact that a feeble murmur is not heard in that position as conclusive against its being so caused. 2. Intensification of the pulmonary sec- ond sound (that is, of the second sound heard at the second left, as compared with the second right costal cartilage3) is undoubtedly present in many of the most marked cases of mitral regurgitant dis- 1 Am. Med. Times, 1862. Quoted in Braith- waite's Retrospect, xlvii. 1863, p. 69. 2 St. Bartholomew's Hospital Reports, 1865, i. p. 13. 3 Dr. Andrew has shown that it is neces- sary, in instituting this comparison, to re- member that the same difference may be due to enfeeblement of the aortic second sound, while the pulmonary second sound is natural; and also that an emphysematous lung over- lapping the heart on one side may modify the intensity of the sound. 1 Med.-Chir. Review, 1861, July, p. 215. ETIOLOGY. 733 ease. Its cause is evidently the increased tension of the blood within the pulmonary system of vessels. But this (as I shall endeavor to show further on) may arise from any cause which prevents the left side of the heart from emptying itself. I cannot see, therefore, how intensifica- tion of the second sound can be indicative of regurgitation through the mitral ori- fice, rather than of other conditions which will then be mentioned. Moreover, I be- lieve that intensification of the pulmonary second sound requires, as a condition of its occurrence, that the right ventricle should be powerful, and that the tricuspid valve should be efficient. I think I have observed that this sign is present chiefly in the early stages of mitral regurgitant disease, before it has begun to tell upon more distant parts. My own views with regard to the inter- pretation of systolic apex murmurs may therefore be summed up as follows :- 1. If such a murmur be audible in the back, it indicates mitral regurgitation. 2. If such a murmur be heard only at the heart's apex, we are unable at the present time to pronounce any positive opinion as to its cause. Should the mur- mur be loud, we may probably conclude that it is not due to mitral regurgitation: since really regurgitant murmurs, when loud, are, perhaps, always audible in the back, though for slight murmurs the same statement may not be tenable. The question still remains, How is a systolic apex-murmur produced when it is not caused by mitral regurgitation ? I have already (vide p. 724) suggested that it may be due simply to dilatation of the left ventricle, as was long ago supposed by many of the earlier writers on auscul- tation. III. A "diastolic" murmur, as has been stated, accompanies the elastic re- coil of the aorta and pulmonary artery. It almost invariably indicates regurgita- tion, through the space that should be closed by one or other set of sigmoid valves into the ventricle ; and in the im- mense majority of cases the valves affected are those of the aorta. The quality of the diastolic murmur of aortic regurgitation varies greatly in dif- ferent cases ; it may be soft and blowing, rough, and attended with thrill, or even musical. It may be so loud as to be au- dible at some little distance from the pa- tient ; or so slight as to require the utmost vigilance for its defection. The seat of this murmur is somewhat variable. As a rule, it is very plainly audible over the base of the heart; its point of maximum intensity is generally stated to be at the sternal end of the sec- ond right costal cartilage, or in the second right interspace ; and it is carried down- wards along the length of the sternum (apparently in consequence of the fact that osseous substance is a good conduc- tor of sound), so that it may often be loudly heard near the ensiform cartilage. This fact has been especially insisted on by Dr. Gairdner.1 Again, this murmur is frequently plainly audible at the heart's apex, and sometimes it is louder there [Fig. 103. (Gairdner.)] than at the base. Lastly, it may be con- ducted along the arteries, sometimes, to a surprising distance: according to Dr. Gee, as far as the radial arteries. In discussing the theory of murmurs in general, I have pointed out the conditions upon which some of the varieties in the seat of this bruit appear to depend (see p. 724). If the views there stated are correct, the fact that in a particular case an aortic diastolic murmur is transmitted upwards along the aorta may be interpreted as in- dicating that tbe valves are so free from serious damage that, although they do not meet, they nevertheless project inwards into the aorta to a greater or less extent; while in those cases in which the murmur is solely carried downwards it may be concluded that the valves are more com- pletely destroyed. A further refinement in regard to dias- tolic murmurs has lately been suggested by Dr. Balthazar Foster^ of Birmingham. He believes that when such a murmur is heard at the apex of the heart it is due to incompetency of the left aortic segment, 1 Clinical Medicine, p. 587. 2 Med. Tinies and Gazette, 1873, ii. pp. 658, 686. 734 DISEASES OF THE VALVES OF THE HEART. so that the regurgitant blood-stream falls upon the mitral curtain and is carried downwards; and, on the other hand, that a similar murmur propagated towards the ensiform cartilage indicates defect in the right and posterior segments, by which the blood is thrown upon the sep- tum. lie alludes to cases corroborative of his views, to which he further attaches considerable importance as regards prog- nosis. lie thinks that incompetency of an aortic segment must specially interfere with the flow of blood into the coronary artery contained within the corresponding sinus (which flow he, in common with many other authorities, believes to occur during the recoil of the aQrta), and so must tend to impair the nutrition of the heart. Now the left aortic segment has no coronary artery in relation with it. Dr. Foster therefore infers that, cseteris paribus, life is more likely to be prolonged when this segment is affected, or (in other words) when the murmur is audible at the apex. But my belief has hitherto been that the murmur is propagated in this direction especially when the regurgitant stream is large : and if so, one would sup- pose that the prognosis must be particu- larly unfavorable. I think that the point is one which needs further observations. It has been stated that in the im- mense majority of cases a regurgitant murmur has its seat at the aortic orifice. In fact a pulmonary regurgitant bruit is so rare as scarcely to need considera- tion. In 1865 Dr. Wilks exhibited to the Pathological Society1 a specimen of dis- ease of the valves in question, in which a double bruit had been heard during life: and one or two other cases are re- But the great rarity of such disease led to its rejection as a diagnosis. Indeed, one can hardly expect in future to attain to greater accuracy: for (as we shall pre- sently see) the pulse may fail to be char- acteristic of aortic regurgitation even when this disease exists; and the ten- dency of aortic diastolic murmurs to be transmitted downwards along the sternum must always prevent a pulmonary regur- gitant murmur from being identified by its being heard over the right ventricle. Still, acquired disease of the pulmonary valves is so exceedingly rare (and in con- genital disease I do not know that marked regurgitation ever occurs), that one hardly needs to make a reservation on account of it in attributing diastolic murmur to aortic regurgitation. The real necessity for reservation lies in the fact that aortic aneurism sometimes causes such a mur- mur, probably because it receives blood during the elastic recoil of the aorta, as well as during the ventricular systole. It is only when an aneurism arises from the commencement of the arch that its mur- mur could be mistaken for one of regurgi- tation through the valves : and even then the former would perhaps never be trans- mitted to the heart's apex, as is so generally the case with the latter. Very frequently, indeed, the two conditions are combined. Another infinitely rare condition, in which a diastolic murmur, not due to re- gurgitation through the aortic valves may be heard at the base of the heart, is that in which the aorta communicates with the pulmonary artery, either by a patent ductus arteriosus, or through an aneuris- mal sac. Of the former affection I have recorded a remarkable instance.' The murmur (which was in part musical) was audible at the second left costal cartilage, and was transmitted to the left along this cartilage, but not downwards along the sternum. It was not everywhere con- tinuous with the second sound. It had a wavy character, quite unlike anything that I had ever heard before. It was clearly distinguished (during the patient's lifetime) from an aortic regurgitant mur- mur ; and it was thought not unlikely to be due to an opening from the aorta into the pulmonary artery. A case in which an aortic aneurism was correctly diagnosed to open into the pulmonary artery has been related by Dr. Wade,2 of Birmingham. The diastolic murmur was prolonged, and of a hissing character with distinct purring tremor. It was audible over the cartilage of the fourth left rib, and in the neck, back, and upper part of the chest. With these exceptions, a diastolic mur- [Fig. 104. Auricular systolic and ventricular systolic murmurs combined. (Gairdner.)] corded in medical literature. In Dr. Wilks's case the question of disease of the pulmonary artery was considered during the patient's life, for the pulse gave no indication of aortic regurgitation, and the bruit became less marked towards the right, and in the course of the aorta, but was equally distinct, or even somewhat more intense, towards the left, clavicle. 1 Guy's Hospital Reports, 1872-73, series iii. vol. xviii. p. 23. 2 Med.-Chir. Trans, vol. xliv. 1 Path. Trans, xvi. p. 74. ETIOLOGY. 735 mur (as I believe) invariably indicates regurgitation through the aortic orifice into the left ventricle. It may be expected that something should be said as to the not infrequent coexistence of two or more of these mur- murs in the same case. I have already remarked on the rarity of systolic mur- murs indicating actual obstruction of the aortic orifice, unless a diastolic murmur be also present, and discoverable on care- ful examination. It may be added that in disease of the aortic valves the ten- dency is for regurgitation to follow obstruc- tion. In the case of the mitral valves the opposite is observed. Commencing dis- ease appears to produce a regurgitant murmur: and it is only as the orifice be- comes more and more contracted that an obstructive murmur is heard. There is this further peculiarity, that when mitral stenosis causes a marked presystolic mur- mur, it rarely happens that any systolic murmur is at the same time audible. I have scarcely ever heard a systolic mur- mur in association with the rough grating bruit, attended with thrill, that is so characteristic of the more extreme degree of constriction of the mitral valve. A more or less distinctly double murmur at the apex is not, indeed, very uncommon : but in this case both portions of the mur- [Fig. 105. mur are rather of a soft and blowing quality: and the inference probably is that the stenosis is moderate in degree. AX' ith regard to the coexistence of mur- murs developed at different orifices I have nothing particular to say. Their deter- mination must be based on the principles which regulate the diagnosis of each mur- mur separately : guided, of course, by the known liability of particular valves to undergo simultaneous or consecutive changes. The other effects of disease of the car- diac valves-those which affect the pa- tient's health, and are consequently com- monly called the symptoms of such dis- ease-are divisible into three distinct classes. I. We may take first a class of effects, which are of great importance, but which have only recently attracted notice, and probably do not yet receive a due share of attention. The valves of the heart are bathed on all sides by the circulating fluid. When they are inflamed or ulcer- ated, the blood flows directly over the diseased surface. When any portion of their substance, or of the products of in- flammation, becomes disintegrated, the detached fragments necessarily pass into its stream. This is so obvious, that we may well be surprised to find that no one had recognized it until Dr. Kirkes pointed it out in the year 1852.1 And as he showed, the phenomena attendant on this Ventricular-Systolic and Ventricular-Diastolic murmurs combined. (Gairdner.)] process are divisible into two distinct groups:- (a.) Embolism.-In the first place, a mass of some size may be detached, which, passing into the arterial system, sooner or later reaches a vessel which it cannot traverse, and which it consequently plugs. The result is that the circulation is en- tirely arrested in the region supplied by the artery, unless indeed blood from col- lateral arteries enters the obstructed ves- sel beyond the seat of the obstruction. It might have been expected that the region in question would become anaemic. Re- cent observations, however, have shown that such is not the case. Prevost and Cotard,1 and afterwards Lefeuvre,2 have studied this question experimentally. They injected foreign bodies (especially the seeds of tobacco) upwards into the abdominal aorta of dogs, and exposed the kidneys and spleen by opening the abdo- men, so as to make apparent the earliest effects of obstruction of the arteries of those viscera. They found that the re- gions supplied by the blocked arteries in- stantly become of a dark purple color, and in the spleen were distinctly raised above the level of the rest of the region. This 1 Gaz. Med. 1866, p. 202. 2 Etude physiologique et pathologique sur les Infarctus Visc^raux, Thfcse de Paris, 1867. A review of these observations will be found in the Med.-Chir. Review for October, 1871, p. 368. 1 Med.-Chir. Trans, xxxv. p. 281. 736 DISEASES OF THE VALVES OF THE HEART. state of engorgement is believed to be due to a paralysis of the muscular coat of the vessels. They become unable to resist the pressure of the blood in the veins, which consequently flows back into the capillaries and arteries, and distends them up to the point of obstruction. Hemor- rhage then takes place. After a time the effused blood and the elements of the tis- sue undergo fatty degeneration : and the affected part acquires a characteristic yel- low color. This always extends- to the surface of the organ, and penetrates more or less deeply towards its interior in the Fig. 106. Auricular-Systolic, Ventricular-Systolic and Ventricular-Diastolic murmurs combined. (Gairdner.)] form of a wedge or cone, which is gener- ally surrounded by a red halo of conges- tion. Still later, absorption takes place : and in the end nothing is left beyond a deep fissure or puckering. It must be added that sometimes, instead of the whole mass undergoing fatty degeneration and conversion into the peculiar yellow matter, a part of it sloughs: in other cases it breaks down into pus. The changes just described do not occur in all organs alike. They are especially well marked in the spleen and kidneys.1 The reason appears to be that the branches of the splenic and renal arteries anastomose but little or (in the case of the splenic artery) not at all. In the liver, on the other hand, a true infarctus is, per- haps, never met with, apparently because its lobules do not derive their supply of blood entirely from a single source. The mesenteric arteries occasionally become the seat of embola. This occurred in one of Lefeuvre's experiments with tobacco seeds. The affected part became first pale and afterwards of a livid purple color. Embolism of a mesenteric artery has also sometimes been observed as a result of disease in the human subject. The cere- bral arteries are very liable to embolism ; this is believed to occur more frequently in the left middle cerebral than in any other artery, apparently because its course in some way favors the entrance of a de- tached mass. In the brain, the result of arterial plugging is generally white soft- ening of the corresponding part of the brain; but sometimes a firm yellow in- farctus is produced. When embolism oc- curs in one of the arteries of the extremi- ties, the tendency is for the limb beyond the seat of obstruction to mortify. The gangrene is not then always of the dry variety, as was formerly taught. It may be moist, and attended with the formation of bullse. This is doubtless preceded by an hypersemia, like that which we have seen to follow plugging of an artery in the spleen or kidneys, except that as the veins of the limbs are provided with valves, the blood probably comes from the collateral arteries of the limb. In the arteries of the extremities, and indeed in all arteries, embola are especially apt to be arrested at those points where the vessel is divid- ing, or where a large branch is given off, so that the calibre of the channel is sud- denly diminished. Thus in the upper limb, they are most commonly found in the axillary artery, and at the bifurcation of the brachial artery : in the lower limb, at the points of division of the common femoral and the popliteal arteries respec- tively. The left lower limb is decidedly more subject to embolism than the right: and by Virchow1 this is atttibuted to the fact that the left common iliac artery comes from the abdominal aorta in a more direct line than the right. The peculiar wedge-shaped masses in the abdominal viscera appear to have been described in- dependently by Hodgkin,2 Cruveilhier, and Rokitansky. Their association with heart-disease was first noticed by the last- named observer, and has been admitted by all modern writers on morbid anatomy. It is, however, only within the last few years that they have been regarded as possessing any clinical interest, or that their formation has been supposed to be attended with any symptoms affecting the health of the patient. Following Kirkes, 1 According to Sperling (Inaug. Diss., Ber- lin, 1872; London Med. Record, Jan. 1873), the kidney is more frequently the seat of em- bolism than the spleen, in the proportion of 75 to 51. 1 Gresammelte Abhandlungen, p. 444. 2 Med.-Chir. Trans, xxvi. ETIOLOGY. 737 Virchow1 is the writer to whom credit is especially due for having drawn attention to this subject: and recently several French memoirs and papers have been written on it, in which the affection is described as a special disease, under the title of " Ulcerative Endocarditis." The clinical features observed in these cases are of two kinds. In the first place, there are the direct efforts of intercepted blood-supply to the part served by the obstructed vessel. Thus, as we have seen, a limb may mortify as the result of embolism of its main artery. Many of the cases of spontaneous gangrene in young subjects that come under the care of the surgeon are of this kind ; and, with the stethoscope, the existence of disease of the valves of the heart may often be recognized without difficulty. It may be worth while to note that the embolism in these cases is not always derived from the diseased valve itself; sometimes it comes from the auricle or ventricle, having been one of the little rounded ante-mortem clots which are so apt to form in the heart's chambers behind any obstruction.2 Embolism of the cerebral arteries, again, may give rise to a great variety of symptoms, according as one or another part of the brain is deprived of its due supply of blood. The most frequent effect is the production of right hemiplegia, with or without aphasia. This corresponds with the fact that the left middle cerebral artery is especially apt to become plugged. Embolism of the retinal arteries leads to changes which can be studied with the ophthalmoscope. It has already been stated that in the viscera, instead of the usual yellow wedge- shaped masses or infarctus being formed, suppuration, oreven sloughing, sometimes occurs in the regions supplied by an artery that has become the seat of embolism. It is perhaps doubtful whether these changes ever in themselves produce any appreci- able influence on the patient's health, or on the symptoms from which he suffers. But they may set up a peritonitis, and this will usually be attended with a great aggravation of his complaint, and even with danger to his life ; and embolism of a mesenteric artery may cause severe en- teritis, which may be quite capable of clinical recognition. (b.) Infection.-But in almost all these cases the effects of the occurrence of em- bolism in particular arteries are compli- cated with, and probably overpowered by, those which depend upon a general contamination of the blood, as it passes over the surface of the diseased valve. This was ^clearly pointed out by Dr. Kirkes, in his classical paper already more than once referred to; and of late years many observers have worked at the subject, in the hope of explaining it more fully. So severe and rapidly fatal are some of these cases, that Virchow has given them the designation of Endocarditis Maligna. A principal symptom in these cases is the presence of fever. The temperature is raised two or three degrees, or more, above the normal standard. Dr. Good- hart1 mentions one case in which it was several times noted at 104° ; and in a case which I recently examined it reached 105'8°. Not rarely there are repeated at- tacks of shivering : indeed, the illness is often ushered in by a sudden rigor. The pulse is quickened ; the tongue is often dry. Extreme prostration, delirium, and somnolence, are occasionally present. Ac- cording to Dr. Wilks, articular pains are often complained of. Vomiting and diar- rhoea are common. The spleen is greatly enlarged, and is sometimes tender on pressure. The skin has an icteroid tinge, and there may even be jaundice, of which Lancereaux2 has recorded several exam- ples. Petechise may be present, or even distinct purpuric blotches.3 Ecchymotic spots may also be found on the surface of the pleura and pericardium, and on the mucous membranes lining the larynx, stomach, intestines, and urinary bladder. The liver after death is found to be pale, supple, and flabby. The tissue of the spleen (which is many times larger than natural) is soft and pulpy. When a patient is known to be suffering from disease of the cardiac valves, there is but little difficulty in assigning to their true cause the symptoms just enumerated. By carefully examining the heart several times at short intervals, one may be able to detect such variations in the physical signs as may demonstrate the fact that acute changes in the valves are going on. Charcot and Vulpian4 mention one case in which the most marked signs of aortic insufficiency became prominently devel- oped within a week. But in many instances there is nothing to draw the physician's attention to the state of the valves; and the real nature of the case may then be easily overlooked. The valves may previously have been quite healthy. And since palpitation, prsecordial pain, and oppression of the breathing may all be absent, there may 1 Gesammelte Abhandlungen, pp. 636-729. 2 Such, an ante-mortem clot may, when a valve is stenosed, be the direct cause of sud- den death: getting washed into the blood- current, it may completely occlude the nar- rowed orifice. See a case recorded by Dr. Van der Byl, Path. Trans, ix. p. 91. vol. n.-47 1 Guy's Hosp. Reports, xv. p. 415 2 Gaz. Med., 1862, p. 662. 3 Path. Trans, xxi. p. 109. 4 Gaz. Med. 1862, p. 388. 738 DISEASES OF THE VALVES OF THE HEART. be nothing to suggest the necessity of ex- amining the heart. The case is thus very likely to be mistaken for one of enteric fever, or, if there be much shivering, of idiopathic pyaemia, or even ague; or again, if there be marked jaundice, for one of pylephlebitis. The relation to purulent infection has been especially in- sisted on by Dr. Wilks, and he has pro- posed to designate the affection an " ar- terial pyaemia." In the previous paragraphs it has been taken for granted that the diseased valves are those on the left side of the heart, and that the phenomena of embolism or of in- fection therefore show themselves in the course of the distribution of the systemic arteries. However, when the tricuspid valve is diseased, or the pulmonary valves, precisely similar effects show themselves ; but, of course, within the lungs. A strik- ing case of this kind has been recorded by Charcot and Vulpian,1 which was diag- nosed during life. One flap of the tricus- pid valve was softened and perforated, and presented numerous vegetations. The lungs contained scattered abscesses. Other instances have been related by Dr. Kirkes and Dr. Moxon.2 Dr. Moxon's case occurred in a woman, within a month after her delivery. The precise nature of the process of Infection in the cases under consideration has been much discussed of late years, and even now it has not been fully ascer- tained. In almost his earliest paper on the subject, Virchow related some experi- ments that he had made of injecting dif- ferent substances into the jugular veins of dogs. And he proved that while por- tions of caoutchouc simply produced ob- struction of branches of the pulmonary artery into which they were carried, ani- mal substances (pieces of muscle, fibrin, &c.) set up severe inflammation of the corresponding tracts of hmg tissue, lead- ing to suppuration or even to sloughing. Hence he concluded that the phenomena of infection are not merely of mechanical origin, but must result from some chemical action. The same fact has since been in- sisted on by Peltz3 of Strasburg, who main- tains that solid elements by themselves never carry infection : this is always pro- pagated by septic fluids. Another writer, Panum of Kie4 endeavored to show that the immediate cause of irritant effects is the decomposition, within the bloodvessels, of the masses by which they are plugged. By Lancereaux, again, stress was laid on the opinion that the poisoned state of the blood in these cases is due to the altera- tion and transformation of the connective tissue of the valves themselves, and never to the mere disintegration of fibrinous concretions. These speculations have, however, been almost superseded by observations of a different order. As far back as 1855, Virchow1 found that a small coagulum upon the mitral valve (in a case of ery- sipelatous perimetritis with a diphtheritic inflammation of the large intestine) con- tained a number of small white miliary bodies, which consisted almost entirely of fine closely aggregated granules, em- bedded in a gelatinous substance. These granules were insoluble in potash, acetic acid and hydrochloric acid, but were dis- solved by chloroform, so that he regarded them as probably of a fatty nature. Char- cot and Vulpian2 afterwards insisted on the peculiar micro-chemical relations of the detritus of diseased valves, shown in their power of resisting strong acids and alkalies. But still more recent observa- tions have tended to show that the prop- erties of these minute granules are not due merely to their chemical constitution, and that they are in fact living organisms. Prof. Winge, and Prof. Heiberg,3 of Christiania, appear to have been the first writers to express this view in a decided form : it has since been adopted by no less an authority than Virchow himself. It is proposed by these writers to give to the affection in question the name of My- cosis Endocardii. Winge's case, which occurred in 1869, was that of a man, set. 44, who died with symptoms of blood- poisoning apparently dependent on a suppurating corn. On the aortic valves there were certain grayish masses, the size of peas or beans, which could be easily picked off, leaving the surface slightly uneven and ulcerated. The tri- cuspid valve presented similar masses. With a microscope of moderate power these appeared to consist of a fine net- work of fibrin threads. But under a higher objective these threads were seen to be made up of rod-like or spherical bodies, arranged in chains, and thus re- sembling leptothrix. There were also a number of fine rounded or rod-shaped bodies, some of which were probably bac- teria, others fat granules. Similar bodies were found in the cylindrical plugs in the smaller arteries of the kidney, correspond- ing to infarctus. Heiberg's case was that of a girl, set. 22, who died six or seven weeks after delivery, with symp- toms of blood-poisoning. The mitral valve was perforated by a recent ulcer, * Gaz. M4d. 1862, p. 428. 2 Path. Trans, xxi. p. 107. 3 Trait6 clinique et experimentale des em- holies capillaires. 2^meed. Strasbourg, 1870. 4 Experimentelle Untersuchungen zur Phy- siologie und Pathologic der Embolie, &c., Berlin, 1864. * Op. cit. p. 709. s Gaz. M^d. 1862, p. 385. 8 Virchow's Arch. Ivi. 1872, p. 409. ETIOLOGY. 739 the margins of ■which and the chordae were coated with vegetations. These contained numerous minute granules, ap- parently simple detritus : and in addition, many rod-shaped bodies resembling bac- teria, and a considerable number of rows of granules, of uniform size, arranged in chains of greater or less length, which Heiberg therefore regarded as lepto- thrix. These, and many of the isolated bodies, resisted the action of even boiling caustic potass. Specimens from both these cases were forwarded to Virchow, who confirms the accuracy of the ac- counts given by the Swedish writers, and states that he has no doubt as to the para- sitic nature of the bodies in question. He is not yet prepared, however, to admit the propriety of using the name lepto- thrix for them. Eberth,1 of Zurich, has since recorded another case of the same kind, which differs from those previously referred to, in the fact that there was no evident external source of blood-poison- ing. lie entitles it "Diphtheritic Endo- carditis."2 It occurred in a young man, previously healthy, who died after little more than two days' illness. Two of the aortic valves were ulcerated through, and the disease extended into the muscular substance of the heart, penetrating al- most to the endocardium lining the right auricle. The margins of the affected valves were covered with soft vegetations. These consisted mainly of a finely granu- lar substance: and the individual gran- ules were shining spherical bodies of uni- form size, some of which exhibited slight movements, the majority being motion- less and embedded in a gelatinous material. Neither boiling alcohol nor boiling alkalies affected these granules, beyond making them slightly paler. Tinc- ture of iodine and sulphuric acid gave them a yellow color. It is therefore al- most certain, says Eberth, that they were really spherical bacteria. So far as I am aware, no similar ob- servations have as yet been published in this country. But my colleague, Dr. Goodhart, informs me that he has in three instances detected minute organ- isms in the fungating masses attached to ulcerated valves. In each case he found, besides innumerable spheroids, rod- and dumb-bell-shaped bacteria, as well as some which formed beaded strings. Most of these had feeble oscillatory movements. Vertical sections of the deepest part of the diseased valves showed a cell growth, to a small extent, such as is described at page 708. On this was deposited a hya- line clot in small rounded masses : and upon these, and in the crevices between them, the bacteria clustered. Dr. Good- hart, however, considered that the ap- pearances which he observed were strongly suggestive of the view that the bacteria were derived from the elements of disintegrating blood-clot. The precise scope and bearing of these observations are, as yet, imperfectly un- derstood ; but I think there can be little doubt that they will hereafter be found to play an important part in the explanation of blood-poisoning now under considera- tion. Heiberg, indeed, expressly states that he does not attribute all cases of ulcerative endocarditis to a Mycosis, since he has failed to find any parasitic organ- isms in specimens of this disease pre- served in the Museum of Christiania. And when bacteria are present in the tis- sues of diseased valves, it is as yet quite impossible to say what relation they bear to the processes of embolism and infec- tion to which the disease gives rise. This question is in fact only a part of the much wider one which concerns the relations of these minute organisms to pyaemia, sep- ticaemia, and allied processes. The theory advocated by Eberth1 is that the bacteria originally enter the blood from without, and then become aggregated together into a sticky mass, which adheres to the sur- face of the cardiac valves, when it is brought to them in the stream of the cir- culation. In confirmation of this opinion, he appeals to observations showing that the ante-mortem coagula in the appen- dices of the auricles are likewise often coated with a complete layer of bacteria. The valves and chambers of the heart thus form a kind of halting-place for the microphytes, which multiply, and subse- quently distribute to all the arteries of the body masses of bacteria in the form of embola, which set up suppuration wherever they are deposited. In the ar- teries of the kidneys especially, agglome- rations of this nature have been demon- strated : and also within the glomeruli and the uriniferous tubules of the affected parts of these organs. II. Another series of effects produced by diseases of the cardiac valves consist in the modifications that they tend to in- duce in the circulation of the blood, and 1 Virchow's Arch. Ivii. 1873, p. 228. 2 This designation has also been frequently used by Virchow. It is important for English readers to remember that German writers use the term diphtheritic in a sense very different from that to which we are accustomed in this country, applying it to inflamed structures of which the most superficial layers, infil- trated with inflammatory materials, are gan- grenous. 1 In a large number of recent cases of py- aemia Eberth has constantly found micro- phytes, not only on the surface of the wound, but also in the subjacent tissues, sometimes to a considerable depth. 740 DISEASES OF THE VALVES OF THE HEART. in the consequent morbid changes which arise in the several cavities of the heart, in the bloodvessels, and in distant organs. To these effects we must now turn our attention, and as they are both numerous and varied, it is needful that we should arrange them in as orderly a manner as possible. Each of the cardiac valves may be viewed as separating from one another two of the chambers of the circulatory system, and when any one of the valves is diseased, we may consider that (1) the primary effect of the disease is exerted upon that chamber which lies immedi- ately behind the valve in the order of the circulation, and wdiich w'as protected by the valve when in its normal state. From the chamber in question, again, disturb- ance of the circulation is, or may be, propagated in two directions:-(2) for- wards, or with the blood-stream ; and (3) backwards, or against the blood-stream. The effects of disease of the several valves have, therefore, to be considered under these three heads. A. It will be found convenient that we should begin with diseases of the aortic valves. These, as we have seen, may be of two kinds, obstructive and regurgitant; but in the immense majority of cases ob- struction and regurgitation coexist. (1) The primary effect of diseases of the aortic valves may be said to occur in the left ventricle, Which is of course the chamber that lies behind the valves in the order of the circulation. Now in aortic stenosis or obstruction the blood cannot be forced into the aorta so easily nor so quickly as in health. The ventricle, therefore, tends to be overloaded with blood, and its walls become stretched or dilated ; at the same time it has to exert increased force to propel its contents on- wards ; and it consequently becomes hy- pertrophied. In aortic regurgitation the ventricle may empty itself readily enough during its systole, but in its diastole it not only has to receive the blood flowing on- wards from the auricle, but also that which is poured back into it from the aorta ; it therefore becomes both dilated and hypertrophied. The changes which occur in the left ventricle are thus the same in the two conditions of stenosis and regurgitation respectively. They consti- tute the compensation by which these sev- eral morbid changes are more or less completely prevented from further dis- turbing the circulation. But there is a distinction of some importance, which has not, I think, been noticed by writers on this subject. In aortic stenosis, hyper- trophy of the ventricle is all that is needed to restore the balance ; dilatation is di- rectly injurious, tending to impair the power of the chamber, and to render still more hypertrophy necessary. But, in aortic regurgitation, dilatation is the main requirement, since the ventricle has to accommodate the blood that enters it from both sides during its diastole ; hyper- trophy is needed only secondarily, and because a dilated ventricle has to exert more force than one of normal size, in order to propel its contents onwards. The dilatation and hypertrophy of the left ventricle in cases of aortic disease may be extreme in degree. The heart then acquires a peculiar pointed form, the right ventricle often looking like a mere appen- dage. The organ often weighs between 20 and 30 ozs., and many instances have been observed in which it has been even heavier. In one case which I have my- self examined-that of a young man, set. 26-the heart weighed 48 oz. I am not sure whether this is not the largest heart on record ; the next largest being one weighing 46| oz., which Dr. Bristowe ex- hibited at a meeting of the Pathological Society. These changes, of course, require time for their development; but Dr. Peacock has adduced evidence to show that they may take place more quickly than might have been expected. Valvular affections themselves often arise gradually ; and the compensatory processes are induced pari passu with the disease. On the other hand, when the valves give way or are lacerated suddenly, time may not be al- lowed for the ventricle to become dilated and hypertrophied; and this is probably one of the main reasons why in such cases the fatal termination is often rapid. Again, either obstruction or regurgitation may of course be so extreme as to render compen- sation impossible. Lastly, when perfect compensation has existed for a consider- able time, it may begin to fail; and then further effects arise which will be con- sidered hereafter. It is generally sup- posed that this is due, either to the pro- gressive increase in the valvular changes (with which the compensatory processes are unable to keep pace), or to the occur- rence of fatty degeneration in the hyper- trophied ventricular wall.' 1 Dr. Allbutt has recently given another explanation of loss of compensation, which is certainly of great interest. It was first sug- gested to him by Mr. Busk, who compared the change in question to that which occurs in the arms of file-cutters. These men con- stantly practise rapid flexions of the elbow- joint, and the biceps enlarges greatly. But after a few years the muscle again wastes, and falls far below the normal value. This is so certain a consequence, that the file-cut- ters receive high wages, calculated upon the average duration of an hypertrophied biceps. ("On the Effects of Overwork and Strain upon the Heart and Great Vessels," p. 43, Macmillan and Co., 1872.) ETIOLOGY. 741 (2) The onward effects of disease of the aortic valves consist in changes in the blood current in the aorta and its branches ; in other words, in changes in the arterial pulse. These are not the same in aortic obstruction, as in regurgitant disease ; and the two affections must therefore be con- sidered separately. In aortic stenosis the character of the pulse appears to be but little altered, un- less the obstruction to the blood current is extreme, in which case Walshe says that "the pulse, though regular in force and rhythm, is small, hard, rigid, and concentrated." Dr. Wilks has mentioned to me that in certain cases he has ob- served the number of pulsations of the heart, per minute, to be greatly reduced. In illustration of this fact, I find in the notes of post-mortem examinations at Guy's Hospital two cases recorded by Dr. Wilks himself. One1 is that of a man, set. 68, in whom " two of the aortic valves were adherent and bony; the aperture was reduced to a very narrow chink ; the edge of one valve slightly overlapped the bony margin of the other, and thus no doubt prevented regurgitation. The pulse during life had been 40 per minute, very small, and sometimes hardly perceptible." The other2 is that of a youth, set. 19, in whom the pulse was said to have been " small and slow. The aortic orifice would only admit a catheter; all the valves were adherent together, leaving only a small rounded hole in the middle." Such cases are doubtless exceptional; but, as has already been stated, aortic stenosis, without regurgitation, is decidedly a rare affection. In regurgitant aortic disease the pulse presents characters so remarkable that they have led to its receiving several special designations, and that they often enable the physician to diagnose the na- ture of the case without aid from any other source. A passage has already been quoted from Vieussens (1715)^ in which the peculiar character of pulse that is now known to belong to this affection is clearly indicated. So far as I am aware, the next writer to mention it was Dr. Hodg- kin, who, in his paper on " Retroversion of the Aortic Valves,"4 published in 1829, says that in one case there was "inordi- nately violent arterial action, which was very rapid and frequent, although regular, there was a remarkable thrill in the pulse, and the carotids were seen violently beat- ing on both sides." But it was Sir Dom- inic Corrigan,5 who in 1832 first laid stress on the peculiarity of the pulse in this disease, a fact connnemorated in the designation of " Corrigan's pulse," which is commonly applied to it both on the con- tinent and in this country. The feature on which Corrigan espe- cially insists, as indicating "inadequacy of the aortic valves," is the existence of visible pulsation in the arteries of the head and superior extremities. He de- scribes the subclavian, carotid, temporal, brachial, and even palmar arteries as being "suddenly thrown from their bed, and bounding up under the skin." In the arteries of the lower extremities, even of larger size than those which present it about the head and neck, pulsation is not (he goes on to say) seen to any compara- tive degree, and generally not at all, while the patient is sitting or standing. The pulsation of the brachial and palmar ar- teries is increased in a most striking de- gree by merely elevating the arm above the head : and the same effect is produced in the lower limbs by lying down and elevating them on an inclined plane. In addition to these points, it may be added that, in aortic regurgitation, the arteries are elongated during their pulsa- tions much more than in health, and can be seen in many positions to become dis- tinctly flexuous with each beat of the heart. Consequently, one name for the pulse in question is that of the "locomo- tive" pulse. But these visible characters of the pulse of aortic regurgitant disease are after all of little consequence in comparison with those which can be felt. To the touch, the pulse in question gives a sensation of peculiar largeness or fulness, immediately followed by an equally peculiar collapse. Instead of the artery slowly receding be- neath the finger, it falls as rapidly as it rose. The pulse is, therefore, often spoken of as "jerking," "splashing," or "col- lapsing;" or as the "water-hammer" pulse, from the well-known scientific toy of that name. Lastly, the pulse of aortic regurgitation differs from that of health in travelling along the arteries much more slowly. Normally, even the radial pulse follows very quickly upon the ventricular systole ; in the disease under consideration, it may almost be synchronous with the second sound of the heart. There is little difficulty in explaining the peculiarities that have been enumer- ated. We have seen that when the aortic valves allow of regurgitation, the ven- tricle is greatly, often enormously, dilated and hypertrophied. The quantity of blood injected into the aorta is, therefore, much increased. No wonder that the pulse feels full and large, that the arteries lengthen, and seem to bound from their seats, beating much more plainly than in 1 Inspection 109, in the year 1859. 2 Inspection 72, in the year 1862. 3 CEuvres Francoises. 4 London Med. Gaz. vol. iii. p. 438. 6 Ed. Med. and Surg. Journal, April 1, 1832, p. 225. 742 DISEASES OF THE VALVES OF THE HEART, health. Then comes the elastic recoil of the larger arteries. Under normal con- ditions, this is gradual. The aortic valves are closed, and the blood moves slowly onwards into the small arteries and capil- laries, meeting considerable resistance. But when the valves in question are dis- eased, and allow reflux to take place through them, there is nothing to support the column of blood in the aorta and its branches d uring their recoil; the blood is rapidly driven out of them, part one way and part another ; and the pulse as sud- denly collapses. Since the invention of the sphygmo- graph, no description of the peculiarities of the pulse in any morbid state can be regarded as complete unless full reference is made to the results obtained with that instrument. And probably diseases of the aortic valves were among the first in which the sphygmograph was applied. It cannot, indeed, be said that those who have specially devoted themselves to this subject have as yet come to a complete agreement in reference to the indications which it affords. But I believe that the existing state of our knowledge is fairly expressed in the following account of the matter:- In aortic stenosis, one might expect that, in proportion as the aortic orifice is obstructed, the exit of blood from the ventricle would be impeded. The up- stroke of the sphygmographic tracing should, therefore, be oblique, or sloping. According to Mahomed, this is the case. I append (Figs. 107 and 108) copies of two tracings given by this observer in the Medical Times and Gazette for 1872,1 which show well the sloping upstroke and the rounded summit, indicative of the fact that " the influence of percussion is lost; the tidal wave alone remains." Fig. 107. Fig. 108. Fig. 109. Very similar to this is another diagram (Fig. 109), which is a copy of one given by Jaccoud.1 According to Mahomed, however, another very different form of pulse may accompany aortic obstruction. It is illustrated in the following diagrams (Figs. 110, 111, 112), which are copied from those given by him.2 It will be ob- served that there is a marked separation between the percussion and tidal waves. It ought perhaps to be mentioned that, in the case from which the tracing No. 112 was taken, there was a double murmur over the aorta, but the existence of con- siderable aortic obstruction was made out, not only from the characters of the pulse, but also from the fact that a tracing obtained from the heart showed the con- 'tractions to be very slow and gradual. It is to be borne in mind that only extreme degrees of aortic stenosis can be expected to affect the pulse in the ways described by Mr. Mahomed. He himself gives a tracing from a case in which "consider- able obstruction was produced by the ad- herence of two of the aortic valves ;" in this tracing no sign of the obstruction is apparent. In aortic regurgitation, the sphygmo- graphic tracings of the pulse present pecu- liarities which correspond in a very strik- ing way with what might theoretically have been expected. The percussion- wave is strongly marked, and the upstroke is therefore high. On the other hand, the dicrotic wave (or "diastolic expansion") is wanting, in consequence of the aortic valves failing to support the column of blood in the aorta during its recoil. Lastly, a high pressure is required to bring out the characters of the pulse fully; this being the result of the hypertrophy of the left ventricle, which is constantly present in cases of aortic regurgitation. The three following figures, which are copies of tracings given by Mr. Mahomed,2 illustrate these points. It ought perhaps to be added that Marey originally laid great stress on a little peak or point at the summit of the long upstroke, as indic- ative of aortic regurgitation ; but this was soon shown to be a mistake. At the pres- ent time, there seems to be a fair agree- ment among different observers as to the characters in a sphygmographic tracing which point to the disease in question. In some cases of aortic regurgitation the pulse does not present its peculiar characters in any marked degree, whether to the touch or to the sphygmograph; and > Loc. cit., Pl. V., Figs. 17, 18, 19. 2 Loc. cit., Plate V., Figs. 7, 4, 6 respect- ively. In Fig. 118 (Fig. 4 in Mr. Mahomed's plate) there are also indications that the ar- teries are atheromatous. » Plate V., Figs. 12 and 13, p. 142. 2 Traite de Pathologie Interne, quatrium Ed. tome i. p. 676. ETIOLOGY. 743 this, although the diastolic murmur may be loud and prolonged. This may be due either to the circumstance that the reflux of blood is really small in amount, or to the fact that mitral regurgitation is also present. Mr. Mahomed gives in his papers in the Medical Times and Gazette some very valuable illustrations of the Fig. 110. Fig. 111. Fig.112. way in which the sphygmograph may be used in cases of this kind, both to deter- mine the degree of valvular incompetency, and to gauge the amount of compensatory hypertrophy of the left ventricle; and also to decide which of two coexistent affections-mitral and aortic-is of pre- ponderating importance. It is in the solu- tion of such questions as these that the great value of the instrument appears to lie, so far as diseases of the cardiac valves are concerned. The mere detection of valvular incompetency can be effected more easily, and perhaps as surely, by the Fig. 114. Fig. 113 Fig. 115. stethoscope ; but in prognosis the sphyg- mograph seems to lend great assistance. The onward effects of diseased condi- tions of the aortic valves are not neces- sarily confined to the arterial system. The capillaries may be imperfectly supplied with blood, and both the nutrition and the functions of the different organs may in consequence be greatly impaired. This is perhaps especially marked in the case of the brain. Attacks of giddiness are far from uncommon in aortic regurgitation, and are ascribed to failure in the due sup- ply of arterial blood to the nervous centres. Aneemia and wasting of the whole body are also frequent symptoms : the former being in fact so constantly present as to be a marked feature in the physiognomy of the disease. (3) Backward effects of aortic disease are absent, so long as the changes in the left ventricle above described enable the heart to do its work efficiently, even though this result should be attained at the expense of increased labor and fric- tion, and under augmented frequency of beats. And since patients with aortic re- gurgitation very often die suddenly while these conditions are fulfilled, backward effects are not rarely wanting to the last. But whenever the compensatory processes fail, so that the arteries no longer receive for transmission onwards their full supply of blood per minute, the necessary result is that the quantity discharged into the ventricle by the left auricle must also be deficient. The inevitable consequence of this, again, is the development of a fresh series of changes, which we are about to study in detail, as the effects of primary disease of the mitral orifice. It is often stated that in affections of the aortic valves these changes occur only when the mitral valve has been stretched, so as to allow of regurgitation through it-this being probably a common result of the dilatation of the left ventricle. But I conceive that the statement in question is an error, and that backkward effects must necessarily arise in the way I have indi- cated, even though the closure of the mi- tral valve may still remain perfect.1 B. Diseases of the mitral valve, again, are of two kinds-obstructive and regur- 1 So far as post-mortem evidence can be brought to bear upon this question, I believe that such evidence is favorable to the view expressed in the text. Thus I find in my notes one case (in which I made an autopsy in July, 1873) of aortic disease with retrover- sion of one of the valves. Dropsy occurred before death, and the lungs contained apo- plectic patches. The mitral valve appeared to be quite healthy; and, after death, it did not allow regurgitation to occur. The left auricle was dilated and hypertrophied, and the right auricle was still more so. 744 DISEASES OF THE VALVES OF THE HEART. gitant: which will to some extent require to be considered separately from one an- other. (1) The primary effect of diseases of the mitral valve may be said to be exerted upon the left auricle. In mitral stenosis the effect in question is well marked. The cavity becomes dilated, often enormously so.1 The appendix is elongated-in one instance I find it noted as 2| inches long by Dr. Moxon-and acquires a peculiar curved form ; and its aperture of commu- nication with the auricle is much wider than natural. The walls of the auricle also become much hypertrophied; they no longer collapse when the cavity is cut open, but support themselves stiffly: the muscular substance may in places be from | to | of an inch thick. The endocardial lining is said to be more opaque than usual. These changes are almost constantly met with in cases of mitral stenosis. And were the current doctrines in regard to mitral regurgitation true, they would doubtless be found no less uniformly in cases of the latter affection just as dila- tation and hypertrophy of the left ventri- cle occur equally in aortic obstruction and in aortic incompetency. However, this is not so. Definitely marked hypertrophy of the muscular wall of the left auricle is seldom present in cases of the so-called mitral regurgitant disease. It is true that the cavity in question is often found to be dilated; but then all the other cardiac cavities are generally enlarged at the same time. I shall endeavor to explain these facts further on. (2) The onward effects of diseases of the mitral valve are of course seen first in the left ventricle. In mitral stenosis this chamber is very generally found to be small, and its muscular substance is no thicker, and may perhaps even be thin- ner, than under normal conditions. The aorta too is often small and thin-walled. But in some cases of mitral stenosis and in almost all cases of " mitral regurgita- tion" the left ventricle is large and fleshy, and not infrequently it is as much dilated and hypertrophied as in aortic regurgita- tion. Various explanations of this have been given. By Friedreich2 it is sup- posed that the augmented tension in the systemic venous system (which we shall presently show to be one of the conse- quences of mitral diseases) causes an in- creased resistance in the systemic arteries likewise. But, apart from the difficulty of admitting that the effects of obstruction thus traverse the complete circuit of the circulation, a fatal objection to this theory is that it would require dilatation of the left ventricle to be the rule in fatal cases of mitral stenosis, instead of its being quite exceptional. Another view is that when the ventricle is enlarged in mitral disease, this is not really due to the val- vular affection, but depends upon some other cause. Thus, in rheumatic cases many other conditions generally exist (such, for example, as diseases of other orifices, or thick pericardial adhesions) to which the change in the ventricle may be ascribed. Indeed, according to some ob- servers, primary dilatation of the left ven- tricle commonly occurs in the course of acute rheumatism, and may persist after the subsidence of that disease. But, again, in very many cases of so-called " mitral regurgitant disease" the valve is itself healthy : and the imperfection in its working (if we are to assume that it does close imperfectly) is itself the result of ventricular dilatation. There is, however, one class of cases in which it certainly ap- pears that mitral imperfection leads to enlargement of the left ventricle-I refer to those cases in which rupture of the tendinous cords of the valve occurs in persons who had not previously exhibited any symptoms of cardiac disease.1 It may indeed be objected that both the ventricle and the valve were possibly af- fected with latent disease before the sud- den rupture took place : but of such dis- ease there is no evidence, and to suppose its existence is to abandon in favor of an arbitrary hypothesis the direct interpre- tation of the facts observed. The expla- nation, indeed, seems to be sufficiently easy. In such cases, the ventricle has greatly increased labor ; a good deal of the blood which enters it having to be expelled twice over from its cavity. On the other hand, in cases of uncomplicated mitral stenosis, the work thrown upon the left ventricle is in no way augmented, if it be not even less than under normal conditions : and, as I have already stated, ' This condition was long ago described as "trne aneurism of the left auricle" by Dr. Thurnam (Med.-Chir. Trans, ser. ii. vol. iii. 1838, p. 244), who expressly insists on its association with contraction of the mitral ori- fice, and mentions that the lining membrane is opaque and rough, and in some cases even ■ossified, and that it is lined with fibrinous layers very similar to those met with in ar- terial aneurisms. 2 Op. cit. pp. 161 and 227. 1 Thus in Dr. Dickinson's case (Path. Trans, xx. p. 150) the heart weighed 20 oz.; all the cavities were dilated to at least three times their natural capacity; the auricles and right ventricle were thinned. The left ventricle was hypertrophied to such an ex- tent as to retain, notwithstanding its dilata- tion, about its normal thickness. And in the report of the post-mortem examination of a similar case that occurred in Guy's Hospital under Dr. Habershon's care, Dr. Moxon states that "all the cavities were dilated." ETIOLOGY. 745 I believe that in such cases the left ven- tricle is always small, and its muscular substance no thicker than natural. The arterial pulse in mitral diseases may present very varied characters, the variations depending not merely upon the nature of the valvular lesion, but also upon the changes secondarily induced by it in the heart's chambers. Formerly, it was supposed that in mitral stenosis the pulse is always small; but since the pre- systolic murmur has enabled this con- dition to be diagnosed before severe symp- toms set in, it has been found that the pulse is often perfectly natural. Indeed, there is no reason why it should be other- wise, so long as the hypertrophied auricle keeps the ventricle duly supplied with blood. In a very large proportion of cases in which a presystolic murmur is audible, the pulse is perfectly regular, and has ample volume and force. According- ly, Mr. Mahomed says1 that "in this dis- ease the sphygmographic tracing does not necessarily present any diagnostic char- acteristics." I have already quoted this writer as having demonstrated that car- diographic tracings, taken at the heart's apex, often afford proof of the existence of mitral stenosis (or, at least, of hyper- trophy of the left auricle), by showing that the auricular systole commences at an earlier period in the ventricular dias- tole than is normal. He further main- tains that in some cases this premature contraction of the auricle stimulates the ventricle to contract likewise ; and that in this way the tracing of the pulse at the wrist may indicate a second ventricular systole, alternating with the main beat, but very much less forcible. The accom- panying diagram is copied from one of Mr. Mahomed's tracings, taken from a patient of mine who was suffering from mitral stenosis, and in whom the double Fig. 116. ventricular systole was made very marked by the administration of digitalis. Both contractions were felt in the pulse at the wrist, the beats of which were alternately strong and feeble. I have observed a sim- ilar double rhythm in several other in- stances of valvular disease ; but I am un- able to say whether they were or were not all of them cases of mitral stenosis. In the later stages of the disease-when the peculiar murmur can often be no longer detected-the pulse assumes very different characters. It is now rapid, soft, small, and very irregular, both in volume and force. The accompanying tracings (Figs. 117, 118, 119) copied from Jaccoud,1 show the sphygmographic character of a pulse of this kind; they are very much what might have been expected from the im- pression which it gives to the touch. It has long been known as the mitral pulse; and, in fact, it is met with, not only in the Fig. 117. Fig. 118. Fig. 119. advanced stages of mitral stenosis, but also in those cases which are commonly grouped under the heading of " regurgi- tant mitral disease." Whether it is of any diagnostic value, as indicating that the valve in question is impaired in struc- ture or function, is a very difficult ques- tion to answer. I have already stated more than once that " regurgitant mitral disease" has no constant pathological ap- pearances, but that it includes a variety of conditions, in some of which the valve certainly admits of regurgitation, while in others there is doubt whether this oc- curs. I must now add my belief that for the production of the so-called "mitral pulse" the mitral valve need not be either narrowed or incompetent. The same kind of pulse probably arises whenever the ventricle does not empty itself com- pletely during its systole, so that the stream of blood projected into the aorta is greatly diminished. Now it would ap- pear that such a perversion of the heart's action is far from being uncommon, being liable to occur in the course of various cardiac and pulmonary diseases without presenting any characters peculiar to one rather than to another of these diseases. The condition in question was first de- scribed by Beau, who gave it the name of 1 Op. cit. No. 6, p. 569. ' Op. cit. No. 21, p. 678; No. 9, p. 616; No. 7, p. 615. 746 DISEASES OF THE VALVES OF THE HEART. asystolie; and most recent French writers have adopted this designation. Dilatation of the heart appears to be the morbid change which is most constantly present in cases of this kind; but very frequently valv- ular disease also exists. The sphygmo- graphic tracings (Figs. 117 and 118), which I have copied from Jaccoud as illustrative of the "mitral pulse," are given by that writer as indicating the existence of a condition ot "asystole." (3) Backward Effects.-So long as the left auricle can duly empty itself, and re- ceive its full supply of blood from the pul- monary veins, tlie parts of the circulatory apparatus behind the auricle are in no way affected by the existence of mitral disease, whether obstructive or regurgitant. But, except in the earlier stages or slighter degrees of such disease, the compensatory action of the auricle is very seldom thus complete; and whenever it fails, the ne- cessary consequence is an augmented ten- sion in the pulmonary system of vessels and in the chambers of the right side of the heart. It has already been stated that the same result occurs also in dis- eases of the aortic valves, as soon as com- pensatory changes fail to enable the left ventricle to carry on the circulation prop- erly. This increase of tension in the pulmo- nary vessels soon leads to changes in their walls, which become thickened, or hypertrophied. In the main trunk of the pulmonary artery this is particularly no- ticeable. The records of post-mortem examinations at Guy's Hospital contain notes by Dr. Moxon of the case of a boy, set. ten years, in whom the coats of the pulmonary artery were nearly twice as thick as those of the aorta at its thickest part; and less striking examples of the same kind are very commonly met with. The artery also becomes greatly dilated. Another result of the increased tension of blood within the pulmonary artery is the fact that in these cases the branches of the vessel are very apt to become atheromatous, although under normal changes they are but little liable to such a change. Perhaps the most striking in- stance of this that could be quoted is one which Dr. Conway Evans' has recorded, and which occurred in a boy, who died of dropsy, consequent on mitral stenosis, at the age of fourteen years. It would ap- pear that Dittrich2 was the first to point out the frequency with which atheroma of the pulmonary artery is found in cases of this kind, and that he described it as occurring especially in the smaller branches, and as being the immediate cause of the patches of "pulmonary apo- plexy" which are so commonly met with under such conditions. The explanation of pulmonary apoplexy, however, is still open to doubt. The branch of artery leading to an apoplectic patch is gener- ally, perhaps always, plugged with fibrin; and this has led many modem observers to regard the affection as of embolic origin. In the first volume of the " System of Med- icine," Dr. Bristowe has discussed this question at considerable length. The pulmonary tissue is also liable to assume a peculiar appearance, which is generally known to German pathologists under the name of "brown induration." In this volume of the present work, at p. 274, Dr. Wilson Fox has given a de- tailed account of this affection; but he seems to have laid hardly enough stress on the dilated and varicose state of the pulmonary capillaries, which Buhl has shown to be present, and which is so striking a proof of the increased pressure upon these vessels. I have found that this dilated state of the capillaries is re- cognizable without difficulty, even in un- injected specimens. Before leaving the subject now under consideration, I must not omit to mention another way in which the left lung suffers from cardiac disease-namely, from the dilated left auricle pressing directly upon the bronchus. Mr. Wilkinson King' first pointed this out, in the year 1838, and his preparations, which are now in the museum at Guy's Hospital, show that the anterior surface of the tube may in this way be rendered quite flat, and its calibre diminished by one-half. But the most remarkable instance is one recorded by Friedreich2 in which narrowing of the left bronchus was diagnosed four years before the patient's death, from the pres- ence of a loud humming sound accom- panying both the inspiration and the ex- piration, heard most plainly over the root of the left lung, near the spine, but also audible over the whole left side of the chest. There was extreme stenosis of the mitral orifice with enormous dilatation of the left auricle. Virchow made the au- topsy ; and the left main bronchus was found to be compressed, so that only a small narrow channel was left. The cavities of the right side of the heart also become greatly dilated and hypertrophied under the conditions now being considered. The muscular tissue of the right ventricle grows much harder than natural-indeed, it is peculiarly hard/in comparison even with the sub- stance of an hypertrophied left ventricle. The tricuspid orifice is stretched. C. & D.-It is at this point that we 1 Trans, of the Path. Soc. xvii. p. 90. 2 Ueher den Laennec'schen Lungen-Infark- tus. Erlangen, 1850. 1 Guy's Hospital Reports, series i. vol. iii. p. 178. 2 Op. cit. p. 30. ETIOLOGY. 747 ought to consider the effects of primary disease of the pulmonary and the tricus- pid valves respectively. But such dis- eases are so rare (excepting malforma- tions, which are treated of separately) that they need scarcely interrupt us in tracing out the backward effects of dis- eases of the valves of the left side of the heart. It will suffice to state that (1) the primary effect of disease of the pulmonary valves is to cause dilatation and hyper- trophy of the right ventricle ; and that that of disease of the tricuspid valve (if primary chronic disease of this valve ever occurs) would probably be to cause dila- tation and hypertrophy of the right au- ricle ; (2) Concerning forward effects of the disease in question, no definite state- ments could perhaps be made ; (3) Their backward effects must be the same as those which more remotely arise from un- compensated diseases of the mitral and aortic orifices, and to these our attention may now be directed. Taking first the vena cava superior and the veins from which it arises, we find that they are enlarged and gorged with blood. Hence the livid countenance, the turgid cheeks, the purple ears, checks, and lips, that are so commonly seen in patients suffering from affections of the cardiac valves. The veins of the upper limbs are also distended ; the hands and nails acquire a livid purple color, and the hands, and often even the arms, become cedeinatous. The lividity may approach, if it may not even equal, that which is seen in cases of malformation of the heart, in the condition known as cyanosis. A further consequence of the congestion of the upper limbs which exists in these cases, is that the finger-ends often become enlarged, or (as it is usually termed) "clubbed." Dr. Dobell' has recently stated that the clubbing of the fingers from heart disease differs from that which is due to phthisis, in the circumstance that the sides and tips of the nails are not at the same time incurved; the reason for this difference being, that in heart dis- ease wasting of the adipose tissue is ab- sent, which wasting he believes to be the cause of incurvation. At the root of the neck the jugular veins, besides being enlarged and unnat- urally full, present another phenomenon which requires further consideration- they can often be seen to pulsate with each beat of the heart. This seems to have been first noticed by Lancisi.2 Jugu- lar pulsation is commonly taken as a cer- tain indication of regurgitation through the tricuspid orifice ; and the frequency of its occurrence, when the circulation through the right side of the heart is im- peded, is supposed to bear out Mr. Wil- kinson King's views of the existence of a physiological safety-valve action, by which reflux is allowed whenever the right ventricle becomes unduly charged with blood. It has, however, been shown by Friedreich that the matter is by no means so simple. In the first place, when the jugular veins are distended they often exhibit rhythmical movements synchro- nous with the respiratory acts. Each ex- piration causes an increased pressure upon the large venous trunks within the thorax ; and even though the valves at the root of the neck may close perfectly, the blood that is pouring in from the veins of the head and upper limbs is stopped, and ac- cumulates behind the obstruction. An apparent pulsation may thus occur with- out any blood really regurgitating into the jugular veins from below. So, again, it is possible that when these veins are very full, variations in their size may oc- cur, synchronously with the heart's move- ments, from the temporary arrest of the onward flow of blood during the closure of the tricuspid valve, quite independ- ently of reflux. In this case, however, compression of the veins in the middle of the neck will at once stop the apparent jugular pulsation. When jugular pulsation is really due to regurgitation of blood, it is of course necessary that the valves at the junction of the subclavian and jugular veins should be incompetent. Dr. Parkes1 is said to have taught that this is due to rupture of these valves : but as Dr. Walshe points out, it is doubtless sufficient that the veins should be greatly distended, so as to pre- vent the edges of the valves from touch- ing one another. According to Friedreich it is possible for a true jugular pulsation to be produced by the pressure of the as- cending aorta, when dilating during the ventricular systole, upon a distended vena cava superior. But this explanation ap- pears far-fetched, and unnecessary. Fried- reich will not allow that tricuspid regur- gitation is present, unless a systolic mur- mur is audible. I shall presently show, however, that almost any kind of valvular defect may exist, without the correspond- ing murmur: and my belief at present is that regurgitation through the tricuspid orifice exists in all cases in which the jugular veins really pulsate. Indeed, I cannot even agree with Friedreich that if pulsation disappears when the vein is compressed higher up, the existence of regurgitation is absolutely disproved : for this procedure may simply prevent the wave being transmitted upwards in the empty vessel. The most that can be said 1 On Affections of the Heart and in its neighborhood, 1872, p. 17. 2 De motu Cordis et aneurysmatibus. Rom. 1728, Lib. ii. Propos. 57. 1 Walshe, op. cit. p. 138. 748 DISEASES OF THE VALVES OF THE HEART. is that it renders the occurrence of reflux doubtful. Friedreich gives sphygmographic trac- ings of the jugular pulse, which appears to be dicrotic, the beat due to the ven- tricular systole being preceded by a smaller elevation accompanying the contraction of the auricle. It must be added that pulsation is gen- erally more distinct in the right than the left jugular vein. In exceptional cases the veins of the face, arms, and hands have been seen to pulsate: and also the thyroid and mammary veins. Turning now to the vena cava inferior and its tributaries, we find that these veins become greatly dilated as a conse- quence of distension of the right auricle. Senac1 mentioned a case in which the cava was as thick as an arm. The hepatic veins also become much enlarged, running as wide open channels through the sub- stance of the liver, and opening into the cava by orifices much larger than natural. These facts are of some importance, as throwing light on the epigastric pulsation, which is often observed in cases of chronic disease of the heart. It was long ago suggested by Allan Burns2 that this is due to regurgitation of blood along the inferior cava, and into the vessels of the liver. And Friedreich at the present time maintains the same view.3 English writers in general, however, describe the dilated right ventricle as giving a shock to the neighboring parts which can be felt in the substernal notch: and some have even spoken of the heart as "beating in the epigastrium," the impossibility of which it did not need the labors of Hamernyk to point out. The probability that epigastric pulsa- tion is often due to reflux into the hepatic veins is increased by the fact that the liver itself is greatly enlarged under these conditions. It is also much congested and fatty, presenting a peculiar mottled appearance, which has gained for it the name of the nutmeg liver. At the same time it is very liable to a chronic inflam- matory process, attended with an increase in its connective tissue, approaching that which occurs in cirrhosis. The conges- tion is transmitted through the liver to the portal vein and its radicles. The spleen becomes enlarged and its tissue very hard, in this respect contrasting with the still larger but soft spleen which is found in association with ulcerative diseases of the cardiac valves. The veins of the omentum and mesentery are gorged with blood. The stomach has its lining intensely reddened and coated with mu- cus : hemorrhage takes place into its sub- mucous tissue, and the ecchymosed spots often become exposed by solution of the mucous membrane over them, forming the so-called "haemorrhagic erosions." The intestines are also greatly congested and lined with mucus : and haemorrhoids are often developed. These changes in the digestive organs are attended with more or less marked symptoms: partial jaundice; dyspepsia, nausea, sickness, even haematemesis; constipation. The engorgement of the veins lying beneath the peritoneum leads to ascites, often of considerable amount. Nor do the other veins that open into the inferior vena cava escape. Thus the renal veins become distended ; and the kidneys are deeply congested, a condition which easily passes into one of chronic inflam- mation, and often leads to the presence of albumen in the urine. The return of blood from the lower limbs is impeded: the veins are gorged, and very often thrombosis of the femoral veins arises, which, as has already been stated, is per- haps the remote cause of the development of pulmonary apoplexy. This engorgement of the veins of the lower limbs, although we mention it last in tracing backwards the consequences of disease of the cardiac valves, is in fact often one of the first effects of such disease to be observed ; manifesting itself by the transudation of serum through the walls of the most distant venous radicles, and the production of oedema of the ankles and feet. The anasarca, slight at first, may increase until the whole of the lower extremities, the abdominal parietes, and even the genital organs, have become dropsical in the highest degree. As a rule, however, the genital organs remain comparatively free : and in this respect cardiac dropsy differs from that which occurs in renal disease, and the distribu- tion of which is not in the same way de- pendent upon simple mechanical condi- tions. On the other hand, the icteroid tinge of the skin, which is generally present in cases of heart disease, is want- ing in other forms of dropsy. III. A third series of effects, produced by diseases of the cardiac valves, consist in sensations of various kinds experienced by the patient. These are the subjective symptoms of the diseases in question. They may present all degrees of intensity ; they may even be entirely absent. Pain may be felt either over the heart itself, or in the left shoulder; or it may extend down the inner side of the left arm 1 Friedreich, p. 41. 2 Op. cit. p. 265. 8 My colleague, Dr. Frederick Taylor, has observed distinct pulsation of the liver in four cases of chronic cardiac disease. When one hand was placed in the epigastrium and the other in the right loin, the organ could be felt to expand with each beat of the heart. Guy's Hosp. Rep. (vol. xx. 1875). DIAGNOSIS. 749 to the elbow, or even to the fingers. It may either be a constant aching, or have a "shooting" or "stabbing" character. It is often distinctly paroxysmal, espe- cially in cases of aortic regurgitation, in which it frequently assumes all the fea- tures of true angina pectoris. Pain in the arm and hand is sometimes accompanied with numbness : and sometimes (accord- ing to Dr. Dobell) these parts are deadly white while the numbness lasts. In some cases the pain is limited to the little and ring fingers, following the distribution of the ulnar nerve to these fingers: but in other cases it affects all the fingers, and even the thumb. Sometimes the pain also passes from mid-sternum to the right shoulder and down the right arm: but when pain occurs in these parts earlier than in the cardiac region, Dr. Dobell thinks that the presumption is in favor of disease of the aorta rather than of the heart. A very important character of the re- flected pains due to cardiac disease is that they are generally aggravated by anything which disturbs the heart's action, and especially by muscular exertion. Not un- frequently, pain is absent so long as the patient is at rest, but comes on at once as soon as he attempts to walk. Another point, on which Dr. Dobell has particularly'insisted, is that the pain of heart disease is often greatly increased by distension of the stomach with food or gas. Hence, when dyspepsia is present, it may easily be regarded as the cause of pain really due to heart disease ; and re- lieving the indigestion may prevent the return of the pain. Not infrequently, instead of pain, the patient speaks rather of a fluttering sen- sation in the prsecordial region : or simply of palpitation. But it is to be observed that a spontaneous complaint of palpita- tion is heard far more often when the pa- tient is suffering from one of its indirect causes, than when any of the cardiac valves are diseased. Indeed, as a rule, the subjective symptoms of valvular affec- tions are subordinate to the other symp- toms. And it may be said that when a patient comes to the physician complain- ing of pain in the heart, and fearing that he has heart disease, the great probability is that that organ is perfectly healthy. Another morbid sensation, belonging to the diseases under consideration, is dys- pnoea. Very often, indeed, the first thing that suggests a suspicion that there is any- thing wrong with the patient is that he is conscious of shortness of breath after mounting stairs, or making some mode- rate muscular effort. When he is at rest, he may be able to breathe comfortably enough; but this freedom from distress often continues only so long as he sits up. As soon as he lies down on an ordinary bed or couch, he becomes aware of un- pleasant feelings, which compel him to change his posture. Thus, even in the slighter forms of cardiac valvular disease, it will generally be found that the patient lies at night with his head raised, employ- ing two or three pillows, whereas a man in health would only require one. And in the more severe degrees of such disease, the patient is often utterly unable to lie down, or even to recline backwards. This condition has received a special name, that of Orthopnoea. It doubtless depends upon the circumstance that in the re- cumbent posture the diaphragm is pressed upwards by the contents of the abdomen (themselves greatly augmented in size), so that the enlarged heart is embarrassed in its movements.1 Orthopnoea is in many respects a serious symptom. By prevent- ing sleep, it greatly taxes the patient's strength, and diminishes his power of re- sisting the disease. Moreover, as Dr. Do- bell has pointed out, it fatigues the lumbar muscles, and makes the backache. It keeps the lower limbs at right angles with the trunk, and so, leading to compression of the veins and lymphatics in the groins, increases the oedema of the legs. Scarcely any condition is, in fact, more pitiable than that of a patient in this plight; and any mechanical appliance by which it can be remedied must certainly be an unspeak- able boon. For this purpose Dr. Dobell has contrived a "Heart Bed," of which he has given a description and a figure in his book ; and from his account it seems to be well worthy of trial in these distress- ing cases. There are other subjective symptoms, belonging to the various secondary effects of diseases of the cardiac valves; but space fails me to describe them in detail; most of them have been incidentally re- ferred to in other parts of this article. Diagnosis.-Under this heading I do not propose simply to recapitulate facts that have already been stated in previous paragraphs; nor shall I attempt to con- struct any tables which might aid the student in distinguishing diseases of the cardiac valves from other affections with which they may be confounded. In my opinion such tables are scarcely ever made use of in practice ; indeed, I do not think that they are applicable to really doubtful cases, in which the difficulty of diagnosis most commonly depends upon either a deficiency of symptoms, or their ambiguity: their being, in fact, such as might belong indifferently to any one of several maladies; or else their being in part such as commonly occur in one dis- 1 Even when the heart is healthy, the po- sition of its impulse may be higher or lower, according as the patient sits up or lies down, if there be an enlargement of the liver. 750 DISEASES OF THE VALVES OF THE HEART. ease, in part such as belong rather to another disease. In cases of this kind, diagnostic skill is a matter of judgment and experience; and all that could be said under the present heading could do but little to further it. There are, however, some important questions in reference to the detection of affections of the valves of the heart which have not yet been touched upon. In dis- cussing each kind of murmur, I have en- deavored to indicate all the causes to which it may be due, and to point out how these may be distinguished from one another. But of the absence of murmur I have as yet said nothing. I now pro- pose to consider this question, and to dis- cuss whether abnormal sounds or bruits are constantly present in the various dis- eases of the different cardiac valves. And first, with regard to the aortic valves. It may almost be said that in practice the diagnosis of aortic regurgita- tion depends wholly upon the discovery of a diastolic murmur, audible at certain parts of the thoracic parietes. If such a murmur is heard, the stethoscopist re- gards it as certain that regurgitation ex- ists. If no such murmur can be detected, there is perhaps no combination of symp- toms (unless it be by the aid of the sphyg- mograph) that would justify the physician in asserting that the aortic valves fail to close. It is therefore a most important question whether a diastolic bruit can always be detected in those persons in whom after death the valves are found to have been incompetent. Now, on looking through the records of post-mortem ex- aminations at Guy's Hospital, I have found that this condition was discovered in 40 cases during the years 1870-71. And on referring to the clinical reports attached to these cases, it appears that in 26 of them regurgitation was positively diagnosed during life ; and that in 11 out of the remaining 14 cases the patients came from the surgical division of the hospital, or were less than seven days in the wards (some having been dying at the time of admission, or brought in dead), or had no notes taken of the auscultatory signs which they presented. Thus the proportion of cases of this disease that may be said to have resisted diagnosis was very small. It has been stated that several of the cases in which the aortic valves wrere found incompetent after death during the period named were cases of surgical dis- ease or injury, in which one may presume that there were no obvious symptoms of cardiac disease. This accords well with the fact that aortic regurgitation is more frequently than any other valvular affec- tion discovered by the auscultator when the patient's history and symptoms had not previously suggested any suspicion of its existence. Dr. Walshe relates the case of a man about 35 years old, the very pic- ture of robust health, who had never had a symptom of disease connected with any organ of his body, and who presented him- self for life insurance. Almost as a matter of form, Dr. Walshe put his stethoscope to the chest; his attention was at once arrested by a loud diastolic murmur. The man dropped dead in the street within a fortnight. I lately saw a bank clerk, aged 32, whose sole complaint was a pain in the chest about the ensiform cartilage, with occasional pain in the back, such as might have been due to any trifling cause. On listening to his chest I heard a well- marked diastolic bruit.1 It might be supposed that there would often be a difficulty in distinguishing be- tween the to-and-fro sounds of pericardi- tis and of those of disease at the aortic orifice. And for my own part I believe that this difficulty would arise oftener than it does, w ere not for the very differ- ent clinical history and course and other symptoms belonging severally to these two diseases. The comparatively super- ficial seat of pericardial friction-sounds, their want of definite localization at the spots where valvular murmurs are most 1 A very striking instance, in which the patient discovered the murmur, has just come under my notice in a young medical man, a friend of my own. On January 23d, 1875, he had gone to his brother's for a day's shoot- ing ; and while at lunch, he noticed a strange noise, which he thought came from his stom- ach. He forgot all about it, and went out shooting for two hours. After dinner he heard the noise again. On the next day, while stand- ing in his dining-room, he became conscious of a loud sound in his chest; and his wife, who was three or four feet off, heard it also. During four days it remained audible at a distance. He consulted a medical friend, who discovered valvular disease. Dr. Wilks saw him two weeks afterwards, and kindly sent him to me. His health remained per- fectly good. He would not have known that anything was the matter with him, except that when he made any exertion he could feel a vibration in his chest. A loud diastolic murmur was audible over an extensive area. There was no excessive impulse; but the apex beat was situated below the sixth rib ; and the heart's dulness extended downwards and outwards for six inches. In this case I think it is clear that, whatever may have been the original cause of the sudden devel- opment of the transitory murmur heard at a distance from the patient's body, the valve had previously been diseased. He had, how- ever, been apparently in perfect health: able to ride, shoot, and run as well as ever. The only sudden effort that he remembered mak- ing on the day when he first noticed the mur- mur was that he had lifted his wife out of a high dog-cart; but this he had done many times before. DIAGNOSIS 751 marked, their intensification by pressure with the stethoscope, and their failing to correspond accurately with the cardiac rhythm, are all valuable points of distinc- tion ; but as a matter of pure ausculta- tion, I think that doubt would sometimes be admissible ; and as a matter of fact I have occasionally experienced this diffi- culty, especially when (as in cases of Bright's disease at an advanced age) the presence of either chronic pericarditis or disease of the aortic coats would accord with the other features of the case. The diagnosis between a presystolic and a diastolic murmur is not generally difficult to those who are well acquainted with the seat and quality of these mur- murs respectively. But I have sometimes found it to be far from easy ; and a dis- tinguished physician, who has himself written much on the subject of heart dis- ease, has informed me of one case in which he confidently asserted the exist- ence of a presystolic murmur, but in which the aortic valves proved to be un- sound, while the mitral valve was healthy. The mistake most likely to happen to the unpractised or careless auscultator is that of supposing the murmur of aortic regur- gitation, when it happens to be loud at the apex of the heart, to be a mitral regurgitant bruit. To commit this error is completely to misunderstand the rhythm of the heart in the patient under exami- nation. But I have nevertheless seen it committed more than once. Either no pains at all were taken to determine the period of the ventricular systole ; or the radial pulse was employed as a guide to it. Now it has been already stated that in aortic incompetency the radial pulse is often delayed, so as to be almost syn- chronous with the recoil of the aorta; or, in other words, with the regurgitant bruit. Hence by feeling the wrist in cases of this kind one may easily mistake a dias- tolic for a systolic murmur. It still remains to be mentioned that an aortic regurgitant murmur is sometimes hard to detect. I well remember that, when I was a student, I had very great difficulty in hearing the murmur in more than one case in which my teachers spoke confidently of its presence. And I now find that I in my turn discover murmurs which my pupils cannot hear, even when I tell them what to listen for. When such a murmur is once heard, it often seems so distinct that one wonders that one could have overlooked it. In other instances the sound is really very slight, and it is thus drowned by any little noise, although plainly audible at night, or when a ward is very quiet. Lately I had a patient under my care, in whom the existence of an aortic regurgitant murmur was matter of the most lively discussion. I was sure that I had heard it two or three times, but on every other occasion I failed to de- tect it. After death the valves were found to be obviously incompetent. There is of course norelation between the amount of reflux and the loudness of the murmur. The diagnosis of mitral disease is far from resting on so satisfactory a footing as that of aortic obstruction and regurgi- tation. We may first take the compara- tively simple case of mitral stenosis. I have already said that a presystolic mur- mur, when heard at the heart's apex, is pathognomonic of this affection. But we have now to approach the subject from the opposite point of view, and to inquire in what proportion of cases such a mur- mur is audible. Some years ago I col- lected for the Guy's Hospital Reports all the instances in which mitral stenosis was found after death during a period of some years. They amounted to forty-seven ; and in only seven (or perhaps six) of them had a presystolic murmur been detected during life. It is true that from them a considerable number (fifteen or twenty) had to be subtracted, as having proved fatal soon after admission, or as having been cases of surgical disease or injury, or as having in some other way failed to afford an opportunity for diagnosis. But there still remained at least three cases of mitral stenosis without presystolic mur- mur, to one in which such a murmur was recognized. At that time the whole question of pre- systolic bruits was comparatively a new one ; and I thought that, with further experience, the number of undiagnosed cases of mitral stcgiosis would diminish. I am bound to say that this appears not to be the case. I have not indeed sub- mitted to numerical analysis the observa- tions that have been made since my paper was written ; but my impression is that, in the very large majority of the cases in which mitral stenosis is found after death, there is no record of the presence of a presystolic murmur during life. Some observers, I know, hope to reduce this proportion of failures in diagnosis, by the more frequent detection of a short pre- systolic murmur preceding the systolic murmur of mitral regurgitation. I must confess that my own experience in this direction has not hitherto been very en- couraging. In more than one instance in which I thought I had detected such a second murmur, the mitral orifice has been found after death of its natural size. It remains to add that, even when a presystolic murmur has once been de- tected, it may often cease for a time to be audible, or even altogether disappear. In the later stages of the disease, when the heart is beating quickly and irregularly, it is almost always absent. Thus, at first there was some difficulty in verifying the correctness of the modern view with re- 752 DISEASES OF THE VALVES OF THE HEART. gard to the rhythm of presystolic mur- murs by post-mortem evidence; and in the majority of cases that have terminated fatally soon after the diagnosis of mitral stenosis, some accidental complication lias been the cause of death. Again, when the patient is prostrated by any de- pressing intercurrent disease, the murmur may become temporarily inaudible, re- turning with convalescence. Of this Dr. Sutton has related a capital instance.1 In other cases, no murmur can be heard as long as the patient remains perfectly quiet; but muscular exertion or eflbrt soon makes it audible. Sometimes even making the patient sit up in bed will bring out a presystolic murmur that had a mo- ment before been absent; sometimes it is necessary that he should walk two or three times the length of a ward, or even go quickly upstairs. One can never safely assert the absence of a presystolic mur- mur when one has examined the patient only in a recumbent posture. It may be added, parenthetically, that in aortic stenosis (the chief other form of obstruc- tive disease at a cardiac orifice), a loud murmur may sometimes be brought out by making the patient run upstairs, al- though none had previously been audible. I state this on the authority of Dr. Wilks.2 From the remarks that have already been made with regard to the so-called mitral regurgitant disease, it will be evi- dent that there can be no question here as to the frequency with which its diag- nosis is effected during life. I believe that a systolic murmur, louder at the apex than elsewhere, and audible at the angle of the left scapula, proves the existence of mitral regurgitation; but it is certainly present in comparatively few of the cases that are commonly placed in this category. There is, in fact, a large residue of cases of valvular disease in which either no murmur is audible at the time of observa- tion, or only a systolic murmur, confined to the apex. These cases constitute the sandy desert of cardiac pathology-not, indeed, unexplored, but with a surface so precarious and shifting as to have hitherto prevented the laying down of roads across it, much less the division of it into terri- tories by fixed boundary lines. As we have seen, the cases in question do not differ at all, so far as stethoscopical evi- dence goes, from others in which the presence of valvular disease is altogether doubtful. It may be true that, since ad- vanced organic changes in the mitral valve almost always lead to stenosis, the diagnosis of stenosis becomes exceedingly probable in any case which can be shown to be primarily one of organic disease of this valve. But it is precisely here that the difficulty arises ; and for such cases I think that the diagnosis of "morbus cor- dis" is often the most exact that can be given. I may refer, for example, to a series of cases of fibroid disease of the heart that I have recorded in the Pathological Trans- actions for 1874, vol. xxv. p. 64. In sev- eral of these cases there was a systolic apex murmur ; and it is probable that, at least in some of them, the mitral valve was really inefficient, since the fibroid change often invaded one of its fleshy col- umns. Now, during life, there was nothing to distinguish these cases from those of ordinary " mitral regurgitant dis- ease," and even in the other cases, in which no murmur existed, valvular dis- ease might really have existed, and been latent. Since my cases were published, it has occurred to me that perhaps one positive indication of the presence of fibroid disease of the heart, rather than of any affection of the valves, may be found in its resisting treatment with greater obstinacy. When a considerable part of the wall of the left ventricle has had its muscular substance replaced by fibrous tissue, it appears reasonable to suppose that the remedies which would be useful in a case of valvular disease should prove to be altogether powerless. I have still to lay stress on the impor- tance of watching, with great care, for the occurrence of those changes in valves al- ready diseased which have already been described, and the recognition of which is so important for purposes of prognosis. The development of incompetency in aortic valves that had hitherto simply obstructed the onward current, the pro- duction of stenosis in a mitral valve pre- viously the seat of regurgitation alone, the rupture of the chordae of a diseased mitral valve, the tearing down of a softened aortic segment, the supervention of acute inflammation in valves long thickened, atheromatous, or calcified, - all these might probably be discovered much of- tencr than is now the case, were the phy- sician to pay more regard to the proba- bility of their occurrence. Nor should the liability to intercurrent pericarditis, and to the development of changes in the heart's muscular tissue, ever be forgotten by those who would have their diagnosis complete for the post-mortem examination. Prognosis.-To determine the proba- ble duration of life in a patient affected with valvular disease of the heart, and the chance that existing symptoms may be relieved or removed, is generally very 1 Lond. Hosp. Rep. vol. iv. 1867-68. The patient was very much weakened by frequent vomiting during the time when the murmur disappeared. 2 Dr. Walshe taught this clinically twenty- five years ago. See his "Diseases of the Lungs and Heart," 1851, p. 217.-Editor. PROGNOSIS. 753 difficult; and it can hardly be discussed systematically in an article of this kind, since it requires that all the circumstances of the case should, one after another, be taken into consideration. But some lead- ing points may be briefly stated. And in the first place, can a diseased valve ever recover its normal structure and functions ? In reference to the acute affections of the valves, arising in rheum- atic fever or in chorea, some facts have already been adduced which indicate that this is possible. And a further argument in favor of the same view may perhaps be found in the circumstance that in each of the diseases in question a systolic mur- mur is heard, which in many cases disap- pears after recovery. If such a murmur, when audible at the heart's apex, be re- garded as proof that the mitral valve is affected, it would seem to follow that en- docarditis is curable. Such an opinion has, in fact, been recently maintained by Dr. Peacock, who, in an analysis' of 146 cases of acute rheumatism that had been under his care, found that " the propor- tion of cases of recent cardiac complica- tion (which he states to have consisted in endocarditis more frequently than in per- icarditis) entirely cured was 41'5 per cent." But the conclusion, of course, depends for its validity upon the question whether the determination of the cause of the murmur is accurate. And this I am not prepared to admit unreservedly. A valve once affected with chronic dis- ease is no doubt almost always damaged beyond possibility of repair. Thickened and calcified aortic valves can never again become thin and supple.2 Nor is it pro- bable that a stenosed mitral orifice can become widened. Friedreich has indeed suggested that in young subjects this may not be impossible : but in proof of it he can only refer, in general terms, to cases in which there were at one time symptoms of extreme stenosis, but in which these gradually diminished, and after death the mitral orifice was found capable of admit- ting two fingers. There is, however, no doubt that thirty years ago the most practised auscultators of the day condemned, as the victims of organic valvular disease that would soon destroy them, children who have since grown up to be men and women, and who to all appearance enjoy excellent health. It is probable that they attached too ab- solute an importance to the existence of a murmur, and that they also committed the error of supposing that the louder the murmur, the worse the disease. One cannot insist too strongly on the fact that between these two things there is no re- lation whatever. The prognosis in the cases under consideration must be based not upon the physical qualities of the murmur, but upon a determination of the degree to which the disease disturbs the circulation ; or, if compensation be com- plete, upon the degree of increased strain thrown upon the heart. I have already pointed out how com- pensation is in many cases effected by dilatation and hypertrophy of certain of the heart's chambers. According to Jaksch there is another kind of compen- sation, consisting in conservative changes in the valves themselves, which absolutely prevent diseases of the valves from pro- ducing their natural consequences. When one cusp of the mitral valve is diseased, he imagines that the other may grow broader, and its chord® may lengthen until it meets its fellow. When one aortic valve is puckered up, the others may gradually become deeper and wider, so as to fill up the gap. The change last men- tioned is one which I have myself seen ; but it doubtless occurs only in very young patients. It has already been stated more than once that in valvular diseases of the heart the development of serious symptoms is often very long delayed. Dropsy may first show itself in a person advanced in years, and destroy life in a few months : but the mitral disease which is rightly re- garded as the cause of the dropsy may be traceable to an attack of rheumatic fever twenty or thirty years back : and in the interval the patient may either have had excellent health, or may always have suf- fered more or less from dyspnoea on exer- tion, which has shown that the heart was defective. It is a question discussed by almost all writers on Heart Diseases, whether a pro- longed existence, and delay in the de- velopment of serious symptoms occur in all forms of valvular disease alike, or be- long especially to any one group of cases. Considerable interest would indeed attach to the determination of the relative prog- nosis of the various affections of dif- ferent valves: and although statistical accuracy is not to be looked for, a general concurrence of opinion on the subject might fairly be expected. The case is not so, however. According to one of the most recent French writers, Jaccoud,1 stenoses in general are more serious than regurgitations: and mitral stenosis is more so than aortic stenosis. Again, Friedreich, the author of perhaps the latest German monograph,2 says that "as * Clinical Society's Transactions, ii. p. 221. 2 The analogy of scleroderma, however, perhaps suggests that even this is not abso- lutely out of the question. vol. ii.-48 1 Traite de Pathologie Interne, tome i. p. 657. 2 Krankheiten des Herzens, Handbuch der spec. Path, und Ther. 2te Aufl. 1867, p. 2S2. 754 DISEASES OF THE VALVES OF THE HEART. a rule the prognosis in obstructive forms of valvular disease is less favorable, and the duration of life shorter, in obstructive than in regurgitant affections." Now, according to all English writers this is absolutely incorrect. Walshe places "the chief valvular derangements in the follow- ing descending series on the basis of their relative gravity,-that is, estimating this gravity not only by their ultimate lethal tendency, but by the amount of compli- cated miseries they inflict :-Tricuspid regurgitation : mitral constriction and re- gurgitation : aortic regurtitation ; pulmo- nary constriction; aortic constriction." Thus Dr. Walshe regards aortic stenosis as admitting of a far better prognosis than aortic regurgitation: and Dr. Pea- cock agrees with him, stating that in the former disease life may be prolonged for many years, and a large amount of health and vigor be enjoyed ; whereas in aortic incompetency it is very rare to find life sustained for a considerable period. Dr. Peacock, indeed, differs from Dr. Walshe and from most other English writers in believing the prospects of longevity to be actually less in persons who labor under aortic regurgitation than in those who have mitral disease. I confess that I am unable to reconcile these conflicting state- ments. It is evident that the discrepancy is in great part due to the uncertainty which still attaches to the interpretation both of auscultatory phenomena and of morbid appearances. I have shown that, according to experience at Guy's Hospi- tal, aortic stenosis, without regurgitation, is far more rare than has generally been supposed: and certainly it would not within the last few years have been possi- ble to make any observations that would have allowed of a numerical comparison between its mortality and that of regurgi- tant disease of the same orifice. The latter disease, however, is undoubtedly a very fatal one. I find from the clinical records at Guy's, that from 45 to 50 per cent, of the patients who have aortic re- gurgitation die within the comparatively short period during which (under ordinary circumstances) they are allowed to remain as in-patients. But then it is to be ob- served that the fact of their admittance implies the existence of severe symptoms at the time: and the observations in question are not incompatible with the fact that the disease often exists for a lengthened period before such symptoms show themselves. I have already re- marked that changes in the aortic valves, allowing regurgitation, have often been found in persons who have presented themselves for life assurance, or in the dead bodies of those who have been killed by accident. Instances of this kind ap- pear to be fairly comparable with the case, on which Dr. Peacock lays so much stress, of a woman, set. 76, who died of strangulated hernia, and in whom two of the aortic curtains were completely blended into one, and the orifice reduced to a mere slit, although she was not known to have had any symptoms of dis- ease of the heart. Unless we agree with Dr. Peacock in supposing that disease of this kind always originates in congenital malformation, there is no proof whatever that in the case in question the disease had existed longer than in the examples of unsuspected regurgitant aortic disease which are so common. But while thus criticizing some of the evidence brought forward in proof that aortic stenosis is a less serious disease than aortic regurg- itation, I nevertheless believe that this is really the case. Again, it is very difficult to institute a comparison between the duration of life in mitral stenosis and mitral regurgitation respectively. For, as we have seen, the cases included under the latter designa- tion present no one pathological lesion, but rather a variety of more or less allied conditions. Many cases of mitral stenosis, with marked presystolic murmur, remain under observation for some years, and are admitted into the wards again and again, without the symptoms undergoing any great increase of severity, and with- out there being at any time reason to ap- prehend an immediately fatal issue. And on the other hand, it is well known that the systolic murmur of mitral regurgita- tion may be detected by auscultation for years before any serious symptoms show themselves. Lastly, I doubt whether any data exist from which one could accurately deter- mine the relative gravity of regurgitant aortic, and of regurgitant mitral disease. For, in addition to other points that have already been noticed, there is between these two affections an important distinc- tion in the fact that one of them is far more constantly traceable to a past at- tack of rheumatic fever than the other. Hence, while one can often with confi- dence say, in the case of mitral regurgi- tation, that the cardiac affection began years before, when the patient had acute rheumatism, one is commonly obliged to refer the commencement of aortic disease to the date when the patient first began to suffer from definite symptoms of heart- disease. Now it is certain that aortic disease sometimes exists for a long time without any symptoms at all; but whether this is the rule or the exception we have no means of knowing. There is, however, one particular mode of death which appears beyond doubt to occur in regurgitant aortic disease far more frequently than in any other affec- tion of the cardiac valves ; and it is one which for many persons has especial ter- rors,-namely, that in which the fatal termination is sudden. It is a curious TREATMENT. 755 circumstance that the contrary is stated by Corrigan, in the interesting paper which is almost the first that was written on this subject. In permanent patency of the mouth of the aorta, he says, li the fatal result is never sudden." "Under proper restrictions the patient is not only able to lead an active life for years, but is actually benefited by doing so." All re- cent writers, however, recognize the ten- dency to the occurrence of sudden death in the disease in question. Thus Dr. Walshe says" Taken as a group, val- vular impediments cannot fairly be cited as frequent causes of sudden death : but there is one among the number, of which the tendency to kill instantaneously is so strong that the fact must always be borne in mind in estimating its prognosis, and that is aortic regurgitation. . . . The manner of death is clearly syncopal: but the immediate mechanism, whether me- chanical or dynamic, is difficult enough of comprehension. I have known death take place during the act of walking, of eating, of speaking,-while the patient was emotionally excited, and, per contra, at a moment when he was perfectly calm. " Further on, Dr. Walshe appears to im- ply that the liability to sudden death is greater when the heart itself is perfectly healthy than when it presents dilatation and hypertrophy of the left ventricle or other morbid changes. But in this he differs from Dr. Peacock, who says2 that " in cases in which the heart is most re- markably enlarged, sudden death is yet of common occurrence," and who cites two instances of the kind, in which the hearts weighed 40 oz. and 46 oz. respectively. With regard to the prognosis of the dis- eases of the valves believed to originate in injury, all that can be said is that in recorded cases the duration of life has been very variable. Dr. Peacock states that the period of death in the different cases of injury to the aortic valves col- lected by him was "twenty-one days, three months and a half, thirteen months, two years, twenty-seven months, and three years and a half: and two persons were still surviving after five months and five years had elapsed" in their respec- tive cases. " In the cases of rupture of the mitral valve, the patients lived nine days, and twenty months : and two still survived eighteen months, and two years, after the occurrence of the accident." Treatment. - The prophylaxis of acute affections of the cardiac valves be- longs to the treatment of those diseases in which such affections are most apt to arise; and if endocarditis can really be prevented by medicine, this is, in fact, the most important part of the treatment of the diseases in question. But at pres- ent I do not know that one can really say any more about it than that rest should be strictly enforced, and that the chest should perhaps be protected from cold by a layer of cotton-wool. Scarcely less important is the preven- tion of the development of chronic dis- ease in valves that have once been dam- aged by acute inflammation. I have already adduced facts which tend to prove that endocarditis not rarely subsides with- out leaving any injurious effects behind it; in particular, that a large proportion of the cases of rheumatic inflammation of the aortic valves in women must termi- nate in the restoration of the normal structure of the valves. The compara- tive immunity of the female sex from the more remote changes which so frequently arise in the male sex can only be ascribed to the fact that women lead less active lives than men, and are not compelled to endure such continuous exertion, or to make such violent muscular efforts. The plain inference is, that in either sex the way to prevent chronic disease of the valves, after endocarditis in rheumatism or chorea, is to keep the patient for many months-or even some years-as perfectly as possible at rest; to insist on abstention from violent exercise, athletic sports and games, of all kinds; to direct the choice of a light, sedentary employment, and to urge the avoidance of all emotional excite- ment. General hygienic conditions should at the same time be carefully attended to. I think, too, that it may hereafter be shown that medicines are useful. I have pointed out how the anatomical charac- ters of chronic disease of the valves differ from those of acute endocarditis; that the vegetations disappear, but that the edges of the valves become thickened and fused together. Surely it is possible that iodide of potassium, mercury, or arsenic, may be able to arrest or prevent these changes, as much as those which belong to certain skin diseases, or the chronic inflammations of parts accessible to the sight or touch of the surgeon. Similar principles must be applied in the endeavor to prevent those forms of valvular disease which are from the first of gradual origin. A very large propor- tion of the cases of aortic regurgitant dis- ease that occur so commonly in laboring men past middle life, are due to the fact that these men have gone on with work involving straining efforts, which can with safety be made only by younger individ- uals, whose tissues are still elastic and supple. Dr. Peacock and Dr. Allbutt have indeed shown that such diseases of the cardiac valves frequently occur at an earlier period of life than has generally been supposed ; but even then they are 1 Op. cit. p. 390. 2 Croonian Lectures, p. 108. 756 DISEASES OF THE VALVES OF THE HEART. perhaps favored by some particular dia- thetic condition, or by habitual excessive indulgence in alcoholic drinks, which pro- motes degenerative changes in the tissues. It may hereafter be possible for the phy- sician to select certain individuals as es- pecially liable to suffer from the harder kinds of labor, and to recommend for them less arduous employments. Among the higher classes, again, chronic disease of the cardiac valves appears very fre- quently to be due to men forgetting that they are advancing in years, and to their continuing to take violent exercise long after they have ceased to be fit for it. This is especially apt to occur in profes- sional men, whose habits are generally sedentary, and who, during an occasional holiday, often run great risks. The phy- sician should always be on the lookout for the earliest signs of tissue-degenera- tion in such persons, and should be ready to warn them of the necessity that they should avoid too great exertions or strain- ing efforts. It is no longer believed that the signs in question are an early arcus senilis, and the fact that the hair has turned prematurely gray ; and I am my- self inclined to doubt whether tortuosity of the temporal arteries, or an apparent rigidity of the radial arteries to the touch, is to be much relied on, as indicative of degeneration of those vessels ; but, taken with other points, they are probably of value; and it seems that the sphygmo- graph may here lend very valuable assist- ance. Even when valvular disease is fairly es- tablished, the prophylactic measures al- ready referred to by no means cease to be applicable. Probably such disease is al- most always progressive; and it is, more- over, liable to become complicated at any period of its course by the supervention of acute endocarditis. But the treatment of diseases of the cardiac valves, properly so called, reduces itself to the treatment of their effects. To these we must therefore refer in brief detail. 1. Very little, and perhaps nothing, is known ot any effectual treatment for the contamination of the blood with morbid materials, which is so apt to occur in the more acute forms of valvular disease, or for the occurrence of embolism in the larger vessels. Quinine would seem to be indicated in the former condition, and may perhaps be of some service ; but Lancereaux observes that its failure has often been demonstrated in cases that had been mistaken for ague, and had there- fore been treated with this drug. The mineral acids are recommended by Fried- reich. I am not aware that any evidence is to be obtained as to the use of the sul- phites or hyposulphites, as recommended by Polli in septic conditions, but I should conceive that there is, at any rate, more chance that they might be useful in the cases under consideration than in the specific fevers against which they have chiefly been employed. Cases in which "typhoid" symptoms occur, with hemor- rhages into the skin and mucous mem- branes, &c., are probably of necessity fatal; and it is almost useless to adminis- ter the ammonia, ether, and musk, which are generally recommended, and which at once suggest themselves to the mind as the drugs that can be most appropriately given. When there is evidence of the occur- rence of embolism in any particular ar- tery, it is possible that the administration of ammonia, as suggested by Dr. Richard- son,1 may favor the solution of the coagu- lum-if indeed he is right in attributing success to this treatment in cases of fibri- nous deposition within the heart. The plan which he recommends is the admin- istration of ten-minim doses of the liquor ammoniae in iced water, every hour, with three to five-grain doses of the iodide of potassium every alternate hour. 2. The changes which diseases of the cardiac valves induce in the circulation of the blood, and in the several chambers of the heart, are capable of being modi- fied in a very remarkable degree by va- rious medicines and modes of treatment; and to these we must now turn our atten- tion, following as far as possible the same order which was adopted in the account of these changes given in pages 394 to 404. In cases of aortic regurgitation, so long as the state of the ventricle is such as perfectly to compensate for the valvular defect, medicinal treatment is scarcely applicable. Patients admitted into an hospital sometimes lose all their symp- toms as a consequence of the rest which they obtain, and which is so essential to them. The avoidance of all violent or straining efforts should in fact be insisted on in this, even more than in other forms of cardiac disease, on account of the marked tendency to sudden death, which must always be borne in mind. For the less severe effects of aortie re- gurgitant disease, the slighter degree of malaise and discomfort caused by it, senega is the common remedy. It is diffi- cult to say how this drug acts; and as ammonia is generally given with it, this has been supposed to be the really effi- cient remedy. I have, however, repeatedly prescribed it alone, and patients have sometimes declared that it has given them distinct relief. I am therefore disposed to believe that it is of value, and the more so, as the late Dr. Barlow (a physician of much experience in such matters) used to teach that in many cases only moderate 1 Med. Press and Circular, Nov. 20, 1872. TREATMENT 757 doses could be borne. The dose usually given is half an ounce to an ounce of the infusion, with or without half a drachm or a drachm of the tincture, and perhaps the same quantity of the aromatic spirits of ammonia, or five grains of carbonate of ammonia. When compensation fails in aortic re- gurgitant disease, we have seen that effects are developed which are identical with those that occur in mitral disease. They require the same treatment, which I shall describe in the next paragraph. In the treatment of a case of "mitral disease"-using that term for the moment in its widest sense-the primary point is the due regulation of the contractions of the left ventricle, for which we have in digitalis a remedy of wonderful power. Within the last few years a great change has taken place in our views as to the ac- tion of this herb, and our knowledge is very much more accurate than it for- merly was. The older opinion was that it enfeebled the power of the heart,1 and therefore that dangerous effects might in certain cases follow its administration, from its tendency to cause fatal syncope. It is true that Dr. Withering in the last century stated it to be most useful in those cases of dropsy in which the pulse was feeble or intermitting, declaring also that it seldom succeeded in men with a tight and cordy pulse. But its good ef- fects in such cases were attributed to its diuretic action, not to its having any power of strengthening a feeble heart. Within the last few years, however, it has been demonstrated that the action of digitalis on the heart is in fact that of a tonic. The proofs of this are varied. In cold-blooded animals, in which the car- diac pulsations can be watched after ex- posure of the organ, digitalis causes spasm of the left ventricle, beginning at isolated points in its wall, and finally affecting its whole substance, so that its beats cease, and it remains rigidly contracted and white. In conjunction with Dr. Steven- son, I some years ago performed a num- ber of experiments on frogs, in which this result was uniformly observed.2 In the higher animals it is less easy to study di- rectly the action of digitalis on the heart, but according to Fothergill,3 Handfield Jones and Fuller have noticed similar effects as regards the state of the heart after death in mammals. The present doctrine with regard to digitalis, then, is that it strengthens the heart's contractions. It is true that when very large doses are given, the pulse may become weak, frequent, and intermittent; but this is supposed to be due to the fact that the ventricle is in a state of spasm, and therefore that its beats are imperfect, and throw but a small quantity of blood into the arteries. Thus the cases of heart disease in which digitalis is most useful are those in which the organ beats feebly and irregularly, in which a condition of "asystolie" exists, and in which the pulse presents the sphygmographic characters indicated at p. 745. In such cases the action of the remedy is to diminish the frequency of the cardiac pulsations, to make them reg- ular, and to increase their force. Among affections of the cardiac valves, "mitral regurgitant disease" is that one which most commonly presents the indi- cations for the administration of digitalis ; and in a large proportion of cases of this kind, great relief is afforded by the rem- edy ; the symptoms may for a time be entirely removed, and the patient restored to a state of apparent health. On the other hand, it is often useless and perhaps injurious in cases of mitral stenosis; for the left ventricle in the earlier stages of this affection generally contracts regularly and with due force, as is apparent from the normal character of the pulse. At a later period in the course of mitral steno- sis, digitalis is often very useful; but the physical characters of the diseases are then less distinctive ; it is often difficult or even impossible to determine its exact nature. Again, in aortic regurgitation, when the hypertrophied ventricle is car- rying on the circulation vigorously, digi- talis often aggravates all the symptoms ; and if the patient should die suddenly, it is liable to the charge of having caused the fatal result, a charge which cannot be refuted, and is probably often justly made against the drug. But Dr. Binger has shown that the existence of aortic dis- ease does not contraindicate the use of digitalis, if the symptoms suggest its ad- ministration. When there is dilatation of the heart (rather than hypertrophy), and the pulse is feeble, frequent, fluttering, and (above all) irregular, it may be given with a fair expectation that it will afford relief. The dose of digitalis is a matter of some importance ; a drachm of the infusion is enough to begin with, or five or ten min- ims of the tincture. According to Dr. Fothergill, the injurious effects of digitalis in aortic disease, with hypertrophy of the left ventricle, may be avoided by employ- ing very minute doses, which will in such cases do as much good as is produced under ordinary circumstances by larger quantities of the remedy. It is doubtful whether any other reme- dies are capable of exerting the same ac- 1 Pereira's Mat. Med., 4th ed., 1855, vol. ii. p. 536. 2 Proc, of the Roy. Soc. 1865 ; Guy's Hosp. Rep. 1866. 3 1 ' Digitalis: its mode of action and its use," 1871. 758 DISEASES OF THE VALVES OF THE HEART. tion as digitalis on the diseased human heart. Dr. Stevenson and I found that squill and two species of helleborus (II. viridis and niger) produced the same pe- culiar effects in the healthy frog. Vera- trum viride is often supposed to resemble digitalis in this respect; and in America it has been largely used to diminish the frequency of the heart's beats. But in frogs its action is the very opposite of that of digitalis ; it rather resembles aco- nite, paralyzing the heart, which, when it stops, is dilated and of a deep purple color. The treatment for the backward effects of diseases of the valves of the heart must of course aim at reducing the increased tension in the pulmonary and venous sys- temic vessels, upon which these effects depend. And there are two principal ways in which this can be done. The first is the removal of a portion of the ve- nous blood by venesection, leeches, or cup- ping. Now, if we take into consideration the fact that blood is forced into the veins from the capillaries in a continuous stream, we shall not at first suppose that much benefit is likely to accrue from the abstrac- tion of a few ounces of blood from one part of the venous system. It seems like taking a cupful of water from a pail that is run- ning over with the supply from a spring. We cannot help imagining that the veins will almost instantly become again dis- tended. But there is abundant evidence to show that such a supposition is erro- neous. Thus the haemoptysis which ac- companies pulmonary apoplexy often re- lieves the patient's breathing for several days or even weeks; and nausea and vomiting, due to congestion of the stom- ach, are frequently removed for a consid- erable time by an attack of hsematemesis. It is clear that the relations, as regards tension, of the different parts of the cir- culating system can be much more stead- ily maintained than one would at first sight have imagined. Equally decided are the therapeutical proofs of the same fact. The withdrawal of a small quantity of venous blood is often attended with the most beneficial results in cases of heart disease. Perhaps the most striking ex- ample that I can cite is one, recorded by Dr. Dickinson,1 of a man who had rup- tured almost all the chordae of the poste- rior flap of the mitral valve. " This pa- tient was frequently relieved temporarily by the abstraction of blood. He was fre- quently cupped, always with apparent re- lief of the dyspnoea and distress. To- wards the close of his sufferings, when, though there was much cardiac action, the pulse was nearly imperceptible, and the patient was approaching a condition of collapse, with much dyspnoea and blue- ness of the face, eight ounces of blood were taken by venesection, with imme- diate and decided relief, the pulse recov- ering itself as the blood flowed, while the distress of the patient was much lessened. The improvement, however, was only temporary. The patient died the follow- ing night." The extreme gravity of the lesion in this case seems to render it worthy of being quoted. If the removal of blood could give relief when one-half of the mi- tral valve " had lost all valvular action, and swung uselessly from its base," there is hardly any case in which one need de- spair of its doing good. In the ordinary forms of valvular disease it is often use- ful, and the relief afforded by it is some- times maintained for several days, or even weeks, so as to allow time for the opera- tion of other remedies. The application of leeches to the epigastrium relieves the sickness and nausea due to congestion of the stomach; probably they would be still more useful if applied near the anus. The other method of relieving the en- gorged pulmonary and venous systemic circulation is by removing, not blood itself, but its watery part alone ; in other words by giving purgatives and diuretics. Among the former remedies, the hydra- gogues are of course to be preferred; jalap, or even elaterium, scammony, sa- lines, &c. As regards diuretics, it has already been observed that one of the principal indications of the favorable ac- tion of digitalis is its increasing the flow of urine, sometimes to an enormous ex- tent. Whatever view may be taken of the theory of its action, there is no doubt about the fact. Other remedies which are supposed to act as diuretics in the diseases under consideration are squill, juniper, broom, and cream of tartar. Co- paiba is sometimes very useful. I have notes of one case of mitral disease which had previously resisted various kinds of treatment, and in which ascites and ana- sarca rapidly vanished under the admin- istration of a simple copaiba mixture. I shall never forget the gratification of the patient as the loops of string that held his trousers together soon became unne- cessary, and the buttons themselves had to be moved again and again, in adapta- tion to the rapidly-decreasing girth of his belly. Dr. Wilks has recently found the resin of copaiba no less effectual, as it is certainly more pleasant. 3. The third group of effects of disease of the cardiac valves-the symptoms sub- jectively experienced by the patient-are frequently capable of great relief by med- ical treatment, but too often resist all the physician's efforts, and make the termi- nation of a case of this kind almost more distressing and painful than that of any other disease. 1 Path. Trans, xx. p. 151. ATROPHY OF THE HEART: HISTORY. 759 The obvious remedies for dyspnoea, pal- pitation, and the sense of pressure and weight in the epigastrium, are the ethers and ammonia, especially when combined with digitalis, if the nature of the disease should be such as to indicate its employ- ment. The application of a large bella- donna plaster to the cardiac region often gives considerable relief to local pain and to palpitation. Hyoscyamus is commonly given as an anodyne in these cases ; but I have not seen it do very much good. Opium is generally said to be inadmissible, or to be used only with great caution. On the other hand, it would appear that the sub- cutaneous injection of morphia may be employed with safety, and with the most marked results. Its use has been espe- cially advocated by Dr. Allbutt.1 He uses the hydrochlorate, in doses of one- tenth to one-third of a grain. It is espe- cially useful, he says, in cases of mitral regurgitation, " when the head is full of venous blood, and distress and stupor seem striving together. An injection of morphia three or four times a week, by tranquillizing the heart, and allowing the circulation to recover its freedom, sets free also the organs that are oppressed. . . . Directly and immediately the in- jection seems to affect the chest almost alone. The face generally becomes less turgid, and its expression calmer. The heart becomes tranquil and rhythmical. . . . The insufferable prsecordial dis- tress ceases. . . . The quick, shallow, anxious cardiac dyspnoea gives way to a deeper, slower, and easier movement. . . . The patient, who has been toss- ing in misery, feels the first tranquil sleep he has enjoyed for weeks." The attacks of angina-like pain, which form so important a part of the symptoms in many cases of aortic regurgitation, re- quire essentially the treatment of neu- ralgias. I have more than once found the regular administration of arsenic able to prevent their recurrence. The parox- ysms themselves are often arrested by the inhalation of ten drops of nitrite of amyl, or of a few whiffs of chloroform ; or again by the subcutaneous injection of morphia. In one case that I saw-in which all these were used in succession- the patient preferred the morphia, as giv- ing him the highest amount of relief. ATROPHY OF THE HEART. W. R. Gowers, M.D. Synonym.-Phthisis of the Heart (old writers). Definition.-Diminution in the size and weight of the heart, consequent on diminution in the amount of muscular tissue contained in its walls. Of these characters the diminution in weight is the most important. An atrophied heart, according to the common use of the term, is one the weight of which is less than the average weight for a person of the same stature, ft is said that, in very rare instances, a heart, the total muscular tissue of which is lessened, and the weight below the normal, may be larger than natural, owing to the dilatation of its cavities. The occurrence of such instances is, by some authorities, denied. If they occur, dilatation is their conspicuous fea- tur£S and they come more accurately un- der that head. Diminished bulk remains a character of those forms of atrophy which may most conveniently be consid- ered under this designation. On the other hand, the muscular tissue of the heart may be lessened in quantity, may have undergone atrophy, when there is increase of other elements in the cardiac wall. In such cases the weight of the heart is, as a rule, not diminished, and these instances are considered „under the head of the special degenerations. Only those rare examples will be here alluded to in which the weight of a heart so changed is less than normal. History.- The important functions always attributed to the heart rendered its atrophy a more anomalous condition, in the eyes of the earlier observers, than its enlargement. Accordingly we find that this condition early attracted attention. Pliny states that the kings of Egypt noted its occurrence. Riolanus alluded to it, and ascribed it to deficiency of the peri- cardial fluid. A well-marked case was recorded by Soumain at the beginning of 1 Practitioner, iii. p. 342. 760 ATROPHY OF THE HEART. the last century.1 Senac, in 1749, de- scribed it carefully in his treatise on the heart,2 which probably remains the longest monograph yet written on cardiac ana- tomy and pathology. Allan Burns, in 1809, described some very characteristic examples.3 It is not mentioned by Cor- visart, who wrote nearly at the same time. Merat, in 1813,4 alluded to seve- ral instances which he had seen, and Ber- tin, in 1824, gave a full occount of it, while by his editor, Bouillaud,5 varieties were subsequently discriminated, which have since been recognized by most writers on the subject. Varieties.-Forms of cardiac atrophy have been distinguished corresponding to the varieties of cardiac hypertrophy. Thus, reduction in the weight of the heart due to mere attenuation of the walls, the cavities remaining of normal size, was termed by Bouillaud, simple atrophy. Reduction in size of the heart, with diminution in the size of its cavities, so that they still bear the normal proportion to the heart, is the concentric atrophy of Bouillaud and Walshe,6the simple atrophy of Hayden.7 Attenuation of the cardiac walls and diminished weight of the heart, with in- crease in the size of the cavities, is the eccentric atrophy of Bouillaud, Forster, Walshe, and others. These cases, as just stated, came more properly under the head of dilatation. Hayden applies the term "eccentric atrophy" to a condition of heart, examples of which must be very rare, in which the walls are attenuated, the whole heart smaller, but the cavities larger than normal. As " concentric atrophy" he classes hearts which are smaller than normal, have the walls rela- tively thickened, and the cavities reduced in capacity. This variety was described by Merat in 1813. It may be doubted whether either of these two varieties has any real existence : they probably repre- sent only states of contraction or relaxa- tion in atrophied hearts. Chomel distin- guished two varieties according to the cause of the atrophy-the congenital and accidental.8 [Allied to cardiac atrophy, is atony of the heart; tending, of course, towards atrophy. This is met with, sometimes, as a result of overwork, producing cardiac exhaustion. During the civil war in the United States, cases of this kind were ob- served and reported upon, about the same time, by Drs. Stille, Da Costa, and my- self,1 as seen and treated inU. S. General Hospitals in Philadelphia. Soldiers who had been (particularly in the "peninsular campaign" of McClellan in Virginia) ex- posed to severe over-exertion in march- ing, with deficiency both of rest and food, were rendered unfit for duty, without evi- dence of any organic disease. In these cases, the pulse was small, abnormally rapid (85 to 100 beats per minute) when quite at rest, and greatly accelerated (up to 120 or 130) even by slight exertion, such as walking slowly across a room. Any considerable effort would cause dys- pnoea and general distress. On physical examination, the impulse of the heart was found to be feeble. Dulness of reso- nance upon percussion was not unusually extended. The sounds of the heart wrere not altered, except in the diminution of the duration and force of the first sound, making it more than normally like the second sound. From the absence both of symptoms and physical signs to prove the existence of any ordinary form of heart disease, some of these patients were, under medical in- spection, suspected of malingering. When sent back to duty, however, a short time sufficed to show their real disability. Rest for a considerable period with good food and tonics resulted in gradual im- provement. No fatal case occurred to give opportunity for autopsy. "Irritable heart" is the expression pre- ferred by some who have studied these cases, to describe their condition. Myers,2 Parkes, and others have noticed in the soldiers of the British army a greater tend- ency to functional disorders of the heart than exists in the same class of men in civil life. Faulty accoutrements are rea- sonably blamed for this. Some of the cases described by these authors recall the historv of those just mentioned, as exam- ples of cardiac exhaustion and atony. It is not hard to account for the patho- geny of such an affection. Increase of the work imposed upon the muscular tissue of the heart is familiarly known, under ordinary conditions, to produce hyper- trophy. This follows the general law of muscular exercise and nutrition. But, when overwork of the heart is compelled, as by rapid marching, with accoutre- 1 Relation de 1'ouverture d'une femme presqne sans coenr. Paris, 1728. 2 Trait6 de la Structure du Coeur, de son action et de ses maladies. Paris, 1749, tom. ii. p. 393. 3 Allan Burns, Observations on Diseases of the Heart. Edinburgh, 1809, p. 110. 4 Dictionnaire des Sciences Medicales, Art. Coeur. s Trait6 clinique des Maladies du Coeur. 2ieme edition. Paris, 1841. 6 Diseases of the Heart and Great Vessels. Fourth edition. London, 1873, p. 276. 7 Diseases of Heart and Aorta, 1875, p. 585. 6 Dictionnaire en 30 volumes. [• Amer. Journal of Med. Sciences, July, 1864.] [2 Prize Essay on Diseases of the Heart among Soldiers. London, 1870.] CAUSES-PATHOLOGICAL ANATOMY. 761 ments, etc., to carry, for many days, per- haps weeks, together, and, at the same time, not only little chance is left for sleep, but food is deficient in quantity and quality, instead of increase of power, ex- haustion must result. The time required for recovery of the tone and energy of the heart, under such circumstances may be extended through several months.-H.] Causes.-Smallness of heart may be a congenital or an acquired condition. A. Congenital atrophy is usually well marked. The heart of an adult other- wise free from disease may not exceed that of a child six or seven years old, as in an example mentioned by Allan Burns. The immediate causes of this condition are unknown. Hereditary influence has not, hitherto, been traced. It is said to be more common in women than in men. The subjects of it may be in other re- spects well formed, but sometimes it has appeared to be part of a more general arrest of development, shown by a childish aspect and defective development of the sexual organs. Parrot1 doubts the con- genital nature of these cases, and believes them to be due to a simultaneous arrest of the growth of the heart and of the sexual organs, occurring at puberty. B. Acquired atrophy may be the result of general or local causes. The chief general causes are chronic wasting diseases, in which the heart frequently undergoes diminution in size. This may occur in cancer, phthisis, syphilis, chronic suppu- ration, diabetes. According to the statis- tics of Quain,2 the heart is small in about half the cases of phthisis, and the diminu- tion in size is rather more frequent in women than in men. Out of 171 cases, it was small in 53 per cent, of the males, in 67 per cent, of the females. There is no evidence of any special influence exercised by these diseases on the heart. The organ apparently wastes in common with the rest of the body, in consequence of the defective nutrition. The local causes are such as influence directly the nutrition of the heart. Nar- rowing of the coronary arteries is said to be an occasional cause. The influence of this condition is to be more distinctly traced in the production of local degener- ation. Walshe, however, regards the in- fluence of pressure in causing local atrophy as due to its effect on the blood supply. Compression of the heart is apparently, in some cases, a cause of its atrophy. The heart has been found small in long-con- tinued pericardial effusion, and the condi- tion has been compared to the contraction of a lung in long-continued effusion into the pleura. Pericardial adhesions have been supposed in some cases to have caused cardiac atrophy. The association of the two conditions was first pointed out by Chevers.1 Hypertrophy and dilatation are more frequent consequences. Ken- nedy2 found atrophy in only five out of ninety cases of pericardial adhesion with- out valve disease. The contraction of tough lymph, resulting from pericarditis, has in some cases been associated with very distinct atrophy of the subjacent portion of the heart.3 Walshe corrobo- rates this, but believes that the effect is due to pressure upon the arteries. Com- pression by fatty tissue sometimes leads to atrophy of the muscular fibres, especially when the fat is infiltrated among them. The instances of this change in which the heart is smaller than the normal are very rare. Wilks and Moxon mention such a case as an example of " fatty atrophy. " The heart weighed only 5| oz. Local atrophy, affecting one part of the heart, is due most commonly to the last- described condition, to local infiltration with fat. Occasionally, the limited posi- tion of contracting lymph, or narrowing of one coronary artery, may have the same effect. Pathological Anatomy.-A heart the subject of atrophy is, as already stated, lessened in weight. The heart of an adult may weigh only six, five, or even four ounces. Quain mentions an instance of the heart weighing only 1 oz. 14 drs. in the case of a girl aged fourteen, who died of phthisis.4 Its size is also lessened. The circumference at the base may be only six inches. Chomel has recorded an instance in which the heart of an adult did not exceed in size a hen's egg. The thickness of the walls depends chiefly on the condition of the heart, whether con- tracted or relaxed. The degree of con- traction may be estimated by the size of the cavity. In cases of acquired atrophy almost all the adipose tissue has disap- peared from the surface, on which the vessels stand out conspicuously. There is often serous infiltration of the fibrous tissue from which the fat has been re- moved. The texture of the heart may be little changed, or it may be pale in color and softer than natural. On the other hand, it may be dark, dense, and tougher than natural. The change depends on the presence and form of degeneration, whether fatty or fibroid, partly also on the accumulation of pigment granules 1 Dictionnaire Encyclop6dique des Sciences Medicales, 1876, art. Coeur. 2 Lumleian Lectures, 1872. Abstract in Lancet, vol. i. p. 426. 1 Guy's Hosp. Reports, vol. vii. 2 Edin. Med. Journal, 1858. 3 An observation of this kind was recorded by Malpighi. 4 Lumleian Lectures, loc. cit. 762 ATROPHY OF THE HEART. within the fibres. The microscope shows the primitive bundles to be lessened in size. The fibres are often fattily degen- erated ; their striation is lessened, some- times indistinguishable.1 The fibrous tissue between the bundles may be in- creased in quantity. Occasionally, espe- cially in the old, brownish pigment may encircle the nuclei of the fibres, or be uniformly distributed through their sub- stance. When it occurs, the pigmenta- tion is usually generally distributed through the heart, and gives its substance a reddish-brown tint. Rindfleisch2 has described it as a special form of atrophy -' ' brown atrophy. ' ' Friedreich believes that the pigment is derived from the col- oring matter of the muscle. Associated conditions, causing the atro- phy, may coexist. The various general conditions, cancer, phthisis, &c., may be present. Pericardial changes, effusion, lymph, plates of calcification, fatty accu- mulation, may compress the heart, or there may be from some cause obvious reduction in size of the coronary artery. The pericardial fluid is, according to Bam- berger, often increased in quantity as a consequence of the cardiac atrophy. Symptoms.-The physical signs of atro- phy depend on the lessened bulk and diminished force of the heart. The extent of dulness, especially the deep dulness, is smaller than normal. To be significant the diminution must be independent of emphysema or any lung condition obscur- ing the cardiac dulness. The impulse is weak, and felt over a small area. The sounds may be lessened in intensity, or they may be unchanged. The latter has been the case in Walshe's experience. The pulse is small, the patient weakly. When due to a local cause the symptoms of the local causative condition, pericar- dial effusion, &c., are often present. Pal- pitation, dyspnoea, and dropsy, are said to occur in cases of acquired atrophy from local malnutrition. The quantity of blood remains unchanged, and the small heart obstructs the circulation. When due to a general state, the heart suffers in common with the blood and the rest of the system, so that the special failing is unnoticed. The general conditions associated with atrophy of the heart were, in part at least, attributed by the earlier writers to the influence of the cardiac state. Phthisis especially was believed to be entirely due to the small size of the heart, so often found associated with it. It is customary now, as already stated, to regard the small size of the heart as secondary to the general state, and to attribute to it no causative influence. Diagnosis. - In determining, post mortem, the existence of atrophy, weight should be taken as the test. The error of mistaking contraction for atrophy will thus be avoided. Burns suggested, as a means of avoiding the same error, a com- parison between the size of the heart and of the pericardium. The size of the body should always be taken into consideration. It is rarely that atrophy of the heart can be diagnosed during life. It may be sus- pected when a weak impulse and dimin- ished dulness coincide with signs of car- diac failure and with some recognized causal condition. Prognosis. - Little can be done to remedy the condition, even when its ex- istence is recognized. The prognosis is therefore unfavorable, but it is always subordinate to that of the condition to which the atrophy is secondary. Treatment.-The treatment is in the main that of the causal state. In general wasting diseases the atrophy of the heart corresponds to its diminished use, and needs no special treatment beyond general tonics, cod-liver oil, nux vomica, &c. When secondary to local changes, little can be done by treatment beyond the re- moval as far as possible of the fluid press- ing on the heart, or the diminution, by dietetic management, of accumulations of fat. 1 The "yellow atrophy" of Rindfleisch is fatty degeneration. 8 Pathologische Gewebelehre, 1875, p. 126. HYPERTROPHY OF THE HEART: HISTORY. 763 HYPERTROPHY OF THE HEART. W. R. Gowers, M.D. Synonyms.-Enlargement of the Heart, 1 Dilatation of the Heart (old writers); Ac- tive Aneurism (Corvisart); Uniform En- largement of the Heart, distinguished from dilatation (Allan Burns); Hypersar- cosis Cordis (Lallemand). Definition.-An overgrowth of the muscular tissue which forms the walls of the heart. Besides muscular tissue the > heart contains connective tissue and adi- pose tissue. An increase in either of these constituents may be, and has been, spoken of as an element in cardiac hypertrophy. Thus "fatty hypertrophy" and "con- nective tissue hypertrophy," or "false hypertrophy," of the heart have been de- scribed. It seems more in accordance with the nomenclature applied to other organs to consider these changes as allied to degenerations, and to confine the term "hypertrophy" to increase in the muscu- lar tissue of the heart. Increased thick- ness of the endocardium and pericardium, which often coexists with muscular hyper- trophy, and is sometimes regarded as part of it, is described separately in the articles "Endocarditis" and "Pericarditis." History.-The earliest allusions to en- largement of the heart appear to be those of Nicolaus Massa in 1559' and of Vesa- lius. Enlargement with thickening of the walls was described in the seventeenth century by Albertini, by our own country- man Mayow, and by Blancard. Its origin in overwork due to obstruction in the cir- culation was clearly pointed out by Mayow, who in 1674 described the dependence of hypertrophy of the right ventricle on mi- tral constriction.2 Vieussens' in 1715 alluded to the origin of hypertrophy of the left ventricle in the overwork caused by constriction of the aortic orifice, and the effect of obstruction in causing enlargement was systematically described by Senac in his treatise published in 1749.2 Enlargement from overgrowth without dilatation was mentioned by Morgagni3 in 1779, by Burserius in 1798,4 and later by Corvisart in 1806, and distinguished by Allan Burns in 1809, who recorded an example of a heart "weighing several pounds, in which the cavities were not more capacious than natural." Corvisart gave a clear description of the various forms of hypertrophy with dilatation, and recognized the frequency with which the left ventricle is affected. Although he mentioned the occurrence of hypertrophy without dilatation, he did not include it in his account of the forms of enlarge- ment,5 but described all enlargements of the heart as "aneurisms," classifying them as " active" or " passive," according as there was or was not hypertrophy. Bertin, in a memoir read before the Aca- demic des Sciences in 1811,6 pointed out beyond the rest." Mayow, Tractatus medico- physici, Oxonii, 1674. De Motu Musculari, cap. vii. The translation is that of Cockle, On Insufficiency of the Aortic Valves. Lon- don, 1861. 1 Trait4 du Cceur, 1715. 2 Traite de la Structure du Coeur, de son action et de ses maladies, par M. Senac. Paris, 1749. Tom. ii. p. 408. 3 "Ventriculus dexter corveam quidem secundum naturam, sed crassissimas parietes habebat." De sedibus et Causis morborum. Epist. xvii. art. 22. See also Epist. xxix. art. 20. 4 The Institutions of the Practice of Medi- cine, by J. Baptist Burserius, of Kamfeld, 1798. Translated by Cullen Brown. Vol. v. p. 312. Edinburgh, 1803. 6 This accounts for Laennec's assertion that the occurrence of hypertrophy without dila- tation escaped the notice of Corvisart. Ber- tin pointed out that the condition is described by Corvisart in a case of aneurism of the aorta. " The left ventricle, without being so dilated, had much stronger and thicker pari- etes than usual." On Diseases of the Heart, Hebb's Translation, p. 283. 6 Mem. de l'Academie Royale des Sciences, 1811. 1 Nicolaus Massa, Anatomise Liber Intro- ductorius. Venice, 1559, p. 56. 2 "Inasmuch as the blood, on account of the obstruction, could not pass freely into the left ventricle, it necessarily happened that the vessels of the lungs, and also the right ventricle, were distended with blood; as a consequence the heart, particularly the right ventricle, would have to contract more vio- lently, in order that it might as far as possi- ble propel the blood through the lungs on to the left ventricle. This again explains why the walls of the right ventricle were so strong and dense, since this chamber, being submit- ted to mcwe violent action, would be enlarged 764 HYPERTROPHY OF THE HEART. the special character of hypertrophy and its isolated occurrence. It was also care- fully distinguished by Kreysig in 1816.1 But in France the nomenclature of Corvi- sart continued in use by Merat, Cloquet,2 and Cruveilhier until, and indeed long after, the publication of Bertin's treatise on diseases of the heart3 in 1824 gave cur- rency to his distinction of the "con- centric," "simple," and "eccentric" forms of hypertrophy. Bertin also dem- onstrated by microscopical examination that the increase of the heart's substance in hypertrophy depends on an overgrowth of muscular tissue, and also endeavored to show, by a chemical examination of the tissue of the two ventricles, that the quan- tity of fat in the hypertrophied muscle was less than in the normal portion.4 He also ably vindicated hypertrophy from some of its supposed consequences. Avenbrugger in 1763 first employed percussion as a means of ascertaining and estimating enlargement of the heart. The example was followed by Corvisart, who translated Avenbrugger's work. Bertin advocated auscultation as a means of dis- tinguishing the "concentric" and "ec- centric" forms. The alterations in the heart-sounds in hypertrophy were, how- ever, first accurately stated by Laennec.5 Varieties.-The hypertrophy may be general, when each portion of the heart is affected, or local, when only part of the heart is changed. When the result of the change is a simple increase in the thick- ness of the wall, without any change in the size of the cavity, the hypertrophy is called " simple when there is dilatation of the cavity as well as hypertrophy of the walls, the hypertrophy has been termed " eccentric.'1'1 u Hypertrophy with dilatation," or "dilated hypertrophy" are other names which have been applied to this condition. If, on the other hand, the cavity is lessened in size, the hyper- trophy has been termed "concentric." The existence of this form is doubtful; it is probable that the supposed permanent reduction in the size of the cavity is merely the result of a strong contraction. "Mixed" hypertrophy was the designa- tion given by Bertin to the condition in which one part of a ventricle is thinned and another thickened. Causes and Pathology. - A. Pre- disposing Causes.-Strictly speaking, hy- pertrophy of the heart cannot be said to have any morbid predisposing causes. It is a healthy reaction against a morbid influence, and the conditions which permit its occurrence are those of health. Every divergence from a state of health, which does not immediately excite hypertrophy of the heart, tends to hinder its occur- rence. The only general or distant mor- bid states which are concerned in its pro- duction are the antecedents of its exciting causes, and these cannot, strictly, be re- garded as "predisposing." Hereditary taint, sex, and age influence the occur- rence of the exciting causes of hypertro- phy, and render the condition twice as frequent in males as in females (Walshe), and frequent in proportion to age, because men are by occupation and exposure liable to the causes of hypertrophy more than women, and hypertrophy is frequently the result of degenerative changes, the tend- ency7 to which increases with age. Four conditions of health may be con- sidered as especially predisposing to hyper- trophy. (1) General nutritive energy of the sys- tem. This influence is shown in the tendency of the normal tissue elements to increase, under certain local stimuli; its defect by their tendency to waste, to de- generate, and give place, under the local nutritive stimulus, to tissue elements of lower vital capacity. This influence is greater in the young than in the old. Its effect in determining the occurrence or the degree of hypertrophy is masked by the greater frequency and greater force of the causes of hypertrophy in later life. It is seen, however, in the rarity with which considerable hypertrophy is developed in old age. (2) Nutritive quality of blood. The influence of this condition is obvious, and is seen in the distinct increase in hyper- trophy which often follows the adminis- tration of hsematinics, as iron, and a good supply of food. (3) "The supply to the cardiac walls of a due quantity of blood. The force of the circulation within the cardiac walls is proportioned to the distension of the aorta.1 Hence, whatever interferes with 1 This was very clearly taught by Corvi- sart. "The heart . . . will have to drive forward, through the narrow artery, too great a column of blood . . . which will necessarily react upon the agent which impels it. . . . Finally, the coronary arteries as well as the capillaries of the heart, remaining in a permanent state of fulness, will supply more nourishing matter to the fleshy substance of this organ ; whence arise, without doubt, the increase, at least in part, of its vital energy . . . the greater con- sistence of the parietes, and the more vigor- ous action of the organ.''-Loc. cit. p. 60. 2 Die Krankheiten des Herzens, Theil ii. Abt. i. p. 460. 2 Diet, des Sciences M^d., art. Coeur. 1813. 3 Traite des Maladies du Coeur et des Gros Vaisseaux, by R. J. Bertin. RedigS par Bouillaud. Paris, 1824. 4 Loc. cit. p. 300. 8 A Treatise on Diseases of the Chest, Forbes' Trans. 1821, p. 372. VARIETIES. 765 the quantity of blood entering the aorta lessens, cceteris paribus, the capacity of the heart for overgrowth ; whatever increases the quantity of blood sent into the aorta, and increases the tension of the blood in it, increases the blood-supply to the heart, increases its capacity for overgrowth. This is no doubt one of the conditions which determines the great hypertrophy so common in aortic regurgitation. The distension of the aorta at the end of the ventricular systole, when the coronary arteries are being filled, is, in that disease, extreme.1 (4) The greater (within limits) the pro- portional amount of rest of the heart, the more perfect is its nutrition. The period available for nutrition is greater when the contractions are infrequent than when they are frequent. The systole is nearly of the same duration at different fre- quencies ; increased frequency in con- traction is at the expense of the diastole. Hence infrequent contraction favors the development of hypertrophy when its ex- citing cause exists. The actual influence of this condition is obscured by the in- crease in the exciting cause, overwork, which frequency of action involves. B. Exciting Causes.-As far as is at present known muscular hypertrophy has but one immediate cause-increase of work. The operation of this cause, the " physiological stimulus," as it has been termed, may be traced in almost every instance in which hypertrophy is found. Each apparent exception becomes con- formable to the rule when the conditions under which the hypertrophy began are accurately known. The over-action of the heart is the cause of its over-growth. Such over-action may be primary, or it may be secondary to an increased resist- ance to its action. Primary over-action commonly takes the form of increased frequency of contraction. Secondary over-action is in the form of increased force of contraction. But the distinction is not absolute, as will appear imme- diately. Other causes have been assumed to ac- count for hypertrophy in cases in which the influence of increased work could not be clearly traced, An irritative influence of the blood on the heart, leading directly to its overgrowth, has been assumed in order to account for some cases of hyper- trophy. But there are at present no facts to support the idea that any blood state, any nutritive influence other than the physiological stimulus, ever leads to over- growth of muscular tissue.1 I. Simple Over-action of the Heart, the conditions of the circulation and heart entailing no increased resistance, i. e. no primary increase of work-is always the consequence of deranged innervation. Its nervous mechanism is at present ill-under- stood. It is extremely doubtful whether a simple increase in the force, without change in the frequency, of the heart's action, ever results from this influence. Increased frequency is the common re- sult. The more frequent contractions are often apparently more forcible. Such over-action of the heart is well seen in simple nervous palpitation, and most strikingly in exophthalmic goitre. Con- tinuous emotional excitement is a power- ful cause of it. It is produced also by the influence of many agents, such as alco- hol, tea, and coffee. It is produced also by general muscular effort. Effort acts, it must be remembered, in another way, by causing increased resistance to the movement of the blood.2 1 The conditions of overgrowth in different tissues no doubt vary widely. In some, hyperplasia of the proper tissue elements is induced by any local irritant. This has suggested a generalization which asserts a common basis for hypertrophy and inflamma- tion. The conclusion, true of some tissues, is quite inapplicable to muscular fibres. (Vide Moxon, Med. Times and Gazette, Nov. 26, 1870.) But the theory has obtained in Germany wide currency and application, so that a recent writer (Zielonko, Virchow's Ar- chiv, 1872) gives, as an example of hypertro- phy of the heart, the enlargement which resulted from the insertion of a seton in its substance, although microscopical examina- tion showed only ordinary inflammatory pro- ducts as the cause of the enlargement. Henry Green (Clin. Soc. Trans, vol. ii.) has sug- gested that hypertrophy of the heart may sometimes be due to the irritative influence of the blood in rheumatism, but the evidence which he has adduced is chiefly clinical, and possesses little weight in comparison with the almost uniform significance of pathological facts. 3 Les mouvemens violents donnent souvent plus de masse au cceur de meme que les mala- dies : nous reduirons ces mouvemens aux exercises fatiguants, a 1'agitation qui suit les exc^s du vin, et it celle qui causent les pas- sions (Senac. loc. cit. tom. ii. p. 400). Cor- visart recorded his conviction that the pas- sions were the most powerful cause of organic diseases of the heart, and instanced the influ- ence of the French revolution in causing the malady (loc. cit. pp. 322 and 323). Statistics furnished by Farr, and given by Quain in his Lumleian Lectures, show that the deaths of males at all ages from heart disease have in- creased fifty per cent, on the increase in 1 Milner Fothergill (Diseases of the Heart, p. 65) maintains that the blood-supply to the heart walls is deficient in aortic regurgitation, because the tension in the aorta so soon falls. But, from the short course of the coronary arteries, their distension must be rapid, and related, in degree, to the degree of the ten- sion of the aortic blood, rather than to the duration of the tension. 766 HYPERTROPHY OF THE HEART. Such increased frequency of contraction tends to cause hypertrophy only in so far as it increases the total work of the heart. It does this, however, in more than one way. (1) Part of the work of the heart consists in the movement of its own mass. No doubt this is but a small fraction of its total labor, but it is a definite quantity, and increases directly as the frequency of contraction. (2) Although simple increase in the frequency of contraction of the heart does not necessarily increase that part of the heart's work which consists in the propulsion of the blood, it does prac- tically effect such an increase. If a heart contracts at twice the normal frequency, and the blood enters the heart at the nor- mal rate, only, say, one-half of the normal quantity of blood will at each diastole enter, and at each systole be discharged. The work of the heart in propelling the blood would thus remain the same. Prac- tically, however, increased frequency of contraction tends to quicken the whole circulation, so that under the circum- stances assumed, more than half the normal quantity of blood would at each contraction enter and leave the heart. Hence the tension of the arterial blood becomes increased, and the pulse fuller and less compressible. Reflex relaxation of the peripheral arterioles, the natural effect of increased tension, relieves, but often in- completely, this increased tension. Thus intra-ventricular pressure and the work of the heart are increased. (3) The heart, acting thus with excessive frequency, may act also with excess of force. The in- creased force may be felt under such cir- cumstances. The heart "thumps"against the ribs. In the pulse the increased force often is unnoticed on account of the smaller quantity of blood which leaves the left ventricle at each contraction. It should be remembered that many circum- stances which increase the frequency, also, at the same time, increase the force of the heart's action. Muscular effort is one of these. This then is the mechanism by which increased frequency of contraction may cause hypertrophy. Its total influence is not, however, great. Increase in fre- quency of contraction is rarely of long duration under circumstances of due nu- tritive energy, and it is not often that hypertrophy can be ascribed with prob- ability to simple primary over-action of the heart. II. Increased Resistance to the Action of the Heart is unquestionably the chief cause of its hypertrophy. Such resistance may be in the form of (1) traction from with- out, or of (2) pressure within the contract- ing organ. (1) As a matter of fact pericardial ad- hesions are frequently associated with cardiac hypertrophy and, according to Wilks,2 with hypertrophy of the right ventricle much more frequently than of the left. It is easily conceivable that such adhesions may oppose the diminu- tion in size, and change of shape, which the heart undergoes during its contrac- tion. But for such adhesions to hinder a contracting heart, the external surface of the pericardium must be connected with more than usual firmness to the adjact nt structures. It is not certain, moreover, that resistance to contraction applied from without has the same effect as resistance applied within the heart, and the con- ditions are so complex that it is impos- sible to trace the direct influence of the adhesions in causing the hypertrophy. Dilatation is invariably, under such cir- cumstances, associated with the hyper- trophy of the heart. It would seem to be a more direct result of the pericardial adhesion than the hypertrophy, both as the simple effect of the external traction, and as the result of the weakening of the wall of the heart by the sub-pericardial changes. But dilatation tends in itself, as will be shown immediately, to produce hypertrophy, and the hypertrophy in an adherent heart, without other cause of hypertrophy, is commonly not more than the dilatation might account for. The effect of pericardial adhesions is consid- ered at greater length, in the article on Dilatation of the Heart. Their direct in- fluence in causing hypertrophy must be regarded as possible, but unproved. (2) Increased blood-pressure within the heart during its systole is the common cause of its muscular over-growth. This is the element which underlies most of the conditions capable of giving rise to hypertrophy. This increased pressure may be due to one of two causes ; (a) the mass of blood to be moved may be ab- normally large; (6) there may be an ab- normal obstruction to the movement of the blood. The effect of each condition is to augment the resistance to be over- come by the contracting fibres-to in- crease the work of the heart. (a) The mass of blood to be moved may be abnormally large. This condition exists in all forms of over-distension of the heart. Dilatation cannot exist with- out an increase in the work of the heart. Hence hypertrophy is its almost invari- able concomitant-invariable when the nutritive conditions are such as to render growth of muscular fibre possible. population, and that this increase affects adult life almost exclusively (Lancet, 1872, vol. i. p. 392). 1 As Morgagni, Beau, Hope, and others have especially noticed. 2 Guy's Hosp. Reports, vol. xvi. p. 202. VARIETIES. 767 The mechanism of over-distension is considered fully in the article on Dilata- tion of the Heart. It may be direct or indirect. It is direct when a cavity is over-filled by the contraction of an over- distended chamber behind it. Thus in mitral regurgitation the left ventricle is over-filled by the contraction of the over- distended left auricle, and becomes di- lated and hypertrophied ; or the over-dis- tension may be indirect, the result of a supply of blood to the chamber from a double source-the regurgitation of blood into the chamber and its supply in the normal course of the circulation. Thus the left ventricle becomes over-distended, dilated, and often enormously hypertro- phied in aortic regurgitation; and the left auricle becomes dilated and hypertro- phied in mitral regurgitation. So, too, in dilatation from the weakening of the wall consequent on pericarditis, hypertrophy commonly ensues. No doubt in these conditions of dilatation the whole of the blood is not always expelled from the ventricle at each systole, but the intracar- diac pressure during the systole is still in- creased and with it the work of the heart. Plethora has been supposed to cause cardiac hypertrophy. Niemeyer points out that the transient plethora induced by a hearty meal with much fluid may, if habitually repeated, have such an in- fluence. The action of the kidneys com- monly prevents any permanent distension of the vessels from this cause. (6) There may be an obstruction to the movement of the blood superadded to that which exists in health. This ob- struction may be situated within or with- out the heart. Within the heart, it may be at the orifice by which the blood leaves the chamber affected. Thus an obstruc- tion at an auriculo-ventricular orifice will cause hypertrophy of the corresponding auricle ; obstruction at the orifice of the pulmonary artery will cause hypertrophy of the right ventricle ; obstruction at the aortic orifice will cause hypertrophy of the left ventricle. In all these cases di- latation may be conjoined with the hyper- trophy, and increase its amount. The obstruction may be outside the heart. It may be in the larger arteries, the aorta and pulmonary artery. Their calibre may be reduced by pressure upon them (as by an aneurism of another ves- sel), or by constriction due to changes in their walls? The hypertrophy which oc- casionally occurs in long-continued dis- placement of the heart, whether from pleural effusions or deformities of the thorax, consequent on curvatures of the spine, &c., is probably due chiefly to the increased obstruction in the great ves- sels from their displacement and altered course.1 Aortic aneurism has been regarded as a cause of hypertrophy of the left ventri- cle since the days of Corvisart. The asso- ciation of the two has frequently been noted, and has been referred by Niemeyer to the law in physics according to which the resistance encountered by a liquid moving through a tube is increased if the tube be suddenly expanded, just as if it be contracted. But it is a matter of con- siderable doubt whether hypertrophy does occur as a simple consequence of aortic aneurism. Senac long ago expressed a doubt upon the subject.2 Stokes affirmed that "we have no reason to believe that the existence of aneurism in any portion of the aorta throws additional labor on the heart, and hence we commonly find a small heart coexisting with a vast aneur- ism."3 Walshe also regarded the hyper- trophy as an occasional consequence, and not invariable even when the sac of the aneurism was situated near the sigmoid valves. The observations of Axel Key,4 indeed, suggest the question whether hypertrophy of the heart is not more com- mon when the aneurism is far from, than when near the heart. He has recorded eighteen cases of aneurism near the heart, in not one of which was there hypertrophy of the left ventricle. In most of the cases, indeed, the muscle was more or less thinned, with or without slight dilatation, especially of the lower part of the cavity. Considerable dilatation seemed related to disease of the aortic valves, not to the aneurism. In several cases the cavity of the ventricle was positively diminished in capacity, although the walls were thinned. In some instances the muscle of the conus arteriosus was thick, while the rest was thin. The atrophy of the muscular tissue was most marked in some cases in which the aneurism lay near the heart. He suggests as an explanation of this sin- gular atrophy of the left ventricle, the pressure of the aneurism on the pulmonary artery, lessening the amount of blood, reaching the left ventricle, and the with- drawal from the circulation of the blood contained in the sac of a large aneurism. 1 See Hilton Fagge, Path. Trans, vol. xvii. 2 " It is certain that the dilatation of these vessels (aorta and pulmonary artery) have not always the consequence (of causing en- largement of the heart)." He goes on to describe a case in which the aorta was dilated to the size of a head, from the arch to the diaphragm, in which the volume of the heart was normal. Senac, Traite, &c., 1749, tom. ii. p. 407. 8 Diseases of the Heart and Aorta, p. 579. 4 Nord. Med. Ark. 1869, I. 4, Nr. 22, and Schmidt's Jahrbuch, vol. 150. p. 21. 1 Hypertrophy of the left ventricle has been produced artificially by Zielonko, in the guinea-pig by tying a ligature round the aorta, and thus reducing its calibre. Vir- chow's Archiv, Bd. 62, Heft I. p. 22. 768 HYPERTROPHY OF THE HEART. Degenerative changes in the arteries cause a considerable increase in the total work of the heart, and are effective causes of hypertrophy. The increased resistance which they produce is due to the loss of elasticity in the vessels, their more tor- tuous course, and the increased friction from roughening of their inner surface. In health the elastic vessels yield before the blood which is thrown into them. When elasticity is lost the vessels approx- imate to rigid tubes, and the resistance they present is consequently increased. By the increased tortuosity of the vessels, due to the loss of elasticity, their absolute length becomes greater, and the friction of the blood against the wall of the vessel is also increased. These degenerative changes are usually found, in greater or less degree, after middle life, and are probably the cause of the increase in the thickness of the left ventricle, which has been said by Bizot1 to occur during the later period of life. Degenerative changes may be a consequence as well as a cause of cardiac hypertrophy, the result of the increased strain to which the vessels are exposed. This fact, which will be con- sidered presently, must not be forgotten in estimating the significance of the asso- ciation. The obstruction may be situated in the minute arterioles and capillaries. In cer- tain diseases of the lungs obstruction from this cause may be traced. In em- physema many vessels are destroyed, and those which remain are elongated and narrowed by the over-distension of the air-cells. The obstruction to the passage of the blood through the lungs is thus very much increased, and hypertrophy and dilatation of the right ventricle result, and may be carried to a high degree. Hypertrophy of the heart is not infrequent in phthisis ; Quain states that in 171 cases it was present in 25 per cent, of the males, 7 per cent, of the females. The condi- tions of lung to which it is related have not yet been ascertained, but in cirrhosis of the lung it is especially frequent ; the compression and destruction of the minute vessels by the contracting tissue produce the obstruction. Compression of the lung tissue by pleural effusion is said to have a similar effect. In all these conditions, if long continued, hypertrophy of the right ventricle may occur. Long-continued muscular effort entails cardiac hypertrophy. As Clifford Allbutt and Myers have shown, the influence of this cause can often be distinctly traced, especially (Milner Fothergill says) among those who work with the arms. Animals frequently afford instances of the remark- able effect which this cause is capable of producing. The most celebrated instance is that of the celebrated Irish greyhound "Master Magrath," the heart of which bore three times its normal proportion to the body-weight, and no cause for the enlargement but extreme and long-contin- ued exertion could be discovered.1 The increased work in which the hypertrophy arises is probably in part the result of the increased frequency and force with which, in consequence of the respiratory needs, the heart acts. But it is in part the re- sult of the compression of the capillaries of the muscles by the contracting fibres, and also the result of the compression of the arterial trunks by the rigid muscles. The total resistance to the action of the heart is thereby considerably increased. This resistance is not a matter of conjec- ture. Increase in arterial pressure during general muscular contraction has been demonstrated experimentally by Traube. During pregnancy the addition of the placental to the systemic circulation in- volves a considerable addition to the work of the heart. Larcher2 found, on examination of the hearts of 100 women who died in child-birth, that the wall of the left ventricle was invariably thick- ened. The average thickness was *015 m. (about | inch). His observations have been confirmed by the clinical investiga- tions of Duroziez, who found that the greater the number of pregnancies the more permanent is the enlargement. He asserts that the enlargement continues through the whole of the lactation period. Friedreich, however, expresses some doubt on the subject.3 The remarkable hypertrophy of the heart which is met with in Bright's dis- ease must be considered among those which result from obstruction to the flow through the minuter vessels. It occurs in all forms of chronic kidney disease, most frequently in the contracted kidney, least frequently in the lardaceous form. According to Grainger Stewart, it is in- variable in the last stage of the acute in- flammatory affection, in which, the dis- ease having assumed a chronic form, the kidney undergoes reduction in bulk. The hypertrophy which occurs in this condition is confined to the left ventricle, and is often uncomplicated by dilatation. It is frequently considerable in amount. Among such hearts the best examples of simple hypertrophy are met with. After death the heart often remains firmly con- tracted, and the characters of a concen- tric hypertrophy are simulated. Dilata- tion may coexist with the hypertrophy in consequence of coincident degeneration. 1 Haughton, British Medical Journal, Jan. 20, 1872. 2 Archives G^n. de Med., Mars, 1859, and note by Larcher appended to a paper by Meniere, Ibid., tom. xvi. 1828, p. 521. 3 Herzkrankheiten, p. 288. 1 Memoirs de la Soci^te Medicale d'Observ. de Paris, 1836. VARIETIES. 769 The association of this hypertrophy of the heart with kidney disease was iirst pointed out by Bright in 1827' as so re- markable that some causal connection between the two must exist, and he after- wards, in 1836,2 expressed his opinion ''either that the altered quality of the blood affords irregular and unwonted j stimulus to the organ immediately, or I that it so affects the minute and capillary circulation as to render greater action necessary to send the blood through the distant subdivisions of the vascular sys- tem." The latter theory is that which has obtained general acceptance, with certain modifications to be alluded to more fully. Modern investigation, while it has extended our knowledge of the con- ditions under which the hypertrophy arises, has scarcely carried us further in our explanation. The most important addition to our knowledge is certainly the fact that in- creased tension of the arterial blood com- monly occurs in those cases of Bright's disease in which hypertrophy of the heart is so often found. The Hardness of the pulse in such cases had long been re- marked, but its significance was not gen- erally recognized until the sphygmograph, by supplying a measure of its degree, drew attention to its importance as sup- plying independent evidence of an obstruc- tion to the movement of the blood through the smaller vessels. Traube,3 who first called attention to the significance of the increased arterial tension, assumed, in effect, that the in- creased resistance within the kidney was the cause of the obstruction. The theory has been largely accepted in Germany, but its manifest inadequacy has prevent- ed it from meeting even partial accept- ance in this country. It is said4 that Traube himself before his death ceased to hold it in its original form. In the smaller arteries a remarkable change of structure was pointed out by George Johnson in 1850 as hypertrophy of the muscular coat.5 First discovered in the kidney, the change was soon found to be general throughout the system. The occurrence of such increased thickness of the walls of the arteries is now generally admitted, and the view that the thicken- ing is due to hypertrophy of the muscular coat has received very wide confirmation. Muscular over-action being the only known cause of muscular hypertrophy, Johnson at first ascribed the vascular change to the same cause as the hyper- trophy of the heart-the resistance to the movement of the blood through the capil- laries. It was assumed that the arteries by their contraction aided the circulation of the blood, and over-acted to overcome the increased resistance. But with the fall of the theory of arterial propulsion, this explanation became untenable. The function of the muscular coat of the ves- sels being, as far as is known, the adjust- ment of the calibre of the vessel, perma- nent spasmodic contraction became the only explanation of the hypertrophy, and has been for many years ably maintained by Johnson. That such spasm exists is, on Johnson's facts, highly probable, and may, the writer believes, be actually seen in the arteries of the retina in most cases of Bright's disease in which a high arte- rial tension exists. The effect of such spasm must be an increased resistance to the movement of the blood in the arte- ries, an augmentation of its tension. In- stead of aiding, it thus directly opposes the action of the heart. That it is the sole cause of the increased resistance may be doubted. Even if it were the only cause, the difficulty is not lessened, for we are almost as ignorant of its origin as we are of any obstruction due to the changed composition of the blood. The natural effect of increased arterial tension, in- creased endocardial pressure, is imme- diate relaxation of the minute arteries, and freer circulation. The spasm of the vessels under these circumstances is therefore a phenomenon very difficult to explain. Ludwig asserts on experimental grounds that it is due to the action of the retained urinary salts on the vaso-motor centre. [The difficulty of this explana- tion has arisen from the decline, above alluded to, of the theory of arterial pro- pulsion ; and when this theory is, as there is good reason to believe it will be, re- stored to physiology, the explanation first adopted by G-. Johnson will prevail satis- factorily. Admitting, with Sir Charles Bell,1 and, later, Legros and Onimus,2 1 Med. Reports, p. 23. 2 Guy's Hosp. Reports, vol. i. p. 397. 3 Zusammenhang zwischen Herz u. Nieren- krankheiten, Berlin, 1856. 4 By Milner Fothergill, Diseases of the Heart, p. 286. The inadequate character of Traube's theory led Bamberger into a denial of Traube's facts, relative to the increased obstruction to the movement of the blood, and consequently increased arterial pressure. But these facts may now be considered to be established, and the details of the controversy between Traube and Bamberger have ceased to be instructive. 5 Med.-Chir. Trans.,vol. xxxiii. 1850,p. 107. VOL. IL-49 [' Essay on the Circulation of the Blood. I have elsewhere argued this question at length; in Transactions of the American Medical Association (Prize Essay on the Ar- terial Circulation, 185(5; On the Present Con- dition of Vaso-mofoT Physiology, 1872); and in the American Journal of Med. Sciences, July, 1868, p. 289.-H.] [2 Journal de 1'Anatomie et de la Physiol- ogic, 1868-70.] 770 HYPERTROPHY OF THE HEART. that there is a true arterial systole, by which the arteries aid the heart in the onward movement of the blood, it is easy to un- derstand how the same cause (local ob- struction) will produce hypertrophy of the muscular tissue both in the smaller arteries and in the heart.-II.] The existence of the hypertrophy of the muscular coat of the arteries has, how- ever, been denied by Gull and Sutton,1 who ascribe the thickening to a "fibro- sis," and attribute the resistance to the movement of the blood to the obstruction in the vessels due to the inelasticity of this tissue. They do not regard the fibrosis as the consequence of the renal disease, but as a primary general change, of which the affection of the kidney is only one local instance. This theory of the primary general character of Bright's disease accords very well with the phe- nomena of some cases, but as an explana- tion of all cases of contracting kidneys it is open to some objections apart from the weight which must be attached to John- son's observations. In many cases of contracting kidney there is certainly fibroid over-growth to be found widely distributed, but the degree of change in the kidney is incomparably greater than that in other organs, so as to suggest strongly the idea of a primary affection of the kidney. Another fact to be taken into consideration is that, whatever be the cause of the hypertrophy of the heart in the contracted kidneys, a similar hypertrophy results as a remote conse- quence of kidney disease unquestionably local in its origin. In later stages of an acute nephritis, hypertrophy of the heart is even more frequent than in the primary contracting kidney, and is associated with the same increased arterial tension. The conclusion then seems to be that hypertrophy of the heart occurs in kidney diseases as a result of increased arterial blood-pressure, the result of some ob- struction to the movement of the blood in the minute vessels ; that such obstruc- tion is in many cases the indirect conse- quence of the kidney disease ; that it is accompanied in most cases with a morbid state of the smaller arteries, to which it is in part to be ascribed. Lastly, in some cases, the obstruction causing the hypertrophy of one ventricle may be situated, not in the vessels, large or small, but beyond them, in the other side of the heart. Thus in mitral ob- struction, the right ventricle is very con- stantly hypertrophied ; in obstruction in the pulmonary system and right side of the heart, the left ventricle may become hypertrophied. The obstruction may even be on the same side of the heart, and act through both systems of vessels, the pul- monary and the systemic. Thus mitral regurgitation may, as Friedreich has re- marked, cause not only congestion of the lungs, distension of the right side of the heart, over-filling of the systemic nervous system, but increase on the tension of the arterial blood, and thus cause an increase in the work of the left ventricle, and an increase in its hypertrophy. It is not easy to understand the mechanism by which this arterial distension is effected, but as a clinical fact it is unquestionable, and occurs especially in cases of mitral regurgitation, in which the left ventricle is greatly dilated and hypertrophied. It is perhaps to be ascribed to the effect of the secondary dilatation of the right side of the heart in augmenting the mechani- cal obstruction. A tracing from a pulse in such a condition is shown in Fig. 121, p. 777. It may be convenient to group the causes of hypertrophy which have been described, first, according to their po- sition (Table I.), secondly, according to their effect (Table II.). > Med.-Chir. Trans, vol. Iv. 1872. VARIETIES. 771 EXCITING CAUSES OF CARDIAC HYPERTROPHY. TABLE I. Over-action, primary Nervous palpitation, effect of alcohol, tea, coffee, &c., muscular effort (in part). Exocardial ........ Pericardial adhesions. Over-action secondary to increas- ed resist- ance. Increase in mass of blood to be moved Dilatation of heart, prim- ary or secondary to re- gurgitation, &c. Within the heart, acting immediately, Contraction of orifices. Endo- cardial Arteries large, r Constriction of aorta, or pulmonary artery, aneur- [_ ism(?), displacement. Increase in obstruction to move- ment of blood, situated, Arterial system generally, Degenerative changes, loss ' of elasticity, atheroma, &c. Outside the heart, Emphysema, cirrhosis, pleural ef- fusions, Pulmonary, acting on right ven- tricle. Arterioles and capillaries, Muscular ef- fort (in pt.) pregnancy, Bright's j disease, j General, acting on left ven- tricle Within heart, acting cir- cuitously, through cir- culation, Valvular disease, &c. TABLE II. CAUSES of hypertrophy. Affecting- All parts of Heart- Over-action from nervous and toxic influences. Dilatation of cavities. Displacement of heart. Left Ventricle- Mitral regurgitation. Constriction and regurgitation at aortic orifice. Constriction or compression of aorta. Aneurism of aorta (?). Degeneration of arterial system. Renal disease. Pregnancy. Muscular efforts. Valvular disease of right side of heart, and all causes of dilatation of right ventricle. Left Auricle- Mitral constriction and incompetence. Right Ventricle- Constriction or regurgitation at pulmonary orifice. Constriction of or pressure on pulmonary artery. Degeneration of pulmonary arteries. Lung diseases, obstructing, compressing, and destroying vessels. Chronic bronchitis. Emphysema. Cirrhosis. Pleural effusion. Affections of mitral orifice. Right Auricle- Regurgitation and constriction at tricuspid orifice. 772 HYPERTROPHY OF THE HEART. By what mechanism the increased work leads to muscular over-growth we have little knowledge. The theory has been put forward that the effect depends on re- flex dilatation of the coronary arteries. Increased blood-pressure within the heart is known to inhibit, by the depressor nerve, the vaso-motor system, causing di- latation of the minute arteries, and freer circulation. The coronary arteries are believed to participate in this effect, and the readier circulation through them has been thought to be the cause of hyper- trophy. That such an action occurs is most probable, and it is probable that thus the nourishment necessary for over- growth is supplied. But that it is not the sole cause is almost certain, from the fact that if the work of a muscle remains the same, a larger supply of blood to it has no power to increase the muscular tissue. We are driven to assume a direct influ- ence'of the increased contraction on the growth of the fibre. The average force exerted habitually by a muscle is far be- low its possible maximum at any moment. It would seem as if this average force, and the bulk of the muscle, were propor- tioned, that an increase in the habitual force leads, in due nutritive conditions, to muscular over-growth. Whether this over-growth is the result of the direct mechanical stimulus to the contracting fibre, or whether it is the result of a re- flex influence exerted through the nerv- ous system, and excited by the increased pressure on the endocardium or by the increased tension on the contracting fibres, we do not know. One condition is, however, essential for the development of hypertrophy-time. A certain period is necessary for growth of old, or for the development of new tissue. Dilatation may occur quickly ; hypertrophy can only take place slowly. Hence the rapidity with which an in- creased resistance is developed largely influences the resulting condition of heart. Obstruction is usually slowly developed, regurgitation may occur rapidly, and this is one reason why the former entails so much simpler an hypertrophy than the latter. So, too, in the obstruction which is developed in the most gradual manner, that of Bright's disease, uncomplicated hypertrophy is commoner than in any other morbid state. The related condi- tions of origin of hypertrophy and dilata- tion are considered more fully in the article on Dilatation. A few cases of hypertrophy have been recorded in which no mechanical cause for the hypertrophy could be discovered. Their proportion to the cases of hyper- trophy in which a mechanical influence can be traced is very small, so small that it is probable that some such cause may have existed and have escaped observa- tion. Some of the cases were recorded before the relation of hypertrophy of the heart to kidney disease was well known, and the existence of the latter may easily have been overlooked. In Bristowe's case of "hypertrophy without sufficient cause," recorded in the Path. Trans., vol. v. p. 82, the heart, which weighed twenty-seven ounces, was uniformly en- larged and hypertrophied without local disease, but the kidneys were reduced in size, and granular, and presented atrophy of the Malpighian bodies. In other cases the increased bulk of the organ is due to an increase in the fibrous, as well as in the muscular tissue. Such was the case in a heart weighing forty ounces, pre- served in St. George's Hospital Museum, and supposed to be an example of true hypertrophy, until Quain examined it, and discovered its real nature. Pathological Anatomy. - Hyper- trophy may occur in each division of the heart, but varies in different parts, both in the frequency of its occurrence and in the degree commonly attained. The comparative affection of the different parts of the heart depends partly on the frequency and degree with which the causes of hypertrophy affect the different portions, and partly on the amount of muscular tissue each part possesses, and by which it is enabled to resist rather than yield to the internal pressure, which is the cause of the hypertrophy. The left ventricle is that affected most fre- quently, and in the greatest degree. Next in frequency and degree comes the right ventricle ; then the left auricle; lastly, the right auricle. It is rare for the hy- pertrophy to be general, and to affect all parts of the heart. More commonly it is partial, affecting one part only. The in- crease in the weight of the heart is the invariable characteristic of hypertrophy. Since the healthy heart consists almost exclusively of muscular tissue, over- growth of that tissue cannot occur at the expense of any other constituent, and must result in an absolute increase in the weight of the heart, proportioned to the hypertrophy. There is also in most cases an increase in the size of the heart. If the cavities of the heart are unaltered, the increase in its size is proportioned to the hypertro- phy. This is the case in the so-called "simple" hypertrophy. The cavities rarely, however, remain unchanged. They are believed by some authorities to be oc- casionally diminished in size. The heart then may be of normal size, or may be very slightly enlarged. The increased thickness of the walls is at the expense of the cavity, which may become reduced to very small dimensions, it is said incapa- ble of containing a walnut. This con- PATHOLOGICAL ANATOMY. 773 stitutes the concentric hypertrophy of Bertin. Lastly, the cavity is, in the ma- jority of cases, dilated, and the dilatation adds greatly to the size of the heart. This constitutes the eccentric variety of Bertin. untenable, and is not verified by the effect of post-mortem decomposition, which should relax completely the con- traction of rigor mortis. Dechambre and Forget maintained that such hearts could not be expanded, as simply contracted hearts can be. The balance of recent pathological evi- dence is certainly opposed to the occur- rence of concentric hypertrophy. It is to be noticed that the careful pathological observation of recent years has brought to light few supposed examples of this change. One specimen only has been brought before the Pathological Society.1 There is in the museum of University College a specimen (No. 2,140) which has been described as itself establishing the existence of the change. But on close examination the characters are far from satisfactory evidence - it is obviously merely an example of the permanent con- traction of a heart the subject of simple hypertrophy.2 The known mechanism of [Fig. 120. 1 By Wickham Legg. Trans. Path. Soc. vol. xxv. p. 105. The specimen presented contraction of the mitral orifice. Details of measurement and weight of the heart are not given. 2 The specimen in question has been ap- pealed to as decisive, and illustrates so well the characters which have led to the estab- lishment of this variety, that it is worth de- tailed description. In the circular glass jar in which it had been preserved for many years it certainly had striking proportions. The walls appeared of great thickness, and the cavity "scarcely capable of containing a hazel-nut." When removed from the jar it appeared considerably smaller. Its weight, with the root of the aorta, is 11| oz., but it has been kept for many years in spirit. The external length of the ventricle is 4 inches. The heart has been divided transversely mid- way between the base and apex of the left ventricle. The diameters of the section are antero-posterior 2| inches, lateral 3 inches. It is evidently a firmly contracted heart, for the cavity of the right ventricle is a mere curved line. The cavity of the left ventricle is, on close examination, stellate ; from the centre three linear branches radiate, and can be opened up. Between them lie the enlarged papillary muscles. On measurement with a wire, the circumference of this stellate cavity, following its branches but excluding the loose papillary muscles, is 4| inches. But the most conclusive evidence is afforded by the thickness of the walls measured at the extremities of the radii of the cavity. On the left side the wall measures f of an inch, in front and behind just | inch in thickness. After every allowance has been made for the effect of the spirit, it seems clear that the thickness of the wall is only a little above the normal. The increased weight is proof that the extent of the wall cannot have been below the normal. It is clear also, from the state of the right ventricle, that the heart is Hypertrophy of left ventricle.] Concentric hypertrophy of the heart has, in most recorded examples, been local, and confined to the left ventricle. Its existence has, however, been the subject of much discussion. It was thought to be common until Cruveilhier, in 1833,1 pointed out how perfectly its characters were simulated by hearts the subjects of simple hypertrophy and post-mortem con- traction. When the heart is at the time of death in systole, the final contraction is fixed by the rigor mortis, the thickened walls are, by their contraction, further increased in thickness, and so remain, and the cavity is reduced to very small dimensions. The resemblance of such a heart to "concentric hypertrophy" is ad- mitted by all authorities. Cruveilhier maintained that all cases of the supposed change are thus explicable, that the cavity of such a ventricle can always be opened out with the fingers, and in this he has been followed by Budd2 and many later pathologists, who urge further that the contraction of the cavities supposed to occur is incompatible with the absence of symptoms of impeded circulation of the blood. Other authorities believe that concentric hypertrophy does rarely occur. Skoda, Rokitansky, Bamberger, Forster, Walshe are all of this opinion. They assert that hearts are occasionally met with, the cavities of which are so small that the hypothesis of mere contraction is 1 Diet, de Med. et de Chir. Prat. art. Hy- pertrophic. 2 Med.-Chir. Trans. 1838. 774 HYPERTROPHY OF THE HEART. hypertrophy renders the origin of this form of over-growth scarcely conceivable. If hypertrophy is the result of increased work, increased intra-ventricular pressure, the volume of the blood within the ventri- cle can scarcely have been lessened ; but without such lessening, reduction in the size of the cavity cannot have occurred. Thus the increased thickness of the wall and lessened size of the cavity are, on etiological grounds, almost incompatible. Moreover, post-mortem decomposition relaxes hearts, firmly contracted, in a very imperfect manner. Concentric hypertrophy of the right ventricle has been described as an occa- sional consequence of some congenital malformations of the heart. Eccentric Hypertrophy.-The thickening of the wall in eccentric hypertrophy is not always conspicuous. The cavity is di- lated, and the superficial area of the wall increased, and the increase in tissue may be only enough, or even not enough, to maintain the normal thickness of the wall. Thus the wall of the left ventricle may be so hypertrophied as to lead to a considerable increase in the weight of the heart, and yet may be only of the average thickness. In estimating the presence and amount of hypertrophy, therefore, the size of the cavity must always be taken into consideration. In one of the heaviest hearts recorded, a heart much dilated, the thickness of the wall of the left ventricle was not more than is common in less di- lated hearts of only half the weight. The increase in the size and weight of the heart is often very considerable. In estimating them it should be remembered that the normal average weight varies according to the sex, age, size of the in- dividual. These are considered else- where (art. "Size and Weight of the Heart."). A heart which exceeds 9 oz. in a man or 8 oz. in a woman, probably pos- sesses an excess of some constituent, in most cases of muscular tissue. A com- mon weight for hypertrophied hearts is 12-16 oz. Hearts are occasionally seen of much greater weight, especially when dilatation extends the area, and hyper- trophy the thickness of the cardiac walls. Under these circumstances the enormous " bovine" hearts are met with. Walshe has met with one weighing 40 oz. ; Lan- cisi mentions one which weighed, emptied of blood, two pounds and a half; Croker King one of 44} oz. ; Austin Flint one of 46 oz., while hearts weighing 46| oz. have been shown by Bristowe and by David at the Pathological Society. The enormous weight of five pounds, men- tioned by Lieutaud, must be regarded as doubtful. How much more then the "quinze livres" of Marchetis I1 The shape of the heart is altered ac- cording to the part affected. If one ven- tricle is more affected than the other, that which is the more hypertrophied forms a larger share of the apex than in health, and the chief enlargement of the heart is on the side of the affected ventricle. Thus in simple hypertrophy of the left ventricle, the extremity of that ventricle extends beyonds the other, so as alone to consti- tute the apex, while increased width re- sults from the lateral enlargement. The resulting shape resembles an obtuse-an- gled triangle when the heart is relaxed, an elongated ovoid when partially con- tracted. In hypertrophy of the right ven- tricle the extremity of that ventricle extends to the apex of the heart, but does not usually pass beyond the other. Hence the apex is much rounder than in health, and may be indistinguishable. When dilatation is joined to the hypertrophy, the width of the heart is much increased, and the transverse may exceed the verti- cal diameter. This is especially the case when the right ventricle is affected, when the heart may assume an almost spherical shape. Hypertrophy of the auricles is never sufficient to alter the shape of the heart; the effect of their dilatation is con- sidered elsewhere. The increase in the thickness of the ■wall is in direct proportion to the amount of hypertrophy, but in inverse proportion to the amount of dilatation. The hyper- trophy is usually so much in excess of the dilatation as to cause an absolute increase in the thickness of the wall. This is com- monly greater in the outer wall than in the septum. In the ventricles the trabe- cula} and papillary muscles usually par- ticipate in the hypertrophy, and, it is said, to a greater extent in the right than in the left ventricle. Sometimes they are thinned, when the heart is dilated. In health the thickness of the ventricu- lar wall varies considerably in different parts. The average thickness of the wall of the left ventricle is about half an inch 1 Quoted, by Senac, loc. cit. tom. ii. p. 408. Bellingham is said, by several writers, to have met with a heart weighing 80 oz. The only ground for the assertion seems to be that Bellingham states that he had seen a heart preserved in the museum of St. George's Hospital which was said to weigh five pounds. This seems to refer to the large heart alluded to by several writers and mentioned above (p. 772) as lately examined by Quain and found to weigh 40 oz. firmly contracted, and also that the circum- ference of the inner surface of the left ventri- cle-the test of the actual reduction in size of the cavity-is little, if any, less than the normal. It seems, therefore, to be merely an example of firm contraction in a heart the subject of moderate simple hypertrophy. The history of the specimen is not known. PATHOLOGICAL ANATOMY. 775 in men, rather less in women. The mea- surement should be always exclusive of the papillary muscles, and the place at which the measurement is made should always be specified. The increase is usually greater towards the base than towards the apex. Hope pointed out that the greatest thickening is a little above the middle of ventricle, at the place where the columns carnese are inserted. Thence it decreases suddenly towards the aortic orifice, gradually towards the apex of the heart. Occasionally the reverse obtains, especially in aortic regurgitation (Walshe), and the wall is thicker towards the apex than towards the base. When the wall of the left ventricle measures three-fifths of an inch in thick- ness it may be considered hypertrophied. An increase in the average thickness to three-quarters of an inch, or an inch, is not uncommon. An inch and a quarter is occasionally reached, and it is said, an inch and a half, or even two inches. The larger dimensions were probably in cases in which there was little dilatation, and the heart was contracted. In the large heart described by Bristowe, the weight of which was forty-six and a half ounces, the wall of the left ventricle was only jths of an inch in thickness at the base; the length of the cavity of the ventricle being six inches. The right ventricle yields readily to in- ternal pressure, and presents a marked increase in the thickness of the wall much less frequently than the left; simple hyper- trophy is very rare. The average normal thickness of the wall is two-and-a-half lines in men, two lines in women. When hypertrophied it is often a third, or half an inch in thickness, and even in rare instances three-quarters of an inch, an inch, and even, it is said, an inch and a quarter (Bertin, 88th case, "eleven to sixteen lines.") The numerous column® carne® are commonly much thickened. The cavity is usually enlarged, but may be lessened in rare cases ; probably, how- ever, only in cases of malformation. When the ventricle is thus hypertrophied, and the left ventricle is dilated, the two may, as Morgagni and Bertin remarked, seem to have become transposed. The left auricle is not unfrequently hypertrophied. The average normal thick- ness of its wall is one line and a half; where hypertrophied it may reach two to three lines. The right auricle is rarely hypertrophied, and always in least de- gree. The average thickness of its walls is one line ; when hypertrophied it may attain one-and-a-half or two lines. The auricles have never been found to present contraction of their cavity. In pure hypertrophy the part changed is of firm consistence, firmer than the nor- mal heart, so that the walls do not col- lapse when cut across. It presents little deviation from the normal color, it is sometimes a little darker. Such unmixed hypertrophy is rare. More commonly the tissue has undergone degeneration, and is paler and softer than normal, sometimes generally, sometimes partially. Roki- tansky points out that in the hypertrophy of the ventricles the changed wall of the right ventricle is always tougher than that of the left. The hypertrophied wall of the heart usually contains more fibrous tissue than the healthy wall. The tissue lies between the primitive bundles, separating them, and here and there forms more extensive tracts. This change, when more consid- erable, is considered as "fibroid degen- eration." It is more abundant in the wall of the right ventricle than in that of the left, and doubtless is the cause of its greater consistence. The nature of the change in the mus- cular fibre in hypertrophy has been the subject of much discussion. Does the in- crease in the size of the heart depend on an increase in the size, or in the number of fibres ? The evidence, in some degree conflicting, is on the whole strongly in favor of the view that the increased thick- ness of the wall is due solely to increase in the number of the fibres constituting it, i. e., to the formation of new fibres. The chief evidence of an increase in the size of the fibres is obtained from the measure- ments of Hepp,1 still quoted as authorita- tive, and who asserted, and gave measure- ments to show, that the average thickness of the fibres in hypertrophy is about four times the thickness of the fibres in health. This conclusion, however, by itself sug- gests a fallacy, since the average thick- ness of the wall in hypertrophy is less than double the average normal thick- ness. Vogel and Henle, Rindfleisch and Walshe conclude that there is no increase in the size of the fibres, while Robin thinks that there is a slight increase, al- though not enough to account for the in- creased size of the heart. Wilks and Moxon are convinced that the chief share in the increase in size is due to increase in number. Considerable weight must be attached to the careful observation of Zielonko,2 who finds that the average of a large number of measurements of the fibres of hypertrophied hearts is a little less than the average of the normal fibre. His observations also corroborate the fact (long before stated by Forster) that the normal fibres are smaller in early than in later life, and are increased in size by good general nutrition. The writer has found on direct enumeration of the fibres in a transverse section of the wall that 1 Zeitschrift fiir rat Med. 1854, p. 257. 2 Virchow's Arch.lv, BcL 62, Heft. I. p. 29. 776 HYPERTROPHY OF THE HEART their number is in the main proportioned to its thickness. The conclusion appears justified that there is no increased size of the fibres in hypertrophy, that the over- growth of the heart is entirely dependent on the development of new and less per- fectly nourished tissue elements. Rind- fleisch suggests that they may arise by fissuring of the pre-existing fibres. He has observed that the square cells, of which the muscular fibres of the heart have been shown to consist, contain seve- ral nuclei, instead of a single nucleus, as in health.1 Symptoms.-Cardiac hypertrophy gives rise to certain distinctive physical signs, and may be accompanied by certain defi- nite symptoms. These signs and symp- toms depend on the increased size of the heart, and on the increased force with which it acts. They vary according to the part of the heart which is affected, and according to the amount of dilatation which is associated with the hypertrophy. It will be convenient to consider sepa- rately the symptoms of the change in each division of the heart, beginning with the left ventricle. In it the change is carried to the greatest degree, and gives rise to the signs and symptoms commonly understood as those of hypertrophy of the heart. When hypertrophy is considerable, the heart, unless fixed by adhesions, lies, in consequence of its greater weight, lower in the thorax than in health. The weight of the base is said to increase the natural obliquity of the organ, so that it may as- sume a nearly transverse position. Left Ventricle.-Physical Signs.- The increased bulk of the heart may cause precordial bulging, noticeable chiefly in the area between the nipple and the left edge of the sternum. The intercostal spaces are widened, and the surface of the chest is more prominent than is the corresponding part on the opposite side. This bulging is most marked in hyper- trophy occurring in early life. The area of dulness is increased. The superficial dulness is usually more exten- sive, the deep dulness invariably larger, and the increase is chiefly to the left. The left edge of the deep dulness, instead of passing from the middle of the third left cartilage to the apex, extends from the inner extremity of the third rib to the nipple, or even to the anterior axillary line, one, two, or even three inches out- side the nipple. It may also, although less commonly, extend upwards to the sec- ond interspace. Its shape is thus usually more oval than in health.2 Resistance on percussion is greater than in health. In extreme enlargement the resonance in the left back is defective, and Walshe has even known the dulness to be so marked, and respiration so weakened by pressure upon the lung, that pleural effusion was simulated. The apex-beat, marking ap- proximately the limit of the heart, is moved outwards and downwards, with its enlargement, into or outside the vertical nipple line, and into the sixth or seventh interspace, into the latter probably only in dilated hypertrophy (Walshe). The increased form of action manifests itself by increased impulse.1 The area of impulse is increased ; it may be felt in the fourth, fifth, and sixth interspaces. A larger portion of heart comes in contact with the chest wall, and the increased force aids also in producing a more ex- tensive impulse. In pure hypertrophy a maximum apex-beat is still perceptible, bearing a normal proportion to the rest of the impulse. But the impulse is not only more forcible, it presents a special change; it is slower, more deliberate as well as more forcible, and hence has been for long termed "heaving." In dilated hypertrophy the impulse is more abrupt than in simple hypi rtrophy, in which the slow heave is carried to its greatest de- gree. The extension of the impulse is often visible, and the whole left front of the chest may be raised by it. It was spoken of as "jarring" by old writers, and still is occasionally so described. But a "jar" implies vibration, and although a vibratory character is often felt in the im- pulse of a hypertrophied heart, it is due to coexisting valvular disease, not to the over-action of the heart itself. Occasion- ally a double impulse can be felt with the presence of extreme emphysema, an accu- rate and. convenient measure of the enlarge- ment of the heart. By many authorities it has been strangely undervalued. Niemeyer's assertion that percussion often fails to reveal hypertropy of the left ventricle is comprehen- sible only in consequence of the guide em- ployed being the superficial dulness, which depends much more on the state of the lung than on the state of the heart. For a very full and clear account of the relations and significance of the diminished resonance caused by the heart in its various conditions, see Balfour, Clin. Leet, on Diseases of the Heart, 1876, Leet. 1. 1 According to old writers, Fern el, &c., the impulse of a hypertrophied heart had been known to fracture the ribs! All the in- stances, however, seem to have occurred in convents or monasteries. Caesalpinus and others assert that two ribs of St. Philip de Neri were torn from their cartilages by the palpitation of his heart. Senac wisely doubted the occurrence of such fractures, unless the ribs had been previously weakened by dis- ease. 1 Pafhologiste Gewebelehre, Vierte Aufl. 1875, p. 193. 2 The deep cardiac dulness is, except in SYMPTOMS. 777 each beat of the heart. Rarely it is a double systolic impulse (Walshe), the ori- gin of which is obscure. More commonly the second and slighter impulse corre- sponds with the commencement of dias- tole, at the end of the " sinking back," as Hope expressed it, who first pointed out the phenomenon. He explained it as due to the sudden filling of the ventricles with blood. Hayden, who adopts a similar ex- planation, has pointed out the coincidence of this second impulse with the second sound. Walshe remarks that the move- ment is rather a succussion than an im- pulse against the chest walls. This char- acter, and the obvious coincidence with the second sound, have, in several cases, suggested to the writer the probability that the impulse is really due to the shock communicated to the whole heart by the closure of the aortic valves, a closure ren- dered more forcible by the greater disten- sion of the aorta. It is in accordance with this explanation that, as Hope and Walshe both point out, this second im- pulse may occur in simple hypertrophy, but is most marked in dilated hypertrophy (in which the distension of the aorta is greatest), and that it is absent in simple dilatation. The sounds of the heart are altered. The first sound is rendered less loud, but longer, the change being especially marked over the ventricle. The sound may be normal at the base and ensiform cartilage (Walshe). Sometimes the muffling of the sound amounts almost to extinction. The second sound is usually loud. When di- latation is added to the hypertrophy the first sound becomes louder and clearer. The post-systolic silence is shortened, as Laennec noted, in consequence of the lengthening of the first sound. Laennec thought that this lengthening may amount to a faint murmur, apart from valve dis- ease or hsemic state, and Walshe corrobo- rates the opinion. During attacks of pal- pitation the first sound may be much more distinct than when the heart is acting uniformly. Reduplication of the first sound is occa- sionally met with in hypertrophy : rarely according to Walshe; almost invariably in eccentric hypertrophy, according to Hayden. It is certainly frequent in some forms of hypertrophy, especially in that due to Bright's disease (Sibson). Irregu- larity in force is not common, in fre- quency very rare, except in association with dilatation and degenerative changes. Symptoms, proper.-A great number of morbid phenomena have been ascribed to the influence of cardiac hypertrophy. The list, however, has been shortened accord- ing as the symptoms of the causes of hypertrophy and of the other associated consequences of those causes, are distin- guished from the symptoms directly due to the hypertrophy itself.1 Almost all the consequences of dilatation of the heart were formerly ascribed to the conjoined hypertrophy. The credit belongs to Bouil- laud of having first vindicated hypertro- phy from its supposed influence in causing dropsy and other consequences of cardiac failure. Fig. 121. Tracing from pulse in great hypertrophy and dilatation of left ventricle in a case of mitral regurgitant dis. ease, with general venous distension and ultimate increase in arterial tension. Artery large and incompres- sible. Tracing taken at very high pressure, which did not modify its character. Subjective symptoms of cardiac hyper- trophy may be absent, when the hyper- trophy is moderate, with little or no di- latation, and is adequate to overcome the obstruction which has produced it. In such cases, however, the varying force of the heart's action, the varying amount of the obstruction, and the common conjunc- tion of relative weakness with absolute strength, lead to sensible evidence of de- rangement. Consciousness of the increased force with which the heart acts is a more or less frequent symptom in all except the slightest forms of hypertrophy. Under excitement the conscious beating may amount to "palpitation." Slight irregu- larity may increase the discomfort, but 1 Senac, in speaking of this subject, says: " Rien n'est plus ordinaire que les b6vAes des observateurs dans la recherche des causes ; tout ce qu'ils trouvent dans les cadavres ils attribuent souvent a la derniere maladie, ou & celle qui a attire leur attention." Loc. cit. tom. ii. p. 398. 778 HYPERTROPHY OF THE HEART. much irregularity or considerable palpita- tion is rare, except in dilatation, and to that the symptom is to be ascribed. Pain, as Walshe points out, is extremely rare in simple hypertrophy, and anginal attacks are almost confined to cases in which the dilatation is considerable. The force with which the left ventricle contracts has an immediate effect on the arterial pulsa- tions. The carotids throb visibly. The pulse is large, full, hard, and sustained. When dilatation is conjoined with the hypertrophy, the pulse is still full, but is softer and more compressible and less sustained. The sphygmogram shows these characters in a sudden and high rise, and, where the hypertrophy is sim- ple, there is a high and often sustained tidal wave. Where there is coexisting dilatation, the tidal wave may not be sus- tained in consequence of the imperfect emptying of the ventricle (Fig. 121). Aortic obstruction may, however, modify considerably these characters, rendering the pulse smaller, while it remains hard, sustained, and incompressible. If con- siderable, it also renders the contraction slow, and the percussion stroke may be lost in a slowly rising tidal wave, as in the accompanying tracing:- Fig. 122. Tracings from infrequent and slow pulse of aortic obstruction, with coexisting mitral disease, and hyper- trophy of the left ventricle. The slowness of the contraction had been increased by the administration of digitalis. Taken at a high pressure ; pulse small but almost incompressible.1 The force with which the blood is driven into the smaller vessels may modify the function of certain tissues and organs. The face is often flushed. Tinnitus au- rium, flashes of light, and muscse volitantes may be complained of. Headache and mental dulncss are sometimes observed, but as a rule the intellect is unaffected. The general nutrition also suffers little. Organic functions are little interfered with. Increased arterial pressure might be supposed, as Walshe remarks, to modify considerably the urinary secretion, in- creasing the quantity of water. The urine presents, however, no distinctive change. Swelling of the bronchial mucous mem- brane, and increased secretion are con- nected by Niemeyer with the active dis- tension of the bronchial arteries. Short- ness of breath on exertion is common, and is by Walshe connected directly with the hypertrophy. True cardiac dyspnoea is rare; and any considerable shortness of breath is probably to be ascribed to the cause of the hypertrophy, or to concurrent dilatation. The pressure exerted on the lungs by an enlarged heart may cause some interference with their function and increase the dyspnoea. Consequences of Hypertrophy. - A long train of evils which are met with in more or less frequent association with hyper- trophy, were formerly regarded as its con- sequences. Many of them are in no way related to its occurrence, but are the re- sult of the dilatation, or remotely of the cause of the hypertrophy. Such are oedema, capillary engorgement, venous congestions, passive hemorrhages. These were enumerated by Hope as consequences of hypertrophy. Bertin long before taught clearly that they cannot be regarded as such, since they are absent when hyper- trophy exists in its most simple form, and occur in proportion as the hypertrophy is complicated by other conditions, such as valvular disease, dilatation of the ventri- cle, &c., themselves capable, without hypertrophy, of causing the symptoms. Not only does hypertrophy not produce these effects, but its tendency is to pre- vent their occurrence. Its power of ar- resting the mechanical effects of its causes is very great, and proportioned to its de- gree. Disease of the aortic orifice, for instance, as long as the hypertrophy is great and unweakened by degeneration, produces no backward effect. So in mitral obstruction, hypertrophy of the left auricle may for a long time save the lungs from passive congestion. So, too, hypertrophy of the right ventricle may prevent any over-distension of the venous system from obstruction to the circulation through the lungs or the left side of the heart. The only morbid effects of hypertrophy which can accurately be thus regarded, are those which result from the greater force with which the blood is driven into the arterial system. These consequences are seen best when there is no impediment to the escape of blood from the ventricle, and especially when the cause of the hy- pertrophy is occasional or is situated in front of the arterial system. The ten- dency is for the due proportion between the contents of the arteries and the veins to 1 These two tracings were taken for me by Mr. H. R. O. Sankey. SYMPTOMS. 779 be disturbed, for the arteries to become over-filled, the veins and the pulmonary system under-filled with blood. It has been said that the whole circulation is accelerated, but this can only be the case when the action of the heart is for the time being more than enough to overcome the resistance which has evoked it. It has been supposed that the increased supply of arterial blood may lead to the overgrowth of organs, but the conjecture is unsupported by observation. A more direct effect upon the vessels may often be traced. When the obstruc- tion is situated beyond the arteries, their walls are exposed to a greatly increased pressure. The same effect occurs when the obstruction is at the aortic orifice, and the action of the heart is from any cause (as dynamic excitement, or the cessation of another cause) in excess of the obstruc- tion. Both the large and small arteries suffer under these circumstances. The increased pressure on the aorta may cause its dilatation, although, as Senac observed, the enlargement from this cause is not often considerable. A more frequent con- sequence of the pressure to which the arteries are exposed is seen in the degene- ration of the vessels.1 Modern observa- tion has established the frequent associa- tion of so-called endarteritis deformans (atheroma) with increased strain. The change is seen in the aorta, in the pul- monary artery, and in the smaller vessels, especially in those in which the relative pressure is the greatest, as in those at the base of the brain. But degeneration is not the only effect of the increased strain upon the vessels ; they not unfrequently give way, and hemorrhage results. Hemorrhage into the brain is, on account of its frequency, magnitude and importance, that form to which attention has been chiefly directed. The frequent association of apoplexy and enlargement of the heart led Corvisart first to assume a causal relationship be- tween the two.2 In this he has been fol- lowed by most subsequent writers-Ber- tin, Hope, Bouillaud, Andral, Burrows, and others. But the conclusions of the earlier observers require some abatement in the light of modern knowledge of the frequency with which apoplectic attacks result, by another mechanism, from car- diac disease. Embolism may give rise to symptoms not unlikely those of cerebral hemorrhage, and embolism is almost con- stantly associated with hypertrophy of the heart. But even when these cases are eliminated from the discussion, the pathological evidence of the association of apoplexy and hypertrophy of the heart is still impeachable. In sixty-five cases of apoplexy collected by Quain1 the heart was enlarged in two-thirds, and in one- half there was no valve disease. The significance of the latter fact is that in these cases the cause of the hypertrophy was probably situated away from the heart, in or beyond the arterial system, which would thus have to bear the whole force of the over-acting heart. But this is the condition in which arterial disease is produced; the small vessels degene- rate, and, becoming weaker, are less able to bear increased pressure to which they are exposed. This is the case, notori- ously, in Bright's disease, especially in the contracted kidney, with which cere- bral hemorrhage and cardiac hypertrophy are so constantly associated. In primary degenerative changes in the smaller ves- sels the same result is seen-a like obstruc- tion may cause hypertrophy, and a like weakness yield before the increased pres- sure. The same sequence is sometimes seen when the cause of the obstruction is situated beyond the arteries and capilla- ries, and acts, it may be, through both systems of the circulation. Mitral dis- ease may lead to extreme blood tension in the arterial system, as the sphygmo- graphic tracing on page 777 shows. Cere- bral hemorrhage sometimes occurs in such cases, even in the young, from the rup- ture of an overstrained artery. All authorities are agreed as to the causal relationship between hypertrophy of the heart and the rupture of diseased vessels. But to this some, as Watson, Eulenberg, Rokitansky, would limit the connection. It must be considered still doubtful whether an over-acting heart can rupture a healthy artery. It is true the large arteries of the brain are often found healthy in cases of cerebral hemorrhage, but this affords only slight evidence of the condition of the smaller vessels of the cerebral substance. These are frequently diseased when the vessels at the base of the brain appear healthy. Statistics on this point corroborate, but do not extend, the conclusion from iso- 1 Pointed out by Kirkes in 1857, Med. Times and Gaz. No. 370, 371. 2 ' 'Where apoplexy takes place in a person in whom there is an excess of muscular sub- stance and strength in the heart, it is easy to conceive that the resistance of the vessels of the brain is not in unison with the extraordi- nary impetus which the heart impresses on the blood; it necessarily follows that the smaller vessels of the brain become more permeable to this fluid, or that they give way and cause effusion and apoplexy." Cor- visart, 1. c., p. 164. It, however, would seem to have been first suggested by the death of Malpighi, who died from cerebral hemorrhage, and whose heart was found greatly hypertrophied, "the parietes of the left ventricle were two fingers in thickness." (Baglivi.) 1 Lumleian Lectures, loc. cit. 780 HYPERTROPHY OF THE HEART. lated observations. Quain found that dis- eased vessels are more common in cases of cerebral hemorrhage when the heart is healthy than when it is hypertrophied. They are present in two-thirds of the former, and only in about half of the lat- ter. The inference suggested is that, since extensive disease of vessels shown by the implication of the larger trunks is less common, in cerebral hemorrhage, when the heart is hypertrophied than when it is healthy, an over-acting heart needs less diminution in the strength of the vessels, in order to effect their rup- ture, than a healthy heart. The occasional, though rare, occurrence of cerebral hemorrhage in the young does not help to decide the question. Disease of the cerebral vessels is now known to be not uncommon in early life, and some of the cases occur in the subjects of heart disease, in whom there exists circuitous increase of arterial tension just described. Moreover in such subjects cerebral aneu- risms, perhaps from imperfect embolism, are frequent, and in many cases it has certainly been by the rupture of such an aneurism that cerebral hemorrhage has occurred. Concentric Hypertrophy of the Left Ven- tricle.-The symptoms are as uncertain as the existence, of the malady. Theoreti- cally, the signs of simple hypertrophy might be expected, and with them some dyspnoea in consequence of the impedi- ment which must be presented to the passage of blood through a heart so much lessened in capacity. Right Ventricle.-Considerable in- crease in the size of the right ventricle causes prominence of the lower part of the sternum, epigastric fulness, and often bulging of the lower left cartilages adja- cent to the sternum. The superficial car- diac dulness is little changed, but the deep dulness extends further to the right than normal, the right edge being one or two fingers' breadth to the right of the sternum. This dulness is partly depend- ent on the enlargement of the ventricle, partly on over-distension of the auricle, which always accompanies the change in the ventricle. Pulsation may be felt at the epigastrium. The apex-beat is in its normal situation, or moved a little to the left, extended as far as, but not beyond, the nipple line. It is frequently changed, being obscured and diffused when the right ventricle lies in front of it. A dis- tinct impulse may be felt over the right ventricle, i. e., over the lower part of the sternum,1 and in the adjacent left inter- spaces. In health a distinct impulse is very rarely to be felt in this situation. In hypertrophy the impulse may have considerable strength, but it is generally quick, rarely of the slow, heaving charac- ter which hypertrophy of the left ventri- cle produces. It may sometimes be felt as far as the base. Little alteration in the sounds of the heart is caused by hy- pertrophy of the right ventricle. The pulmonary second sound is usually inten- sified by the increased tension within the pulmonary artery. Sometimes the second sound is reduplicated. Jugular pulsation has been associated with hypertrophy of the right ventricle by Lancisi, Laennec, Hope, and others. It is doubtless due to actual regurgitation through the tricuspid orifice, and coexisting dilatation of the ventricle is necessary for its production. Few symptoms proper can be associated with the condition. The pulse is natural. The venous system shows no signs of en- gorgement. It is remarkable how com- pletely hypertrophy of the right ventricle will prevent the development of dropsy, and other signs of venous stagnation, by an obstacle in front of it. The lungs or left side of the heart usually present evi- dence of the condition causing the hyper- trophy, emphysema, disease of the mitral orifice, &c. Dyspnoea is common, as Walshe points out, but is more frequently the result of the cause of the hypertrophy, than of the hypertrophy itself. Consequences of Hypertrophy of the Ricjht Ventricle.-The immediate effect of over- action in the right ventricle is to over-dis- tend that part of the pulmonary vascular system which lies between the ventricle and the obstruction which has caused the hypertrophy-the pulmonary arterial sys- tem, when obstruction is in the tissues of the lung, the pulmonary veins also, when the obstruction is on the left side of the heart. Atheroma of the pulmonary ar- tery frequently exists in conjunction with this condition, and has been regarded as causal, but in few cases have the two been observed except in conjunction with some other recognized cause of such hy- pertrophy, and it seems more reasonable to conclude that the degeneration is the result of the increased strain to which the pulmonary artery is exposed. Where the degeneration is considerable and of old standing, as in cases in which the ar- tery is found calcified, it may be the only discoverable cause of a moderate hyper- trophy of the ventricle. Pulmonary congestions, oedema, and especially pulmonary apoplexy, have, since the days of Bertin, been commonly ascribed to hypertrophy of the right ven- tricle. Where the obstruction causing the hypertrophy is situated on the left side of the heart, the increase in the strength of the right ventricle will add considerably to the strain upon the dis- tended pulmonary vessels, and may con- stitute the efficient cause of their rupture. 1 This was pointed out by Burggrave in 1754 (Act. Acad. Nat. Cur. vol. x. p. 140). AURICLES - DIAGNOSIS. 781 Modern pathological research, however, has shown that diseases of the right side of the heart frequently cause pulmonary apoplexy in another way, by leading to pulmonary embolism. We are only be- ginning to learn how large a proportion of pulmonary apoplexies is due to this cause. When such embolism occurs, hy- pertrophy of the right ventricle will in- crease very much the strain on the collat- eral circulation, and, in consequence, will augment the amount of hemorrhage. Auricles.- Hypertrophy of the Left Auricle is usually attended with evidence of its enlargement, i. e., dulness, com- monly relative only, in the inner part of the second left interspace. Less fre- quently a distinct impulse is to be recog- nized in this situation, preceding in time the ventricular impulse and due to the auricular systole. Evidence of mitral disease is commonly present, a systolic or presystolic murmur. Dilatation of the auricle invariably coexists. No symp- toms are known to be associated with the hypertrophy. Its tendency is to prevent the mitral mischief from influencing the pulmonary circulation. Hypertrophy of the Right Auricle is very rare, and is always associated with dilata- tion. Its signs are dulness to the right of the sternum in the third and fourth in- terspaces, and, in very rare cases, an im- pulse, presystolic in rhythm, in this situa- tion. It is often attended with marked jugular pulsation, and with the evidence of disease of the right ventricle or of the tricuspid orifice. Diagnosis.-The diagnosis of hypertro- phy depends on the recognition of in- creased force of impulse, and especially, in the case of the left ventricle, by the deliberate heaving character which indi- cates the contraction of a large mass of muscle. In the case of right ventricular and of auricular hypertrophy, the in- creased force is indicated by impulse, where in health none is present. Evi- dence of enlargement of the heart, by percussion dulness, or by movement of the apex-beat, or by extension of the im- pulse, is usually also obvious. In left ventricular hypertrophy the character of the pulse assists the diagnosis. Where doubt remains, the presence of a morbid state, capable of causing the hypertrophy, may afford evidence of its probable exist- ence. In judging of the existence and degree of hypertrophy the condition of the lungs must always be taken into consideration. Considerable emphysema may conceal all the signs of a hypertrophy of high degree: The impulse may be imperceptible, the dulness masked, and the heart-sounds weakened. The existence of hypertrophy must then be inferred from the condition of the arterial system. There are certain conditions from which hypertrophy has most frequently to be distinguished. Undue Exposure of the Heart in very flat- or narrow-chested persons, with small lungs, may simulate hypertrophy. The heart comes into more extensive contact with the anterior wall of the chest than in health. Its impulse is felt over a larger area, and may appear to have undue force. A maximum apex-beat is still preserved. The superficial duluess is more extensive than in health. The dis- tinction from hypertrophy rests on the absence of a heaving character in the im- pulse, on the normal or nearly normal po- sition of the apex-beat (it is never outside, though it may be in the nipple-line), on the natural extent of the deep dulncss, on the unchanged pulse, on the absence of any causal condition, and on the recogni- tion of the short antero-posterior or trans- verse diameter of the chest. The difficulty of diagnosis in such cases is sometimes increased by the presence of an exocardial murmur, produced by the undue friction of the heart against the bony chest wall, and, by the circumstance, that patients with very flat chests are often weakly and ansemic, and suffer from shortness of breath and extreme consciousness of any dynamical heart-disturbance. Dynamical Disturbance of the Heart may be mistaken for hypertrophy. Under ex- citement the heart may beat with appa- rently increased force, and be brought into abnormal contact with the wall of the chest, so that there is an increase in the area as well as in the force of the impulse. Sometimes the increase in force is more apparent than real, and the pulse is small and weak. Frequently, however, the rapidly-acting heart distends the arte- ries, and the pulse becomes hard and full. There is an entire absence of the delibe- rate heave of hypertrophy, and of evi- dence of permanent change in the form of the heart; there is no bulging, no in- creased dulness. Best in the recumbent posture soon reduces the impulse to the normal. It must not be forgotten that an hypertrophied heart readily palpitates under excitement, and any irregularity in the excited action is ground for sus- picion. Displacement of the Heart may lead to an apparent extension (really a move- ment) of the impulse and dulness in a given direction. Displacement to the left, moving the apex outside the nipple line, may simulate hypertrophy of the left ventricle; and displacement downwards, rendering the impulse of the right ven- tricle perceptible at the epigastrium, may resemble dilated hypertrophy of the right ventricle. But under these circumstances HYPERTROPHY OF THE HEART. 782 there is no alteration of the character of the impulse as there is in hypertrophy; the opposite boundary of the heart may be found to have undergone a correspond- ing change of position, and a cause of the displacement will be discoverable. Dilatation of the Heart resembles hyper- trophy in causing increase in size, shown by extension of dulness and increased area of impulse. The impulse is, how- ever, diffuse and weak; the proportional intensity of the apex-beat is lost, the pulse is soft, and the action of the heart often irregular. The distinction between the two conditions can rarely be absolute, since they are usually, in varying degree, conjoined. Pericardial Effusion may cause bulging and an increase in the area of dulness. The impulse, however, is less, instead of more forcible; and the apex is raised, instead of being moved outwards or downwards. The dulness extends up- wards in the pyramidal form, and its left boundary is beyond, instead of cor- responding to, the left limit of the impulse. Apart from the auscultatory signs, the acuteness of the symptoms in pericarditis, sudden pain, dyspnoea, fe- ver, will usually prevent an error in diagnosis. In auricular hypertrophy, the extension of dulness above the normal limits of the cardiac dulness is usually slight. If sufficient to stimulate peri- cardial effusion, a pre-systolic impulse will, in most cases, be detected. Aneurism has been confounded with hypertrophy, but the conditions under which such a mistake could arise must be very rare. The double centre of pul- sation usually affords a sufficient distinc- tion. Local diagnosis of the part of the heart affected with hypertrophy has been al- luded to in describing the symptoms pro- duced by the change in the several cham- bers of the heart. The chief difficulty arises in some cases of ventricular hyper- trophy. In hypertrophy of the right ventricle, slight hypertrophy of the left ventricle may be concealed or simulated by the strong impulse of the anterior right ventricle and the displacement out- wards of the apex-beat consequent on the enlargement of the right side. The diag- nosis of the state of the left ventricle must then depend on the character of the apex- beat-on the presence or absence of a dis- tinct heaving impulse. On the other hand, considerable hypertrophy of the left ventricle may cause an impulse over the position of the right ventricle. In such a case the impulse of the left ven- tricle possesses great force, and the diag- nosis must be based on the relative pro- portion of the impulse over the two ventricles. In all cases a comparison of the extent of causal lesion, with its mechanical ef- fects, will often suggest an accurate opinion as to the existence and degree of hypertrophy when the part affected is not accessible to physical examination. For instance, congestion of the lung is the necessary mechanical effect of mitral con- striction. The absence of such conges- tion, when considerable mitral constric- tion exists, is valid ground for suspecting compensatory hypertrophy of the left auricle. So, too, we sometimes find that such compensation has not occurred- that the lungs are constantly overloaded with blood, but that the general venous system has not suffered; the jugular veins are undistended: there is no ana- sarca or albumen in the urine. In such a case we may be sure that there is hyper- trophy of the right ventricle. Prognosis.-The difficulty of extricat- ing hypertrophy from the various condi- tions with which it is associated has led authorities to entertain very different opinions regarding its influence on the life and well-being of the patient. The gravest consequences of hypertrophy (as formerly described) are now known to be those of its attendant conditions; the "conservative" character of hypertrophy, as a healthy reaction against a morbid influence, is generally recognized, and its prognosis is admitted to be, as a rule, favorable ; any unfavorable element being due rather to coexisting dilatation, or to other effects of the cause of the hypertro- phy, than to that condition itself. it is rarely that evil results can be traced directly to the overgrowth of the heart. The unpleasant sensations at- tending the action of a hypertrophied heart suggest many possible evils which experience rarely justifies. It may pro- duce hemorrhage, especially into the brain, when vessels are rotten, but prob- ably does not rupture healthy vessels; it may render inflammations more severe, but never initiates them. Most observers will share Walshe's profound doubt whe- ther in its most extreme forms, hypertro- phy can never per se lead to death. Does hypertrophy ever diminish or dis- appear ? It is probable that hypertrophy lasts as long as its cause exists. Many facts on record support the opinion that, if the cause of simple hypertrophy cease to act, the heart gradually resumes its normal size. Atrophy may occur in an hypertrophied as readily as in a normal heart. Whether a heart the subject of dilated hypertrophy ever regains its nor- mal volume is doubtful. The occurrence of the so-called concentric atrophy, in which the size of the cavities lessens, and also the disappearance of the dilatation of atony, support the idea that a moderately- dilated heart may regain its normal size. TREATMENT 783 The prognosis in hypertrophy must, therefore, largely depend on the extent to which its cause is removable. For practical purposes the work of the heart in these cases may be divided into three categories: (1) that which is required to carry on the healthy circulation, the body being at rest; (2) superadded work, tem- porary and variable, such as is involved in muscular exertion, emotional excite- ment, local inflammation, pregnancy, &c. ; (3) some permanent abnormal re- sistance to the movement of the blood, increasing the pressure within the cavity affected. The second of these is alone amenable to treatment. The chance of removing or curing hypertrophy depends on the extent to which causes of this class constitute the work of the heart. Where hypertrophy is developed when the work of the second class is as slight as possible, where no avoidable exertion is made, and where no occasional causes of obstruction exist, the chance of removing or lessen- ing hypertrophy is small. In the rare cases in which the whole increase over the normal work of the heart depends on causes of the second class, the prognosis is the most favorable. Such cases are sometimes met with among athletes, as in an instance Walshe records. The probable permanence of the hyper- trophy on the one hand, the likelihood that it may give place to dilatation on the other hand, must influence the prognosis in any individual case. This probability must be estimated by the degree to which the causes of dilatation are, or are likely to be, in operation. Impaired general health, or the presence of degenerative tendencies, local or general, render the prognosis less favorable. Where the cause of hypertrophy is per- manent, the influence of the hypertrophy varies, and with it the prognosis. In cer- tain conditions the increased force with which the heart acts may lead, directly or indirectly, to evil consequences, and in such cases the presence and degree of the hypertrophy may entail, per se, a corre- sponding increase in the gravity of the prognosis. In all forms of valvular dis- ease in which the hypertrophy depends on direct obstruction to the escape of blood from the cavity, the hypertrophy is purely beneficial in its effect; it secures a due supply of blood to the parts beyond the obstruction ; it saves the vessels and or- gans behind from suffering from the im- pediment. It is only when hypertrophy is due, in part, to a variable cause beyond the obstruction, that it may be occasion- ally in sufficient excess to produce preju- dicial arterial distension. In cases of regurgitation, in which the heart has to exert undue force in the pro- pulsion of an undue quantity of blood, the hypertrophy is less simply beneficial in its influence. The muscular force with which the ventricle contracts tends to in- crease the amount of blood regurgitated, and so increase its own repletion. This is the case directly in aortic regurgitation, indirectly in mitral regurgitation. The degeneration of the arteries is hastened by the strain to which they are exposed by the action of the hypertrophied ven- tricle in aortic regurgitation; while in mitral regurgitation, although the stronger action of the ventricle may drive a larger quantity of blood into the aorta, it also increases the amount regurgitated through the incompetent valves. But it must be remembered that in these cases the hy- pertrophy is a substitute for dilatation, and may be accepted as the less of the two evils ; or it counteracts the influence of dilatation which coexists. When the obstruction causing the hy- pertrophy is situated in the vascular sys- tem, pulmonary, or systemic, whether the consequence of degeneration, Bright's disease, &c., the hypertrophy is also less simply beneficial, since the increased strain to which the vessels are subjected increases their liability to degeneration and rupture. In Bright's disease this danger reaches its height, since degeneration of the strained vessels is very apt to occur and renders their rupture easy. In senile changes cardiac and vascular degenera- tion often correspond, and the hypertro- phy which at first is evoked by the change in the vessels yields to dilatation, by which the blood-tension is lessened. But this retro-compensation is not without new risks. In all cases, however, it is still true that the prognosis of the hypertrophy is sub- ordinate to that of the lesion causing it, and also to that of coexisting dilatation. Once established as the result of a perma- nent cause, it usually increases, and bears a simple proportion to its cause. It is ex- tensively employed in prognosis, but is used rather as an indication of the extent and gravity of the lesion causing it than as affording in itself much information. As far as it goes, its presence renders the prognosis of the causal lesion better. Com- pensatory in its action, it wards off evil and promotes health. Treatment.-Current opinion as to the treatment of hypertrophy has under- gone great changes, in accordance with the altered ideas of its relation to the common consequences of organic heart disease. When most of these were con- sidered to be the direct effects of the over- acting heart, every effort was made to diminish its over-action and to lessen its over-growth. Low diet and frequent 784 HYPERTROPHY OF THE HEART. bleedings are the measures which Alber- tini and Valsalva handed down to a long series of their successors ; and the effects of their doctrine is even now to be traced, although perhaps rather in the pages of text-books than in practice. Even after the purely consecutive nature of hyper- trophy was clearly recognized by Bertin, the same treatment was advocated. The judicious management of hyper- trophy depends on the recognition of the fact that it is sometimes purely beneficial, usually welcome as a substitute for its too frequent associate, dilatation, and rarely directly prejudicial. No universal rule for the treatment of hypertrophy can therefore be laid down, since the proper course may be sometimes to foster its oc- currence, sometimes to lessen its excess, or, failing that, to prevent its increase. Hypertrophy of the heart being the re- sult of two factors, nutritive activity and increased work, its increase may be to some extent prevented, and its amount diminished, by lessening each factor in its production. The nutritive activity of the heart can be lessened only by diminishing that of the general system by low diet, bleeding, &c. But to attempt this while the causes of hypertrophy continue, is to substitute dilatation for hypertrophy. The system has been advocated, however, in conjunction with causal treatment, from the time of Bertin. It may be ques- tioned whether the causes of established hypertrophy can ever be sufficiently re- duced to permit the safe employment of "antiphlogistic" measures. Moreover they can rarely be necessary. We see in the voluntary muscles that reduction of work is invariably followed by reduction in size of muscle. Every analogy sug- gests that cardiac hypertrophy will rapid- ly subside when the condition which ex- cited it has lessened or has ceased. It is not often that this result can be proved to occur in the case of the heart, but in- stances are not infrequent in which it seems to take place. The reduction of the causes of hypertrophy, i. e., the work of the heart, to a minimum, constitutes, then, the main object in the treatment of hypertrophy. This work is partly of a constant, partly of an occasional nature. The normal work of the circulation must be carried on ; the permanent organic cause of the hypertrophy can rarely be lessened; but the occasional addition to the heart's work involved in violent mus- cular exercise, increased frequency of con- traction from alcohol or emotion, in- creased obstruction from remediable states of blood or local inflammations, may all be to a large extent removed. Rest of body and mind is therefore the first and most essential element in treatment. All exercise which quickens the pulse must be absolutely forbidden.1 Emotional tran- quillity must be as far as possible secured. The utmost temperance in food and alco- hol should be enforced. A fair amount of nitrogenous food, and a very little light wine with it, constitute the best diet. If food is well taken without alcohol, the latter may often with advantage be pro- hibited. The digestive organs should be carefully attended to. Nothing disturbs the action of the heart so readily as a dis- tended stomach. Food must be moderate in amount, and every cause of transient plethora avoided. The secretions must be carefully regulated, and impaired ac- tion of the kidneys or the skin must be supplemented by mild purgation or diu- resis. Local inflammations, bronchitis, &c., must be carefully guarded against, and when they occur, removed as speedily as possible. Too often, however, the amount of ob- struction which can by these means be removed bears but a small proportion to the total against which the heart has to contend. Can this permanent obstruc- tion be further reduced ? To some extent the work of the heart can always be lessened by reduction in the total quantity of the blood. This formed an important element in the old system of treatment, and it was partly with this object that frequent and repeated bleedings were re- commended. Their condemnation in the present day is superfluous. It may be doubted whether occasional leeching, which still finds advocates, is justified by its ultimate results, although its imme- diate effect is to give relief to the heart. Restriction of fluids has been suggested. It is at any rate a harmless measure ; but the rapidity with which urinary secretion regulates the volume and density af the blood renders it doubtful whether more than a very transient effect is produced. It will be gathered from these state- ments that the conditions under which an attempt at the removal of hypertrophy is indicated are very rare. Whenever the hypertrophy can act immediately on the causal resistance, its influence is always, on the whole, and sometimes entirely beneficial. Only when the over-action of the heart is primary, or is due to a cause which has ceased to operate, is it to be attacked directly. In the rare instances in which violent exercise has called out persistent hypertrophy, or some obstruc- tion has been removed, the condition may call for immediate treatment to reduce its effect. Where the obstruction is situated far from the heart, and degenerated ves- 1 ' ' On doit regarder le repos comme un remede pr^servatif; mais ce repos n'exclut pas un exercice moderS, lorsque les grands accidents sont calmes."-Senac, 1. c. p. 419. TREATMENT. 785 seis are interposed which have to bear the full force of an over-acting ventricle, as in Bright's disease, the question also some- times arises of the chances of evil from vascular rupture, on the one hand, and from a weakened heart on the other. The certain, slow, but sure evil of a weakened heart will generally counterbalance the possible catastrophe, and any attempt to lessen the cardiac strength will be avoided. The use of drugs in hypertrophy is a subject on which various opinions have been held.1 Most observers agree with Walshe, that the reduction of the bulk of the heart is beyond the direct power of any drug. The chief role of medicine lies in regulating the cardiac contractions and in freeing the circulation from removable causes of embarrassment. Frequent ac- tion involves a great increase in the work of the heart. Force is needed, it has been stated already, to move the heart, apart from the movement of the blood. The minimum frequency consistent with the due supply of blood to the system gives the heart its best conditions of action. Moreover, very frequent action may fill the arteries to repletion, and so increase their distension as greatly to augment the intra-cardiac pressure. Lastly, frequent action lessens the total rest of the heart, and favors degeneration. No remedy has been discovered which lessens the undue frequency of the action of the heart so effectually as digitalis. But digitalis strengthens the cardiac action, and hence its use in hypertrophy has been discoun- tenanced by most modern writers, and by some strongly condemned. The experience of clinical observers is not, however, in complete accord with theoretical conclusion. By many the value of digitalis in hypertrophy is strongly as- serted. One explanation for this may lie in the fact that hypertrophy is so rarely simple. Almost invariably, dilatation is conjoined with it. In dilatation, digitalis is of extreme value, and its use in hyper- trophy is to a great extent proportioned to the existence and amount of dilata- tion. Moreover all irregular action of the heart involves waste of force, involves useless work. Too frequent contraction does the same. Each may generally be controlled by digitilas. Even where there is no irregularity and little dilatation, the cardiac action may be below the actual needs of the system ; the compensation is insufficient, and the additional strength of contraction imparted by digitalis is purely useful. The dose of digitalis needed in these circumstances is smaller than that required in dilatation. Five minims of the tincture, or a drachm of the infusion, three times a day, will usu- ally effect all that is required. A larger dose, is, as Milner Fothergill states, much more frequently deleterious than in dilata- tion, in which large doses are borne, not only with impunity, but with advantage. In pure hypertrophy, digitalis is rarely necessary. Veratrum viride has been used, especially in America, to reduce the strength of the heart, when in hyper- trophy its force appears beyond the pres- ent need of the system. Doses of five minims of the tincture may be given three times a day. Both the force and fre- quency of the heart's action are reduced. Inunction of Ung. Veratrise has also been employed for the same purpose. Where hypertrophy is not pure but is great, and acts directly on the vascular system, or tends to increase its cause (as in aortic regurgitation), it may be neces- sary, by similar measures, to reduce the force of the heart to a minimum neces- sary for the work of the circulation. Di- gitalis has been employed in small doses and recommended strongly by B. Foster, but most authorities discountenance its use under these circumstances, and Ringer1 points out that the same end may be attained by small doses of aconite. A combination of aconite and veratrum is recommended by H. C. Wood.2 The consciousness of the cardiac con- tractions, which constitutes so troublesome a symptom of hypertrophy, is only in part due to the force with which the heart acts. It is much more frequently the result of irregular or too sudden con- tractions, and related to coincident dilata- tion rather than to hypertrophy. It is commonly controlled by rest and digitalis. For the relief of cardiac pain, direct sedatives may be needed. Opium, or mor- phia, is very effectual. Aconite is strongly praised by Walshe. Belladonna, Indian hemp, hydrocyanic acid are also useful in some cases. The Virginian prune bark, which contains hydrocyanic acid, is some- times useful, but its tonic properties ren- der it more suitable for dilatation. Cold locally applied to the cardiac region is strongly recommended by Niemeyer. The treatment of hypertrophy of the right ventricle must be conducted on the same general principles as that of the left. It is almost always united with di- latation, and is never excessive. Hence it needs as far as possible to be strength- ened, both absolutely by tonics, digitalis, &c., and relatively by diminishing its work, by lessening as far as possible the 1 Their possible use seems to have occurred to the French school of physicians at the be- ginning of this century, although the chief cardiac medicine, digitalis, had long before been employed in this country. VOL. II.-50 1 Handbook of Therapeutics, fifth edition, p. 427. 2 Philadelphia Med. Times, 1874, Nov. 14 and 21. 786 DILATATION OF THE HEART. obstruction to the movement of blood through the lungs, and by the avoidance of over-exertion, &c. Hypertrophy of the auricles rarely calls for special treatment. Never simple, the conjoined dilatation always predominates. The more detailed treatment of dilated hypertrophy is described in the next article, on Dilatation of the Heart. DILATATION OF THE HEART. W. R. Gowers, M.D. Synonym.-Enlargement of the Heart (old writers); Aneurism of the Heart (Baillou, Lancisi); Passive Aneurism, or Passive Dilatation (Corvisart) ; Herzer- weiterung (Freysig) ; Cardiectasis (Jac- coud). Definition.-Increase in the size of one or more of the cavities of the heart. Such increase in size may or may not be attended with obvious thickening or thin- ning of the cardiac walls. History.-Dilatation of the heart re- ceived much attention from the earlier pathologists, being rightly regarded as the chief cause of its enlargement. In the middle of the sixteenth century, Vesalius gave an account of a heart, the left ven- tricle of which contained two pounds of blood, and Baillou1 mentioned one that equalled in size a man's head. Harvey2 also in 1628 alluded to this condition. Dilatation of the auricles was described by Willis. Dilatation of the right ventricle and left auricle, as the result of mitral constriction, was described by Mayow in 1674. Vieussens,3 in 1715, described a case, observed in 1695, of extreme dilata- tion of left ventricle, the consequence of aortic regurgitation. Peyer, Lancisi, and all successive writers alluded to, or re- lated instances of the condition. The first systematic account of its mechanism and causes was given by Senac4 in 1749, who distinguished dilatation with and without thickening of the walls. Morgagni,5 in 1779, described very clearly its origin, and effect on the circulation. Several cases were related by Ferriar,6 in 1792, and the general causes and symptoms of dilatation were described by Allan Burns, in 1809. In France, after the writings of Lancisi had given the word currency, Baillou's term "aneurism," had been used to de- signate enlargements of the heart, as well as of the great vessels. Corvisart, in his description of dilatation in his work, pub- lished in 1806, designated the two varieties described by Senac, "active" and "pas- sive" aneurism, with a subprotest against the application of the term to conditions with such different tendencies. He de- scribed accurately, as far as the descrip- tion went, the different symptoms ' and tendencies of the two conditions, and pointed out the association of dropsy, or the "serous diathesis," with dilatation, rather than hypertrophy. A further ac- count of dilatation of the left auricle as a mechanical consequence of mitral con- striction was given by Abernethy in 1806.1 Dilatation consequent on carditis, and associated with adherent pericardium, was described, as the result of articular rheumatism, by Sir W. Dundas in 1808.2 Its varieties were recognized a little later by Kreysig. Bertin, in 1811, distinguished the conditions and processes of dilatation and hypertrophy (in the sense in which the words are now used), and Laennec's work on Auscultation, published in 1819, gave the terms authoritative use. In Bertin's systematic treatise, edited by Bouillaud in 1824, the chief varieties were distinguished which have since been gene- rally recognized. The detection, by percussion, of enlarge- ment of the heart, of which dilatation is the chief cause, is due to Avenbrugger (1763); that of the altered impulse by pal- pation, to Corvisart (1806); that of the auscultatory signs, to Laennec (1820). Varieties.-From the condition of the cardiac walls, their increase or dimin- 1 Epidemics et Ephemerides, 1574. Yvaren's Trans., Paris, 1858, p. 289. 2 De motu cordis et sanguinis. 3 TraitS du Cceur. 4 Traits de la Structure du Coeur, &c., tom. ii. 5 De Sed. et Caus. Morb., Epist. xxvii. 6 Medical Histories and Reflections, by John Ferriar, M.D., vol. i. 1792, p. 144. 1 Med.-Chir. Trans, vol. i. p. 27. « Ibid. p. 37. CAUSES. 787 ution in thickness, certain varieties have long been distinguished. (1) Dilatation with Hypertrophy (active aneurism of Corvisart), in which the walls are increased in thickness, as well as the cavities in size. (2) Dilatation with Attenuation (passive aneurism of Corvisart), in which the cavi- ties are increased in size, while the walls are reduced in thickness. To these Bertin proposed to add that of simple dilatation, in which the dilated walls preserve their normal thickness, and mixed dilatation, in which the walls are in one place increased, in another diminished, in thickness. These varieties have been adopted by most subsequent writers. The name, " simple dilatation," cannot, however, be consid- ered an accurate designation of the condi- tion which it denotes, dilatation without hypertrophy of tissue. If a heart be di- lated only, its walls, extended in area, are necessarily lessened in thickness. For the normal thickness of the walls to be preserved when the cavity is dilated, over- growth of tissue must occur. Thus the condition of " simple dilatation" neces- sarily produces dilatation with attenua- tion, while the state to which the term is applied is really dilatation with moderate hypertrophy: this was shown clearly by Stokes. Forget applied to the condition the term hypertrophic dilatoire. Many writers have suggested, and Wilks and Moxon maintain, that pure dilatation never occurs, that hypertrophy is the in- variable accompaniment, as the increased weight testifies, and that recorded exam- ples of hearts dilated and not increased in weight have been examples only of relaxa- tion. They prefer the simple distinction into dilatation with thickening, and dila- tation with thinning. Other varieties which have been distin- guished are those of general dilatation, in which all four cavities of the heart suffer, and partial dilatation, in which the change is confined to one or some of them. It has also been proposed by Hayden1 to designate those cases in which an obvious active cause of dilatation can be distin- guished, consecutive, and those in which no such causes exists, primary. Lastly, dila- tations have been classified as temporary or permanent. Bertin suggested that the latter only should be included under the term, the temporary forms being rather examples of distension than of dilatation. Causes.-The maintenance of the nor- mal size of the heart ultimately depends on the existence of a due proportion be- tween its elastic and contractile force, and the blood-pressure to which it is ex- posed in passive resistance and active con- traction. A disproportion between these two forces is the ultimate cause of its dila- tation ; such disproportion may result from a change in the amount of either factor, an increase in the blood-pressure, a decrease in the cardiac strength. Often the two conditions are conjoined ; a weakened heart yields before an increased pressure, and ,thus becomes over-dis- tended ; and the conditions being perma- nently dilated. To these two causes must, probably, be added the effect of traction from without, which acts by les- sening the effect of the contractile force of the heart, and so corresponds in its action with the weakening of the wall. Thus diminished strength of the walls of the heart constitutes a predisposition to dilatation, and the causes of that weaken- ing may be considered as the predisposing causes of dilatation ; the endocardial pres- sure being regarded as the exciting cause of the dilatation. But, as is the case with many predisposing causes of disease, the weakness of the wall of the heart may be the only morbid antecedent. Moreover, the action of these two causes of dilata- tion is not simply predisposing and excit- ing. It will be convenient, however, to consider the mechanism of their action after they have been described in brief detail. The antecedents of the predispos- ing and exciting causes may be spoken of as the remote causes of dilatation. It must be remembered also, that in- creased endocardial pressure is the imme- diate cause, not only of dilatation, by its mechanical effect, but of hypertrophy, by the vital reaction which it induces. Its effect in producing dilatation is influenced in part by the existence of the predisposi- tion (weakness of the cardiac wall), in part by the conditions under which it acts, and which may be regarded as deter- mining causes. Commonly, however, the double tendency of the increased pressure results in the double effect, and hyper- trophy and dilatation are conjoined. We have thus four classes of causes to con- sider, the remote, predisposing, exciting, and determining causes. (A.) Remote Causes.-The general con- ditions of hereditary influence, age, sex, occupation, previous illness, etc., enter largely into the causation of dilatation of the heart, as the antecedents of the conditions on which it immediately depends. They can only be fully un- derstood when the immediate causes are known. Hereditary taint has a powerful influence in disposing to special degene- rations and to certain diseases, such as acute rheumatism, on which the imme- diate causes largely depend. Age has a similar influence. Degenerative changes are concerned in the production of both causes of dilatation, and hence the dis- ease increases in frequency with advanc- 1 Diseases of Heart and Aorta: Dublin, 1875, p. 558. 788 DILATATION OF THE HEART. ing years. Sex influences the occurrence of dilatation by determining exposure to one of the commonest causes of increased endocardial pressure, muscular exertion. Degenerative changes in the vascular sys- tem are largely due to the same influence, and are causes of dilatation. Hence the disease is more frequent in men than in women. Occupation has a similar influ- ence : all those occupations which involve considerable effort tend to cause dilatation of the heart. (B.) Predisposing Causes.-Conditions of weakness of the cardiac walls may con- sist in acute or chronic changes in the muscular fibres, or in destruction of those fibres and their replacement by tissue ele- ments which yield more readily to the pressure of the blood. Morbid states of the muscular fibres are, (1) Atony, in which the relaxation of the fibres at rest is more absolute, their contraction less com- plete. (2) The granular degeneration of acute disease. (3) Fatty degenera- tion, resulting ultimately in the actual destruction of fibres. (4) Fatty over- growth, in which the muscular fibres undergo secondary atrophy. (5) Fibroid degeneration, the sequel to an acute in- flammatory change or the result of a chronic perversion of nutrition. (6) Spe- cial degenerations and growths. (7) Weakening of the fibres due to the state of dilatation. Beau pointed out that the fibres common to the two ventricles may be so weakened by dilatation of one, as to lessen considerably the contractile force of the other ventricle, and so to aid its dila- tation. (8) Lastly, it has been stated by Niemeyer1 that the muscular fibres may so lose their contractile power as to per- mit dilatation when no structural change in the cardiac wall, or in the fibres them- selves, can be detected by the microscope. Seitz2 has lately advocated the same view. In all the recorded examples, however, over-exertion has been the exciting cause of the dilatation, and the cases appear to have been characterized rather by insuffi- cient power to react against the aug- mented pressure, than by any primary degeneration. The conditions by which these patho- logical process are produced constitute the predisposing causes of dilatation. The most important of these conditions are : (1) Anaemia and chlorosis, in which the general mal-nutrition results in atopy, and, it may be, granular degene- ration of muscular fibre throughout the body. (2) Acute febrile diseases, espe- cially rheumatism, erysipelas, pyaemia, typhus, typhoid fever, &c., having a similar effect. (3) Inflammation, pri- mary or secondary to endo- or peri-carditis, the inflammation in the latter case invad- ing the adjacent layer of the heart. (4) Obesity, with local overgrowth of fatty tissue. (5) Chronic degenerative changes in the system, as yet ill-defined, but often due to chronic alcoholism, and causing fatty and fibroid degeneration of various organs, including the heart. (6) De- rangements of the blood-supply to the walls of the heart. Chronic and inter- mitting passive congestions cause, as Sir William Jenner points out,1 degeneration of the heart, toughening its walls and les- sening its contractile power. Diminished blood-supply is a common cause of fatty and granular degeneration. It may be due to imperfect distension of the coro- nary arteries in consequence of the defec- tive distension of the aorta, or it may re- sult from narrowing of those vessels by the contraction of lymph outside the heart, or by degeneration, atheromatous and calcareous, of their walls. (7) De- fective nerve-powrer probably in some cases leads to inefficient contraction and dilatation of the heart. Dr. Dobell be- lieves that sexual excesses are powerful causes of cardiac weakness. Traction from without, the result of peri- cardial adhesions, is sometimes a cause of dilatation of the heart. The two condi- tions are constantly found associated, but in the majority of cases there exists also endocardial mischief sufficient to account for the dilatation. Hence, Morgagni and many subsequent writers doubted whether the state of the walls was not always the consequence of the coexisting valvular disease. But cases are not infrequent in which dilatation exists, and no morbid condition can be found to explain its oc- currence except an adherent pericardium. Beau,2 arguing from a small number of such cases, inferred that dilatation was the invariable result of pericardial adhe- sion. The same view was very strongly maintained by Hope.3 Wider observation showed, however, that adhesions were frequent enough with no morbid state of the heart's walls. Laennec, Bouillaud,4 Barlow, Stokes, and others maintained, therefore, that pericardial adhesionshave no direct effect in causing dilatation. The same view has been still more recently maintained by Hayden.5 Gairdner,6 how- ever, emphasized the fact that in a minor- 1 On Congestion of the Heart, Med.-Chir. Trans, vol. xliii. 2 Arch. Gen. de Med. ser. ii. tome x. 1837, p. 425. 3 Diseases of the Heart, p. 192. 4 Traite Clinique, &c., 1835, p. 454. 5 Diseases of the Heart and Aorta, p. 363. 6 Edin. Med. Journal, February, 1851. 1 Text-book of Practical Medicine, American Trans, vol. ii. p. 320. 2 Zur Lehre von der Ueberanstrengung des Herzens. Deutsches Archiv fur kiln. Med. 1873, xi., xii. CABSES. 789 ity of cases no other cause can be discov- ered for the changes in the walls of the heart. At the same time he showed that, in other cases, the adhesions not only do not tend to cause dilatation, but they do not prevent the reduction in size which accompanies chronic wasting diseases. The most extensive statistical evidence on the question is that furnished by Ken- nedy,1 of Dublin, who collected ninety cases of adherent pericardium without valve disease, and found that the heart remained healthy till death in thirty-four, and was enlarged in fifty-one. But some of his cases were from museums, into which hearts of the normal size would be little likely to find their way, and it is probable, therefore, that his proportion of healthy hearts is too small. Dr. Hayden has collected twenty-three cases of adhe- rent pericardium, without valve disease, and found that in seven there was enlarge- ment without any other discoverable cause.2 Putting together these facts, and those recorded by other authorities, it seems fair to conclude that adherent peri- cardium causes enlargement of the heart in one-third of the cases. The difference in the effect of the adhe- sion is not to be explained by difference in its extent. The most marked hyper- trophy and dilatation was due, in one of Gairdner's cases, to a firm adhesion of very limited extent, near the apex of the left ventricle. In other cases in which no influence was exerted, the adhesion was universal. Dr. Wilks3 has pointed out that, when general adhesion is associ- ated with dilatation, the effect is more marked on the right ventricle than on the left. This is no doubt due to the thin- ness of the muscular wall of the right ventricle. In estimating the effect of pericardial adhesions it must be remem- bered how frequently they are associated with another cause of dilatation, the dam- age to the subjacent portion of the cardiac wall by the extension to it of the pericar- dial inflammation. For the settlement of the question of their influence more facts are needed which shall embrace not only the state of the heart's walls, and the fact of adhesions, but the extent, firmness, and probable duration of the latter, the extent to which the pericardium is con- nected with parts around, and the extent to which the muscular fibres of the heart have suffered from the inflammation. Dr. Gairdner4 has maintained that when the expansion of the lungs is interfered with by their atrophy, the inspiratory efforts to distend them, which he regards as the great cause of emphysema, may lead to over-distension of the heart. He believes that it is by this mechanism that emphysema is associated with dilatation of the heart, and appeals in support of the theory, to the fact that the dilatation is not confined to the right side, but af- fects in slighter degree and a little later in time the left side also. This view de- pends for its probability on the inspira- tory theory of emphysema. If, with Sir William Jenner and most modern author- ities, emphysema is believed to arise chiefly, not from primary atrophy of the lung, but from its over-distension during expiratory efforts, this explanation of the origin of dilatation of the heart falls to the ground. No dilating influence by trac- tion can result from violent expiratory efforts, and when emphysema is once es- tablished the inspiratory effort which can be made is far less than in health. If the dilatation of the right ventricle in these cases is referred, as is generally taught, to obstruction to the flow through the lungs, the simultaneous affection of the left side can be explained in another way. (C.) Exciting Causes.-Increase in the endocardial blood-pressure has been men- tioned as the chief exciting cause of dila- tation of the heart. Such increased pres- sure opposes the contraction of the heart, and leads, by a mechanism to be presently described, to its dilatation. It depends on increased resistance to the movement of the blood, the result of an increase in its mass, or an obstruction in the orifices or vessels through which it flows. This increased pressure leads to two results, directly to dilatation, indirectly to hyper- trophy. The causes of the increased pres- sure, which are more fully considered in the article on hypertrophy, are as fol- lows :- (1) Increase in the mass of blood to be moved, consequent on over-distension of the heart. Thus regurgitation through an orifice causes dilatation of the chamber behind. Thus, too, the dilatation tends to its own increase, a process which is only arrested by the occurrence of hyper- trophy. (2) Resistance to the movement of the blood in consequence of narrowing of the orifice by which it leaves the affected chamber. The influence of this condition in causing dilatation is not great. The obstruction is gradually developed, and unless associated with weakness of the cardiac walls, the latter become hypertro- phied to overcome the increased resist- ance. In aortic obstruction, for instance, dilatation is rare. (3) Resistance to the movement of the blood through the vascular system is a powerful cause of dilatation, and is most effective when suddenly developed or in- 1 Edin. Med. Journal. 2 Loc. cit., table on p. 362. 3 Guy's Hosp. Rep. vol. xvi. p. 202. 4 British and Foreign Medico-Chirurg. Rev., July, 1853, p. 212. 790 DILATATION OF THE HEART. termitting, and especially when the con- dition in which it arises is such as to im- pair the nutrition of the walls of the heart. Disease of the large vessels, aorta and pulmonary artery, rarely causes dilata- tion. Obstruction of the smaller vessels is a more effective cause, and especially those forms of obstruction which affect the pulmonary circulation alone, or in conjunction with the systemic vessels. Long-continued and severe muscular efforts are, as Ferriar' pointed out, a pow- erful cause of dilatation and hypertrophy. The resulting condition of heart depends largely on the existence of the conditions which favor the occurrence of one or the other state. The effect of effort is to ob- struct the circulation through both the general and pulmonary system. Its in- fluence on the left ventricle has been de- scribed in relation to hypertrophy. Clif- ford Allbutt has especially pointed out the direct effect on the right ventricle and the influence of undue smallness of lungs on its occurrence. The obstruction to the pulmonary circulation by the pressure of the air on the inner surface of the air cells obstructs the escape of blood from the right side of the heart. The compres- sion of the heart itself interferes with the entrance of blood from the veins, tends to their over-distension, and when the pres- sure is removed, to the over-distension of the right auricle and ventricle. Thus the intermitting obstruction causes intermit- ting over-distension of the right side of the heart, and that intermitting conges- tion of the walls of the heart which leads to the degeneration of its substance and renders dilatation permanent. It is by a similar mechanism, according to the views generally accepted, and fully stated by Sir William Jenner in the present volume of this work, that emphysema of the lungs causes dilatation of the heart. Intermittent distension results, as just described, from the violent expiratory ef- forts with closed glottis, which constitute the efficient cause of emphysema; and as the latter condition is developed, degene- ration, elongation, and destruction of ca- pillaries render the obstruction perma- nent, which before was occasional. The right side of the heart undergoes dilata- tion, sometimes to an extreme degree. Hypertrophy is usually also produced. The congestion of the cardiac wall dis- poses the left ventricle to yield before the increased pressure of the aortic blood, which is an ultimate effect of the venous distension acting through the capillary system. Other forms of pulmonary change have a slighter tendency to cause dilatation of the heart than emphysema. An excep- tion must, however, be made for cirrhosis of the lung, which produces, in a large number of cases, hypertrophy and dilata- tion of the right side. Such a change was present in one-third of the cases of cirrho- sis collected by Bastian.1 Mechanism.-The consideration of the mechanism by which dilatation is effected is necessarily, in the main, theoretical. It has, perhaps on this account, received little attention, and has even been some- times dismissed as useless. But any clear conception of the way in which a morbid state is related to its causes, if correct, must afford a clearer view of its pathologi- cal significance, and of the way in which by treatment it may best be met. The dilatation of the heart is produced, in every case, by its over-distension with blood. Just as the various causes of hy- pertrophy involve, as the efficient cause, overwork, so the various causes of dilata- tion involve over-distension. The imme- diate cause of this over-distension is, in each case, the existence at the end of the diastole of an endocardial pressure dispro- portioned to the resisting power of the wall of the heart, and before which the wall yields. The act of dilatation thus occurs during the diastole of the heart. This circumstance lessens the simplicity of the relative action of the exciting and predisposing causes of dilatation, since, as will be immediately explained, each may act by producing a similar effect. Three sources of over-distension may thus be recognized. (1) The mass of blood entering in the normal course of the circulation may be abnormally large; simple over-distension. (2) Blood may enter the cavity from an abnormal source (regurgitation), and being added to that entering it in the normal course of the circulation, increases the mass of blood and so the distension of the chamber: over-distension from regurgitation. (3) The whole of the blood previously in the chamber may not be expelled from it dur- ing contraction, the residual blood being added to that entering from behind in- creases the distension of the chamber; over-distension from imperfect contraction, or residual over-distension. (1) Simple over-distension is the result of over-distension of the source from which the blood enters the affected chamber. It is well seen in the effect of mitral regurgi- tation on the left ventricle. The over- distended auricle drives an abnormal quantity of blood into the ventricle, into which probably an increased quantity has already passed in consequence of the heightened tension of the blood within the auricle. It is probable that a large quantity of blood enters the ventricle during diastole, enough to equalize, or almost to equalize, the pressure within 1 Med. Hist, and Ref., vol. i. 1792. 1 Art. Cirrhosis of Lung, vol. iii. CAUSES. 791 the ventricle and within the auricle,1 be- fore the auricular contraction effects the actual distension or over-distension of the ventricle. The pressure to which the in- ner suface of the ventricle is exposed at the end of the auricular systole is very great, for in accordance with the well- known law of hydrostatics it is multiplied directly as the area of the inner surface of the ventricle exceeds that of the au- riculo-ventricular orifice. Simple over- distension may occur, especially in the auricles, in conditions of acute weakening of the cardiac walls. The lessened tone of the muscular fibres allows them to yield unduly before the pressure of the incoming blood, and as the current is con- tinuous, they thus become directly over- distended. Similarly the flaccid ventri- cles may yield unduly before the current which enters during diastole, and the systole of the auricles may over-distend the ventricles. This mechanism has been described by Beau2 as dilatation sans asys- tolie. But the conditions are those under which contraction is imperfect, and the small pulse renders it probable, in many cases, that such imperfection occurs. Re- sidual over-distension will then increase the dilatation. (2) Over-distension from regurgitation is one of the most efficient causes of dilata- tion. The cavity is filled with blood from a double source. That which enters into the normal course of the circulation is added to that which has regurgitated into the cavity, and over-distension results. In aortic regurgitation, for instance, it is the addition of the contents of the auricle to the blood regurgitating into the ven- tricle from the aorta, wfliich actually dis- tends the chamber and dilates it until, ultimately, the dilating process is met by compensating hypertrophy. In perma- nent patency of the semilunar valves the intra-ventricular pressure at the end of the auricular systole must be very great, since the pressure of the aortic blood will be added to that produced by the contrac- tion of the auricle. (3) Over-distension from imperfect con- traction; residual over-distension.-When- ever, from any cause, systole is incom- plete, blood must remain in the chambers and render the entrance of the normal quantity of blood an over-distending agent. Incompleteness of contraction is theoretically possible from two causes, diminished contractile force, and in- creased resistance to contraction. It is probable that each of these does actually prevent complete contraction, since each is found to be an efficient cause of dila- tation. (a) The various conditions -which weak- en the cardiac walls, already considered, must tend to render the heart incapable of overcoming all the resistance that is opposed to it, whether that be normal or increased. Hence the contraction is im- perfect, and the residual blood is the ulti- mate cause of over-distension. To this condition Beau gave the name of asystolie. This weakening of the wall not only leads to over-distension, it also renders the ef- fect of the over-distending force greater in degree and in duration, for the weak wall yields more to the increased pressure, and the yielding of the degenerated wall is permanent. Among the conditions weakening the heart must also be reck- oned the state of dilatation. The dilated heart has increased work, for it has to move an increased mass of blood, to over- come a greater pressure. To this it is even less competent than a healthy heart. Hence the dilatation itself renders the contraction additionally incomplete, and is thus perpetuated and increased. The influence of dilatation is of course here considered apart from that of the hyper- trophy commonly conjoined with it, and to some extent counteracting its effect. It is by interfering with contraction that pericardial adhesions must be con- sidered to exert whatever influence they possess in causing dilatation of the, heart. Connections of the pericardium with parts around, consequent on the extension of inflammation to its outer surface, may cause the adhesions to the heart to oppose considerably the reduction in size during systole, and thus to render the contrac- tions incomplete.1 Moreover, a similar effect may be produced by the interference with the approximation of different parts of the surface during contraction, which must occur if a thick inelastic membrane covers the heart. Such an influence will interfere chiefly with the contraction of the thin-walled right ventricle, and this may be one reason why it suffers most. 1 That this is the case is highly probable, from a phenomenon sometimes to be observed in cases of mitral constriction. When dias- tolic and presystolic murmurs are both pres- ent, the former due to the slow passage of blood through the orifice in consequence of the tension of the blood within the auricle, the latter due to the contraction of the auricle, there may be. during an occasional prolonged diastole, an interval of silence between the two murmurs. When the diastolic murmur is loud, this silence can only be explained by a cessation, or almost cessation, of the flow of blood, which means, of course, an equaliza- tion of the pressure in the two cavities. 2 Beau, Traite d'Auscultation. Paris, 1856. 1 Thus in Gairdner's case, already men- tioned, in which marked hypertrophy and dilatation of the left ventricle were associated with, as the only discoverable cause, a local adhesion near the apex, a corresponding ad- hesion connected the other side of the peri- cardium with the left lung. 792 DILATATION OF THE HEART. The effect will be to cause a residual over- distension, just as does the simple weak- ening of the cardiac wall with which the adhesions are so often associated. (6) Increased resistance from some ob- struction to the circulation is another cause of incomplete contraction. Such increased resistance may interfere with the contraction of a healthy heart, but probably rarely does this unless great and suddenly developed. The reserve of power usually prevents imperfect con- traction, and compensating hypertrophy gradually renders the heart efficient. But when suddenly developed, or when the nutrition of the heart is interfered with, the chamber dilates. This dilatation was formerly, and is still by some, ascribed to the direct effect of the increased pres- sure on the contracting fibres.1 It was compared by Senac to the effect of an extending force in elongating a cord.2 Niemeyer3 pointed out that such an explanation is entirely inapplicable to the conditions of the phenomenon. In- crease in the capacity of a contracting chamber from increased pressure within it during contraction, is inconceivable. Such increased capacity can only be ex- plained by an increased quantity of blood entering it under a pressure sufficient to overcome the resistance of its walls. The influence of increased resistance to con- traction may be to weaken the muscular fibres, to lessen the elasticity of the walls, and to render over-distension easier, but more than this it cannot di- rectly effect. (D.) Determining Causes.-The exciting causes of dilatation and hypertrophy are thus to some extent the same ; the occur- rence of the result is influenced not only by the predisposition already described, but also by certain determining conditions. (1) The rapidity of the development of the increased blood-pressure, i. e., the rapidity with which the valvular disease, or the systemic or pulmonary obstruction is produced. Time is necessary for the production of that hypertrophy which alone can prevent dilatation, and a sud- denly-developed obstruction invariably leads to dilatation. (2) The small amount of muscular tissue normally existing in the wall of the affected chamber of the heart. This is naturally proportioned to the work of each segment of the heart, i. e., to the blood- pressure, to be by it passively resisted and actively overcome. The extra pressure induced by the abnormal obstruction or regurgitation bears no necessary propor- tion to the normal blbod-pressure, and be- fore absolute equal increments of pressure, the smaller the normal amount of muscu- lar tissue, the more readily does dilatation occur, because the systole is the more readily rendered imperfect, and residual over-distension produced. Each cavity of the heart affords an illus- tration of these influences, and although our knowledge is still very imperfect, we can understand something of the origin of the condition found in each instance, and it is worth while to recapitulate briefly the way in which the different results are brought about. In aortic obstruction, the left ventricle is commonly hypertrophied, less commonly dilated. The left ventricle, containing the greatest amount of muscular tissue, possesses a large reserve of force, and can overact so as to overcome a moderate in- crease in resistance, and so prevent resid- ual over-distension and dilatation. The development of obstruction is usually slow, and thus there is time for hyper- trophy to occur. In aortic regurgitation there is always dilatation, and usually much, often very much, hypertrophy. The regurgitant blood causes the ventri- cle to be overfilled, and the patent aortic orifice transmits to the interior of the ven- tricle, during its passive state, the intra- aortic pressure. The regurgitation is usually slowly developed, and the mus- cular tissue of the ventricle considerable, and hence hypertrophy occurs. This is favored by the abundant blood supply to the heart, consequent on the great disten- sion of the aorta. In mitral disease, obstructive and re- gurgitant, the left auricle undergoes dila- tation and hypertrophy, the former pre- dominating in regurgitation, from the direct over-distension and frequently rapid development of the pathological state. Hypertrophy of the auricle is usually more frequent in obstruction from the slowness with which the lesion is developed. Dila- tation is always, however, conjoined, from the ease with which the contraction of the weak auricle is rendered imperfect by ob- struction. In mitral regurgitation, the left ventricle is hypertrophied and dilated, and the dilatation is usually considerable, in consequence of the direct over-distension of the chamber, and perhaps also of the * Lately by Chirone in Lo Sperimentale, August, 1874. 2 "La contraction qui resserre les ven- tricules est peut-etre 1'instrument qui aug- ment les dimensions, que le sang soit en trop grande quantite dans ces reservoirs; qu'il trouve quelque barriere que 1'empeche d'en sortir avec la liberty qu'il a ordinairement, Paction des fibres sera plus forte : or cet exces de force doit n6cessairement les allonger: un raccourcissement force produit le meme effet qu'une action qui tire et qui tend une corde, ses Elements doivent necessairement s'ecarter, et me se sSparer, s'ils sont tires avec trop de violence."-Senac, Traite, &c., 1749, tom. ii. p. 397. 3 Loc. cit. vol. ii. p. 316. PATHOLOGICAL ANATOMY. 793 imperfect distension of the coronary arte- ries and consequent damaged cardiac nutrition. The right ventricle, in disease of the left side, usually undergoes dilatation, from its small amount of muscular tissue, but often is also hypertrophied, in conse- quence of the slowness with which the obstruction in the left side tells back upon the right. The hypertrophy is usually less and the dilatation as much marked, when the obstruction is situated in the pulmonary system, in consequence of the directness with which such obstruction affects the ventricle, the rapidity with which it is frequently developed and in- creased, and the damage to the cardiac nutrition, which results from the extreme and sudden passive congestion to which the heart is, in these cases, very often liable. In obstructions to the systemic circula- tion, hypertrophy is the common change in the left ventricle, and often, especially in Bright's disease, is wholly unattended with dilatation. The extreme slowness with which the obstruction is developed is, no doubt, a chief factor in determining the occurrence of hypertrophy rather than dilatation. Occasionally, however, dilata- tion occurs instead of hypertrophy. Such cases are perhaps instances of simultane- ous cardiac and vascular degeneration, in which the increased blood tension is the result of the latter, and the damaged heart is incapable of resisting the abnormal pressure. The sequence of the conditions of hy- pertrophy and dilatation varies under different circumstances. It is certainly not uniform, as has been maintained by some writers. When an increased resist- ance or a cause of over-distension is sud- denly developed, dilatation results at once, and hypertrophy slowly, when time allows overgrowth to occur. This is fre- quently seen in aortic and mitral regurgi- tation. The order is the same when the initial state is one of defective power in the walls of the heart ; dilatation pre- cedes and is the cause of hypertrophy-as in that which results from carditis. On the other hand, dilatation may be second- ary. Degeneration occurs in the hyper- trophied tissue more readily than in the healthy heart. Nutritive influences fail from impaired health or advancing years.1 Again, the coronary vessels suffer from undue strain, degenerate, and lessen the blood supply. This, as pointed out by Mauriac, is a frequent occurrence in aortic regurgitation. Under all these conditions the degeneration weakens the cardiac wall, and dilatation occurs at a later period than the hypertrophy. Pathological Anatomy. - Dilata- tion may affect all the chambers of the heart or only some of them. It has been a subject of rather unprofitable discussion whether general or partial dilatation is the more common. It is rare for one chamber to sutler considerably alone. When the cause of the dilatation is dis- ease of an orifice, the chambers behind the orifice are usually alone affected. An exception is mitral regurgitation, in which the cavity in front of the orifice is dilated also. The chamber immediately behind the diseased orifice commonly suiters more than the others. In mitral constriction, for instance, the left auricle is most di- lated. In all diseases of the left side of the heart, the right side may ultimately become dilated. Hence the most widely distributed change occurs when the ob- struction is in front of the left ventricle, and affects each part of the heart succes- sively. In aortic regurgitation, for in- stance, enormous hearts are met with, in which every cavity is dilated. Occasion- ally a similar result follows obstruction in the aortic system. The dilatation, as already stated, is rarely simple. Hypertrophy is usually present, and varies in amount according to the conditions described in the last article. From the variations in the amount of dilatation and associated hy- pertrophy very different effects on the form and size of the heart are produced. The amount of dilatation is estimated by comparison with the normal capacity, by measurement of the external size of the heart, the thickness of the walls, and the length and mid-circumference of the cavity. In estimating it, regard must be had to the age of the patient, and to the state of fhe body. The capacity of the heart naturally increases with age. In decomposition the relaxation of the heart is extreme, the cavities present their maximum capacity, the walls their mini- mum thickness. The existence of de- composition, which in some cases is very rapid, must therefore induce caution in inferring actual dilatation from a flaccid and apparently dilated state of the heart. A heart, the subject of general or par- tial dilatation, is increased in size and al- tered in shape. The increase in size may be considerable ; the circumference being two, three, or four times the normal. Occasionally the left ventricle is so large as to be "capable of containing another heart"-a favorite comparison since the time of Malpighi. The left auricle may be dilated, in disease of the mitral orifice, to very large dimensions. In a case re- corded by Cruveilhier, it had four times its normal dimensions. The greatest di- 1 Niemeyer pointed out how frequently from this cause the hypertrophy which results from senile vascular degeneration gives place to dilatation. 794 DILATATION OF THE HEART. latation, however, oocurs on the right side. Both ventricle and auricle may be very large. The right auricle, as Bur- serius1 remarked, may undergo greater dilatation than any other part of the heart. Stokes2 mentions a case in which the auricle was so capacious as to contain a pound of blood. The shape is altered according to the part of the heart affected. In general di- latation the heart is increased in width, so that it has a more globular shape. This depends especially on the dilatation of the right chambers, and is marked when these alone are affected. Consider- able dilatation of the auricles may alter considerably the normal shape of the heart. Thus in the case mentioned by Stokes, the dilated right auricle "formed a vast purple tumor, which concealed the whole of the anterior portion of the right lung." In pure dilatation the weight of the heart is normal. Instances of this are, however, to say the least, very rare. As a rule the weight of the dilated heart is greater than normal, in consequence of the almost invariable coexistence of hyper- trophy. The walls of the heart the subject of simple, or nearly simple, dilatation are flaccid, and collapse when cut across. They are thinner than normal in propor- tion to the amount of dilatation, and to its freedom from accompanying hypertro- phy. In most cases the attenuation, however considerable, is the result of the extension of the wall. In rare cases the wall may actually be atrophied. In the ventricles the thinning is most marked towards the apex. The wall of the left ventricle may be reduced to one-sixth of an inch at the middle and one-twenty- fifth of an inch at the apex. The walls of the auricles may, in extreme dilatation, be reduced to an almost membranous condition. Very frequently, coexisting hypertrophy prevents noticeable diminu- tion in the thickness of the walls, even when the dilatation is very great. The thickness of the wall may even be above the normal, notwithstanding the dilata- tion, especially when the latter is moder- ate in degree. The muscular tissue is sometimes nor- mal in appearance, sometimes pale or mottled. Under the microscope it usually presents evidence of degeneration, espe- cially when the dilatation is compara- tively pure. The muscular fibres present indistinct striation, or granular or actual fatty degeneration. The connective tis- sue between the fibres is often increased, and may also present granular degenera- tion. The endocardium may be thicker or thinner than normal; it is often irregu- larly thickened and opaque, especially in the auricles. The pericardium is stretched in proportion to the dilatation, and is also often unduly opaque. The orifices participate in the dilata- tion of the cavities of the heart. The auriculo-ventricular orifices undergo the greatest extension, especially when the cavities on each side of them are dilated. The ultimate result is that the valves be- come incompetent to close the orifice, in consequence of the disproportion between their area and that of the enlarged orifice. This effect is increased by the removal of the bases of the papillary muscles to a greater distance from the orifice, in con- sequence of the extension of the wall. For a time the incompetence may be averted. The segments of the valves may undergo some amount of dilatation so as to close the enlarged orifice, and the papillary muscles may undergo at their apices transformation into fibrous tissue, which, being incapable of contraction during the systole, effects a practical elon- gation of the muscle, and so helps to counteract the effect of the removal of their points of attachment. Ultimately, however, the dilatation of the orifice ex- ceeds the influence of these compensa- tions, and incompetence of the valves results. This is the case especially in the right side of the heart, in which the di- latation of the two cavities is usually simultaneous and considerable, and is the common cause of tricuspid incompetence.' In dilatation of the auricles, the large venous trunks opening into them, unpro- tected by valves, commonly participate in the dilatation, and may be greatly en- larged, so that their openings into the auricle may be hard to determine. The auricular appendices are also much di- lated. Certain associated conditions are com- monly met with in cases of dilatation. Some of these are causal, such as valvu- lar disease, pericardial adhesions, emphy- sema of the lungs, kidney disease. Others are sequential, such as passive congestion of organs, and its consequences in altera- tion in their texture. Consequences.-From the incompe- tence of the valves due to the dilatation of the orifices, regurgitation of blood with all its consequences, results. Before, how- ever, sequential regurgitation is devel- oped, the same consequences, although in less degree, may result from the dimin- ished power of propelling the blood. The 1 This was first insisted on by Forget, Ga- zette Medicale de Paris, 1844, p. 657. The dilatation of the orifice was pointed out by Corvisart, loc. cit. p. 154. 1 The Institutes of the Practice of Medicine, 17D8. Cullen Brown's Trans, vol. v. p. 312. 2 Diseases of Heart and Aorta, p. 275. CONSEQUENCES. 795 resistance of a larger quantity of blood has to be overcome, and the power of moving it is absolutely diminished by the dilatation. Hence, unless compensatory hypertrophy assist, less blood leaves the dilated chambers at each systole. The amount of residual blood may be so large that the quantity which can enter in the normal course of the circulation is less than in health. Hence, as Morgagni pointed out,1 the dilatation acts as an ob- struction to the onward movement of the blood, the vessels behind (venous system) become overfilled, the vessels in front (arterial system) underfilled. The effect of dilatation of a cavity may thus come to be the same as that of ob- struction at the orifices of the heart by which the blood should enter the cham- ber. If the chamber affected be a ven- tricle, the first effect is the over-disten- sion of the corresponding auricle, and its consequent dilatation and perhaps hyper- trophy. The veins by which the blood enters the auricles are over-distended, and when valvular incompetence is added, the pulmonary and larger systemic veins may be enormously dilated. I have known the right internal jugular to be so large, in dilatation of the right side of the heart, as to be mistaken for an aneurismal di- latation of the common carotid artery. Pulsation may be communicated to the veins as a result of the valvular incom- petence (see article on Diseases of the Valves). The venous congestion affects alike the general tissues, causing various dropsies into the cellular tissue and serous cavities, and the organs, especially the lungs, brain, liver, portal system, and kidneys. Lastly, the other side of the heart may be overloaded and dilated, and ultimately even the side of the heart first affected, by the transmission of the in- fluence through both systems of circula- tion. The last effect, which occurs only when the primary disease is at the mitral orifice, is perhaps due to the secondary dilatation of the right side. The effect of this venous congestion is to overload the venous radicles of the organs with blood, and cause their permanent dilata- tion. The proper tissue-elements of the organs undergo atrophy, or it may be granular, or fatty degeneration, partly in consequence of the pressure upon them of the distended veins, partly from the im- perfect supply of arterial blood. Lastly, the connective tissue of the organs over- grows, and their consistence is thereby in- creased. The effect of these changes is somewhat modified by the characters of the organ affected. The heart itself may suffer from the mechanical congestion of its walls, the consequences of which have been already pointed out. The mechanical congestion, however, it is believed, affects the heart later and less than the other organs, in consequence of the obliquity of the open- ing of the cardiac veins which produces a valve-like effect. The lungs are overloaded with blood, and serosity exudes from their walls into the air-cells and minute bronchi, and probably blood corpuscles migrate into the parenchyma. Ultimately the capillaries becomes varicose,1 the blood-pigment col- lects in the cellular elements of the lung, giving it a brown color, and the connective tissue is increased in quantity,2 augment- ing considerably the consistence and to a slighter extent the size ofthe lung, and pro- ducing ultimately the condition of " brown induration." The brain undergoes slighter changes, no doubt in consequence of the effect of gravitation in opposing the movement of the blood. Its venules are enlarged and the distension of the surface veins may be very great. The pressure of the dis- tended vessels in the interior may lead to their rupture into the perivascular sheaths, or to atrophy of the adjacent brain substance. The consistence of the brain is often lessened. Induration does not result. Corvisart maintained that rupture of large vessels and cerebral hem- orrhage might result from venous conges- tion, but his opinion has not received much confirmation. The liver is congested, in a very high degree, from the directness with which the hepatic vein suffers from increased distension of the inferior vena cava. The organ becomes uniformly enlarged, first and mainly from the distension of the radicles of the hepatic vein, and after- wards by fatty degeneration of the liver tissue, or by fibroid overgrowth around the vessels and between the lobules, by which the organ may become indurated. On section, the distended venules are very conspicuous, and their enlargement is such that the hepatic tissue is com- pressed between them, and the appear- 1 Morgagni, speaking of a case of aortic re- gurgitation, says: "Some portion (of the blood) returned into the left ventricle of the heart when the ventricle ought to receive the blood that was coming in from the lungs, it would necessarily happen that the returning portion, as well as the portion which had not been extruded just before, must occupy some part of that space which, from the design of nature, was entirely due to the blood that was coming in from the lungs, which circum- stance finally could not but overload the lungs and heart." De Sedibus et Cansis Morborum, 1779, letter 23, art. 12. As trans- lated by Cockle, loc. cit. 1 Buhl, quoted by Wilson Fox, vol. iii. art. Brown Induration of the Lung, p. 801. 2 Rokitansky, Wilson Fox, loc. cit. 796 DILATATION OF THE HEART. ance is produced of lobules lying between the distended venules, and thus a portal congestion is simulated. The liver tissue is frequently pale from fatty or fibroid de- generation, and, contrasting with the dark vessels, the so-called " nutmeg liver" is produced. Ultimately the liver may un- dergo reduction in size from atrophy of the proper elements and contraction of the fibrous tissue (Murchison).' The flow through the liver capillaries is necessarily impeded, and thus the ob- struction is transmitted to the portal sys- tem. The spleen is enlarged, and, like the liver, may be the seat of fibroid over- growth, causing its induration. The peri- toneal and intestinal vessels are distended, and fluid may be effused into the perito- neal cavity. The fibroid overgrowth in the liver may ultimately lead to compres- sion of the portal venules, and consequent portal congestion, out of proportion to the congestion which results simply from the cardiac state. The kidneys suffer similar congestion, and present the appearance which was produced artificially by ligature of the hepatic vein, by Robinson.1 They are enlarged, smooth, and dark in color from the venous distension. The cortical and pyramidal portions preserve their relative proportions. At first their consistence may be lessened, and the capsule separate readily; after a time fibroid overgrowth occurs and the kidneys become indurated. Ultimately this tissue may contract, the organs becoming smaller and harder, their surface slightly granular, and the capsule unduly adherent. The veins of the body generally are also over-distended. Serum escapes from them into the connective tissue and accumu- lates in the more depending parts. Usu- ally the condition comes on gradually, and the oedema commences in the legs. It is first noticed in the evening, and dis- appears during the night, when the legs are raised ; but it continues increasing, until, although lessened, it is not removed by the horizontal posture. If the patient be in bed it may be first noticed in the lower part of the back. It may increase until the distension of the legs is extreme, and the skin, if not relieved, may slough. Lastly, coagulation may occur in the dis- tended veins, but this accident is not common. The amount of congestion va- ries from time to time in dependence upon accidental causes of increased obstruc- tion, due sometimes to variable cardiac strength, more frequently to variations in the cause of the dilatation in the hmgs, &c. A<jain, the manifestations of venous congestion are not uniform in different cases. An accidental cause, a local in- flammation, may determine a large effu- sion of serum in some special position, as the pleural or peritoneal cavity. Some accidental obstruction may lead to local oedema. A special predisposition to dis- ease in some one organ, as the liver or the kidney, may cause that organ to suf- fer in undue degree and give a special character to the symptoms. Moreover a vicarious action is often observable be- tween the vessels of the organs and of the limbs and cellular tissue. The extreme affections of organs, the very large livers, the extreme albuminuria, are often seen where the general oedema is slight; whereas when the anasarca is extreme there may be even to the last only a trace of albu- men in the urine, and the enlargement of the liver may be trifling. Fibroid over- growth in organs may hinder the disten- sion of their vessels, and so throw an ad- ditional strain upon those of the general system. The over-distension of the venous sys- tem, on which so many of the symptoms depend, can only be in part ascribed to the dilatation of the heart. It is in large part due to the cause of. the dilatation. Dilatation of the right ventricle permits the obstruction in the lungs, which exists in emphysema, to tell back upon the ve- nous system. But it also adds to the obstruction. When due to no increased resistance, but to muscular degeneration, it will give rise to similar symptoms. So in the latter case, degeneration of the car- diac wall, the weakness in its contractile power which permits dilatation, is itself, as Niemeyer pointed out, a cause of the impaired circulation. The resulting dila- tation, by its mechanical influence, inten- sifies what may be called the potential obstruction which results. Symptoms.-The existence of dilatation is declared by certain symptoms and physical signs. Some difficulty in their determination has arisen from the circum- stance that pure dilatation is so rarely met with; dilatation is usually accompa- nied by hypertrophy. But pure hyper- trophy is not uncommon, and by compari- son of these cases with those in which dilatation coexists, and especially with those in which dilatation predominates, the symptoms of the latter condition have been ascertained. They are most marked and characteristic in general dilatation. The Physical Signs depend on the in- creased size and lessened strength of the heart. The area of dulness, both deep and superficial, is increased. The deep dulness may extend from the anterior axillary line, to two fingers' breadth to the right of the sternum, even in rare cases as far as the right nipple ; upwards it may reach to the first rib, and down- 1 Clinical Lectures on Diseases of the Liver, 1868, p. 120. * Med.-Chir. Trans. 1843, p. 51. SYMPTOMS. 797 wards to the seventh rib. It inclines to squareness of outline, in consequence of the lateral increase in the size of the heart. The greater the dilatation, the greater is the lateral increase in the dulness. The impulse is perceptible over an abnormally large area. It may be felt from the epi- gastrium to the axilla. It is also diffused. A maximum apex-beat may or may not be perceptible. It is always less distinct than in health. When it cannot be felt it may sometimes be seen (Walshe). The impulse is weak and sudden in proportion to the amount of dilatation and to its purity, i. e., its freedom from associated hypertrophy. It may be somewhat undu- latory in character, in consequence of dif- ferent parts of the heart striking the chest wall successively, not simultaneously. Successive beats may be unequal in strength, and may also strike the chest- wall at different points. Bulging of the chest-wall is slight in dilatation, and is said to be always absent when there is no hypertrophy; now and then in a large dilated and slightly hypertrophied heart it is very distinct. Displacement of or- gans occurs in the hypertrophied form, the lungs are pushed but of the way, the liver may be displaced downwards, so that its rounded upper surface is visible beneath the ribs. The sounds of the heart are weakened, the first sound is shortened and its tone raised. As Flint1 puts it, the valvular element in the sound predominates. When there is coexisting hypertrophy, the first sound may be clear and ringing, but the sound becomes weaker in proportion to the amount of dilatation. The shortening may cause the first sound to resemble in its characters the second sound, so that, as Stokes2 pointed out, it may not be easy to distinguish between them. Laennec taught that clearness of the first sound is a sign of dilatation. Stokes and Gaird- ner3 showed that this clearness exists only when hypertrophy is combined with the dilatation. Reduplication has been noticed in some cases, and may be due to the asyn- chronous contraction of the two ventricles. In dilatation of the ventricle, especially of the left ventricle, a systolic apex mur- mur is frequently heard. In a large num- ber of cases it depends on incompetence of the auriculo-ventricular valves, primary (in the case of the mitral valve), or due to the extension of the orifice in the dila- tation of the heart. In many cases, how- ever, no incompetence can be discovered after death, although a systolic apex mur- mur was heard during life. But the post- mortem tests for incompetence of the mitral valve are not very satisfactory. Slight inefficiency may remain undetected, and on the other hand, slight regurgita- tion cannot be accepted as conclusive evi- dence of functional incompetence. In each case the action of the papillary mus- cles during life may vitiate the post-mor- tem conclusion. lienee some authorities believe that such a murmur, when heard in dilatation of the ventricle, is always due to auriculo-ventricular regurgitation. Others, among whom are Stokes' and Walshe, believe that a murmur is occa- sionally to be heard in cases in which the post-mortem evidence of valvular compe- tence is so conclusive that regurgitation is a very improbable explanation. They consider that the contraction of the ven- tricle alone may throw the blood into audible vibrations. The conditions are certainly such as to render the result con- ceivable. It is probable that the systole of a dilated ventricle is never complete. A considerable amount of blood remains in its cavity. The spaces between the various projections into the cavity,-the trabecuke, papillary muscles, the cuspid valves,-are larger than in health, and remain unoblitcrated at the end of the ventricular contraction, and the eddies into which the blood is thrown must be considerable. Moreover, the irregularity of the blood current is no doubt sometimes increased by irregularity in the contrac- tion of the ventricles. By these means it seems probable that a murmur may be produced within the ventricle, the conse- quence and the sign of dilatation only. The pulse is weak in proportion to the amount and purity of the dilatation. It is sometimes of moderate size, sometimes small; its size is largely influenced by the condition of heart to which the dilatation is secondary. It is often quick, and is unduly quickened by exertion. Some- times it is infrequent, either because the heart's action is infrequent, or because the irregularity in force is so great that every systole does not influence the pulse. Thus the effect of intermission is produced. Actual intermissions may also occur. Dilatation of the left ventricle alone, is attended by the changes in the impulse which have been already described as among the most conspicuous signs of gen- eral dilatation. The impulse is diffused, and both impulse and dulness are extended to the left. The first sound is weak ; the pulse presents the characters just de- scribed. Sooner or later the mitral ori- fice is stretched to incompetence of the valves; then general dilatation, with all its symptoms, quickly follows. Dilatation of the left auricle may lessen the resonance at the inner end of the 1 On Diseases of the Heart, second edition, p. 86. 2 Op. cit. p. 260. 3 Edinburgh Medical Journal, July, 1856, p. 56. 1 Diseases of the Heart and Aorta, p. 261. DILATATION OF THE HEART. 798 second left interspace, and a feeble presys- tolic impulse may be perceptible there. Pressure on the left bronchus may inter- fere with the expansion of the left lung (Barlow). Dilatation of the right ventricle causes pulsation to be transmitted to the epigas- trium, and extension of dulness to the right of the sternum in the fifth and sixth interspaces; the apex of the heart is in the normal position. Jugular fulness is common, and pulsation consequent on tri- cuspid incompetence is not rare, and, as tricuspid incompetence is rarely due to any other cause, it affords additional evi- dence of the existence of dilatation of the right ventricle. The pulse may, as Lan- cisi pointed out, be little changed. Dilatation of the right auricle causes dul- ness to the right of the sternum, where pulsation may sometimes be detected, generally presystolic, rarely systolic in consequence of the tricuspid insufficiency (as in a case of Dr. Stokes,' in which an aortic aneurism was simulated). Jugular pulsation, systolic in rhythm, occurs, and may be in rare cases diastolic also. Symptoms.-Dilatation of the heart affects, secondarily, almost every organ in the body, and its symptoms, direct and indirect are very numerous. They vary widely, however, in distribution and de- gree, in different cases. Cardiac discomfort is frequently pre- sent ; it varies from mere uneasiness to acute pain, constant or paroxysmal (pseudo-angina). Palpitation is very com- mon. The sudden contraction of the en- larged heart is perceived unduly by the patient, especially when irregularity in force or rhythm is superadded. The heart is easily excited to frequent con- traction by slight causes-muscular exer- tion, emotional excitement, or mechanical disturbance, as by a distended stomach. The general strength is always les- sened. The patient complains of lassi- tude and languor and faints easily. All parts of the general system present evidence of passive congestion. The venous stasis is seen in the distended superficial veins and the cyanotic tint. Subcutaneous oedema is often present and may be considerable. Its occurrence is influenced, not only by the cardiac ob- struction, but by the state of the blood. In anaemic persons the normal blood-pres- sure may suffice to cause slight oedema of the feet, and a similar state of blood assists very much the effect of the in- creased venous pressure in cardiac dilata- tion. The local dropsies, effusions into the pleural, pericardial, or peritoneal cavities are attended by their special symptoms. Their occurrence may alter the character, and add much to the gravity of the symptoms present in a given case. Special symptoms result also from the congestion of organs. The congestion of the lungs is indicated by cough, dyspnoea, cyanosis. Cough is often a very trouble- some symptom. It may be paroxysmal and independent of any bronchial secre- tion, or a small amount of mucus may ex- cite an excessive cough. Secretion is often, however, abundant enough from the congested vessels, and the sputa may be abundant, watery, or mucous, often stained with blood. The congested bron- chi arc liable to inflammation, by which all the symptoms are increased. Dyspnoea is a very constant symptom, due chiefly to the imperfect pulmonary circulation and deficient aeration of the blood. At first it is slight, and is felt only when exertion increases the need for oxygen : especially on ascending a hill or stairs. Later on it may be constant, and be increased when the body is recumbent (probably because the descent of the dia- phragm is impeded by the weight of the abdominal viscera). Respiration may be quickened to thirty or forty acts per minute, and is panting in character, with noisy expiration. It varies in intensity, sometimes in correspondence with cardiac failure, sometimes without apparent cause. The patient, never free from a sense of want of breath, may from time to time start up in an agony of dyspnoea, undo the clothes upon his chest, and grasp convulsively at any object within his reach. Often even the reclining pos- ture with the head backwards cannot be borne, and the sufferer can only rest or sleep sitting up with his forehead sup- ported. Sometimes a rhythmical char- acter may be observed in the dyspnoea, analogous to, though not identical with, the Cheyne-Stokes breathing. Brier attacks of panting dyspnoea commence suddenly, and gradually subside to com- parative, perhaps dozing, calm, with which they alternate. These spasmodic forms of dyspnoea may be singularly out of proportion to the interference with the aeration of the blood, as estimated by the amount of cyanosis. The congestion of the brain causes fre- quent headaches. Vertigo is common. The patient sleeps and dreams much. He dozes during the day, and at night is disturbed by restless starts. Corvisart pointed out that the passive congestion sometimes causes a "sub-apoplectic" state during the last hours of life. Deli- rium is not uncommon, and may be vio- lent ; a state of approaching chronic mania sometimes results. The congestion of the liver is indicated by an icteric tint of skin, by pain and weight in the right back, right shoulder, 1 Diseases of the Heart and Aorta, p. 275. DIAGNOSIS. 799 or hepatic region, and by abdominal dis- comfort due to the increased size of the organ. Frequently the enlargement can be both seen and felt. Pulsation may be felt in it, either communicated to it directly by the heart, or, it is said, trans- mitted through the venous system. The liver is very constantly depressed as well as enlarged. More urgent symptoms re- sult from the transmitted obstruction in the portal system. The functions of the stomach and intestine are interfered with by the mechanical congestion of their walls. Vomiting is a common, and often a most troublesome, symptom. It is probably due to the mechanical conges- tion of, and direct pressure upon, the stomach. Possibly, in some cases, it may, as Walshe suggests, be the reflex result of an irritation of the pneumogas- tric nerve. It sometimes results from a catarrhal condition, which is easily ex- cited in the congested organ. The dis- tended vessels may give way, and haemate- mesis result. Piles are common. The hemorrhage from them may relieve the congestion and prevent other symptoms. In other cases, from the mechanically congested vessels, serum escapes into the intestinal canal, or the peritoneal cavity, causing diarrhoea or ascites. In the for- mer the stools are copious and watery, and give little pain. Such diarrhoea may constitute the earliest symptoms of car- diac mischief. All these symptoms of portal congestion may, in the later stages, be intensified by an increase in the ob- struction due to secondary changes in the liver itself. The mechanical congestion of the kid- neys produces changes in the urine, which becomes scanty, dense, high-colored, often loaded with lithates, and may contain albumen. The quantity of albumen varies, and does not always correspond, as might be expected, with the amount of venous congestion. Roberts* suggests that it de- pends on the pressure to which the arteries are exposed in the congested state, and he points out that it is often greater, the stronger the force with which the heart acts. Tube-casts are frequently present in the urine, and are generally hyaline or slightly granular, and of medium size. The ultimate effect of general dilata- tion is to act through the venous and capillary system on the arteries and the left ventricle, increasing the tension of the pulse and the effect on the left side of the heart. The variation in the amount of obstruction at different times produces great alterations in the organic symp- toms. As Stokes pointed out, attacks of dyspnoea due to cold, &c., maybe accom- panied with a rapid increase in the size of the liver, which will descend in a short time far into the abdomen, partly from the enlargement, partly from displace- ment, and on the subsidence of the attack will return to its ordinary volume. The albumen in the urine may undergo a simi- lar modification, although in less simple dependence on the venous stasis. Diagnosis.-The essential sign of di- latation, by which its existence and de- gree may best be ascertained, is the diffu- sion of the cardiac impulse, its comparative uniformity over the whole area in which it can be felt. In proportion to the purity of the dilatation the first sound is tone- less, high pitched, and short and weak; the pulse is small and feeble, and the lungs and general system suffer from the second- ary consequences of the cardiac failure. Obscuration of impulse may simulate dif- fusion, and thus lead to a mistaken diag- nosis of dilatation. A thin layer of over- distended lung may intervene between the heart and the chest-wall, and so ren- der the apex-beat indistinct and appar- ently diffused. The increased resonance over the cardiac area will indicate the cause of the indistinctness. Dilatation may also be simulated, as Niemeyer pointed out, when the apex strikes against a rib, and the impulse is felt equally in the interspace above and below the point of contact. This is most frequent in nar- row-chested persons, whose ribs are near together. A mistake may be avoided by noticing this conformation of thorax, and by observing that the apex-beat is nearly in the normal situation, and that the ap- parent diffusion is vertical only ; there is no lateral extension of the impulse. From hypertrophy the diagnosis can rarely be one of absolute distinction. Some hypertrophy usually coexists with dilatation, and often confers on the dif- fused impulse increased force, and some- times the pathognomonic "deliberate," heaving character. In proportion to the predominance of the dilatation, the im- pulse is weak and sudden, the precordial region is not bulged, the cardiac dulncss is increased laterally rather than verti- cally, the impulse is extended laterally rather than lowered, and the pulse is weak rather than strong. From pericardial effusion dilatation is principally to be distinguished by the di- rection of the increase in dulness which occurs in each condition-in dilatation laterally, in pericardial effusion upwards. The pyramidal apex of the latter, when distinct, is not simulated by the dulness of the dilated heart. The impulse of the heart and the dulness are conterminous, to the left at all events, in dilatation ; while the dulness of pericardial effusion may extend beyond the impulse. The apex-beat is not raised in dilatation, and 1 On Urinary and Renal Diseases, third edition, p. 356. 800 DILATATION OF THE HEART. the sounds of the heart are as loud over the precordial region as at the top of the sternum, where in effusion they are most distinct (Walshe). Lastly, there is no friction-sound, and far less displacement of organs or precordial bulging, than in pericardial effusion. But precordial bulg- ing and obliteration of intercostal spaces may be present in dilated hypertrophy, and in extreme dilatation the sounds may be much weakened. In a case recorded by Evans the right ventricle was actually tapped under the idea that it was a peri- cardial effusion. ' From fatty degeneration dilatation may be distinguished by the evidence of en- largement of the heart, by the diffusion of its impulse, and by the proportion between its diffusion and its weakness. In fatty degeneration, when it exists alone, there is no enlargement of the heart, and the change in the impulse is a simple weaken- ing without diffusion. Often the two conditions are conjoined. Prognosis.-The prognosis in dilata- tion of the heart is always grave. Unless compensated for by hypertrophy, its di- rect effect is to interfere with the func- tion of the heart, and to lead to those serious results to which death is often due. Hence the gravity of the prognosis is proportioned (1) to the purity and ex- tent of the dilatation; (2) to the exist- ence of a tendency to degeneration rather than to growth, and of states of general malnutrition, defective food-supply, &c., which interfere with the occurrence of hypertrophy ; (3) to the extent to which the dilatation is due to causes beyond con- trol, to the amount of irremovable work which the heart has to perform. Must the state, once established, be regarded as permanent ? The relative amount of dilatation may certainly be lessened by the development of hypertro- phy. There is some reason to believe that apart from the development of hy- pertrophy a dilated heart may lessen in size. It was long ago asserted by Beau and Larcher that dilatation is sometimes temporary when due to a temporary cause, and it has been said that a similar diminution may occur when, by absolute rest, the work of a recently dilated heart is reduced to a minimum. Individual cases have conveyed this idea very strongly to careful and unbiased observers. Milner Fothergill has lately brought forward strong evidence to show that such reduc- tion in size may occur. He has shown that diminution in the cardiac dulness may correspond with the disappearance of the symptoms of dilatation, and afford evidence that the condition is itself di- minished. The same conclusion is indi- cated by the completeness with which the acute dilatation of adynamic diseases, such as fever, may pass away. Treatment.-The object of treatment in dilatation of the heart must be to re- store as far as possible the disturbed bal- ance between the cardiac work and the cardiac strength. The increased blood pressure, to which the dilatation may be primarily due, must be reduced to the minimum compatible with the work of the circulation. Accidental causes of ob- struction must be removed. Bronchitis must be got rid of as soon as possible. Especially, exertion must be avoided. Best, mental, moral, and physical, is of the greatest importance. Muscular exer- tion involves a large increase in the work of the heart, and its cessation will often suffice to restore the disturbed balance. In extreme dilatation, confinement to bed or the couch for a time is a wise measure, and will not seldom remove most of the troublesome subjective symp- toms, and even some grave objective signs of dilatation. Where this cannot be se- cured, or is unnecessary by reason of the moderate degree of dilatation, the rigid avoidance of all needless and severe exer- tion should be enforced. The blood-pressure may also be lessen- ed by the reduction of the total volume of the blood. This may be accomplished in. more than one way. The most ready method is by the abstraction of blood by venesection or cupping. The relief which it affords is often immediate and striking. The ultimate effect, however, is that the volume of the blood is soon reproduced, while the heart is permanently weakened. Hence it must only be employed when the need for immediate relief is para- mount, and renders the danger of the ultimate damage a secondary considera- tion-that is to say, when the patient is in imminent danger of death. It is espe- cially useful when the right heart and venous system are overloaded. The quantity of blood taken need not be large. In less urgent cases the same end may be obtained by other means, by pur- gation and diuresis. The former must not be severe, or the subsequent depres- sion is not easily rallied from. Diuresis is often of great service in these cases, even where there is no dropsy.* The amount of fluid taken as drink should be small. The power of the heart should be in- creased so that it may resist the blood- pressure, and may contract completely, so as to expel the whole of its contents. To this end the general nutrition must be, 1 "In morbis pectoris, semper ducendum esse ad vias urinae." Baglivi, quoted by Ferriar. 1 Clin. Soo. Trans. 1874-75. TREATMENT. 801 as far as possible, improved. A dry bracing air is useful, and gentle exercise should be taken which does not increase materially the work of the heart; food must be nutritious and easily digested. Iron is of great service, and seems to aid directly the production of the needful hy- pertrophy.1 Excited action of the heart must be calmed by avoiding the causes of excite- ment, and by sedative medicines. Moral emotion must, as far as possible, be avoid- ed, and the sources of gastric disturbance guarded against or relieved. A distended stomach easily excites an attack of palpi- tation. Of drugs having a direct action on the heart, none is so useful as digitalis, which increases the tone of the heart, lessens the frequency and increases the force of the contraction. There has been much discussion as to the action of digitalis, and the condition of heart in which it is of most service, but there is at present a consensus of opinion that its action is tonic, and that in dilatation its most marked beneficial effect is produced.2 The heart's action is reduced in fre- quency and increased in force; irregu- larity in force and rhythm is lessened or removed. The sphygmographic tracing shows this effect. The grave conse- quences of dilatation are lessened, venous congestion, dyspnoea, and oedema, general or local, are all diminished.3 Concerning its modus operand^ there is still some difference of opinion. The less- ened frequency of contraction probably lessens the work of the heart by diminish- ing that part which.consists in moving its own mass, and at the same time the longer periods of rest probably conduce to the perfectness of the cardiac nutrition. Frequency of action is at the expense of rest, for the length of the systole remains nearly the same at various degrees of fre- quency of contraction, increased frequency being obtained at the expense of the dias- tole. It has been calculated that the time of rest to the heart which is con- tracting 144 times per minute, is increased by one-third if the pulse is reduced to 72.1 Moreover, the smaller cardiac vessels, arteries, and veins, as well as capillaries, must be emptied of blood during the car- diac systole.2 A certain time must elapse on each diastole before the capillaries can be filled with blood and transudation of nutritive fluid through their walls can take place. This period will be nearly the same in every diastole, and hence the total period of rest available for cardiac nutrition, will on this account also be greater the less frequent the contraction.3 Digitalis appears to act also by increas- ing the completeness of the contraction of the heart. Under its influence the heart of an animal becomes firmer at the end of systole. Such contraction insures the expulsion of the whole of the blood con- tained in the chamber. Every approxi- mation to this is, in dilatation, a direct gain. It not only assists directly the cir- culation, but it arrests a process which is probably the main mechanism of the ori- gin and increase of dilatation, viz., the over-distension of the chamber in conse- quence of the addition of residual blood to that which enters it from the ordinary source. Increased firmness of contrac- tion will not only lessen the tendency to further dilatation, but will improve the condition of the cardiac walls,4 and in- 1 Chalybeate waters were recommended by Senac in commencing dilatation (Traits, 1769, t. ii. p. 330), and his recommendation was endorsed by Ferriar (Med. Hist, and Ref., vol. i. 1792, On Dilatation of the Heart, p. 168). 2 Withering pointed out that digitalis "sel- dom succeeds in men of great natural strength," but does much good "if the pulse be feeble or intermitting, the countenance pale, the lips livid, the skin cold. ' ' An Ac- count of the Foxglove, &c. Birmingham, 1785. 3 "I do not intend to say how this medi- cine (digitalis) acts, but I can, from observa- tion, declare, that it has a very powerful ef- fect in obviating the urgency of the symp- toms in dilatation of the heart" (Allan Burns, 1809, loc. cit. p. 57). Ferriar had previously largely used digitalis in dilatation. The verbal accord between these writers and those of the present day is more complete than is that of their meaning. Dilatation of the heart was to the former synonymous with its enlargement and over-action, and they valued digitalis for (and believed that it did good by) its supposed power of lessen- ing such over-action, when it was really strengthening the heart's defective power. VOL. n.- 51 1 Milner Fothergill, Diseases of the Heart, p. 4. 2 Harvey observed that the substance of the heart becomes pale during its contraction. 3 Assuming, for instance, that the period required for the vascular distension of the heart, and not available for nutrition, to be uniform at different frequencies of contrac- tion, and to amount at each contraction to one-tenth of a second, the total period then available for nutrition would be increased about three per cent, from this cause only, by a reduction in the frequency of the pulse from 100 to 80. But it is probable that the time needed for the vascular distension of the heart is shorter the greater the distension of the aorta, and hence that it is shorter the less frequent the contraction, and the actual increase in the period available for nutrition will be rather greater than is represented by the above estimate. 4 Partly, no doubt, by rendering perfect the expulsion of the blood from the cardiac veins, as Dr. H. C. Wood points out (Phil. Med. Times, 1874, Nov. 14, 21). 802 DILATATION OF THE HEART. crease the tendency to compensatory hy- pertrophy. Digitalis acts also by steadying the heart, diminishing its irregularity. Dr. Kinger1 suggests that its main effect in dilatation of the left ventricle accompany- ing mitral regurgitation is thus produced. By preventing irregular contraction it arrests that part of the regurgitation which depends on the irregular action of the papillary muscles, and so relieves the over-distension of the auricle, and indi- rectly of the ventricle. Five to fifteen drops of the tincture of digitalis may be given with advantage three times a day. Most observers have found the tincture convenient and relia- ble, but the infusion is believed by Ringer to be a surer preparation, in doses of one or two drachms. Much larger doses have been given, but these should be employed with caution. Ringer recommends strong- ly that the minimum effectual dose should be employed in the first instance, since an increase after a time is often necessary. The Virginian prune has long been em- ployed as a cardiac tonic in America, and was introduced into this country by Clif- ford Allbutt,2 who has found it very use- ful in cardiac dilatation. I have found its power as a tonic, although marked, in- ferior to digitalis ; but it is of much value for the relief of continuous cardiac discom- fort, and may with advantage be given for a time, while digitalis is omitted. Twenty or thirty minims of the tincture may be given three times a day. Nux vomica and strychnia are also useful in improving the cardiac tone. Arsenic has been recommended for the same purpose. Treatment of Special Symptoms.-Car- diac discomfort, in various forms, whether as pain or palpitation, is the source of much distress. The tranquillizing influ- ence of digitalis on the heart relieves much of the pain. Aconite is of use in the same way, and is of most service when "ex- treme irritability of contraction coincides with great weakness of beat" (Walshe). Half a minim or a minim may be given ; its effects being watched. Drawing a few deep breaths will often arrest an attack of palpitation (Brown-Sequard). Bella- donna may be given internally in doses Tftv to Tftxv three times a day, and is often of much service. Belladonna plas- ters have been condemned by some au- thorities as useless, but they certainly give relief to the cardiac discomfort. Pa- tients constantly ask for their repetition. The tincture of the Virginian prune some- times gives very marked relief to continu- ous pain, and will sometimes stop for a time slight pseud-anginal seizures. Opium has the same power over cardiac as over other pains. Hypodermic injections of morphia give quick relief, but their use has been discountenanced in grave heart diseases, on account of the fear of too profound a sedative influence on the heart. But Clifford Allbutt and Ringer have employed them extensively, and as- sert that T'rt or | of a grain may be in- jected with perfect safety, even in grave dilatation. The relief to the patient is certainly in many cases most striking. A very small quantity will sometimes pro- cure sleep, in cases of cardiac insomnia, when sedatives given by the mouth fail altogether. Tolerance of sedatives by the mouth in these cases does not always im- ply a corresponding tolerance of the hy- podermic injection, and the first injection should therefore always be very small. For paroxysmal pains, antispasmodics may also be given. Nitrite of amyl in inhalation, so useful in true angina, also gives relief to the pseud-anginal seizures, and to the sense of suffocation, which is sometimes troublesome. If necessary, it may be employed diluted with spirit. A few drops of chloroform, or what is more convenient, half a teaspoonful of chloric ether, inhaled with steam, is also useful. Attacks of increased cardiac failure need general stimulants and antispas- modics. Alcohol, given with hot water, is one of the most rapidly diffusible stim- ulants. Sal-volatile and ether, with tinc- ture of lavender, are the most convenient and most effective drugs. Stimulation of the ends of the pneumogastric nerve in the stomach seems to have some influence in exciting the heart's action, and effer- vescing drinks and carminatives are use- ful in that way. In syncopal seizures the head should be placed low, and the remedies just enu- merated should be employed. Active respiratory movement should be restored as quickly as possible. It is thus, and by arousing consciousness and will, that cold affusions and stimulating applications to the nostrils are of service. The lung complications of dilatation of the heart, bronchitis, oedema, congestion, need the most stimulating special treat- ment for each variety. Stimulating ex- pectorants, as ammonia, are necessary for the bronchitis ; and congestion is best re- lieved by the cardiac tonics and stimu- lants already described, and by mild counter-irritation. Cough is often an exceedingly trouble- some symptom in these cases, it may be paroxysmal or constant, and out of all proportion to the expectoration. Morphia is generally necessary to control it ; one- twelfth of a grain may be given by the mouth, and with it a few minims of the tincture of belladonna. 1 Handbook of Therapeutics, 5th ed. p. 421. 2 Medical Times and Gazette, Feb. 16 and March 2, 1867. TREATMENT. 803 Dyspnoea is among the most obstinate, as well as the most distressing, symptoms of dilatation. Its chief treatment is that of the cardiac failure, and the same dif- fusible stimulants are needed. The par- oxysmal form is relieved most effectually by more direct sedatives: opium, Indian hemp, belladonna, lobelia inflata. Dry- cupping, and a few leeches to the pre- cordial region, are recommended by Walshe when there is palpitation as well as dyspnoea. Posture is important; the head' should be well raised, and Walshe recommends an attitude leaning forward, with the forehead supported by a sling. When the dyspnoea is dependent on pul- monary oedema, relief is often only to be obtained in the sitting posture.1 Headache is not often a troublesome symptom except in dependence on the cough. It is best relieved by posture, and by bathing the forehead with hot water. Sleeplessness is often a distress- ing symptom. Rest is disturbed by sud- den starts, or the patient wakes up in a sudden fright with a sense of great dis- tress. Such symptoms may usually be removed by tne administration of the third dose of digitalis at bedtime in com- bination with bromide of potassium. Indian hemp (gr. 3 of the extract or H] x. of the tincture), will also, though less uniformly, give relief. Actual insomnia may be relieved by chloral, chloral and bromide, and morphia by the mouth or skin, employed with caution. The congestion of the liver may be lessened to a marked extent by mer- curials. Every relief given to the portal congestion no doubt lessens immediately the pressure upon the hepatic lobules. Vomiting is sometimes a very trouble- some symptom. Effervescing ammonia, with bismuth and hydrocyanic acid or morphia, is the most useful. The amount of ammonia need not be large ; gr. x of the carbonate with gr. xj of citric acid is sufficient. Ice should be sucked, and food given in small quantities. Counter- irritation to the epigastrium is sometimes useful. Any portal congestion must be relieved, the bowels being kept open. Diarrhoea sometimes demands treatment, and should be moderated rather than re- strained. If constipation is present, mod- erate doses of hydrogogue purgatives are most useful, as Piillna or Hunyadi Janos water, colocynth, or podophyllin. Flatu- lence is often very troublesome, and adds much to the cardiac and general distress. Hot fomentations externally and carmina- tives internally give most relief; sal- volatile, peppermint, chloric ether, spirit of horse-radish, are all useful. The relief which is afforded to the sufferers from dilatation of the heart by the removal or diminution of their gastric troubles is often very great. Dobell has lately drawn attention specially to this subject.1 The scanty urine consequent on the kidney congestion may call for treatment. Mild diuretics, with digitalis for its dou- ble action, often suffice to relieve the kidneys. Often, however, this long- continued congestion induces tissue changes in them, and dry-cupping to the loins, or stronger diuretic treatment- broom, juniper, &c.-may be necessary. Stokes2 remarks that diuretics often suc- ceed after a mercurial, where they have previously failed. Dropsy is almost invariably a trouble- some symptom in the later periods of a case. It is dependent partly on the blood-state, favoring osmosis, partly on the mechanical congestion, increasing the pressure of the blood in the small vessels, and increasing it to the greatest extent in the most depending parts, where gravita- tion aids the cardiac failure. It can only be effectually combated by treating each of these causes, first by strengthening the heart, and secondly by improving the blood-state. Hsematinic and cardiac ton- ics are needful for this. But it may be lessened by other measures. No remedy can promote, directly, the absorption of the effused fluid from the cellular tissue back into the bloodvessels, but reduction in the volume of the blood exercises a marked influence. The abstraction of blood will be necessary only when acute pulmonary oedema threatens life, and then cupping on the chest is preferable to venesection. Often purgation is suffi- cient, and hydrogogue cathartics, bitar- trate of potash, elaterium, jalap, are the most effectual. Where there is evidence of enlargement of the liver, a dose of a mercurial is stated by Hayden to increase the effect of the purge upon the dropsy. Diuresis occupies a position hardly second to purgation for the removal of dropsy ; copaiba, iodide of potassium, nitrate of potash, juniper, broom, nitric ether, and especially digitalis, may be given. The dose of digitalis for the removal of dropsy by its diuretic action needs to be larger than when its tonic action alone is needed, 3ij or $iv of the infusion, or 1T[x or xx of 1 On Affections of the Heart, 1872. The value of carminatives has long been known. Albrecht relates that Sylvius removed all symptoms in a case of cardiac dilatation by their use. According to Pliny, the Egyptians believed the juice of horse-radish to be the only cure for atrophy of the heart. 2 Loc. cit. p. 263. 1 A reclining-chair, with a cross rest on which the forehead can be supported, has been for some years in use at University Col- lege Hospital, and a "heart-bed" for the same purpose is described and recommended by Dobell. 804 FATTY DISEASES OF THE HEART. the tincture, may be given twice a day. Dry-cupping over the kidneys sometimes, it is said,increases the effect of the diuretic. In severe cases all these means, success- ful at first, may ultimately fail to remove the dropsy, and it becomes necessary to relieve the distended limbs, or sloughing will occur. It is necessary to anticipate this and to scarify or puncture the skin, and allow the limb to drain. Scarifica- tion is the more effectual, but is said to be attended with greater risk of erysipe- las. Erysipelas will rarely occur when the precaution is taken to wrap up the limbs in flannel, wrung out of warm water, immediately after the scarification, re- newing it every two hours during the first two days. A harelip pin is a conve- nient instrument for the punctures. Jaccoud1 recommends, as a substitute for punctures, friction each day with cro- ton oil: in a day or two the characteristic eruption is produced, and from it the se- rum escapes abundantly. The frequency with which a slight inflammation is the starting-point of a slough makes it diffi- cult to believe that the risk of gangrene is lessened by this method. In all cases of dropsy, as little fluid as possible should be taken. When the kid- neys are underacting from congestion, its effect is, as Milner Fothergill1 has insist- ed, only to throw an increased strain upon the heart. [The propriety of so absolute a dictum in regard to fluid, may be questioned. Dilution of the blood, by lessening its stimulating quality, tends to diminish congestion of the kidneys, and thereby to favor secretion. Of all agencies employed in practice for diuretic effect, much ex- perience shows that water is, ordinarily, the most potent; and hardly any diuretic will act well unless considerably diluted with water. Thirst is, no doubt, usually the best guide in this matter.-II.] FATTY DISEASES OF THE HEART. By W. R. Gowers, M.D. Fatty degeneration of the heart con- sists in the substitution of fat for its mus- cular substance. This result may be reached by two processes of different pathological and clinical relations. The one process effects simply the molecular substitution of fat for the proper substance of the muscular fibres. The other con- sists in the overgrowth of the normal fatty tissue of the heart among the muscular fibres, so as to compress, and ultimately to destroy and replace them. The former process needs the microscope for its dem- onstration ; the latter is obstrusively con- spicuous to the naked eye. The one is an indication of diminished vitality, and may be its initial stage, a necrosis; the other is at first a growth. Some varieties of the two processes present common pathological features, and their effect on the function of the organ is the same; but their diverse conditions of origin and anatomical characters need separate de- scription. In pursuing this course the example is followed which was set by Dr. Quain2 in a memoir on the subject, which has served as a model for most subse- quent writers. The hypertrophic form of " fatty inliltration" will first be described, and then the "necrobiotic" process of fatty degeneration. Fatty Overgrowth. Synonyms.-Fatty Infiltration (Roki- tansky) ; Fatty Growth, Fatty Hypertro- phy (Quain); Adipose Cardiaque, Sur- charge Graisseuse, Obesite du Coeur (French writers). Definition.-An abnormal develop- ment of adipose tissue on and in the sub- stance of the heart. Fatty tissue is always present on the surface of the heart, and varies in amount according to the age, and the nutritive conditions and tenden- cies of the individual. In abnormal de- velopment this fat may become so excess- ive that mechanical interference with the function of the organ is the result. It is a local "instance of the extension into 1 Pathologie interne, 4th ed. vol. i. p. 621. 8 On Fatty Diseases of the Heart, Med.- Chir. Trans, vol. xxxiii. 1 The Progress of Heart Disease, Lancet, vol. i. 1875. HISTORY - PATHOLOGICAL ANATOMY. 805 the domain of disease of the physiological process of growing fat."1 History.-Some of the symptoms of obesity, which are in part cardiac, were among the earliest medical observations. Hippocrates noticed the tendency of fat persons to earlier death than others, and both he and Celsus observed the dyspnoea which is associated with obesity. Harvey described an excess of fat around the heart of Old Parr. Since that time almost every writer on diseases of the heart has alluded to or described a similar con- dition. Kerkering,2 in 1717, noted its oc- currence at so early an age as two years. Seuac3 in 1749 described carefully the nor- mal variations in the quantity of fat ac- cording to time of life, &c. Morgagni4 recorded examples of hearts so loaded with fat that no muscular tissue could be seen. Portal5 noted the concurrence of fatty overgrowth in the heart with a simi- lar condition in the voluntary muscles. The state was fully described by Corvi- sart, who suspected that it might be a cause of sudden death. Morgagni thought that the muscular fibres of the heart suf- fered in this condition of fatty growth. The microscope, long after, showed that this is actually the case. It was inferred, however, from the apparent substitution of the fatty for the muscular1 tissue, and from the evidence of cardiac weakness. Hearts subject to this mixed change were described, and the disease ably discussed, by Duncan (1816), Cheyne (1818), Town- send (1832), and R. W. Smith (1838).6 Causes.-Excess of adipose tissue on the heart is usually associated with excess of adipose tissue elsewhere, and is due to the same causes. Quain found that in almost every case of fatty growth about the heart there was general obesity. The converse holds good to a less extent. King Chambers7 records that of thirty-six corpulent persons a considerable excess of fat at the base of the heart was found in twelve. On the other hand, in 165 bodies not remarkable for fat, there was excess of fat about the heart of four only. Hereditary predisposition exercises a marked influence on the occurrence of obesity, and no doubt also on the occur- rence of fatty infiltration of the heart. In two-thirds of the cases of general obesity it is found that hereditary or col- lateral obesity exists. Sex also influences its occurrence. If the statistics of Quain* be combined with the cases of fatty growth contained in the valuable tables of Hayden,2 we have thirty-five cases of this condition of which twenty-five were men and ten women. The condition is therefore more than twice as common in the male as in the female sex. Age also exercises a distinct influence. At birth, as Seuac pointed out, the heart is free from fat, and the amount increases as years go on. After six years fat is always present between the auricles and the ven- tricles. Fatty infiltration follows the same law and commonly occurs after middle life.3 The combined cases of Quain and Hayden illustrate this very clearly. Under 20 there was but one case, between 20 and 30, three cases; be- tween 30 and 40, none; between 40 and 50, four ; between 50 and 60, eleven ; be- tween 60 and 70, nine ; and over 70, seven cases. Sedentary habits increase the tend- ency to this condition. Food is an effec- tive agent if the disposition to grow fat exists. Starchy, saccharine, and fatty foods are the chief fat-forming elements. Their effect is the supply to the system of a quantity of carbon in excess of the res- piratory needs, and this carbon is stored up as fat. But if the oxygen supplied be in considerable deficiency, nitrogenous food may yield fat by its imperfect oxida- tion. Alcoholism also exercises a re- markable influence. Malt liquor seems to be more effective in causing fatty growth than spirits, but any form of alco- holism conduces to it; the blood in chronic alcoholism has been found to contain far more fat than in health. Sudden changes in the conditions of the system seem sometimes to determine the overgrowth of fat, general and local. An acute ill- ness, and confinement to bed owing to an accident, are among the causes which Chambers mentions as having set the obese tendency in operation which has continued after the cause ceased to act. Pathological Anatomy.- The fat normally present on the heart exists chiefly in the auriculo-ventricular and in- ter-ventricular sulci, extending thence on to the ventricles, especially on to the sur- face of the right ventricle. When exces- sive it may conceal from view almost the whole of the muscular tissue of the heart. It may remain confined to the surface, 1 Hayden, Diseases of Heart and Aorta, p. 596. 2 Opera Omnia Anat. 1717, p. 134. 3 Traits, &c., vol. i. p. 187. 4 De Sed. et Cans. Morb. Ep. iii. Obs. 20; xxvii. 2 ; xxx. 18. 5 MSm. de l'Acad. des Sciences, 1784. 6 See Fatty Degeneration-History. 7 On Corpulence, 1850, p. 92. 1 Loc. cit. 2 Diseases of the Heart and Aorta, p. 648, et seq. These Tables are compiled from the Transactions of the Pathological Societies of London and Dublin, and from Dr. Hayden's own case-books. 3 The case which is described by Kerkering stands almost alone. 806 FATTY DISEASES OF THE HEART. but when considerable it usually invades the substance of the heart, passing in be- tween the muscular fibres. On section the muscular substance appears nar- rowed, its junction with the surface fat being much nearer to the inner surface of the wall than in health. Streaks of fat may extend into the muscular tissue. Sometimes the latter is reduced to a thin endocardial layer, and even, as Laennec pointed out, the papillary muscles may appear to arise from a mass of fat. The muscular fibres are not really destroyed so completely as they appear to be: un- der the microscope they may still be seen in considerable number among the fatty tissue by which they are separated and displaced, and often pressed upon. Fatty degeneration of the fibres does, however, occur in a very large majority of the cases. Of the twenty cases contained in Hay- den's table, in two only were the muscu- lar fibres stated to be healthy. The fat does not, however, always form such extensive and continuous layers. A follicular variety of fatty overgrowth was described by Laennec, and has since been generally recognized. In it the fatty tis- sue occurs in minute areas, which can be seen as specks in the substance of the [Fig. 123. Fatty In filtration of Heart.-A sec tion from the more external portion of the left ventricle of the heart showing the growth of tat between the muscular fibres. The fibres are in some places atrophied and com- mencing to undergo fatty metamorphosis. X 200. (Green.)] heart, especially beneath the endocar- dium. In all conditions of fatty growth the fat is contained in oval and round cells, having an average diameter of inch, and very similar to those which con- tain flit elsewhere. In cases of fatty over- growth upon the heart there is usually also an excess of fat outside the pericar- dium. Symptoms.-A considerable increase in the amount of fat upon the surface of the heart may be unattended by morbid signs. This was remarked by Corvisart and Laennec, and their observations have since been abundantly confirmed. Where the fat has invaded the substance of the heart, is infiltrated in the muscular tissue, the effect is a simple weakening of the heart, identical with that presently to be described as the result of the fatty degen- eration, which is so frequently combined with the fatty growth. The impulse and sounds of the heart are weakened. The apparent weakening is greater than that which actually exists, because the subcu- taneous and mediastinal fat obscures the impulse and dulls the sound. From the same cause the slight increase in the size of the heart which commonly exists is rarely to be detected. The actual dimi- nution in the strength of the heart is often considerable. The pulse is weak, but may be perfectly regular even to the last, Dyspnoea is frequent, and syncope, and even rupture of the heart, may occur. The tendency to sudden death is verv marked. Out of thirty-four cases in which the character of the death was noted it was sudden in twenty-four. Of these a third died from rupture of the heart, and another third from syncope. In every case of rupture, and in most of those in which syncope occurred, there was fatty FATTY DEGENERATION. 807 degeneration of the remaining muscular fibres. Diagnosis.-The diagnosis of fatty overgrowth in this condition depends on the recognition of the association of car- diac weakness and general obesity. The signs and symptoms arc those of fatty de- generation. With such signs, if general overgrowth of fat is present, we are justi- fied in suspecting the existence of fatty overgrowth and infiltration of the heart. Treatment.- The treatment is essen- tially that for the general obesity of which the local overgrowth is but a part. The main object is to lessen the supply of the fat-forming hydrocarbons, and to increase their consumption in the system. The amount of food taken, if excessive, should be restricted ; and fat, starch, and sugar should be, as far as possible, excluded from the diet. As much exercise should be taken as is practicable without putting undue strain upon the weakened heart. It is doubtful whether drugs possess any power of lessening the local accumulation of fat. Alkalies are believed by Cham- bers to diminish general obesity: what- ever beneficial influence they exercise on general obesity they will also exert on the local state. In other respects the treatment of fatty overgrowth is the same as that of fatty degeneration of the heart presently to be described. Fatty Degeneration. Synonyms. - Ramollissement (Corvi- sart, Laennec), Softening of the Heart; Carditis (Bouillaud) ; Greasy Degenera- tion (Hope) ; Fatty Metamorphosis (Ro- kitansky); Atrophic Graisseuse (Parrot) ; Steatose Parencymateuse (Blachez). Definition.-A change in the muscu- lar fibres of the heart, by which the trans- verse strife are at first obscured, and afterwards disappear, being replaced by granules and globules of fat. This gran- ular and fatty degeneration of the heart, as far as we at present understand it, has nothing in its nature of specific character, but is simply the expression of defective nutrition of the proper substance of the fibre. Hence, as might be expected, the conditions with which it is associated, and to which, directly or indirectly, it is due, are widely different in their nature and mode of action. So diverse are they that it is evident that the condition of the heart is rather a common consequence, than a special disease. It has, however, its own symptoms and its own consequences, and so needs special description. History.-Fatty degeneration was a late discovery in cardiac pathology. Mor- bid appearances, such as are now known to result from bitty degeneration, were mentioned by Robert Fludd1 in the be- ginning of the seventeenth century, and by Lancisi a hundred years later, but re- ceived little attention. Overgrowth of the surface fat, and its invasion of the muscular tissue, were indeed described by Morgagni and many other writers, as has been already stated, and there can be little doubt that, in some of the instances recorded, true fatty degeneration of the remaining fibres was present. Such a change in voluntary muscles was discov- ered by Haller and Vicq d'Azyr ; and some French pathologists at the begin- ning of the present century suspected that a similar process might be the cause of some morbid appearances in hearts which did not present the ordinary char- acters of fatty growth. Corvisart,2 who was perfectly familiar -with the latter, had heard of this opinion, and considered the explanation plausible, although he had not himself seen the change referred to. In 1816, Andrew Duncan3 described a heart which was probably an example of the mixed change, fatty growth and de- generation, and a similar case was re- corded by Cheyne4 in 1818. The naked eye characters of the simple degeneration were first accurately distinguished by La- ennec5 in 1819, who described the change in a limited area in very exact terms, rec- ognized its identity with the degeneration described by Haller and Vicq d'Azyr, and gave to it the definite name of " fatty de- generation of the heart. "6 Bertin,' quot- ing Laennec's description, believed he had noticed the change in question, but ad- mitted that he had confounded it with chronic softening, "of which," he said, "it is perhaps only a variety." General softening of the heart was described by Bertin as the effect of carditis.8 It was 1 Senac quotes from Fludd an account of a heart so soft and brittle that the fingers could be placed in its substance. It is said that the man from whom it was taken had played at cards two days before his death. (Senac, TraitS, &c., vol. ii. pp. 382, 389.) 2 Diseases of the Heart, Hebbs' Transla- tion, p. 168. 3 Edinburgh Medical and Surgical Journal, 1816. 4 Dublin Hosp. Rep. vol. ii. 1818, p. 216. 5 On Diseases of the Chest, Forbes' Trans- .ation, 1821, p. 229. 6 It is difficult to believe that Laennec did not recognize the identity of "softening" and fatty degeneration, for he described the two conditions in identical terms. i Traite des Maladies du Cceur, 1824, p. 431. 8 Bertin noted (p. 400) as symptoms of "softening" many which are now ascribed 808 FATTY DISEASES OF THE HEART. thus described also by Bouillaud.1 The combination of fatty overgrowth with softening and degeneration of the remain- ing fibres was especially noted by Adams2 in 1827, Elliotson3 in 1830, Townsend4 in 1832, and Latham in 1839. Simple fatty degeneration was described and distin- guished from fatty growth by Hope5 in 1839, and by Williams6 in 1843, who com- pared it to the formation of adipocere. Fresh interest was given to the subject in 1844 by the publication of Rokitansky's observation of the microscopical charac- ters of the degenerated fibres.7 In 1845 Peacock8 published similar observations, made apparently in 1843, independently of Rokitansky's discovery. In 1847 a very clear description of the process in its wider associations was given by Paget,9 and of its chemical pathology by Vir- chow.10 In 1850 a series of cases illus- trating the facts previously ascertained, were published by Ormerod'1 and by Ken- nedy,12 and in 1805 Quain13 contributed the very full account of the whole subject of fatty diseases of the heart, which has been already mentioned. Varieties.-According to the appear- ance of the fibres, whether they contain granules or globules of fat, the two stages have been distinguished of granular and fatty degeneration, and it has been held that these two varieties are sometimes distinct forms of degeneration. There are, however, reasons for regarding them as stages of the same process, and both forms will be considered here. For con- venience' sake the single term "molecu- lar degeneration" may be used to denote them. "Primary" and "secondary" de- generations were distinguished by Quain, the former occurring without, the latter dependent on, preceding inflammation. Ponfick14 would divide the degeneration into two forms, according as the muscular tissue of the heart was or was not in a preceding abnormal condition, and would further divide the cases in which the mus- cular tissue presents no other change than the degeneration, into " toxamic," " se- nile," and "ancemic" varieties, according to their supposed causes. Etiology.-( a ) Predisposing Causes. -Hereditary Influence.-A few facts are on record which suggest that fatty degen- eration of the heart may own an inherited cause, and thus be transmitted. The cause may be a tendency to early decay of the muscular fibres, due to their defect- ive vitality, or it may be a predisposition to one or other of the exciting causes of fatty degeneration, to be immediately de- scribed, especially to fatty overgrowth or arterial disease. Sex has a marked influence. This is established by all the statistics which have been collected. The disease is at least twice as frequent in men as in women. Quain found the proportion 4 to 1, Orme- rod about 3 to 1, Hayden more than 2 to 1. Ponfick states that the fatty degenera- tion which results from general anaemia is an exception to the rule, and is more common in women than in men. Age.-Fatty degeneration of the heart may occur at any age. It has been found in the foetus, and has been met with at every period of life from infancy to old age. But it is much more common in the second than in the first half of life. It is itself a degeneration, and it owns, as its frequent exciting causes, other degen- erations, and is thus most frequent during the degenerative period. About three- quarters of the cases occur after forty years of age. Habits ef Life have probably less influ- ence in causing fatty degeneration, than on the occurrence of fatty growth. The condition is more common among the lower classes than among the upper-the reverse of the proportion that obtains in cases of fatty growth. Sedentary habits predispose to imperfect nutrition of the muscular fibres, and some occupations act also by rendering the individuals liable to the exciting causes. Depressing Emotions are believed by Quain to predispose, in some cases, to fatty degeneration. Moral emotion or long-continued physical pain is said to have such an influence. Nutritive Influences.-The tendency to the formation of fat, which has so marked an influence on fatty growth, has appa- rently much less effect in causing fatty degeneration. Quain found that the dis- ease occurred with almost equal frequency in fat and in thin persons. (b) Exciting Causes.-The exciting causes of fatty degeneration of the heart comprehend all those conditions which to fatty degeneration, such, as weakened or inappreciable impulse, dulness of sound, and extreme frequency or slowness of the pulse. 1 Traits Clinique des Maladies du Coeur, Ed. Quinzieme, tome i. p. 615. 2 Dublin Hosp. Rep. vol. vi. 398. 3 Lumleian Lectures, p. 32. 4 Dublin Journal of Medicine, 1832, p. 165. 6 Diseases of the Heart, p. 348. * Principles of Medicine, 1843, p. 304. 7 Handbuch. der Path. Anat. Bd. ii. 1844, p. 463. 8 Monthly Journal of Medical Science, Jan. 1845, p. 20. 9 London Med. Gazette, 1847 (lect. vi.). 10 Virchow's Archiv, Bd. i. p. 152. 11 London Med. Gazette, 1849. 12 Dublin Med. Press, vol. xxi. 15 Med.-Chir. Trans, vol. xxxiii. 14 Berlin Klinische Wochenschrift, 1873, Nos. 1 and 2. EXCITING CAUSES. 809 can interfere directly with the nutrition of its fibres. They are very diverse in character, but fall naturally into the two groups-general and local. They may act in conjunction with, or apart from, the predisposing causes. I. General Conditions causing molecular degeneration of the heart are numerous, and various in their character. The tend- ency to degeneration may (1) be primary, or (2) it may be secondary to other mor- bid states, of which the most important are certain causes of general impairment of nutrition, certain states of poisoned blood, and certain poisons introduced from without. (1) Fatty degeneration of the heart may own as its only cause the tendency to general degeneration which is natural to old age and which may occur at a much earlier date. This constitutional tendency is undoubtedly one of its chief causes. The degeneration is rarely con- fined to the heart; it is in most cases more widely spread and is seen in the in- elastic skin, the rigid vessels, the white hair, the arcus senilis. But the tendency of such degeneration to unequal distribu- tion is well known and maybe manifested by disproportionate degeneration of the heart, especially when the conditions of life are such as to put an undue strain upon the organ. This degenerative tend- ency may or may not be associated with overgrowth of fatty tissue, and thus two types of degeneration are met with, the pathological tendencies of which Paget long ago pointed out. (2) Fatty degeneration may be the re- sult of some general condition of imper- fect nutrition. Ancemia both quantitative and qualita- tive may cause it. The influence of re- peated losses of blood in causing this de- generation has long been observed as a clinical fact,1 and it has been recently studied experimentally by Perl.2 It can be readily produced in dogs by repeated bleedings, but much more readily by occasional large bleedings than by more frequent smaller bleedings. It was espe- cially marked when the loss of blood amounted to three per cent, of the weight of the body. The papillary muscles of both ventricles are said to suffer first, then the walls of the left ventricle, and lastly the walls of the right ventricle. Stokes pointed out that depressing treat- ment may act in a similar manner. In idiopathic anaemia fatty degeneration of the heart also occurs. Biermer3 has re- marked that fatty degeneration of the bloodvessels often coexists. In preg- nancy, intense anaemia sometimes occurs, and in such cases fatty degeneration of the heart has been fouud.1 Wasting Diseases were noticed first by Ormerod, to have as one of their conse- quences fatty degeneration of the heart. Those in which it is most frequently met with are phthisis, cancer, and chronic suppuration. In each condition the amount of degeneration may be consider- able. In cancer it has seemed to the writer to be sometimes associated in de- gree with the degree of the fatty degenera- tion in the new growth. In Addison's disease it has also been met with.2 Toxoemic Influences constitute another group of causes. Fatty degeneration may result from many acute and some chronic blood changes. These include the various acute febrile conditions, spe- cific and non-specific, and certain chronic diseases which alter the constitution of the blood. In acute febrile diseases, molecular de- generation of the heart has been noticed by a large number of observers. Its naked-eye characters were distinguished by Laennec, and its conditions of origin and consequences were carefully studied by Louis and Stokes. Laennec pointed out that it occurred especially in those cases in which marks of " putridity" were present. By most writers the change has been regarded as inflammatory, as due to " myocarditis." It is certain that actual inflammation, as by extension from the pericardium, causes a similar degenera- tion. But in most of these cases, as Louis and Stokes pointed out, other evi- dence of inflammation is wanting ; there is no purulent infiltration, no effusion of lymph on the pericardium; and Stokes pointed out that local inflammations are rare in the conditions in which this change occurs. Moreover, identical changes may occur from other influences with equal rapidity, in which there is no suspicion of inflam- mation, but proof of a profound alteration in the state of the blood-as for example in phosphorus poisoning. Simple eleva- tion of the temperature of the body has been shown capable of producing a simi- lar degeneration.3 Many acute diseases are attended with this molecular degeneration. In acute rheumatism the condition is usually asso- 1 Gusserow, Archiv fur Gyneekologie, 1871, ii. 2, p. 218. 2 E. Wagner, Die fette Metamorphose des Herzfleisches. Leipsig, 1865. 3 Iwaschkewitsch, Journal fiir Militararzte, 1870, and Virchow's Jahresh. 1870, i. 179. Wickham Legg, Path. Trans, vol. xxiv. 1873, p. 226. 1 Ormerod, loc. cit. p. 832. 2 Virchow's Archiv, lix. 1. Similar ex- periments had also been made by Tschud- nowsky. Botkin's Archiv, Bd. ii. 1866-67. 3 Bericht Uber der 42en Versammlung dent. Naturforscher u. Aerzte. Dresden, 1868. 810 FATTY DISEASES OF THE HEART. dated with undoubted inflammation out- side or inside the heart, and is confined to the adjacent fibres, and other evidence of inflammation is to be found where the change is most intense. But in other cases in which the blood-change is pro- found, a simple degeneration may extend through the whole thickness of the wall and be apparently related to the pyrexia or to the degree of the blood-change, as in other febrile diseases, rather than to the special form of the toxaemia. The other diseases in which the change occurs are the various febrile affections, and especially those in which any pyo- genic influence is at work. It is com- mon, for instance, in erysipelas, puerperal fever, and smallpox. In the last it has been found to be very frequent.1 It oc- curs also in yellow fever,2 and malarial fevers.3 In typhus and typhoid fevers,4 it is also common, although other forms of degeneration are also found in the heart as well as in the voluntary muscles in these diseases. In typhus Stokes found that it marked some epidemics much more than others, and that it gen- erally commenced about the sixth day. In typhoid, Wagner5 found extensive fatty degeneration in nine cases out of fifty-nine. In diphtheria the change is also common. G. llomolle found it in six out of fourteen cases which he exam- ined, and Parrot found it in almost as large a proportion.6 In measles also Parrot found it present in about one-fourth of fifty-four fatal cases, In one case it was extreme. Ex- treme degeneration of the heart has also been met with in acute atrophy of the liver. Chronic alterations in the blood may cause fatty degeneration of the heart. It occurs in gout, as Charcot has pointed out.7 At first it is slight, but as the dis- ease progresses it may become very con- siderable and become a cause of sudden death. In the altered state of blood, which results from chronic renal diseases, it also occurs. It has also been found in purpura, scurvy, and the hemorrhagic diathesisin the latter perhaps as a re- sult of the loss of blood. It has also been seen in trichinosis. Certain poisons possess a remarkable power of inducing fatty degeneration of the heart in common with that of other parts. Foremost among these must be placed phosphorus, which has a very rapid action on the heart, liver, kidneys, and other organs, causing marked fatty degeneration in a few days. In a case recorded by Habershon, on the fifth day after a dose of five grains of phosphorus all the organs wrere the seat of fatty de- generation. The heart becomes yellowish or reddish-gray, soft, and friable, the fibres being filled with fat drops. Ac- cording to Schraube2 the affection of the heart is almost invariable in phosphorus poisoning. Arsenious acid, lead, and antimony3 are said to cause a similar molecular degeneration. In poisoning by sulphuric and other acids it has also been found ; and it occurs in greater degree the more readily the acid can get into the blood.4 Alcohol is, if not the most powerful, at any rate the most frequent toxic cause of fatty degeneration. In chronic alcohol- ism the blood is loaded with fat. The habitual use of ether and chloroform is said to have a similar effect. II. Local Causes.-All local causes of atrophy of the heart (q. v.) may also cause the fatty degeneration of its fibres. This is, indeed, partly the mechanism by which the atrophy is produced. External pressure may have this effect. Compression by fluid rarely causes molec- ular degeneration, but pressure by the contraction of lymph, limited in area, or by the pressure of calcified plates, may produce it. It is possible that the effect is in many cases produced, not by the di- rect pressure on tlie muscular fibres, but, as Walshe suggests, by the compression of the arteries and consequent defective supply of blood, a powerful cause of fatty degeneration. Interstitial pressure on the muscular fibres may certainly, however, be an im- mediate cause of this fatty degeneration. It is seen in fibroid and fatty overgrowth. It is well seen in the effects of syphilitic and other growths in the heart. In each condition the fibres are compressed di- rectly by the new tissue which is devel- oped between them. In fatty overgrowth 1 P. Sick quoted in Canstatt's Jahresbericht, 1866, ii. 39. Desnos and Huchard. Senao noted the frequency of syncopal death in this disease. Trait6, &c. 1749, ii. 551. 2 Bat. Smith, quoted in London Med. Rec- ord, 1874, p. 517. 3 Ponfick, loc. cit. ; Vallin, L'Union M6d. 1874, No. 23. 4 Stokes, Diseases of the Heart, p. 366 ; Murchison, On Fever, pp. 256, 631. 6 Loc. cit. 6 Diet. Encyclopedique des Sciences M6d. vol. xviii. 1876, art. Occur. It has also been observed in diphtheria by Bengelsdorf (Berl. Klin. Wochenschrift, 1871), and Bouchut (Gaz. des Hop. 1872, p. 117). 7 Maladies des Vieillards et Maladies Chro- niques. Paris, 1868. 1 Wagner, loc. cit. 2 Schmidt's Jahrb. 1867, 209. 3 Salkowsky, Virchow's Archiv, xxxiv. 1 and 2. 4 Munk and Layden, Berlin Klin. Wochen. schrift, 1865, Nos. 49 and 50. PATHOLOGICAL ANATOMY. 811 they may be little changed, but they fre- quently suffer, presenting narrowing and indistinctness of striation, sometimes sim- ple atrophy, sometimes very distinct fatty degeneration. This latter occurs espe- cially when any predisposing cause of fatty degeneration coincides in operation, such as congestion of the heart in fibroid overgrowth, sedentary habits, degenera- tive tendencies, or alcoholism in fatty overgrowths. Local Ancemia from vascular obstruc- tion is a frequent cause of extreme fatty degeneration. The obstruction is usually gradual, and due to atheromatous changes in the walls of the coronary arteries, cal- cification, &c.; sometimes it is sudden from thrombosis, or less frequently em- bolism. The left coronary artery is said to be affected more frequently than the right. The degeneration is limited to that part of the heart to which the dis- eased vessel is distributed. This connec- tion was noticed by Quain, and his obser- vations have since been abundantly confirmed. He found diseased coronary vessels present in thirteen out of thirty- three cases, and pointed out that the effect depends on the absence of anasto- moses with other vessels, by which a col- lateral circulation could be established, the "terminal character" of the arteries, as it would now be termed, first demon- strated by Swan.1 Congestion of the walls of the heart is, as Jenner2 pointed out, a cause of fatty degeneration of the muscular fibres. The degeneration is rarely simple, more or less fibroid growth is usually conjoined. The chief cause of such congestion is dilata- tion of the right side of the heart and obstruction, consequent on the distension of the auricle to the escape of the blood from the coronary sinus. Hence fatty degeneration of the heart is frequent in emphysema, long-continued pleural effu- sion, and diseases of the left side of the heart, which overload the right cham- bers. Inflammation of the substance of the heart, "carditis," is also attended -with molecular degeneration of the fibres. The effect is clearly seen in cases of pericar- ditis in which the inflammation invades the subjacent layer of muscular tissue. The depth to which the change extends varies according to the degree and dura- tion of the inflammation. Sometimes only a sixteenth, sometimes a quarter, or more, of the whole thickness of the heart is thus damaged. Wagner found fatty degeneration of muscular fibres present in seventeen out of thirty-five cases of severe pericarditis which he examined. In other forms of carditis the muscular fibres suffer in the same way. In the rare cases of suppurative carditis the degeneration pro- ceeds to the complete destruction of the fibres. It has been already stated that inflammation has been regarded as the mechanism by which the heart suffers in the acute febrile disease, and that these cases cannot justly be regarded as inflam- matory. Defective vitality of the muscular fibres of the heart has already been described as part of a general proneness to degenera- tion ; it may also occur as a local con- dition. This influence is seen in the proneness of the fibres of certain individ- uals to undergo such degeneration, apart from any other exciting cause. It is seen also in the tendency of hypertrophied hearts to undergo this change. Other hypertrophied muscles have been said, after a certain period of use, to fail and undergo degeneration.1 Fatty degenera- tion occurs with undue readiness in the newly-formed fibres, and in the majority of cases hypertrophied hearts present de- generation of some of the fibres. This is the case especially in conditions of valvu- lar disease which entail venous conges- tion of the walls of the heart, but it is also found in other conditions of hyper- trophy. In that which occurs in Bright's disease, for instance, E. Wagner found fatty degeneration in one-third of the cases (twelve out of thirty-five). Pathological Anatomy. - In con- sidering the pathological anatomy of fatty degeneration it will be convenient to re- verse the usual order and to describe first the microscopical changes in the fibres, and afterwards the alterations in the naked-eye characters which result from the minute changes. The first indication of the degeneration is the appearance of minute black gran- ules within the substance of the fibres. At first they may coexist with the normal transverse striation and seem to lie in rows between the primitive fibrillie. As they increase they appear to replace the transverse striae, which diminish in dis- tinctness and finally cease to be recog- nizable. Often from the first no regular- ity can be observed in the disposition of the granules; they are scattered uni- formly through the primitive bundle. As the degeneration progresses the gran- ules increase in size, and become translu- cent in the centre, being, in fact, globules of fat. These become larger, but rarely, as Quain observed, exceed the size of a blood-corpuscle. A linear arrangement of these fat globules is frequently to be observed : some are scattered throughout 1 Med. Gazette, xlii. 751. 2 Med.-Chir. Trans, vol. xliii. 1 The hypertrophied hiceps of the file-cut- ter is said by Clifford Allbutt, on the authority of Busk, to waste after a certain time. 812 FATTY DISEASES OP THE HEART. the substance of the fibre, while others are arranged in rows. Ultimately they may occupy the whole area of the fibre : sometimes they are aggregated in one part of it, and the remaining space is clear, free from granules or striae. The globules constantly appear to accumulate outside the primitive bundles; whether by the coalescence of granules formed there, or by migration from within the fibres, is not clear. The appearance is too constant to be accounted for by the accidental escape of globules when the section is being made. The muscular fibres are ultimately left clear; empty fibre sheaths appear to remain in their place. The existence of a sarcolemma to the muscular fibres of the heart has been denied : if absent, the appearance of the empty sarcolemma is simulated by the unchanged fibrous tissue between and separating the primitive bundles. The affection of different fibres is rarely uniform. Some may contain many fatty globules, and others only minute granules, while others are still healthy. Similar de- grees of affection may be observed in the course of the same fibre: one part may be healthy, in another part the granular stage may be present, and in another there are only globules of fat. The globules and larger molecules of fat are soluble in ether and resist acetic acid. It is necessary to rupture the fibre in order to apply this test. There is some doubt whether the finer molecules at the earliest stage of the degeneration are all soluble in ether. It has been affirmed by some writers, but lately denied by Rind- fleisch,1 who maintains that at the com- mencement of a true fatty degeneration the granules are insoluble in ether. The point will be alluded to in its bearing on the pathology of the process. To the last the molecules and globules of fat main- tain their appearance. They never blend into uniform masses such as occupy the cells in fatty overgrowth. The effect of this molecular degenera- tion is to modify considerably the naked- eye characters of the affected part. It is changed in color. The granules and globules reflect light strongly, and ren- der the tint paler. It becomes gray, ashy- gray or grayish-yellow. Laennec aptly compared the color often seen to that of a faded leaf. In the degeneration which occurs in acute diseases, the substance of the heart may be dark in color, from the rapid staining of the tissues consequent on the decomposition of the blood-corpus- cles, and the escape and transudation of their coloring matter. At the same time the consistence is changed. The affected part is soft and flabby. The fibres become brittle and break up easily into short pieces, so that a scraping from a cut section shows much shorter fragments of fibres under the mi- croscope, than does that from a healthy heart. The effect of this brittleness of the fibres is to render the tissue friable and easily broken under the finger, and sometimes the change is so great that the tissue softens and breaks down in a lim- ited portion, or the substance may be torn by a violent contraction of the heart. This diminished consistence may be the most conspicuous feature, and hence the change was described as "pale soften- ing." The part so changed may have a greasy aspect and feel, and may actually grease paper which is applied to it. The in- crease in the quantity of fat contained in the tissue is, however, smaller than might be expected. Hermann Weber, indeed, affirmed that there was no increase ; and it has been established by other investi- gators that in slight fatty degeneration only the same amount of fat is to be ob- tained from a heart fattily degenerated as from a healthy heart. But it has been shown that in more considerable fatty de- generation, the amount of fat is increased from two or three per cent., to four or five per cent, over the quantity contained in a healthy heart.1 The distribution of the change varies. In the form which is secondary to acute diseases, the degeneration is often distrib- uted uniformly through the whole heart. But frequently, as Louis and Stokes pointed out, the left ventricle is affected much more than the right. When sec- ondary to pericarditis only the superficial layer is affected, adjacent to the inflamed pericardium. Occasionally, in fever, ac- cording to Stokes, the change may affect only the superficial layer. When arising from a chronic process it may be confined to the inner layer beneath the endocar- dium, or may be greater in that than in the superficial layer.2 More commonly it is widely distributed through the heart, generally in the form of minute foci of degeneration, pale spots, lines, crescents, in apparent isolation, or connected, and forming, as has been said, a plexus of de- generated areas throughout its substance. The resulting mottling appears on section or may be visible through the endocar- dium. This form is often presented by the degeneration which succeeds hemor- rhage. Lastly, a limited area of the heart's wall, generally near the apex, may be affected intensely and uniformly ; the affected region is sometimes sharply 1 Biittcher, Virchow's Archiv, xii.; Kry- low, ibid. 1868, xliv. 4. Stevenson, quoted in Wilks' and Moxon's Pathological Anatomy, p. 119. * Ormerod, loc. cit. p. 832, case vii. 1 Path. Gewebelehre, 1875, p. 16. PATHOLOGY. 813 limited. It was this variety which first attracted the attention of Laennec. This form commonly results from vascular dis- ease. Not rarely a diseased vessel may be traced passing directly into the area, as in cases which have been described by Quain and others. When degeneration affects part of the heart the frequency varies with which different portions suffer. The ventricles are affected much more frequently than the auricles. Indeed, Ormerod doubted whether the auricles are ever affected : they are certainly occasionally the seat of this degeneration, and their wall may be affected in a limited area through its en- tire thickness. Quain found that in about half the cases both ventricles are affected, and that where one ventricle only is af- fected the left is diseased twice as fre- quently as the right. The size of a heart the seat of fatty de- generation may seem to be increased, but this is due to the diminished firmness of the organ, in consequence of which it does not maintain its shape when placed on a table. In pure fatty degeneration the size of the heart is normal or only in- creased slightly by the occurrence of sec- ondary dilatation, and not rarely it is di- minished. A wall partially degenerated may be bulged out so as to cause a local dilatation of the cavity. Fatty degenera- tion, however, may and often does occur in hearts previously enlarged. Hypertro- phied tissue, as already stated, undergoes degeneration more readily than healthy fibres. Associated changes may be found in other organs, especially those which are causes of this condition or are other re- sults of a common cause. Those most frequently met with are degenerated vessels, and fatty degeneration in other organs. Ormerod thought the fatty de- generation in other organs was more com- monly associated with fatty degeneration of the right than of the left ventricle. It has been already stated that hearts, the subject of fatty growth, frequently present fatty degeneration of the remain- ing fibres. In all seats of fatty degeneration cal- careous salts are apt to be deposited, but this seems to occur less frequently in the substance of the heart than in some other seats of degeneration. Most cases of "ossification of the heart" are cases of calcareous deposits in subpericardial in- flammatory tissue. (See "Adherent Peri- cardium. ") The papillary muscles are occasional seats of calcification of degene- rated tissue. In rare cases calcareous deposits are found in the substance of the heart. Ina case mentioned by Renauldin1 the substance of the left ventricle of a man, aged 33, was infiltrated with grains of calcareous matter, larger to- wards the cavity of the ventricle. Some of them were as large as the tip of the finger. Two remarkable forms of calcifi- cation have been described by Coats1: in one the fibres were dotted with spherules of calcareous matter like globules of oil; in the other the process had resulted in a "petrifaction" of the fibres without change of form. The blood has been said to contain fat in some cases of fatty degeneration. R. W. Smith stated that he had seen globules of fat visible to the naked eye in the blood after death, and Stokes noted the same thing. Some doubt attaches to these ob- servations from the difficulty of avoiding the escape of fat from the divided tissues into the blood. Dumenil and Pouchet,2 however, state that they found a consid- erable quantity of fat in the blood of a person, the subject of chronic alcoholism, who, on subsequent death, was found to have fatty degeneration of the heart and liver. Magnus Huss also affirmed that he had seen fat in the blood of drunkards. Pathology.-The significance of this molecular degeneration is clear; it is a sign of lessened vitality, sometimes of ac- tual death. But the nature of the process has been the subject of much discussion, and is still, to a considerable extent, ob- scure. It seems probable that the first step in fatty degeneration is a molecular change in the muscular fibre, by which the fat which exists within it in an invisible form, combined with the protein constitu- ent, is separated and precipitated in visi- ble granules and globules. Invisible fat, to be detected by chemical analysis only, exists in the blood, the heart, and, in fact, all the animal tissues,3 and is be- lieved to be combined with the nitrogen- ous material, because it is found that the different nitrogenous substances have their own special forms of fat; that the fat of fibrin, for instance, is different from the fat of serum.4 In the healthy heart the fat thus combined amounts to about two or three per cent. In moderate fatty degeneration, even when granules and some globules of fat are visible under the microscope, chemical analysis shows that there is no increase in the total quantity of fat.5 It would thus appear that the first step of the degeneration is a separa- 1 Glasgow Med. Journal, August, 1872. 2 Gaz. Hebd. de M6d. et Chir. 1862, p. 32. 3 Virchow, in his Archiv fiir Path. Anat. i. 1847, p. 156. 4 Lehmann, Physiological Chemistry; Vir- chow, loc. cit. 6 Hermann Weber, Ormerod. 1 Journal de Med., Jan. 1816. Quoted by Laennec, p. 231. 814 FATTY DISEASES OF THE HEART. tion and precipitation of the combined fat. It is probable also that the granules, which constitute the first stage of degen- eration, are not all of a fatty character ; that some of them are of protein nature. Virchow suggested that the protein material may ultimately be changed to a soluble extractive and pass away, leaving the precipitated fat. But in more advanced fatty degenera- tion the quantity of fat is greater than this explanation will account for. Fibres arc seen to be filled with globules of fat, and analysis shows that the amount of fat in the tissue is actually considerably increased, often to double the normal quantity. What is the source of this additional quantity of fat ? It must be either formed in the fibre or introduced from without. The former is the simpler explanation ; by it the fat is supposed to arise by a chemical change, an imperfect oxidation, of the nitrogenous constituent of the fibre. This is the explanation which harmonizes well with the visible characters of the change, since the trans- verse striation disappears as the fat is formed. Rindfleisch1 points out that the stage of "cloudy swelling" of cells, in which they are filled with minute granules soluble in acetic acid, if it does not resolve, passes into one in which the granules re- sist acetic acid and dissolve in ether. This view was suggested by Fick2 and Rokitansky,3 and has been adopted by Virchow, Paget, Quain, and others. It is certain that fat may be formed from nitrogenous material. The vegetable world affords many instances of this. Butyric acid, a fatty acid, may be formed by the decomposition of fibrin (Wurtz). Chemistry supplies other examples of the same class. If the fat, in molecular de- generation, is not formed by a change in the protein matter, it must be introduced from without. But the increase in the fat is sometimes found in situations in which it cannot have been introduced from without. Prolonged maceration in dilute nitric acid, for instance, will pro- duce such a degeneration in healthy mus- cular fibres; a similar change is often seen in preparations preserved in dilute alcohol. Doubtless this is chiefly due to the separation of the combined fat, and it has accordingly been found that there may be no increase in the total quantity of the fat contained in the fibre before and after the occurrence of the degeneration. In some cases, however, a considerable increase in the amount of fat has been found ; that is to say, there has been a considerable formation of fat. Ilandfield Jones' found the increase of fit to amount to nearly fifty per cent., and as any acces- sion of fat from without is impossible it can have arisen only by the decomposi- tion of the protein material. The forma- tion of adipocere is another illustration of the same process, but this substance seems somewhat variable in its character and mode of formation. Ormerod, in- deed, maintained that its composition al- ways agrees with the composition of the fat of tlie animal, and that its fatty ele- ment is due to a change in, and infiltra- tion of, the normal fat into the muscular and other tissue. But he found that one specimen consisted of at least half pure fat, and Quain found that adipocere from the muscle of a horse was almost entirely soluble in ether. Other evidence, although less conclu- sive, of the origin of the fat from the protein matter, is drawn from the occur- rence of extreme fatty degeneration in parts to which the blood cannot gain ac- cess. It is seen, for instance, in "infarc- tions." The area from which the blood- supply is cut off by embolism is the seat of intense fatty degeneration. It is seen also in the experiments (performed first by Wagner) in which portions of animal tissue have been inclosed in the peritoneal and other cavities of living animals, and have become changed to masses of fat. But these experiments are deprived of some of their significance by the fact that the inclosure of the fragments in an im- permeable coating prevents any increase in the fat beyond that present in the healthy tissue (Burdach). Inorganic substances permeable to the animal fluids become charged with fat in just the same way as the organic tissue. These facts, indeed, negative ail the significance of these experiments as proof of the trans- formation of protein substance. They do not, however, exclude the possibility that some of the fat may have arisen in this way, since an impermeable coating will prevent the access of oxygen, without which the oxidation of the protein mate- rial, imperfect though it be, cannot occur. The fatty degeneration found in phos- phorus poisoning, in poisoning by acids, and intense ansemia, has been regarded as further evidence of the formation of fat by imperfect oxidation of nitrogenous material, since it is believed that all these conditions act by a common mechanism, the diminished supply of oxygen to the tissues consequent on the diminished number of blood-corpuscles. The dimin- ished oxidation is also indicated by the fall in the temperature of the body. These facts prove that in fatty degen- 1 Pathologische Gewebelehre, p. 16. 2 Muller's Arch. 1842, p. 19. 8 Path. Anat. 1 British and Foreign Medico-Chirurgical Review, July, 1853, p. 59. 815 CONSEQUENCES-SYMPTOMS. eration some of the excess of fat present in the fibres may be, and probably is, due to a chemical change in the protein con- stituent of the fibre. They do not how- ever, exclude the entrance of some of the fat into the fibre from without. It has been argued, indeed, by Robin' and Ormerod,2 and the view is supported by Walshe, that all the fat seen in the fibres in fatty degeneration enters them from without, that it is essentially an infiltra- tion of the fibres with fat, derived directly from the blood, and replacing the protein constituent of the fibres, which has been removed by a process of atrophy. There are two ways in which such infiltration of fat is conceivable. Minute fatty globules may enter the fibre from the blood, pass- ing through its wall as fat, just as the fatty molecules of the portal blood pass into the liver cells adjacent to the portal canals.3 Or the fat may enter the fibre in invisible combination with the liquid pro- tein material which must, in the normal course of nutrition, always permeate the fibres. Within the fibre this fat may be separated and precipitated by a process similar to that concerned in the sepa- ration and precipitation of the fat contained originally in the muscular tissue, the nitrogenous material passing out as "extractive." The constant repe- tition of such a process may fill the fibre with fat globules. There is some reason, as just stated, to believe that most of the fat which is found after a time in pieces of tissue inclosed in the peritoneal cavity of another animal passes in from without. If this is so with regard to substances separated from all structural continuity with the living tissues, it may be the same with the fat which is found in such excess in areas in which, in consequence of arrest of blood-supply, necrosis has oc- curred. The permeation of these areas with fat-containing plasma, from the ad- jacent healthy region, must constantly go on. The analogy of calcification, which often succeeds fatty degeneration, affords some support to this theory. Normally, the blood, heart, and other organs contain a small proportion of calcareous salts, probably combined with the protein sub- stance. No transformation of the other elements can produce the lime salts which are found in the calcified tissue. They must enter the tissue from without, with the blood plasma, from which they are separated and deposited, while the nitro- genous element passes away. This pro- cess, continuing during a long time, ulti- mately effects a complete infiltration of the tissue with calcareous matter. A consideration of all the facts of fatty degeneration make it probable, then, that, as Handheld Jones suggested, each pro- cess may be concerned in the production of the excess of fat which is found in ad- vanced fatty degeneration ; that the fatty material at first seen in the fibre is merely separated and precipitated in visible form, and that the subsequent excess arises in part by a transformation of the protein material, and in part by the entrance of fat from without. Consequences.-The effect of fatty degeneration on the function of the heart is to lessen its propulsive power, and thus to lead to imperfect filling of the arterial system, and consequent visceral anaemia. This effect is much more marked than is the correlative venous distension, which is so prominent an effect of dilatation of the heart. The relative defective supply to the arterial system is recognizable in the symptoms which it causes during life, rather than by any pathological conse- quences which can be observed after death. These symptoms are described further on. The fatty degeneration of the fibres may not only affect the function of the heart, it may lead to changes in its con- dition which have their own results. The weakened walls may yield unduly before the pressure of the blood, and the heart may become dilated. Such dilatation is rarely very great. Its mechanism and conditions have been already considered (Art. "Dilatation"). But the weakness which fatty degeneration produces may have a much graver result. The brittle- ness of the fibres may lead to their rup- ture, and when the degeneration extends through the whole thickness of the wall of the heart, the whole wall may give way. This accident, "rupture of the heart," is of such gravity and import- ance as to need detailed consideration, and it is therefore described at the end of this article. Symptoms.-The physical signs and the symptoms which attend fatty degen- eration of the heart are usually indistinct and never distinctive. All are common to other morbid states. They depend on the diminished power of the heart, which modifies the signs of its action, and affects the function of other organs. As the size of the heart in simple fatty degeneration is little changed, the area of dulness presents no alteration. The slight dilatation, which is the conse- quence of the fatty degeneration, rarely leads to the signs of enlargement of the heart. In a considerable number of cases the dulness is increased, but this increase depends rather on pre-existing hypertro- phy or dilatation, or else it is due to con- current fatty growth. 1 Chimie Anatomique. 2 Brit. Med. Journal, 1864, ii. p. 152 ; St. Barth. Hosp. Rep. vol. iv. 1868, p. 30. 3 Fatty "degeneration" (infiltration) of the liver was produced artificially by Magendie and Gluge injecting fat into the portal vein. 816 FATTY DISEASES OF THE HEART. Diminished force of impulse is the most important physical sign of cardiac degen- eration. The area of impulse, like the area of dulness, is only increased by co- existing conditions. As long as the im- pulse is perceptible, the apex-beat may, in most cases, still be felt. When dilata- tion has occurred in consequence of the weakening of the cardiac wall, the im- pulse may be diffused and peculiar in character, resembling, as Stokes re- marked, rather the slight, general im- pulse of an aneurism than the normal impulse of the heart. When the patient is thin, and the lungs are small, so that the impulse of the heart can be well felt, a partial change in impulse may be ob- served to correspond to a partial degen- eration. Stokes, for instance, observed that in fever, when the left ventricle was much more degenerated than the right, while an apex impulse might be lost, an impulse in the lower sternal region, due to the right ventricle, might be still per- ceptible. The sounds of the heart are weakened in correspondence with the weakness of the impulse. The first sound, to which the contraction of the heart directly con- tributes, is that which presents the great- est change. It is usually toneless, shorter, and relatively high-pitched, and may be- come aimost or even quite inaudible at the apex, only the second sound remaining. The first silence is longer than normal in consequence of the shortening of the first sound. The second sound is also weak- ened in consequence of the deficient dis- tension, and therefore deficient recoil, of the aorta and pulmonary artery. When the first sound is shortened and raised in pitch it may resemble the second. The sounds of the foetal heart are then very closely simulated, especially if the heart acts rapidly. When the degeneration is local, the sounds may be modified locally, just as the impulse. In the acute degen- eration of fever, Stokes observed that the first sound might be lost over the left ven- tricle when it was still audible over the right, in cases in which the post-mortem examination showed the left ventricle to be the more affected. Walshe has ob- served a similar alteration of intensity in chronic disease under similar circum- stances. According to Stokes, if, after ceasing to be heard for a time, the first sound reappeared, it was heard first over the right ventricle and afterwards over the left. In one case both sounds were inaudible for thirty-six hours before death. Stokes believed that a systolic basic murmur might exist during the early stage of the degeneration. Other ob- servers have noted the occurrence of an apex murmur due to regurgitation, and have ascribed it to fatty degeneration of the papillary muscles. The rhythm of the heart's action varies much. It may be regular throughout, but is often irregular, chiefly, Walshe thinks, when dilatation coexists; some- times it is frequent, even to an extreme. It may be slower than natural, and the diminution in frequency may proceed to a degree met with in no other affection. This was first pointed out by Adams. It may fall to forty, thirty, or twenty beats per minute. In rare cases it has sunk as low as eight or ten beats per minute for hours before death.1 The pulse is weak and small, in proportion to the cardiac failure. Its rhythm, as a rule, cor- responds with that of the heart; rarely it is less frequent than the heart's contrac- tions, in consequence of the weaker beats of the heart failing to send a wave along the vessels sufficient to be felt. Pain is not a common symptom, but now and then is complained of, and is sometimes very troublesome. It may be confined to the cardiac region, may be re- ferred to the sternum, or may extend down the arm. It may be paroxysmal, and simulate angina pectoris in its char- acters. Occasionally true anginal seizures occur, but no direct relation is known be- tween their occurrence and the fatty de- generation of the heart. Syncopal attacks, as might be expected from the nature of the disease, are not rare ; they are usually produced by some effort. They vary in intensity, sometimes amounting only to a sense of faintness, sometimes to loss of consciousness. They may be accompanied by a sense of great distress, as if death were impending. Death does not unfrequcntly occur in such an attack. Often in this condition cere- bral symptoms are associated with those of cardiac failure. Convulsions may occur. Vertiginous sensations are not unfre- quent. Walshe mentions a case in which loss of memory for recent events preceded each attack of syncope. Or the loss of consciousness, commencing as apparent syncope, may continue, and deepen, slowly or rapidly, to coma, with stertorous breath- ing. These "pseudo-apoplectic" seizures, as they have been termed, are usually brief, and leave no paralysis. They have, however, a great tendency to recur. They were referred by Adams and R. W. Smith to congestion of the brain, but Stckes pointed out that their association is with a deficient supply of arterial blood, and that they are probably due to cerebral anaemia, the immediate cause of the syn- copal seizures. In confirmation Stokes mentioned a case in which they could be averted at their onset by hanging down 1 Ormerod thought that infrequency was associated rather with fatty infdtration than with fatty degeneration. Loud. Med. Gaz. 1849, p. 917. " SYMPTOMS. 817 the head so that it nearly touched the floor. When death has occurred in these attacks, the brain has appeared free from organic disease. It is needless to remark that apoplexy from actual organic changes in the brain may occur in subjects of fatty degeneration of the heart. Other occa- sional symptoms on the part of the nerv- ous system are numbness and formication, such as have been attributed to anaemia of the spinal cord. Dyspnoea is a common symptom. It may be slight, felt only on exertion, espe- cially on ascending an incline or on making some other effort. Or the dys- pnoea may be severe, constant, amounting to a continuous sense of suffocation. Con- siderable dyspnoea is said to be present in one-half of the cases of pronounced fatty degeneration. Occasionally it has a spe- cial form. Sometimes frequent sighing is observed, as Stokes pointed out. Some- times the dyspnoeal breathing possesses a peculiar rhythm of striking character, which has attracted much attention since it was first described by Cheyne.1 It was very carefully studied by Stokes,2 and by him especially associated with fatty de- generation of the heart, although further observation has shown that it is by no means confined to that affection. This form, which has been termed the "Cheyne-Stokes dyspnoea," or "ascend- ing and descending respiration," is char- acterized by recurring series of respiratory acts, first increasing and then decreasing in intensity. In the intervals breathing seems to have almost or entirely ceased ; then slight respiratory movements are noticeable, which gradually become deeper and deeper, until an acme of very deep and labored breathing is reached, after which the respirations gradually become shallower until they subside into the same apparent apnoea, which is again broken by the gradual onset of another series. In the classical case recorded by Cheyne, the cycle included about thirty respira- tions and lasted a minute. In most of the other cases recorded it has occupied a shorter time. Hayden has found the pulse unchanged during the paroxysms. As just stated, this form of dyspnoea is by no means confined to fatty degenera- tion of the heart. It has been seen in other forms of heart disease, especially in valvular disease with dilatation3 and in atheroma of the aorta.4 It has been met with even more frequently and at all ages in affections of the nervous system, in cer- ebral hemorrhage,5 in tumors of the brain, uraemia, and tubercular meningitis.1 It has frequently been seen in cases in which affections of the heart and brain coexist. It has been produced artificially in ani- mals by Filehne2 by the injection of mor- phia and subsequent inhalation of ether and chloroform. It has also been observed in a case of fatty degeneration of the heart, during the narcosis which followed a fatal injection of morphia, and also in chloral narcosis. Its probable explana- tion lies in a lowered sensibility of the respiratory centre in the medulla oblon- gata, as was suggested first by Walshe,3 and after him by Laycock and Traube. A form of dyspnoea which has in seve- ral instances been described as that of Cheyne, is that in which the dyspnoea subsides slowly into dozing apnoea, to be broken after a few seconds by a sudden rouse to conscious, or half-conscious, dys- pnoea, which, after a few seconds, slowly subsides. This occurs rather in dilatation than in fatty degeneration of the heart. It seems readily explicable on the theory of diminished sensitiveness of the respi- ratory centre which requires a voluntary or half voluntary reinforcement. The latter is only excited by a stronger degree of the physiological stimulus ("anoxae- mia") than the former ; the blood, when well aerated by the dyspnoeal respirations, ceases to excite it; sleep gradually with- draws the reinforcement, and the respira- tory centre ceases to act; the apnoeal ve- nosity of blood increasing, at last awakes the higher mechanism to renewed action. But the true Cheyne-Stokes breathing differs from this in the very gradual in- crease in the breathing, from shallow to deep, as the dyspnoea comes on.4 has also seen it in one case of cerebral hemor- rhage, and has been informed of two other cases in which it was marked. 1 Traube, Roth. 2 Berlin. Klinische-Wochenschr. 1874, Nos. 13, 14, 32, 35. 3 Diseases of the Heart and Aorta. Third Ed. 1862, p. 345. 4 Several theories have been framed to ex- plain the details of the phenomena. Traube accounted for the slow accession of the dys- pnoea by supposing that the venosity of the blood first excites the terminal branches of the vagus in the lungs, which, it is known, can liberate only slight reflex respiratory movements, too slight to prevent accumu- lating venosity and general stimulation of the afferent nerves, producing the intenser dys- pnoea. The gradual onset of the returning respiration is not, however, difficult to ex- plain, for it is the natural form in which the physiological stimulus manifests its returning action after it has been withdrawn by the abundant aeration of the blood in the dys- pnceal breathing. A state of apnoea may easily be produced in health by a series of very deep respirations. The highly oxyge- ' Dubl. Hosp. Rep. 1818, p. 216. 2 Dubl. Journal of Med. Science and Dis- eases of the Heart, August, 1846, p. 324. 3 Seaton Reid, Dub. Hosp. Gaz. 1860. 4 Hayden, loc. cit. p. 632. 5 Laycock, M. Fothergill, &c. The writer vol. ii.-52 818 FATTY DISEASES OF THE HEART. In some cases there may be from first to last no embarrassment of the breathing. Walshe has pointed out that this freedom from dyspnoea may accompany even the syncopal and apoplectic seizures. Cough is sometimes present without bronchitic or other cause. The other symptoms referable to the general system are in the main those of defective blood supply. The skin is pale, the muscular power deficient, the surface and extremities cold ; the mind is weak, often depressed. The digestive organs suffer; anorexia is common. Symptoms of over-distension of the venous system are rare. Slight oedema may occur, but marked dropsy probably never occurs as a consequence of the fatty degeneration. It sometimes results from coexisting dila- tation, especially when primary. It is only under such a condition that the urine contains albumen. In simple fatty degeneration of the heart the urine pre- sents no deviation from the normal. Co- existing degeneration of other organs often modifies the general characters of the symptoms of fatty degeneration. [Absence of symptoms of fatty degen- eration of the heart must be rare, but it is sometimes met with. In the case of a lady well known to me, who died at about sixty years of age, nothing occurred to show failure of health until the last day of her life. Her physique was fine ; she was accustomed to walk two or three miles a day, and to go up several flights of stairs without inconvenience. Autopsy1 showed rupture of a decidedly fatty heart.-H.] Course and Terminations.-The course of molecular degeneration of the heart varies according to the circum- stances under which it arises, and espe- cially as it occurs gradually as a slow de- generation, senile or premature, or acutely in consequence of blood-poisoning. In senile degeneration the symptoms are gradual in onset, and may be marked, or may be very obscure. The duration of the affection may be long, sometimes twelve to fifteen years. In these cases other causes often increase the effect of age, and may be to some extent remova- ble, and the extension of th£ degeneration may be arrested for a considerable time. Sooner or later the cardiac failure comes ; late, if the conditions of a tranquil unemo- tional existence can be secured ; soon, if the sufferer has still to face the storms of life, physical and moral. In an acute ill- ness, preceding degeneration of the heart prejudices very much the patient's state. The pulse becomes weak and irregular, often, as Kennedy showed, extremely fre- quent ; and, if the acute disease be at all severe, syncopal failure occurs. Under other conditions the end may come as slow failure, or sudden stoppage from loss of power, or from rupture. The lat- ter occurs in a considerable proportion of the cases in which the disease is well marked. When the coronary vessels are diseased and the heart degenerated, the sudden complete obstruction of a large branch will stop the damaged heart.2 The more acute degeneration commonly oc- curs in the course of some pyrexial affec- tion. It is characterized by more or less sudden failure of the heart's action, out of proportion to the other evidences of in- tensification of the general disease. The condition usually corresponds with a high temperature, and often occurs before the primary disease has begun to subside. When the patient recovers, and the py- rexial stage is over, the action of the heart may become very infrequent or may remain unduly frequent. The form of degeneration which suc- ceeds a hemorrhage is marked by more nated blood no longer stimulates the respira- tory centre ; no besoin de respirer is felt, and, except by a voluntary effort, no respiratory movement is made, until, after a few seconds, the slowly increasing state of blood causes respiratory movements, slight at first, after- wards deeper, until the normal respiration is reached. To explain the degree and dura- tion of the dyspnoea, as well as its gradations, Filehne assumed that vaso-motor spasm causes continued stimulation of the respiratory cen- tre, until that spasm is slowly relaxed by a degree of aeration of the blood which ceases to stimulate the respiration, and thus the slow relaxation of the spasm causes a slow diminution, and finally cessation, of the re- spiratory movement. He found that by simple alternate compression and relaxation of the arteries in a guinea-pig (right innominate and left subclavian) he could produce perfect Cheyne-Stokes respiration. In further con- firmation of his theory he states that he has arrested the characteristic breathing by in- halation of nitrite of amyl. It is not difficult to understand the origin of this form of respiration in cerebral diseases, in which the lowered sensitiveness of the respiratory centre is likely, and the with- drawal of higher influence may leave its tendency to rhythmical action free to modify a series of its actions. Its connection with cardiac diseases is less easy to understand. Little's theory of unequal action of the ven- tricles is certainly unsupported. Hayden suggests that the etiological condition is athe- roma of the aorta interfering with the supply of arterial blood to the peripheral vessels. Tliis explains the occurrence of dyspnoea bet- ter than its rhythmical cessation. Long-con- tinued over-stimulation of the respiratory centre may possibly lead to its diminished sensitiveness. [' This case occurred in the practice of Dr. Lodge, of Merion, Penna.-H.] 2 Payne, Brit. Med. Journal, Feb. 5th, 1870. DIAGNOSIS-PROGNOSIS. 819 gradual sinking, the patient becomes weaker and weaker, and dies asthenic at the end of a few days or a week or two, from the loss of blood. Diagnosis.-It will be gathered from the preceding remarks that the diagnosis of fatty heart is never easy and is often difficult or impossible. The opinion of Latham that the existence of the disease does not admit of positive recognition, only of probable conjecture, is that of most later authorities. Many of the symp- toms which are the most uniformly con- nected with fatty degeneration of the heart, are also due to so many other con- ditions, that they have not, even conjoint- ly, much significance. The diagnosis, as far as it can be made, depends on the fol- lowing points:- (1) On the Simple Loss of Power.-A very similar loss of power may be due to dilatation, but dilatation diffuses the im- pulse and enlarges the heart; neither effect belongs to degeneration, unless dila- tation is associated with it, and then the muscular degeneration can rarely be de- tected. Such simple loss of power may, however, occur in either a normal or a hypertrophied heart. In each it has the same significance, but in the latter the weakness is commonly relative only. It needs in all cases to be carefully distin- guished from concealment of impulse in consequence of over-distension of the lung. A mistake may be avoided by attention to the other signs of emphysema, and especially to diminution or obliteration of the superficial cardiac dulness, which al- ways occurs when a distended lung pushes the heart away from the chest wall. Weakness of the first sound of the heart is also most valuable, in the absence of emphysema, as concurrent evidence of the diminished force of its contraction. Other symptoms of fatty degeneration are of less significance, except perhaps slowness of pulse, which is, however, rare ; the spe- cial forms of dyspnoea are also too rare, and they are also too equivocal, to be of much value. Some weight has been at- tached to the syncopal seizures which occur in this disease, and especially to the mixture of syncopal and cerebral symptoms. Mental depression has also received attention as adding weight to other symptoms. Pallor of the surface has a similar significance. (2) On the Presence of Similar Degene- ration elsewhere.-Senile degeneration is in some persons local, much more com- monly it is general, and its wider mani- festation may give significance to cardiac symptoms, which alone would be of little import. Of these degenerations the most important are those of the vascular sys- tem, of which the heart is part. The smaller vessels are accessible to direct examination, and their degeneration is manifested by hardness and tortuosity. Perhaps of next significance is the change in the cornea known as "arcus senilis,'' and which, since it was shown by Canton to depend on fatty degeneration, has at- tracted much attention as convenient indi- cation of a diathetic tendency to such a change. That it has such significance in some cases is unquestionable,1 and it has been thus accepted by Quain, Barlow, Paget, and others. But its value may easily be over-rated. Like every other local degeneration, it may be part of a similarly wide-spread change or it may be an isolated phenomenon. The latter is the case perhaps, more frequently than the former, and has led many observers to deny that any weight can be attached to it as evidence of fatty degeneration of the heart. Haskins2 has recorded twelve cases with no affection of the heart. A wider observation has shown that the truth lies between the two extremes, and that the arcus senilis, as already stated, may give weight to other characters but alone is of little significance. Other evi- dences of degeneration are of still less value ; but grayness of hair is probably a stronger evidence of degenerative tenden- cies than is its loss. (3) The existence of a recognized cause of fatty degeneration is also of considerable value as an aid to diagnosis. Of the va- rious causes, chronic alcoholism is that which is most frequently associated with the degeneration; and most frequently assists the diagnosis. Prognosis. - Molecular degeneration of the heart is always serious, but its gravity varies much under different cir- cumstances. The condition to which danger is especially related is the persist- ence of the cause of the degeneration. As long as the cause lasts, the degeneration continues and increases. Life depends on the maintenance of the functional power of the walls of the heart, and pro- gressive degeneration must sooner or later produce death. If the cause of the de- generation ceases to act, the disease ceases to progress, and if moderate in de- gree, may, it is probable, even be recov- ered from. When a certain point of damage has been reached, the condition seems to preclude more than partial resto- ration of Structure. The forms of degeneration which occur in acute diseases are those in which the immediate danger is greatest, but at the same time the ultimate prognosis is usu- ally favorable. It is immediately grave, because the heart is often unable to resist the prostrating influence of the general 1 Luithlen, Virchow's Archiv, 1871, p. 91. 2 Am. Jour. Med. Sciences, January, 1853. 820 FATTY DISEASES OF THE HEART. disease. It is ultimately good, because the causal disease soon ceases, and often before the change in the heart has reached an irreparable degree. After the acute illness is over, the patient may die from the subsequent slow failure of the heart, but frequently he recovers, sometimes completely, sometimes with some perma- nent damage to the substance of the heart. In chronic degeneration the immediate prognosis is less grave, but the ultimate prognosis is worse than in the acute cases. Those are the most hopeful in which there exists a removable cause of degeneration, such as the consumption of alcohol. Where the malady has arisen as a senile degeneration, or as a widely-spread idio- pathic change, and the conditions of life are unalterable for good, the prognosis is very unfavorable. It is worse also the earlier in life the patient is attacked, since, as Quain pointed out, early age often entails an inability to obtain that rest which alone can ward off the conse- quences of the disease. The fatty degeneration of the heart which coexists with a like degeneration in the vessels has been regarded as being not without advantages : adapted, in senile atrophy, to the lessened mass of blood,1 and diminishing, by the lessened strength of contraction, the strain to which rotten vessels are exposed.2 Treatment.-Advanced fatty degen- eration of the heart is generally an irreme- diable condition. Something may be done to ward off its effects, but little to restore the heart to its normal state. In slight degeneration, improvement, even perhaps recovery, may take place. The great end to be aimed at is the removal of the cause. In the acute degeneration of pyrexia there is, as stated, every reason to believe that a state of granular degeneration may be recovered from, when the cause has ceased to act. A chief object in treat- ment must therefore be to maintain the strength of the patient, to keep his heart going by judicious stimulation until the disease is over. General tonics will then aid recovery. Strychnia has been thought by many to be of great use. In the chronic forms of degeneration there is frequently little room for thera- peutics. The change is too often due to conditions beyond the influence of any means at our disposal. All removable causes, however, such as chronic alcohol- ism and gout, must be carefully searched for, and their influence, if possible, re- moved or neutralized. A fair amount of nitrogenous food is necessary. Restric- tion of fat is of more doubtful benefit. Tonics are useful-iron, quinine, or strych- nine. Digitalis has been recommended to strengthen the fibres which are weak- ened but not destroyed. Walshe says it is most useful where the pulse is frequent and dilatation coexists. If the degenera- tion can be arrested, hypertrophy of the remaining fibres may occur, and help to restore the functional power of the heart. In every form of degeneration care must be taken not to overtax the heart. Its weakened texture is easily damaged still further, and approximate health de- pends on the avoidance of exertion, &c. Effort with closed glottis must be espe- cially avoided, such as pulling on boots, lifting weights, straining at stool; the lat- ter has in several instances been the im- mediate cause of cessation of the heart's action. All causes of syncope must also be carefully avoided. In acute illness, the horizontal posture must be carefully maintained as long as the cardiac failure continues, and it must be left off with caution. The general health must be carefully attended to. A life in the open air is strongly praised for such cases by Stokes. The digestive organs must be put right, and the heart preserved from every cause of embarrassment to its action. Stimulants are needful for the cardiac failure, and a diffusible stimulant may be kept at hand for the syncopal attacks. Coffee has been strongly praised by Des- nos and Huchard in the degeneration of smallpox. Hayden has found the nitrite of amyl of service in the paroxysms of rhythmical dyspnoea. It is equally useful in the at- tacks of suffocative oppression or anginal pain. Pain may be relieved by sedatives such as have been recommended for the pain in dilatation of the heart. But equal caution is needful respecting the use of opiates, especially by hypodermic injec- tion. I have known half a grain of mor- phia, injected hypodermically, followed by death, of which there was no premoni- tion. Ormerod relates a case in which the same quantity was taken by the mouth, and death occurred during the ensuing sleep. Chloroform should not be inhaled ; ether should be employed instead. In a large majority of cases of death while under the influence of chloroform, tatty degeneration of the heart has been found. Rupture of the Heart. This accident occurs in a considerable proportion of the cases of fatty degenera- tion, both simple and associated with overgrowth of fat. Conversely, fatty de- 1 Crisp, Treatise on the Bloodvessels, 1851, p. 363. 2 Sir W. Jenner, Address to the British Med Association, 1869. RUPTURE OF THE HEART. 821 generation is by far the most common cause of rupture. Spontaneous rupture never occurs in a healthy heart, and the number of cases due to any other cause, as abscess, or aneurism, or deep endocar- dial ulceration, is very small. Out of one hundred cases of rupture collected by Quain,1 in seventy-seven fatty degenera- tion was detected by the microscope, and of the remaining cases, in all but two either softening was noticed, or the state of the heart was not mentioned. It is thus probable that in at least nine-tenths of the cases of rupture fatty degeneration is the condition of the cardiac wall to which the accident is due. The degeneration which permits rup- ture is rarely uniform throughout the whole of the cardiac walls. Uniform de- generation causes uniform weakening; the force of contraction is lessened, and there is no spot specially incompetent to bear the lessened strain. It is when the degeneration, as is so commonly the case, is unequal, and especially when the de- generation in a limited area reaches a high degree, that rupture takes place. The contraction of the more healthy por- tions of the cardiac wall puts upon the more rotten portion a strain which the former can bear, but which the latter is quite unable to bear. This unequal change is the form which is associated, as its immediate cause, with local and de- generative, rather than with general or inflammatory causes. It rarely, for in- stance, results from the damage to the cardiac wall, from endo- and pericarditis, or from pyrexia; whereas it is common in the degeneration secondary to unequal fatty growth and infiltration, and still more frequent in that which results from vascular obstruction, chronic or acute. It is not uncommon to find a degenerated or thrombosed branch of the coronary artery going straight into a patch of in- tense fatty degeneration in which the rupture has occurred.2 The sudden oc- clusion of a vessel by embolism may cause a similar patch of softening.' There is another way in which rupture has sometimes been produced by the asso- ciation of diseased vessels and fatty change. The degenerated vessels may give way; the resulting extravasation readily tears its way in the softened tissue, and may reach the surface, being assisted, no doubt, by the contractions of the heart. The systole of the heart empties its ves- sels of blood, and when a hemorrhage has occurred into the substance of the wall, the contraction must compress the effused blood, and force it in the direction of least resistance. It is not uncommon to find more than one extravasation in the wall of the heart.1 Such hemorrhages are said to be sometimes the result of embolism. The chief other causes of rupture, an- eurism of the heart, cysts in its walls, &c., are considered elsewhere. The influence of the degenerative con- ditions is seen in the effect of age on the occurrence of rupture of the heart. The accident occurs chiefly in the old. Of the cases collected by Quain, two-thirds were over 60. The mean of forty-eight cases has been found to be 68 years.2 Most collections of cases have shown the acci- dent to be more frequent in the male sex, but Quain's statistics give an equal num- ber of cases in each sex. Occasionally, hereditary predisposition has appeared to influence the occurrence, and even the seat of rupture, perhaps by similarity of vascular distribution. A classical in- stance is the death of George II. and his relation, the Princess of Brunswick, of rupture of the right ventricle. In primary rupture of the heart the immediate cause of the tear is probably a contraction of undue strength, the strain upon the fibres being greater than the de- generated texture can resist. Thus the accident has commonly occurred during conditions of excited action of the heart, during unusual effort, such as running to catch a train, lifting a weight, cough, straining at stool,3 or during emotional excitement. Of twenty-four cases col- lected by Barth, in five death occurred during the act of defecation. Sometimes no undue exertion can be traced, the symptoms come on suddenly while the patient is at rest, even during sleep.4 All parts of the muscular substance of the heart are liable to rupture. It has occurred in the walls of each ventricle, of each auricle, in the septum between the ventricles, and in the papillary muscles. It is, however, far more frequent in the left ventricle than elsewhere. All statis- tics agree in showing that the left ventri- cle is the seat of rupture in three-quarters of the cases, and that it is at least twice as frequent in the anterior as in the pos- terior wall. The usual seat is near and parallel to the septum, and not far from the apex. About twelve per cent, of the cases occurred in the right ventricle, 1 Colin, Gaz. des Hopitaux, 1867, p. 104. 2 In the few cases on record of rupture of the heart at earlier ages, most were due to other causes than fatty degeneration. In rupture of the left ventricle, for instance, in a woman aged 49, described by Gregorie (Vir- chow. Jahresb. 1870), the cause was the per- foration of a circular ulcer, probably, since the woman was the subject of constitutional syphilis, due to a softened gumma. 3 Arch. G€n. de Med. 1871. 4 Quain, Path. Trans, i. 62. 1 Lumleian Lectures, Lancet, 1872. 8 Quain, Path. Trans, iv. 80. Simon, Berl. Klin. Wochenschrift, 1872, No. 45. 822 FATTY DISEASES OF THE HEART. about six per cent, in the right auricle ; while only two or three per cent, have occurred in the wall of the left auricle and in the septum. The size of the rupture varies from a point scarcely recognizable to an inch in length. It may be larger on the inner surface than on the outer surface. Some- times it is larger outside, and the inner opening may be small, and concealed among the columnte carnese. When the latter is the case, Blaud thought that the rupture had occurred from without in- wards. The course of the rent is often oblique, so that inner and outer openings do not correspond. It is usually parallel to the muscular fibres, less frequently across them. The rupture is usually sin- gle ; sometimes there are several partial ruptures, and one complete. A coagulum usually lies between the lips of the rent, and the cavity of the pericardium is usually filled with clot. A morbid state of the heart, to which the rupture may be ascribed, is always present. In the rare cases in which fatty degeneration or softening, or other change, has not been detected, degeneration of the coronary arteries has been found when looked for, and the rupture has probably been produced by interstitial hemorrhage. Symptoms.-Sudden, intense pain usu- ally marks the occurrence of the rupture. The pulse becomes at once extremely weak and irregular, and soon impercept- ible. There is pallor qnd coldness of the surface, consciousness is lost, the patient may vomit, respiration ceases, ami death occurs in a few moments. Sometimes consciousness is lost before any manifes- tation of pain can be made. The person falls, pallid and unconscious, a few breaths are drawn, and he is dead. In seventy- one out of one hundred cases of rupture, collected by Quain, death was thus rapid. Occasionally the patient lives for several hours, even for a few days, with intense cardiac distress, and evidence of cardiac failure. The pain may extend down the left arm, sometimes down the right arm also. Vomiting is troublesome, and has been referred to the irritation of the fibres of the pneumogastric by the slowly pro- gressing rent. It may be accompanied by diarrhoea so intense that an attack of cholera is simulated.1 In a few cases the course of the symptoms is less regular. Some improvement takes place, and then the symptoms recur. Walshe believes these stages represent the rupture of suc- cessive layers of the cardiac wall. In a case recorded by Crisp2 vomiting and pain for several hours were followed, before death, by the cessation of the pain. Five cases out of one hundred collected by Quain lived forty-eight hours. One lived a week. In some of the cases in which the patient lived for a few days the rup- ture was through the septum only.1 A case is on record of rupture through the posterior wall in which the patient lived for six days. When the patient lives sufficiently long to allow a physical examination of the chest to be made, the pulsations of the heart are found to be imperceptible, in- crease in the cardiac dulness may be rec- ognized just before death, or for some hours previously.2 Probably in such a case the rupture is at first small, blood escapes into the pericardium, slowly, and chiefly at the period of complete disten- sion of the heart, and the accumulation of blood in the pericardium lessens the de- gree of diastolic distension of the heart, and of the escape of blood. A fall of tem- perature of 3 j° C. was observed in Liou- ville's case. Rupture of the papillary muscles and chordae tendineae give rise to sudden but less urgent symptoms, and are described in the article on Diseases of the Valves of the Heart. Diagnosis.-From simple syncope, and from all forms of cerebral loss of conscious- ness, rupture of the heart is distinguished by the sudden, intense pain. Where pain is absent death is usually too rapid to per- mit diagnosis. The cessation of the pulse is peculiar to rupture, and distinguishes it from other less grave causes of cardiac pain, as angina pectoris. From rupture of an aneurism, that of the heart may be distinguished only by the rapidity of the symptoms, and by the absence of the physical signs of pericardial effusion. The pain and vomiting may cause a slow case to be mistaken for gastric disturbance ;2 the profound syncopal symptoms, and the seat of the pain should prevent such an error. Prognosis.-Complete rupture of the heart is of necessity fatal. It is rarely, indeed, that the occasion for a prognosis presents itself. In cases of slower rup- ture, where the tear is at first incomplete, the prognosis is scarcely less certain. No case is on record in which a spontaneous rupture has been shown to have healed. The manner in which wounds of the heart sometimes heal suggests the possibility of a like result in rupture ; but the diseased state of the walls which permitted the 1 De Barry, Arch. f. Klin. Med. vii. 152. 2 Liouville, Gaz. de Paris, 1868, No. 50. Simon, Berl. Klin. Wochenschrift, 1872, No. 45. 3 Thompson, Lancet, 1871, ii. 635. 1 Land, Norsk Maga, fiir Laegevidsk, Bd. 23, p. 103. Virchow, Jahresb. 1870, ii. 96. 2 Path. Trans, i. 62. FIBROID DISEASE OF THE HEART. 823 rupture seems to preclude any attempt at cicatrization. It is just possible, how- ever, that a partial rupture of a compara- tively healthy heart, by interstitial hem- orrhage, may, with careful treatment, heal. One or two cases are on record in which the symptoms of partial rupture passed away, and it is possible that they may have been of this character. Treatment. - In complete rupture death is too speedy to permit treatment. Where the symptoms are of slower prog- ress, and the rupture partial only, an at- tempt may be made to prevent its exten- sion. The tearing force being, in all probability, due to the contractions of the heart, these must be reduced to a mini- mum. Absolute rest should be secured. Aconite may be given for the double pur- pose of thus lessening the force of the heart, and of relieving pain. No stimu- lants should be given. Ice should be sucked and stimulating applications to the epigastrium, such as chloroform, or spongo-piline, or camphor liniment, may lessen the vomiting and afford some relief to the pain. There is only too certain reason to fear a steady increase in the symptoms. fibroid disease of the heart. W. R. Gowers, M.D. Synonyms.-Fibroid Infiltration; Fi- broid Transformation (Ormerod); Con- nective Tissue Hypertrophy (Quain); Cir- rhosis of the Heart; Induration of the Heart; Chronic Myocarditis ; Schwielen des Herzfleisches. Definition.-Fibroid disease of the heart, cardiac fibrosis, as it may be termed, consists in an increase in the interstitial connective tissue, without, or more com- monly with, a secondary atrophy of the muscular fibres. The change may affect the whole heart in slight degree, or a limited portion in a high degree. Increase in the interstitial fibrous tissue of the heart may result from chronic inflammation, and all forms of fibroid disease are, therefore, by some au- thorities, regarded as forms of myocar- ditis. But the condition may certainly arise by a slow chronic process, in which no characteristic of inflammation can be traced. History.-Induration of the heart, when considerable, is so obvious a morbid state that it early attracted attention. It is said to have been described in 1529 by Benivenius, a Florentine physician. Senac and Morgagni noticed its occur- rence. Fothergill recorded a case in which the heart was examined by John Hunter.1 Corvisart described an exam- ple in which the ventricles sounded like horn when struck, and grated under the knife. Laennec, Bertin, Bouillaud, Hope, all described it, and the last three ob- servers regarded it as an effect of chronic inflammation. Rokitansky described it in its relation to aneurism of the heart. Many cases have been brought before the Pathological Society, and the disease has been the subject of special study in this country by Quain1 and Hilton Fagge,2 in Germany by Skoda,3 Dittrich,4 and Skrzeczka,5 and in France by Pelvet.6 Etiology.-The causes of fibroid de- generation are still little known. It is certainly more frequent in men than in women, and chiefly occurs during or after middle life. The right side of the heart is said to be affected occasionally in foetal life. It is not commonly associated with fibroid degeneration of other organs, and it seems not specially related to the habits or conditions of life of the individual. Walshe believes, however, that it is some- times due to chronic alcoholism. Its oc- currence is chiefly influenced by local causes. Long-continued intermitting con- gestion of the heart causes, as Jenner7 showed, toughening and induration of the organ, with increase in the interstitial tissue. The frequent existence of fibroid 1 Lumleian Lectures, 1872; Lancet, 1872, vol. i. 2 Path. Trans. 1874, p. 64. 3 Wiener Wochenschrift, 1856. Med. Zei- tung, 1869. 4 Prager Vierteljahreschrift, 1852. 6 Virchow, Archiv, 1857, xi. 176. 6 Des An^vrysmes du Cceur. Paris, 1867. 7 Med.-Chir. Trans, xliii. 1 Med. Obs. and Inq. v. 1774, p. 252. FIBROID DISEASE OF THE HEART. 824 overgrowth in hypertrophy of the heart is probably due to the congestion which results from the cause of the hypertrophy. Local inflammation may result in fibroid change, as in the superficial layers of the heart after pericarditis. Where the fibro- sis is limited in area, it has also been ascribed to an extension to the wall of adjacent endo- or pericarditis, but Hilton Fagge has suggested that the traces of inflammation which are found may be secondary to the fibroid change, and can- not be taken as proof of such an origin. Injuries, blows on the precordial region, have been assigned, in some cases, as the cause of the symptoms. Lastly, there is clear evidence that syphilis is capable of causing local indurations of the heart; most probably by the transformation into fibrous tissue, of gummatous growths. Pathological Anatomy.-The slight- er diffused form of fibrosis may affect the whole heart, or only one chamber. The intenser form is usually limited to a por- tion of one chamber. Occasionally a high degree of fibroid growth may extend around the heart, and has been described as a true "stenosis of the heart."1 In the fibroid change secondary to pericar- ditis the outer layers of the heart are most affected, and sometimes one-half of the thickness of the wall may be trans- formed into fibrous tissue. The local forms of fibrosis affect the papillary muscles more frequently than any other parts. These may be entirely transformed into fibrous tissue of tendinous aspect. More rarely the wall of the heart is the seat of circumscribed changes, es- pecially the neighborhood of the apex. They are also found in the septum, and in the posterior wall at the base. In the right ventricle the degeneration is usually near the base. The local forms are com- monly most marked towards the inner surface of the wall. If the -whole thick- ness of the wall is affected, it is rendered thinner, even apart from aneurismal bulg- ing. The endocardium over the degene- ration is often thickened. The diffuse fibrosis renders the wall of the whole heart tougher, more resistant to the fingers and knife. Sometimes, when the new tissue is soft, and the mus- cular fibres are degenerated, the consist- ence may not be increased, may even be diminished. The change may alter very little the naked-eye appearances, or the enlarged intermuscular septa may be visi- ble in the cut section. The localized change usually presents a glistening fibrous appearance, gray or white, sometimes of a greenish or bluish tint. The section may have a spongy appearance. (Hilton Fagge.) Where" less advanced, whitish bands and tracts of fibrous tissues may be seen in the muscular substance. In some cases several separate areas are affected. Occasionally calcareous deposits have been found in the changed tissue. Under the micioscope the localized forms present well-developed fibrous tis- sue with nuclei. In more recent cases a fusiform cell-growth has been found, de- veloping into fibres. It is said to begin around the bloodvessels, in the intermus- cular septa, with an infiltration of nuclei and leucocyte-like cells. Sometimes, it is said, the new substance appears very ob- scurely fibrillated or amorphous, and may undergo fatty degeneration. Pelvet has seen much elastic tissue in some speci- mens. Through the fibrous tissue the muscular fibres may be seen passing, lessened in number, sometimes narrowed by pressure, or the seat of fatty degenera- tion. It is rare for them to disappear entirely. Occasionally the degeneration is in excess of the development of fibrous tissue, and the affected area softens. Consequences.-The effect of fibrosis on the form and size of the heart varies. Hypertrophy and dilatation usually co- exist with the diffuse change, and some- times the overgrowth of the muscular and fibrous tissues, advancing pari pat-su, may enlarge the heart to vast dimensions, as in the specimen preserved in St. George's Hospital and described by Quain.1 The increase in the fibrous tissue which re- sults from congestion is commonly greater in the right ventricle than the left. Lo- calized fibrosis also often occurs in hyper- trophied hearts, although it may be found in hearts which are normal in size. The cavity may present little change, or it may be generally dilated. More com- monly the wall of the affected spot is bulged out into an aneurism. (See Aneu- rism of the Heart.) Symptoms. - The necessary effect of fibrosis of the heart will be, as Corvisart clearly taught, to lessen its contractile power. The diffused form, therefore, pro- motes dilatation or lessens the effects of the hypertrophy which it accompanies. The symptoms of the localized form, in marked cases, have commonly been those of cardiac weakness. Dyspnoea and dropsy have been the chief troubles, and in their general character the symptoms resemble those of dilatation of the heart. The im- pulse is weakened.2 The first sound is 1 Lumleian Lectures, loc. cit. 2 Laennec taught that induration increases the firmness of the heart's contraction ; but this was probably a hasty conclusion from the firmness of hypertrophied and strongly- contracted hearts. 1 Dittrich, loc. cit. FIBROID DISEASE OF THE HEART. 825 weak and toneless, and it has been no- ticed to be much weaker over the left than over the right ventricle, when the former was most affected. A systolic murmur has been present in many cases, due, in some, to regurgitation from fibro- sis of papillary muscles. The pulse is weak, and has been, in some cases, very infrequent; only thirty beats per minute have been noted. Cardiac pain is present in a considerable number of the cases. In many instances, however, the symp- toms have been entirely latent. These differences depend no doubt partly on the extent and position of the fibrosis, affect- ing the action of the rest of the muscular tissue more in some cases than in others. Death in many instances has been sudden, apart from the rupture, or even the exist- ence of an aneurism. Diagnosis. - Fibroid degeneration of the heart is at present hardly more than a pathological curiosity, for it is doubtful whether it has ever been recognized dur- ing life. Its detection, apart from the signs of aneurism of the heart, must de- pend on the symptoms of cardiac dilata- tion without its physical signs. Treatment.-The treatment needed is that for cardiac weakness-for the dila- tation which it resembles in its effects. Rest, the avoidance of all strain on the circulation, and the administration of digitalis, to strengthen the remaining fibres, are the chief measures. If there is any suspicion of syphilis, iodide of po- tassium should be given, although it is doubtful whether the stage of induration can be modified by that drug. DISEASES OF THE ORGANS OF CIRCULATION.-Continued. B. Associated Organic Changes. Mediastinal Tumors. ON MEDIASTINAL TUMORS. By R. Douglas Powell, M.D., F.R.C.P. The Mediastinum is that central space situated behind the sternum and between the pleurae which is occupied by the heart and'the great vessels connected with it, the trachea and its main divisions, the pneumogastric and phrenic nerves, and the thymus and bronchial glands. Tiie lungs with their pleural coverings are closely applied on either side of this region, their anterior margins overlapping it in front to an unequal extent on the two sides, so that in health the dulness on percussion that the solid contents of the mediastinum would naturally yield is in a great measure obscured, and permitted to become apparent only at the upper part of the sternum and over the triangular area of the heart's dulness. In emphy- sema of the lungs the mediastinum may be yet more completely covered up ; in other pulmonary affections attended with diminution of bulk, it may become un- covered on one side or on both, giving rise to some singular, and at times perplexing, distortions of the mediastinal dulness without any corresponding disease within the space itself. The division of the in- terpleural space into anterior and pos- terior mediastinum is entirely arbitrary, the former term being loosely applied to that portion of the space in front of the trachea and the roots of the lungs, the latter to that portion situated behind this plane. The mediastinum is in health altogether obscured to us from behind by the spine and the thick posterior margins of the lungs closely in contact with it. Our present concern being only with morbid growths affecting the mediasti- num, we shall refer to such other diseases as aneurism, abscess, pericardial effusion, &c.,-only in so far as they affect diag- nosis. Varieties, Etiology.- Carcinoma,' sarcoma, and lymphoma are the three varieties of morbid growth which may give rise to tumor in the mediastinum. Since the time, only a few years ago, when attention in this country began to be more closely directed to the finer distinc- tions, based on anatomical structure, which separate true cancers from other tumors, and these from one another-an inquiry first entered upon by Professor Virchow, and largely stimulated and promoted by the labors of the Morbid Growths Committee of the Pathological Society of London-the rarity of primary carcinoma of the mediastinum has be- come more evident, and a large propor- tion of the cases that only a short time ago were designated scirrho-encephaloid, or scirrhous, or soft cancer, would now be classed amongst the sarcomata or the lymphomas. Still, cases of true cancer primarily affecting the deep-seated parts of the mediastinum do now and again oc- cur ; e.g., one such case is recorded by Dr. C. T. Williams in the Pathological Transactions, vol. xxiv., its cancerous nature being confirmed, on minute ex- amination, by Mr. Arnott. Even as a secondary growth, cancer rarely affects the mediastinum, save when, as, however, not uncommonly happens, it directly pene- trates through the chest wall from a can- cerous breast. Sarcoma, too, as a primary disease, is most rare in this situation ; when it oc- curs it usually arises secondarily to some similar or associated growth situated i Throughout this article the terms "carci- noma" and "true cancer" are applied to that form of new growth whose typical structure is met with in the scirrhous breast. 826 ON MEDIASTINAL TUMORS. 827 elsewhere. Nor is it always clear how a secondary growth arises in the mediasti- num ; its path of transmission is not in all cases evident. We cannot always ob- tain evidence of a lymphatic connection' between the primary and secondary growths, nor, on the other hand, is it easy to see how a disease germ could be conveyed from a distant part to the medi- astinum through the circulation without first involving the lung; and in view of this difficulty, it is worthy of remark how frequently the disease, although mainly mediastinal, involves also one lung to a greater or less degree. It is very possible that, in some of these cases, the secondary growth may have really been conveyed to some portion of the lung or pleura first, and formed a small nodule there ; but that, the bronchial glands becoming early infected, the disease in them proceeds with such great rapidity as soon to out- strip and obscure its pulmonary origin, and to give the case the clinical and even post-mortem features of primary mediasti- nal disease subsequently involving the lung. This explanation at least occurred to me as best accounting for a case of osteo- sarcoma of the mediastinum and lung, occurring subsequently to the removal of a shreddy sarcomatous growth from the knee-joint.1 There will always remain, of course, the possibility of the disease of the mediastinum, though secondary in point of time, being due to a recurrence or a continuance of the same constitu- tional dyscrasia which led to the produc- tion of the first. Experience has, how- ever, of late years, gone against the validity of such an hypothesis. Of morbid growths affecting primarily the mediastinum, lymphoma or lympho- sarcoma, or, as it is sometimes designated, lymphadenoma, is by far the most com- mon. It was Dr. Murchison who first recognized lymphadenoma as a distinct variety of morbid growth, in a case of disease affecting the intestines, liver, mesentery and heart, &c., which he brought before the Pathological Society of London in November, 1868,2 and of the minute character of which an ample report is appended to his description by the Morbid Growths Committee. In the same volume, p. 102, Dr. Church has also described a case of "Carcinoma of the pericardium, anterior mediastinum, and lymphatic glands, in the thorax and ab- domen," which he recognized as different in minute structure from true cancer, and regarded as more correctly "ranked among the mediastinal sarcomatous tu- mors mentioned by Virchow3 as approach- ing so closely to the structure of lymphatic glands as to be with difficulty separable from them." In the next volume (xxi. of the Transactions, p. 358), is recorded as such by myself the first case of lympho- sarcoma or lymphadenoma of the medias- tinum, although there are many cases in earlier volumes related as instances of cancer which would be undoubtedly more correctly included under the newer term. In subsequent volumes examples of the disease are given by Drs. Murchison, Ben- nett, Payne, Dickinson, and others. In most cases, the growth originates in the lymphatic glands, either in the ante- rior mediastinum or at the root of the lung, the connective tissue surrounding the glands becoming quickly implicated. In a case, however, reported by Dr. Church, and in another by myself, the thymus gland appeared to have been the original seat of the disease. The growth invades other tissues, the neighboring glands, the lungs, the heart, and even the vessels. It does not, however, incorporate to itself with the same avidity as cancer does all the tissues with which it comes in contact, but prefers to creep along the bronchial or vascular sheaths, and to in- volve organs more slowly, guided by the lymphatic paths into their interior. The calibre of large bronchi, veins, or even the auricles of the heart, may, however, be invaded by flattened projections of this growth, which by the unaided eye could not be distinguished from cancer. As a local disease, then, lymphoma in this situation is decidedly malignant, but in an intensity rarely as great, and some- times much less, than that of cancer. It is sometimes, however, a part of a more general disease, affecting more or less the whole glandular system, and in one re- markable case, which was for several months under my observation both as an out-patient and in the wards of the Bromp- ton Hospital, and which subsequently terminated fatally in the Middlesex Hos- pital under the care of Dr. Murchison,1 the disease, mainly affecting the glands of the neck, mediastinum, and axilla, and the spleen, was marked by periodical at- tacks of fever, accompanied by intumes- cence of all the affected glands and of the spleen, which gave to it an altogether peculiar character. After death, almost every organ was found disseminated with lymphatic growths identical in structure 1 A description of the clinical characters presented by this case while in the Middlesex Hospital, with an account of the autopsy and an admirably summary of the literature of the subject, is given by Dr. Murchison in the Path. Trans, vol. xxi. p. 372, and to it is appended an account of the microscopical ex- amination of the diseased structure by Dr. Sanderson. 1 Path. Trans, vol. xxiv. p. 28. 2 Vide vol. xx. p. 192. 3 Die Krankhaften Geschwulste, Band ii. p. 376. 828 ON MEDIASTINAL TUMORS. with those already described. In this case then was seen exemplified the highest degree of malignancy conceivable, only comparable to that of disseminated cancer or miliary tuberculosis. Age. - Growths in the mediastinum may be met with at almost any period of life, but they are more prevalent before the middle period ; and it is useful to re- member this fact, since, if we meet with a case of mediastinal tumor of doubtful nature in a patient under the age of 25, it is more likely to be malignant than aneu- rismal, this probability being increased as the age is earlier. Of six cases which have fallen under my personal observa- tion, all but one were under 30-viz., one at the age of 6, two at 20, one at 27, and one at 29 ; the sixth case being aged 49. Of seven cases specially referred to by Dr. Bennett as mediastinal, two occurred at the age of 11, one at 17, one at 20, one at 23, one at 40, and one at 60. So that if we might fairly strike an average from such limited numbers we should get 24'8 as the mean age for the occurrence of this disease. Sex.-As regards Sex, five out of Dr. Bennett's seven cases quoted were fe- males, and five of my six cases were also females. On the other hand, however, of six cases specially referred to by Dr. Symes Thompson in a pamphlet on Me- diastinal Tumors, published in 1865, all were of the male sex. We must, then, for the present, say that these growths may occur in either sex, with perhaps a slight preponderance in favor of the fe- male sex. When a mediastinal growth invades the lung secondarily, it appears to have a special but not exclusive prefer- ence for the left lung, the other lung as a rule wholly escaping. In four of Dr. Ben- nett's cases one lung was invaded, and in each instance the left. Of the three of my cases in which one lung was invaded, it was in two instances on the left side. Symptoms.-The Symptoms of medias- tinal tumors are little influenced by the kind of growth (and the same remark ap- plies to physical signs), they are due to compression or obliteration of vessels and nerves, of the air-tubes or (esophagus, or to the invasion of the heart or the lungs or other structures on the confines of the space. They therefore closely resemble those presented by aneurismal tumors, and the diagnosis between the two is often perplexing. In cases of tumor, deep-seated pain in the chest or back is not so prominent a symptom as in aneurism ; there is often no pain experienced until the growth ap- proaches the surface, when it assumes the pleuritic character. The characteristic stabbing pain of cancer is occasionally complained of. If it is borne in mind that malignant growths, cancer, lymphoma, sarcoma, differ from aneurismal tumors hi two important respects-viz. (a) they tend to incorporate to themselves the structures they encroach upon, thus in- vading and replacing more, and com- pressing and displacing less than aneu- rism ; and (b) a change in the direction of expansion, so common in aneurism, is much less so in them, and is not attended with that relief to symptoms dependent on local removal of pressure-it will be more readily understood why the pressure symptoms should as a rule be more insidi- ous, yet when present more constant and persistent with them than with aneurism. The Dyspnwa depends upon the size and seat of the tumor, and increases day by day with its growth ; but severe par- oxysmal attacks of dyspncea are occasion- ally witnessed in tumor as in aneurism. These paroxysms are usually due to direct pressure upon the trachea or a main bronchus, and are more frequently ob- served among the later symptoms of the disease. Cough, dry, ineffectual, or at- tended with only scanty mucous or frothy expectoration, is an early and very con- stant symptom, and, together with a cer- tain sense of constriction or pain about the sternum, constitutes the complaint for which the patient usually first seeks ad- vice. The cough may have a clanging laryngeal character, and may be attended with huskiness of voice or aphonia. These symptoms are, however, less frequent than in aneurism. Sanguineous expectora- tion may be present, and is a sign that the tumor has invaded the lung. Profuse hcemoptysis is rare, but has been met with as an early symptom. In the later stages of the disease profuse hjemoptysis some- times occurs, and is followed by marked relief to pressure symptoms ; it then be- comes an important sign of tumor. In a large proportion of cases, however, no haemoptysis occurs throughout the disease. Dysphagia is in mediastinal growth a far more common and prominent symptom than in aneurism. It is more constant when present, although, as in the case of dyspnoea, it too may be increased by paroxysms, more especially in the earlier stages of the disease. Physical Signs.-At the time of seek- ing advice patients with mediastinal tumor are not as a rule emaciated ; they often indeed appear to be well nourished, although on inquiry it will be invariably found that they have of late lost flesh ; nor do they ever evince as the disease progresses that degree of emaciation so commonly seen in chronic phthisis, save in those cases in which the oesophagus is involved or pressed upon. The face is PHYSICAL SIGNS. 829 usually pale, with often some lividity of lips, and in most, perhaps in all instances, there is a certain anxiety of expression, a slight contraction of the brow, giving an aspect of distress which is often sufficient to mark off the case as one not of ordinary chest disease. A slight staring of the eyes, with noticeable puffiness of face, commonly present, may, as the disease advances, be intensified into the aspect of semi-strangulation, characteristic of a tumor pressing upon the great veins. The temperature, unless there should be some inflammatory complication, is not raised. In the exceptional case already referred to the periodical attacks of fever were but phases in the progress of a gen- eral disease affecting the whole glandular system. In further considering the physical signs of mediastinal tumor it must be re- membered that, as has already been in- cidentally remarked, these growths very commonly involve sooner or later one of the lungs. The lung thus secondarily affected is most frequently, but not al- ways, the left. On inspecting the chest, some alteration in shape is frequently to be observed. The upper sternal region may be unduly prominent, or one side of the chest may be both to eye and measurement larger than the other, the enlargement being perhaps more decided above than below the nipple level. The side, however, which yields most evidence of disease is not always the larger, it may be smaller, to measurement; and this negative sign, taken with other positive ones, e. g., dis- placement of heart, would be very signifi- cant of tumor. Cases have been observed by Dr. Pollock, Mr. Holmes, and others, in which the tumor has projected through the sternum and cartilages. Some en- larged glands at the root of the neck, or in the axilla, mobile in adenoma, fixed in cancer, may give us a clue to the nature of the disease. The superficial veins of the chest are frequently found distended, more frequently and more decidedly so than in aneurism. They may be more distended on one side of the median line than on the other, and one upper ex- tremity may show venous obstruction and cedema. Displacement of heart is one of the most important signs of intra-thoracic tumor ; it is a result of direct pressure, and its direction is, generally speaking, deter- mined by, and is an important index of, the seat of the tumor. The growth may occupy the upper part of the anterior mediastinum, and extend downward in front of the pericardium, covering it with a thick, solid apron, or, growing from be- hind, it may push forward the heart against the sternum ; or again, encroach- ing forwards from the root of the lung (a common site) between it and the pericar- dium, it may press aside the heart. We should endeavor, therefore, in all cases, by palpation and auscultation, to ascer- tain the exact and relative position of both the apex and base of the heart. In certain rare cases-one such came under my notice in Dr. Cotton's wards, at the Brompton Hospital, in 1866-the heart is fixed in situ by the growth extending on both sides of it. The mediastinal growth may extend downwards between the lung and heart to the diaphragm, forming a large mass between it and the base of the lung. Some downward displacement of the liver or stomach, with hardness and bulging of the hypochondrium, are then to be observed. Increased dulness on percussion is an essential sign of mediastinal tumor. It may amount to only a patch of lessened resonance at one sterno-clavicular angle or in one interscapular space, or there may be three or four square inches of dul- ness over the upper sternum continuous below with that of the heart area. Again, the toneless percussion may and often does extend beyond the confines of the mediastinum, so as to include the whole or a greater part of one side ; in consequence of the growths involving by direct invasion, or indirectly, by the de- struction of its main bronchus, the lung on one side. Several questions in diag- nosis arise from this fact, and it is curious how invariably the disease in such cases is mainly one-sided, and how frequently the other lung altogether escapes. Sup- posing the dulness to be thus extended, its quality and distribution become mat- ters of great importance in diagnosis. Its quality is essentially hard and resisting-• often unequally so at different parts, so as to have a lumpy character, being more toneless and resisting over small scattered areas than in the intervening parts. Above the clavicle, in the outer scapular region, and at the acromial and axillary regions of the chest, a resonant note may still be obtained-in fact, a mediastinal growth, when it invades a lung, almost invariably does so from its hilus, extend- ing out yards so as to occupy the whole middle part of the lung, coming to the surface in rounded prominences and leav- ing the remoter "corners" of the thorax, so to speak-the summit, humeral, and scapular regions, and the base-to be last involved. It will be remembered that in pleural effusion the dulness advances steadily from below upwards, the circum- ferential parts of the chest first becoming toneless, the central-sternal and inter- scapular regions-being last affected. Displacement of heart away from the affected side is common to both condi- tions. If the base of the lung, however, becomes the seat of secondary pneumonia, 830 ON MEDIASTINAL TUMORS. or is collapsed by some attendant effusion, the validity of the contrast just drawn is somewhat obscured. On auscultation the heart's sounds are found to be unduly conducted over the dull region in front and too audible in the interscapular region behind. When the tumor is mainly seated in the anterior mediastinum, the conduction of the heart's sounds may be intense in this region, and may be attended with an impulse dis- tinctly appreciable to the ear. The im- pulse is, however, in such cases knocking, not expansile ; but it sometimes closely resembles that yielded by an aneurismal sac thickly lined bycoagulum. A systolic murmur is sometimes audible over some portion of the dull region; it has, how- ever, the simple, short, blowing character distinct from the rasping or expansive bruit which would most likely accompany an aneurism of similar superficial dimen- sions. In cases of tumor growing from the posterior mediastinum, the heart pressed against the sternum may yield to the ear a very peculiar sensation, analo- gous to that experienced by the hand when laid upon a struggling bird. In an ob- scure case which came under my notice three years ago, the presence of this sign, together with displacement of the apex towards the ensiform cartilage, enabled me correctly to surmise the nature of the case before any other positive sign could be detected. The pericardium and the heart, more particularly one of the auri- cles, very often become involved in the growth, and a cardiac murmur or friction sound may thus be given rise to. The respiration is commonly bronchial over the tumor, or it may have a stridu- lous or sibilant character. Stridor is less common than in aneurism, and for the reason before named, that growths tend to occlude rather than compress the tubes with which they come in contact. The observation of very well marked stridor has so often led me carefully to examine for a tumor which has proved not to exist, that the sign has, for me at least, lost much of the value often ascribed to it. Still it would not be safe to disregard it, especially when localized at one part of the chest. When the growth, however, occupies the anterior mediastinum, and is of considerable thickness, no respiratory sound may be audible over it, more or less bronchial respiration and rales being heard in the outer subclavicular regions. It is indeed in parts of the chest distant from the tumor in the mediastinum that we often get auscultatory signs most sug- gestive of its presence, e. g. there may be observed at one base marked feebleness of respiration, amounting to a mere mus- cular struggle without any accompanying respiratory sound, yet the percussion dul- ness is perhaps little if at all impaired. quite insufficiently so for effusion ; there is no tegophony, the vocal resonance is diminished, or altogether annulled. On the opposite side the respiratory murmur is normal or exaggerated. Here is a grouping of signs very confirmatory of a tumor compressing or obliterating a main bronchus. When the dulness extends from the mediastinum over one side of the chest, it is accompanied by enfeebled or even annulled respiration, and we may have many of the signs most significant of fluid effusion into the pleura-displacement of heart dulness, absence of respiration, and even of vocal fremitus, with enlargement of the side. The diagnosis between the two is only made with extreme difficulty, and without puncture of the chest, is often indeed impossible. In this dilemma, however, attentive auscultation will often discover here and there over the affected side a slight grating friction sound, a sign which becomes of the greatest import- ance, showing the pleural surfaces still to be in apposition. Moist rhonchi-mucous or gurgling rales-are never to be heard in any abundance over the dull region, as would be almost inevitably the case in any simi- lar extent of consolidation from scrofulous disease. This remark is not the less true al- though after death we do occasionally find softened patches in a lung which has be- come invaded by a growth, the softening having as a rule been preceded by oblite- ration of the bronchi leading to them, so that they yield no sign during life. In- deed, on making a section of a lung whose root has been invaded by a tumor, we frequently find a striking appearance as of multiple abscesses dispersed through the organ, and the condition has been re- peatedly so described. In truth, how- ever, these "abscesses" are generally nothing more than bronchial tubes which have become enormously distended with secretion in consequence of obstruction at the main bronchus, collapse and slow in- flammation of the surrounding pulmonary tissue being also present. The distended tubes, with their opaque contents, shine through the pleural surface of the lung as yellow spots, giving to it a remarkable appearance. No doubt some of the alveoli become filled and yield before the accu- mulating pressure of the bronchial secre- tion. Sir George Burrows many years ago related, to the Medico-Chirurgical Society, a case of carcinoma of the lungs in which the right bronchus was ob- structed, and some bronchial tubes in dif- ferent parts of the lower lobe "when cut across were found distended with thick, yellow, tenacious pus, giving the appear- ance of small abscesses." A typical case of the kind, too, is described by my col- DIAGNOSIS. 831 league, Dr. C. T. Williams, in the twenty- fourth volume of the Pathological Trans- actions, and I have seen other instances, the most remarkable one being from a case of aneurism compressing the left bronchus, of which I made the autopsy in July, 187u. An extract from my note- book states as follows :-" Left lung very large, consolidated throughout. Bron- chial tubes much congested and dilated, many presenting terminal dilatations, filled with muco-purulent secretion. Lung studded throughout with nodules of yellow pneumonia, having for their centres bron- chial tubes which exude their secretion on pressure. Surrounding these nodules the tissue is in a condition of gelatinous pneu- monia, so that the total result is a solid lung. Some of the broncho-pneumonic centres have broken down into small cavi- ties filled with muco-purulent fluid. Right lung healthy, but in a state of active congestion. Dr. Budd1 regards the secondary in- flammatory changes-thickening and ad- hesion of pleura, and inflammatory de- struction of lung-that occur in a lung whose root is invaded by cancer as due, not to irritation of the invading new growth, for cancer per se has little ten- dency directly to cause inflammation of the surrounding parts, nor for the most part to obstruction of veins and arteries (pulmonary and bronchial) which might cause gangrene or atrophy of the lung, but he thinks that these changes result "from the tumor involving and destroy- ing all or a great part of the nerves with which the several tissues are furnished." In one of his cases Dr. Budd regards the pericarditis present as due to the same cause. I have seen one case to which this explanation might very well apply. It was one that occurred at the Brompton Hospital under the care of Dr. Pollock in 1868, in which there was found after death a tumor invading the left lung from its root to about one-third of its extent, the rest of the lung being shrunken from inflammatory softening; encroaching upon the summit and also upon the base were found two pleural cavities occupied by purulent fluid : the left main bronchus was almost, but not quite, obliterated by the growth. It is readily conceivable that partial destruction of the pulmonary nerves may, by lowering the vitality of the lung, render it more liable to the oc- currence of inflammatory changes, and that complete destruction of these nerves at their origin might directly induce in- flammatory destruction of the organ. In the main, however, I should feel disposed to regard the mechanical obstruction at the main bronchus as being, in most cases, sufficient to account for such sec- ondary lesions as we find. In some of the cases which I have quoted the secre- tion from the bronchial membranes went on with a vigor undiminished by any im- pairment of nervous influence, and the pneumonic changes present were, appa- rently, directly due to obstruction to the escape of this secretion. It is very possi- ble that pressure upon the nerves may give rise to muscular paralysis of the bronchial tubes, as suggested by Dr. Bennett, without affecting their secreting power. Diagnosis.-In relating the symptoms and signs of mediastinal tumors in the present chapter and in the succeeding section on aneurism, much has been said incidentally respecting the diagnosis of these tumors from other diseases. We have still, however, to summarize and dis- cuss the most important difficulties that may arise in the way of diagnosis. These difficulties vary somewhat, according as the disease is (a) purely mediastinal, or (6) involves the lungs secondarily. (a) Growths which are purely or mainly mediastinal may closely simulate aneu- rism. The following are the chief con- siderations which would tend to decide the question in favor of the tumor being a morbid growth :- The age of the patient being under 25. The presence or history of tumors else- where. The absence of marked disease of the vessels. The absence of characteristic pulsation or bruit, especially when combined with The presence of local venous engorge- ment, and Extensive area of superficial dulness. "Extensive area of dulness must in aneurism mean a large sac, and with such a large tumor we should almost inevitably get marked expansile pulsation. Again, aneurismal sacs, before they produce ex- tensive dulness of any portion of the parietes of the chest, point, as it were, in some particular direction, becoming dis- tinctly prominent and producing an ec- centric motion around them in conse- quence of the thoracic parietes being ab- sorbed, or yielding at the point of greatest pressure."1 In the early stages, however, of the disease, it may be extremely difficult, nay, impossible", to make the diagnosis with certainty. We must duly consider and weigh the probabilities in each case, there being no further rules of sufficient general value to be worthy of mention here. 1 "On some of the effects of Primary Can- cerous Tumors within the Chest." Med.- Chir. Trans, vol. xlii. 1859. 1 Graves' Clinical Lectures, 1848. 832 ON MEDIASTINAL TUMORS. Mediastinal abscess is very rare, at least of such dimensions as to simulate tumor. Such an affection would usually be accom- panied with scrofulous abscesses else- where, and probably with hectic symp- toms. Sub-sternal thickening may cause many of the signs of tumor, particularly when associated, as in one case which has been for some time under my notice, with oesophageal spasm. The effect of treat- ment (antisyphilitic) upon such cases soon discovers their real nature. A variety of chronic pericarditis has been described by Prof. Kussmaul1 under the name of callous mediastino-pericarditis, in which the pericardium becomes greatly thickened and its cavity completely oblit- erated by the tough products of a chronic inflammation, which, moreover, extends to the cellular tissue of the mediastinum, indurating it and surrounding the great vessels with a contractile tissue which constricts and distorts them. The in- creased mediastinal dulness and other signs attendant upon this condition closely simulate those of tumor, but Kussmaul states that there are two signs which are characteristic of this lesion,-viz., a com- plete, or almost complete, failure of the radial pulse during inspiration, and, simultaneously, visible swelling of the great veins of the neck instead of the collapse that usually takes place during this portion of the respiratory act. Ad- hesion of the great vessels to the sternum, either directly or through the medium of the pericardium, is supposed to account for these phenomena. Certain cases of phthisis, in which chronic disease at one apex has led to exposure of the mediastinum from retrac- tion of the margin of the lung on one side, may be mistaken for mediastinal disease. Such cases, however, especially some cases of so-called senile phthisis, are more apt to be confounded with cancer of the lung or with aneurism. They have al- ready been referred to in the previous chapter. (6) A mediastinal growth secondarily invading the lung on one side may pre- sent more difficulties in the way of diag- nosis than one more strictly confined to its original site. Deeply seated, invading the lung at its hilus, and, as it were, functionally choking it, such a tumor may simulate chronic pneumonia, local or general empyema, or aneurism of the de- scending aorta. The close resemblance between certain cases of mediastinal growth spreading through a lung and effusion into the pleura has already been referred to. The signs in favor of tumor may be thus summarized :- 1. An unconformity of increased meas- urements to those which would be occa- sioned by fluid accumulation. 2. The presence of large tortuous veins and oedema of upper extremities or head. 3. Dulness marked at the mediastinal region becoming less uniform in tone and firmness at the circumferential parts of the chest, where patches of resonance may be found which could hardly coexist with fluid. 4. The loud transmission of the heart's sounds (Walshe). 5. The detection of pleuritic friction- sound over parts dull on percussion. (It must be remembered that there may be some effusion which has supervened upon the mediastinal disease, and that this effusion may be general or limited.) 6. Haemoptysis or "currant-jelly" ex- pectoration would negative the disease being one simply of effusion. 7. The presence of the signs of pressure upon central parts (Walshe). This last-named consideration is cer- tainly of value, but it may mislead ; e. g., I have myself seen two instances in which considerable effusion into the pleura has been attended with that peculiar laryn- geal cough and husky voice which I re- garded as significant of tumor in addition to the effusion, and which in one case led others of great experience also into the same error. These signs both, however, disappeared after the removal of a large quantity of purulent fluid. Another pressure sign I have seen exemplified in a case of simple effusion, which might sug- gest some associated mediastinal tumor, though more probably of aneurismal than malignant kind, viz., increased size, tor- tuosity, and throbbing of the radial and brachial arteries on the affected side. The case was under the care of my colleague, Dr. Tatham, and the best conclusion we could come to was that the phenomenon was due to hardening and hypertrophy of the vessels from increased resistance to circulation through them, in consequence of impediment to venous return from the limb. There was no oedema of the limb, however, and after the removal of the fluid the thickening remained ; no sign or symptom of tumor has since occurred. 8. In all cases of doubt, and when the dyspnoea is at all urgent, an exploratory trocar should be inserted. Cases of mediastinal growth invading the lung from its root have often been mistaken for chronic pneumonia. Dr. Walshe lays stress upon the follow- ing signs as distinguishing tumors from chronic exudative pneumonia :-1 1 Berliner klinische Wochenschrift, 1873, Nos. 37, 38, and 39. An abstract of these papers is given by Dr. M. Bruce in the Medi- cal Record for December 17th, 1873. 1 Diseases of the Lungs, 4th Edition. DIAGNOSIS. 833 1. A tendency to increase instead of | diminution of bulk of the affected side. 2. Implication of the mediastinum. 3. The more serious change in the re- sults of percussion. 4. Emaciation is of earlier appearance and more marked in chronic pneumonia than in tumor. 5. Dyspnoea out of proportion to extent | of consolidation favors the diagnosis of tumor. These five signs would be of equal I value in distinguishing between chronic pneumonia in its less restricted sense of chronic inflammatory consolidation of the lung affecting the lower lobe, and medi- astinal growths secondarily affecting the lung. Dr. Walshe gives three further distinctions, viz.:- 6. The failure or disappearance of vocal fremitus, ■which remains in chronic pneu- monia ; 7. The different characters of respira- tion in the two diseases ; 8. The presence of haemoptysis and red jelly-like expectoration which never occur in chronic pneumonia. These do not, however, help us in eliminating those chronic basic consolidations which do not clear up, and which are therefore most apt to come before us for diagnosis from tumor. I have for instance so repeatedly I seen cases of chronic pneumonia in which I from great thickening of the adherent pleura the vocal fremitus has been much deadened or almost annulled, that I can- not but regard the distinction No. 6 as apt to mislead. The respiration, too, in such cases is remarkably feeble. The di- agnosis would, under such circumstances, be cleared up in favor of tumor by finding with these signs tolerably limited to the lower lobe the heart displaced towards the opposite side. I have had also under my observation for some years a patient with consolida- tion of the base of the right lung who has had decided haemoptysis on several occa- sions, and two years ago he expectorated a currant-jelly-like sputa more or less con- tinuously for nearly three months, which induced me several times to seek carefully for signs of malignant disease, but without result; and the patient is now greatly better, all symptoms being in abeyance. My own experience would indeed lead me to say that haemoptysis is not very uncom- mon in chronic basic pneumonia. In the diagnosis of mediastinal growth from aneurism compressing the root of the lung, and setting up in it secondary in- I flammatory disease, we must have regard to the distinctions to be laid down between tumor and aneurism. Haemoptysis would by no means necessarily decide the ques- tion in favor of tumor. In endeavoring to come to a conclusion as to the nature of the morbid growth which we have ascertained to be present in the mediastinum, an inquiry so far as we at present know of no great practical impor- tance, we may bear a few general facts in mind. 1. If the disease be primary in the me- diastinum, it will be almost certainly lymphoma. 2. The younger the patient the more likely is it to be of this nature. 3. The presence of enlarged movable glands in the neck, or in other parts of the body (which may suppurate, but do not ulcerate) are also favorable to the di- agnosis of lymphoma. 4. If the disease be secondary to a growth elsewhere, it will be of the same nature as the primary disease, or allied to it within the range of pathological varia- tion, e. g. If the disease makes its ap- pearance subsequently to a limb having been removed, or a joint resected for a malignant growth, we may feel confident that it is one of the sarcomata, either soft oval or spindle cell, or osteo-sarcoma, or enchondroma. If a fixed, nodulated, hard tumor were present in the neck or had been removed from the breast, we might expect the disease in the mediasti- num to be cancerous. 5. So far as invasion of the lung goes, this feature is common to all these growths. Prognosis.-The prognosis is unfortu- nately in all these cases at present equally fatal. But we cannot say whether in the case of lymphoma some remedy may not hereafter be found to exercise some con- trol over the growth. The duration varies according to the parts involved by the tumor, it is rarely greater than a few months. Treatment.-There is no treatment to be adopted in these diseases, save to combat so far as is possible such symp- toms as pain, restlessness, anaemia, &c. By attending to these points and to the digestion, by local depletions when indi- cated, or in the case of complication with hydrothorax, by tapping, the lives of the unfortunate sufferers from these dire mala- dies may be certainly prolonged and ren- dered more endurable. VOL. IL-53 diseases of the organs of circulation.- Continued. C. Diseases of the Vessels. Aorta. Pulmonary Artery. Coronary Arteries. Systemic Arteries. Veins. Cardiac Concretions. Lymphatics. THE DISEASES OF THE AORTA. R. Douglas Powell, M.D., F.R.C.P. In the ensuing articles, the term "tho- racic aorta" will be used inclusively as applying to that portion of the main ar- terial trunk which is contained within the thorax, having its origin at the left ventricle of the heart, and escaping through the diaphragm to become con- tinuous with the abdominal aorta at the level of the last dorsal vertebra. In its passage from the ventricle to the left side of the third dorsal vertebra, the aorta de- scribes a somewhat twisted curve, and this arch of the aorta is divided for con- venience of anatomical description into an ascending, a transverse, and a de- scending portion. That portion of the vessel extending between the third dorsal vertebra and the diaphragm, to which the term thoracic vertebra is sometimes ex- clusively applied, is better described as the descending thoracic aorta. The function of the aorta-that of re- ceiving and distributing, in more equable currents, and with the least possible con- version of motive force, the blood impelled into it with each systole of the left ven- tricle-is mainly performed by the arch, and for the most part mechanically, by virtue of its being a curved elastic tube furnished with appropriate valves. But the anatomical structure of its walls, the organic muscular fibre they contain, and the phenomena occasionally witnessed in disease, forbid our regarding the whole function of the aorta as being quite so simply discharged. We have organic muscular fibre nowhere else in the body save where the property of muscle is ap- preciably exercised, at least to that ill- defined extent which we characterize by the term tonicity. It is by the local depri- vation of this unobtrusive form of mus- cular activity through nervous agency that we may most reasonably explain those violent aortic pulsations which are occasionally met with in nervous people ; and no doubt mental depression and anx- iety exert largely through this means what influence they have in predisposing to aortic aneurism. Aortitis. Acute inflammation of the aorta, in the sense of an acute exudative inflammation, is a disease of very doubtful, if not im- possible, occurrence. Professor Lebert,1 after detailing the symptoms that have been ascribed to the disease by Frank, Bizot, and others, confessed that, in the course of twenty years' experience, he has not seen one case, either clinically or anatomically, corresponding to it. Pro- fessor Rindfleisch2 observes that, "apart from thrombotic arteritis and phlebitis, there is hardly such a thing as acute in- flammation of the walls of the vessels," save, as he proceeds to explain, in so far as their external coats, which must be re- garded as part of the general connective tissue, may partake in any contiguous in- flammation. But even in this partial 1 Virchow's Handbuch der spec. Path., Krankheiten der Blut- und Lymph-gefasse, 1855. 2 Pathological Histology, vol. i. p. 249, Dr. Baxter's translation for Sydenham Society, 1872. 834 AORTIC ENDARTERITIS, ATHEROMA. 835 manner the aorta is very slow to share in such processes, and when it does so the inflammation is very chronic and limited, giving rise to no special symptoms. On the other hand, it must not be de- nied that such a disease as acute inflam- mation may affect those portions of the walls of the aorta which are vascular in the usual way, and involve the non-vas- cular inner coat in an irritative and dis- orderly cell proliferation, after the man- ner in which acute inflammation affects such tissues. Such cases have not, how- ever, yet been distinguished by definite clinical symptoms. The very striking cases of aortitis related by Dr. (now Sir Dominic) Corrigan, in the Dublin Medical Journal for 1838, would, in the light of a newer pathology, be regarded as exam- ples of atheroma of the vessel running a rather rapid course.1 The case which most nearly perhaps of any on record presented the symptoms which have been ascribed to acute aortitis-viz., fever, rigors, tu- multuous action of heart, with intense and painful throbbing of the aorta, and embolic infarction of distant organs-is that related by Mr. Moore in the " Medi- co-Chirurgical Transactions." vol. xlvii. p. 129, in which he endeavored to pro- mote consolidation of an aortic aneurism that was rapidly making its way through the thoracic parietes, by the insertion into it of numerous coils of fine iron wire, but after death the inflammation was found to be confined to a secondary sac of the aneurism which had perforated the chest-wall. In a remarkable case re- corded by Dr. Parkes in the Medical Times and Gazette, February, 1850, there was post-mortem evidence of recent in- flammatory disease, affecting a large por- tion of the descending aorta, which, how- ever, appeared to have supervened upon disease of old standing which had doubt- less much modified the anatomy of the walls of the artery and the ultimate dis- tribution of its nutritive vessels. The dis- ease in this case was not attended with any characteristic symptoms during life, the absence of which might, however, have been due to the almost insensible condition of the patient while under observation. It would be unprofitable to dwell fur- ther upon a disease of the existence of which, as a primary affection, there is, we think it may be said, as yet no sufficient clinical or post-mortem evidence. Aortic Endarteritis, Atheroma. The inflammatory process by which the aorta is commonly affected is necessarily of a slower kind from its attacking pri- marily a non-vascular tissue-the internal coat of the vessel. It consists essentially of proliferation of the cell elements of this coat, commencing in its deeper layers and [Fig. 124. Atheroma of the Aorta.-Showing the cellular infiltration of the deeper layers of the inner coat, and the consequent internal bulging of the vessel. The new tissue has undergone more or less fatty degeneration. There is also some cellular infiltration of the middle coat. i. internal, m. middle, e. external coat of vessel. X 50, reduced £. (Green.)] extending sooner or later to the middle and external tissues. The pathology of this process is minutely described in another article; its effects upon the walls of the aorta-which are spoken of collectively as atheroma-may be referred to in three stages or degrees- (1) patchy thickening, with some soften- ing, mainly affecting the inner coat, un- evenness of the inner surface, and dimin- ished elasticity of the vessel; (2) fatty 1 The cases described by Norman Chevers, Guy's Hosp. Rep. 1841, are so difficult to recognize in accordance with the pathology of the present day, and so complicated with other diseases, as to be useless for clinical illustration. 836 THE DISEASES OF THE AORTA. degeneration of the affected tissues, fibroid thickening of the whole vessel wall; (3) crumbling down, or infiltration with cal- careous salts, of the degenerated internal or middle coat; great consequent rough- ening of the inner surface of the aorta, and increased brittleness of the vessel. In the earlier stages of aortic endar- teritis there is sometimes narrowing of the calibre of the vessel from the intrusion of its thickened walls ; but dilatation almost always takes place later on in the disease. The later stages of atheroma,softening,and calcification,are little more than the effects of imbibition and chemical change acting upon a part which has lost its vitality. Atheroma may then be defined as de- generation of the coats of the aorta, the result most commonly of preceding inflam- matory change (endarteritis), but, it must be added, sometimes occurring primarily as fatty transformation from senile decay. The seat of the disease is most commonly at the commencement of the aorta, and this is the portion most affected even in those cases in which other parts of the vessel are involved. Moreover, we can rarely obtain clinical evidence of atheroma affecting the aorta beyond its ascending or transverse portion. Etiology.-It is of some importance clinically to bear in mind respecting the pathology of atheroma, with which we are now concerned, that the slow inflamma- tory changes which lead to its production are, in the majority of instances, of a de- generative kind from the first-that is to say, they are associated with some con- stitutional cachexia or with senility. Even in those eases in which the disease occurs in earlier life, and apparently as the result simply of undue arterial strain, there may usually be strongly suspected some antecedent impairment of nutrition to account for that sensitiveness or want of resilience to strain which leads to the setting up of atheroma. It has, however, been shown very clearly by the clinical observations of Dr. Clifford Allbutt and Mr. Myers, and the patholo- gical inquiries of Dr. Moxon and others, that aortic atheroma is particularly com- mon among those who are engaged in oc- cupations of a constantly laborious kind- strikers, bargemen, those who work heavy pumps, &c.; and Dr. Allbutt regards daily continued heavy labor as much more effi- cacious in producing this result than inter- mittent toil of even a more severe kind, such as the athletic sports of the higher classes ; but he also lays stress upon his opinion that depressing circumstances of life, bad air and food, greatly favor athe- roma arising from strain.' Rheumatism, gout, syphilis, and kidney diseases are the maladies most predispos- ing to atheroma. Intemperance and hereditary tendency hasten its appear- ance. Of senile changes, atheroma is one of the most constant, but it only rarely comes under our clinical observation, from the diminishing activity and vigor of the circulation with advancing age rcn- dering the results of atheromatous change in the aorta less likely to manifest them- selves. Mr. Francis II. Welch of Netley has in a recent paper read before the Medico- Chirurgical Society of London (1876) con- tended that nodular disease of the aorta (endarteritis) is one of the most frequent internal lesions of the syphilitic virus and also one of the earliest produced-a view supported by some high military authori- ties. Mr. Welch found that out of 56 cases of syphilis terminating fatally from specific lesions 60'7 per cent, showed aortic nodulations. Again of 34 cases dead of aortic aneurism 50 per cent, at least were strongly infected with syphilis. Mr. Welch's important paper did not pass without criticism, and it will no doubt do much to hasten the solution of a very complex question as to the real potency of syphilis in developing atheroma. The main issue rests upon what is regarded as evidence of syphilis both during life and after death. Symptoms and Physical Signs. - The symptoms of atheromatous change in the aorta are always obscure ; and exten- sive disease may exist without any symp- toms being complained of; nor on the most minutely careful physical examina- tion can we in all cases assert that there is or is not atheromatous disease of the main vessel present. The secondary re- sults of atheroma are, in the first place, mechanical-viz., dilatation, aneurism or rupture of the vessel, or embolism from the conveyance of masses of fibrine which have been entangled by the roughened surfaces to distant parts ; and it is only when such secondary phenomena begin to arise that symptoms or signs of disease present themselves. Our object must then be to discover, at the earliest possible mo- ment, the commencing secondary conse- quences of atheroma, so as to be on our guard, so far as it is possible, against their further extension. Attacks of angina or of palpitation, oc- curring independently of effort, but readily brought on by exertion, are suggestive of this form of the disease ; but it as often happens that some casual symptom which, so far as symptoms are yet classi- fied, might mean anything or "dyspep- sia," in the man before us directs our attention to the heart. The patient is of an age at or beyond that of middle life, 1 On Overwork and. Strain of the Heart, and Aorta. DURATION-TREATMENT. 837 which is in favor of the probability that such cardiac attacks may be dependent upon dyspepsia (or, in the case of women, climacteric hysteria), and the presence or absence of these conditions must of course be carefully ascertained ; but their exist- ence must not be regarded as sufficient to exclude the graver malady, for they fre- quently coexist with and complicate aortic disease. There is nothing characteristic in the appearance of the patient; he may be thin and cachectic looking, or the re- verse ; but whether his appearance sug- gests such questions or not, rheumatism, gout, syphilis, and intemperance should be inquired for, and the urine repeatedly examined for albumen or morbid deposits. On examination, the radial and brachial arteries will commonly be found more rigid and inelastic than natural. Although during an attack of dyspnoea the heart's action is tumultuous and the pulse alarmingly irregular, yet at the time the patient comes under observation the cardiac movements may be quite steady, with perhaps an occasional inter- mission, there is some evidence of hyper- trophy of the left ventricle (increased im- pulse with muffled sound), and perhaps nothing else can be discovered; from these patients being big-chested and more or less emphysematous, it is also some- times difficult to judge of the cardiac hy- pertrophy. In more marked cases, how- ever, there is With indistinctness of the first sound, accentuation of the second and a short systolic, or rather post systolic, murmur over the aorta beyond the valves. It may be that this murmur is only dis- coverable when the heart is acting strongly as from excitement, or after taking a few turns up and down the room-and in sus- picious cases this exercise prior to a sec- ond auscultation should never be omit- ted ; the murmur does not displace the first sound, but is superadded to and im- mediately follows it. In other cases there is a partial replacement of the second sound by a fine diastolic murmur. These latter physical signs are often not to be found for the first few months, during which the patient has presented suspicious symptoms, and their supervention in this way is the most significant feature in the history of such a case for diagnosis. In the upper sternal region both the cardiac sounds are accentuated, and may be at- tended even with slight shock to the ear; in order correctly to value this sign, how- ever, a reverse precaution to that men- tioned above should be adopted - we should note that the patient be quite calm, and if possible, make a second ex- amination after he has been lying down for a short time. At a later period, signs of decided dila- tation may become apparent, there may be some dulness over the aortic region, and some pulsation-rather flapping than thrusting-may be felt by the finger at the second interspace close to the ster- num. The bruit becomes more distinct, sometimes very rough and accompanied by fremitus, when calcareous degenera- tion may be presumed to be present. The dyspnoea increases, and the anginal at- tacks may become more frequent and se- vere ; or, on the other hand, they may disappear ; but palpitation is always more persistent. The symptoms of embolism may now come on, among which hemi- plegia, rigors and hsematuria, superficial hemorrhages, and gangrene may be enu- merated ; or sudden pain, dyspnoea, and faintness may announce the commence- ment of a sacculated aneurism, or death may suddenly take place from cardiac syncope or rupture of the aorta. In other cases sacculated aneurism may imper- ceptibly arise. The acute symptoms signalizing the formation of a dissecting aneurism may be the first to announce to us the exist- ence of long preceding atheroma, and it is unnecessary to say that the disease, the phenomena of which are thus related in chronological order, may first present itself to our notice at any of the stages referred to. In all cases of suspicion the general state of the circulation should be carefully examined, the aid of the sphyg- mograph being sought. Duration". - The duration of aortic endarteritis or atheroma cannot be pre- cisely stated, from the insidious manner in which the disease commences. It may be considerably, perhaps indefinitely, pro- longed by careful management, hence the importance of its early recognition. The disease proceeds to its fatal termination either by simple progress leading to rup- ture of the vessel, or by embolism of the brain or other organs from conveyance of debris or fibrinous plugs ; or by dilatation of the aorta, or direct involvement of its valves, giving rise to incompetency with its attendant cardiac results, or, finally, by the formation of a sacculated or dis- secting aneurism. In calculating the ^prog- nosis, the present duration of the disease and the progress it has already made in one or other of these directions has to be considered. Treatment.-The treatment of aortic degeneration is purely palliative. A care- ful regulation of the diet so as to avoid both overloading of stomach and too long fasting, is of the first importance ; stimu- lants should be reduced to a minimum, or dispensed with a ltogether, and the hepatic function should be carefully attended to. A mild but bracing climate with level 838 ANEURISM OF THE THORACIC AORTA. walks and carriage exercise are desirable. Of drugs the aromatic stimulants and antispasmodics are most useful during the attacks of dyspnoea. The subcuta- neous injection of morphia is very useful in warding off the attacks, when, as is not infrequently the case, they show any ten- dency to recur at definite times. ANEURISM OF THE THORACIC AORTA. R. Douglas Powell, M.D., F.R.C.P. Aneurism at the Sinuses of the Aorta. Aneurism affecting the very com- mencement of the aorta, either at or im- mediately above one of the sinuses of Valsalva, rarely attains a sufficient size to assume special characters of its own before death takes place, either from its rupture into the heart or pericardium, or indirectly from the grave derangement of the valves and orifices at the base of the heart it has occasioned. It may there- fore be more conveniently considered here than among the larger aneurisms affecting the rest of the aorta. The aneurism oc- curs usually above the right coronary valve, next most frequently"above the in- tercoronary valve or between these two (Sibson). It is also always of the saccu- lated variety. The pouch necessarily projects in most cases into the right side of the heart at or near the commencement of the pulmonary artery. Symptoms and Physical Signs.-In a certain number of cases there are no symptoms to attract our notice to the heart, until the patient suddenly dies from rupture of the sac. In other cases the symptoms and signs are those of athe- roma, with some dilatation of the first portion of the aorta. The expansion of the portion of the aorta forming the base of the aneurism, tends to displace down- wards the attachment of the aortic valves, and if situated above the junction of two of these valves necessarily occasions great incompetency, with all the signs and symptoms of aortic regurgitation. The pouch by projecting, as it most commonly does, towards the base of the pulmonary artery, tends also to displace its valves or narrow its orifice, and hence there may be a systolic or a diastolic murmur situated in the pulmonary region. This latter sign in particular might lead us to suspect the disease. Hypertrophy of the left ven- tricle, with or without a similar affection of the right, is usually present. In two cases which have come under my own observation, the hypertrophy and dilata- tion of the right side of the heart were very marked. Diagnosis.-The diagnosis can rarely be made with certainty. It is almost im- possible to single out from among the symptoms which may be accounted for by the many attendant lesions, those pecu- liar to an aneurism rarely exceeding the size of a filbert, and buried in the base of the heart. Yet, where we have evidence of these lesions-of aortic atheroma with some dilatation, and of regurgitation through the valves-the existence of an- eurism should always be reckoned upon as possible; and if there be any murmur detected ovtr the pulmonary artery, ac- companied by marked hypertrophy and dilatation of the right side of the heart, the presence of aneurism may be fairly assumed. The termination of the disease is usually by rupture into the pericardium or right side of the heart. Death may ensue, however, from the valvular derangement occasioned by it, or in some other way from the extensive disease of the vessel by which it is most commonly accom- panied. The general treatment of this disease is identical with that of atheroma. Aneurism of the Thoracic Aorta BEYOND THE VALVES. Aneurism of the aorta is a preternatural dilatation of that vessel at some portion of its course. The dilatation may be general, involving the whole circumference of the vessel for a certain length, and such an aneurism may assume the fusiform, cylin- drical, or globular shape. The aneurismal expansion of the vessel is more commonly partial, from the yielding before the blood- pressure of some circumscribed portion of the arterial wall previously weakened by disease, which bulges outwards from the ETIOLOGY. 839 vessel as a bud, or nil de sac, of gradually increasing dimensions. This variety is spoken of as the sacculated aneurism ; it is always associated, however, with some general enlargement of the arterial chan- nel. These varieties of aneurism are more easily classified in the museum than dis- tinguished clinically. Among the circum- scribed aneurisms of which the sacculated variety is the type and form of most fre- quent occurrence, we must also include, affects the first portion of the aorta, and, when extensive, yields many of the signs of aneurism presently to be described. Etiology.-Speaking generally, what- ever increases the pressure of the blood within the aorta or impairs the resisting power of that vessel, favors the produc- tion of aneurism. Increased propelling power of heart and increased resistance to the escape of blood from the aorta, into the vessels beyond, are the two conditions which, separately or combined, augment the pressure of blood within the vessel: disease of the walls of the vessel, of what- ever kind, diminishes its power of resist- ing the normal or enhanced blood-pres- sure. In discussing more minutely the etiol- ogy of aneurisms of the aorta, we must refer separately to the disease as occurring as a result of senile changes, and as being prematurely produced by artificial or acci- dental circumstances. Senile decay of the arterial wall is one of the natural causes of aneurism. In the normal pro- gress of age, degeneration commences in the large vessels, and probably too in the smaller ones, before the tissue of the heart suffers in nutrition;1 indeed, the first effect of this arterial decay is, as is well known, a certain increase in the muscular power of the left ventricle to compensate for the increased resistance to the circulation through more rigid vessels ; and it is at this period of ad- vanced middle life that aneurism is most frequently met with-but sometimes age in these special tissues is hurried on by favoring disease. Beyond the period of advanced middle life the tendency to sac- culated aneurism is lost, the bulk of the blood is diminished, the nutrition of the heart begins to suffer and the vigor of the circulation becomes correspondingly lessened ; a lower activity of life is thus necessitated which is quite normal to ad- vancing age and in harmony with the changes taking place in the tissues. In old age, however, it sometimes happens that the senile atheromatous change-no doubt aided by some, attendant (second- ary ?) inflammation-proceeds to actual softening and erosion of the inner tunic of the aorta, and the blood then insinu- ates between the coats of the vessel, and a dissecting aneurism arises. Subacute and chronic arteritis, the varying stages and modifications of which [Fig. 125. Section of Arch of Aorta, with Aneurism.] for purposes of description, the globular1 aneurism, and those aneurisms strictly speaking perhaps of the dissecting kind, i. e., commencing suddenly with rupture of the internal coat, but in which the lesion is limited, and the further progress of the disease is by gradual expansion. No doubt more aneurisms, regarded even post-mortem as sacculated, originate in this way than is generally supposed. The ordinary fusiform aneurism is in its slighter degrees more commonly spoken of under the simpler name dilatation of the aorta, and has already been referred to in speaking of atheroma. It usually 1 This is perhaps the best term to apply to those cases in which the dilatation affecting the whole circumference involves only a com- paratively limited portion of the length of the aorta. It is not a new one, being used by Dr. Walshe in the same sense, though the cases referred to he regards as of extreme rarity. An aneurism of this globular form presents all the physical signs and clinical phenomena of a sacculated aneurism, even to perforation of the thoracic parietes, as in Dr. Murchison's case related at page 849. One or two instances of this variety, which seems to be more frequent in the descending thoracic aorta, have lately appeared before the Patho- logical Society. 1 This statement, it must he admitted, is based rather upon general clinical experience than upon any exact inquiry into the natural relative progress of age in the different tissues, which is as yet wanting in medical literature. It is, I believe, however, in accordance with the impression of most physicians, and is in all probability exactly true. 840 ANEURISM OF THE THORACIC AORTA. have already been referred to as account- ing for the production of most of the appearances recognized under the term atheroma-thickenings, scars, erosions, calcifications, &c.-is the diseased condi- ism, or may, under some severe effort, suddenly give way with those acute symp- toms which occasionally usher in the obvious disease. Hereditary predisposi- tion has not been found to exist, save in exceptional cases, in aneurism. One re- markable case came under my own obser- vation seven or eight years ago, in which there was a tolerably trustworthy history of a mother and four sons dying of inter- nal aneurism. Dr. Fuller1 relates the case of a gentleman whose paternal grandfather, uncle, and father, had all died from aneurism, and whose sister was laboring under that disease. Although rheumatism is usually enu- merated among the diseases predisposing to aneurism, it has hitherto been included among such general causes as syphilis and renal disease, on the tacit under- standing that the " rheumatic diathesis" is favorable to the occurrence of prema- ture arterial decay. Whether this be the case is at least, I think, a question for further inquiry ; but rheumatism must in a more definite sense be regarded as a possible cause of aneurism, if I may judge from the history of some cases which have come under my own observation.2 It has been found in certain cases of rheu- matic fever with aortic valve disease, that the aorta beyond the valves has pre- sented patches of arteritis corresponding with the impingement against it of vege- tations fringing the margins of the valves. Does the rheumatic endocarditis ever ex- tend beyond the valves to produce endar- teritis affecting the aorta at its commence- ment ? I have only seen clinical evidence in one case which would lead me to answer this question in the affirmative. The case was that of a lad aged 17, in whom aortic aneurism occurred traceable to two attacks of rheumatism occurring at the ages of eleven and twelve. No other cause for the aneurism could be made out, and the patient was too young for degeneration of the vessel, save of an acute kind, such as might possibly be occasioned by rheumatic fever. The operation of aortic regurgitant dis- ease of the heart, left behind by rheumatic endocarditis, as a cause of aneurism, may be readily conceived in persons at or be- yond middle life. I have met with three examples of aneurism, the histories of which will, I think, admit of no other in- terpretation ; and in two other cases I have had reason to suspect the disease to have arisen in this way. Greatly in- creased power of cardiac systole is re- quired in aortic regurgitant disease to carry on the circulation with an aorta whose action is crippled through imper- fection of its valves ; the whole shock of [Fig. 126. Aneurism of arch of the aorta.] tion most commonly preceding aneurism ; indeed, it is through the intervention of arteritis that all the known causes of aneurism of the aorta, and, perhaps, of other vessels, become effective. The con- stitutional states, then, which tend to produce atheroma, also favor the occur- rence of aneurism-hereditary predisposi- tion, rheumatism, gout, syphilis, kidney disease, alcoholism. Even strain, with but rare and violent exceptions, leads to the production of aneurism, not simply by rupturing any of the coats of the aorta, previously healthy, but by overstretching, or too violently exercising them, and thus setting up local atheromatous disease of the slow inflammatory type. Dr. Moxon1 has brought together so many arguments to prove the direct effect of strain in pro- ducing atheroma as to have, I think, set- tled the question. He shows how the disease affects first the aorta in the region of the valves and at its ascending portion, and that the inflammatory degeneration occurs in points arranged longitudinally in the course of the vessel. Thus arising, it is not difficult to understand how any of these little disease "rifts" may slowly widen to the production of a large aneur- 1 Guy's Hospital Reports, series iii. vol. xvi. p. 448 ; also recent work on Pathological Anatomy by Wilks and Moxon, chap. " An- eurism." 1 Diseases of the Chest, p. 656. 2 Vide Clinical Transactions for 1874. ETIOLOGY. 841 this extra power is received of course by the ascending portion of the aorta. More- over, instead of the unduly forcible im- pulse of blood being received by an aorta already containing a certain residuum of blood sufficient to diminish the shock, the great vessel is, on the contrary, more empty and flaccid than natural at the moment of ventricular systole, the blood in regurgitant disease escaping back into the ventricle. The effect of this increased impulse, or shock, upon the aorta must be to predispose it to the occurrence of atheromatous disease and of subsequent expansion. Intemperance, mental emotion, and violent exercise operate as causes of aneu- rism by increasing the blood pressure within the aorta. Dr. Rendle's statistics of cases of internal aneurism occurring among the female convicts in the Queen's Prison, Brixton, conclusively show the effect of mental depression and excite- ment in predisposing to aneurism. As already hinted, loss of muscular tone of the vessel, through nervous influence,1 may take a more important part in such cases in the origin of aneurism than is at present allowed. Mechanical impedi- ment to the circulation through the great vessels beyond the aorta is, however, per- haps the most important cause of aneu- Mr. Myers1 gives the statistics of In- spector-General Lawson ("Army Medi- cal Report," 1866), showing that the deaths from aortic aneurism are in the army eleven times greater than among the civil population ; and he accounts for this enormous disproportion by the tight- ness of the dress and accoutrements of the soldier occasioning greatly increased blood-pressure within the aorta during any violent exercise, by compressing the great vessels of the neck and upper ex- tremities. In proof of this Mr. Myers gives one set of 703 cases of aortic aneu- rism from Dr. Sibson, in 420 of which (59'7 per cent.) some portion of the as- cending aorta was involved. He also gives-in support of Dr. Sibson's view that that portion of the aorta on which there is most strain is most often affected with aneurism--109 other cases, culled from the Netley Hospital records, and from those of his own regiment, in 75 (about 70 per cent.) of which the disease affected the ascending portion or arch of the ves- sel. He thus successfully endeavors to locate the cause of the disease in soldiers from its point of manifestation being dis- proportionately more frequent in them at that portion of the aorta which is at or above the origin of the great vessels of the neck and upper extremities.2 As further evidence of the effect of strain in producing heart disease among soldiers, Mr. Myers mentions the significant fact that among them aortic valve disease is twice as frequent as mitral, whereas in civil life mitral disease is slightly the more frequent. He also refers to the very large proportion of valvular heart disease in the army, which are not trace- able to either rheumatism or albuminu- ria, the two diseases answerable for most such cases occurring in civil life. It must, of course, be remembered that wherever the obstruction may be, the aortic at its origin must be most import- antly affected ; for it is here next to the ventricle, that the supplementary force is gathered to overcome it, and perhaps the great and almost sudden change in the mode of life on entering the military ranks -from that of the slow-moving, slouching, ill-fed farmer's lad, or the [Fig. 127. Aneurism of Aorta.] rism, with special reference to which the malady will be found to prevail more at certain ages, among those following cer- tain occupations, and, with some reserva- tions, in the male sex. In an exhaustive essay on the etiology of diseases of the heart among soldiers, 1 On the Etiology and Prevalence of Dis- eases of the Heart among Soldiers. London. 1870. 2 Taking the whole of Dr. Sihson's 880 cases, of which in 460, or 52'3 per cent., the disease was situate at either the ascending or transverse aorta, or between the two, and further making allowance for the fact that these cases were of all ages, whereas those quoted by Mr Myers were within the age of effective service, the preponderance of the affection in ascending aorta, among soldiers appears still more considerable. 1 Niemeyer refers to palsy of the vasomoter nerves as a questionable cause of aneurism, though he gives Rokitansky's opinion in fa- vor of it. 842 ANEURISM OF THE THORACIC AORTA. loafer from among the unhealthy recesses of large towns, to that of the smart, straight, large-eating and more or less plethoric soldier-should be also taken into account, as well as his disadvantages in dress, in considering the effects of the soldier's occupation in predisposing to aneurism.1 However this may be, it will be readily perceived that arterial strain tending through the medium of atheroma to produce aneurism among other diseases of the heart and aorta, is the common re- sult of many of the conditions of the sol- dier's present life and training. Sailors, with an equal liability to great physical effort, and affected in about equal propor- tion with the taint of syphilis, although more subject to aneurism than civilians, are less so than soldiers, their greater amenity in this respect appearing due mainly to their looser dress and more gradual training. The occupations of hammermen, lightermen, smiths, and others, necessitating long-continued mus- cular effort, predispose to aneurism. Age.-Aneurism of the aorta may oc- cur at any age ; it is, however, extremely rare before twenty, and is most prevalent between the ages of forty and fifty. A small number of cases, 5 or 6 per cent., occur before thirty. Professor Lebert2 finds the disease most prevalent between the ages of forty-five and sixty. In Dr. Crisp's3 tables, 132 out of 175 cases oc- cur between the ages of thirty and sixty, this wide margin being, as before ex- plained, accounted for by certain habits and constitutional states anticipating by disease the effects of age upon the ves- sels. The great majority of aneurisms occurring between these periods of life are of the circumscribed sacculated or fusi- form kind ; in advanced life, on the other hand, those cases which do occur are most commonly of the dissecting kind (Peacock4). Sex.-Males are much more liable to true aneurism of the aorta than females, though the latter are by no means exempt from the disease. Of circumscribed an- eurism of the aorta from two-thirds to four-fifths of the cases occur in males (Crisp, Peacock, Blakiston) ; on the other hand, dissecting aneurism appears to be of as frequent occurrence in women as in men. That this disproportion between the sexes is due entirely to the difference in their habits of life is apparent from the statistics of Dr. Rendle, already referred to. Mr. Holmes1 remarks that "internal aneurisms seem equally if not more com- mon among women when their way of life exposes them to the vascular excite- ment consequent on intemperance, vice, and mental emotions." Though aneurism appears to prevail more in Great Britain than in other coun- tries, this excess is attributable to our rougher mode of life rather than to any climatic influence. Symptomatic History and Symp- tomatology.-As a rule the commence- ment of aneurism of the aorta is unmarked by symptoms, and the disease may con- tinue latent up to the time of death. The so-called exciting causes of aneurism, tho;- e acts or accident- which seem immediately to determine the commencement of the disease, cannot well be classified ; when recognizable they consist either of some temporary exaggeration of usual daily toil, or of some shock, or fall, or blow, violently affecting the circulation. Such causes are, however, but rarely sufficient to account for internal aneurism if we at- tempt to isolate them from the predispos- ing, i. e. the true causes of the disease. In the sacculated or circumscribed forms the history, when any can be discovered, may be referred to one of the following types. In one case there may long have been signs of failing health and nutrition, and positive signs of degenerative disease of the aorta may have previously been detected. In another the patient has perhaps enjoyed robust health and in- dulged in active pursuits and free living until, after a fall from a horse, or a blow, or a sudden violent effort, he feels a momentary pain in the chest and faint- ness, soon passing out of memory but re- called by the consciousness, on subse- quently assuming his wonted exercises, of a gradually increasing shortness of breath and palpitation, with deep-seated pain in the chest; the dyspnoea becomes habitual, and he is ever conscious of too great a pulsation within the chest which disturbs his rest. He then seeks advice. Some- times the symptoms come on more acutely -e.g., a tailor on lifting while in the "squat- ting" posture the heavy seam press he has been accustomed to wield for years in the same way, is seized with agonizing pain in the left breast, prolonged faint- ness and violent palpitation, and soon a pulsating tumor appears in the aortic region, where he had felt "something 1 It is a fact worthy of note that severe gymnastic exercises have only been in vogue in the army within comparatively recent years. I have, however, met with aneurism in several soldiers who have never been sub- jected to them. 2 Virchow's Handb. der spec. Path., Bd. v. abth. ii.; Krankheiten der Bint- und Lymph- gefasse, p. 25. 3 Diseases of the Bloodvessels, p. 135. 4 On Dissecting Aneurism. Edin. Surg. and Med. Journal, vol. lx. p. 291, 1843. System of Surgery, vol. iii. p. 419 SYMPTOMATIC HISTORY AND SYMPTOMATOLOGY. 843 give way." The symptoms in other cases come on almost imperceptibly with cough, dyspnoea, and partial aphonia, attributed to cold, yet the patient will, on being questioned, perhaps date them back to some protracted labor or "heavy job," as in the case of a blacksmith or lighterman. At the time of applying for advice the symptoms vary in their nature and inten- sity with the seat of the tumor and the direction in which it is growing. They are all due to pressure upon the neighbor- ing parts causing their displacement or erosion, interference with the patency of air and food tubes, irritation or destruc- tion of nerves, and they may be thus enumerated nearly in the order of their frequency - Pain, dyspnoea, cardiac or pulmonary, or both, persistent in greater or less degree, but often associated with paroxysmal attacks ; voice altered, husky, uncertain, or whispering; cough, dry, hoarse, or ringing, laryngeal, stridulous breathing, headache, disordered vision, loss of power or positive paralysis of lower extremities. Few if any ^f the symptoms as thus enumerated can be regarded as specially distinguishing aneurism from other tu- mors in the chest, their significance rests rather upon their grouping and upon cer- tain characters about them which require further consideration. The existence of an aneurism may sometimes be inferred from the presence of certain symptoms whilst the physical signs are as yet most obscure, and otherwise insignificant. The pain in aneurism is of a wearing, aching, or burning character, correspond- aneurism is of various kinds and grades, and has many causes. (1) The mechan- ism of the circulation being disordered, any effort giving rise to an extra demand upon the heart occasions dyspnoea. (2) The simple fact of there being a tumor within the chest compressing and dis- placing its other contents necessitates some degree of dyspnoea. The fact of the tumor being pulsatile and of dimensions varying slightly from time to time witli the fulness of the circulation may serve to give a distinguishing feature to the dys- pnoea, viz., its more marked sensitiveness to conditions tending to disorder circula- tion than in the case of other tumors. A certain deep-seated throbbing is some- times complained of after effort or excite- ment. But (3) the dyspnoea most charac- teristic of aneurism occurs in paroxysmal attacks, in one of which the patient not unfrequently dies. Much dispute has arisen as to the mechanism of this form of dyspnoea, and upon the views we hold respecting it will depend our treatment of cases of impending suffocation from this cause. The pneumogastric nerve is sometimes affected in the disease ; it may be either compressed and flattened by the tumor, or destroyed and incorporated with the sac by inflammatory change. More com- monly one or both of the recurrent branches are affected, the left most fre- quently so by direct compression, or the right indirectly by dragging of the tumor upon the origin of the subclavian. Either paralysis or irregular spasm of the laryn- geal muscles on one or both sides may thus be occasioned. Among those who attribute these attacks of dyspnoea to dis- turbance of the innervation of the glottis, some regard them as due to spasmodic closure of the glottis, others to paralytic closure. Spasm of the glottis is the cause to which the dyspnoea is most commonly attributed. It is generally held that, to quote the words of Dr. John Reid,1 "all the mus- cles which move Mie arytenoid cartilages receive their motor filaments from the in- ferior or recurrent laryngeal nerves. And as the force of the muscles which shut the larynx preponderates over that of those which dilate it, so the arytenoid cartil- ages are carried inwards, when all the fil- aments of one or both nerves are irri- tated." This is the view upon which those who hold the spasm theory mainly [Fig. 128. Aneurism of Aorta, which burst into the Trachea ] ing in position with the seat of the tumor. It is a fixed pain, but associated with paroxysmal pains of an evidently neural- gic character, radiating in the course of contiguous nerves. The first onset of the disease is occasionally ushered in, as be- fore said, by very acute suffering'. The dyspnoea present in cases of thoracic 1 Physiologies! Posearches, No. iv. Ex- perimental investigations into the functions of the eighth pair of nerves, 1848. Dr. San- derson (Handbook of Practical Physiology, p. 298) regards all the intrinsic muscles of the larynx as expiratory, the widening dur- ing the inspiration being a condition of gen- eral relaxation. 844 ANEURISM OF THE THORACIC AORTA. rely. M. Krishaber1 observes, as the re- sult of some experimental inquiry, that in paralysis of the chords either from de- struction of the recurrent nerves or di- vision with the knife of one or both of them, there is no dyspnoea, the glottis being actually more patent under such circumstances than natural. This view, however, is entirely opposed to the con- clusions drawn from similar experiments by others. The experiments of Legallois and John Reid distinctly show that on section of the recurrent nerves the paral- yzed chords are sucked together with each inspiratory effort, giving rise to suf- focation or great dyspnoea. Some experi- ments 1 have myself made on the cat en- tirely confirm in this respect those of Le- gallois2 and Reid, while in another par- ticular, the effect of irritation of these nerves upon the larynx, they, so far as they have gone, lead me to hesitate in ac- cepting the conclusions of these and other experimenters. For while the cat was in a state of urgent distress from the suck- ing together of the paralyzed chords with each inspiration, first one inferior laryn- geal nerve, then the other, and then both, were galvanized with a weak current, and in each case the corresponding arytenoid cartilage was powerfully rotated outwards, so as to widely open the glottis and in- stantly relieve the dyspnoea.3 While, then, I think that further experimental inquiry will tend to show that spasmodic closure of the larynx may not in man be caused by irritation of the recurrent nerves, clinical observation is also in favor of the dyspnoea of aneurism, so far as it is laryngeal, being due to paralysis. When the larynx is at all affected, paral- ysis-denoted by the altered voice, and observable by the laryngoscope-is the lesion usually present.' Dr. Habershon1 has found actual atrophy of the laryngeal muscles on the affected side. Dr. George Johnson and Dr. Baiimler in the 23d and 24th volumes of the Pathological Trans- actions respectively, have each recorded a case in which bilateral paralysis of the chords was found during life, and post mortem the laryngeal muscles on both sides were found to have undergone atro- phic changes. In these two cases the trunk of the vagus, as well as the recur- rent nerve on one side, was found com- pressed by the tumor, the nerves on the other side being free. Dr. Johnson con- siders that the bilateral paralysis in these cases may have been due to the compres- sion directly paralyzing the muscles on the same side through the recurrent, and caus- ing refiex paralysis of the muscles on the opposite side through the trunk ot the pneumogastric and the efferent nerves in relation with its centre. Dr. Johnson holds that bilateral spasm may be occa- sioned in a similar way.1 But how does paralysis of the chords give rise to occasional paroxysms of dys- pnoea ? The mechanism of these attacks of dyspnoea seems to be either (a) that owing to sudden enlargement of the aneu- rism from excitement of heart, after a full meal, or from mental emotion or physical exertion, the increased pressure on the nerve renders a partial paralysis complete, and a paroxysm of dyspnoea occurs from sucking together of the flaccid chords ; or, (6) as one may observe in some cases in [Fig. 129. Aneurism of aorta, which produced caries of ver- tebiTB.j winch the chords have been destroyed by ulcerative disease, so when they are pa- ralyzed, effectual cough being impossible, mucus collects at the glottis, and gives rise to dyspnoea. And moreover we must remember that-as may be well seen in experimenting with animals-during any excitement of breathing, the dyspnoea al- ready present from paralysis of the chords necessarily becomes more urgent; the more powerful the inspirations the more completely is the glottis closed by atmo- spheric pressure. But there are at least two other causes of paroxysmal dyspnoea in aneurism, affecting the trachea or bron- chi. Dr. Bristowe, in a valuable commu- nication to the St. Thomas's Hospital 1 Comptes Rendus des Stances de la Society de Biologie, October, 1866, d' I'Opportunit^ de la Trachiotomie dans les Anevrismes de la Crosse de l'Aorte. 2 Snr le Principe de la Vie, 1812. 3 These experiments were made in the summer of 1874 with the kind help of Dr. M. Bruce and Mr. Schafer. 4 Medico-Chirurgical Transactions, vol. xlvii. 1 Vide Medico-Chirurgical Transactions, for 1875. 845 PHYSICAL SIGNS. Reports for 1S72, expresses his belief that the dyspnoea of intrathoracic tumor is only purely laryngeal, and contends that it is most commonly due to direct narrow- ing of the trachea by the pressure of the aneurismal or other tumor, and to accu- mulation of mucus at the point of stric- ture, acting merely mechanically by plug- ging the narrowed opening, and perhaps causing in addition some spasmodic con- traction of the tube. lie illustrates his view by several cases; and there are many others, one of which has lately come under my own observation, which bear no other interpretation ; and I think the explana- tion will be found applicable to those cases in particular in which there is marked stridor on one or both sides of the chest, according as the trachea or one main bronchus is pressed upon. In such cases of course all idea of relief by trache- otomy must be abandoned. Again in some cases of aneurism, particularly when affecting the third portion of the arch, pa- roxysms of dyspnoea, closely resembling those of asthma, may be occasioned by compression of the small branches of the pneumogastric forming one of the pulmo- nary plexuses. (Gairdner.) Direct press- ure upon the trachea may also, however, as I have seen in one remarkable instance, give rise to dyspnoea having very closely the characters of asthma. Palpitation, or cardiac dyspnoea, is usu- ally an intermitting rather than a con- stant symptom in aneurism; it is gen- erally complained of on slight exertion. Attacks of true angina pectoris are some- times witnessed in cases of aneurism af- fecting the first portion of the aorta, and probably arise from pressure on the car- diac plexuses (Gairdner). There is usu- ally more functional disturbance of the heart when the disease is thus situated. Acceleration of pulse is sometimes, how- ever, a persistent symptom: in the case of a woman for many months under my notice with aneurism of the first portion of the arch, the pulse was constantly beating at a rate of between 130 and 140 per minute, the patient complained of palpitation, and assured me that the heart's action was not quickened from excitement at the times of my repeated observations. Dysphagia, although often present, is a less constant symptom in aneurism than in other tumors in the same situation.1 I have seen two or three instances in which an aneurismal tumor has caused a circular perforation of the wall of the oesophagus, without any distress having been com- plained of from difficulty of swallowing.1 There is sometimes a spasmodic character in the dysphagia, which is regarded as of reflex origin. Headache and disordered vision are occa- sional symptoms, the former referable to obstructed return of blood from the head, the latter to pressure upon the sympa- thetic affecting the size of the pupil. Haemoptysis., though it may occasion- ally, and to a slight extent, occur in the course of aneurism, from bronchial con- gestion or lung irritation, as a rule only presents itself as the final symptom in those cases in which rupture of the aneu- rism takes place into the trachea, oesoph- agus, or one of the great bronchi. Some- times this final gush is preceded for a few days by a sanguineous tinging of the scanty expectoration, and Dr. Gairdner mentions a case in which this expectora- tion preceded death by a considerable interval. Dr. Blakiston2 has recorded a case in which fragments of discolored coagula were expectorated with blood two or three weeks before death, which materially aided the diagnosis of an aneu- rism of the descending arch communicat- ing with the left bronchus. Physical Signs.-It is by the physical examination of the patient before us-the observation of all the signs discoverable by the eye, the hand, the ear, aided by the stethoscope, the laryngoscope, and the sphygmograph-that we clinch the diagnosis as to the existence and probable seat of the aneurism which the symptoms present have led us to look for. The physical signs of aortic aneurism vary greatly in the distinctness with which they are manifested according to the position and size of the dilatation. It is, practically speaking, true that an an- eurism may be present and give rise to death by rupture without having ever presented any distinctive signs. Such signs, however, even in obscure cases, are more often overlooked than absent, and may usually be discovered on diligent ex- amination. We will first enumerate all those that may be found in tolerably ob- vious and typical cases. Summary of the Physical Signs that may be Observed in Aneurism of the Ascending or Transverse Aorta3-It is in a consider- 1 For a good example of this, ride case of aneurism by Dr. Quain, Path. Trans, vol. xvii. p. 110. Dr. Fuller also refers to the occasional occurrence of severe lesion of the oesophagus from aneurismal pressure without any corresponding dysphagia. Diseases of Chest, 1862. 2 Diseases of the Heart, p. 56, case 24. 3 These aneurisms are specially referred to here, not only because they are the most 1 M. Leudet observes that dysphagia in compression of the oesophagus by aneurism of the aorta is often absent. "Recherche sur les Lesions de 1'CEsophagie causes par les Anevrismes de l'Aorte." Compte Rendus de la Soc. de Biol., 3me sSr. 1863, p. 180. 846 ANEURISM OF THE THORACIC AORTA. able proportion of cases at once evident on inspection of the patient stripped to the waist, that he is suffering from aneurism of the aorta. We observe the veins large, full, and tortuous in the humeral region and neck on one side, more rarely on both, a certain fulness, and deepening of the antero-posterior diameter of the up- per chest near the sternum on that side, or the superior portion of the sternum itself is rounded and prominent, marbled with blue veins. At the most prominent portion of the costal or sternal bulging, there is distinctly visible pulsation, or there may be a more confused but rhythmic shock apparent with each beat of the heart. Sometimes the pupil on one side corresponding with the pulsating tu- mor is notably smaller than the other. On now employing palpation, one hand being applied to the scat of the apex beat, which is usually shifted a little down- wards and to the left, and the other placed on the tumor, we feel two centres of pulsation, synchronous or nearly so, within the chest-a very significant sign of aneurism. More carefully noting the character of the morbid impulse, we may observe it to be distinctly heaving, expan- sile, spreading out from some central point. Thrill, either systolic or diastolic, or both, may be perceptible over the tu- mor ; it is only very rarely, however, to be observed in sacculated aneurism. It may very often be found on comparison that the pulse is more feeble at one wrist than the other, or it may be obliter- ated on one side altogether.1 Some hard- ening from degeneration of the vessels may perhaps be observed at the same time. On percussion, which must always be performed with great gentleness, the note is found to be dull, over the unusual prominence; the dulness includes the sternum, extending laterally on one or both sides to gradually fade into lung res- onance. It may be continuous with the cardiac dulness which is lowered or sepa- rated from it by a band of resonance, or it may encroach upon the sterno-clavicu- lar or episternal regions. Together with the dulness there may usually be noticed increased resistance or hardness over the seat of the tumor, and this is especially marked in cases of large aneurism con- taining much coagulum. Some dulness may also be detected on percussion in the upper interscapular region on one or both sides. On applying the stethoscope to the sus- pected region, the first thing which at- tracts attention is the impulse or systole' shock, which may be intense to the ear when it is not perceptible to the eye, and only barely so to the most attentive pal- pation. This systolic shock may be ac- companied by a bruit usually grave, rough, expansive, more distinct over the centre of the tumor than over the aortic valves. The second sound, clear and ringing at the base of the heart, may over the tumor be accompanied by a peculiarly abrupt shock or second impulse to the ear, which impulse may be even apparent also to the hand. Sometimes a diastolic bruit is audible, in which case the second shock sound is usually ob- scured or lost. All the auscultatory sounds of aneurism are most audible di- rectly over the tumor ; they may be con- ducted along the course of the aorta, and become very audible at one or both inter- scapular regions. Over the tumor the respiratory murmur is absent, but on passing the stethoscope aside to the acro- mial region, the breath-sound is found to be more or less bronchial, and the voice- sound to be more bronchial, though true bronchophony is rare. In the interscapu- lar or supra-spinous region of the corre- sponding side, the respiration may also have a tubular quality. Over one lung, more rarely over both, the breath-sound has often communicated to it a peculiar sonorous vibrating quality, probably by conduction from the laryngeal stridor present.2 The respiratory murmur is often weakened, and it may be completely annulled at one base, though this is rare with the obvious aneurismal tumors we have now principally in mind. With the laryngoscope no alteration may be found in the condition of the cords, or they may be lax and act feebly with respiration, or one (usually the left) may be completely paralyzed and motionless. In rare cases both vocal cords have been found para- lyzed. The employment of the laryn- goscope and sphygmograph would be quite superfluous in the presence of half the signs above enumerated. They be- common, but because of them alone can any general description including all the essential phenomena of the disease be given. Aneu- risms in the other situations present one or more of the same signs obscured by their greater depth from the surface; such could only be treated of as individual cases, and will be referred to more particularly in dis- cussing the diagnosis of thoracic aneurism. 1 It is usual, but perhaps scarcely neces- sary, here to warn the too eager observer against mistaking abnormal distribution of radial or contraction of pupil from old iritis for signs of aneurism. 1 In speaking of the systolic and diastolic phenomena of aneurism, I refer to those signs presented synchronously (or nearly so) with the systole and diastole of the heart respect- ively. 2 Professor Stokes attaches great importance to this sign. "Diseases of the Heart and Aorta," 1854, p. 556. PHYSICAL SIGNS. 847 come useful aids in certain obscure cases, however, to which we shall presently refer. Such are the signs of aneurism which may be present in cases in which the di- latation is situated near the surface, at the ascending or transverse aorta - its favorite seats. We must, before consid- ering the less certain signs presented by aneurism more obscurely placed, discuss the mechanism and diagnostic value of the more important of tnose above enu- merated. The unequal pupils, venous obstruc- tion, local bulging of the chest wall, dis- placed heart, percussion dulness, and the auscultatory phenomena of tubular, en- feebled, or annulled respiration, are mere pressure signs common to aneurismal or other tumors within the chest. The un- equal pulses, the rhythmic pulsation, bruits, and shock signs, are specially char- acteristic of aneurism, though some of them may be produced or simulated by solid growths. Inequality of pupils is not a very com- mon sign of aneurism, although when present it is a very striking one. The affected pupil is usually contracted and immovable, and corresponds with the side on which the aneurism is situated. Of thirty-six cases of aneurism of the arch, of which I have notes, the pupils were unequal in four only. Dr. Walshe has observed the affected pupil vary within a few days, being " now equal to, now no- tably, now slightly smaller, now larger, than the other in size," and in one of the four cases above mentioned the pupil varied from day to day in a similar man- ner. The cause of the affection of the pupil is admitted to be pressure upon the sympathetic, paralyzing it and permit- ting the unopposed action of the third nerve upon the pupil, or irritating it and producing the rarer phenomenon of dila- tation of the pupil by excited sympathetic action (Walshe). The degree of displace- ment of heart depends upon the position and size of the aneurism. The apex beat when the first or second portion'of the arch is affected is lower and more or less displaced to the left. This displacement may be extreme in aneurism of the first portion, the tumor taking up the whole of the normal position of the heart, and being readily mistaken for it. The base of the heart is also lowered, so that the organ lies more transversely in the chest than natural, and there is commonly pul- sation at the epigastrium, which must not be hastily received as evidence of di- latation of the right ventricle. The car- diac impulse may be increased in force ; it is often, however, not stronger than natural, and may be enfeebled. It is re- markable how much less common hyper- trophy of the left ventricle is than one would expect.1 The cause of this is not clear, unless it be deficiency in the coro- nary circulation, for one would suppose there must be increased resistance to sys- temic circulation in all cases of aortic aneurism. The heaving expansile impulse, distinct from that of the heart, is diagnostic of aneurismal tumor, which, however, must be near the surface to give this sign. It is very frequently present in aneurism of the first and second portions of the arch, and it may also be present in large aneu- rism of the descending arch, but only in the later stage when erosion of the ribs and vertebral processes has enabled the tumor to present as a pulsatory swelling in the left interscapular region. In cases in which the wall of the sac is greatly thickened by fibrinous laminae, the expan- sile thrust may be entirely lost, and a knocking impulse alone felt which it is impossible to distinguish from that com- municated to a solid tumor by the aorta underlying it. The position of the tumor and the nature of the diastolic sounds will greatly assist the interpretation of this sign. In all cases where the impulse is obscure, the plan suggested by Dr. Stokes will be found of great value, viz., to " make pressure with the flat of the hand on the anterior part of the chest, while the other hand is placed between the shoulders during expiration." By this means an obscurely and deeply expand- ing character of the impulse may be de- tected which will favor the probability of its aneurismal origin. There is sometimes to be felt a distinct thrill with the beat of the tumor. This " fremissement cataire," stated by some authors to be almost al- ways present, is in reality not of frequent occurrence. Of eight cases in which I have myself observed marked thrill, in one accompanying also the diastole, in four the aneurisms were secondary to regurgitant disease of rheumatic origin, and they were all probably of the fusiform kind.2 The systolic bruit, often absent,3 though occasionally to the experienced ear very characteristic of aneurism, is by no means, as a rule, a reliable sign, except in those cases in which it is localized at some por- tion of the aorta distant from the heart, 1 Hypertrophy of the Heart was present in 8 only of 22 cases carefully recorded by Dr. Blakiston, in his work on diseases of the heart. 2 Dr. Hope had never seen a case of aneu- rism with thrill. Dr. Walshe states it to be more common in "peripheral dilatation" than true aneurism. 3 Lebert states it to have been present among the earlier signs in half his cases. Loc. cit. It existed in 22 out of my observed 36 cases, in 12 instance the bruit being double. 848 ANEURISM OF THE THORACIC AORTA. as in the right or left interscapular region or along the left side of the spine. A diastolic bruit most audible at the site of the suspected aneurism, while the second sound is clear at the base of the heart, is an important sign ; a murmur replacing the second sound at the base of the heart is of value in diagnosis when there is also evidence of a thoracic tumor, the nature of which is otherwise obscure ; its value consisting in such a case in its indicating disease within the aorta, and so render- ing the aneurismal nature of the tumor very probable. The importance of ascer- taining whether a bruit replaces one of the sounds of the heart, or is superadded to it, being, as it were, heard through it, has been well pointed out by Dr. Parkes in at least a third of the cases, however, of obvious aneurism of the thoracic aorta there is no bruit at all audible, and when we take into account obscure cases the proportion becomes much larger. The peculiar diastolic shock sound when once heard, or rather felt by the ear, is not easily forgotten. It is, when present, most significant of aneurism, and when succeeding to a more or less distinct systolic impulse, I believe absolutely so. It is only to be heard in aneurism affect- ing the first and second portions of the aorta, and when the tumor is very near the surface the shock is not infrequently so great as to communicate a second im- pulse to the hand. Of the thirty-six cases I have already referred to this sign was present in fourteen ; and in ten of these there was no murmur present, although in the majority of them other .signs of percussion, impulse, and pressure ren- dered the diagnosis clear. In a few in- stances, however, and notably in three, the diagnosis (speedily verified by death) was very difficult, and depended mainly upon the importance attached to this sign. This phenomenon has been variously ex- plained, and has given rise to much in- genious discussion.2 It is no doubt of complex mechanism, and is made up partly of the conducted second sound which is accentuated in these cases, but is chiefly caused by the transmission of a wave to the surface with the closure of the aortic valves. The sac of the aneurism becomes fully distended a little later than the aorta itself, so that the systole of the vessel commences a trifle sooner than that of the aneurism. The aortic valves close at the moment of aortic systole, and at the instant of their closure the shock wave is transmitted through the aneurism. If there be any imperfection of the aortic valves so as to give rise to appreciable regurgitation, the shock-sound or impulse is either not developed or very imperfectly so. Diagnosis.-Having given at some length the general symptoms and signs of aneurism, keeping in view more particu- larly those cases in which the disease affects that portion of the aorta occupying the anterior mediastinum, we have to take also into account in the diagnosis the question as to the part of the aorta affected by the aneurism, and, if possible, how to distinguish between aortic aneurism and dilatation of the innominate, subclavian, carotid, and pulmonary arteries respect- ively. In aneurism of the ascending aorta, but beyond the heart, the signs are grouped about the second right space close to the sternum as their centre. Greater displace- ment of heart, and interference with its function, with cyanosis and dropsy of the upper half of the body from pressure upon the innominate vein, are more often met with when the disease is in this situation. The rule is nevertheless for the aneurism to extend towards the surface rather than deeply, so that the vein often escapes se- rious compression. As the disease ad- vances, the downward displacement of the base of the heart becomes more decided, and the area of pulsation enlarges down- wards and to the right (Sibson). When the transverse portion of the arch is af- fected, the manubrium sterni is the central region of disease signs, which have a ten- dency to extend, however, more to the left than the right of the sternum. There is frequently no external tumor from the aneurism projecting backwards from the arch. The signs of pressure upon the air and food tubes, and their functional dis- turbance through involvement of the pneumogastric nerve, are most common in this variety, inequality of pulses also shows extension of the disease to this por- tion of the arch. In aneurism of the de- scending portion of the arch the signs usually present themselves most distinctly on the left side of the spine in the upper interscapular region, although the tumor may present at the second left space near the sternum. The pain is severe in the back and shoulder, the dyspnoea is usually pulmonary, either paroxysmal, assuming the character of asthma, or constant from pressure on the left bronchus, or partaking of both these characters. Diminished respiration with dulness at the base of the left lung is commonly to be observed. There may be partial or complete para- plegia from erosion of the vertebrae and pressure upon the cord. Aneurisms af- fecting the descending thoracic aorta are comparatively uncommon, and unless very large, difficult to detect. If very large, 1 Clinical Lectures. Med. Times, Feb. 1850. 2 See a criticism of the opinions of Drs. Bellingham and Lyons and M. Guerin, in Dr. Stokes's book above quoted, p. 546. DIAGNOSIS. 849 there may be curvature of the spine, dis- placement of the heart forwards and to the right, local dulness and possibly pul- sation. The whole side may be dull with | absence of respiration, from pressure upon the bronchus and subsequent blocking of the lung by retained secretions. A bruit localized in the back is almost diagnostic of aneurism in this situation. Persistent pain is always present, and is often the only sign of the disease. Laryngeal pres- sure signs are not present. It would be a matter of great practical importance to be able to say whether an aneurism affecting the innominate, sub- clavian, or carotid artery involved the arch of the aorta, since, if the aorta be distinctly included, the slender hope of permanent relief which might otherwise be entertained from operative procedure is still further diminished. It may also come to be of considerable importance to know whether in a given case the disease principally affecting the aorta involves one of these main vessels at its origin, as affording the chance of temporary arrest by checking circulation through that ves- sel. Unfortunately, the diagnosis in both these respects is in many cases beset with the greatest difficulties. There is no ab- solutely diagnostic sign separating aneu- rism of the innominate (the vessel with regard to which the question most often arises) from that of the aorta. If, how- ever, the aneurism has its centre of pulsa- tion or other signs below the second rib, or if it encroach upon the sternum with- out also presenting behind the sterno- clavicular articulation and the episternal notch, the presumption is, that the arch of the aorta is decidedly involved. A well-marked shock-sound would be also very significant of the disease being mainly aortic. We may also get some informa- tion from a comparison of the state of the pulse at the two radials; and this naturally leads us to consider the value of the sphyg- mograph in the diagnosis of aortic aneu- rism. For the purpose of showing the kind of information yielded by the use of the sphygmograph, we will take one or two tolerably well-marked cases. Fig. 130. Pulse in Aortic Aneurism. In Case I., that of Eliza B , from which the above pulse-tracing (Fig. 130) was kindly taken for me by Dr. Burdon Sanderson, there was a circumscribed aneurism of the ascending aorta, present- ing its distinguishing signs-local bulging, dulness, systolic impulse, and faint dias- tolic bruit-at the second right intercostal space near the sternum. Here it will be seen that the systolic wave, A C D, is prolonged, occupying a greater proportion of the tracing than it should do-i. e., there is a prolonged effort on the part of the left ventricle to overcome increased resistance. The impaired elasticity of the arteries is also shown by the blunted, elbow-like point at A, at the commence- ment of the systolic upstroke. The shock or percussion wave, A B C, of the pulse, is at the same time somewhat diminished; but as this phenomenon is general, not limited to one radial, it has no signifi- cance, since it may be produced by many other conditions; it is, however, very commonly, but by no means constantly, met with in aneurism of the main vessel. The only evidence we gain in this case, therefore, is that of the presence of arte- rial disease. Case II., in which the tracings were also taken by Dr. Sanderson, Dr. Murchi- son has kindly allowed me to make use of to illustrate some further points respect- ing the use of the sphygmograph. (Fig. 131.) In this case the pulsations were different in the two radials. Thomas J , a coachman, was admit- ted into the Middlesex Hospital, under Dr. Murchison, in November, 1868, with a pulsating tumor in the chest, most prominent at the third right interspace, where a double bellows murmur was audi- ble. There was scarcely any difference to be detected by the finger in the two- pulses, but the right was" thought to be slightly the smaller. It was for this rea- son only, there being no doubt about the diagnosis, that Dr. Sanderson was re- quested to take tracings of the two pulses. In the left radial tracing, the lengthened, systole, A C D, is the only noticeable fea- ture ; in the right, on the other hand, we have superadded to this sign of general increased resistance to circulation, others indicative of local interference with the arterial movements. The systolic vibra- tion, or percussion wave, A B C, very marked (rather exaggerated) in the left pulse-tracing, is almost lost in the right. The dicrotism is also more distinct in the left than the right. At the same time the right pulse is not notably smaller than the left. Hence from the pulse alone we find evidence (1) of arterial dis- vol. ii.-54 850 ANEURISM OF THE THORACIC AORTA. ease, in the prolongation of the systole : vibratile impulse (percussion wave) in the (2) of a tumor pressing upon or dilatation right radial, without diminution in the of the artery, in the local effacement of size of the pulse. Fig. 131. Had this latter phenomenon been due to extension of a coagulum, so as to par- tially occlude the innominate, the pulse would have been much smaller on the right side. But a saccular dilatation of the vessel, or a solid mass in contact with it, might act as an inefficient damper in destroying the vibratile shock, without affecting the. size of the pulse. In this case the aneurismal tumor in- vaded the thoracic parietes, and pre- sented to the right of the sternum, but the patient died of an intercurrent attack of pneumonia. After death, the aneurism was found to be globular, as large as the two fists, and involving the whole circum- ference of the aorta, from its commence- ment to the origin of the right subclavian, which came off as a separate trunk. The aortic orifice was incompetent. It has been observed that evidence of arterial disease coexisting with that of a tumor within the chest strongly favors the presumption that the tumor is aneu- rismal. Thus the intelligent use of the sphygmograph may prove in certain cases of considerable value in helping the diag- nosis of aneurism, although it should be clearly understoood that alone it is nearly useless for that purpose.1 Another sign of aneurism, much in- sisted upon by some authors, is postpone- ment or delay of pulse in one wrist. Strictly speaking, it is not correct to say that the pulse is postponed, for it begins and ends at the same time in the two wrists ; but the sense of delay may be oonveyed by the finger through the initial shock or percussion wave being oblite- rated on one side, while it is well marked on the other. Thus, in Case II., we can readily understand that the shock wave, Bight and Left Badial Pulse in Aneurism of Aorta. ABC, constituted the pulse wave, as appreciated by the finger of the observer when applied to the left radial, while on the right side this wave was annulled, and the true systolic wave, A C D, alone appreciable. Hence the pulse on the right side might have appeared to the ob- server postponed (this point is, however, not entered in the notes of the case). This point of delay in the pulse, then, is, when present, of some practical value in diagnosis; it means the appreciation by the finger of the deficiency of shock wave on one side. The distinction of aneurism of the tho- racic aorta from other tumors in the same situation, from mediastinal abscess, local empyema, uncovered aorta from con- tracted lung disease, dilated heart, peri- cardial effusion, aortic valve disease, laryngitis, asthma, and angina pectoris, requires a few further remarks. The leading features which separate aneurism from other mediastinal tumors have already been incidentally referred to in speaking of the value of the individual signs present in aneurism, and have been more specially considered in the diagno- sis of mediastinal tumors. We may, however, briefly mention a few other con- siderations of some importance to bear in mind in cases of difficulty, as affording, when taken in association with the signs of tumor, additional evidence for or against aneurism. 1. If the age of the patient be under twenty-five, in the absence of any history of direct injury, the chances are against aneurism. 2. Great emaciation in the absence of intense prostrating pain, is against aneu- rism. 3. Great displacement of heart, in the absence of marked signs of a large pulsat- ing tumor, is against aneurism. 4. Female sex of the patient is against aneurism. 5. On the other hand, severe pain, con- 1 In the Med. Times and Gazette for 1873, pp. 141 and 122, will be found valuable original papers, by Dr. F. A. Mahomed, on the use of the sphygmograph in the diagnosis of aneurism. PROGNOSIS 851 stant, with occasional exacerbation, is in favor of aneurism. 6. The more inconstant the distal signs of pressure-unequal pulse, irregular pupils, laryngeal and bronchial dyspnoea, dysphagia-the greater the probability of the disease being aneurismal. 7. Dr. Walshe observes that " the ab- sence of symptoms and signs, indicative of ordinary affections of the heart and lungs, in an individual suffering from persistent anomalous disturbances within the chest, even though he does not, or rather because he does not, exhibit any failure of general health, affords strong motive for suspecting aneurism." In the diagnosis of pulsating empyema from aneurism, very rarely required, the pres- ence of fluid impulse without bruit or shock sound, the extension probably of the effusion beyond the limits of an aneu- rism, the pointing of the abscess, and the presence of irritative fever, would be the distinguishing signs. Cases not infrequently occur of diseases affecting the apex of one lung, causing the retraction of its margin away from the base of the heart and aorta. Such cases present many of the signs of aneur- ism-dulness, forcible local pulsation, sometimes a bruit, with palpitation and dyspnoea.1 The history of such a case, the evidence of distinct disease of the lung, and of enlargement of the opposite lung, with elevation rather than depres- sion of the heart's apex, and the absence of other pressure signs, will usually pre- vent error in diagnosis. In some cases, aneurism of the descend- ing aorta, compressing the left bronchus, and leading to collapse of the lung, or to its blocking by catarrhal products, be- comes so masked by the secondary affec- tion, and from the depth of the tumor in the mediastinum, as to make the diag- nosis from chronic pneumonia or pleurisy most difficult. In such cases, however, the urgency of the dyspncea, especially on excitement, and the deep-seated pain and palpitation, will usually awaken at least grave suspicion in the right direction. Dr. Hope lays some emphasis on the possibility of aortic regurgitant disease being mistaken for aneurism. The sym- metrical pulsation of all the vessels and the seat of the murmur will usually pre- vent such an error. Dilatation of the commencement of the aorta is not unfre- quently occasioned, however, by regurgi- tant disease, and the locomotion of the vessel being always increased, the signs of the dilatation are thereby much exag- gerated. Laryngeal symptoms are apt to be pres- ent in the most obscure forms of aneurism, projecting deeply from the back of the arch. Such cases may be mistaken for laryngitis ; but the inconstancy and par- oxysmal character of the symptoms, so rare in adult laryngeal affections, should at once arouse suspicions, and laryngo- scopic examination with a minute explora- tion of the chest will then usually solve the difficulty. Prognosis.-In aneurism of the aorta, the prognosis is within a brief and uncer- tain space of time fatal. It is the uncer- tainty as to the time of death, and the suddenness with which it may at any time occur, that gives to this disease its peculiar terror. It is this peculiarity, moreover, which should make us so ex- tremely careful not to make a wrong diagnosis; and when there is any doubt, as there often must be, we should give the patient or his friends only a sufficient insight as to his critical condition to in- sure the due settlement of his affairs. Duration.-From six months to four years from the time of detection of the aneurism (Lebert).1 This limit has been extended in certain cases. The main characteristic of the duration of aneur- ism, however, is its uncertainty. The aneurismal wall may be obviously thick- ening by fibrinous deposit at one point while fatal erosion is taking place at an- other. Mode of Death.-Rupture is by far the most common termination of aneurism, and the more latent the aneurism, the more uniformly does death occur in this way. Dr. Sibson2 remarks, " It will be observed throughout, that the greater the proportion of ruptures in any group of aneurisms of the aorta, the smaller is the proportion of instances in which the dis- ease is indicated by symptoms during life, and vice versa. " The rupture may take place into the pericardium, left or right pleura, bronchi or lungs, trachea or oeso- phagus, or externally or more rarely into the vena cava, right auricle, &c. Dis- secting aneurism, most commonly affect- ing the first portion of the aorta, almost invariably bursts into the pericardium. Circumscribed aneurism of the ascending aorta most commonly also gives way into the pericardium, of the transverse aorta into the trachea or oesophagus, of the de- scending into the left pleura, left bron- chus, or oesophagus, or into the abdomen. A certain small number of patients die of exhaustion, fewer still of syncope or as- 1 I have met with several cases of the kind which might readily have heen mistaken for aneurism; and in one case the error had heen actually made, and the diagnosis of aneurism communicated to the patient by an observer of some experience. 1 Loc. cit. Analysis of 30 cases. 2 The Aorta and the Aneurisms of the Aorta. 852 ANEURISM OF THE THORACIC AORTA. phyxia (apart from hemorrhage), or from acute intercurrent disease.1 Treatment.-The objects we have in view in tlie treatment of thoracic aneur- ism are, firstly, to diminish the strain upon the injured vessel as much as possi- ble ; secondly, to encourage the deposi- tion of fibrine within the aneurism. We have further, by the administration of anodyne remedies internally or locally, to lessen suffering. In carrying out these objects, rest as far as is possible for the circulation is of the first importance, and the conditions most necessary to secure this rest to the circulation, are strict muscular repose, mental quietude, and regulated diet. It requires much intelli- gence on the part of the patient, and tact on that of the physician, to maintain these conditions for a sufficient length of time to be of service, even when surrounding circumstances are favorable. The recumbent posture, or that most nearly approaching it and yet comfortable to the patient, should be preserved, all excitement avoided, and the nutrition maintained by a diet restricted in quan- tity, but enriched in quality. Blood rich in nutritive elements more readily depos- its fibrine, and favors those efforts at re- pair which result in a welding together of the fibrinous layers nearest the arterial wall, while, mechanically speaking, it has no more pressure effect upon the weak- ened vessel than blood deficient in these elements. On the contrary, we daily find that whenever an anaemic condition is present the circulation is hurried and more easily disturbed. Evidence of a rapid softening down of the laminae which had almost blocked an aneurism may sometimes be found post mortem in those who have subsequently to careful treat- ment again been subjected to the debili- tating circumstances of a life of poverty. Fluids must be only very moderately par- taken of; milk, soft puddings, eggs, and a moderate quantity of meat may be allowed. Mr. Tufnell,2 whose treatment of large internal aneurisms has been re- markably successful, restricts the food taken to 2 oz. of bread-and-butter and 2 oz. of new milk for breakfast; 2 or 3 oz. of bread and 2 or 3 oz. of meat for dinner with 2 oz. to 4 oz. of milk or claret; and 2 oz. of bread-aud-butter with 2 oz. of milk for supper. In his first recorded case he maintained this treatment, com- bined with absolute rest, for nearly two months with complete success. Mr. Tuf- nell would of course allow a certain slight variation from this diet measure to suit individual cases: his treatment is more- over only applicable to cases of sacculated aneurism. Dr. Sibson1 also advocates the regulation of the diet in conjunction with rest, but is content to limit the quantity of fluid taken per diem to within one pint. Let me repeat, rest in the re- cumbent posture is of the utmost import- ance to the success of this treatment; Mr. Tufnell reckons that in some of his cases this alone lessened the number of distensions of the aneurismal sac by more than 20,000 a day I2 Stimulants, or I should rather say stimulation, must be absolutely interdicted. During this treat- ment too frequent examinations are to be avoided, but the circulation and the aneurismal impulse, when within our reach, should be carefully watched. Cer- tain drugs-chloral, opium, digitalis, ver- atria, and aconite-are useful to allay ex- citement of circulation. They are none of them efficacious without rest, but they, and particularly chloral and opium, may help in diminishing the restlessness and impatience of persons naturally irritable who have great difficulty in submitting to the treatment by diet and recumbency. Belladonna applications may be employed for the purpose of relieving pain, but when this is acute the subcutaneous in- jection of morphia is the best remedy. The continuous application of an ice bag, suspended from above the patient, to the tumor when prominent externally will often greatly relieve pain, reduce inflam- mation, and perhaps even help to promote consolidation within the sac. Gentle laxatives or saline purgatives must be given to prevent any effort in relieving the bowels. When, as sometimes hap- pens on the patient first coming under notice, there is any undue fulness of ves- sels present, free purgation with salines will be attended with marked relief up to a certain point. In cases of urgent dys- pnoea with engorgement of vessels, vene- 1 See on this point the statistics of Dr. Crisp, Dr. Sibson, and Professor Lebert. The above general remarks are more espe- cially founded upon the very careful and complete Tables of Dr. Sibson-584 cases. Lebert's statistics are on this head less trust- worthy, the numbers being much smaller; thus of 41 cases he finds 4 rupture externally, Drs. Crisp and Sibson finding this termination in about 4 per cent. Lebert also gives no cases of rupture into oesophagus, whereas this is rather a frequent termination of cases of aneurism-of transverse and descending aorta-about 5 per cent. (Sibson). 2 Thoracic Aneurism successfully treated by restricted Diet and the application of Ice. Dublin Hospital Gazette, January, 1858 ; also on the Treatment of Thoracic and Abdominal Aneurisms, by J. Tufnell, F.R.C.S.I., Army Med. Rep. for 1862, and Medico-Chir. Trans- actions for 1874. 1 Croonian Lectures, Lancet, 1870. 2 See an able review of the modern treat- ment of aneurism in the Medical Times and Gazette for December 20, 1873. TREATMENT. 853 section should be promptly employed; repeated blood-letting after the manner recommended by Valsalva1 in the last century, combined with the lowest possi- ble diet, is not likely to find favor in the present day. Various internal remedies have been administered with the view of favoring the formation of coagulum within the aneurism, either by rendering the blood less watery-e. g., saline purgatives, diu- retics ; or by affecting it or the aneurismal wall in some specific way-e. g., acetate of lead, iodide of potassium, ergot. The free administration of iodide of potassium in aneurism has been pretty extensively tried. It seems to have been first intro- duced by Nelaton2 in 1859, and subse- quently tried by Drs. Bouillaud,3Chucker- butty4 of Calcutta, Roberts5 of Man- chester, and Balfour6 of Edinburgh ; and the concurrent testimony of these several observers is very favorable to the drug as a valuable agent in the treatment of this disease. Dr. Balfour holds that "no treatment for aneurism, and especially for internal aneurism, holds out anything like an equal prospect of relief, if not of cure, with that by the iodide of potassium." The drug must be given in large doses (gr. xx) and continued for many months. Its mode of action is unknown ; Dr. Bal- four7 thinks that it is not by increasing the coagulability of the blood, but by its seda- tive action upon the heart and " by some peculiar action on the fibrous tissue, by which the contraction of the sac is aided and its walls are strengthened and con- densed." Langenbeck8 having observed the great value of ergot, particularly when used subcutaneously as ergotin in arresting hemorrhage, tried the drug in the same way in aneurism, and with considerable success in a case of the disease affecting the innominate and subclavian trunks. He injected | gr. of the watery extract, increasing to 3 grs., every three days. It is difficult to say how far in this, as in other instances of the reputed efficacy of drugs in the treatment of circulatory dis- eases, the attendant rest may have aided in producing the amelioration of symp- toms. Rest and recumbency, with the aid of drugs, failing or being impracticable for the obliteration of aortic aneurism, the question arises, whether any operative measure can be adopted to control the cir- culation through the sac so as to favor its gradual obliteration by laminated clot. M. Velpeau,1 in 1839, seems to have been the first to entertain the question of liga- ture of one or more of the main branches of the aorta for the cure of aneurism, and this treatment has been most recently ad- vocated by Dr. Cockle2 and practised by Mr. Christopher Heath.3 The exact value of this method of treatment, and the rules which should guide us in adopting it, cannot be regarded as yet thoroughly ascertained. In cases in which one of the great vessels-most commonly the in- nominate-proceeding from the arch is largely involved, or in which the aneurism is at least extending in the direction of one of these main branches while there is no evidence of extensive arterial degene- ration, the distal ligature may be most appropriately tried, the principle of the ligature being to greatly enfeeble the cur- rent through the sac by arresting the cir- culation through the branch principally involved or most nearly proceeding from the aneurism. Ligature of the right carotid or subclavian, or both, or of the left carotid, must be decided upon accord- ing to the direction of the growth of the aneurism. Distal pressure upon the great vessels of the neck has been employed, and though most difficult to effectually carry out, is yet, perhaps, worthy of a further trial. The common object of the different kinds of treatment we have hitherto con- sidered, viz., rest, diet, compression, and ligature, has been that of encouraging spontaneous coagulation within the aneu- rismal sac, whether by lowering the cir- culation generally, or by locally arresting it entirely, or lessening its force or alter- ing its direction. Mr. Moore4 in 1864 proposed a new 1 For the most modern authoritative infor- mation on the surgical treatment of aneurism, vide Lectures delivered by Mr. Holmes, at the College of Surgeons, 1872. Lancet, July, 1872, lect. ii. 2 Further Contributions to the Pathology and Treatment of Aneurismal Tumors of the Neck and Chest, by John Cockle, M.D. Lan- cet, 1869, pp. 422 and 489. See also Clinical Transactions for 1872. 3 On the Treatment of Intra-thoracic Aneu- rism by the Distal Ligature, by Christopher Heath, F.R.C.S., 1871. * On a New Method of procuring the Con- solidation of Fibrine in certain Incurable Aneurisms. Med.-Chir. Trans, vol. Ivii. p. 129 et seq. 1 Vide Observations on Aneurism, by Mr. Erichsen, Syd. Soc. 1844, pp. 239 and 261. 2 Clinique Europdenne, July, 1859. 8 Idem, August, 1859. 4 Iodine of Potassium in the Treatment of Aneurism. Brit. Med. Journal, July, 1862. 5 Clinical Lecture on the successful use of Iodide of Potassium in the Treatment of Aneurism. Idem, January, 1863. 6 On the Treatment of Aneurism by Iodide of Potassium. Edinb. Med. Journal, July, 1868. 7 Idem, January, 1874, p. 645. 8 Idem, November, 1869. Abstract from the Berliner klinische Wochenschrifl, March, 1869. 854 ANEURISM OF THE THORACIC AORTA. treatment of aneurism, by the insertion into the sac of a foreign body (fine iron wire) to act as a nucleus for rapid and firm coagulation. The result in the case to .which he applied this treatment-a case of aneurism of the thoracic aorta rapidly perforating the chest-wall-was discouraging, inflammation of the sac, embolism of distant vessels, and great in- crease in the sufferings of the patient being occasioned. The same idea has since, however, found favor among a few bold operators, who have severally tried needle punctures, the introduction of car- bolized catgut, watch-spring (14 inches 1), and iron wire, with uniformly deplorable results. The latest and most rational method of the kind adopted is that of Dr. Levis of Philadelphia,1 who lias intro- duced through a capillary trocar a great length of fine horsehair into the sac of a subclavian aneurism. I think it must be allowed, however, that this mode of treat- ment is wrong in principle, and must, therefore, in the majority of instances fail in practice. If direct coagulation of blood within the sac be aimed at, it is only thus accomplished in a dangerous and imper- fect manner, the clot formed being sub- divided and soft, and entangled round a foreign body in the centre of the sac in- stead of being laminated and firm, and deposited around its circumference; hence danger of inflammation of the sac, of capillary or larger embolisms, and of blood-poisoning from rapid disintegration of the clot. If the object be to determine coagulation within the sac by setting up a certain degree of inflammatory action, or if the fear of inflammation resulting from these procedures be disregarded on this ground, the practice must equally be condemned as dangerous, if not unjusti- fiable, for we have no means of controlling the inflammation when induced in the main blood-channel. It must further be borne in mind that by producing suddenly coagulation within an aneurism without that local or general lowering of the cir- culation which would favor its natural occurrence, we necessarily run great risk of causing rapid extension of the disease in some other, perhaps more fatal, direc- tion. These objections, it must be con- fessed, have, too, a certain force when applied to the somewhat less modern practice of galvano-puncture, which has recently, in common with all other methods of treating this deadly malady, been very keenly discussed and tested. There is this striking advantage in gal- vano-puncture, however, that no foreign body is allowed to remain within the aneurism. It has, moreover, been tried with success now in a few instances.1 The idea of employing electricity in the treatment of aneurism seems to have sprung from the physiological experi- ments of Scudamore 1824, Muller 1832, and Ansell 1839, and to have been first applied in practice by M. Petrequin in 1841.2 It was Ciniselli, however, who, in 1846, first employed electro-puncture in the treatment of aortic aneurism,3 and the first definite principles on which to proceed in the employment of this agent were laid down still later by MM. Baum- garten and Wertheimer in 1852,4 as the result of extended experimental inquiry. The experiments of these gentlemen showed (a) that coagulation might be with certainty induced at any point within a large vessel of an animal during life by electrolysis, (6) that this coagula- tion was most firmly5 affected around the positive needle when both were intro- duced : (c) that the best way, however, of producing coagulation was to insert the positive needle only, applying the nega- tive element by means of a moistened sponge or metallic conductor placed on the external surface. Dr. Fraser, in 1867, confirmed and added to these conclusions, observing that, whereas at the positive needle a firm and comparatively small clot was formed, at the negative needle, on the other hand, the coagulum was large and frothy. Dr. John Duncan6 is, however, of opinion that the needles connected with both poles should be introduced, and in this view he agrees with Ciniselli.7 Dr. 1 Of 13 cases treated by Ciniselli's method, between July, 1868, and July, 1870, 6 were "cured." Of them 3 relapsed after 17, 3, and 4 months respectively; the latter case, however, after a second operation, being again "cured" and remaining so, after 8 months. For details of 23 cases, and for a description of Ciniselli's method of employing electro-puncture, see his paper in the Annali Universali di Medicina for November, 1870, p. 292 et seq., Table, p. 625. An abstract of this paper is given in the Jahresbericht for 1870, Bd. ii. s. 109. 2 Vide Essay by Dr. Fraser, of Edinb., on the Action of Galvanism on Blood and on Al- buminous Fluids, 1867. 3 Case related in the Annali Universali di Medicina, 1870, p. 294, and referred to with 22 others in a Table at p. 625. 4 Gazette des Hopitaux, June 19, 1852. 5 Confirming a previous observation by Prof. Schuh, Vierteljahrschrift fur die prak- tische Heilkunde, Bd. i. 1851. 6 On the Surgical Applications of Elec- tricity, Edinb. Med. Journal, 1872, 506 et seq. 7 In this view also Mr. Marcus Beck con- curs : and the comparative effect upon an al- buminous fluid of inserting only one or both 1 Referred to by Mr. Holmes, in London Medical Record, December 17, 1873. TREATMENT. 855 Althaus,1 on the other hand, regards the negative pole as the one to the use of which "we have to look for the cure of aneurism." As to the mode in which electricity effects coagulation within an aneurismal sac, the question whether it may be by the mere passage of the electrical current through the blood, is set at rest by the observation of Dr. Fraser, that although the two needles be separated by an inter- val of blood through which the current must pass, yet coagulation takes place only around each needle separately. A certain amount of inflammation is often set up in and about the sac by this agent, which no doubt, if it do not proceed to a dangerous extent, may help to promote consolidation ; this inflammation is, how- ever, shown by Drs. Duncan and Fraser to be not essential to coagulation, but, on the contrary, to be guarded against as one of the chief sources of danger. The coagu- lation is produced in truth, as pointed out by Steinlein2 and confirmed by others, by (a) electrolytic decomposition of the salts of the blood which are mainly instru- mental in maintaining its fluid state; (b) by the acid elements set free at the positive pole directly causing coagulation there, or combining with the oxidized metal to form salts which precipitate the albumen. This latter action may be in- creased by coating the positive needle with some more oxidizable metal, such as zinc. In the writings of Dr. John Duncan, Dr. Fraser, Mr. Holmes,3 and Prof. Cini- selli already quoted, will be found re- corded the clinical and physiological expe- riences which furnish us with all the knowledge we at present possess on the subject. The valuable records of indi- vidual cases of galvano-puncture in aneu- rism which are gradually collecting are as yet too few to admit of classification. So far as they have gone, however, they do not encourage us to anticipate a very favorable opinion of the operation, for of nine cases of aortic aneurism thus treated of which accounts have appeared in the English journals within the last two years, in only one, that of Dr. McCall Ander- son's, has a decidedly good result been obtained, although in one or two other instances, in Drs. Ralfe and Johnson's case, and in a case of Dr. Bastian's, per- foration of the chest wall has been for a time averted. In other instances, how- ever, this perforation has undoubtedly been hastened by the needle punctures. Appropriate cases in which the operation has been undertaken with the view of curing the aneurism must be classified apart from those in which the puncture is made with the view of temporarily stanch- ing an aneurism already diffused and threatening to burst through the surface, before we can hope to obtain reliable sta- tistics upon which to decide as to the true value of this treatment: moreover we cer- tainly have not yet arrived at the method of operating agreed on all hands as the best. Meanwhile the following appear to be the most important points respecting the operation which the physician should bear in mind:- 1. (ci) The cases of thoracic aneurism which seem most suitable for treatment by galvano-puncture with a view to perma- nent relief are those in which the dilata- tion is presumably sacculated, near to the surface, and advancing outwards, the sac being as yet entire ; (6) the operation may sometimes be performed as a palliative measure to retard rupture through the surface, or to relieve suffering. 2. The treatment by rest, with the aid of restricted diet and appropriate drugs, must have first been fairly tried and proved useless or impracticable before any operative procedure is justifiable, and the same absolute rest and careful diet must be maintained throughout the operation and the subsequent treatment. 3. It is best not to freeze the surface before puncture, although its sensibility may be deadened by cold. Sometimes the operation may be usefully preceded by the administration of a dose of morphia subcutaneously to enable the patient to remain without suffering in one position during its performance. 4. The battery used should be of many (10 to 30) cells with plates of small sur- face. By diminishing the size of the plates and increasing the number of the cells used, a given electrolytic power is obtained with a less intensity of heat than with fewer cells and larger plates.1 needles is well illustrated by a simple ex- periment made by Mr. Beck and Dr. Poore. Into some white of egg held in the hollow of the hand the positive needle connected with twenty cells of Weiss's battery was introduced, a sponge connected with the negative pole being applied to the back of the hand. After five minutes no action upon the albumen had been effected. Both needles were then intro- duced together into the albumen, and in two minutes a firm coagulum of the size of an oat surrounded the positive needle-point, and a frothy mass as large as a pea was found at the negative needle. Lancet, 1873, p. 550. 1 Medical Electricity, 2d edit. 1870, p. 607. 2 Galvanopunctur bei Varicositaten und Aneurysmen-Zeitschrift der k. k. Gesell- schaft der Aerzte zu Wien, 1853. Quoted at p. 471 of Dr. Hammond's translation of "Meyer's Electricity in its Relations to Prac- tical Medicine." 8 Lancet, 1872, vol. ii. pp. 336 and 663. 1 Foveau's improvement of Weiss's instru- ment is now considered the best. Dr. Poore has, however, electrolyzed white of egg by 856 ANEURISM OF THE THORACIC AORTA. 5. The needles connected with both the positive and negative poles and of the dimensions of medium-sized harelip pins, insulated with vulcanite to within a cer- tain distance of their points (according to the size of the aneurism), should be thrust vertically into the aneurism so as to avoid scratching or puncturing its inner surface at any other point. 6. The electrolysis should be continued for twenty minutes or half an hour, or until some decided alteration in the pulsa- tion or bruit of the aneurism has been produced. The withdrawal of the needle must be effected with the utmost caution, to avoid the loosening of the clot should it happily have become adherent to the wall of the aneurism. A second and a third employment of the agent may be made at intervals of several days. The question of tracheotomy occasionally comes before us in cases of thoracic an- eurism, in which death is threatened from paroxysmal dyspnoea. If we accept the views lately advocated by Dr. Bristowe, that not only the constant, but even the paroxysmal dyspnoea is in the majority of cases due to direct pressure upon the trachea, we can expect no relief from this operation. If, however, the view that the paroxysms of dyspnoea may be occa- sioned either by irritation or destruction of the recurrent nerves be still tenable, we may expect to prolong life and to render death less terrible by its performance. There have been cases in which the opera- tion has distinctly though only tempora- rily saved life. Spontaneous Rupture of the Aorta. Spontaneous rupture of the aorta is most commonly the result of antecedent disease of the coats of the vessel, more particularly of the senile atheromatous kind. It may occur, however, in conse- quence of stenosis of the vessel (Roki- tansky), though such cases are necessarily very rare. Even in such cases, too, the proximate cause of the rupture is disease of the vessel wall, either abnormal deli- cacy and thinness (Rokitansky) or athe- roma the result of heightened blood pressure. Rupture of the aorta most commonly takes place at or near its com- mencement (Broca, Peacock). It may at once extend through all the coats of the vessel, causing immediate death from hemorrhage, or, as is more commonly the case, it extends through the internal to the middle coat, and the effused blood tearing apart the layers of this coat, or separating it from the external for a greater or less distance, a dissecting aneur- ism arises. The coats of the vessel may be thus dissected or separated apart throughout the whole length of the aorta, and even along some of its main branches. Dr. Todd1 relates a case where the sepa- ration extended from half an inch beyond the valves to the abdominal aorta and along the innominate and right carotid arteries, causing drowsiness and partial left hemiplegia by compressing the canal of the last-named vessel. There is frequently no discoverable ex- citing cause of the rupture ; in a few cases it has been traceable to great mental emo- tion, or to cardiac excitement from over- distension of the stomach ; external vio- lence, as the shock of a blow or fall, may also give rise to it. Rupture of the aorta may occur at any age after thirty. Dis- secting aneurism occurs mostly in ad- vanced age; it is about equally common in both sexes.2 There are no special symptoms attributable to rupture of the aorta save those of fatal syncope. In cases, however, in which the rupture is incomplete and a dissecting aneurism oc- curs, the symptoms are, acute rending pain in the prsecordial region extending to the left shoulder and spine, severe car- diac dyspnoea, orthopnoea, with profound shock to the system, pallor of countenance, great anxiety, and feeble, irregular pulse. The rupture of the external coat may quickly follow that of the inner, anol death immediately ensue, or the patient may rally for a few hours, or even days, before a second attack proves fatal. In some rare cases, in which the aneurism becomes circumscribed, its future course may closely resemble that of other circum- scribed aneurisms. The treatment of aortic rupture or dissecting aneurism is, of course, merely palliative. Narrowing of the Aorta. In certain rare instances there is a con- genital deficiency in the calibre of the whole aortic system. This general nar- employing a Pulvermacher's chain of fifty- eight elements moistened with dilute sul- phuric acid (one part to thirty); and he suc- ceeded in producing in an hour a firm clot at the positive electrode three-quarters of an inch long, of the diameter of a goose-quill and weighing nine grains. Dr. Poore sug- gests, as well worth a trial, the employment of a similar battery in the treatment of aneu- rism, and thinks it possible that patients might be able to bear the application of a ■current from such a battery for far longer periods than when elements of larger surface are made use of. This is, of course, a ques- tion only to be decided by direct experiment. Vide the book now published. 1 Med.-Chir. Trans, vol. xxvii. 1844. 2 Rokitansksy's cases show a slight pre- ponderance on the male side; in Dr. Pea- cock's it was slightly more frequent among females. NARROWING OF THE AORTA. 857 rowing usually affects mainly the descend- ing aorta, particularly the descending portions of the arch. It is most common in females, and is often overlooked, being attended with no marked symptoms until the period of puberty, when the insuffi- cient general development, with marked deficiency in the sexual system, become apparent. The only physical signs present are those of hypertrophy and dilatation of the left ventricle, and smallness of pulsa- tion in the abdominal and iliac arteries. A more common form of congenital narrowing of the aorta, is that in which the constriction is limited to that portion of the arch beyond the subclavian artery, either at or a little above or below the ductus Botalli. The term "coarctation of the arch of the aorta" is often applied to this condition. The constriction rarely occupies more than half an inch of the length of the vessel. It may be ring-like, as though the vessel had been tied by a moderately thick piece of string, or it may be caused by a fold, more or less deeply projecting into the vessel, or by a scar- like contraction corresponding with the position of the duct; or again, the vessel at this point may be converted into a thickened, impermeable cord. The de- gree of constriction varies from complete closure to a diameter of three or four lines, or a mere narrowing. Only in five cases out of forty collected by Dr. Pea- cock was the obliteration complete. The walls of the aorta at the seat of the con- traction may be natural or thickened or thinned. The ductus arteriosus is usually closed, but in some cases it is open for part of its extent, in others it is more or less pervious throughout; it is affected in one of these ways in about one-sixth of the cases. Above the constriction the aorta is as a rule widened, sometimes greatly dilated ; it may, however, be of natural dimensions; below the constric- tion, it is either of normal size, or more frequently somewhat diminished: occa- sionally, however, it is even widened, and in one case quoted by Dr. Peacock, an aneurism was found immediately below the stricture. A deficiency in the num- ber of aortic valves has been found in one-eighth of the cases, and other cardiac malformations have been mentioned. The great branches of the arch are always en- larged, and by the communication of some of the branches derived from them (the transversalis colli, superior intercostal, internal mammary'), with corresponding branches from the descending aorta (in- tercostal, epigastric), a tolerably free col- lateral circulation is maintained. Hyper- trophy of the left ventricle is a necessary consequence, and is often attended with dilatation and with, no doubt, secondary dilatation and hypertrophy of the right cavities of the heart. This affection is three times more fre- quent in the male than the female sex. In almost every case the deformity is either congenital, or acquired in the first few days of infant life : death however may occur at any age, usually but not al- ways preceded by symptoms of heart dis- ease. There are several theories to ac- count for the occurrence of this deformity of the aorta, of which three are admitted by different authors as applicable to cer- tain cases :- 1. Although the normal process of closure of the ductus arteriosus, which oc- curs within the first week or ten days of life, is simply one of gradual withering and contraction, yet in some instances it is delayed by the formation within the duct of a fibrinous coagulum, which may extend into the aorta and completely oc- clude it at the point corresponding with the entry of the duct. As the clot subse- quently becomes gradually absorbed, the walls of the aorta and those of the duct contract upon it to their complete obliter- ation. Foerster adopts this theory as ap- plicable to those cases in which both the duct and the aorta are completely closed. 2. In other cases, however, the coagu- lum may not extend beyond the duct, the walls of which, thickened from the irrita- tion attendant upon the presence of the clot, contract upon it as it becomes ab- sorbed, puckering the adjacent walls of the aorta in an irregular and scar-like manner, so as partially to constrict the vessel. 3. A more generally applicable explana- tion is, that this deformity is a partial preservation of the foetal condition by which the aorta conveys blood to the head and upper extremities, and the pulmonary artery, continuous through the duct with the descending aorta, supplies the lower extremities and abdominal viscera. It is the view of Reynaud and Rokitansky, and is adopted by Dr. Peacock and most modern authors, and may be described as follows:- At the termination of foetal life, with the expansion of the lungs the blood- stream is diverted from the ductus arterio- sus through the two branches of the pul- monary artery. The blood thus diverted returns to the left ventricle and increases the volume to be transmitted through the first and second portions of the aorta by the amount destined for the supply of the lower half of the body. In the normal condition of things the isthmus of the aorta-that portion connecting the great brachio-cephalic trunk with the ductus ar- teriosus as it joins the descending aorta- now rapidly expands so as to become a part of the main arterial channel, while the starved ductus dwindles. If, however, as sometimes happens, whether from de- fective nutrition, rigidity from inflamma- 858 ANEURISM OF THE THORACIC AORTA. tory thickening, or any other cause, this isthmus fails to widen, the increased vol- ume of blood finds exit through collateral channels into the descending aorta, the branches of the arch expand, and their twigs, communicating with branches from the descending trunk, enlarge so as to supply to it the blood required for the lower limbs and viscera. Thus far the process takes places in the first days of extra-uterine life, but the narrowed por- tion of the aorta, having the extra pres- sure of blood thus removed from it, still further atrophies from disuse, and in course of time may become quite closed, although its channel is probably in these cases never completely obliterated. An increased muscular power of heart is re- quired to compensate for the increased re- sistance to circulation necessitated by the transmission of the blood through circuit- ous and divided routes instead of by one short and broad channel to the descending trunk. It has already been stated, that this de- fect in the aorta is not necessarily attended with any symptoms, and that when they arise they are those of lesion secondary to the aortic deformity, of hypertrophy and dilatation of the heart, rupture of the heart or aorta, or great dilatation of the main vessel above its narrowed portion. It is unnecessary to refer to these symp- toms in detail. Diagnosis. - The diagnosis has not often been made, but when attention is directed to such a case the physical signs pointing to the constriction and its situa- tion, though few, are tolerably significant. They are those of hypertrophy of the heart, most distinctly of the left ventricle, usu- ally attended with some dilatation, throb- bing of the great vessels of the neck and upper extremities; while arteries not usually visible, the transverse cervical, and thyroid, and the small anastomosing vessels at the margin of the sternum and epigastrium are enlarged, tortuous, and pulsating. With this activity of circula- tion in the upper half of the body is con- trasted the febrile pulsation of the abdomi- nal aorta, iliac and femoral arteries, all pulsation in the popliteal and the tibial vessels being often absent. A systolic, or rather post-systolic, murmur may be heard over the aorta and also over the enlarged vessels. The presence of aneu- rism or of some other mediastinal tumor pressing upon the aorta will be excluded by the absence of any other signs of pres- sure upon the nerves, or food or air tubes, or upon the lungs. Prognosis.-In a considerable propor- tion of cases death occurs from some lesion apparently altogether unconnected with the aortic deformity, eleven cases out of the forty referred to by Dr. Pea- cock having died from cerebral disease, bronchitis, pneumonia, &c. But the cir- culation is carried on at high pressure, at least as regards the heart and first por- tions of the aorta, and sudden death, from syncope or rupture of the heart or aorta, occurred in eight of the forty cases. In the rest, the heart in time gives way under its excessive toil, degeneration and dilatation succeed to hypertrophy, and death slowly occurs in the way usual to such affections. Supposing, therefore, that the diagnosis be made while the patient as yet appears to be in fair health, there is a very fair chance that if, bearing in mind the very mechanical nature of the result of this malformation, he be warned against such exercises as increase the circulation, and encouraged in calm intellectual pur- suits and a sedentary profession or busi- ness, he may possibly live to the average period of life. The danger of sudden death should undoubtedly be mentioned to his friends, or to the patient himself. There is, of course, no special treatment other than "expectant" to be adopted, but this palliative treatment is of the greatest importance. The most concise account of this affec- tion of the aorta is contained in an original article by Dr. Peacock in the " British and Foreign Medico-Chirurgical Review" for April, 1870. Dr. Peacock gives a brief abstract of all the cases re- corded up to that time, with full refer- ences to the authors. Rokitansky is the principal authority on the subject. "Path. Anatomy," vol. iv., and his work " Ueber einige der wich- tigsten Krankheiten der Arterien," 1852. See also section on "Coarctation of the Aorta" in Dr. Walshe's work on "Dis- eases of the Heart." In Foerster's " Handbuch der Pathol- ogischen Anatom ie," p. 726, will be found a brief description, with references to fifty-two cases by different authors. ANEURISM OF THE ABDOMINAL AORTA. 859 ANEURISM OF THE ABDOMINAL AORTA. By Dr. William Murray, F.R.C.P. Bond. The pathological anatomy of Aneu- rism, the degeneration of arteries, and the process of erosion in bony structures, are subjects too general to be handled in an article on the diseases of a single bloodvessel: the following remarks will not therefore be so extended as to em- brace those general conditions to which the aorta is subject in common with the whole arterial system. These will be alluded to when they present features pe- culiar to the abdominal aorta; but the discussion of the several diseases to which this lower half of the vessel is subject will chiefly engage our attention. The latter afford so deep a study in pathology, diagnosis, and treatment, that a distinct treatise might well be written on them, especially as they often involve excruci- ating agony to the sufferer, and have in most cases a fatal issue. The Anatomical, Characters of the Disease.- Atheromatous, calcare- ous, or ossific (Virchow) changes in the coats of the aorta are doubtless the chief predisposing causes of Aneurism ; they rob the vessel of its elasticity by destroy- ing its middle coat, where resides the tis- sue on which the dilatation of the artery and its subsequent recoil depend, and thus they lead either to a permanently dilated condition of all the coats of the vessel (at the diseased spot), constituting a true Aneurism, or the degenerated coats give way and a false Aneurism is pro- duced. In addition to this source of origin, a tolerably healthy aorta may be ruptured in its middle or internal coats, and thenceforth an aneurismal pouch may be formed at the seat of the accident; and this fact is worthy of remembrance, because an Abdominal Aneurism arising from muscular exertion or external vio- lence may thus occur in a healthy vessel, and be subjected to successful treatment, whereas the occurrence of the disease apart from straining or violence, points strongly to a diseased condition of the vessel, and augurs ill for the future course of the disease. It is also important to remember that Abdominal Aneurism is much less often complicated by valvular disease of the heart or extensive arterial disease, than is found to be the case in Aneurism of the thoracic aorta and its branches. Simple dilatation of the abdominal aorta is rare, and the cases of true Aneu- rism bear a small proportion to the cases of false Aneurism in this vessel. Dr. Sibson's tables show 60 per cent, of Aneu- risms in the abdominal aorta to have been sacculated, and 10 per cent, non- sacculated ; as we may take it for granted that almost all the sacculated Aneurisms were false, and that some of the non-sac- culated were also false, we see how small the number of true Aneurisms in this situation becomes. The opening into the Aneurism may be at any part of the cir- cumference of the aorta; in sacculated aneurisms it is as frequently on the an- terior as on the posterior aspect of the vessel, and it may be exceedingly small, or as extensive as the size of the vessel will allow; in one case the whole of the posterior aspect of the. vessel had dis- appeared. The coats of the artery in true Aneurism are, of course, continuous throughout; but when, as does occur, the true Aneurism is sacculated, the inner coats become extremely delicate, and the external coat becomes thick and strong. If the inner coats become thickened they are never thereby increased in strength or consistency. In the cases I have ex- amined, when the Aneurism was saccu- lated and of moderate size, the internal and middle coats were prolonged but a short distance into the sac ; here they be- came soft and pultaceous, or rough and adherent to the fibrine or other contents of the sac, and, on tracing them through- out the sac, fragments were here and there discernible in patches. The sac may be empty, or merely lined by a thin layer of fibrine, when the Aneurism is small and communicates with the artery by a large orifice so as to permit a free current of blood through the cavity of the sac. In other cases, where the current has not been so free, concentric laminae of fibrine are found, tough and old, imme- diately beneath the external wall, but softer and stained with blood towards the interior of the sac. The sac may contain coagulated blood in quantities varying ac- cording to circumstances, and some have observed a distinct vascularity in the ex- ternal layers of fibrine. I would lay par- ticular stress upon the presence of lami- nated fibrine and coagulated blood in these Aneurisms, because one or other of these 860 ANEURISM OF THE ABDOMINAL AORTA. in any given case is the chief factor in curing the disease ; they are therefore to be looked upon as the result of nature's unaided attempts to provide a means of cure. In some rare instances the Aneu- rism has been formed by a hernial pouch of the internal coats protruding through an aperture in the external coat; in other instances the blood finds its way between the internal and external coats, and thus forms a dissecting Aneurism. Laennec saw an aorta in which the inter- nal and external coats were thus sepa- rated from the arch to the bifurcation ; and a case is quoted in which the blood thus dissected its way for a few inches and then passed into the original channel of the vessel by another opening just above the bifurcation, and thus establish- ing a fresh course for itself, obliterated the natural channel of the aorta. The natural tendency of the disease is to in- crease, despite the reparative deposition of barriers of fibrine or coagula ; on this account the sac may attain a great size, but in doing so its walls usually give way, and a diffuse Aneurism is formed, in some cases the original walls disappear entirely, and their place is taken by adja- cent textures without the occurrence of any great extravasation of blood. And thus the walls of an Aneurism may come to be formed of fasciae, bones, viscera, layers of fibrine, &c. The changes which occur in the sac are either conducive to the cure of the dis- ease or to the occurrence of rupture. The latter is by far the most common tend- ency ; for, despite the reparative deposi- tion of barriers of fibrine, the Aneurism increases in size under the pressure of a current of blood too rapid to coagulate or deposit fibrine, and eventually the sac gives way, either forming a diffuse Aneu- rism, or destroying existence at once by the loss of blood in large quantities, or by sucessive hemorrhages letting life ebb out more gradually. If a diffuse Aneu- rism be formed, the diffused blood may coagulate, layers of fibrine may be de- posited, and these, together with adjacent parts, may contribute to prevent further extravasation of blood, so that life may be considerably prolonged ; in the end, however, a diffuse Aneurism is almost al- ways fatal, either by the enlargement of the tumor or by its rupture. The other termination to which the disease pro- gresses is that of cure. Hodgson relates a curious case of a small Aneurism which had eaten its wray into the body of one of the dorsal vertebrae, and had there be- come completely filled with layers of fibrine, which presented a smooth even surface to the channel of the aorta. Again, the Aneurism may become so placed as to press upon its aperture of communication with the aorta, and thus may lead to its own cure by compression. From what- ever cause the deposition of fibrine arises it will lead to the safest cure of the dis- ease, but generally the filling up of the sac will be aided by coagulation of blood between or within the layers of fibrine. The sac may become obliterated by in- flammation and suppuration of its walls and contents. Haldane reports a case in which three Abdominal Aneurisms un- derwent spontaneous cure by calcareous degeneration of fibrine which had coagu- lated in their interior.' Seat of the Disease.-We have already said that an Aneurism may commence at any part of the circumference of the aorta, and Dr. Sibson shows that it occurs just as frequently on the anterior as on the posterior aspect of the vessel. Generally the tumor inclines to the left side, but in some cases it has been seen projecting across the front of the spine towards the right side. It may be seated beneath the pillars of the diaphragm, and being em- braced by them, may project into the chest as well as the abdomen. Most fre- quently the disease occurs near the origin of the coeliac axis, and it often involves the orifice of that vessel ; the origin of the superior mesenteric artery is also a com- mon seat-indeed, it may be said with truth that the disease usually occurs above the renal arteries. I have seen several cases, however, in which the dis- ease was seated below the renal vessels, and one in which it must have been as low as the origin of the inferior mesen- teric artery. As a rule, the arteries near the Aneurism become involved in it, and sometimes they are dilated ; when the Aneurism is large they are often stretched over it, and in most of these cases they are obliterated either by pressure or co- agulation of fibrine. Pressure upon other parts occurs as the Aneurism enlarges; it may become doubled on the aorta, and thus compress that vessel itself; or, as already observed, the various branches of the aorta may be compressed and obliter- ated- compression of the bile-ducts may occur, leading to jaundice ; of the duode- num and pylorus, causing nausea; of the cardia and oesophagus, producing vomit- ing and dysphagia ; or of the renal ves- sels (generally without ura?mia, or sup- pression of urine). It is curious that compression of the renal vessels so seldom leads to serious results. I have a speci- men in which the left renal artery is ob- literated, and the corresponding kidney is dwindled to one-third its natural size, while the artery of the opposite side is pervious, and its kidney is hypertrophied to double its natural size.2 In this case 1 Edinburgh Medical Journal, Jan. 1863. 2 See a specimen, in Path. Division of the Newcastle Museum. ANATOMICAL CHARACTERS OF THE DISEASE. 861 no renal disorder manifested itself by symptoms during life. I do not know of any proof that the thoracic duct suffers from compression in the abdomen, al- though such a complication with conse- quent emaciation is highly probable, nor have I heard of the pancreatic duct alone suffering in a similar manner. The left kidney may be considerably displaced, and pushed over to the right, or the liver may be pushed forward, and the disease may thus simulate enlargement of that organ. The vena cava is so far removed from the aorta above the level of the renal arteries, that it is seldom compressed ; and dropsical accumulations, or enlarge- ment of the superficial veins, are on this account rare in Abdominal Aneurism ; lastly, the colon may be obstructed in its descending division with the occurrence of symptoms of obstruction during life. The aneurismal sac will protrude ante- riorly, forming a considerable pulsating tumor, if it spring from the anterior aspect of the vessel: if, on the other hand, it spring from the posterior aspect of the vessel, it will be bound down by fascia} or other structures and protrude but little ; while, however, these posterior Aneu- risms pulsate and protrude but little, they lead to more serious results by pressing on important deep-seated parts. As the nervous pains which form the chief symptoms of Aneurism are the result of this pressure, it may be well to indicate the anatomical relation of anterior and posterior Aneurisms (i. e., Aneurisms springing from the anterior and poste- rior aspect of the aorta) to the nerves in which the pain is chiefly seated. An anterior Aneurism which springs from the anterior aspect of the aorta and pro- trudes forwards, will necessarily compress the ganglia plexuses and branches of the abdominal sympathetic system : a poste- rior Aneurism, which springs from the posterior aspect of the aorta and grows in a posterior direction, presses on the roots or branches of the spinal nerves as they issue from the intervertebral foramina, in close proximity to which the aorta is placed at this part of its course. Corre- sponding with these anatomical facts, Dr. Sibson has shown the rule with re- gard to these aneurismal pains to be : that posterior Aneurisms excite paroxysmal and radiating, as well as continuous pains, in the back and loins in a large number of cases, and pains in the epigastrium in a small number of cases ; while anterior Aneurisms excite pain in the epigastrium in a large number of cases, and pain in the loins with paroxysms of radiating pains in but a small number of cases. Thus, there is established a direct rela- tion between the situation of the Aneu- rism and the seat of the pains produced by the disease, and this is fairly explica- ble by the fact that anterior Anuerisms press ou the sympathetic nerves of the abdomen, while posterior Aneurisms press on the spinal nerves and their branches. All this is said with a full recognition of the fact that erosion of the vertebra} is produced frequently by posterior Aneu- risms, and but rarely by anterior develop- ments of the disease-for the truth is, that no relation whatever can be estab- lished between the pain of these Aneu- risms and the occurrence of erosion. Sib- son found, we admit, that of forty-six cases of sacculated Aneurism, in fifteen there was erosion of the vertebrae, and in every one of these fifteen there was a communication with the aorta on its pos- terior aspect; but Ilabershon and others have clearly established the fact, that as to cause and effect no relation between pain and erosion of the vertebrae exists, for cases are recorded in which there was pain in the loins of the most acute nature, and after death the vertebrae were found to be free from erosion; and a painless illness has more than once been known to precede death when the vertebrae were found to be extensively eroded. The con- clusions to be drawn are these1st. That sacculated posterior Aneurisms, as a rule, produce erosion of the vertebrae, and are generally accompanied by lumbar pain, but cases may occur where by press- ing on the spinal nerves alone, pain without erosion may be produced ; and conversely, sacculated posterior Aneu- risms may in rare cases erode the verte- brae without pressing on the spinal nerves, and therefore without producing pain : in short, you may have pain without ero- sion, and erosion without pain, for the pain depends upon pressure on the spinal nerves, and not upon erosion. Erosion of the vertebrae, occurs chiefly in Aneurisms which open into the aorta on its posterior aspect. By this process the bodies of the vertebrae may be completely destroyed, and then the Aneurism may communicate with the spinal canal, or the vertebral column may be considerably displaced, and angular curvature may be thus produced. In a case already re- ferred to, the body of one of the lum- bar vertebra; was completely hollowed out by a small Aneurism, and the cavity thus formed was lined by a fine smooth mem- brane. I need scarcely say that erosion of bones is a process distinct from caries, consisting of a combination of absorption and molecular destruction under the influ- ence of pressure. True caries of the verte- brae has been observed in connection with aneurismal pressure, and this is not at all to be wondered at, if the aneurism occur in a strumous subject, or if the bone has pre- viously been in an unhealthy condition. The rupture of Abdominal Aneurisms is more frequently followed by the forma- 862 ANEURISM OF THE ABDOMINAL AORTA. tion of a diffuse Aneurism than in the rupture of any other vessel; this is due chiefly to the tough and yielding struc- tures which surround the aorta and its branches. The rupture, and consequent hemorrhage, may take place suddenly and fatally, or gradually, by successive gushes of blood, and without immediate death. This difference in the mode and consequences of rupture is due to a differ- ence in the texture through which it may occur; when Aneurisms open on the cutaneous surface, the skin previously be- comes attenuated, it loses its vitality, a slough forms, and thus an opening is made slowly and by a gradual process ; on the mucous surfaces the opening is formed in the same manner; but in the serous membranes it always occurs some- what suddenly by a rupture or rent. Thus on the surface of the body and in mucous canals, hemorrhage is gradual and at first very slight, sometimes a mere trickling of blood, but it is sudden and complete when the vessel bursts into a serous cavity. When the opening occurs into areolar tissues, whether subcutaneous, submucous, or subserous, a diffuse Aneu- rism generally results before the final or fatal rupture takes place. The following statement will give the best idea of the parts where rupture is likely to take place. Of the cases collected by Dr. Sibson, rupture took place in 77 per cent. Of these, 28'5 burst into the peritoneal cavi- ty ; 8, into the mesentery ; 9, into the left pleura ; 6'5, into the right pleura; 22, behind the peritoneum in the left hy- pochondrium ; 4, behind the peritoneum in the right hypochondrium; 7, into the duodenum ; and in 21 cases of rupture be- hind the peritoneum, 17 of the Aneurisms communicated with the aorta posteriorly, and only 3 communicated anteriorly. Ilabershon, Stokes, and others have no- ticed rupture with extravasation into the iliac fossa beneath the fascia, into the cellular tissue around the aorta (in which case the blood may find its way upwards into the chest), into the small omentum, and into the mesocolon, forming in it, as Stokes says, a pillow of blood. Laennec, Chandler, and Dr. Beatty record cases of rupture into the spinal canal. Rupture may occur into the lungs, and death by luemoptysis may follow; this happened where pleuritic adhesions caused the base of the lung to form part of the parietes of the Aneurism, through which the blood found its way to the less resisting paren- chyma of the lungs. Lastly, rupture into the vena cava is mentioned in Crisp's tabulated cases. Mr. Syme's case of vari- cose Aneurism between the aorta and the vena cava is, as far as I know, unique. The Causation or Etiology of the Disease.-The chief predisposing cause of Aneurism, here, as elsewhere, is degeneration of the arterial coats, but this is not the sole cause, as the aorta in the abdomen, though much less frequently degenerated than the thoracic aorta, is, nevertheless, as frequently the seat of Aneurism as that vessel; this proclivity to Aneurism is due, no doubt, to the posi- tion occupied by the abdominal aorta: closely bound to the spinal column in its most mobile part, it is subjected to every position the body may assume-at one time being greatly on the stretch, at an- other almost bent upon itself-nor are the variety and extent of the movements to which this vessel is subjected the sole causes of this disease, for the rapidity with which they are suddenly performed is often of itself sufficient to lacerate its brittle inner coat. This latter cause is seen to act in cases where the patient has suddenly attempted to regain his bal- ance, or where he has made a sudden start or effort, from which he is often able to date the commencement of his malady. We may, therefore, lay it down that muscular exertion is the chief exciting cause of the disease, and that this may operate in two ways: 1st. By suddenly subjecting the vessel to a severe strain. 2d. By continually subjecting it to a va- riety of movements which increase the strain upon its internal coats. Fully ac- cording with these statements, we find that intemperance, severe privations, ad- vancing age, irregularities of life, and dis- sipation, syphilis, and rheumatism (all of w hich induce gradual degeneration of tis- sue), are frequently adduced as predis- posing causes of the disease. We find that occupations and conditions of life leading to great muscular exertion are prolific as exciting causes of the disease ; for instance, of 49 cases, Crisp found that 47 were between twrenty and fifty years of age, and that 22 of these were between thirty and forty years of age ; so that, while age undoubtedly contributes to pro- duce the disease, it is not old age especial- ly, but a certain time of life (when de- generation may have set in) which is generally accompanied by great bodily activity. In short, a small amount of degeneration accompanied by great bodily exertion more easily leads to the disease than a large amount of degeneration with slow and feeble bodily exertion. Corre- sponding proof of this is found in the fre- quency of the disease in males as com- pared with females. Crisp found 8 female to 51 male cases ; Habershon, 2 females to 11 males. As a rule, when the disease occurs in females they are young, and have led very hard and irregular lives of dissipation. Gairdner mentions such a case in a young woman aged only sixteen years. The occupations which seem to predispose to the disease are all of a labo- SYMPTOMS. 863 rious nature ; the men are smiths, strikers, excavators, navvies, porters, paviors, founders, &c. The disease may occur apart from these exciting causes, and when it does so we may be sure there is more certainty of the aorta being extremely dis- eased, and far less chance of the disease being cured than when it is caused by muscular exertion, &c. In this category of causes we ought to include external injuries, such as blows, by which the disease is not infrequently produced ; and we cannot lay too great stress upon the bad effects of overstrain- ing, such as the following. A healthy young fellow is employed as a pavior, and on lifting his huge wooden rammer for a blow loses his balance ; with the rammer uplifted he makes a vigorous effort to keep his feet, during which he " strains his backfrom that day he begins to complain of symptoms of Aneu- rism, and eventually he turns out to have the disease. Symptoms.-I propose to discuss the symptomatology of the disease under two heads. 1st. Those symptoms and signs which by their presence indicate the disease. These are the positive symptoms. 2d. Those symptoms which by their presence contra-indicate or negative the existence of Aneurism, and by their ab- sence, in doubtful cases, are therefore evi- dence in favor of the existence of Aneur- ism. These are the negative symptoms, and are of course produced by other diseases which closely resemble Aneurism in their main characters; when these symptoms positively present themselves, they often exclude the possibility of Aneurism ; when they are altogether absent, we have an ominous sign that the disease exists. 1st. The positive symptoms. Pain is generally the earliest symptom, the most prominent symptom during the course of the disease, and the symptom which by its increasing intensity gives the severest sting to the patient's dying moments. With regard to its frequency, we may say it occurs in five-sixths, if not in seven- eighths of the cases on record; its fre- quency and its general characters are chiefly determined by the seat of the Aneurism. The absence of pain in some cases is, however, a well-established fact, and when this is combined with an absence of other leading symptoms, the patient may live, till within a few hours of his death, with- out the slightest suspicion that any serious malady exists. Such a case has occurred to my knowledge where rupture and loss of blood were the cause of death. We have before demonstrated the relation which exists between the seat of pain and the seat of the disease, and have shown that pain is a more severe and more fre- quent occurrence in posterior than in anterior Aneurisms. As the nature of these aneurismal pains is peculiar and characteristic, their consideration is of great importance. They are of two kinds. 1st. A continued pain in the back, loins, epigastrium, or hypogastrium, as the case may be. 2d. An intense paroxysmal pain in the back or loins, which radiates to the front of the belly, to the testicle, or down the thigh, according to the spinal nerves through which it may be produced. The first is wearisome, and exhausts the pa- tient by depriving him of his rest; the second is agonizing, and leaves him pros- trate after every paroxysm. The pain is unaccompanied by febrile excitement, ac- celeration of the pulse, rigors, or perspira- tions ; it usually increases as the disease^ progresses, and before death agony of the most acute nature has often to be endured: in one case this was so severe that an ex- hausted and dying patient fairly leaped out of his bed, and in another case it brought on an attack of raving delirium. We conclude that the rule with regard to pain in Abdominal Aneurism is, that it may be seated in the back or in- the belly, indicating in the former site a pos- terior Aneurism, and in the latter an anterior Aneurism, and that in either case it may be of two kinds-paroxysmal or continued. The situation of the pain occasionally varies: it may be seated in the hip, in the iliac regions, changing from one side to the other (Beatty's case) ; it may simulate colic, being increased after eating, or by constipation of the bowels, and may be accompanied by nausea, anorexia, vomiting, or flatulence. The region of the liver may be painful and even tender, with pain about the shoulder and scapula, thus simulating hepatic disease ; the chest maybe the seat of pain with dyspnoea, or the cardiac re- gion with palpitation. One other strong feature of the pain is its tendency to "catch the breath" during the descent of the diaphragm, and in such cases we may suspect the scat of the disease to be un- derneath the crura of the diaphragm.1 The paroxysmal pain may closely sim- ulate that of renal or biliary calculus, lead colic, or simple neuralgia. All these somewhat anomalous pains may seriously complicate the diagnosis, and in such cases a careful consideration of other symptoms will be necessary. Change of posture often affects the pain considerably. Patients usually experi- ence relief by lying on their face or on their right side, by resting on the hands and knees, or by sitting almost double. On the other hand, lying on the back, or standing in the erect posture, are usually 1 See cases by Dr. Ogle, in Lancet. 864 ANEURISM OF THE ABDOMINAL AORTA. painful positions. The pain is almost always increased by bodily exertion, and in some cases even the slightest movement is attended by pain ; pressure usually in- creases it, but in some instances pressure has afforded considerable relief; some- times the surface over the Aneurism is exquisitely tender; but all 1 have seen were quite free from this, and might be manipulated gently with the greatest freedom from pain. The pain varies in character as well as in situation ; the words boring, burning, catching, pulsating, twisting, lancinating, are used by patients to convey to our minds the different kinds of pain felt by them. It is often dull pain when contin- uous, and sharp when paroxysmal. It varies in intensity also,-it is sometimes absent, at other times trivial; in most cases very severe, and occasionally un- bearable. We would urge the great ne- cessity of recognizing the import of pain such as is here described in all obscure cases, and of making it an incentive to a most careful physical examination of the abdomen, in order to determine whether or not an Aneurism exist. A pulsating tunior forms another most important symptom of this disease. The pulsation may be visible even at a dis- tance, forming a distinct heaving projec- tion of the abdominal wall; on the other hand, it sometimes gives no visible evi- dence of its existence. To the applied hand a distinct heaving impulse is communicated, and at the spot a more or less defined tumor can often be felt. The character of the pulsation is very marked ; felt equally in all directions -laterally as well as in front-the tumor seems with each pulsation to expand under the hand, and when the fingers are applied to its sides they are separated with each pulsation. In some cases, where the sac has pressed on the cardiac region, a double shock or pulsation has been communicated to it from the heart. There may be a thrill or vibration with each pulsation, and if by pressure the sac can be emptied, its distension will be ac- companied by a purring thrill. The tumor may be movable when it occupies one of the branches of the aorta, e. g., the sup. mesenteric ; in opposition to this, however, we have cases by Courato and others, diagnosed to be Aneurisms of this vessel by their non-mobility along with the diaphragm: most frequently the tumor is fixed. The site of the pulsation varies considerably; most frequently it occupies the epigastric region and inclines to the side, so as to be covered by the margins of the left false ribs ; in rare cases it inclines to the right side, and in so doing may push forward the right lobe of the liver with each impulse ; it not unfre- quently occupies a spot a little above and to the left of the umbilicus, or it may be so deeply seated in the epigastrium as only to be felt on deep pressure in that region. The mass may present itself in the left lumbar region, or in the groin, simulating lumbar abscess in the one case, and psoas abscess in the other ; or it may project considerably towards the right lumbar region, and so simulate enlarge- ment of the kidney. I have read of one case in which the tumor occupied the position of the spleen, and was mistaken for disease of that organ ; and in another case, under my care, whenever the patient lay upon his left side the tumor fell under his left ribs and entirely disappeared. Added to the difficulties which may arise from the various situations of the tumor, is the established fact that, in some cases, neither pulsation nor tumor can be de- tected. Hope mentions a remarkable case of this kind, where the Aneurism was found to be bound down by the pillars of the diaphragm, the lumbar fascia, and bands of adhesion-an occurrence by no means impossible when the Aneurism is small and projects backwards from the posterior surface of the aorta. As before mentioned, the tumor may sometimes be emptied by pressure, but this will depend upon the amount of fibrine in its interior. The Physical Characters of the Timor.- The tumor may be soft and fluctuating, and in such cases it is easily emptied of its contents by pressure, or it may be dense and resistant to the touch ; its sur- face is generally smooth, although in rare cases it may be lobulated. Percussion does not often afford valuable evidence of the disease, for the presence of intestinal flatus, and the deep situation occupied by the tumor when it is above the renal ar- teries, interfere with its indications. The percussion note is generally dull over the tumor, but this dulness may be limited to one part, such as the summit of the tu- mor, and there is generally a line of reso- nance running between the tumor and the liver. The characteristic expansile pul- sation of the tumor may be replaced by a forcible short or jogging shock communi- cated to the applied hand. A bellows murmur is frequently to be heard in connection with Abdominal Aneurism. It was observed in 25 per cent, of the cases collected by Sibson, but I cannot help thinking that it occurs more frequently than this, for I have never seen a case without it. The character of the murmur varies ; according to Dr. Walshe it may be, 1. A single systolic murmur. 2. A dull, muffled, systolic sound, con- vertible into a murmur by a little pres- sure. 3. A sharp, abrupt, systolic mur- mur, audible at the left lumbar spine, or much more marked there than in front. 4. A systolic murmur below the sac, and none immediately over it. 5. Occasion- SYMPTOMS. 865 ally a dull second sound. Dr. Walshe has never heard a murmur diastolic in time.1 A shock may be perceived by the ear, as well as a murmur ; it may be single and systolic, or double ; the presence of a sec- ond diastolic shock is pathognomonic of the disease ; as before said, a thrill may accompany the murmur. Where murmur is inaudible, pressure with the stethoscope over the Aneurism may produce it, and in all cases the patient should be made to assume the recumbent position, which generally increases both the murmur and the pulsation of the tumor. Dr. Corrigan attributes this development of the mur- mur and pulsation in recumbency, and their disappearance in the erect posture, to the removal of hydrostatic pressure from the walls of the cyst, which permits a more free passage of blood in and out of it, with less tension and more vibration of its walls. The murmur varies in in- tensity : it may be feeble, or so loud as to be audible at a distance, and its intensity sometimes diminishes with the growth of the Aneurism. It is very important to bear in mind, in obscure cases, that all physical signs may be absent-impulse, murmur, and dul- ness ; and in such cases a diagnosis of the exact nature of the tumor cannot possibly be made. Murmur is sometimes the only physical evidence of the disease. In all suspected cases, therefore, the stethoscope ought to be applied, and its application to the spine and left vertebral groove ought not to be neglected, as murmur in that region is of grave import. To these, the cardinal symptoms of the disease, we must add others of less im- portance. Respiration, if the sac be so high or bulky as to interfere with phrenic action, will be quickened and impeded. Sibson found dyspnoea mentioned in eight per cent, of the cases. Cough may be ex- cited when the walls of the thorax be- come in any way connected with the sac, but, as this is rare, we find cough much less frequently present than dyspnoea. Dysphagia was observed in about six per cent. ; and from the close anatomical re- lation which the oesophagus bears to the aorta we need not be surprised at this. Nausea, vomiting, loss of appetite, flatu- lence with spasmodic pain, and constipa- tion, are all common enough occurrences in the course of the disease. Mayo ob- served numbness of the lower limbs ; and in other cases, coldness, formication, pricking, numbness, and even paralysis of the legs has occurred. Ascites or ana- sarca of either limb are exceedingly rare, and, as will be seen, these occurrences are more indicative of the absence of the dis- ease than of its presence, i. e., they are negative symptoms which when present almost preclude the existence of the dis- ease. As the result of pressure, we ought to mention Professor Seaton's curious in- stance of contraction of the right pupil in a case of Abdominal Aneurism ; probably the sympathetic nerves were the channel through which this curious phenomenon was brought about. [Another effect of pressure is the oc- clusion, partial or total, of the thoracic duct. This was diagnosticated during life, and verified after death, in a case which I saw in the Pennsylvania Hospi- tal, under the care of the late Dr. W. Pepper. No doubt the emaciation, in many cases of Abdominal Aneurism, is considerably accelerated by this cause.- H.] It is a curious fact that all these symp- toms may for a time disappear, and the patient get apparently well; it is curious, too, that during seasons of great excite- ment, when the mind is directed to other things, the pains may be completely for- gotten. The cases of the gentleman who spent a day in the hunting-field, and the barrister who made a powerful speech in court, a short time before death, abund- antly illustrate this. As the disease pro- gresses and the pain increases, insomnia and restlessness at night tend to exhaust the body; the patient becomes emaciated, exhausted, worn out, and would doubtless die of slow exhaustion did not death from rupture put an end to his sufferings. 2d. We now come to the negative symp- toms, by which we mean those symptoms which seldom or never occur in Aneu- rism, and therefore negative the exist- ence of the disease; these symptoms being generally present in diseases which simulate Aneurism, are of great import- ance in the diagnosis of doubtful cases. They speak against the existence of Aneurism, and for the existence of other diseases. We first remark the absence of general arterial excitement, with undue fulness or rapidity of the'pulse-78 to 88 seems to be the average rate of the pulse, and the pulse-respiration ratio generally remains at the normal standard. Undue rapidity of pulse is therefore a negative symptom. The temperature of the body is, as far as I have observed in two cases, normal, and from the exhausted state of the pa- tients, it may be below par; great in- crease of temperature indicates some other affection. The heart's action may continue to be quite normal; indeed, we may say disease of the heart is the excep- tion rather than the rule in this disease. Anasarca of the extremities, so impor- tant in many abdominal diseases, is very rare in Aneurism, and only occurs when the cava becomes involved in or commu- nicates with the tumor. Enlargement of the superficial veins of 1 Diseases of the Heart, p. 494, 3d. ed. vol. ii.-55 866 ANEURISM OF THE ABDOMINAL AORTA. the abdomen is also exceedingly rare in Aneurism, and very common in other dis- eases of the abdomen. Ascites is still more rare, and being so common in ab- dominal disease, its absence is seriously significant of Aneurism. Dr. Stokes lays great stress upon the absence of effused lymph and the friction-sound which it produces when it is present in the peri- toneal cavity. Unless the disease press on the emulgent vein of the kidney the urine is healthy; and as, clinically, very few exceptions to this rule occur, the ab- sence of sediment of pus, mucus, and albu- men, ought to prevent us from assigning a renal or vesical origin to the pain. Jaun- dice, want of bile in the stools, general con- stitutional disturbance with complication of other organs, and enlargement of the liver, are opposed to the probability of the existence of Aneurism. Mobility of the tumor rarely occurs in aneurism of the aorta itself, although oc- casionally this is observed in Aneurism of its branches; but mobility is, as we shall see, common enough in some other abdominal tumors. Stokes points out that aneurismal tumor never begins be- low and increases upwards ; this upward growth of a tumor would therefore argue powerfully against Aneurism. The general cachexia of cancer, or the tubercular diathesis, are very rare in Aneurism, as are also deposits of cancer or tubercle ; so that in all doubtful cases, careful inquiry into the history of the pa- tient, and careful physical examination of the body, are necessary. The diseases which may be mistaken for Aneurism are so numerous and diver- sified that it may be well to divide them into- 1. Affections depending on increased aortic pulsations only. 2. Affections wherein a tumor, itself pulseless, receives an impulse from the aorta. 3. Affections wherein pulsation, not derived from the aorta, exists. 4. Affections wherein a pulseless tumor simulates a non-pulsating Aneurism. z 5. Affections where pain without tumor exists. 1. Increased Aortic pulsation is not ex- pansile, the lateral impulse and the move- ment in a forward and slightly downward direction being wanting. Murmur is very rarely present (never occurring over the spine, and scarcely ever diastolic), and the most careful manipulation and per- cussion 'will fail to detect lateral enlarge- ment in calibre. The absence of pain, of the evidence of arterial disease, and the occurrence of the disease in young, anae- mic, and female subjects of nervous tem- perament, or its development during attacks of dyspepsia, flatulence, or con- stipation, and its entire removal by treat- ment, are indications sufficient for our guidance in ordinary cases. In more obscure cases, the most careful inquiry will often fail to produce a decided opinion. 2. Tumors which receive an impulse from the aorta. Under this head are cancer of the stomach and pylorus ; cancer of the pan- creas, liver, and small omentum, involv- ing the duodenum. Tubercular deposits in the mesenteric or lumbar glands; omental tumors or cysts, ovarian tumors, and tumors attached to the uterus, or even the enlarged uterus itself; enlarged kidney, distension of the pelvis of the kid- ney, a movable kidney, distension of the colon from flatus, worms, or feces (the latter being by far the most common), or cancer of the transverse colon, each of these affections may receive an impulse from the aorta, and may compress the vessel so as to lead to murmur also. By attention to the symptoms before deline- ated, many of these may be excluded; and, as the diagnosis in each case will re- quire a full consideration of each suspected disease, all I shall attempt to do here will be to lay down a few general rules for our guidance. A. In but a few of these cases does the impulse possess the heaving, expansile character of Aneurism ; and lateral im- pulse is rare. B. The tumor in most of the above cases is movable, and when moved the murmur is modified thereby; in Aneu- rism of the Aorta itself this is never the case; and in Aneurism of its branches, movement does not cause the murmur to disappear ; by causing the patient to rest on his hands and knees the tumor may fall away from the aorta, and pulsation will then cease if it be not aneurismal. C. In many cases symptoms contra-in- dicating Aneurism will be present. D. In all cases a more careful inquiry into the history of the case, the constitu- tion of the patient, and the character of the tumor, is necessary, for in many cases this will give great aid to diagnosis. E. Clear out the bowels, examine the urine, remove dyspeptic symptoms, regu- late the uterine functions, and in so doing make careful inquiry into the condition of the organs involved. 3. This class of cases includes those tu- mors which possess in themselves a heav- ing impulse, due to their active vascular condition. The relation between a diffuse Aneurism and a vascular cancer is some- times very close, even when external; and when vascular organs like the liver or kidney becoming affected with hsema- toid cancer, acquire a heaving, expansive pulsation, the diagnosis is very difficult. Cancer of the mesenteric and lumbar glands may also simulate Aneurism. It TREATMENT. 867 is in these cases that the presence of con- stitutional disturbance, quick pulse, hot skin, perspiration, and of diathesis, is so useful an aid to diagnosis; the symptoms of disease of the organs involved would also aid us if present. 4. Cases where a pulseless tumor resem- bles a non-pulsating Aneurism. Of this class are psoas and lumbar ab- scess, possibly leading to displacement of vertebrae, like angular curvature, causing pain in the back like that of Aneurism, and perhaps appearing suddenly as if the Aneurism had ruptured. We must in- clude in this class any of the tumors in class 2 which may have acquired the symptoms of Aneurism without pulsation. The absence of murmur in these cases, and the presence of cancer or tubercle in other organs, would aid the diagnosis. The 5th class of cases is a difficult one. It includes all cases of obscure pain in the belly, back, loins, hips and thighs. Cases of lumbago, sciatica, neuralgia of the abdominal wall, intestinal pain, the pain of calculus, various hepatic and ne- phritic pains, spinal pain, &c. &c. In such cases a careful physical examination of the abdomen, for other evidence of the disease, is the best safeguard in avoiding error; but beyond this, and the special symptoms of these diseases which may accompany the pain, I know of no point on which to establish a diagnosis. Course, Duration, and Termination of the disease.-Beginning suddenly, or develop- ing gradually by obscure symptoms, the course taken by the disease varies; it may be so mild as never to betray its exist- ence till the final rupture takes place, or it may entail almost constant suffering on its victim. In pronouncing an opinion it is of great importance to remember that even in severe cases periods of convales- cence occur in which all symptoms disap- pear, and the patient feels quite well. Many cases seem to exist for a long time without serious disturbance, when sud- denly, after the Aneurism has reached a certain size, all the symptoms set in with great severity. The duration of the dis- ease is variable; cases are on record which lasted seven years, and even eight years, but this is far above the average. The practical question seems to be, how long will a patient live after an Aneurism has produced severe or decided symptoms of its existence ? This period rarely ex- ceeds eighteen months, and after the for- mation of a decided pulsating tumor, with paroxysms of pain, the majority of pa- tients die within three months. The ter- mination of the disease has hitherto, in almost all cases, been in death. A few cases are recorded where, without aid, nature managed to fill up the sac by layers of fibrin, &c., and thus to establish a cure. In other cases again, by proper diet and regimen, and the employment of various modes of treatment, the disease has been cured. Death may occur from exhaustion, or from hemorrhage ; and death from hemor- rhage may be sudden or gradual. When gradual, the patient may at first experi- ence relief of his pain, or shock with rigors may be experienced at the time, and last more or less for a few days, during which the heart beats rapidly and feebly, the first sound being almost lost. The pulsa- tion in the tumor, after rupture, becomes weaker, the murmur is lessened, and a new, soft, semi-solid swelling is formed without pulsation or murmur. Dr. Walshe has observed pulsation of ex- pansile character in the extravasated blood, but the rule is, I believe, as stated above. Dr. Lyons found the symptoms of rupture followed by dulness on one side of the chest, and diagnosed rupture into the pleural cavity, which proved to be correct. Hemorrhage into the peritoneal cavity is generally followed by sudden death, and hemorrhage into the lung, stomach, or bowel, will be followed by discharge of blood from those cavities. Convulsion may accompany loss of blood. Dr. Stokes thinks that a sudden loss of blood is more dangerous than the loss of larger quantities by degrees. In one case Dr. Stokes observed fainting on three suc- cessive days before death : he believed them to correspond to successive dis- charges of blood from the Aneurism. When the blood forms a tumor in the lumbar or iliac region, the pulsations in the femoral may be impeded, but this is not always the case. Treatment.-Like most uncured dis- eases, Aneurism of the Aorta has been subjected to various methods of treat- ment. It will be needless to dwell upon those methods which have become obso- lete, and have been rejected by the expe- rience of the profession. Of these the treatment of Valsalva has been most com- monly adopted, for in most cases it af- fords temporary relief, and in some cases seems to have established a cure, where the strength of the patient, aided by his faith and perseverance in the means em- ployed, permitted of a fair trial. We should scarcely have adverted to the plan of Valsalva, had not Tufnell, of Dublin, brought out some rather startling cases showing that a modification of Valsalva's treatment may prove successful. Dr. Tuf- nell's plan is that of Valsalva without de- pletion, and consists chiefly in rest, plain but good diet, and soothing medicines when needed. The patient should be placed in the recumbent position, and this he must maintain for some weeks, or even months. Now, despite the success which has attended Dr. Tuffnell's efforts, I can- 868 ANEURISM OF THE ABDOMINAL AORTA. not think his treatment will ever become popular, for few patients will be found willing or able to rest night and day in one posture for a period of three months, and the irksomeness of the patient's own existence during that time is not the only difficulty, for the patience of relatives will also be severely tested in giving all due attention to the case; however, when no better means can be employed this may be tried. The administration of medicines has hitherto done but little for internal Aneurism, and further researches in this respect are needed. Dr. Owen Rees has given acetate of lead, and Roberts, Bal- four, Begbie, and others have shown how decidedly the symptoms of internal Aneu- rism improve on the administration of large doses of iodide of potassium. In my own experience the iodide has, in some cases, relieved the symptoms; in others, the symptoms have altogether disappeared for a time, and in one case I believe a cure has been effected. This experience, I think, fairly represents that of the pro- fession generally on this subject. When other means of cure fail, or when they are inappropriate, there still remains one procedure which holds out a fair hope of recovery to the patiect. Compression, which has done so much for the cure of Aneurism of other arteries, has acquired a peculiar honor in proving applicable to Aneurism of the Abdominal Aorta ; in other arteries it supersedes another less safe, but equally effectual mode of cure (ligature); but in the aorta it renders curable a disease hitherto entirely beyond our reach. As a student in some of our best hospitals, I never heard so much as a hint that efforts for the cure of such cases were worth entertaining. Now, however, there is hope for many cases. Already the aorta has been successfully compressed several times for the cure of Aneurism-both for Aneurism in its own course, and for the iliac Aneurism. As this method of treatment, though easy in its application, requires much care and attention to details, I propose to add as much information on the subject as we at present possess, in the hope that ere long our experience of the treatment will be much enlarged. Let us premise by a few remarks on the anatomy of the abdominal aorta. The vessel extends from the last dorsal verte- bra to the middle of the fourth lumbar vertebra ; it lies a little to the left of the median line, having the right crus of the diaphragm, the vena azygos and the tho- racic duct between it and the vena cava. The vena cava is nowhere in exact con- tact with the aorta, and gradually diverg- ing as it ascends, at the level of the renal arteries the greater part of an inch inter- venes between it and the end of the aorta. During part of its course the aorta is era- braced by tbe pillars of tbe diaphragm, so that for about two inches only part of its circumference, the anterior aspect, is in the abdominal cavity ; this embraced part of the artery is remarkable for being cov- ered by important organs, and for giving off the most important branches of the aorta. It is covered by the pancreas and the splenic vein, the left renal vein, the third portion of the duodenum, and some of the most important plexuses of the sym- pathetic nervous system. The arteries given off from it are placed as follows : 1. The phrenic-immediately the aorta appears from beneath the dia- phragm. 2. The coeliac axis-one inch from the commencement of the abdominal aorta. 3. The superior mesenteric-three- fourths of an inch below the coeliac axis or one inch and three-quarters from the commencement of the aorta ; and the re- nal arteries, half an inch lower than the mesenteric, or two inches and a quarter from the point at which the aorta enters the abdomen. From this point downwards for three inches at least, no large vessel arises from the aorta, nor is the vessel, during this part of its course, covered by important parts. Lastly, we have the inferior mesenteric artery, a little more than five inches be- low the commencement of the aorta, the vessel itself terminating at the distance of seven inches from its origin. From these facts it will be seen that the aorta may be compressed with the greatest safety and facility in its lower two-thirds, that is, in the last five inches of its course. Let us refer for a moment to tbe points on the front of the abdomen, to which this and other points correspond, so that we may determine from the exter- nal evidence of the site of an Aneurism, how far it is amenable to treatment by pressure, and with what amount of safety pressure may be applied. The aorta extends from the end of the sternum to the umbilicus (seven inches). Allowing one inch for the length of the ensiform cartilage, its tip will correspond to the origin of the coeliac axis. Three- fourths of an inch lower is the superior mesenteric artery, and half an inch lower than it, or four inches and three-quarters from the umbilicus, is the origin of the renal arteries. Allowing an inch for the point on which the pressure is applied, we have here a clear space of more than half the aorta where Aneurisms may be easily and safely treated by pressure, for the in- ferior mesenteric artery being by its anas- tomoses well supplied with blood, can be occluded without the slightest risk. The rule is, that you must not apply the tour- niquet higher than one inch and a quarter from the tip of the ensiform cartilage, the point of origin of the renal arteries; in TREATMENT. 869 fact, you cannot apply it higher than this point, so that we may conclude it is safe to apply it as high as you can. For an account of the vessels by which the circu- lation is carried on inside and outside the abdomen after the aorta is occluded, I must refer the reader to my work on The Rapid Cure of Aneurism, and for a still fuller account of the anastomosis between the lumbar branches of the aorta above and the branches of the internal iliac be- low, I would refer to the researches of Prof. Turner, of Edinburgh. It may not be out of place here to add a few words on the application of pressure to the aorta, as its success depends entirely upon an accurate attention to the details of the procedure. Before proceeding to compress, it is impqrtant to ascertain that the heart, liver, kidneys, and other organs are in a healthy state. It is also important to clear out the bowels both by a purgative and by a stimulating enema, as distension of the abdomen by flatus adds to the difficulty and danger of applying firm pressure. The use of chloroform is abso- lutely essential for more than one reason. It not only enables the patient to bear severe and long-continued pressure, but it also removes the resistance of the ab- dominal parietes. The instrument to be used may be a large Signorini's horse- shoe tourniquet, or Lister's tourniquet for the abdominal aorta, or a tourniquet with a fine adjustment, invented by Dr. G. Y. Heath and myself, and made by Coxeter. The strength of the rack and pinion, or screw of the instrument, is of very great importance in all cases. In applying the tourniquet, complete arrest of the circulation through the Aneurism should be aimed at, as it is of the greatest moment to secure complete stagnation of a mass of blood in the Aneurism for a period of time sufficient to produce coagulation. It is very prob- able that coagulation sets in rather sud- denly when once the conditions for it have been secured, and one object should be to encourage this tendency in the blood by retaining it in a stagnant condi- tion as long as possible without the slight- est movement or disturbance. After considering the experience de- rived from recent cases, I am of opinion that we should proceed as follows in car- rying out the pressure treatment 1st. Apply the pressure for four hours, and if on removing the tourniquet no im- pression has been produced on the pulsa- tion, the first attempt must be considered at an end, but if the pulsation is some- what diminished, the instrument should be reapplied for another hour. In one case when pressure was being applied to the aorta for the cure of an iliac Aneu- rism, when I arrived I found the assist- ants who had charge of the case had just removed the instrument in despair, but perceiving a distinct lessening of the pul- sation, I insisted on a reapplication of the instrument, and in twenty minutes the Aneurism was consolidated, and the pa- tient got well. 2d. If the first attempt has been unsuc- cessful, a few days must elapse before an- other trial is made ; on this occasion the pressure should be maintained for six or eight hours. 3d. If this fail, a final effort must be made, and the pressure extended to a period of twelve hours. There is but little danger if the process be tried in the above cautious manner, as indications of inflammation, exhaustion, or shock would at once put a stop to our efforts. Pres- sure so prolonged as to exhaust the pa- tient, or so frequently applied as to pre- vent perfect recovery in the interval, is specially to be avoided. I need scarcely add that everything depends on the per- sonal superintendence of the surgeon who undertakes to treat the case. He must give up his ordinary work for the day, and devote himself to this alone. Assist- ants cannot be expected to give that con- centrated attention to the tourniquet which is essential to the proper applica- tion of pressure. If we fail to cure the Aneurism by any of the above efforts, we must endeavor to alleviate the sufferings of the patient as much as possible. Leeching and cupping are sometimes useful in relieving the pain of plethoric patients. Rest is an all im- portant condition for the relief of pain. Nocturnal pains and insomnia are best combated by opiates, bromide of potas- sium and cldoral in appropriate doses; belladonna combined with opium is of great use, and liniments of aconite or belladonna and chloroform are useful ex- ternal applications, but the subcutaneous injection of morphia is our best remedy for pain. It is important to keep the patient's mind free from undue anxiety, and to maintain the general health by diet and regimen. Medicines which con- trol arterial excitement, such as aconite, hydrocyanic acid, green hellebore, and digitalis, are often of great use, but in spite of these and all other remedies the patient will often suffer severely before he dies. For much of the pathological anatomy on this subject we are indebted to the labors of Dr. Sibson and Dr. Habershon, and to Mr. Timothy Holmes we are in- debted for the fullest exposition of the surgical aspects of the subject, as well as for the first suggestion that pressure might possibly be applied to the abdomi- nal aorta for the cure of Aneurism. Up to the commencement of 1873 at least twenty Aneurisms had been treated by 870 DISEASES OF ARTERIES. pressing the abdominal aorta, of these only two died, and in them the fatal re- sult was evidently brought about by re- applying the tourniquet too soon. I can- not too strongly urge the importance of avoiding this ; nothing is gained by a speedy re-application, and great risk is thereby incurred. I need not say that the advocates of a new method of treat- ment should, above all things, avoid the arrest of its early development and tender growth, by too rudely or hastily putting it to the test in inappropriate cases, or by pushing it too far. Since the above date several cases have occurred. Before referring to them I ought to mention the case cured by Moxon and Durham in Guy's Hospital, and to the case treated by Sir J. Paget without success. I ought also to refer to the case where Mr. Bryant applied distal pressure with fatal but not altogether discouraging results. A full discussion of the treat- ment used in these cases is contained in Mr. Holmes's "Lectures on the Surgical Treatment of Aneurism.''1 Since 1873 Dr. Headlam Greenhow has successfully carried out the treatment in a case in the Middlesex Hospital, and Dr. G. II. Philipson has succeeded in curing a case in the Newcastle Infirmary. To these might be added one or more cases cured by continental surgeons, and I must not fail to refer to the success of Mapa- thea and O'Fenal in Dublin in applying pressure to the aorta for the cure of ilio- femoral Aneurisms. Most of the above cases illustrate one important point, viz., that an Aneurism often continues to beat for several hours after the pressure has been removed, and then suddenly and finally ceases to do so. To account for this, several suggestions may be offered. It may depend on a gradual contraction of the walls of the Aneurism, fresh laden with barriers of fibrin ; or on the sudden formation of a clot of blood on recently- deposited fibrin, or blood-clot; or on some more obscure alteration of the relationship of the contents of the sac to the blood- current. For a fuller discussion of this interesting question I must again refer you to my work on the rapid pressure treatment. DISEASES OF ARTERIES. John Syer Bristowe, M.D., F.R.C.P. (1) Inflammation.-Arteritis, or inflam- mation of the arteries, is a disease which physicians and surgeons regarded for- merly as of common occurrence ; but they not only included under the term true cases of the disease, but attributed to Arteritis cases in which, though arterial disease was present, it was not inflamma- tory, and probably a still larger number in which there was no arterial affection whatever. They regarded, in fact, mere post-mortem blood-staining of the lining membrane of the arteries as evidence of inflammatory congestion, and all degene- rative changes of the same tissue as the results of the deposition of inflammatory products. It need scarcely be said here that the lining membrane of arteries is now known to be devoid of capillary ves- sels, and incapable, therefore, of vascular injection ; and that any redness it may present is simply due to its imbibition after death of the coloring matter of the blood which has lain in contact with it; and that atheromatous and other degene- rative changes have either no connection with inflammation, or only such a con- nection with it as have cirrhotic and such like deposits in the liver and other organs. Inflammation of an artery manifests it- self chiefly by changes in the outermost and middle, or vascular coats. In the early stage, the cellular coat, which is that in which the vasa vasorum are chiefly distributed, presents changes simi- lar to those which occur in inflamed con- nective tissue of other parts; these are, specially, redness from hypersemia of the capillary vessels, and swelling in conse- quence of inflammatory exudation. Simi- lar changes, though less in degree, affect the outer portion of the middle coat. But the inner layer of the middle coat, and the internal coat, undergo little if any appreciable modification. If, however, the thickening of the walls be at all con- siderable, then the calibre of the vessel becomes diminished, and the lining mem- brane corrugated. The inflammatory changes may become arrested at the point here indicated, and the artery then either revert to its original healthy state, or its walls become permanently indurated and DISEASES OF ARTERIES. 871 thickened ; or, on the other hand, the in- flammation may lead to softening, and even to suppuration-the latter condition affecting specially the outer portion of the arterial parietes. The processes just de- scribed as occurring in the arteries of man, have been proved experimentally, by Virchow and other observers, to be capable of production in the arteries of dogs and other of the lower animals. Associated generally with arteritis, es- pecially with inflammation of arteries less in size than the aorta, we find the deposi- tion of fibrin on the inner surface of the inflamed tract. This soon increases in quantity, and occludes the channel of the artery. A fibrinous concretion is thus produced, adherent to the surface, block- ing up the vessel, sometimes more or less defined and rounded at the extremities, sometimes shading off into ordinary unde- colorized coagulum. After a while such a clot is apt to undergo disintegration in its interior, to become a cyst occupied by puriform fluid, and thus to resemble accu- rately the softening clots which occur so frequently in the interior of the heart. Sometimes, on the other hand, it under- goes changes resembling those which fibrinous deposits in the interior iff an aneurism undergo ; it contracts and hard- ens, and blending with the arterial walls, forms ultimately with them a mere fibrous cord. Sometimes again, the obstructing clot becomes wholly or in part removed, and the channel of the vessel consequently restored. It was formerly supposed that clots forming at the seat of inflammation, in arteries and veins, were due in great measure to inflammatory exudation taking place from the lining membrane of the affected vessel, and the experiments of Gendrin seemed to prove the validity of this explanation. But Virchow's more recent investigations, the results of which seem to have been confirmed by Henry Lee and Callender, show that if a vein, from the interior of which blood is ex- cluded, be irritated, the substance of its walls becomes infiltrated with inflamma- tory products, but no exudation whatever takes place on the surface of the lining membrane. It is certain, therefore, that the lining membrane of veins, and, it may be added, that of arteries, either never furnish any inflammatory exudation, or furnish it rarely and with difficulty, and almost certain, therefore, that the plugs which are associated with arteritis are due to the mere coagulation of blood. But even if it be admitted that these plugs are merely coagulated blood, it by no means follows that they are not in many cases the consequence of arteritis. It is impossible, indeed, on any other view to explain how it is that in Arteritis com- mencing from without, clots form in the interior of the affected portion of vessel. Doubtless the lining membrane of the artery particles in the inflammatory pro- cess and the formation of a clot at the site of inflammation is due to some coagulating influence which the affected wall hence exerts over the blood with which it is in contact. The causes of arteritis are as various as the causes of most other inflammations. Sometimes it is the consequence of irrita- tion acting from within, as when an acci- dental thrombus forms at the part or an embolus becomes impacted there. More frequently it is the result of some cause acting locally, but from without, as when an artery is mechanically or otherwise in- jured, when it becomes surrounded by or imbedded in cancerous or tubercular formations, or when it becomes involved in suppuration of tissue, or in any other process of inflammation. Sometimes again, it is doubtless due to special condi- tions of general unhealthiness ; and there is some reason to believe that certain forms of anaemia, and that syphilis, may be enumerated among them. The results of arteritis are also various. Sometimes, no doubt, the arterial walls return to their original healthy condition; sometimes they become indurated and perhaps thickened, with loss of contractile power and of elasticity ; when obstructed by clot, they sometimes, as before stated, remain permanently obstructed, and if life be prolonged, become reduced to mere fibrous cords; sometimes, on the other hand, their walls become softened and ulcerated, and perforation may take place, followed by hemorrhage, and its conse- quences. The most important results, however, of Arteritis arc generally those secondary phenomena which take place, in conse- quence of the obstruction of the artery, in those tissues or parts to which the ob- structed artery leads. These will be best considered under the head of "Throm- bosis and Embolia." The symptoms, immediately due to Arteritis, may be very briefly enumerated. They consist in a greater or less amount of general febrile disturbance, with (if the artery be within reach) pain and tender- ness at the seat of inflammation, and per- haps fulness and hardness and loss of pul- sation. But these rarely exist in an un- complicated form ; for on the one hand they are often, from the very earliest moment, mixed up with, and masked by, the symptoms of that morbid condition with which they are associated, or out of which they have arisen; while on the other hand, when inflammation affects an artery leading to any important part, the symptoms due to its obstruction soon by their gravity overshadow the symptoms due directly to arteritis. 872 DISEASES OF ARTERIES. The treatment of simple Arteritis may also be dismissed in a very few words. It should consist, first, of such constitutional management as is appropriate for other forms of inflammatory affections, and sec- ond (when the artery affected occupies a limb or is otherwise accessible) of local abstractions of blood by leeches or other- wise, and according to circumstances, of moist warmth, such as may be produced by poultices, or of cold applications, espe- cially of ice. In speaking of Arteritis we have hitherto avoided all reference to those morbid con- ditions of the internal coat which Virchow regards as the results of endo-arteritis, and which are so frequently the seat of atheromatous and other degenerative changes. These consist of cartilage-like, slightly translucent circumscribed thick- enings of the internal membranes, which vary in size, are more or less rounded in outline, and project in a wheel-like form into the arterial canal, and are found under the microscope to be due mainly to over- growth of the cell-elements of the part. This latter fact shows that they are growths, and not, at all events in their earlier stages, degenerations ; and since they are developed slowly, and at the same time (at all events when they are limited to the larger arteries) without ob- vious symptoms, they may doubtless be regarded as chronic inflammatory changes, allied to those which constitute cirrhosis. Again, laminse of true bone are occa- sionally formed in the lining membranes of arteries ; as also in that of veins. And here, as in the last case, wre have ob- viously to deal, not with degeneration, but with growth and development. The laminse are the result of some slow inflam- matory process, or at all events of some process related to inflammation. (2 ) Degeneration.-Degenerative changes occur mainly in the internal and middle coats of arteries, and are for the most part attended with the deposition of fatty or of calcareous particles, and the gradual disintegration of the tissues in which the particles accumulate. Degeneration is sometimes a primary change, but more frequently probably the result of antece- dent chronic endo-arteritis. In the for- mer case the normal structural elements of the arterial walls immediately decay, in the latter the decay takes place in the substance of a something due to the over- growth of such elements. This distinc- tion, which Virchow clearly demonstrates, is undoubtedly a real one; at the same time it is, as yet at all events, of little practical importance; for the twro condi- tions are constantly associated, and they lead to the same issues. Fatty degeneration of arteries usually goes by the name of atheroma. Virchow, who points out the inappropriateness of this term as usually employed of arterial disease, endeavors to limit its use to those cases in which the degeneration occurs in the deeper layers of the internal coat and leads to the formation there of a cavity containing fatty detritus-cases in which, as a matter of fact, the degeneration is almost without exception secondary. And he calls those cases fatty erosions in which the process begins on the free surface, and in which as a rule the degeneration is pri- mary. But for reasons which have been already referred to we shall employ the word atheroma in its ordinary sense. Atheromatous degenerations appear in the early stage as opaque white, or yellow- ish-white spots, seated either in the sub- stance of the internal coat, or between that and the middle coat. They are irregular in size and shape, ;tnd form ele- vations, which encroach more or less on the arterial canal, but present, neverthe- less, a perfectly smooth and polished free aspect. They arc at this time probably few in number and widely scattered, but there are certain situations which they specially affect, among which are the margins of the orifices of origin of branch- es. At a later stage, they have increased in extent, partly by the formation of fresh spots, partly by the coalescence of neigh- boring ones. 'Their thickness has at the same time increased and increased irregu- larly ; so that the inner surface of the af- fected artery assumes an uneven and more or less tuberculated character. If a ver- tical section of the diseased arterial walls be now made, two or three varieties of condition will be observed, existing either alone, or more commonly in combination. In one case, the morbid process will be found to be entirely superficial. In an- other case the degenerations will be found to involve the deeper layers of the inter- nal tunic. The membrane at the seat of disease will then be found thickened to two, three, or four times its original thickness, sometimes to a greater degree still, attaining it may be in the aorta a thickness of a quarter of an inch. It will be found opaque, yellowish-white, softer than natural, pulpy, or even semi-fluid in consistence; and it will, unless, the soft- ening be sufficient to destroy this charac- teristic, be found to consist of superposed laminae, arranged nearly parallel with the surface, and continuous at their edges with the laminae of the healthy portion of the membrane. It will generally be ob- served, also, that a thin layer of compara- tively healthy membrane separates the more diseased tissue from the canal of the artery. In another case, but more rarely, the morbid process attacks the middle coat, and may be limited to that coat. The further changes which take place in atheromatous patches may be briefly stated. The more superficial ones soften DISEASES OF ARTERIES. 873 on the surface, become eroded, and then gradually disappear, leaving an ulcer-like pit or depression. The deeper-seated sometimes soften, and presently discharge their contents through a small orifice in the lining membrane into the channel of the artery. Sometimes it would seem that more or less of the atheromatous material gets absorbed, and the surface assumes in consequence an irregularly depressed, puckered appearance. Some- times the diseased patches undergo creti- fication and the artery assumes in their situation the so-called "ossified" condi- tion. Calcareous degeneration of arteries gen- erally accompanies, or rather follows on, atheromatous deposit. Sometimes, how- ever, it seems to be developed independ- ently of atheroma. Like atheroma, it generally commences in the internal coat, and may be limited to it. It forms hard brittle plates of irregular shape, and of various sizes, which in the first instance are limited for the most part to the deeper layers of the internal coat. At all events, in the early stage, the calcareous plates are separated from the current of blood by a thin layer of the lining membrane. After a while, however, this layer becomes also infiltrated, and the earthy matter comes into direct contact with the blood. The calcareous accumulations then form plates corresponding in their general shape to the portion of the artery in which they have been formed, having a tolerably smooth internal surface, and an outer surface, which is more or less nodu- lated ; occasionally they form nodulated projections even on the free surface. Not infrequently erosion of the artery takes place at the circumference'of such plates, and their rough edges become exposed to the blood; sometimes the plates become detached. In some of the smaller arteries more particularly, as in those of the ex- tremities, calcification takes place in the middle coat sometimes primarily, some- times in association with similar disease of the internal coat. In this case the calcareous matter tends to assume the form of rings, and obviously infiltrates the muscular fibres of the part. Whenever atheromatous or earthy de- position takes place, even if it be confined to the lining membrane, some change in the nutrition of the middle tunic seems either to accompany it, or to follow quickly upon it. For the portion of this tunic which is subjacent to the deposit, even if it looks healthy, loses more or less completely both its elasticity and its con- tractile power. It need scarcely be added, that this loss of power occurs also, and even more markedly when the middle tunic is distinctly involved in degenera- tion. Atheromatous degeneration consists essentially in the transformation of the cellular elements of the tissue into oil (olein) and cholesterine, and the softening and breaking down of the intervening parts. The oil (which is said to be olein) occurs in the form of globules of various sizes, some so small as to constitute mere molecular matter, others so large as to exceed the size of a pus-corpuscle. The cholesterine occurs in two conditions ; in one it forms the ordinary thin imperfect rhomboidal plates; in the other (mixed probably with albumen), it forms globules of various sizes, which, like those in the so-called fatty kidney, present a cross when examined with polarized light. At some period in the course of athe- romatous degeneration, the degenerated patches begin often to be the seat of cal- careous depositions, they shrink probably in thickness and gradually concrete. This earthy transformation consists in the gradual deposition, among the other de- generative products, but chiefly in the intercellular tissues of earthy globules, and at the same time, of the gradual dis- appearance by liquefaction, and absorp- tion probably, of the cholesterine and oil. The earthy globules run together, blend into botryoidal masses, and at length form patches of earthy material which still give evidence of their mode of origin in the persistence of irregular angular cavities, in the nodulated character of their mar- gins, and in the presence of free earthy globules in the neighborhood of these mar- gins. The process of calcification here described is similar to that observed in other forms of pathological calcification, as on the surface of serous membranes in the teeth, and so on : it is similar also to the mode of calcification which Mr. Rainey has shown to be normal in shells, and in various other forms of healthy hard tissues including bones. Pathological calcifications of this kind in many tissues, and even in veins, have been shown to be- come occasionally converted into true bone, so that true ossification of an artery is by no means an improbable event. Virchow, also looking at the question from a somewhat different point of view, considers that the earthy depositions tak- ing place in the lining membranes of arte- ries result in true ossification. When calcareous deposit takes place independ- ently of atheroma, or so much in excess of oily deposit as from the beginning to mask the presence of the latter, the pro- cess of calcification is still essentially the same as that which has been described. The earthy jnatter is deposited, that is to say, in globular particles and masses, which, by further deposition on their sur- face, grow together. When the calca- reous change takes place in the middle coat, the muscular fibres (as has before been pointed out) are the special scat of 874 DISEASES OF ARTERIES. this change and become converted into rigid spindle-shaped bodies. All arteries are liable to the various forms of atheromatous and earthy degene- ration which have just been considered, but they are not all equally liable. Again, although, when the disease is present, there is a tendency for it to become gene- ral, it by no means very infrequently hap- pens that it is limited to one particular section of the arterial system, and attains there even a very advanced condition. Among the arteries specially liable to be affected, and in which as a rule the dis- ease is found most developed, may be enumerated the aorta, the large trunks immediately springing from the aorta, the arteries of the brain, the coronary arteries of the heart, the splenic artery, and the arteries of the extremities. To these may be added, diffused arteries, such as those of stumps, and the arteries dis- tributed in the walls of the senile uterus. When atheromatous and calcareous de- posits are at all extensive, they lead to many more or less important results. Tims, they produce often extreme irregu- larity of surface, and sometimes to these irregularities, clots become adherent, and occasionally undergo that central soften- ing which will be found described in con- nection with cardiac clots often, especially in small arteries such as those of the brain, of the heart, or of the extremities), the lining membrane becomes so much thick- ened, that the passage of the blood be- comes impeded, or even altogether ar- rested ; sometimes, the deposit of calca- reous matter becomes so extreme, that entire arteries are converted into rigid cylinders ; sometimes again, the athero- matous degeneration is so abundant, that the softened lining membrane forms in the interior of the artery a number of undulating partially detached excres- cences, projecting loosely into its interior. And it is worthy of remark, that most of the conditions just referred to occur not simply in arteries of large or of medium size, but even in the minutest arteries and in the capillaries. The latter two kinds of vessel, it is well known, often undergo the fatty form of degeneration ; but they also occasionally undergo the purely calcareous form of degeneration. We have seen them in the brain con- verted into rigid needle-like tubes, in which, under the microscope, the calca- reous matter consisted entirely of calca- reous globules, which were deposited apparently beneath the lining membrane, and had coalesced more or less completely with one another. The causes of these degenerative pro- cesses in arteries arc obscure. It is cer- tain that they constantly attend on old ase ; and then, according to the situation of the vessels chiefly affected, lead to cerebral apoplexy, to senile gangrene of the extremities, to angina pectoris, or other forms of cardiac disease, or to aneu- risms. But it is also certain that they do not attend on old age exclusively; that they are occasionally observed in infancy ; and that they not unfrequently lead to fatal results in adolescence and in the prime of life. There is reason to be- lieve, that in the latter cases, the disease is due to certain cachexiae, inherited or acquired ; and that among these must be included the syphilitic, the gouty, and that which accompanies the various forms of Bright's disease. There is no doubt, indeed, that degeneration of arteries is a constant accompaniment of chronic renal disease ; and Dr. Kirkes has endeavored to account for this, erroneously, we sus- pect, on mechanical grounds. The symptoms, due to degeneration of arteries, simply, are very indistinctly marked. Persons whose arteries are in this condition live often for years while the disease is in progress, and yet sutler little inconvenience from it. The symp- toms, indeed, which call attention to the presence of degeneration are almost en- tirely due to the conditions which compli- cate degeneration, to rupture, to aneurism, to obstruction of arteries, to enlargement of the heart, and so on. Yet, sometimes, when the superficial arteries are the seat of degeneration, the fact that they are so is indicated by their form and their rigidity ; sometimes, when the cerebral arteries are affected, transient brain symptoms point to the presence of this condition ; sometimes, when the aorta is the special seat of mis- chief, something in the rhythm, in the sounds, and in the dimensions of the heart, suggests the presence of aortic disease. There is even less to be said in regard to the treatment of arterial degeneration, than in regard to its symptoms. All that need be stated on this head is, that the patient in whom such arterial disease is suspected should guard against all excite- ment, mental and bodily, that he should give way to no excess of any kind, and that he should endeavor to live quietly, and regularly, and temperately. There is another form of arterial de- generation, known as the waxy, larda- ceous, or so-called "amyloid" degenera- tion, which, so far as we know, has only been hitherto detected certainly in the capillary vessels, and in the minutest ar- teries. So far as this is a disease of the vascular system, it may be regarded in the light of a pathological curiosity only, inas- much as it leads to no symptoms referable to the bloodvessels. It is seen constantly in the kidneys, in the liver, and in the spleen, when these viscera are the subjects of the form of degeneration in question. It seems, indeed, to commence in the capillaries and small vessels, and to in- DISEASES OF ARTERIES. 875 volve subsequently only the other tissues of these organs. The affected vessels be- come thickened and pellucid, and glassy- looking, and absorb iodine with charac- teristic readiness, assuming a peculiar reddish-brown hue. Virchow maintained some years since, that the matter de- posited in waxy degeneration is cellulose ; this view, however, has been disproved, and he has since retracted it. Dr. Ed- mund Montgomery demonstrated several years ago, at the Pathological Society, that the waxy or "amyloid" material contained much cholesterine, combined with albuminous matter. And he re- garded it as identical, or nearly so, in chemical composition with the fatty-look- ing globules, acted on by polarized light, which occur amongst other globules in ordinary atheroma.1 Waxy degeneration is due apparently to the influence of certain conditions of system ; especially of those which attend the later stages of syphilis, and chronic tubercular diseases, and of that which is induced by wasting suppuration, espe- cially when the bones are involved. (3) Changes of Dimension.-Alterations in the calibre of arteries take place very frequently, both as physiological and as morbid processes. As instances of the former may be mentioned, the enlarge- ment of the collateral arteries of a limb in consequence of the obliteration of the main trunk, the alternate enlargement and diminution of the uterine arteries which attend the development and subse- quent shrinking of the gravid uterus ; and the atrophy which ensues after amputa- tion in the arteries and stumps. The latter class of changes, however, the class (that is to say) which includes morbid dilatations and morbid contractions, is that which mainly interests us here. (a) Enlargement.-An artery may be more or less generally enlarged, under which circumstance it is commonly spoken of as being dilated ; or it may be enlarged at one or more distinct points, and the word aneurism is then employed to desig- nate every such enlargement. Dilatation. - Dilatation, in the sense just indicated, is not uncommonly met with in the degenerated arteries of old persons, especially perhaps in the aorta, and in the arteries at the base of the brain. The arteries thus affected are generally somewhat unevenly dilated, and present in consequence an irregularly nodulated or knobby contour. Dilatation is apt to occur also in a series of arteries belonging to some circumscribed locality, when by their aggregation they produce that condition which is commonly known by the name of cirsoid aneurism, or aneu- rism by anastomosis. The arteries in this disease, which are generally in their origin arteries of minute size, become generally and extremely dilated, they elongate and become tortuous, and ulti- mately by the formation of new anasto- moses, or the enlargement of those which originally existed, communicate freely with one another in all directions. This dilatation does not appear to be attended with any structural disease of the arterial walls. They are, however, probably al- ways very much thinner than those of healthy arteries of the same size. Aneurism.-Circumscribed dilatations of arteries, or aneurisms, present many va- rieties of character dependent on their causes, the structure of their parietes, their form, and some other conditions. Hence, in reference to their origin, they have been called idiopathic or traumatic, in reference to their walls, true or false or diffused, and in reference to their form, sac- culated or fusiform ; and they have been classified by different authors in accord- ance with one or other of the plans thus indicated. The several names just enu- merated are in common use. Of them, some are employed only in their literal sense, and scarcely need, therefore, any explanation ; but two or three of them not only convey no very obvious meaning, but have been used in such different, nay opposite, senses by different authors, that their retention is a source of constant con- fusion. The names to which we here specially refer are those of true, false, and diffused aneurisms. By Scarpa, and other earlier writers, the term true was applied to those ordinary forms of aneurism in which, as a rule, the middle coat of the artery is deficient, or in which, at all events, the walls of the aneurism do not include all the layers constituting the ar- terial wall; and the term false was used of that comparatively rare form of aneu- rism, in which the walls are formed of all the arterial tunics. Hodgson, however, and subsequent writers on the subject, have, unfortunately, exactly transposed the use of these words, and have called that true aneurism which Scarpa described as false, and that false which he described as true. The terms true and false are still constantly employed, and generally inexactly. Obviously it would be conve- nient to drop them altogether. The term, "diffused aneurism," again, has been used in various senses. Thus, by some, it has been used to signify that diffusion of blood which takes place when an artery, or an aneurism, ruptures into the cellular 1 Since the above was written, Dr. Marcet has shown that the lardaceous material is es- sentially a form of albumen combined with much less potash and phosphoric acid, and with more soda, chlorine, and cholesterine than an albuminous structure in health. Path. Trans, vol. xxii. p. 1. 876 DISEASES OF ARTERIES. tissue-a condition to which, as Mr. Holmes properly insists, the term of rup- tured artery or aneurism is properly ap- plicable. By others, however, it is em- ployed to designate those cases in which after such a rupture the patient survives sufficiently long for the space into which the blood has escaped to become circum- scribed by inflammatory induration, and thus to be converted into a cavity main- taining a free communication with the ruptured vessel. In this latter sense we shall continue to employ it. An ordinary or Sacculated Aneurism is a circumscribed dilatation of an artery, involving generally a well-defined area of the arterial walls, and limited generally to one side, or a portion of one side only. When small in proportion to the artery from which it springs, it may be more or less hemispherical, or thimble-shaped, its orifice being its broadest part. But sometimes while it is yet small, and gen- erally when it becomes large, it assumes a rounded, or even completely globular form, and then opens into the artery with which it is connected by an oval orifice, less in breadth than the aneurism itself- sometimes very much less-and with its long diameter corresponding in direction with the channel of the artery. Some- times from the enlarging sac yielding more readily at one or more points than elsewhere, the original aneurism may have other aneurisms, as it were, spring- ing from it; sometimes the irregular re- sistance opposed to its growth by sur- rounding parts compels its enlargement in certain directions rather than in others; and from these, or other causes, aneurisms may come to assume almost any variety of shape. Their size varies within very wide limits. As a rule, it may be con- sidered that the largest arteries yield the largest aneurisms ; but this is a rule liable to exceptions, of which, perhaps the most notable is, that aneurisms springing from the commencement of the aorta are almost always fatal from rupture while they are still very small. They vary, roughly speaking, from the size of a child's, or of an adult's, head to that of a pea or less. Their orifice is generally round or oval, though perhaps somewhat irregularly so. Sometimes this is bounded by a well-de- fined or tumid margin; but sometimes the cavity of the artery gradually dilates into the aneurism, and the orifice (though still defined above and below by an abrupt line) is undistinguishable laterally, and formed simply by the divergence in this situation of the arterial walls. Various descriptions have been given of the com- position of the walls of such aneurisms as are under consideration. Some authors, indeed, enumerate every conceivable vari- ety of composition, from that in which it is formed of all three coats, to that in which it is formed of one coat only. We need not follow them. As a rule, an idio- pathic aneurism, when in an early stage of formation, or while it remains small, presents a lining membrane which is con- tinuous at the margins of the aneurismal orifice with the lining membrane of the artery ; and if the artery be macerated, or is slightly decomposed, the membrane may be detached, and will be found to form a complete cast of the cavity. This lining membrane is generally thicker and softer than that of the artery itself, and perhaps more translucent; but it presents little or no structural difference. In larger aneurisms the inner surface is still generally, in the greater part of its extent, more or less polished ; but though still necessarily continuous with that of the artery, becomes for the most part quite inseparable from the tissues which it lines. Very often, even in commencing aneurisms, the middle coat of the artery terminates in the thickened rim which bounds its orifice ; sometimes it may be traced for a variable and even consider- able distance on to the aneurism ; and sometimes flakes, of what appears to be the middle coat, are scattered here and there irregularly over the whole circum- ference of the tumor. It may be stated that, as a rule, the middle coat is either deficient or presents traces of its presence only. The external arterial tunic is that which mainly and most uniformly forms the wall of any aneurism. At first prob- ably it exists there in an unaltered condi- tion. But as the tumor grows, and as this coat becomes stretched, additional connective tissue becomes added to it and incorporated with it, so that it becomes thicker and more resisting than the outer coat of the artery itself. And as the tumor continues to grow and presses upon neighboring organs and tissues, these or portions of them become compressed and indurated, and contribute to the forma- tion of its walls. A Diffused Aneurism may be of any size or any shape ; it may originate as such directly from an artery, and not very un- frequently it becomes superadded to an ordinary aneurism as a consequence of rupture of its walls ; indeed, it is a very common thing to observe, in large aneur- isms, that the proper parietes are here and there, over some wrell-defined area, deficient, and replaced by condensed, blood-infiltrated tissue belonging to the parts in which the aneurism is imbedded. The parietes of a diffused aneurism con- sist simply of the tissues which happen to have limited the escape of blood, and which have become to some extent infil- trated with blood, indurated and, accord- ing to their age, more or less fibrous. A Fusiform Aneurism is an aneurism in which the entire circumference, or the DISEASES OF ARTERIES. 877 greater part of the circumference, of an artery becomes for a limited and tolerably well-defined part of its length, dilated. Such an aneurism is generally more or less irregular in form, and indeed approx- imates in structure and in mode of forma- tion to that condition which we have already described under the head of Dila- tation. It may, however, like an ordi- nary sacculated aneurism, become very large; and this enlargement may be due either to its progressive general increase, or to the superaddition of a sacculated aneurism. As might be supposed, aneu- risms of this kind may comprise in their parietes all the arterial coats, and proba- bly in the beginning always do so; but, in their onward progress, their parietes naturally tend to become identical with those of the sacculated variety. A modification of the fusiform aneurism is occasionally observed in the aortic arch in cases where the aorta is greatly con- tracted or obliterated at the point of en- trance of the ductus arteriosus. The arch in these cases becomes generally and considerably dilated, sometimes so much so as to be capable of containing the fist; the walls undergo great attenuation, but (excepting accidentally) remain free from atheromatous or other unhealthy deposit, and whole. Aneurisms may be produced by acci- dent, or spontaneously ; and perhaps not very unfrequently in the course of the complete development of an aneurism both causes may have operated in various degrees. In other words, accidental oc- currences are more liable to produce aneurisms in arteries which are already diseased, and in a condition favorable to the spontaneous origin of aneurism, than they are in healthy arteries; and when aneurisms have already formed, their en- largement is not very unfrequently in part due to the occurrence of accidental rup- tures. Accidental aneurisms are often met with in the popliteal artery, and other large arteries of the extremities, and in the aorta, as the result of a strain, in which probably the middle coat has been lacerated ; and it may occur in any artery as the consequence of a wound. In cases of idiopathic aneurism, the es- sential cause of the disease is, doubtless, deficiency of resisting power in the mid- dle coat of the artery at the seat of aneu- rism, as compared with the dilating power of the blood to which it is opposed. The operation of this cause is shown in its simplest form in the instance already quoted, in which an aortic arch, other- wise healthy, becomes dilated in conse- quence of the obliteration of its further extremity. But idiopathic dilatation and idiopathic aneurism most commonly arise in connection with atheromatous and os- sific deposits. When these are all exten- sive, the middle coat, even when not ob- viously itself the seat of such deposits, loses both its contractile and elastic powers, and is then apt to yield under the constant impulse of the blood. It becomes attenuated, its fibres separate from one another, and, as the tumor be- comes larger, either wholly or in part disappear. For a time, no doubt, the thickening of the inner coat, due to athe- romatous or earthy change in it, protects the feeble middle coat from the injurious operation of the dilating force. But, after a while, the atheromatous inner coat be- comes eroded and removed, or the athero- matous collection between it and the mid- dle coat becomes discharged into the artery, or the bony plate becomes par- tially or entirely detached ; and in one of these ways, or in some other way, the protecting influence is removed from the enfeebled middle coat, which then begins to expand. It is not, however, absolutely necessary that the removal of the internal coat should even in cases of atheroma precede the formation of aneurism ; it is merely necessary that its own resisting power should not be sufficiently great to compensate for the loss of this power in the middle coat. It may be added, that any other condition tending to enfeeble the middle arterial tunic may be a cause of aneurism. Thus aneurisms arise as a result of inflammation involving the walls of arteries; and Tufnell, Holmes, and J. W. Ogle have all published cases in which aneurisms seem to have supervened in this way from embolia. Sometimes an artery may be opened by ulceration com- mencing from without, and thus a diffused aneurism may be produced. When once an aneurism has begun it almost always undergoes gradual enlarge- ment. Up to a certain point, as has been already shown, its parietes are for the most part derived solely from those of the artery out of which ft has originated ; but soon, in its progress, it begins to press on and displace neighboring organs, and then to appropriate them, as it were, in the formation of its walls. Its enlarge- ment may be almost unlimited when it is developed in the substance of cellular tis- sue, as behind the peritoneum, or when its chief growth is subcutaneous; but when it projects towards serous surfaces, or presses upon mucous channels, it tends comparatively early to open into them. The ultimate tendency, indeed, of all aneurisms is to rupture. Often, as has been pointed out, partial ruptures occur into cellular tissue, and the additional cavities thus formed become circum- scribed and taken into that of the original tumor. Often an aneurism opens by a sudden tear into a serous cavity, as that of the pericardium, the pleurae, or the peritoneum ; but perhaps more frequently 878 DISEASES OF ARTERIES. the rupture takes place into the sub-serous tissue, the blood accumulating therein and finally escaping thence by a subse- quent rupture into the serous cavity itself. Often again an aneurism, after gradually pressing upon a mucous canal, opens into it through the formation and separation of a slough between them. In this way thoracic aneurisms frequently open into the trachea, bronchial tubes,or oesophagus; and abdominal aneurisms occasionally dis- charge themselves into some lower part of the alimentary canal. Occasionally, too (but this is usually a very late event), an aneurism bursts externally, having pre- viously by its pressure caused the forma- tion of a cutaneous slough. In rare cases an aneurism opens into an artery, a vein, or even into the heart itself. These latter events are most common in aneurisms of the aortic arch. But aneurisms produce mischief not merely by bursting and caus- ing fatal hemorrhage. They are apt, by pressing on various organs, to produce effects referable to these organs; thus when developed on the under surface of the brain, they may produce eclampsia, or interfere with vision or with hearing, or lead to some other nervous phenomena; thus when developed in the thorax they may compress the trachea or the oesopha- gus, and so impede respiration or swal- lowing, they may involve the recurrent laryngeal nerve or the sympathetic, and induce certain characteristic symptoms which will be elsewhere detailed; and they may compress, and lead to oblitera- tion of venous trunks, and thus induce dilatation of tributary and anastomotic veins, and oedema of the parts beyond the seat of obstruction. The effect of aneu- risms on bones is curious. It is well known that, as they enlarge and press upon bones, they cause their erosion and gradual disintegration ; that in this way a thoracic aneurism will destroy more or less completely the bodies of two or three vertebrae, and may even, in consequence of this destruction, burst into the verte- bral canal; that it will destroy portions of the sternum, of the ribs, or of the clavi- cles. Whilst this destruction is in pro- gress, the eroded surface of bone lies exposed in the aneurism, forming a seg- ment of its walls; and not unfrequently a partially destroyed clavicle or rib is found projecting into the interior of an aneurism. Occasionally aneurisms undergo spon- taneous cure. To understand this it is necessary to consider the changes which take place within their cavities. Some- times after death aneurisms are found empty, or filled only with perfectly coagu- lated blood or mere post-mortem coagulum. Sometimes, on the other hand, they are lined with laminated clots. These con- sist of a series of more or less imperfect layers, which lie one within the other, concentric with the aneurismal walls. They are pretty firmly attached to one another, hut admit of separation, and the outer one is generally somewhat firmly united with the lining membrane of the aneurism. They consist of a toughish fibrinous material, of which the outer layers are thin and more or less buff-col- ored, the inner becomes thicker and softer and redder as they approach the channel through which the blood is still passing. The amount of these clots varies very much; sometimes there are merely two or three layers, so that the cavity of the aneurism is scarcely encroached on by them ; at other times they fdl the greater part of the cavity; and occasionally they are so abundant as completely to obliterate it: the innermost laminae filling up the orifice of the aneurism and lying flush with the general surface of the artery, or even forming an irregular projection into its channel. Clots of this kind are very commonly observed in sacculated aneu- risms, but they are not invariably present in them, and very large sacculated aneu- risms are sometimes wholly free from them. Fusiform aneurisms arc almost always without them. It need scarcely be said that these clots are distinctly de- posited from the blood. The cause of their deposition is probably twofold. In the first place it is a recognized fact that blood tends to coagulate upon rough or diseased surfaces; thus upon mere athero- matous patches occurring in an otherwise healthy artery coagula are sometimes seen to have formed. In the second place, from the fact that these coagula are far more common in aneurisms which communicate with an artery by a com- paratively small orifice, than in those which are mere fusiform dilatations, it may be taken for granted that stagnation of blood tends to encourage the deposition of fibrine. The formation of these clots depends then, probably, in some cases on one of these causes, in some on the other of these causes, but generally, doubtless, upon the concurrence of the two. It may be added that the presence of a layer of fibrine is probably the most efficient cause of all in determining fibrinous deposition; just as a nucleus of calcareous matter in the bladder attracts to itself similar mat- ter which otherwise would have been re- tained in solution in the urine. The formation of these clots in quantity no doubt frequently opposes an important barrier to the growth of an aneurism; and as has been shown they sometimes form so abundantly as completely to obliterate its cavity. In the latter way a sponta- neous cure may sometimes be effected ; but it is doubtful if such cures would gen- erally prove permanent; for they are mostly observed in persons who have DISEASES OF ARTERIES. 879 been confined to bed some time previous to death, and the clots on which they de- pend are generally not very difficult of detachment. But indeed, on the other hand, it is occasionally in consequence of such a detachment that an aneurism be- comes cured ; the mass of clot, or a por- tion of it, shifts its position, and blocks up the artery upon which the aneurism is seated, leading at the same time to oblit- eration of the arterial canal and of the aneurism. Sometimes, again, an aneurism becomes cured by itself compressing the arterial tube either above or below its orifice. Aneurisms may occur in any artery; but much more frequently in certain ar- teries than in others. Generally, it may be said that those arteries which are most prone to atheromatous and earthy degen- erations are those which are most prone to aneurismal dilatation. Such are the aorta, especially its arch, the innominate, carotid, and subclavian arteries, the cce- liac axis, the common iliacs, and the ar- teries at the base of the brain. But the proneness to aneurism is not solely in proportion to the proneness to degenera- tion ; for in consequence of the compara- tive violence of the impulse to which arteries near the centre of circulation are exposed, these incur a special risk which those further removed escape ; and again, in consequence of the position and con- nections of certain arteries (as the popli- teal) they are exposed to danger of various kinds of violence to which many other ar- teries are exposed little, if at all. But we repeat that aneurisms may arise in almost any artery. Besides those named, or indicated, aneurisms are met with in the mesenteric artery and its branches, in the coronary arteries of the heart, in the ophthalmic artery, and in one case we found one in the course of one of the small arteries in the substance of the cerebellum. The pulmonary system of arteries is very rarely the seat of aneu- risms ; still, they are occasionally met with both in its trunk and in its branches. These arteries are more frequently di- lated. Aneurisms occur much more frequently during middle age and in declining years than in the earlier periods of life ; but they are far more uncommon (in the la- boring classes especially) between the ages of thirty and forty. And still younger persons, even children, do not wholly es- cape. They affect men more frequently than women. This is especially true of aneurisms of the extremities, which are mostly the result of violence. The local indications of an aneurism, when it is seated in some accessible part, consist in the presence of a dilating pul- satile tumor, attended frequently when it is developed in the course of large arteries by a murmur synchronous with the sys- tole of the heart. But in the case of many aneurisms, as of those within the skull, and in other inaccessible situations, these indications fail us entirely. The other symptoms of aneurism can scarcely be usefully considered here, inasmuch as they are in part those due to degenerated arteries generally, in part those which arc due to the pressure of the aneurism on surrounding organs and tissues (and these symptoms will necessarily vary with the situation of the aneurism), and in part also those which may arise from their rupture (and these again must vary ac- cording to the part into, or in connection with which, the rupture takes place). It is difficult also to consider usefully in a short space the treatment of aneurism. Indeed, we are compelled to pass over in silence the important subject of their sur- gical treatment. With regard to aneu- risms which are beyond the reach of sur- gery, the essential objects to be held in view are, first, to prevent their increase ; and second, to promote their obliteration by the deposition of clots within them. These ends can only be attained, so far as we know, by maintaining as much as pos- sible rest of body and of mind, especially by quieting the circulation and prevent- ing any such bodily movements as are likely to affect the aneurism immediately. When aneurisms approach the surface, the application of icc or other sedatives over them, galvano-puncture, and the in- troduction even of foreign bodies, as of threads or wire, may aid coagulation. At one time it was supposed that the fre- quent abstraction of blood, and the use of a low diet, were important adjuncts in promoting the cure or retarding the prog- ress of aneurisms. Such was Valsalva's method. But modern physicians, and among these must be specially mentioned I)r. Stokes, have generally found reason to disapprove of this plan of treatment, and to prefer (as it seems to us with rea- son) the use of a nutritious and even of a generous diet, and abstinence from bleed- ing and other hurtful drains on the system. Before concluding the subject of aneu- rism, it is necessary to consider two or three abnormal conditions of artery to which the term Aneurism is with more or less inappropriateness commonly applied. These are dissecting aneurism, aneurismal varix, varicose aneurism, and cirsoid aneu- rism, or aneurism by anastomosis. Dissecting Aneurism occurs chiefly, if not entirely, in the aorta. It commences (generally in connection with degenera- tive disease, but sometimes when the ves- sel is simply dilated) in a rupture of the internal coat, through which blood is forced between the middle and outer coats, or rather (as Dr. Peacock has 880 DISEASES OF VEINS. shown) into the substance of the middle coat, where it accumulates, separating the internal and external coats from one another. Sometimes the resulting sepa- ration is slight, extending beyond the ruptured orifice ; sometimes it is very ex- tensive, *• dissecting the coats of the aorta from the arch to the bifurcation, and extending even into the iliac arteries. Such an aneurism may after a while un- dergo a further rupture, either externally through the outer coat, or internally through the inner coat, and thus commu- nicate by a second orifice with the inte- rior of the artery. Sometimes the accu- mulation of blood in the substance of the walls is so great that the artery becomes obstructed. Varicose Aneurism and Aneurismal Va- rix, are names which have been applied to the very rare conditions which follow on the establishment of a communication between a neighboring artery and vein. Such a communication may (as the result of disease) take place between an aortic aneurism and the superior cava, and (as the result of accident) between certain of the arteries and veins of the extremities. It used occasionally to result from wound- ing the artery through the vein, at the bend of the elbow, in the operation of phlebotomy. To the case in which the artery opens immediately into the vein, the term aneurismal varfx is applied ; to that in which an aneurismal cavity lies between the communicating vessels, the term varicose aneurism. Of Cirsoid Aneurism we have already spoken. This is sometimes a congenital affection ; sometimes arises without any obvious cause at various times after birth, and even in adult life ; and it may appear in various parts of the body, as in the or- bit, in the fingers, and elsewhere, but most frequently in the scalp. A remark- able case is recorded in the " Pathological Transactions," where nearly the whole of one of the lower extremities was involved. (&) Contraction and Occlusion.-These conditions may be produced in a variety of ways, of which some have already been partially considered. Their more import- ant causes we will here enumerate, leav- ing what little we have to say about the symptoms and treatment of obstruction till we come to consider the subjects of thrombosis and embolia. Occlusion of arteries is sometimes a congenital defect; sometimes it is the result of in jury ; some- times it arises from the pressure of some hard tumor growing external to the ar- tery, or from the artery becoming com- pressed by, or involved in, some carcino- matous or other growth ; not unfrequently it takes place in the course of atheroma- tous and earthy degeneration, as a conse- quence either of excessive thickening of the lining membrane of the artery, or of the partial detachment of diseased patches, or of the formation of clots in connection therewith. To such obstructions of the arteries of the lower extremities, senile gangrene is perhaps always due ; a simi- lar condition of the coronary arteries of the heart leads now and then to local patches of degeneration and to rupture of the heart; and a similar condition of ar- teries of the brain, to circumscribed soft- ening of that organ. Lastly, occlusion is not unfrequently due either to the forma- tion of clots in arteries (thrombosis) at the seat of obstruction, or to the impac- tion in arteries of clots and other matters brought to them from some comparatively remote portion of the vascular system (embolia). These last two causes of ob- struction will be considered under the head of " Thrombosis and Embolia." DISEASES OF VEIKS. By John Syer Bristowe, M.D., F.R.C.P. (1) Inflammation.-The term "Phle- bitis" was formerly used, like the term "Arteritis," in a much wider and much looser sense, and much more inaccurately, than it is for the most part at the present day. It signified then a disease of the gravest import; for it was the common designation of most cases of what is now called pysemia, of many obscure fatal cases in which it was erroneously supposed that inflammation had crept from some distant vein to the heart, and of many cases of what would now be termed thrombosis or embolia. It included also true Phlebitis, or inflammation of the veins: the disease which alone we now propose to consider. Phlebitis, in this latter limited sense, is a morbid condition of vein, due some- DISEASES OF VEINS. 881 times to constitutional, causes, sometimes commencing from within the vein, some- times from without, attended with impor- tant changes in the venous walls, and frequently "with more or less of inflamma- tory mischief external to the vessel, and with coagulation of blood or other morbid phenomena within it. The changes which indicate the pres- ence of inflammation affect the outei- vas- cular region of the venous walls in a far higher degree than they do the inner re- gion which is devoid of capillary vessels. When inflamed, the walls become thick- ened (sometimes several times thicker than in health), congested externally, infiltrated with inflammatory exudation, and softened; sometimes suppuration takes place in them, sometimes they be- come disintegrated, or ulcerated and per- forated, or entirely destroyed. If the inflammation be a chronic process, the exudation in the walls assumes a fibroid character, and the walls get indurated as well as thickened. Generally while these changes are in progress, the connective tissue, with which the vessel is surrounded, partakes in the inflammatory processes, and consequently becomes congested, infiltrated, and, ac- cording to circumstances, indurated and brawny, or the seat of suppuration. At the same time, too, changes for the most part take place within the vessel. Blood coagulates there and clings to its lining membrane ; a clot filling up, and it may be distending and occluding the vein, be- comes thus established, and secondary phenomena due to the arrest of the circu- lation ensue. Clots thus formed undergo various changes, which will be afterwards more fully considered; sometimes they remain solid, and gradually contract and indurate ; sometimes they soften and be- come reduced to a puriform fluid; and sometimes, we believe, they undergo ac- tual suppuration. The causes of phlebitis are very various, and influence to a great extent its degree, its character, and its progress. Thus, in some instances, it is due simply to the affected vessel being pressed upon, or sur- rounded, by some tubercular, cancerous, aneurismal, or other growth. Then gen- erally the walls of the vein become greatly thickened and indurated, and its channel filled with a clot, which is usually hard and fibrinous, and closely adherent to the lining membrane. Sometimes, however, the vessel becomes flattened and so ob- structed, and clots are formed only beyond the seat of obstruction. Sometimes,' too, the portion of vessel chiefly involved be- comes entirely destroyed and no longer traceable. In many cases phlebitis is consequent on the vein being involved in inflamma- tion (erysipelatous or other) affecting pri- marily the organ or tissue in which the vein is included ; and the phlebitis then tends to partake more or less in the char- acter of the surrounding inflammation. The sheath of the vein becomes first in- flamed, and subsequently the inflamma- tory process invades successively the outer, middle, and internal coats ; leading some- times only to their congestion and to their thickening, but sometimes resulting in distinct suppuration. In the latter case the sheath of the vessel may become uni- formly infiltrated with pus, or present more or less isolated collections of that fluid, and pus may be developed in the substance of the outer tunics ; and occa- sionally as a result of this the venous walls undergo erosion or ulceration from with- out inwards, and a communication, or communications, become established be- tween the interior of the vein and the parts external to it. When the inflam- mation extends thus from without, it sometimes happens that the outer walls only of the vein are involved; the walls become thickened in the aggregate, but the lining membrane remains smooth and polished, no coagulum forms, and the channel remains free. More frequently, however, the walls become affected in their whole thickness, and at the seat of the disease a clot forms, which adheres and blocks up the canal of the vein. This clot, as before stated, tends to soften either generally or in certain spots, and thus to assume the character of an ab- scess, or of a collection of pus bounded on all sides by coagulum, or by a layer of inflammatory lymph. There is no doubt that in nearly all these cases the pus- like fluid, and the more solid material bounding it, are simply the consequence of degenerative processes taking place in clots deposited from the blood. But occa- sionally true pus is certainly met with in this situation. Sometimes this is due to the opening of an abscess into a vein and the consequent conversion of a limited portion of the venous system into an ab- scess ; but sometimes it is due, we believe, either to the development of pus from the lining membrane of the vein, or to sup- puration occurring in the substance of the clot. This latter condition we have un- doubtedly observed in cases of erysipelas. Again, phlebitis may result from local irritation, from poisoned wounds, or from other injuries. The inflammation then affects principally the sheath of the ves- sel, which becomes congested and infil- trated with inflammatory products, and sometimes undergoes suppuration ; and it tends to travel along the sheath, so that presently a considerable length of vein, or a system of veins, may become affected. The same changes take place in this case in the venous walls, and in the interior of veins, as have been already considered. VOL. II.-56 882 DISEASES OF VEINS. In other cases, again, the inflammation doubtless commences from within, the outer portions of the walls of the veins becoming involved secondarily to the inner. This is the case, probably, when without any cause, originating, so far as we can see, in the walls themselves, thrombi form in certain veins, as in the iliac veins, for example, of phthisical pa- tients. Such thrombi distend and occlude the vessels which subsequently only to the formation of these thrombi become thickened and give other evidence of in- flammation. There are yet other cases, probably, in which thrombi form, wherein the inflam- mation associated with their formation is a primary inflammation of the venous walls, dependent probably on some con- stitutional affection. Such cases, how- ever, are necessarily obscure, and it is difficult to distinguish them from those which have just been considered. We may add here a few words on the different conditions of system in which phlebitis is most apt to supervene, and on the veins which are most prone to be affected. Phlebitis frequently takes place, as has been already stated, in the soft tissues, in connection with various forms of inflammation, such as erysipelas, diffuse cellular inflammation and carbun- cle. It takes place frequently, too, in connection with inflammation, and espe- cially with suppuration, of bones and joints ; under this head may be included phlebitis of the lateral sinuses of the skull, consecutive to suppuration in the ear. It is peculiarly apt to supervene in the puerperal state, frequently affecting the uterine veins, and frequently also sis and of heart disease. In the former of these affections especially, it is not un- common to meet with it in the iliac veins, and in the venous trunks connected with the upper extremities. It is also discov- ered now and then, both in these diseases and in others, in the renal veins, in some of the veins connected with the liver, and other visceral veins. Lastly, we may point out that phlebitis is liable to arise in veins already otherwise diseased, as, for example, in varicose veins. Just as inflamed arteries, which have become obstructed with clot, lead in con- sequence of this obstruction to secondary affections in organs and tissues to which they are distributed, so inflamed veins, when they have become similarly oc- cluded, produce in consequence of their occlusion secondary phenomena in the regions which they drain. The obstruc- tion of a vein necessarily leads in a greater or less degree to stagnation of blood, first in the veins, and next in the capillaries which form part of its system. This stagnation of blood, with the consequent dilatation of the vessels in which it is stagnant, may be the only secondary phe- nomenon ; and it may soon disappear, provided either the vein becomes pervious again, or the anastomotic veins are suffi- ciently large or numerous to take on readily its suspended functions. In other cases the veins beyond the seat of ob- struction become dilated and tortuous, and scrum exudes into the connective tis- sue, causing anasarca. This dilatation of tributary veins, with localized anasarca, is well seen, in the legs when the obstruc- tion takes place in the iliac veins, in the arms when it occurs in the subclavian and axillary veins, and in the head and neck and arms when the vense innomi- natse are the seat of disease. But the formation of phlebitic clots is attended with a class of dangers different from those which have just been considered, and different from any which attend the formation of clots in arteritis. I allude to the dangers of embolia, to the dangers, that is to say, of the detachment of the phlebitic clots or of fragments of them, of their transference by means of the cir- culation to other parts of the system, of their impaction in small arteries, and of the effects more or less serious to which they may then lead, in the areas which the obstructed arteries happen to supply ; and I allude also to the supervention of pyaemia, which mostly, as before pointed out, has its starting-point in some local phlebitis taking place in connection with some unhealthy inflammatory process. The local symptoms of phlebitis consist in pain and tenderness in the course of the affected portion of vein, with distin- guishable fulness and hardness, if it be superficial, and often with redness or livid [Fig. 132 Thrombus in Saphenous Vein. S.Vein. T. Throm- hus. C. Conical end projecting into femoral vein. At v, v, the Thrombus is softened. (Virchow.)] affecting other of the systemic veins, but more particularly the iliac, producing, or aiding to produce, the condition known as phlegmasia dolens. Phlebitis, too, is very liable to occur in the course of phthi- DISEASES OF VEINS. 883 discoloration in the integuments over it. These symptoms are attended also with more or less general febrile disturbance, and followed soon, generally, by disten- sion of the veins beyond, and by anasarca. If the phlebitis be of that kind which, commencing in the venous sheaths, tends to spread along them from the smaller to the larger veins, the symptoms become altogether more grave ; the pain and ten- derness, the hardness and superficial con- gestion, which mark the seat of disease, are observed to spread and to become extensive ; abscesses may form here and there around the veins, and may even lay open portions of them ; the constitutional symptoms are those of high fever, which tends to assume the typhoid character. The symptoms of phlebitis, however, in complicated cases, are very often difficult, or even impossible, to recognize; some- times, no doubt, because the symptoms themselves are very trivial, frequently be- cause the complications are of so grave a character as to include and mask them. The latter event takes place particularly when the phlebitis occurs as a part of erysipelas, or of diffuse cellular inflamma- tion, or of other kinds of inflammatory affections; it occurs also when pyaemia, or even sometimes when embolia, super- venes on phlebitis. But little need be said in reference to the treatment of uncomplicated phlebitis. If the vein be within reach, leeches, or ice (inclosed in a bladder or India-rubber bag) may, in the early stage of the affec- tion, be applied along its course. At a later stage poultices or warm-water dress- ing may be serviceable. Rest should, of course, be enjoined. The constitutional treatment must be made to depend partly on the character and degree of the consti- tutional symptoms due to the disease, partly on the patient's general condition of health, partly on the special dangers to be apprehended and guarded against. If the general symptoms be trivial, little or no medical treatment is called for; but the more they assume a typhoid charac- ter, the more stimulants and nourish- ment, and medicines tending to the same end as these, are required. If the patient be suffering from tubercle, cancer, or heart disease; from the syphilitic or alcoholic or other cachexy ; or from the effects of privation, the constitutional treatment must have special reference to these con- ditions, to the patient's general condition of health, and to the special dangers to be apprehended and guarded against. (2) Degeneration.-Degenerative changes in veins are infinitely more rare than they are in arteries. Indeed, ordinary athe- roma is probably never met with here; although it would seem that some degree of fatty degeneration, or at least of depo- sition of oily molecules, is not unfre- quently to be seen microscopically in the walls of varicose veins, and in their valves. Depositions of earthy matter, although very rare, are yet, undoubtedly, of occasional occurrence. And it is worthy of remark that one of their favor- ite seats is the walls of varicose vessels ; those vessels in fact in which fatty matter is now and then discovered. The cal- careous deposits form irregular plates (originating apparently in or beneath the lining membrane) almost always consid- erably thinner than the calcareous plates in arteries, and often presenting a nodu- lated or " stalactitic" character towards the channel of the vein on which they tend to encroach. These calcareous plates have the same composition, and doubtless the same mode of development, as those in arteries. They consist mainly of car- bonate and phosphate of lime, are de- posited in globular masses which tend to coalesce, are formed in fact much as bones is formed, and are sometimes converted into unmistakable bone. They are usu- ally observed in small amount, and often a single calcareous mass alone is discov- ered. (3) Concretions. -Phlcbolithes are glob- ular or ovoid or irregular concretions, not unfrequently observed in the interior of veins, especially in the interior of veins which are dilated or varicose. Their most common seat probably is in the veins about the neck of the bladder, and other pelvic veins; they are met with, however, occasionally in the varicose veins of the lower extremities, and in the veins of the lungs and of the spleen. They are sometimes attached at one or more points to the lining membrane, are sometimes inclosed in a capsule formed by the oblit- eration of the vein above, and below the concretion, and sometimes lie loose either in the channel of the vein, or in a pouch connected with it. These bodies vary from the size of a horse-bean downwards, but are sometimes considerably larger. They are of a yellowish-white color, hard and calcareous, and on section appear to be made up of concentric layers like a urinary calculus. They consist chemically of carbonate and phosphate of lime, with some magnesia, and a variable proportion of organic material. How these bodies are formed has been matter of dispute. By some writers it was imagined they were formed externally to the lining mem- brane of the vein, into which they subse- quently became prominent, then peduncu- lated, and finally detached. The more common opinion, however, and that which is doubtless the correct one, is that they originate in transformed clots. And, in- deed, according to Rokitansky, there is commonly a roundish cavity or irregular 884 DISEASES OF VEINS. fissure within the nucleus, which is itself dry and of a rusty brown or dull yellow color. A clot of which this nucleus is the remnant is probably first formed; this undergoes degeneration, collapses, and furnishes a nucleus around which fibrin- ous layers from the blood are successively and slowly formed, and in which calcare- ous salts become deposited. (4) Adventitious Growths.-Veins, like arteries, may be involved in carcinoma- tous and other growths, and like arteries, may become obliterated in consequence. But veins are additionally liable to be- come the actual seat of such growths. Thus, sometimes when a vein gets sur- rounded by a malignant tumor, this gradually invades its walls, and ulti- mately projects into it, and then either forms pedunculated or sessile outgrowths, or fills the channel, renders it impervious, and extends along it. Sometimes, again, secondary cancerous growths originate in the substance of the venous walls, and ultimately form polypi, hanging into the cavity of the vein. We have seen a good example of this condition, in connection with a' trunk of one of the pulmonary veins, in a case where the lung was the seat of carcinoma. The same thing may occur also in connection with tumors which are not malignant. Thus in a case of myeloid disease of the humerus, we once found the veins ramifying in the deltoid muscle, and some of the large veins of the upper arm, filled with mye- loid growth, identical with it. Tubercle, so far as we know, is never met with in the veins. (5) Changes of Dimension.-Veins undergo changes of dimension both from physiological and from pathological causes. To the former class of causes are to be attributed that ordinary enlarge- ment of the veins which attends the growths of the body, that enlargement which takes place in anastomotic branches when a trunk is obstructed, those changes of dimension of the uterine veins which attend the corresponding change of di- mension of the uterus itself, that diminu- tion of size which occurs after amputa- tion in the veins of stumps, and so on. To the latter class of causes must be as- signed the varicose condition of veins which is so often met with, and some forms also of contraction of veins. (a) Enlargement.-Varicose veins are veins which have irregular dilatation. Veins thus affected are elongated and unnaturally tortuous: their diameter is larger than natural, and often very con- siderably larger; and at the same time they present, irregularly distributed over their surface, hemispherical dilatations or aneurism-like pouches, and occasionally even flask-like diverticula communicating with them by a comparatively small ori- fice. In veins furnished with valves the dilatations occur more particularly in con- nection with the sinuses immediately above them. Coincidently with this dila- tation, the walls become attenuated, and the valves (at first perhaps simply ren- dered inefficient by becoming too widely separated from one another) become atrophied and shrivel up. The middle coat of veins is probably that (like the middle coat of arteries) by which dilata- tion is in the normal condition chiefly opposed ; and it is therefore in connection specially with the yielding of this that dilatation occurs. Its fibres become divaricated ; and, as already pointed out, they undergo some degenerative process indicated by the deposition in them of fatty particles. Sometimes, on the other hand, the walls of the dilated veins be- come thickened instead of attenuated, a change which is due to thickening of the outer coat. Dilated veins, like dilated arteries, may, by their pressure on parts external to them, cause the absorption of these parts. In this way the enlarging vessels sometimes approach the surface of the skin, or that of some of the mucous membranes, and even cause the absorp- tion of bone. We have pointed out already that varicose veins are specially liable to become inflamed; they are specially liable also to have coagula de- posited within them. These may occur as casts of veins, blocking them up; or may be produced in the dilatations only ; sometimes, according to Rokitansky, laminated coagula like those of aneu- risms are formed within the pouches. Phlebolithes, as we have already pointed out, are sometimes found in varicose veins, and are probably derived from such clots as have just been described. The vari- cose condition affects veins very variously both in extent, in degree, and as regards the order of veins affected. Sometimes the larger veins only are thus dilated, and when such veins are seated in some super- ficial part, large tortuous, soft, knotty, bluish cords, projecting above the normal level of the skin, indicate their presence. Sometimes the smaller veins only are varicose, and then, if superficial, they form in different situations pencils as it were of reddish or bluish vessels, larger than natural, thickly clustered and radiating, it may be, from a point or line. Sometimes one or two veins only, or portions of them, present the varicose condition ; sometimes nearly all the veins of a limb may be involved in the disease; sometimes there seems a still more gene- ral tendency for the veins to become dilated. The essential cause of the dilatation of veins is the same in principle as that of DISEASES OF VEINS. 885 the dilatation of arteries, namely, inabil- ity of their walls, from deficiency in them of resisting power, to withstand the pres- sure which the blood within them exer- cises upon them. This inability may de- pend either on actual loss of power in the walls, oi' on loss of power due to their over-distension, in consequence of impedi- ment to the onward flow of blood. It may depend therefore on constitutional causes, or on accidental local conditions of disease. But there is an additional circumstance, which has a very important influence in determining the formation of varices, and in increasing their bulk when once they have begun, that is, the pres- sure to which veins are exposed in rela- tion to the height of the column of blood they have to support. It is, we need scarcely say, a well-known hydrostatical fact, that the pressure exerted by a fluid (whether circulating or still) against any point in the walls of a receptacle contain- ing it, is in exact proportion to the height of the column of fluid above that point; and hence it is clear that those portions of the venous system, which are most de- pendent or nearest the ground, are ex- posed to greater pressure from within than those which occupy a higher situa- tion. No doubt this is to a great extent counteracted, in those veins which from their position are most subject to its opera- tion, by the presence in them of valves. Still, it is not wholly counteracted even in healthy veins ; and in those which have become sufficiently dilated to render the valves within them useless, it must act to its fullest extent. It is, doubtless, owing in great measure to the operation of this cause that varicose veins are specially frequent, and become specially large, in the lower extremities. Varicose veins sometimes get well spontaneously, especially after the disap- pearance of the cause which has induced them. Sometimes a cure is effected by the gradual return of the enlarged veins to their normal size, sometimes by an at- tack of inflammation in them leading to the deposition of a clot, and to their ob- struction and subsequent obliteration. Sometimes they remain more or less sta- tionary. But more commonly, if left alone, they continue to enlarge, and tend ultimately to burst externally and to cause dangerous, even fatal, hemorrhage. The presence of varicose veins leads also to unhealthy conditions of the parts with which they are connected. The symptoms due to varicose veins may be gathered from the foregoing ac- count of their morbid anatomy. They consist locally of enlargement of the veins, swelling and oedema of the associated tis- sues, aching pains, sometimes itching, tendency to inflammation of surface, eczema, excoriation and ulceration. To these may be added special symptoms, due to the impairment of function of any organ or part with which the varicose vessels happen to be connected. It is not easy to lay down any general rules with regard to the treatment of this affection. If it arise in constitutional conditions, there is reason of course to suppose that constitutional treatment may be of service. Looking upon the disease then as a disease indicating debility, it is natural to assume that tonics and other remedies tending to give strength may prove serviceable. And in the present state of our knowledge it is no doubt wisest to act on this assumption. If, on the other hand, it depend on any local impediment to the flow of blood, it will be right, if possible, to remove or counteract this local condition. Further, it is gen- erally desirable to support the affected veins, by the application over them of uniform and moderate pressure, in order to obviate the debility of their walls ; and, as far as possible, to maintain the part affected in either the horizontal position, or some other position tending to relieve the vessels from undue pressure of their contents. Before leaving the subject of varicose veins, it is desirable to say a few words in regard to some of the situations in which they chiefly occur, or in which their oc- currence is specially interesting. The most common seat of varicose veins is doubtless the lower extremity. Both legs seem to be equally liable to be affected. The disease here presents great varieties; sometimes a small portion of a vein, or a small group of veins only is affected; sometimes nearly all the veins are in- volved ; and all varieties are met with between these extremes. There seems little doubt that the superficial veins are those which, as a rule, are primarily and principally affected; but it has been pointed out by Briquet and by Callender that the points of chief distension are those in which the superficial veins are joined by branches from the muscular and other subjacent tissues; it has also teen, pointed out that in many eases the deeper- seated veins are equally involved with the superficial veins, and that occasionally the disease is actually limited to those which are deep-seated. Among the conditions tending to produce varicose veins here, and especially, of course, tending to pro- duce them in such persons as are consti- tutionally predisposed to their occurrence, may be enumerated, occupations requir- ing long-continued maintenance of the erect position, pregnancy, ovarian dis- eases, and generally the presence of ab- dominal tumors producing pressure either on the vena cava or on the iliac veins, and probably also cardiac and other diseases in which the free passage of blood from 886 DISEASES OF VEINS. the right to the left side of the heart is impeded. Varicose veins in the leg pro- duce swelling of the leg and sometimes a slight degree of anasarca; they are apt also to lead to inflammatory conditions here, to induration of the cellular tissue, to congestion of the surface, excoriation and eczema, and not unfrequently to ulcers. These ulcers are generally very intractable. It is in the leg. too, more than anywhere else, that rupture of the dilated veins is liable to occur. In the treatment of varicose veins of the leg the constant use of support is very essential. Generally the constant wearing of an evenly applied bandage from the foot to the upper part of the thigh, or of a well- fitting laced stocking, is indicated. Some- times the obliteration of the trunk veins by surgical means becomes imperative. The details of surgical treatment we do not profess to discuss, but we may enu- merate the more important surgical expe- dients, such as the application of pressure in the course of a vein, the tying of veins, the formation of an eschar over them, the introduction of foreign matters such as threads into them for the purpose of pro- ducing coagulation, and the like. When the surface of the leg is congested or in- flamed, the limb should be maintained at rest and in the horizontal position, and cooling and such other applications as are applicable in superficial inflammation should be employed. In the treatment of varicose ulcers support and pressure are of the first importance. If a vein burst, the wound should be treated exactly like the wound after the ordinary operation of phlebotomy. The patient, too, should be placed in the horizontal position and the limb elevated. Varicose veins not unfrequently arise in the spermatic cord, producing the dis- ease termed varicocele. This occurs al- most always upon the left side, and is supposed to be determined here in part by the great length of the left spermatic vein, and in part by the fact that this vessel opens into the renal vein instead of open- ing like its fellow directly into the cava. The veins in this disease become very large and tortuous, and are described as feeling like a bundle of worms ; the tes- ticle to which they belong becomes the seat of much aching pain, and ultimately its nutrition becomes impaired, it shrinks in size and undergoes atrophy. In this affection the testicle should be supported; and, as in the former case, it may be necessary to employ operative measures. Hemorrhoids or piles have generally been regarded as a varicose, condition of the hemorrhoidal veins; and there is no doubt that they are often produced, and always increased, by constipation and by any other condition which impedes the passage of blood along these veins, or the veins into which these empty themselves. Hemorrhoids, however, are not so much varicose veins as they are a hypertrophic condition of the mucous membrane, or of the integuments, in the neighborhood of the anus, attended with much congestion of the capillary and other minute vessels, and in some degree also with a varicose condition of the veins. Varicose veins may occur in other situ- ations besides those which have been specified, and lead to grave results. Thus, there is reason to believe that the veins of the stomach and of other portions of the alimentary canal occasionally become dilated, and induce dyspeptic and other obscure symptoms. We have met with a case in which the veins of the oesophagus were varicose, and where death was due to the rupture of one of them. The veins about the bladder and the prostate are not unfrequently varicose. Those of the labia pudendi certainly often become vari- cose in the course of pregnancy. Again, varicose veins are occasionally observed in the upper extremities, and even in the neck. As the result of actual obstruction of veins, they may in fact be met with in almost any situation ; we have already specially pointed out some cases of this kind, and we may add to the list, the oc- currence of such veins in the abdominal parietes in certain cases of hepatic or of splenic disease, and the dilatation of veins in the neck and upper extremities which follows upon obliteration of the innominate veins, or vena cava descendens, produced by aneurismal or other tumors in the neck. Rokitansky says that the veins of the pia- mater become varicose in drunkards. (6) Occlusion.-Occlusion of veins has been already considered incidentally in various parts of the foregoing account of the diseases of veins. It has been shown to occur sometimes as the result of phle- bitis attended with the formation of clots; to be produced sometimes by the pressure of a tumor growing external to the vein, sometimes by the growth of carcinomatous or other tumors into the interior of the veins. The results of occlusion and its symptoms have also been considered inci- dentally. They are principally, dilatation of the veins on the distal side of the seat of obstruction, enlargement of anasto- matic veins, oedema of the tissues through which the passage of blood is obstructed, and such further phenomena as attend, on the one hand anasarca, on the other hand varicose veins. CARDIAC CONCRETIONS: MORBID ANATOMY. 887 CARDIAC CONCRETIONS. John Syer Bristowe, M.D., F.R.C.P. The condition of the blood in the heart's cavities, at the time of death, as to quantity and quality, and the relation which its varieties of condition bear to the cause of death, are necessarily matters of much pathological interest; they are matters also of some practical interest; and, in both these points of view, have been made of late years the subject of a good deal of careful observation. Yet it is curious that nearly all systematic writers on heart-diseases-and even the more recent of them-have either passed this subject over in almost complete si- lence, or, if they have been tempted to enlarge upon it, have displayed a lack of knowledge in regard to it which the char- acter of their works in other respects would scarcely have permitted us to suspect. It is not proposed, in the limited space which has been necessarily allotted to the present article, to treat exhaustively the subject under consideration, still less to criticize at any length published opinions upon it which seem to us erroneous. It is intended rather to give a general brief account of the whole subject, and to en- large upon those points only which seem to have some special interest and import- ance. Morbid Anatomy.-At the time of post-mortem examination, the cavities of the heart may be found either contracted and empty, or dilated and containing an amount of blood proportionate to their dilatation. And, in the latter case, the blood may be found either quite fluid, or imperfectly coagulated, or coagulated and moulded to the surfaces with which it is in contact, or in the form of "globular concretions," or in a tough laminated con- dition, or mixed, it may be, with concre- tions (emboli) brought hither from remote parts of the vascular system. It may be added, that two or more of the above con- ditions frequently coexist in the same case, and such of them as are not incom- patible with one another, even in the same cavity. It is desirable, however, to discuss them separately. Emptiness of Cavities. - The cavities which are most frequently found empty of blood are the ventricles. This empti- ness is much more common in the left ventricle than in the right; but not un- frequently both cavities are in the same condition. The auricles are generally full, if not distended. Fluid and semi-fluid Blood.-The blood contained in the heart's cavities may be fluid or semi-fluid. That is to say, it may be nearly as fluid as when it freshly es- capes from a vein, it may be more or less treacly, or it may contain floating in it soft loose masses of dark-colored imper- fectly-formed clot. It is in these cases usually that the lining membrane of the heart and large vessels becomes stained with the coloring matter of the blood. Moulded Clots.-The blood may have undergone more or less complete coagula- tion. Its condition, however, varies very considerably in different cases. Some- times the coagula are small, and the car- diac parietes are contracted, or collapsed upon them ; sometimes they are large and distend the cavities to the full; some- times they exist therein alone ; sometimes they are surrounded by a greater or less quantity of serum or of uncoagulated blood ; sometimes they are of a uniform red-black hue ; sometimes they are partly decolorized ; sometimes they are wholly fibrinous. These coagula, whatever their color or consistence, are always accurate, or near- ly accurate, casts of the cavities which contain them, and are generally attached to the surface, not by any organic connec- tion, but by being dove-tailed, as it were, with its inequalities. Those of the corre- sponding auricles and ventricles are con- tinuous through the auriculo-ventricular opening ; and are, moreover, prolonged to a greater or less extent into the venous and arterial trunks. In the aorta they sometimes extend throughout nearly its whole length, in the pulmonary artery to its smallest subdivisions. The prolonga- tions into these tubes are cylindrical, but generally a good deal smaller in diameter than the tubes themselves; and those portions of them which correspond to the arterial valves, have always the form of the valves distinctly impressed upon them. Moulded coagula are sometimes, as has been just pointed out, of a uniform red- black hue. They have then much the appearance and consistence of black-cur- rant jelly, are soft and tremulous, and consist of a uniform mixture of chiefly the 888 CARDIAC CONCRETIONS. fibrine and the red corpuscles of the blood. Sometimes they are partly de- colorized, or, in other words, a partial separation of their component elements has taken place. The fibrine may then have separated, much as it does in the formation of the butty-coat after bleeding, producing a thin almost colorless layer on that portion of the clot which, during its formation, has lain uppermost. Or it may happen that the whole surface of the clot is fibrinous, while the interior remains colored. Sometimes again, and this is the most remarkable case, the whole, or nearly the whole, of the clot is fibrinous. Such clots are sometimes loose in texture and watery and retain more or less of the coloring matter of the blood : some- times straw-colored, jelly-like, and elas- tic ; sometimes close-grained, buff-colored, opaque, and tough. Moulded clots may be found in all the cavities of the heart: but those which are fibrinous are chiefly found in the ven- tricles, and mere frequently in the right ventricle than in the left; they may, how- over, occur in the left ventricle even when they are absent from the right. The clots which extend into the larger vessels are generally in the greater part of their ex- tent identical in character with the car- diac clots, with which they are con- tinuous. But even when almost purely fibrinous, they mostly pass off at their extremities into colored clots. This is especially the case with those occurring in the veins. Softening Clots.-Softening clots, globu- lar concretions, purulent cysts (for all these names, and many others, have been applied to the bodies now about to be de- scribed) are coagula, which have under- gone changes, by which they have become converted into roundish masses, softened for the most part internally into a puri- form fluid, attached firmly to the parietes, and occupying, with scarcely an excep- tion, those portions of the cavities which lie out of the direct current of the blood. These bodies may occur singly in a car- diac cavity, or in considerable numbers, and may vary from the size of a pin's head up to that of a pigeon's egg. They are almost always attached to the surface, and generally spring distinctly from the inter- spaces between the carneae columnae, or the musculi pectenati. Their attachment to the surface, though sometimes in part due to slight adhesions, is mainly effected by this entanglement with the fleshy columns ; and, indeed, where several of these bodies are present in a cavity, they are probably always continuous with one another by means of processes extending beneath those muscular bands which are attached to the cardiac walls by their extremities only. Their free surfaces are sometimes smooth, sometimes more or less ribbed ; generally they have an opaque buff-color, but they may present more or less of a brick-red tint, or may be variegated with irregular streaks of red and white. On section, they present considerable variety of ap- pearance. Sometimes they are solid throughout, and repeat on their sectional surface, the characters already displayed by their external aspect; more commonly, however, they are more or less softened, at one time converted into a thin-walled cyst, at another time broken up irregu- larly into a series of small intercommuni- cating cavities. The walls of the cyst are identical in character with the sub- stance of the unsoftened concretions, but their inner surface is soft and flocculent. The contained fluid is thick and puriform, and varies in color from a pale buff to a brick-red, or even chocolate, hue. Under the microscope the solid portions of these concretions are found to consist of a fibroid network similar to that of or- dinary coagulated fibrine. " This, how- ever, is intermixed with a large quantity of granular matter, which renders the fibroid structure more or less indistinct. They contain also oil, compound granular cells, and a few imperfect cells which ap- pear to be the remains of white corpuscles. In some cases there are many altered blood-corpuscles, and now and then soli- tary and clustered needle-like crystals." " The puriform contents of the cysts pre- sent considerable variety as to their mi- croscopic elements. When white or buff- colored, they consist almost solely, if not solely, of molecular matter, oil, and broken-down corpuscles, with which are frequently mixed compound granular cells, and colorless acicular crystals. When presenting a brick-red or chocolate hue, they exhibit, in addition to the elements just mentioned, numerous blood-corpus- cles, more or less altered, and conse- quently more or less indistinct, and occa- sionally also ruby-colored, rhomboidal, h®matoid crystals." In one instance which we have met with, the fluid con- tents consisted almost entirely of well- marked pus-like corpuscles. It is asserted by Rokitansky,1 that these concretions are almost always limited to the left ventricle. This, however, is an error. They do, it is true, occur here more frequently than in any other one of the cavities of the heart; but they occur much more frequently in all the other cavities collectively, than they do in the left ventricle. They are not unfrequently found in two or three cavities, and occa- sionally in all of them at the same time. In order of frequency they affect, we be- lieve, first, the left ventricle ; second, the 1 Path. Anatomy (Sydenham Society's Translation), vol. iv. p. 217. ETIOLOGY. 889 right ventricle ; third, the right auricle ; and last, the left auricle. With regard to their position in the cavities of the heart, there is no doubt that, with scarcely an exception, they occupy those situations which are most favorable to the stagna- tion of blood. "In the auricles they chiefly affect the auricular appendages, and in ventricles they almost always oc- cupy the spaces and interstices between the carnese columns. '" Occasionally, they are developed around some of the chor- dae tendineae; and one or two cases are recorded, in which they have been found detached. Laminated Clots.-Laminated coagula, such as are found in aneurisms, are of very unfrequent occurrence in the heart, and of recorded cases, the most common are certainly those in which the coagula have formed in the interior of aneurismal dilatations, or of actual aneurisms devel- oped in connection with the ventricles. Still a small number of cases have been met with, in which cavities otherwise healthy have become almost obliterated W'ith coagula of this kind. We are ac- quainted with this condition only as aflect- ing the left auricle, secondarily, to ex- treme contraction of the mitral orifice- under circumstances, therefore, not dis- similar from those which lead to the for- mation of such coagula in the interior of actual aneurisms. In one such case,2 where the mitral orifice was so contracted as scarcely to admit the tip of the little finger, the left auricle was greatly dilated, and full of firm laminated coagulum, which formed two perfectly distinct masses -one extending from the auricular ap- pendage backwards, the other forwards from the posterior and inner part of the cavity. They were slightly adherent to the parietes, and were in contact with one another by their free surfaces, which were consequently flattened. The cavity of the auricle was thus obliterated, or, at least, reduced to the imperfect and irregular channel left between these mutually com- pressed masses. Embolic Concretions.-Sometimes,though very rarely, concretions which have been moulded in remote parts of the vascular system are found entangled amongst ordi- nary cardiac clots. The only instance in which we have certainly met with this condition was a case of scarlet fever with sloughing of the tonsils. In this case small opaque shreds, and portions of cylinders, consisting entirely of corpuscles resembling those of pus, were found in the right ventricle, embedded in ordinary post-mortem clot. We have never met with tubercle or carcinoma in the heart thus conveyed. Etiology.-It is obvious that at the moment of death the heart's ventricles are either contracted, or in various de- grees dilated ; and that their emptiness or fulness of blood at the time of post- mortem examination must be in great measure determined by these conditions. It is obvious, too, that in those cases in which the cavities are found full of blood from the stagnation in them simply of the blood arrested in its course at the moment of death, the state of this blood as to fluidity or coagulation must depend in great measure upon the conditions of sick- ness under which death has occurred. All these are matters of interest, and worthy of investigation; but they are not in- cluded within the scope of our present article, and we are compelled therefore to dismiss them. But of the dots found in the heart after death, some have evidently been formed in it during life, and may possibly have had some influence in destroying life. Amongst these must be included such as are wholly or for the most part fibrinous, globular concretions, and laminated co- agula. How and by what means these are produced we have now to consider. Clots moulded to the cavities of the heart, if they be of uniform consistence and of a uniform reddish-black color, have doubtless in all cases been formed post mortem, from fluid blood contained in the cavities at the time of death ; and the same explanation doubtless holds good of those cases also in which such clots pre- sent a layer of fibrine (a huffy coat in fact) on that part of their surface which has lain uppermost. In all cases, however, where the clots are purely fibrinous, or where the fibrinous element is in excess, or where the fibrine which has separated occupies any other position than the upper surface, the separation of the fibrine and therefore the coagulation of the blood, must have taken place during life, while the blood was still in process of circulation. That this must be so is evident from the consideration that there is no means by which stagnant fluid blood can, in coagu- lating, manifest separation of fibrine ex- cept upon its upper surface, still less achieve the perfect separation of its fibrine from all its other constituents. It is fur- ther proved by Dr. Richardson's exami- nation' of these fibrinous clots, which shows that the amount of fibrine contained in them is several times greater than can be accounted for by the quantity of blood 1 The passages included within inverted commas are quoted from the author's papers, " On Softening Clots in the Heart," contained in the 7th and 14th volumes of the Patho- logical Society's Transactions. 2 See Path. Trans, vol. xi. p. 65. 1 See Dr. Richardson's Lectures in the Brit- ish Medical Journal for 1860. 890 CARDIAC CONCRETIONS. which the heart's cavities are capable of containing. It must not be forgotten, however, that all the fibrine met with in such cases in the cavities of the heart rarely, if ever, exceeds the amount of fibrine contained in the blood which passes through the heart in the course of half a dozen beats; and that, therefore, the whole of a large fibrinous clot may have been whipped out of the blood in the course of the minute or two of circulation which precedes death. It is certain, then, that such clots are formed during life, but by.no means clear how long their forma- tion actually takes. Some of them are doubtless, as has been just suggested, formed in the course of the few moments immediately preceding death ; but it is ex- ceedingly probable that others have taken some considerable time in their formation. What it is that determines this coagula- tion of the blood during life is by no means easy to determine. Dr. Richard- son, in the paper before referred to, enu- merates several classes of cases in which fibrine is peculiarly apt to be deposited during life in the heart's cavities, the most important of his classes being that of acute inflammatory affections, including pneumonia. We have no doubt that, in all the cases which he enumerates, fibrin- ous clots are not unfrequently observed ; but, indeed, they are constantly met with in the post-mortem room, not only in them, but in almost every form of disease. They are by no means constant, even in cases of pneumonia. Mr. Henry Lee believes them to be characteristic of purulent in- fection of the blood. This, however, is obviously an error ; for while it is common to meet with them in cases where no such infection can be suspected, in cases of pysemia they are altogether exceptional. We shall not pretend to offer any satis- factory explanation of the causes of the formation of these ante-mortem clots in some cases, and their non-formation in others. But we may admit generally with Dr. Richardson, that there are diseases in which, from some cause or other, there exists a tendency to the separation of fibrine ; and further we may suggest that slowness in dying may in such cases to some extent determine this separation. With regard to the formation of the rounded concretions, which are generally softened in their interior into a puriform fluid, many fanciful theories have pre- vailed. Thus it has been supposed that they are softened tubercle, or pus, conveyed to the heart from a distance and there en- cysted. Their contents, however, are never tubercular, and rarely if ever purulent; and although they may be occasionally met with both in phthisis and in pysemia,their occurrence in these diseases, especially in the latter of them, is exceptional. Again, it has been supposed that their formation is due to local endocarditis. But, in re- ply to this supposition, it may be pointed out that they rarely, if ever, accompany undoubted cases of endocarditis; and, moreover, that they are almost without exception found in just those parts of the heart's cavities in which true endocar- ditic deposits probably never take place. That they are merely altered clots is evi- dent, both from their microscopical con- stitution and from their identity, in the changes which they undergo, with clots formed in other parts of the body, whether in the vessels or by extravasation. It is evident, too, that the condition in which they are found after death is the result of processes which must have required days, or even weeks, and possibly a still longer time for their completion. It is evident, further, from the mode in which they are attached to the cardiac walls, that they must have been formed in the position in which they are discovered post mortem. The cases in which they are most com- monly observed are cases of heart disease, of renal disease with dropsy, of chronic bronchitis, and of chronic phthisis, cases in which death is often slow, or in which struggles, as it were, between life and death are apt to occur from time to time for some while before death actually su- pervenes. It seems probable that the foundation of these concretions is laid at one or other of these moments of seem- ingly impending death, by the coagula- tion at that time of blood in the cavities of the heart; that the patient rallies from his apparently moribund condition, and that the clots, at once the evidence and the result of that condition, remain ; that the clots then during the remainder of the patient's life gradually undergo those changes, which clots in the brain and elsewhere are liable to undergo ; that they become torn into smaller masses, probably in consequence of the constant move- ments of the cardiac walls; that these masses become rounded partly in conse- quence of the contractile force inherent in the fibrine of which they chiefly consist, partly by the attrition to which they are exposed by the constant movement of the fluid blood over their surface, and that after a while their interior undergoes softening and disintegration. The laminated clots, of which I have quoted an example from the left auricle, are evidently of slow growth, and originate long anterior to death. Indeed, they are obviously formed on the same principle as that which determines their formation in aneurisms, and are the result, as in aneu- risms, of a slow process of deposition from the blood. Symptoms and Effects.-We now have to consider the important question, whether the clots which are formed in the SYMPTOMS AND EFFECTS. 891 heart prior to death have any effect in producing death, and if so, whether their presence during life can be recognized by any characteristic symptoms. All who have enjoyed much clinical, combined with post mortem, experience of disease, will admit, as regards the vast majority of cases in which moulded fibrinous clots are discovered in the heart, that their forma- tion has taken place during the process of dissolution, and as a part of that process, that their formation has been unattended with symptoms referable to themselves, and that if they have exerted any influ- ence adverse to life, it can only have been in the sense of preventing any tendency to rally, in other words, of confirming the act of dying. It does not however neces- sarily follow that cases do not occasionally happen, in which in the course of certain forms of disease, or even apparently in health, such clots form, and by the im- pediment which they oppose to the circu- lation of the blood through the heart, cause death. To the consideration of this point we will shortly recur. Meanwhile we will discuss the effects of those forms of clot-globular and laminated concretions -which beyond all dispute must have been in existence a considerable time an- terior to death. In regard to the lamin- ated concretions, it may be stated, we think with some degree of certainty, that their presence is attended with no special symptoms. No doubt they add to the embarrassment of the heart, but they add only to the embarrassment of an already embarrassed organ ; they merely increase the severity of symptoms which are al- ready severe, and therefore, if combined with mortal disease, merely cause the disease to anticipate its final series of events. It is worthy of remark, however, that life is maintained in these cases even when the auricular cavity is so encroached on as to be no more than a mere channel between the veins and the auriculo-ven- tricular opening. Globular concretions equally as a rule produce no special symp- toms. Certainly they are constantly met with post mortem in cases which have been under continued observation, and have presented no special symptoms indicative either of their formation or of their pres- ence. No doubt their presence in the cavities of the heart has a tendency on the whole to impede the action of the heart and to affect the circulation in- juriously, especially if they be large, or if they occupy certain situations. But im- pediment, real or virtual, to the circula- tion, probably always exists prior to the formation of these bodies, so that their addition tends to aggravate symptoms al- ready established rather than to develop new ones. It seems not improbable that they may now and then interfere with the normal function of some of the valves, and so lead to the production of endocardial murmurs, but with this result we have no practical acquaintance. Again, two or three cases are recorded in which they have been found detached in an auricle, and lodged in, and thus obstructing, a contracted auriculo-ventricular orifice. And it has been surmised that they may occasionally become ruptured, and, by the escape of their contents into the cir- culating blood, produce symptoms of py- aemia. It may be considered, therefore, that, excluding a small number of quite exceptional cases, the presence of these clots in the heart cannot be recognized by peculiar symptoms, but may be surmised, and often correctly, in cases where the struggle between life and death has been greatly protracted, especially if the pa- tients be suffering from any of the diseases in which morbid anatomy shows that these clots are chiefly produced. It is import- ant, however, to bear in mind that al- though these concretions doubtless origin- ate in ordinary fibrinous coagula, there are few if any cases in which the moment in which they were first formed can be even approximately determined. Let us now return to the question as to the influence of moulded clots in produc- ing death. It seems to us that with the facts before us-first, that coagula of this kind are constantly observed in the post- mortem room as the mere accompaniment and result of the dying process ; second, that (as has been showm) whole cavities may become- obliterated by coagula with- out directly causing death ; third, that (as has also been shown) in the majority of cases in which it can be clearly demon- strated that concretions have been formed some considerable time before death, their formation has not produced marked symp- toms, we ought to require very strong testimony indeed to convince us in any case that concretions found in the heart at the time of death, have caused death, still more to convince us that those clots which resemble in every point the clots which are the mere result of dying, have had this effect. It is no doubt convenient and seductive, when we meet with a case of fatal illness, to be able to point to some obvious pathological phenomenon attend- ing it, and to believe that in that we recog- nize the cause of death. Not long ago fatty heart furnished the ready explana- tion of most sudden deaths, now fibrinous concretions in that organ begin to rival fatty heart in popularity. We have no hesitation in stating our conviction that in the great majority of cases w'hich have been recorded of death from the forma- tion of fibrinous concretions in the heart, these concretions have been developed in the ordinary way, and have had no more to do with the death of the patient than the rigor mortis has. We are not pre- 892 THROMBOSIS AND EMBOLIA. pared to deny that death is sometimes actually caused by such a deposition of fibrine, but we can state positively that no such case has come under our obser- vation, and we believe that the great ma- jority of recorded cases are cases in which the sequence of events-cause and effect -have been misunderstood and trans- posed. In the remarks which have just been made, we wish it to be distinctly un- derstood that we refer exclusively to car- diac concretions, and not to concretions blocking up the pulmonary artery and limited to that artery. This latter sub- ject will be discussed under the head of "Thrombosis and Embolia." We may add, for the convenience of those readers who are interested in the subject, that they will find an ingenious account of the symptoms which are supposed to attend the formation of moulded cardiac concre- tions, in Dr. Richardson's lectures, al- ready more than once referred to in the course of this article. THROMBOSIS AND EMBOLIA. John Syer Bristowe, M.D., F.R.C.P. The terms " Thrombosis" and " Em- bolia" (or Embolism) have been intro- duced by Virchow : the former, to signify the coagulation of blood in arteries or veins during life: the latter, to signify the transference either of clots, or of other solid matters appearing within the vascu- lar system, from one part of that system to another part, in the direction of the circulating current, and by means of it. These subjects have already been partly considered under the heads of "Pyaemia," "Cardiac Concretions," "Diseases of Arteries," and "Diseases of Veins ;" wre propose however here to treat them as a whole, and, as they are intimately related to one another, to combine their descrip- tion in a single article. The local phenomena, which attended the coagulation of blood in the vascular system during life, are essentially the same, in whatever part of that system coagulation takes place ; and the changes which clots undergo are also essentially the same, whether the clots occur in the arteries, in the veins, or even in the heart. These have been already in great part de- scribed. A clot, consisting either of nearly pure fibrine or of all the solid ele- ments of the blood combined, forms, and is moulded as it forms, to the surface against which it lies ; to which also it is from the beginning, or becomes ere long, adherent. The changes which such a clot undergoes in the course of time vary. They consist, sometimes in its gradual con- traction and organization ; the fluid mat- ters become absorbed, the cellular ele- ments disintegrate and disappear, the fibrinous portion undergoes condensation, and ultimately the clot becomes converted into, or replaced by, ordinary connective tissue. They consist sometimes in the softening and breaking down of the clot internally ; the central parts become con- verted into a thick puriform fluid, some- times red, sometimes nearly white, con- sisting chiefly of disintegrated cell ele- ments merely-such as granular matter, oil, cholesterine, debris of corpuscles, and perhaps hsematoid crystals ; the clot may thus come to form, either wholly or in part, a mere fluid-holding bag, in which condition it may remain for a consider- able time ; but gradually, here as in the former case, the fluid portion undergoes absorption, the contents dry up and the cyst-walls collapse upon them. Some- times, further, clots become the seat of calcareous transformation ; and this may occur both in those which have softened internally and in those which have main- tained the solid form ; particles of earthy matter are deposited, which gradually in- crease in number, and ultimately by their aggregation transform them into calcare- ous masses. There is reason, as has been already shown, to believe that phlebo- lithes are formed in this way ; and phle- bolithes are occasionally the seat of true ossification. A full account of these clots, as they are met with in the heart's cavities, has already been given. In the aorta and pulmonary trunk they are unfrequent, except where they are met with as fibrinous or more or less col- ored cylinders prolonged from the interior of the respective ventricles or from the neighborhood of the semilunar valves. Such clots, like the corresponding cardiac THROMBOSIS AND EMBOLIA. 893 clots, are manifestly formed during life, though often during the last moments only of life, they always present the im- press of the arterial valves, and, though generally much smaller than the channel in which they lie, sometimes almost fill it. Older clots are sometimes observed in the aorta. These are isolated roundish concretions, adherent to the surface (mostly if not always in connection with points of disease), projecting into the canal, but not materially obstructing it. In other arteries, however, and especially in the smaller arteries, these clots gener- ally form solid cylinders, equal in diame- ter to the vessel in which they lie, adher- ent more or less to its surface, and more or less completely obstructing its channel. The obstruction, however, is generally at first incomplete, and the constant impulse of blood against the proximal extremity of the clot tends gradually to force a cer- tain proportion of blood between it and the arterial walls. In this way, blood in small quantities flows for a time through irregular channels over the surface of the clot; soon, however, it coagulates there, and thus the original clot becomes in- crusted with an irregular layerj of more recent coagulum, the vessel becomes dis- tended and the occlusion becomes com- plete. Further, additional coagulum tends to be deposited in connection with the extremities of the primary clot ; this deposition ceasing generally, on the proxi- mal side, at the point of anastomosis near- est the seat of obstruction. clot at their proximal end, until the vein becomes filled up as far as its mouth, and that, in continuation of this process (from the blood which passes along the trunk vein with which the obstructed vein com- municates), additional coagulumis gradu- ally added to that which has been already deposited, until from the plugged orifice there projects into the interior of the trunk a rounded mass of laminated coagu- lum, which may attain a very consider- able size. The causes of Thrombosis have already been to some extent considered. Some- times the coagulation seems to be con- secutive to mere stagnation of blood, or sluggishness of circulation, occurring in certain conditions of disease. Such prob- ably is the case in regard to softening clots in the heart; such probably, also, is the case in regard to the clots which plug certain of the veins in phthisis and some other affections; and such, also, doubt- less, is the case when arteries, leading to districts of disease in which the capillaries are obstructed, become themselves filled with clot. Sometimes the coagulation is determined by mere roughness of the sur- face over which the blood passes. This is observed when isolated clots become adherent to atheromatous patches, and when extensively atheromatous or ossified arteries become obstructed with clots. Sometimes the thrombus is the result of inflammation of the walls of the artery or vein in which it is found, the coagulation of the blood being consequent on some altered relation between the walls of the vessel and the blood within them. In- deed, phlebitis and arteritis are probably the most frequent causes of thrombosis. Further, the formation of clots in arteries and veins takes place occasionally in the course of some cachectic conditions of system, such as those connected with syphilis or ansemia. It may, of course, be a question, whether or not the coagu- lation in these cases even may not be the result of inflammation. The embolus, or obstructing mass, which, conveyed from a distance, be- comes lodged in some vessel, and, for the most part, occludes it, may consist of any solid material derived either directly from the blood, or from the walls of certain parts of the vascular system. But in order for Embolia to take place, it is obvi- ous that the solid matter must be formed in such a situation as shall admit, first, of its detachment, second, of its convey- ance by means of the circulating fluid, third, of its impaction in some vessel too minute to admit of its further progress onwards. Hence it follows that an embo- lus must always be looked for in some part of the pulmonary or systemic arterial system, or in the portal system, and that [Fig. 133. Diagram of a Hemorrhagic Infarct.-a. Artery ob- literated by an embolus (e). v. Vein filled with a secondary thrombus (th). 1. Centre of infarct which is becoming disintegrated. 2. Area of extravasation. 3. Area of collateral hyperaemia. (O. Weber.)] The brief account which has just been given, applies with almost equal exact- ness to the clots which form in veins. A very important additional fact, however, in regard to these, has been demonstrated by Virchow ; the fact, namely, that they tend to increase by the deposition of fresh 894 THROMBOSIS AND EMBOLIA. its source must be sought for, as a rule, either in the veins or in the heart; occa- sionally in the large arterial trunks. A very frequent source of Embolia is the formation of clots, from whatever cause, in the systemic veins. Thus, sometimes phlebitic or other clots become dislodged, then swept away in mass by the blood, and ultimately fixed in some part of the pulmonary arterial system. More commonly, however, as Virchow has shown, thrombi, which have become friable in texture, undergo disintegration, so that fragments only of them become detached and carried onwards; and he has shown that this process chiefly occurs in connection with those bulbous extremi- ties of thrombi which project from the occluded veins into the trunks with which these veins are connected. In this case the emboli are likely to be numerous and small; and it is likely that many of the smaller twigs of the pulmonary artery will be occluded rather than one or two of the larger branches only. The same processes may take place in connection with the pulmonary veins and systemic arterial tree ; but ThroYnbosis in these veins, and Embolia from this source in the systemic arteries, are certainly not common. Another frequent source of emboli is furnished by the interior of the heart. Sometimes, there is reason to believe, the softening clots, which have been already described, and which it has been shown may be detached, may be conveyed on- wards, and produce arterial obstruction. The most frequent source by far, how- ever, in connection with the heart, is the vegetations which form on the valves in the course of rheumatic and other inflam- matory conditions. Sometimes the soft granulations of recent inflammation, which are often clustered, and often loosely attached, become separated and washed away with the current of blood; sometimes, on the other hand, fragments of older concretions break off-concre- tions which have become condensed and friable, or tough. In either of these cases, it may happen that the detachment of one or two large masses may lead to the blocking up of some arterial trunk, or (and this is more commonly the case) that the separation of a number of small fragments may cause the occlusion of one or many small vessels. Since cardiac vegetations, as the result of inflamma- tion, are much more common on the left side of the heart than on the right side, it necessarily follows that Embolia originat- ing from the heart is much more com- monly met with in the systemic arteries than in the arteries of the lungs. The last source of emboli is the crum- bling away or disintegration of athero- matous or cretaceous deposits, such as one meets with in erosion or ulceration of the lining membrane of the heart or arte- ries. The minute particles, or, at least, some of them, not unfrequently become arrested, like other emboli, in the arterial twigs, and lead to their obstruction. As in the last case, Embolia from this cause is much more frequently observed in the systemic arteries than elsewhere. An embolus, of whatever kind it maybe, and whatever may be its source becomes swept along with the blood, from one vessel to another vessel, until it reaches one which from its size opposes a bar to its further progress; in this it becomes wedged, and obstructs it wholly, or almost wholly. Very often it becomes fixed on the spur formed by the bifurca- tion of an artery. Soon after its arrest the embolus becomes invested in clot; blood gradually coagulates on its proxi- mal side as far back as the next anasto- mosis of the obstructed artery ; it coagu- lates, also, generally on the distal side as well, sometimes only as far as the next branch, sometimes throughout the whole series of vessels which the primarily ob- structed artery supplies. In the case of obstruction of vessels from emboli, equally as in that from thrombi, blood will, in a greater or less degree, insinuate itself for a time between the embolus and the vas- cular wall; this blood, however, generally soon coagulates, and becomes continuous with that at either extremity of the em- bolus. The clot in which the embolus thus becomes imbedded, and which com- pletes the obstruction which the embolus had begun, may vary in character from an ordinary colored clot to a purely fibrin- ous one. At first it is easily distinguish- able from the embolus within it; but, like other deposited clots, it soon under- goes degenerative changes, and gradually approximates, more or less, in character to the embolus itself, which may thus be rendered quite incapable of separate rec- ognition. Generally, at all events in the more obvious cases, the embolus is a definite mass, which becomes impacted in the form in which it had separated. Not un- frequently, however, especially when the more minute arterial twigs become ob- structed, these twigs are found distended with an aggregation of small angular masses, which would seem to be either the debris of a larger embolus, or the minute particles due to the erosion or crumbling occurring at the seat of the primary affection. It seems not improba- ble that both of these latter explanations may hold good of certain cases; that sometimes, as Virchow suggests, an em- bolus which has become impacted breaks up into fragments, under the constant pressure from behind to which it is ex- posed, and that these fragments become THROMBOSIS AND EMBOLIA. 895 then driven onwards into the minuter vessels beyond ; that occasionally also, perhaps the debris, separated from an eroded surface, become in the process of separation loosely cemented together by coagulum, and the soft mass thus formed becomes driven into the minuter arteries, and moulded to them. The local indications of the presence of a thrombus and of an embolus are as nearly as possible identical. In both cases the vessel becomes obstructed and distended; in both, inflammation of the walls (even if it did not previously exist) becomes excited, and they undergo thick- ening ; and in both, if the vessel affected be superficial, it may be felt to be en- larged or hardened, and will probably be found to be painful and tender. The most important results, however, of these affections are those which depend on the obstruction of vessels-results which man- ifest themselves in connection with the parts which lie on the distal side of ob- struction, and especially in those regions, the vessels of which are tributaries or effluents of those which are obstructed. It has already been pointed out generally what these results are. When a vein is obstructed, the return of blood is pre- vented in a greater or less degree, the vessels behind become distended with blood, dilated-it may be varicose-and the tissues behind become the seat of con- gestion and of dropsical effusion. When an artery is the seat of obstruction, the direct passage of blood to and through the parts to which the artery leads be- comes arrested. In some cases, of course, this disturbance of the circulation is tem- porary only; anastomozing branches en- large, and, by transmitting an increased quantity of blood, make up between them for the loss to the circulation of the ob- structed vessel. But in all cases disturb- ance takes place to some extent; the nu- trition of the districts to which the artery leads becomes impaired, the blood stag- nates in its vessels, these become dis- tended with blood, owing to the reflux into them from neighboring vessels, and not unfrequently ruptured so that ex- travasation takes place; sometimes in- flammatory processes, with exudation of lymph, or suppuration, supervene; and very often molecular death and gangrene ensue. The gravity of the consequences of ob- struction of vessels, whether arising from Thrombosis or Embolia, depends partly on the size of the vessel obstructed, partly on the importance to life of the organ or part to which the blocked-up vessel be- longs, partly on the suddenness with which occlusion takes place. Obstruction from one or other of these causes may affect any vessel. As regards obstruction of veins, all that might otherwise have needed to be said here has already been said under the head of Phlebitis, from which venous Thrombosis can scarcely be separated. But some of the more important cases of obstruction of arteries we propose now briefly to consider seriatim. Obstruction of Arteries of Heart, Liver, Spleen and Kidneys.-In each of these cases, what Virchow terms capillary em- boli, derived from cardiac granulations, are far from uncommon. Occasionally large masses become impacted in certain of their vessels ; and occasionally (in the kidneys especially), without any cardiac disease whatever, the larger number of the principal arteries of the organ become obstructed by the formation of firm fibrin- ous adherent clots within them. The consequences of obstruction of the arteries of the organs just enumerated are not very dissimilar from pysemic affections of the same organs ; they may consist in all (but more especially in the heart and kid- neys) of minute abscesses, about as large perhaps as pins' heads, or of minute ab- scess-like points, in which the puriform matter is comp'osed of mere disintegrated material; they may consist also in all (but more particularly in the spleen, kid- neys, and liver), of so-called "fibrinous blocks." These vary in size, but are often very large-a cubic inch or so in bulk. They present, for the most part, well-de- fined limits, vary between a pale buff color and a deep brick-red hue, and ap- pear to consist essentially of the normal tissues infiltrated with some of the ele- ments of blood. The pathological phe- nomena here described are very frequently observed, but the symptoms to which they give rise are not very obvious. Obstruction of Arteries of Brain.-Far more important than the obstructions which have just been considered are the obstructions which, as Dr. Kirkes origin- ally showed, take place occasionally in the arteries of the brain. The obstruc- tions here are, without doubt, frequently embolic, and take place distinctly in the course both of chronic diseases of the aortic or mitral valves, and of acute in- flammatory attacks of these parts. When such is the case the embolic fragment is al- most invariably discovered in one or other of the middle cerebral arteries, or their branches-according to Dr. Kirkes, most commonly in the artery of the right side. But the obstruction also frequently takes place wholly independently of heart dis- ease, and without any possible source of Embolia, and is clearly then due to Throm- bosis of the affected vessel. Such Thrombo- sis may occur in any of the arteries at the base of the brain, and we have seen a case in which the cerebral portions of both in- ternal carotids and the basilar artery be- came thus successively obstructed. The 896 THROMBOSIS AND EMBOLIA. effects of obstruction of arteries on the portions of brain-substance to which the obstructed arteries lead consist, in the first place, of patchy congestion, and, in the second place, of marked softening, at- tended with yellowish, or slightly green- ish discoloration, and the appearance of numerous compound granular cells. The affected portions of brain are usually small and circumscribed, but are sometimes ex- tensive and diffused. They are most fre- quently observed (in connection with ob- struction of the middle cerebral artery), in the corpus striatum. The symptoms of obstruction of the cerebral arteries always appear suddenly. The patient is seized with a kind of " fit," sometimes apparently epiplectic, some- times syncopic, but sometimes unattended with either convulsions or loss of con- sciousness ; and on emergence from this sudden attack he is found to be hemiple- gic. The symptoms which succeed are little, if at all, different from those which attend on apoplectic attacks ; they vary in different cases, as the latter vary, and need not be detailed in this place. Obstruction of Arteries of Extremities.- The arteries of the extremities become occasionally obstructed by clot. Some- times no doubt these obstructions are em- bolic ; but far more commonly we believe they depend on arteritis. In the lower extremity, where this condition is most frequently observed, the seat of obstruc- tion is usually, we believe, either the fem- oral artery in the neighborhood of the origin of the profunda, or the popliteal artery. Occasionally obstruction takes place simultaneously in the corresponding arteries of opposite limbs. The formation of a plug is generally, perhaps always, ushered in by acute pain at the spot which the plug occupies. This is followed by impaired circulation in the limb beyond, loss of pulsation in the distal portion of artery, pallor, coldness, numbness, and ultimately, it may be, gangrene. In cer- tain cases, however, the patient recovers from the effect of the occlusion, as patients recover from that produced by the liga- ture of an artery. Obstruction of Pulmonary Artery.-The branches of the pulmonary artery are the recipients of all the emboli derived from the systemic venous system. Embolia, therefore, is in them of common occur- rence. Thrombosis also not unfrequently takes place in them. The blocking-up of minute arterial twigs in pysemia leads, as has been already shown, to the morbid changes in the lungs indicative of that malady. The formation of clots in some of the arteries, in the course of mitral and other forms of obstructive cardiac diseases, are constant accompaniments of pulmonary apoplexy and probably in most cases precede and cause it. Occa- sionally the impaction of a large embolus in one of the larger branches of the pul- monary artery, or the development therein of a thrombus, leads to inflammatory, and other, mischief of a comparatively large portion of the lung, or even of an entire lobe. We have seen such a case, in which a large portion of lung, the main artery of which was obstructed by an embolus, had become pneumonic, its terminal bron- chial tubes had become destroyed by sup- puration, and thus converted into irregu- lar cavities, and the investing pleura had become inflamed. The most serious cases, however, are those in which, either from Thrombosis or Embolia, the whole, or nearly the whole, pulmonary circulation becomes suddenly arrested, and rapid or sudden death ensues. A good many cases of this kind are recorded, and they seem to be comparatively frequent among puerperal women, though they are by no means confined to them. Occasionally no doubt the transference of a clot which has formed in one of the systemic veins is the cause of this sudden obstruction, either by the clot itself blocking up the pulmo- nary trunk, or by serving as a nucleus, around which, after its impaction, further coagulation takes place. Much more fre- quently, however, we believe, the forma- tion of the obstructing clots commences, and becomes completed, in the arteries in which they are discovered after death. And we ground this belief on the fact that in many cases, where death from this kind of obstruction is unquestionable, the pulmonary clots form an almost con- tinuous system, accurately, or nearly ac- curately, moulded to the channels in which they are found, and in a greater or less degree adherent to them. It is a very remarkable fact that, in some at least of these cases, the deposition of clots in the pulmonary arteries must have taken place, and been completed to the verge of almost total obstruction during a period of nearly perfect health, and that the patient's sud- den death has been due either to an acci- dental shifting of the clot, or to the coag- ulation of the streamlets of blood, by the persistence of the flow of which between the older clots and the arterial walls life had hitherto been maintained. The clots here referred to commence sometimes im- mediately above the pulmonic valves, sometimes at the bifurcation of the pul- monary artery, sometimes separately in each branch of the artery, and are con- tinued more or less uniformly, and for a greater or less distance, along their rami- fications. They possess all the characters of clots formed some while before death, and adhere here and there to the arterial walls. The symptoms which indicate serious obstruction of the pulmonary artery are sudden embarrassment of respiration, THROMBOSIS AND EMBOLIA. 897 great dyspncea, with coldness, and pallor, and clamminess of skin ; pallor, not livid- ity, of face; feebleness, rapidity and irregularity of pulse, followed by death, sometimes after an interval of several days, sometimes quite suddenly. As an example of the formation of clots in the pulmonary arteries, or rather of their presence in these arteries, during appar- ent health, and of sudden death resulting from their presence, we may quote the following case:- A female servant, thirty years of age, was admitted into St. Thomas's Hospital under Dr. Bristowe's care, on the 18th June, 1860, having suffered from slight symptoms of pleuritis on the right side for about ten days. On admission there was distinct evidence of dry pleurisy on the affected side, but the symptoms soon passed away ; the patient got apparently well, and was about to leave the hospital; but before she could leave it, and while assisting in the wards, she was attacked suddenly with faintness and gasping for breath, and in a few minutes was dead. Her death took place seven days after admission. The body was spare, and without cedema. The pericardium was healthy, the heart of moderate size, with parietes, lining membrane and valves all healthy. All the cavities contained dark fluid blood, without a trace of coagulum. The right lung was adherent to the parietes by an exceedingly delicate, easy-to-be- broken down membrane. The organ was small, and its lower lobe partially col- lapsed. Its surface was studded with irregular, and in some cases, large patches of subserous hemorrhage. Its tissue was crepitant throughout, though less so be- low than above. The bronchial tubes contained a large quantity of frothy mu- cus. The branches of the pulmonary artery distributed to the organ were in the greater part of their extent filled with decolorized and slightly adherent cylindri- cal coagula. They commenced, not in the trunk of the pulmonary artery, but in the division of it leading to this lung, formed casts of all the primary branches of this division, and were prolonged thence into many of the secondary and subsequent branches. The coagula, however, did not in all instances form parts of a con- tinuous system; but in many cases the smaller branches, and in a few the larger branches, were occupied by coagula of the same kind as, but having no continu- ity with, those prolonged from the root of the lung. The clots were for the most part cylindrical, and accurate casts of the vessels in which they lay ; still, here and there they presented slight irregularities and enlargements. They were for the most part adherent, though slightly so, to the parietes ; but here and there were free, leaving passages between them and the arterial walls ; which, together with the intervals entirely free from clot, were filled with dark-colored fluid blood. All the clots presented a reticulated fibrinous surface, and a central black-currant-jelly- like axis. They had evidently formed prior to death. The pulmonary veins were empty. The left lung was in pre- cisely the same condition as the right. There was no important disease in any other organ. The blood in the systemic arteries and veins was generally fluid; but in the left internal iliac vein, extend- ing partly into the common iliac, was a cylindrical coagulum, not completely fill- ing the vessel, but adherent to it, and presenting characters identical with those of the clot in the lung. Again, in the left innominate vein, a mass of coagulum was discovered, completely blocking it up; this was unadherent, and was found, on unravelling it, to consist of a branching system of partly decolorized clots, which could not have been formed there, but mnst have been carried thither from some of the smaller tributary vessels. The above case, it may be added, is not adduced to prove that death may take place from the formation of clots within the pulmonary arteries. For the case is one in which there is room for difference of opinion in regard to the source of these clots. We believe, nevertheless, that in this case the clots found in the pulmonary arteries were formed in them ; and we be- lieve it partly in consequence of the form and structure of the clots, partly because there is no valid ground for disbelieving that such clots may be deposited during life, as well in the pulmonary arteries as. in the systemic veins. VOL. II.-57 898 DISEASES OF THE PULMONARY ARTERY. DISEASES OF THE PULMONARY ARTERY. R. Douglas Powell, M.D., F.R.C.P. In any systematic consideration of the diseases affecting the pulmonary artery, that vessel must be separated into two portions, one external to, and one within the lungs. Disease of the pulmonary artery before its distribution in the lungs is so uncommon that, in practice, a mur- mur most audible over the region of this vessel is regarded as of hsemic origin, or this hypothesis failing, as attributable to some congenital defect about the heart, or to pressure from without, and it is only by this method of exclusion that we force ourselves to admit that the disease has its seat in the vessel itself. Atheroma. Etiology.-The etiology of atheroma and aneurism of the pulmonary artery does not essentially differ from that of corresponding affections of the aorta ; but in consequence of the pulmonary vessel being more deeply seated, more lax in its capacity, and therefore less liable to direct injury or effective strain, the results of those constitutional influences, gout, alco- holism, syphilis, which lead to atheroma, are much more rarely developed. The milder degrees of atheroma-fatty degen- eration of the intima-are, however, not unfrequently seen associated with those heart and lung diseases-mitral constric- tion and regurgitation, pulmonary fibrosis, or emphysema with hypertrophy of the right ventricle of the heart-which per- manently increase the tension of the pul- monary circulation. The association of such atheromatous patches in the pulmonary artery with those diseases which cause more or less persistent difficulty in the smaller circula- tion, and which have as their common accompaniment a more or less increased venosity of blood, is, as has been well pointed out by Drs. Wilks and Moxon, a strong argument against the supposition that this artery is protected from athe- roma by virtue of the dark blood circulat- ing through it. That the pulmonary artery is not wholly insusceptible to deeper lesions, however, is apparent from a case, to be presently cited, in which, under the •combined assaults of rheumatism, alco- holism, and hard work, with a very strong suspicion of syphilis, this vessel, in com- mon with the aorta, became affected with atheromatous disease resulting in loss of substance. Dr. Hope1 refers to a case in which the vessel was dilated and rigidly- ossified, even beyond its primary divis- ions in the lungs. Symptoms.-No symptoms have hither- to been traced as referable to atheroma of the pulmonary artery. Dilatation. Aneurism. Under circumstances of great pressure within the pulmonary circulation, as in cases of marked narrowing of the mitral orifice, with great hypertrophy of the right heart, a certain general enlargement of the pulmonary artery may take place. Dr. Sydney Coupland has recorded the case of a naval pensioner, aged 75, in whom there was an extreme degree of this general dilatation of the artery and its branches. In this case the main trunk was found dilated to a circumfer- ence of 6| inches, the valves being incom- petent and the walls of the artery greatly thinned. There was in this case great hypertrophy and dilatation of the right heart, marked emphysema of the lungs, and patchy superficial atheroma of the intra-pulmonary branches. Although some degree of patency of the foramen ovale was also present, Dr. Couplaud re- garded the emphysema as the real cause of the general dilatation of the vessel.2 Dr. Conway Evans, in the Pathological Transactions for 1866, describes a case in which there was both general dilatation of the artery and hypertrcphic thickening of its walls, with atheroma of the internal coat, associated with a contracted mitral orifice. Dr. Evans refers to other similar cases, recorded by Drs. Quain, Peacock, and Bristowe, in all of which, as in the case he describes, marked hypertrophy of the right ventricle was present. No case of aneurism of the main trunk of the pulmonary artery is referred to in Dr. Peacock's index to the Pathological Transactions, for vols. xvi. to xxv. inclu- sive ; and Mr. Erichsen, in his selected 1 Diseases of the Heart, 4th edit. p. 394, 1849. 2 Path. Trans, vol. xxvi. 1875. NARROWING OF THE PULMONARY ARTERY. 899 observations on aneurism, only refers to one case, described by Ambrose Pare, in which there was aneurismal dilatation and ossification of this vessel, from rup- ture of which the patient died suddenly. Dr. Crisp had met with no recorded case.1 Narrowing of the Pulmonary Artery. Etiology.-Constriction of the pul- monary artery is most commonly situated at its commencement, and is generally a congenital disease, associated with other congenital malformations of the heart, especially with imperfect septum ventri- culorum and patent foramen ovale and ductus Botalli (Lebert).2 Endocarditis affecting the pulmonary valves and caus- ing them to adhere by their margins, and so as partly to close the orifice, or myo- carditis., leading to constriction at the conus arteriosus, are the most common causes of narrowing of the pulmonary ar- tery : and these causes come into action before the end of the third month of intra- uterine life. Symptoms : Diagnosis.-Dyspnoea and cyanosis becoming obvious as soon as the infant commences active movements, with the physical signs of great hypertrophy of the right side of the heart and a systolic murmur heard over the pulmonary carti- lage and conducted upwards and to the left, are the principal points to be ob- served in the diagnosis of this malady. A more full consideration of its clinical and pathological features will be found in the section on congenital diseases of the heart. Narrowing of the pulmonary artery be- yond the valves is, like other diseases affecting this vessel, of rare occurrence. The most common cause of such local diminution of calibre is compression by a tumor, either aneurismal or from medias- tinal growth, or possibly consisting of enlarged bronchial glands. As the following case well illustrates the principal symptoms of compression of the pulmonary artery, and also presents other features of interest, I may perhaps be allowed to relate it here. T. D., aged 38, a fireman in a pottery manufactory, came under my observation at the Charing Cross Hospital in October, 1874. He was in his work exposed to great changes of temperature, sometimes working at a tem- perature of 2000 or more, and also to pigment fumes and coal-dust, etc. To these causes he attributed a constant cough from which he had suffered for some time. He stated that he often had to lift heavy weights, as much as 2 cwt., which he would carry in his arms supported against the lower chest. No dis- tinct history of syphilis was elicited; three children were living out of a family of nine. Patient had a severe attack of rheumatic fe- ver in 1856 which lasted sevente.en weeks, but had since then continued his work with- out difficulty up to six weeks previous to his attendance at the hospital. He had only for two weeks been quite disabled from work, on account of palpitation and breathlessness. The following notes were taken a month before his admission into the hospital, where he continued under my care in the temporary absence of Dr. Silver. The patient was a short, stout man, with a somewhat bloated face, of a dusky pallid hue, with decided lividity of lips. On exposing the chest an enlarged vein was observed coursing from the left shoulder along the second intercostal space to the sternum, the veins generally of the neck were full, and the carotids throbbed visibly. Pupils and pulses equal. The chest was expanded. The heart's apex beat at the sixth rib one inch outside nipple line, and, as indicated by shading in the diagram, the cardiac impulse was diffused from this point below the nipple to the epigastrium, and above the nipple to the second cartilage. Over a circular space b, having its centre at the third cartilage close to the sternum, and extending to the cartilage above and below, an impulse was felt synchronous with the apex-beat but more prolonged and attended by a marked thrill. Immediately succeeding this a second short impulse or shock coin- cided with the second sound of the heart. At the 2d, mid-sternum, a, the systolic im- pulse was slight, without thrill, and the diastolic shock more faint. The superficial cardiac dulness was bounded, as indicated in the diagram, by a line extending from the second left cartilage near the sternum to the apex beat, and skirting the region of thrill and the left nipple. To the right the area of dulness reached half way to the right nipple at the level of the fourth rib. A systolic rough bruit was heard most loudly over the region of thrill, b, and was succeeded by a second sound so accentuated as to communi- cate a shock to the ear. The blowing mur- mur was loud also at the base of the heart with marked accentuation of the second sound, and (?) a very slight diastolic bruit. Sibilant rales were heard over the chest; at the left posterior base there was some dulness extending round to the lower axilla with weakened respiration and subcrepitant rale. The systolic bruit was more audible at the left than the right suprascapular region. The legs were cedematous, the liver en- larged, and the abdomen somewhat full, though not containing any considerable amount of fluid. This patient continued under observation in the hospital until his death in December. Increasing dyspncea with severe paroxysms, marked cyanosis, and extreme anasarca of the abdominal walls and lower extremities without much increase in the amount of fluid 1 Diseases of the Bloodvessels, 1847. 2 Vide Clinical Lecture, Medical Times and Gazette, January, 1870. 900 DISEASES OF THE PULMONARY ARTERY. in the peritoneum, oedema of the lungs, in- creased congestion of the veins of the head and neck, with some regurgitation through the jugulars, were the principal signs of in- gravescing disease. The physical signs about the heart did not materially change. The patient became intensely cyanotic shortly before death. Bearing in mind the extreme rarity of aneurism affecting the main pulmonary ar- The left ventricle was greatly hypertrophied. The aorta was slightly contracted at its ori- fice, but immediately beyond the valves, which were healthy, it was dilated, and from the left side a wide-mouthed pouch extended behind the pulmonary artery, so as to pro- ject for three-quarters of an inch beyond it in contact with the left auricular appendix. Several shallow secondary pouches were to be seen on the inner surface of the sac, one projecting into the calibre of the pulmonary artery, and another having given way into it, forming the aperture above described. The liver showed lesions referable to drink and perhaps to syphilis. This case is of pathological interest in- asmuch as it is an example of a rare dis- ease-atheromatous erosion of the pul- monary artery. Clinically, the symptoms and signs were principally those of stenosis of the pulmonary artery and aneurism of the aorta. In this case the most important signs and symptoms were those most character- istic of constriction of the pulmonary artery beyond the valves. The systolic bruit most intense over the pulmonary cartilages, and here accompanied by sys- tolic impulse and thrill with great accent- uation of the second sound, were signs attributable to aortic aneurism; but the marked evidence of hypertrophy and dila- tation of the right heart, the general venous engorgement with regurgitation through the veins in the neck and general dropsy, pointed to an obstruction to the exit of blood from the right ventricle. In simpler cases the systolic murmur is char- acterized as pulmonary by its being con- ducted upwards and to the left, or to the left interscapular region. Accentuation of the second sound is insisted upon by Professor Quincke' as of importance in distinguishing constriction of the vessel beyond the valves from stenosis at or within the ventricular orifice when the second sound is obscured. There may be dilatation of the vessel above the point of constriction. Dr. Peacock2 in a tabulated collection of thirty-three cases of aortic aneurism opening into the heart or great vessel in- cludes fifteen cases in which the com- munication was with the pulmonary ar- tery. The aortic aneurisms in those cases arose with one exception from the ascend- ing aorta, and in most instances immedi- ately above the valves ; the perforation of the pulmonary artery took place, with two exceptions, within an inch and a half of the valves. In two instances the ves- sel was perforated below its bifurcation. These cases suffice to show that aortic aneurism is the most common cause of Fig. 134. tery, yet having regard to the signs of aneu- rism present, and to the evidence also, in the marked hypertrophy and dilatation of the right ventricle, of obstruction at the pulmo- nary artery, the diagnosis of aneurism of the aorta pressing upon and narrowing the pul- monary artery was inevitable. From the po- sition of the dulness and thrill, and from the absence of any regurgitant murmur, it was assumed that the aneurism must be projecting forwards from the third portion of the arch. This, however, proved not to be the case. At the autopsy an aneurismal pouch was found arising from the aorta a little above the valves, extending behind the pulmonary ar- tery so as to project three-quarters of an inch beyond it, coming in contact with the left auricular appendix. This aneurism was found to have opened into the pulmonary artery. The left ventricle was greatly hyper- trophied, the aorta atheromatous throughout, and from its inner surface several shallow pouches extended, each presenting a thick- ened margin. The right ventricle was much dilated and hypertrophied, the pulmonary valves being natural. An oval well-defined aperture half an inch in diameter was found at the distance of three-quarters of an inch above the junc- tion of the left and posterior valves. The vessel was somewhat stretched around the aperture and pouched inwards. Above the anterior valve at the same level was found a depressed smooth surface of irregular outline, having a raised, hard, puckered margin. 1 Ziemssen's Cyclopaedia, vol. vi. Diseases of the Bloodvessels. 2 Path. Trans, vol. xix. p. 126. PULMONARY ARTERY WITHIN THE LUNG. 901 pressure upon the pulmonary artery. The degree of pressure from this cause must vary infinitely, and the cases must differ correspondingly in the relative intensity of the symptoms referable to the aneurism and to the compression of the pulmonary vessel. In the case above related the rupture of the aneurism only accelerated by a few hours the death of the patient, which was rapidly approaching, from symptoms referable to dilated right heart and obstructed venous circulation. Murmur Over the Pulmonary Artery. A pulmonary murmur systolic in time, soft in quality, and of medium or low pitch, is commonly heard over the second and third left cartilages close to the ster- num without there being reason to sus- pect any disease of the vessel. This murmur is very local-not conducted in any direction. It is heard most frequently in young women and children, being then associated with arterial bruits in the neck, and with the venous hum audible over the jugulars (more especially over the right jugular, in which vessel a thrill may commonly be felt). Whatever the exact mechanism of the murmur may be ame- mia is its most common cause. "The pul- monary artery at its commencement is very superficial, and it is readily conceiv- able how the rush of a thin watery blood through an orifice so close under the ear should cause an appreciable sound. In children, and even in adults whose cartilages are tolerably resilient, the mur- mur may be produced or much intensified by pressure with the stethoscope ; and it may be removed by such full inspiration as lifts the cartilages and ribs from press- ing upon the vessel. In extreme anjeinia murmurs of the same kind may be heard all over the cardiac region, being generated at the several orifices of the heart. In cases of retracted left lung from old- standing disease a murmur is frequently audible over the pulmonary artery, prob- ably induced by the flattening of the chest wall bringing the cartilages in contact with the vessels. The tension of blood within the artery is always increased in these cases, as shown by the accentuation of the second sound, and sometimes in marked cases of fibrosis of the lung the division of the artery as it enters the affected organ is positively constricted and wrinkled. In other cases an enlarged and hardened gland will intrude upon the calibre of the vessel as it enters the lung. In displacement of heart from fluid effu- sions or other causes a systolic murmur may be heard over the pulmonary artery. Pulmonary Artery within the Lung. Although disease of the main trunk of the pulmonary artery is exceedingly rare, atheroma and even aneurism of its branches within the lung are frequently met with, but only, with equally rare ex- ceptions, in cases of disease disorganizing the lung, uncovering its vessels, and in- volving their walls in its destructive pro- cesses. It is in the course of excavation of the lung in phthisis that thickenings, ero- sions, dilatations or actual aneurism of the branches of the pulmonary artery are most commonly met with. We have at once under these conditions the three most important determining causes of atheroma and aneurism, viz.: increased blood pressure, on account of the many vessels which are occluded, local loss of support from breaking down of the tissues around, and softening of the arterial wall by inflammatory changes, also quite of a local character. In acute ulcerative destruction of the lung such vessels as do not become oc- cluded in good time are apt to become softened or eroded, and, by their rupture, to give rise to copious and sometimes fatal hemorrhage. In cases in which the de- struction of the lung is less acute and violent, cavities form with more or less trabeculated -walls, the trabeculae con- sisting partly of bronchi, but chiefly of vessels surrounded by a certain thickness of condensed tissue. These vessels are as a rule occluded, but exceptions are occa- sionally met with. We frequently find in chronic cavities a large branch of the pul- monary artery which is quite patent, oc- cupying a trabecula, or coursing along the wall of a cavity immediately beneath the limiting membrane. Such vessels, miss- ing their wonted support on the cavity side, become strained by the blood-pres- sure. At first the arterial wall thickens, -not from hypertrophy, as Dr. Rasmus- sen has suggested,1 for the thickening is limited to the side exposed, and has a uniform smooth section in which nothing but a commingling of connective tissue elements affecting the ■whole thickness of the wall and obscuring all distinctions be- tween the coats can be seen. It is evi- dently an inflammatory process of the nature of endarteritis which affects these vessels, and although the thickening ap- pears hard and fibroid, it nevertheless yields before the constant blood-pressure, the calibre of the vessel commencing to dilate at this point. Dilatation goes on 1 Edin. Med. Journ., paper translated by Dr. Moore, vol. xiv. 902 DISEASES OF THE PULMONARY ARTERY. in the usual way of aneurism, the origin- ally thickened coat thinning as it becomes spread out before the increasing intru- sion of blood, until it forms a brittle, soft, papery layer which cannot be recognized from a fibrinous lamina. Thus a most typical sacculated aneurism may form, projecting into a cavity more or less occu- pied by laminated fibrin, and which may rupture at any period of its formation. The more chronic the cavity the more suitable the conditions for the formation of a sacculated aneurism. In chronic cavities which have from ex- posure to some evil influences become in- flamed or ulcerous, vessels imbedded in the walls, or occupying trabeculae are rapidly laid bare, and may either become perforated or may dilate into irregularly shaped fusiform aneurisms. An attempt (often successful) at occluding such ves- sels may frequently be observed in the formation of a firm oat-shaped coagulum which is attached to the internal surface of the artery corresponding with the point of exposure. This plug may gradually enlarge and close the vessel. There are some specimens in the Brompton Hospital' Museum, showing sacculated aneurisms projecting into and occupying bronchial dilatations. Etiology. - The etiology of these aneurisms is included in their pathology. They are of strictly local origin, and it is doubtful if any constitutional conditions influence their production. Age and Sex.-These conditions also only affect the occurrence of aneurism according as they influence the pulmonary disease. In fifteen cases which I have tabulated1 the ages of the patients varied from fourteen to forty. I have since, however, met with a case of fatal haemop- tysis in an infant seven months old, from erosion of a dilated pulmonary vessel in a cavity.2 Three of the above cases were females and the rest males: the infant just alluded to, however, was a female, and probably the preponderance of males in so small a number is of accidental occurrence. Symptoms and Signs.-Copious- hae- moptysis, repeated at short intervals, occurring in a case in which there is ex- cavation of the lung, is the most charac- teristic symptom of the rupture of an aneurism, or a large vessel, within the lungs. The first gush of blood is of a dark venous color but quite pure and unmixed. No other symptom or sign indicates the presence of these lesions of the pulmonary artery save in exceptional cases. In one case that fell under the notice of the author but a few hours before) death, a very peculiar interrupted form of amphoric breathing was explained post mortem by a small aneurism project- ing into the chief bronchus at its point of communication with a large cavity. Diagnosis.-This can be made with tolerable certainty from the character of the haemoptysis, as above explained. The more chronic and quiescent the cavity the more likely is sudden haemop- tysis to be derived from this source. Sometimes the excavation containing an aneurism is of very small dimen- sions. Prognosis.-Always of course very grave, but by no means necessarily fatal. Cases of the most profuse and oft-re- peated haemoptysis sometimes completely recover. Treatment. - Absolute and pro- longed rest with full doses of ergot give the best results. A very nice discrimina- tion is needed in the management of these cases, especially as regards stimu- lants. It is at the moment of fainting that the best opportunity of coagulation occurs, and one must not be in a hurry to restore the force of the circulation. These patients, too, often recover and make blood very rapidly, and then are apt to get a return of their haemoptysis. A restriction of diet, especially as regards butcher's meat, is often useful, and no stimulants should be allowed. 1 On the Pathology of Fatal Haemoptysis. Path. Trans, vol. xxii. 1871. 2 Ibid. vol. xxv. Dr. Fagge has since re- ported a case similar to aneurism occurring in a female child aged 2f years. Ibid. vol. xxviii. ON DISEASES OF THE CORONARY ARTERIES. 903 ON DISEASES OF THE CORONARY ARTERIES. By R. Douglas Powell, M.D., F.R.C.P. The coronary arteries may be affected with any of those lesions-atheroma, fatty degeneration, calcification, occlu- sion, dilatation, or aneurism-to which other similar vessels are liable : and, as is also the case with like vessels going to important parts, the phenomena indica- tive of disease are all referable to dam- aged nutrition and disordered functions of the organ, in the present instance the heart, to which the vessels are distri- buted. The diagnosis of disease of the coronary vessels is therefore a pathologi- cal inference which is helped by no symp- toms directly attributable to alteration in them. Extensive disease may exist without giving rise to any suspicious signs; indeed a moment's consideration of the conditions of the coronary circula- tion suffices to enable us to see that they may be varied or interfered with inde- pendently of disease affecting the vessels themselves. The coronary arteries are, unlike other systemic vessels, filled at the moment of cardiac relaxation by the systole of the aorta forcing the blood back upon the closed aortic valves. If the aortic valves be damaged so as to admit of free regur- gitation, the pressure of blood in the coronary arteries is thereby more or less diminished, and the vigor of the circula- tion through them lessened. Again, atheromatous disease of the aorta at its origin not unfrequently leads to almost complete closure of the coronary vessels at their commencement. Other morbid conditions, such as an undue rigidity of the aorta or aneurism affecting it may by interfering with the rebound or systole of the vessel materially influence the coro- nary circulation. Hence those disease- phenomena, such as angina, or irregular or failing heart's action with syncopal attacks which, when no more definite physical signs are present, are regarded as being due to fatty degeneration of the heart in consequence of a diseased condi- tion of its vessels, may equally be due to disorder or derangement of the circulation through the vessels arising from some one of several other causes. Atheroma, calcification.-Angina pectoris is frequently connected with cal- cification of the coronary arteries, but by no means necessarily so. Of three of the most rapidly fatal cases of angina ever recorded, viz., those related by Dr. Latham,1 in only one was disease of these vessels present to any appreciable extent. Dr. Dickinson, in the seven- teenth volume of the Pathological Trans- actions, calls attention to occlusion of the coronary arteries at their commencement as a cause of angina. He relates three cases in which " soft atheroma spread- ing under the lining of the aorta" had caused great narrowing or complete closure of the mouths of the vessels which were otherwise quite healthy. The mus- cular substance of the heart was in each case slightly fatty but not atrophied. A similar case is recorded by Mr. Spenser Watson in vol. xix. of the same Society's Transactions. Professor Gardiner has more fully treated of this subject else- where in this System of Medicine. Dr. Quain2 has shown in how large a propor- tion of cases of true fatty degeneration of the heart the faulty nutrition is traceable to diseased vessels. Thrombosis.-Dr. Hayden3 refers to the occasional occurrence of thrombosis affecting the coronary vessels as a cause of acute fatty degeneration of the heart. In a case of Dr. Quain's,4 in which the aorta was dilated, the left coronary artery was found to be completely obliterated at the first part of its course and occupied for an inch further by an adherent clot, apparently the result of thrombosis. In this case great cardiac agony was experi- enced by the patient, only relieved by sedatives for two months before death ; there was however only a slight amount of fatty degeneration present. Aneurism.-Aneurism, of the coronary artery has been met with as a "museum curiosity" in several instances. Dr. Gee records a remarkable case in the St. Bar- tholomew's Hospital Reports, vol. vii., in which three aneurisms were found upon these arteries in a boy aged seven years,, who had died with scarlatinal dropsy, pneumonia and meningitis. In the St. 1 Diseases of the Heart, New. Syd. Soc. Edit. p. 450 et seq. 2 Med.-Chir. Trans, vol. xxxiii. 3 Diseases of the Heart and Aorta, p. 1017- 4 Path. Trans, vol. xxiii. p. 57. 904 HEMOPHILIA. Thomas's Museum Catalogue1 a specimen is described showing aneurismal dilata- tions along the course of the coronary arteries varying in size from that oi a pea downwards, sacculated, some empty, others completely filled by adherent bull- colored clot. The heart was removed from a man aged 22, who had died of pul- monary apoplexy and hemorrhage into the kidneys, and who therefore was pre- sumably the subject of general arterial disease. The materials are not at present avail- able for any further clinical consideration of diseases of the coronary arteries. In minute anatomy these diseases present no peculiarities. [HEMOPHILIA. Henry Hartshorne, M.D. Tins is often designated as the hemor- rhagic diathesis. Its characteristic is, a tendency to spontaneous hemorrhages from various parts of the body, and a dis- position to bleed copiously, or for a long time, from very slight wounds. Lancing the gums, for instance, in a heemophilic child, may be followed by a serious flow of blood, hard to arrest. Later in life, the extraction of a tooth may endanger life in the same way. In married women, who are " bleeders," coitus may be followed by hemorrhage from the vagina; and, during lactation, the nipples have been known to bleed at the time of suction. Ecchymoses, in such persons, take place upon occasion of the slightest bruises. Sometimes purpuric vesicles form upon the skin, which burst, discharging blood. Epistaxis is common in those who suffer from Haemophilia, and may be fatal in spite of treatment. The most trifling surgical operations are dan- gerous to such persons. A well-known clergyman in Philadelphia, a few years ago, lost his life by hemorrhage following the excision of a small wen, no larger than an olive, from his side. Haemophilia is usually hereditary. Sev- eral children of a parent so affected may exhibit the diathesis; although it is not rare for some of them to escape. A mother belonging to a haemophilic family may herself be free from the tendency, which reappears in her offspring. It is a common statement with authors, that women are much less subject to Haemophilia than men; and that, in members of "bleeding" families, preg- nancy is not especially liable to dangerous hemorrhages. This last statement is of doubtful accuracy. Investigations by two German pathologists, Borner1 and Keh- rer2, have brought to light facts showing that very dangerous post partum hemor- rhages do occur in women of such fami- lies ; and that such a hereditary proclivity probably accounts for many deaths by uterine hemorrhage, for which some other explanation has been accepted. Dr. Borner believes that reproductive activity intensifies the haemophilic predisposition, which, before puberty, may have been latent. Menstruation, however, in such persons, is not apt to deviate greatly from the conditions belonging to health. Some- times menorrhagia occurs, and, in a few cases, vicarious hemorrhagic discharges. Abortion is not frequent in haemophilic subjects; but, when it takes place, it is always dangerous, and often fatal, from profuse hemorrhage. The climacteric period, in haemophilic women, is sometimes attended by violent menorrhagia ; in other instances the ces- sation of the menses is delayed to a late period of life. Immermann3 asserts, on the basis of statistics, that Haemophilia is more com- mon in Germany than elsewhere in Europe ; next, in Great Britain; then, successively, in Sweden, Norway, Den- mark, North America, Holland, Belgium, Switzerland, Russia, and Poland. More rare in France, it does not appear to have been known in Italy, Spain, Portu- gal, Greece, or Turkey. Such a negation, however, of knowledge concerning its oc- currence may perhaps be explained by its having been, so far, overlooked in some countries, from the attention of the pro- [i Wiener Medicinische Wochenschrift, Aug. 17 to Sept. 21, 1878.] [2 Archiv fiir GynSkologie, Band x.] [3 Ziemssen's Cyclopaedia, vol. xvii.J 1 Vol. iii. No. 81. HEMOPHILIA. 905 fession not having been specially called to it. Immermann also states that persons of Jewish descent are particularly liable to it, whatever may be the locality of their residence. This seems to point to a comparatively small influence of climate in its production or promotion. Of the pathology of Haemophilia, diverse views are held. Formerly, it was sup- posed that the blood was deficient in red corpuscles and fibrin. When it is exam- ined after considerable hemorrhage has taken place, such a deficiency is probably often found. But, at other times, there seems to be rather a disposition to plethora in haemophilic persons. They bear great losses of blood wonderfully well, and rapidly make them up. Before attacks of spontaneous hemorrhage, moreover, local congestions are sometimes apparent. Congenital weakness and thinness of the walls of the bloodvessels is, by some pathologists, believed to account for the excessive facility of extravasation of blood. Sir W. Jenner says that "the tissues are soft and bruise easily; the blood is slow in coagulating, although it coagulates as firmly as in health ; that is, blood is formed rapidly, and there is a tendency to plethora of the small vessels, so that when the patient is looking his best, injuries have the worst effect, and spontaneous hemorrhages are most likely to occur." P. Kidd, in a paper read before the London Royal Medical and Chirurgical Society,1 reported a microscopical exami- nation of the aorta, vena cava, and small vessels of the mouth of a child, six years of age, which died from spontaneous oral hemorrhage. The coats of the aorta and vena cava were normal in appearance. The small arteries, veins and capillaries of the mouth, especially the smallest veins, were extensively altered. The morbid change consisted chiefly in a great proliferation of the epithelioid cells lining the vessels. This was observed in the vasa vasorum even of the aorta and vena cava. Some of the smaller arteries had also undergone degeneration of the mus- cular tissue of their middle coat. Other investigators have asserted that, in Haemophilia, there is an unusually superficial distribution of the cutaneous and subcutaneous vessels; also, in the absence of actual degeneration, marked thinness of the vascular walls. Again, in a certain proportion of cases, hypertrophy of the heart has been found to exist. If an opinion in regard to the pathol- ogy of this affection may be ventured, it must be, that congenital and hereditary delicacy and defect of resistance of the walls of the bloodvessels is the main cause of pro- clivity to hemorrhage, and difficulty in its suppression. Hypertrophy of the heart may be induced by the absence, in great part, of the assistance which should be given by the smaller arteries in the circu- lation of the blood ; obliging the heart to increase its own efforts to accomplish the round of blood-distribution. Local con- gestions may then easily occur, because of the dilatability of the weakened vessels ; and, in their state of distension, a slight disturbing cause may cause rupture of the vascular coats and hemorrhage. This will be more or less serious, according to its seat and amount. Treatment.-For the diathesis of Haemophilia there can be, we must sup- pose, no specific remedy ; nor do we know of any therapeutical measures likely to do much towards insuring its removal or cor- rection. Immermann objects to the use of iron (on account of the frequently plethoric condition of haemophilic per- sons), except as a restorative tonic after loss of blood has been sufficient to produce temporary anaemia. J. Wickham Legg, in his work upon the subject, advises cau- tion in the suppression of spontaneous hemorrhages ; considering that this should be delayed until the distended vessels have obtained relief. For the arrest of excessive hemorrhages, in haemophilic subjects, the same general and local remedies are appropriate as in other hemorrhagic cases. Rest is impera- tive in every instance. Pressure is some- times available ; styptic applications, such as are described in works on surgery, ought to be promptly and perseveringly used. Ice, in some cases, and the hot water douche (110° to 120° Fahr.) in others, will answer a good purpose. Ergot, tincture of chloride of iron, acetate of lead, tannin, &c., may be given internally. Hypodermic injection of ergotin has been found efficacious in several instances.1 For dental hemorrhage, particularly, Verneuil2 advises quinine, internally, one or two grammes daily. Of course this treatment cannot be long continued. Certain precautions are of importance with haemophilic persons. Wounds and abrasions of all kinds must be sedulously avoided. Surgical operations, even of the most apparently trifling kind, should not be performed upon such persons, unless from urgent necessity, for the saving of life. Violent exercise, and even great emotional excitement, ought to be guarded [■ Porak, reported, in La Tribune MSdioale, quoted in Phila. Med. Times, Aug. 16, 1879. His formula was, Bonjean's ergotin, two grammes, glycerin, thirty grammes. Twenty drops were hypodermically injected in cases of epistaxis, into the lip or cheek.] [2 Journal de Medecine et de Chirurgie, June, 1879.] [' British Med. Journal, May 25, 1878.] 906 INFLAMMATION OF THE LYMPHATIC VESSELS. against, on account of the danger of per- turbation of the circulation. Legg, Immermann and others consider that the marriage of haemophilic persons should be discouraged or forbidden, so as to interrupt the transmission of so fatal an inheritance. Such a restriction, even if sustained by legislation, would be very difficult to enforce, and would sometimes work to social disadvantage. We can scarcely insist upon it absolutely, since, when one of the parents has an entirely untainted constitution, each generation has a prospect of greater and greater at- tenuation of the inherited morbid pro- clivity. Certainly, cousins, even of the second or third degree, in hsemophilic families, ought never to be allowed to marry. An extreme manifestation of the diathesis, moreover, ought, in any case, to prohibit marriage.] INFLAMMATION OF THE LYMPHATIC VESSELS. J. Russell Reynolds, M.D., F.R.S. Affections of the system of lymphatic vessels are closely associated with diseases of the skin, of the glandular apparatus, and of other organs which may be the seats of dyscrasic and diathetic disease ; and hence the major part of their pathol- ogy as well as of their clinical history will be found in the articles on Erysipelas, Hodgkin's Disease, Leucocythsemia, and Pyaemia. Sometimes, however, from so- called "accidental" conditions, an in- flammatory process may occur, indepen- dently of any one of those more general Changes in the organism ; and this may exist in such form in the lymphatic ves- sels as to merit a separate notice. Synonyms.-The terms Adenitis, An- geioleucitis, Lymphangitis, and Lymph- adenitis, have been used to denote this otate. Causes.-These may be placed in two categories: (1) those which are simply accidental, such as exposure to cold, wounds, bruises, strains; and (2) those which carry with them some toxic agent which affects the body generally, and, it may be, mainly through the lymphatic vessels. When the lymphatic vessels are the seat of inflammatory change, as the result of "accidental" injury, it is to be found that the constitutional state is un- satisfactory. There is to be traced some taint, either hereditary or acquired since birth, which disposes the individual to lymphatic disease, and without which a mere bruise or wound would have been inoperative. Occasionally rapid inflam- mation has occurred after a simple injury ; when some poison has been introduced into the body and has become the start- ing-point of Lymphangitis, the body may have been previously healthy, but the impression so made upon it may be such as to lead to most mischievous results. The most common causes are injury to the nails, especially of the foot, chronic ulcers of the skin, stings, punctured wounds, bites, the introduction of un- wholesome animal matter from wounds, abraded mucous surfaces, morbid mucous secretions, or any tissue undergoing un- healthy change. The surface of the wound may absorb some poison from the air ; diphtheria has been followed by this disease; the vessels in proximity to cancerous, tubercular, or other morbid growths, may become the seat of inflam- mation. Symptoms.-The classical signs of in- flammation are those which constitute the local indications of Lymphangitis, viz., pain, tenderness, redness, and swelling. These are obvious when the superficial vessels are inflamed, but less distinct when the more deeply seated lymphatics are especially involved. The pain is not, as a rule, severe ; there may be only stiff- ness, or a stinging and burning sensation. The tenderness is in proportion to the superficiality of the inflammation and its association with dermatitis, either simple or specific, and it is sometimes very great. The redness, sometimes of vinous hue, is observed to run in long narrow lines along the course of the vessels, and often form- ing a network extending from the peri- phery towards the trunk, and reaching laterally beyond the lymphatics. The swelling of the vessels may be distinct; they are hardened, knotted, and enlarged, but the changes they exhibit do not pass downwards. The glands into which the lymphatics pass become speedily inflamed, inflammation of the lymphatic vessels. 907 and the skin and cellular tissue are in- volved in a general inflammatory process, usually of erysipelatous sort. The in- flammation of the vessels usually stops at the gland nearest to the seat of injury, and oederaa of the skin and subcutaneous areolar tissue exists beyond the site of inflammation. The course of the disease may be rapid ; and, when associated with some classes of poisons, rapidly fatal, passing into sup- puration, sloughs, or gangrene ; but, on the other hand, the inflammation may be resolved ; or it may pass into a chronic state, with much induration of skin, and hypertrophy of some of its elements. The general symptoms, like those of erysipelas, vary with the nature of their cause. They may be slight when second- ary to a merely local injury; but severe and of adynamic character when the result of poisonous infection. Usually there is a feeling of chilliness, rather than a rigor, at the onset, followed by irregular alternations of heat and cold, with trembling of the limbs. The pulse is always frequent, but variable in force and volume. There is nausea and prse- cordial discomfort, followed by vomiting, insomnia, and delirium. Such febrile symptoms may precede the appearance of local changes, and become aggravated as the latter are developed. Rigors, at- tended with profuse sweating, and ac- companied by distension of the abdomen, dyspnoea, very frequent pulse, and mut- tering delirium, are the signs of approach- ing death by blood-poisoning. Diagnosis. - Phlebitis may resemble Lymphangitis in its mode of origin and in many of its symptoms, but differs at its commencement in the more distinctly localized character of the ailment, in the larger size and smaller number of the red lines which mark its existence, in their greater hardness, and less frequent tend- ency to become associated with changes in the cellular tissue. The swelling is less, the pain not so severe, and the gen- eral disturbance less pronounced. " It must be remembered, however, that the two conditions may coexist. From erysipelas this disease may be distinguished by the presence of those special vascular changes which are ob- served in inflammation of the lymphatics, and which are not present in erysipelas. The latter affection is of relatively shorter duration, exhibits more general inflam- mation of the skin, and is frequently as- sociated with general toxaemia, much more highly marked than in Lymphan- gitis. It is sufficient to say that Lymphangitis has been sometimes mistaken for simple erythema or erythema nodosum, to put the practitioner on his guard against a repetition of such errors. Structural Changes.- Thickening of the walls of the vessels, infiltration of the connective tissue in their neighbor- hood, pus in and about them, glandular suppurations, and sloughs, are the most common appearances. The skin is often covered with phlyctense, or with spots of gangrene, while the central organs may present no departure from health, or only such as are common to all toxeemic and adynamic states. Secondary abscesses are sometimes found in liver or in lung, and phlebitis is by no means uncommon. The General Treatment of Lym- phangitis requires no special notice, as it differs in no respect from that which is required for the various maladies of which it forms a part; and the local treatment of its complications is such as falls into the province of the surgeon, and requires no description here. INDEX OF VOL. II. ABDOMEN, tympanitic dis- tension of the, a cause of displacement of the heart, 370, 377, 440 collapse of the, also affects the position of the heart, 438 Abscess of the heart, 662 a cause of aneurism of the heart, 455 of rupture of the heart, 821 Abscess of the lung, 830 mediastinal, 832 Abscesses, multiple, in the lungs, from embolism, 738 Acetate of lead, in treatment of haemoptysis, 141 of acute pneumonia, 216 Acetate of methylamine, in treatment of pleurisy, 351 Aconite, value of, in the treat- ment of hypertrophy of the heart, 785 of dilated heart, 802 of pneumonia, 212 Adenitis, 906 Adherent pericardium, article on,607 pathological anatomy, 608 physical signs, 609 Adventitious growth in the veins, 884 Adventitious products in the heart, article on, 462 Age, influence of, in asthma, 97, 100 in cancer of the liver, 145 in cirrhosis of lungs, 278 in phthisis, 104 predisposing cause of bron- chitis, 318 in laryngitis, 18, 20 in chronic laryngitis, 22 in acute pneumonia, 205 in chronic pneumonia, 248 influence of, on the position of the heart, 416 on the weight of the heart, 365 on the area of pericardial dulness, 546 influence of, on mortality in tracheotomy in croup, 67 on occurrence of croup, 48 Age, predisposing to aneurisms, 879 to aneurism of the aorta, 839, 841 to aneurism of the abdominal aorta, 862 to aneurism of the heart, 459 Age, predisposing- to aneurism of the pulmo- nary artery, 902 to angina pectoris, 673 to arterial atheroma, 874 to atheroma of the aorta, 836 to dilatation of the heart, 787 to fatty overgrowth of the heart, 805 to fatty degeneration of the heart, 808 to fibroid disease of the heart, 823 to hypertrophy of the heart, 764 to mediastinal turners, 828 to renal pericarditis, 590 to rheumatic pericarditis, 475 to rupture of the aorta, 856 to rupture of the heart, 821 to tubercular pericarditis, 463 Air, effect of, in asthma, 106 Albumen in the exudation of croup, 62 Albuminuria, a cause of pneu- monia, 286 see also Bright's disease. Alcohol, in treatment of asth- ma, 106 in treatment of pneumonia, 214, 215 Alcoholic excess, habitual, a cause of dilatation of the heart, 788 of fatty heart, 805, 810 of fibroid disease of the heart, 823 of valvular disease of the heart, 756 predisposes to the occurrence of delirium in rheumatism, 525, 528 Alcoholic stimulants in croup, 66 in secondary croup, 70 [Alum, in croup, 65] Ammonia, value of, in the treatment of angina pec- toris, 697 of chronic bronchitis, 336 of dilated heart, 802 of chronic valvular disease of the heart, 756, 759 of pneumonia, 213 use of, in croup, 66 in pleurisy, 351 Amyl, nitrite of, value of, in the treatment of angina pectoris, 689, 699, 759 Amyl, nitrite of, in treatment- of dilated heart, 802 of fatty heart, 820 occasional alarming effects of, 701 mode of administration, 701 Amyloid degeneration of ar- teries, 874 Anaemia, predisposes to dilata- tion of the heart, 788 to fatty degeneration of the heart, 809 to thrombosis, 893 Anaemic murmurs, so-called, mode of production, 723, 730 Anaesthesia, of larynx, 24 Anasarca, see Dropsy. Aneurism, of the abdominal aorta, 859 of the coronary arteries, 903 of the thoracic aorta, 838 compression of the pulmo- nary artery by, 899 intra-thoracic, diagnosis of, from mediastinal tumor, 833 diffused aortic, 860, 862 dissecting, of the aorta, 856, 860, 879 a result of atheroma, 837, 839 of the pulmonary artery, 898, 901 Aneurism of the aorta, a cause of displacement of the heart, 438, 451 of angina pectoris, 671 of hydrops pericardii, 664 of hypertrophy of the heart, 767 of pericarditis, 593 Aneurism of the heart, 786 acute, 662 false consecutive, 453, 455 Aneurism, lateral or partial, of the heart, article on, 452 aneurism of the left ventri- cle, 452 of the left auricle, 460 of the valves, 460 Aneurism of the cardiac valves, 460 mode of origin of, 619, 710 of the mitral valve, 460 of the aortic valve, 461 Aneurismal varix, 880 Aneurisms, classification of, 875 sacculated, 876 diffused, 876 fusiform, 876 909 910 INDEX OF VOL. II. Aneurisms- etiology, 877 rupture of, 877 symptoms and treatment, 879 Angina pectoris, article on, 665 symptoms, 665 diagnosis, 670 etiology, 673 pathology, 686 prognosis, 595 treatment, 697 Angina pectoris, due to aneu- rism of the aorta, 845 to atheroma of the aorta, 836 relation of, to disease of the coronary arteries, 903 to the neuralgia), 691, 695 Angina sine dolore, 684 Antimony in croup, 64, 65 Aorta, the abdominal, aneurism of the, article on, 859 anatomical characters, 859 etiology, 862 symptoms, 863 diagnosis, 866 prognosis, 867 treatment, 867 Aorta, acute inflammation of the, 834 atheroma, 835 rupture of the, 856 congenital narrowing of the, 857 Aorta, arch of the, anatomical relations of, in front, 411 at sides, 416 at back, 422, 426, 435 variations in the position of, 372, 428 position of the, affected by respiration, 406, 411 by shape of chest, 414 Aorta, the ascending, variation in the position of, 383 in the length of, 374 Aorta, the descending, rela- tions of, in the chest, 426 Aorta, root of the, connections of, in the chest, 413, 431, 436 variations in the position of, 383, 384 Aorta, the thoracic, aneurism of, article on4 838 etiology, 839 symptomatology, 842 physical signs, 845 diagnosis, 848 prognosis, 851 treatment, 852 Aortic aperture, the, size of, in health, 363 extreme enlargement of, 367 Aortic endarteritis, 835 etiology, 836 symptoms and physical signs, 836 prognosis and treatment, 837 predisposes to aneurism, 839 rheumatic, 840 Aortic murmurs, diagnosis of, from pericardial friction, 556, 750 systolic anasmic murmur oc- curs in rheumatic endocar- ditis, 639, 642 Aortic obstruction, characters of murmur, 729 rarely uncomplicated by re- gurgitation, 712 effects of, on the heart, 792 a cause of hypertrophy, 740 prognosis of, 753 Aortic regurgitant disease, a cause of aneurism of the aorta, 840 a result of aneurism of the aortic sinus, 838 frequency of, among soldiers, 841 diagnosis of, from intra-tho- racic aneurism, 851 Aortic regurgitation, a conse- quence of rheumatic endo- carditis, 641 earlv characters of murmur, 642, 643 signs of established disease, 644, 733 late appearance of, 646 effects of, on the heart, 792 a cause of dilatation of the heart, 740 of angina pectoris, 684 diagnosis of, 749, 751 prognosis of, 753, 754 treatment of, 756 use of digitalis in, 751 Aortic sinuses, the, position, 386, 388 Aortic stenosis, see Aortic ob- struction. Aortic valves, disease of the, due to atheroma, 719 to rheumatic endocarditis, 493, 494 effects of, on the heart, 740 a cause of hypertrophy of the heart, 367 predisposes to endocarditis, 657 Aortic valves, the, relations of, 386, 388, 432 mode of action of, 619 aneurism of, 461 atrophy of, 713 congenital disease of, 715 endocardial inflammation of, 620 chronic changes in, 711 Aortic vestibule, the, 386 AortitiSj acute, 834 Apqx of the heart, the position of, during life, 410 after death, 371, 382, 428 a common seat of aneurismal dilatation, 456 change in the position of, caused by respiration, 406 by habit of body and nature of occupation, 414 by pericardial effusion, 497, 568 by hypertrophy of the heart, 776 Apex-beat of the heart, changes in, caused by rheumatic endocarditis, 634 by adherent pericardium, 614, 617 by dilatation of the heart, 797 Apex-beat of the heart,displace- ment of, in intra-thoracic aneurism, 847 Apex-beat of the heart- in mediastinal tumor, 829 Apex-murmurs, systolic, clini- cal significance of, 730, 752 a sign of dilatation of left ventricle, 797 sometimes present in fibroid disease of the heart, 752, 825 Aphonia, due to mediastinal tumor, 828 Apneumatosis, article on, 306 definition, 306 history, 306 pathological anatomy, 307 etiology, 310 symptoms, 314 prognosis, 316 diagnosis, 316 treatment, 317 Apnoea in croup, 55 [Apomorphia, in croup, 65] Apoplexy, cerebral, a conse- quence of hypertrophy of the heart, 779 pulmonary, connection of, with embolism, 780, 896 Arcus sinilis, value of, in diag- nosis of cardiac degeneration, 819 Arsenic, value of, in the treat- ment of angina pectoris, 704, 759 Arterial pyaemia of Wilks, 738 Arterial tension, increase of, during the anginal paroxysm, 689 Arteries, diseases of the, article on, 870 inflammation, 870 degeneration, 872 amyloid disease, 874 aneurismal dilatation, 875 contraction and occlusion, 880 calcification of, 873 Arteries, thickening of the walls of, in Bright's disease, 769 Arteritis, pathology of, 870 etiology, 871 symptoms, 871 treatment, 872 a cause of thrombosis, 893 a result of thrombosis, 895 predisposes to aneurism, 877 Arteritis deformans of Vir- chow, 720 Aryteno - epiglottidean folds, distension of, in croup, 61 Ascarislumbricoides in glottis, 56 Ascites, a cause of displace, ment of the heart, 442 a consequence of chronic heart disease, 748 rarely due to abdominal aneurism, 866 Asphyxia, death by, in croup, 55 treatment of, 64 Aspirator, use of the, for tap- ping the pericardium, 605 Asthma, article on, 93 definition of, 93 symptoms of paroxysm, 93 varieties, 97 causes, 98 pathology, 101 INDEX OF VOL. II. 911 Asthma, article on- treatment, 102 [hypodermic use of morphia in, 104] Asthma, spasmodic, a cause of vertical displacement of the heart, 438 Asystolie of the heart, 746, 791 treatment of, 757 Atelectasis, 307, 309 Atheroma, a cause of incom- petence of cardiac valves, 719 a consequence of hypertrophy of the heart, 778, 780 Atheroma, arterial, pathology of, 872 etiology, 874 symptoms and treatment, 874 predisposes to aneurism, 877, 879 a cause of embolism, 894 of occlusion of vessel, 880 Atheroma of the aorta, 835 predisposes to aneurism, 839, 859 to rupture, 856 of the coronary arteries, 903 a cause of dilatation of the heart, 791 of fatty degeneration of the heart, 811 of the pulmonary artery, 898 a consequence of mitral ste- nosis, 746 Atmosphere, effect of the, in treatment of phthisis, 135 [Atony of the heart, 760] Atrophy of the heart, article on,759 definition and history, 759 varieties and causes, 760, 761 pathological anatomy, 761 symptoms, 762 treatment, &c., 762 Auricle, the left, position of, 419 movements of, during life, 411 aneurism of, 460 signs of dilatation of, 797 of hypertrophy of, 775, 781 hypertrophy of, a conse- quence of mitral stenosis, 744 Auricle, the right, position of, 376 dimensions of, 379, 430 movements of, 407 signs of dilatation of, 798 Auscultation, value of, in diag- nosis of mediastinal tumors, 830 Bacteria, found in the heart in acute ulcerative endocarditis, 738 relation of, to embolism, 739 Bath, use of the, in rheumatic hyperpyrexia, 514, 519, 521 Bathing, in treatment of phthi- sis, 138 Baths, warm, in croup, 64 Belladonna, value of, in treat- ment of angina pectoris, 705 of aortic aneurism, 852, 869 of dilated heart, 802 Belladonna-■ external application of, in rheumatic endocarditis, 660, 661 in pericarditis, 603 in chronic valvular disease of the heart, 759 Benzoin, in treatment of acute laryngitis, 20 Black phthisis, 112 Bleeding, value of, in treat- ment of aortic aneurism, 852, 869 Blisters, in treatment of acute bronchitis, 330 of croup,66 of pneumonia, 213 value of, in the treatment of hydrops pericardii, 665 of pericarditis, 604 Bloodletting, for the relief of angina pectoris, 702 in croup, 65 in dilation of the heart, 800 in hypertrophy of the heart, 783, 784 in chronic valvular disease, 758 in treatment of acute pneu- monia, 208, 213, 214 of acute laryngitis, 21 of pleurisy, 352 [Bloodletting, occasional, in pneumonia, advocated, 210, 243 in pleurisy, 352] Brain, the, changes in, caused by dilatation of the heart, 795 by embolism due to valvular disease, 736 by capillary embolism due to endocarditis, 532 embolism of, 895 Bright's disease, effects of, on the heart, 793 a cause of endocarditis, 618, 654 of pericarditis, 589 of hypertrophy of the heart, 366, 768 complicating angina pectoris, 673 predisposes to hydrops peri- cardii, 664 Bright's disease, chronic, a cause of atheroma, 874 of atheroma of the aorta, 836 of aneurism, 840 Bronchi, morbid anatomy of, in croup, 62 Bronchiectasis, 280 Bronchitis, a cause of displace- ment of the heart, 438 of hypertrophy of the heart, 366 Bronchitis, article on, 318 definition, 318 synonyms, 318 acute catarrhal, 318 causes of, 318 symptoms of, 320 varieties, 320 physical signs, 325 duration and termination, 326 diagnosis, 326 prognosis and mortality, 327 Bronchitis, article on- pathology, 328 morbid anatomy, 328 treatment, 329 chronic bronchitis, 332 causes, 332 symptoms, 332 diagnosis, 334 prognosis, 334 pathology and morbid ana- tomy, 334 treatment, 335 Bronchitis, occurring in con- nection with chronic lung and heart disease, 324 with croup, 55, 62 with blood diseases, 324 with exanthemata, 324 Bronchorrhoea, 333 Bronchus, the left, partial ob- struction of, by the left auri- cle, from extreme mitral ste- nosis, 746 Brown induration of the lung, article on, 274 synonyms, 274 morbid anatomy and patho- logy, 274 symptoms, 276 treatment, 276 Bruit, systolic, a sign of ab- dominal aneurism, 864 of aortic atheroma, 837 of intra-thoracic aneurisms, 846, 847 of mediastinal tumor, 830 flALCIFICATION of arteries, V 873 of the walls of the heart, 470 a mode of cure of aneurism of the heart, 459 of the valves of the heart, 710 of veins, 883 [California, Southern, a resort for chronic bronchitis, 337] Calomel, in croup, 65 Cancer, a cause of fatty de- generation of the heart, 809 of hydrops pericardii, 664 of pericarditis, 599 Cancer of the heartf 464 Cancer of the lungs, article on, 144 literature, 144 pathology, 145 symptoms, 146 diagnosis, 149 differential diagnosis, 150 prognosis and treatment, 151 Cancer of mediastinum, 826 a cause of lymphangeitis, 906 Carbolic acid, in treatment of chronic laryngitis, 23 Cardiac asthma of Stokes, 684 treatment of, 699 Cardiac concretions, article on, 887 morbid anatomy, 887 etiology, 889 symptoms and effects, 890 Cardiograph, the, indications of, in mitral stenosis, 727, 745 in aortic stenosis, 742 912 INDEX OF VOL. II. Carditis, article on, 661 etiology, 662 pathological anatomy, 662 symptoms, 662 diagnosis, &c., 663 Caries, of the vertebrae, a result of aneurism of the aorta, 861 Carnification of lung, 225 Carotid artery, ligature of the, for the cure of intra-thoracic aneurism, 853 Carotid artery, the left, position of, in the chest, 411 Catarrh, diagnosis of, from croup, 57 Catarrhal croup, 70 Catarrhal pneumonia, 217 Causes of croup, 48 Cell-products, their origin in inflammation, 237 Chalmers, Dr., sudden death of, 677 Chest, alteration of the shape of the, due to mediastinal tumor, 829 pain in the, a symptom of angina pectoris, 666 of pericarditis, 505 of chronic valvular disease, 748 shape of the, affects the po- sition of the heart, 414,421 Cheyne-Stokes respiration, or rhythmical dyspnoea, 685 (note), 816 Child-crowing, diagnosis of, from croup, 56 Chill, a cause of pneumonia, 157 Chloral, in dilated heart, 803 in the treatment of angina pectoris, 698 in the treatment of aortic aneurism, 852, 869 in the treatment of pneumo- nia, 213 Chloric ether, inhalation of, for the relief of pseudo- angina, 802 Chloride of sodium, its reten- tion in system, and presence in sputa in acute pneumonia, 236 Chlorine, in treatment of chronic bronchitis, 336 Chloroform, danger of, in fatty heart, 820 external application of, in rheumatic pericarditis, 604 in endocarditis, 660 use of, in tracheotomy for croup, 69 in the treatment of angina pectoris, 699 in treatment of asthma, 104 of acute laryngitis, 21 of pneumonia, 179 Chordae tendineae of the heart, rupture of the, 709 Chorea, complicating rheuma- tic pericarditis, 532 with non-rheumatic pericar- ditis, 536 numerical summary, 536 connection of, with cerebral embolism, 532 relation of, to endocarditis, 618, 651, 717 Chronic ulcerative pneumonia, 260 Cirrhosis of the heart, 823 Cirrhosis of the lung, article on, 277 nature and history, 277 pathological anatomy, 281 pathology, 285 etiology, 294 symptoms, 298 physical signs, 301 diagnosis, 303 prognosis, 304 treatment, 305 Cirrhosis of the lung, a cause of displacement of the heart, 447 of dilatation of the right ventricle, 790 of tricuspid regurgitation,731 Cirsoid aneurism, 875, 880 Class, influence of, as a predis- posing cause of pneumonia, 155 Climate, influence of, as a cause of croup, 49 Climate, in treatment of phthisis, 136 a predisposing cause of bron- chitis, 319 Clots, in the arteries, 892 in the heart, 887 in the veins, 893 distinction between ante- and post-mortem clots, 889 changes in, during life, 892 Cod-liver oil, in treatment of phthisis, 132 of chronic pneumonia, 268 Cold, exposure to, a cause of inflammation of the lymph- atics, 906 influence of, in production of pleurisy, 341 [Cold air, in pneumonia, some- times apparently beneficial, Cold compresses, in treatment of broncho-pneumonia, 232 in treatment of pneumonia, 212 Collapse of lung, description of, 225 Coma, occurrence of, in cardi- tis, 663 in croup, 55, 63 in acute pneumonia, 173 in rheumatism with endocar- ditis, 519 with pericarditis, 515, 526 without heart affection, 520, 527 Compression, cure of abdomi- nal aneurism by, 868 Concentric hypertrophv of the heart, 764, 772 Congenital atrophy of the heart, 760 Congenital disease of the valves of the heart, 713 Congenital narrowing of the aorta, 856 of the pulmonary artery, 899 Conium in treatment of acute laryngitis, 20 Conjunctivae, injection of, in croup, 53 Constitution, influence of, in pneumonia, 156 Contagion, a cause of phthisis, 116 Conus arteriosus, position of the, 381, 386 relation of, to the lungs, 400 Convulsion, a symptom of car- ditis, 663 of pericarditis, 537 Convulsions, in acute bron- chitis, 324 in acute pneumonia, 173 Copaiba, value of, in dropsy from chronic heart disease, 753, 803 Copper, sulphate of, in croup, 70 Coronary arteries, diseases of the, article on, 903 atheroma, 903 thrombosis, 903 aneurism, 903 Coronary arteries, origin of the, 388 atheroma of, a cause of dila- tation of the heart, 788 of fatty degeneration of the heart, 811 embolism of, a cause of rup- ture of the heart, 821 ossification of, a cause of an- gina pectoris, 671, 673, 687 (note) Corrigan's pulse, 741 Costermonger's sore-throat, 25 Cough,in croup, 53 characters of, in apneumato- sis, 314 in chronic bronchitis, 332 in idiopathic bronchitis, 321, 323 in cancer of the lung, 147 in cirrhosis of the lung, 299 in croup, 54 in acute laryngitis, 18 in mediastinal tumors, 828, 832 in phthisis, 122,124,126,127, 140 in pleurisy, 343, 349 in acute primary pneumonia, 165 in chronic pneumonia, 261 croupal, in hysteria, 60 croupal, pathology of, 60 Cough, a troublesome symptom in dilated heart, 798 Counter-irritation, in treat- mant of apneumatosis, 317 of phthisis, 141 of pleurisy, 353 Cracked-pot sound, 128 Cracked voice, 22 Creasote in gangrene of the lung,217 in chronic bronchitis, 336 Crisis in acute pneumonia, 180 Croup, article on, 46 definition, 46 diagnosis, 56 etiology, 48 history, 46 morbid anatomy, 61 name, 46 pathology, 60 prognosis, 63 symptoms, 53 synonyms, 48 treatment, 63 varieties, 70 INDEX OF VOL. II. 913 [Croup, distinct from diphthe- ria, American authors upon,48 mucous rille in, a favorable sign, 55] Croup, formerly confounded with diphtheria, 47, 70 with hooping-cough, 46 Cupping, value of, in the treat- ment of angina pectoris, 702 of dilated heart, 800, 803 of phthisis, 141 in chronic valvular disease, 758 Cysts in the heart, 465 Cysts, purulent, in the heart, 888 mode of formation, 890 DEATH, mode of, affects the size of the heart, 364, 773 the position of the heart, 370, 378 mode of, in abdominal aneu- rism, 867 in atheroma of the aorta, 837 in croup, 55 in intra-thoracic aneurism, 851 in stenosis of the aorta, 858 Death, sudden, in cases of an- gina pectoris, probable cause of, 693 from aneurism of the heart, 459 from aortic regurgitation, 754 from embolism of pulmonary artery, 896 from fatty heart, 806, 818 from fibroid disease of the heart, 825 from "heart disease" gene- rally, 675 from rupture of the heart, 822 Decubitus in pleurisy, 343 Delirium, characters of, in acute pneumonia, 172 treatment of, in acute pneu- monia, 214 Delirium, a symptom of cardi- tis, 653 of endocarditis, 628 of dilated heart, 798 occurs in rheumatism with pericarditis, 515, 527 with endocarditis, 519, 528 without heart affection, 520, 528 melancholic, 530 in non-rheumatic pericardi- tis, 534 Delirium tremens, complicat- ing rheumatism, 516, 525, 528 Delusions, occurrence of, in rheumatic patients, 529 [Dental hemorrhage, treated by quinine, 905] Diaphragm, the, movements of, affect the position of the heart, 404 affections of, causing pericar- ditis,'601 Diarrhoea, in dilated heart, 799, 803 Diarrhoea- in rheumatic hyperpyrexia, in phthisis, 123, 126 in acute pneumonia, 172 Diastole of the heart, see Heart, movements of. Diastolic murmurs, causes of, 725, 733 Diet, errors of, in croup, 66 Diet, in treatment of aneurism, 879 of aortic aneurism, 852 of aortic atheroma, 837 of acute bronchitis, 331 of haemoptysis, 902 of phthisis, 118, 132 of chronic pneumonia, 267 Digitalis, in treatment of acute bronchitis, 332 of chronic bronchitis, 335 of pneumonia, 211 value of, in the treatment of chronic valvular disease of the heart, 757 in dilated heart, 801 in fatty heart, 820 in hypertrophy of the heart, 785 Dilatation of the heart, article on, 786 definition and history, 786 etiology, 787 pathological anatomy, 793 consequences, 794 symptoms, 796 diagnosis, 799 prognosis, 800 treatment, 800 Dimensions of the heart, in health, 364 in disease, 367 Diphtheria, a cause of endo- carditis, 720 of acute fatty degeneration of the heart, 810 of inflammation of the lym- phatics, 906 Diphtheria, formerly con- founded with croup, 47, 70 diagnosis of, from croup, 58 Diphtheritic endocarditis of Eberth, 739 Diseases, constitutional, influ- ence of, on the size of the heart, 366 acute febrile, a cause of fatty degeneration of the heart, 809 Dissecting aneurism, 856, 860, 879 Diuretics, value of, in the treatment of dilated heart, 803 of hydrops pericardii, 665 of pericarditis, 607 of pleurisy, 353 of valvular disease of the heart, 758 Dropsy, a consequence of an- eurism of the heart, 458 of dilated heart, 795, 798 of fatty heart, 818 of chronic valvular disease, 748 symptoms of, 796 treatment, 803 Dropsy, ovarian, effect of, on the action of the heart, 443 Ductus arteriosus, patent, a rare cause of cardiac mur- murs, 734 Dulness on percussion, area of, from dilatation of the heart, 796, 799 from hypertrophy of the heart, 776, 782 from pericardial effusion, 545 Dulness on percussion, value of, in diagnosis of intra- thoracic aneurism, 846 of mediastinal tumor, 829, 831 Duration of angina pectoris, 696 of croup, 54, 55 of fatty degeneration of the heart, 818 of dilatation of the heart, 800 of hypertrophy of the heart, 782 of rheumatic pericarditis, 491 of effusion into the pericar- dium, 497, 543 Dysphagia, 148 causes of, 148 caused by pericardial disten- sion, 508 in cancer of the lung, 148 occasional in croup, 54 a symptom of aneurism of the aorta, 845 Dyspnoea, in apneumatosis, 314 in acute bronchitis, 321, 823 in cancer of the lung, 148 in cirrhosis of lung, 300 in croup, 53, 54 of abdominal aneurism, 865 of mediastinal tumor, 828 Dyspnoea, a symptom of aneu- rism of the aorta, 843 causes of, 844 a symptom of angina pectoris, 668 of atheroma of the aorta, 837 of carditis, 662 of dilated heart, 798 of fatty heart, 685, 806, 817 of heart disease, 7-19 of hydrops pericardii, 664 of hypertrophy of the heart, 778 causes of, in pericarditis, 507 from obstruction of the pul- monary artery, 899 treatment of, 803 Eccentric hypertrophy of the heart, 764 pathology of, 774 Effort, violent muscular, a cause of aneurism of the aorta, 840, 842, 862 Electricity, use of, in the treat- ment of angina pectoris, 702 in treatment of emphysema, 90 value of, in the treatment of aortic aneurism, 854 Emaciation, in cancer of the lung,147 Embolism, a consequence of valvular disease of the heart, 735 VOL. IL - 58 914 INDEX OF VOL. II. Embolism- pathology of, 709, 735 a cause of pulmonary apo- plexy, 746, 780 of the cerebral arteries, a probable cause of chorea and rheumatic insanity, 531, 532 connection of, with hyper- trophy of the heart, 779 of the coronary arteries, a cause of rupture of the heart, 821 Embolism, definition of, 892 causes, 893 symptoms, 895 due to atheroma of the aorta, 837 signs of, in the cerebral ar- teries, 895 in the pulmonary, 896 Emetics, in treatment of asth- ma, 102 in acute bronchitis, 330 in croup, 64 in acute laryngitis, 21 Emotion, violent mental, a cause of aneurism of the aorta, 841 Emphysema of lungs, in croup, 63 Emphysema, pulmonary, a cause of displacement of the heart, 437 of dilatation of the heart, 790 of hypertrophy of the left ventricle, 768 Emphysema, pulmonary, arti- cle on, 71 definition, 71 varieties, 71 Emphysema, pulmonary vesi- cular, article on, 72 definition of, 72 causes, 72 varieties, 76 complications, 87 treatment, 90 works consulted, 92 Emphysema, large-lunged vesi- cular, 78 symptoms, 82 Emphysema, small-lunged vesi- cular, 85 symptoms, 86 Empyema, a cause of displace- ment of the heart, 443 Endarteritis deformans, 779 see Atheroma. Endo-arteritis, of Virchow, 872 Endocarditis, a common cause of embolism, 894 Endocarditis, article on, 618 pathological anatomy, 618 physical signs and symptoms, 620 prognosis, 644 diagnosis, 647 treatment, 659 Endocarditis diphtheritica, 739 maligna, of Virchow, 737 secondary to acute rheuma- tism, 618 to Bright's disease, 654 to chorea, 651 to pyaemia, 654 to chronic valvular disease of the heart, 648, 655, 710 Endocarditis, recurrent, pa- thology of, 655 symptoms of, 658 diagnosis of, in cases of old valvular disease, 648 Endocarditis, rheumatic, com- parative frequency of, in relation to joint affection, 474, 660, 717 increased liability to, after first attack, 491, 495 relation of, to pericarditis, 494 predisposes to aneurism of left ventricle, 452, 454 Endocarditis, ulcerative, etiol- ogy of, 719 pathology of, 619, 709 symptoms, 737 diagnosis, 737 treatment, 756 relation of, to pyaemia, 718 Entozoa, in the heart, 466 Epidemics, influence of asso- ciated, on croup, 51 Epigastrium, pulsation at the, causes of, 437, 748 a sign of dilatation of right ventricle, 798 of hypertrophy of right ven- tricle, 780 of adherent pericardium, 615, 617 of intra-thoracic aneurism, 847 pain at the, a symptom of pericarditis, 503 Epiglottis, condition of, in croup,54 inspection of, in croup, 64 Epistaxis, in acute pneumonia, 172 Ergot, value of, in the treat- ment of aneurism of the aorta, 853 of haemoptysis, 902 [Ergotin, local use of, for hem- orrhage, 905] Erysipelas, a cause of acute fatty degeneration of the heart, 810 a cause of phlebitis, 882 diagnosis of, from croup, 59 diagnosis of, from lymphan- gitis, 907 [Ether, added to cod-liver oil, 135] Ether, value of, in the treat- ment of angina pectoris, 698 of dilated heart, 802 in chronic valvular disease of the heart, 758 Exercise, an aid to diagnosis of heart disease, 752 beneficial in cases of fatty heart, 807 in treatment of phthisis, 137 Exertion, a cause of pneumo- nia, 158 Expectoration, characters of, in asthma, 95 in cancer of the lung, 126, 147 in a cute idiopathic bronchitis, 322, 323 in acute pneumonia, 165, 237 in chronic bronchitis, 332 in chronic pneumonia, 262 Expectoration, characters of- in cirrhosis of the lung, 299 in morbid growths of larynx, 26 in phthisis, 122, 123,126,127 microscopical characters of, in acute bronchitis, 322 in phthisis, 123 in acute laryngitis, 19 in chronic laryngitis, 23 Expectoration, sanguineous, a symptom of intra-thoracic aneurism, 845 of mediastinal tumor, 828 Expiration, character of, in croup, 53 Expiratory type of chest, 417 External jugular, bleeding from, for croup, 65 Exudation, in croup, on larynx and trachea, 61, 62 Exudation, its origin in inflam- mation, 238 FACE, the, expression of, in angina pectoris, 669 in endocarditis, 627, 640 in mediastinal tumor, 829 in rheumatic pericarditis, 510 cyanosis of, from dilated heart, 798 from distended pericardium, 513 from chronic valvular dis- ease, 747 flushing of, in hypertrophy of the heart, 778 Fainting, see Syncope. Fatty degeneration of the heart, article on, 807 definition and history, 807 varieties, 808 etiology, 808 pathological anatomy, 811 symptoms, 815 [without symptoms, 818] diagnosis, 819 prognosis, 819 treatment, 820 Fatty overgrowth of the heart, article on, 804 causes, 805 pathological anatomy, 805 symptoms, 806 treatment, 807 Fibrin, deposit of, from the blood in inflamed arteries, 871 in aneurisms, 852, 859, 878 artificially induced by elec- tricity, 854 Fibrinous deposits in the heart, 468 on the cardiac valves, 708 Fibro-cartilage, the central, of the heart, 387 Fibro-cartilaginous degenera- tion of the walls of the heart, 469 Fibroid degeneration of the lung, 247 Fibroid disease of the heart, article on, 823 definition and history, 739 etiology, 823 pathology, 824 symptoms, &c., 824 INDEX OF VOL. II. 915 Fibroid phthisis, 247 Fifth left costal cartilage, vari- ations in relative position of, 371 Fingers, clubbing of the, a re- sult of chronic heart disease, 747 First sound of the heart, see Sounds of the heart. [Florida, a resort for chronic bronchitis, 337] Fluid, in the pericardium, phy- sical signs of, 545 effects of, on neighboring or- gans, 540 on the heart itself, 541 diagnosis of, from dilated heart, 799 from hypertrophy of the heart, 546 characters of the, in hydrops pericardii, 664 Food, in treatment of asthma, 107 insufficient, predisposes to aneurism of the aorta, 862 to atheroma of the aorta, 836 Foreign bodies, causes of pneu- monia, 158 Fremitus, the friction, of peri- carditis, see Thrill. Friction, pleuritic, complicat- ing pericarditis, 504 Friction-sound, the, of pericar- ditis, time of its appearance in acute rheumatism, 492, 557 auscultatory signs of, 556 area of, 560, 565 spots of greatest intensity, 567, 578 Varieties, 561 decline and disappearance of, 573, 580 diagnostic characters of, 582 effects of pressure on, 584 diagnosis of, from endocar- dial murmurs, 556, 750 relation of, to amount of effu- sion, 545, 558 characters of, in pericarditis from Bright's disease, 593 Fungus huematodes of the lung, 145 Fungus melanodes of the lung, 145 Furrow, the interventricular, 381, 425 the auriculo-ventricular, 381, 397, 422 GALLIC ACID, in treatment of haemoptysis, 141 Galvano-puncture, cure of aortic aneurism by, 854, 855 Gangrene of the limbs, from embolism, 737, 895, 896 Glottis, foreign bodies in, diag- nosis from croup, 56 imperfect closure of, in croup, 61 cedema of, diagnosis of, from croup,61 spasms of, 56, 57 spasms of, due to aneurism of the aorta, 843 Gout, predisposes to atheroma of the aorta, 836 Gout, predisposes- to aneurism, 840 Gout, chronic, a cause of fatty degeneration of the heart, 810 predisposes to angina pecto- ris, 673, 703 Granulations, on the cardiac valves, in endocarditis, 619, 708 further changes in, 719 " Grape cure," in cancer of the lung, 152 HABIT, predisposing cause of bronchitis, 319 [Haemophilia, article on, 904 pathology of, 905 symptoms of, 904 treatment of, 905] Haemoptysis, due to aneurism of the aorta, 845, 862 to mediastinal tumor, 828 Haemopytosis, in acute pneu- monia, 216 in chronic pneumonia, 262 in cancer of the lung, 150 in cirrhosis of the lung, 300 in plastic bronchitis, 338 treatment of, 141 Hallucinations, occurrence of, in rheumatic patients, 529, 531 Hay asthma, 96, 98, 325 Head, oscillatory movements of the, a rare symptom in peri- carditis, 538 Headache, characters of, in pneumonia, 172 Headache, due to aneurism of the aorta, 845 Headache, from dilated heart, 798 treatment of, 803 Heart, abscess of the, 662 abscess in the, due to embo- lism, 895 acute aneurism of, 662 lateral or partial aneurism of, article on, 452 clots in the, 887 • displacement of the, due to mediastinal tumor, 829 Heart, adventitious products in the, article on, 462 tubercle in the heart, 464 cancer, 464 cysts, 465 entozoa, 466 fibrinous deposits, 468 fibro-cartilaginous or osseous „ degeneration, 469 polypoid growth, 470 Heart, affection of, in croup, 63 [Heart, atony or exhaustion of, 760] Heart, atrophy of the, article on, 759 Heart, dilatation of the, article on, 786 a cause of angina pectoris, 686 a consequence of aortic re- gurgitation, 740 diagnosis of, from pericardial effusion, 799 Heart, dimensions of the, in health, 365 Heart, dimensions of the- in disease, 866 Heart, displacement of the, due to abdominal disten- sion, 370, 377 to angular curvature of the spine, 767 to ascites, 442 to asthma, 448 to aortic aneurism, 438, 451 to bronchitis, 438 to cirrhosis of the lung;, 302, 447 to diaphragmatic hernia, 602 to deformities of the thorax, 767 to pulmonary emphysema, to empyema, 443 to hypertrophy of the heart, 776 to enlargements of the liver, 378, 443 to mediastinal tumors, 440, 449 to pericardial effusion, 497, 542 to pleuritic effusion, 440, 443, 447 to pneumothorax, 447 to distension of the stomach. 440 see, also, Heart, position of. Heart, fatty degeneration of the, a cause of angina pec- toris, 672, 686 of suduen death, 806 predisposes to rupture of the heart, 820 Heart, fatty disease of the, ar- ticle on, 804 fatty overgrowth, 804 fatty degeneration, 807 Heart, fibroid disease of the, article on, 823 a cause of mitral regurgita- tion, 752 Heart, gout in the, 673 Heart, hypertrophy of the, ar- ticle on, 763 effects of, on size and weight of the heart, 367 a consequence of aortic ste- nosis, 740 relation of, to pericarditis in Bright's disease, 591 . predisposes to pericarditis in acute rheumatism, 600 relation of, to dilatation of the heart, 792 Heart, impulse of the, see Im- pulse, cardiac. Heart, irregular action of the, due to aneurism of the aorta, 845 to atheroma of the aorta, 837 Heart, malpositions of the, ar- ticle on, 437 vertical displacements, 437 lateral, 443 forward, 551 backward, 451 Heart, movements of the, de- scribed, 401 relation of, to the normal sounds and to abnormal bruits, 725 Heart, ossification of the, 813 916 INDEX OF VOL. II. Heart, pain in the region of the, see Pain. Heart, position of the, during life, 406 variations in the, vertical, 370 lateral, 378 due to age, 416 to position of patient, 379 to respiration, 404, 421 to sex, 416 to state of health and nature of occupation, 414 to shape of thorax, 420 to mode of death, 370, 378 Heart, rapid enlargement of the, 367 relation of, to spinal column, 419, 422, 435 Heart, rupture of the, article on, 820 a result of carditis, 662 of fatty degeneration of the heart, 816 Heart, state of the, after death from angina pectoris, 671, 694 Heart, syphilitic affections of the, 468 Heart, weight of the, in health, 364 in general diseases, 366 when itself diseased, 367 when atrophied, 761 when hypertrophied, 740, 774 Heat, in the treatment of croup, 64, 66 Hemiplegia, right, a common result of cerebral embolism, 737 [Hemorrhage from the mouth, excessive, treatment for, 905] [Hemorrhagic diathesis, 904] Hemorrhoids, origin of, 886 Hereditary predisposition, to aneurism of the aorta, 840 to dilatation of the heart, 787 to fatty heart, 805, 808 . to rupture of the heart, 821 Herpes of mouth, common in acute pneumonia, 175 Horsehair, use of, for the cure of aortic aneurism, 854 Humidity, a cause of phthisis, 118 Hunter, John, illness and sud- den death of, 681 Hydatic cysts in the heart, 466 Hydropericardium, hydroperi- carditis, 663 Hydro - pneumo - pericarditis, diagnosis of, 474 Hydrops pericardii, article on, 663 etiology and pathology, 663 symptoms, 664 treatment, 665 Hydrothorax, article on, 358 definition, 358 history, 358 symptoms, 358 pathology, 358 diagnosis, 359 prognosis, 359 treatment, 359 Hyperesthesia, of the larynx, 24 Hyperesthesia- local cutaneous, in rheumatic pericarditis, 501 Hyperpyrexia, occurrence of, in cases of rheumatism with pericarditis, 514 with endocarditis, 519 without heart affection, 520 without delirium, 521 general summary, 523, 527 occurs also in sunstroke, &c., 524 Hypertrophy of the heart, ar- ticle on, 763 definition and history, 763 causes, 764 pathological anatomy, 772 symptoms, 776 diagnosis, 781 prognosis, 782 treatment, 783 Hypophosphites, in the treat- ment of phthisis, 132 {MPULSE, aneurismal, cha- racters of the, in intratho- racic aneurism, 846, 847 in aneurism of the abdomi- nal aorta, 864 importance of, in diagnosis, 866 Impulse, carjiac, character of the, in abdominal aneu- rism, 865 in intrathoracic aneurism, 847 changes in the, caused by mediastinal tumor, 830 Impulse, the, of the heart, character of the, in cardi- tis, 663 in dilated heart, 797, 799 in fatty heart, 816, 818 from hypertrophy of left ven- tricle, 776 of right ventricle, 780 changes in, caused by adhe- rent pericardium, 552, 580 by endocarditis affecting mi- tral valve, 633 by pericarditis with effusion, 548 , 571, 577 value of, in diagnosis, 781, 799 Infarction, hemorrhagic, of the spleen, 895 Infection, a cause of phthisis, 142 Inhalations, in acute bronchi- tis, 331 in plastic bronchitis, 338 in chronic laryngitis, 24 . Injury, a cause of pneumonia, 158 Injury, external, a cause of an- eurism of the aorta, 842, 862 Injury, local, a cause of acute rheumatism, 499 Innominate artery, aneurism of the, diagnosis of, from aortic aneurism, 849 Innominate artery, position of, in the chest, 411 Insanity, temporary, a sequela of acute rheumatism, 529 Insomnia, from heart disease, treatment of, 803 Inspiration, characters of, in croup, 53, 54 effect of, on the heart, 405 see Respiration. Inspiratory type of chest, 414 Intemperance, habitual, a cause of atheroma of the aorta, 836 of aneurisms, 840, 841 of aneurism of the aorta, 862 Intercurrent pneumonia, 217 Interlobular pneumonia, 243 Intermittent fever, a predispos- ing cause of pneumonia, 157 Intra-thoracic tumors, a cause of displacement of the heart, 449 Invasion, of croup, 53 Iodide of potassium, in treat- ment of aneurism of the aorta, 853, 868 of angina pectoris, 705 of chronic bronchitis, 235 of acute pneumonia, 211 of chronic pneumonia, 268 of chronic valvular disease of the heart, 755, 756 Iodine, external use of, in croup,66 Ipecacuanha, in broncho-pneu- monia, 232 in croup, 64, 65 in pneumonia, 213 Iron, in chronic bronchitis, 335 in croup, 70 in phthisis, 142 in pleurisy, 351, 353 Iron, value of, in the treatment of carditis, 662 of dilated heart, 801 Iron wire, use of, for the cure of aortic aneurism, 854 r TABORANDI, for pleuritic ['J effusion, 353] Jactitation, muscular, in peri- carditis, 538 Joints, the, first affected in acute rheumatism, 499 Jugular veins, bleeding from, in croup, 65 fulness of the, from dis- tended pericardium, 509, 513 from dilatation of right ven- tricle, 798 pulsation in the, a sign of tricuspid regurgitation, 747 KIDNEY, characters of, in pulmonary emphysema, 82 embolic infarction of the, 895 multiple abscesses in the, a result of embolism, 895 Kidneys, chronic disease of the, see Bright's disease. Kidneys, congestion of the, due to dilated heart, 796, 799 to chronic valvular disease of the heart, 748 treatment of, 803 Kidneys, displacement of the, by aneurism of the abdomi- nal aorta, 861 INDEX OF VOL. II. 917 [T ACTIC ACID inhalation in L Li croup, 69] [Laryngeal dyspnoea, various forms of, 70] Laryngeal muscles, paralysis of the, in aneurism of the aorta, 843 Laryngismus stridulus, article on, 32 definition of, 32 synonyms, 32 causes, 32 symptoms, 33 diagnosis, 34 pathology, 34 prognosis, 34 treatment, 34 varieties, 35 Laryngismus stridulus, diag- nosis of, from croup, 56 Laryngitis, a cause of displace- ment of the heart, 438 Laryngitis, acute, article on, 17 definition, 17 synonyms, 18 causes, 18 duration, 19 symptoms, 19 diagnosis, 19 morbid anatomy, 20 pathology, 19 prognosis, 20 therapeutics, 20 varieties, 21 Laryngitis, chronic, article on, 22 definition, 22 synonyms, 22 causes, 22 symptoms, 22 course and terminations, 23 diagnosis, 23 pathology and morbid an- atomy, 23 prognosis, 23 therapeutics, 23 varieties, 24 Laryngitis, following small- pox, diagnosis of, from croup, 59 Laryngitis, secondary to ery- sipelas, 37 to measles, 36 to smallpox, 36, 59 to scarlatina, 37 to typhus and typhoid, 37 to syphilis, 42 ■Laryngitis, secondary to phthi- sis, 38 synonyms of, 38 definition of, 38 causes, 38 symptoms, 38 diagnosis, 39 pathology, 39 morbid anatomy, 40 prognosis, 41 therapeutics, 41 caries of the cartilages, 40 Laryngorrhcea, 23 Laryngoscope, article on, 43 definition, 43 history, 43 illumination by reflection, 44 direct illumination, 44 method of examination, 44 laryngeal image, 45 introduction of instruments, 45 Laryngoscope, article on- infraglottic, 45 Laryngoscope, use of the, in diagnosis of intra-thoracic aneurism, 846, 851 Laryngoscopic signs, in acute laryngitis, 18 in chronic laryngitis, in tumors of the larynx, 26 Larynx, article on diseases of, 17 division of, 17 Larynx, condition of, in croup, 60, 61 injury of, diagnosis of, from croup, 57 Larynx, morbid growths in, ar- ticle on, 25 definition, 25 synonyms, 25 natural history, 25 symptoms, 25 laryngoscopic signs, 26 course and termination, 26 diagnosis, 27 pathology, 27 morbid anatomy, 27 prognosis, 28 therapeutics, 28 Larynx, neuroses of, article on, 29 accounts of bilateral paraly- sis of adductors of vocal cords, 29 of unilateral paralysis of ad- ductor of one vocal cord, 30 of bilateral paralysis of ab- ductors of vocal cords, 30 of unilateral paralysis of ab- ductor of one vocal cord, 31 of spasm of the muscles of the vocal cords, 32 Larynx, cedema of, secondary to Bright's disease, 43 Larynx, polypus of, diagnosis of, from croup, 57 smallness of, in childhood, 60 spasm of, in croup, 56 ulceration of, in secondary croup, 61 Leeches, use of, in the treat- ment of dilated heart, 803 of endocarditis, 660, 661 of acute laryngitis, 21 of pericarditis, 603 of phthisis, 141 of pleurisy, 352 of pneumonia, 213 in chronic valvular disease of the heart, 758 [Limewater inhalation in croup,69] Liver, changes in the, caused by chronic valvular dis- ease, 748 by dilatation of the heart, pathology of, 795 symptoms, 798 treatment, 803 displacement of the, due to mediastinal tumor, 829 enlargement of, a cause of displacement of the heart, 378, 443, 450 multiple abscesses in the, a result of embolism, 895 Lobelia inflata, in treatment of asthma, 103 of croup, 66 Lobular pneumonia, see Apneu- matosis. Lungs, abscesses in, from em- bolism, 738 brown induration of, a con- sequence of mitral steno- sis, 746, 795 cirrhosis of the, a cause of displacement of the heart, 447 of dilatation of the right ven- tricle, 790 of tricuspid regurgitation, 731 embolism of, 746, 781, 896 sarcoma of the, invading the mediastinum, 826, 829 syphilitic affections of, article on, 270 Lungs, the, relations of, to the heart, 398, 412 relative size of, 399, 430 relative size of, affects the position of the heart, 378 Lymphadenoma, a common form of mediastinal tu- mor, 827 distinction of, from carcino- ma, 827 Lymphangitis, 906 Lymphatic glands, state of, in croup, 54, 63 Lymphatic vessels, inflamma- tion of the, article on, 906 causes, 906 symptoms, 906 diagnosis, 907 treatment, 907 Malformations, congeni- tal, of the aorta, 856 Measles, diagnosis of, in occa- sional cases, from croup, 58, 59 Mechanical bronchitis, 325 Mediastinal tumors, article on, 826 etiology, 826 symptoms, 828 physical signs, 828 diagnosis, 831 prognosis and treatment, 833 Mediastinum, anatomical rela- tions of the, 826 tumors in the, affect the posi- tion of the heart, 440, 449 Melancholia, following acute rheumatism, 529 Mercury, in croup, 65 Microscopical appearances, in endocarditis, 708 in fatty degeneration of the heart, 811 in fibroid disease of the heart, 824 of lung, in pneumonia, 191 Mineral acids, in chronic bron- chitis, 335 Mineral waters, in chronic laryngitis, 24 Mitral disease, chronic, causes of, 720 pathology of, 710 rarely congenital, 71 due to chorea, 652 918 INDEX OF VOL. II. Mitral disease, chronic- a cause of hypertrophy of the heart, 368 effect of, on the cardiac im- pulse, 554 predisposes to secondary en- docarditis, 657 Mitral orifice, the, circumfer- ence of, in health, 364 in disease, 366 variations in the position of, 393 anatomical relations of, an- terior, 414 posterior, 424 Mitral regurgitation, charac- ters of murmur, 625, 630, 729 causes of, 731 diagnosis of, 732, 751 diagnosis of murmur from pericardial friction, 557, 631 not always audible at back, 425 effects of, on the heart, 792 guides to prognosis in early stage, 632 relation of, to pericarditis, 600 treatment of, 757 Mitral stenosis, a cause of en- docardial clots, 889 Mitral stenosis, frequency of, characters of murmurs, 726 effects of, on the heart, 793 diagnosis of, 751 prognosis, 754 treatment, 757 see, also, Presystolic mur- murs. Mitral valve, the, description of, 391 relations of, 414, 433, 436 action of, 402, 619 aneurism of, 461 endocardial inflammation of, 619 frequently attacked by rheu- matic endocarditis, 494 Moisture, influence of, on mor- tality of croup, 49 [Morphia, in advanced phthi- sis, 141] in treatment of cardiac dys- pnoea, 838 of cancer of lung, 151 of pleurisy, 351 of pneumonia, 213 of pneumothorax, 362 Morphia, subcutaneous injec- tion of, in aneurism of the aorta, 852,869 in angina pectoris, 699 in dilated heart, 102 in late stages of mitral dis- ease, 759 caution necessary, 820 Mortality in croup, 48, 63 Movements, involuntary mus- cular, in pericarditis, 537 Murmur, endocardial, mode of production, 722, 723 variability of, a sign of en- docarditis, 648 pericardial characters of, 556, 581 Murmur, systolic, in the aorta, due to intra-thoracic aneu- rism, 846, 847 to abdominal aneurism, 864 to atheroma of the aorta, 837 to mediastinal tumor, 830 in pulmonary artery, due to anaemia, 901 Muscular fibres of the heart, anatomical arrangement of, 387 Muscular strain, habitual or long-continued, a cause of dilatation of the heart, 790 of hypertrophy of the heart, 768 of chronic valvular disease, 720 Mycosis endocardii, 738 Myocarditis, acute, 661 chronic, 823 a cause of fibrinous deposits in the walls of the heart, 468 of irregular action of the heart, 506 relation of to fatty degenera- tion, 809 NAILS, injury to the, a cause of inflammation of the lymphatics, 906 Nervous system, symptoms affecting the, in angina pectoris, 661 in endocarditis, 628 in n on-rheumatic pericardi- tis, 534 in rheumatism with pericar- ditis, 513, 526 with endocarditis, 519, 526 without heart affection, 520, 527 connection of, with high tem- perature, 514, 523 with remission of joint affec- tion, 517, 528 with suppression of perspira- tion, 517, 519 with alcoholism and nervous exhaustion, 525 [Night croup, 55 treatment of, 64] Nitrate of silver, in acute laryn- gitis, 21 Nitre paper, in asthma, 105 Nutmeg liver, the, a result of chronic heart disease, 748, 796 OBESITY, effects of, on the action of the heart, 442 predisposes to dilatation of the heart, 788 to fatty heart, 805 Occupation, influence of, on the position of the heart, 414 on the joints first affected in acute rheumatism, 498 predisposing to angina pec- toris, 674 to aneurism, 839, 841 to aneurism of the abdomi- nal aorta, 862 to atheroma of the aorta, 836 Occupation, predisposing- to dilatation of the heart, 788 to fatty heart, 805, 808 to hypertrophy of the heart, 768 to phthisis, 118 to acute rheumatism, 476, 498 to rheumatic pericarditis, 476, 498 to chronic valvular disease of the heart, 720 to varicose veins, 885 (Edema glottidis, diagnosis of, from croup, 59 (Egophony, in pleurisy, 344 (Esophagus, disease of the, a cause of pericarditis, 601 perforation of the, a cause of pneumo-pericardium, 472, 473 Oleum picis, in chronic pneu- monia, 268 Opiates, value of, in the treat- ment of angina pectoris, 697, 698 of dilated heart, 802 of rheumatic endocarditis, 661 see, also, Morphia, Opium. Opisthotonos, in angina pec- toris, 670 in pericarditis with nervous complications, 539 Opium, value of, in treatment of aortic aneurism, 852,869 of cancer of lung, 152 of croup, 66 of phthisis, 140 of chronic pneumonia, 268 Orthopnoea, from chronic val- vular disease of the heart, 749 from dilated heart, 798 see Dyspnoea. Ossification of the heart, 469, 813 of the coronary arteries, 671, 681 Over-exertion, a cause of hy- pertrophy of the heart, 367, 768 of chronic valvular disease, 720, 755 Oxalates, in urine of croup, 54 PAIN, character of the, in an- eurism of the abdominal aorta, 861, 863 in angina pectoris, 666 seat of, 666 causes of, 691 in cancer of the liver, 148 in intra-thoracic aneurism, 843 value of, in diagnosis, 850 a symptom of lymphangitis, 906 of mediastinal tumor, 828 Pain, in left arm and shoulder, a symptom of chronic valvu- lar disease of the heart, 748 Pain, in the region of the heart, a symptom of carditis, 663 of dilatation of the heart, 767 of endocarditis, 628, 650 INDEX OF VOL. II. 919 Pain, in region of the heart- a symptom of fatty degene- ration of the heart, 816 of fibroid disease, 825 rare in hypertrophy, 778 of rheumatic pericarditis, 493, 500, 503 sudden, from rupture of the heart, 822 Palpitation of the heart, in rheumatic pericarditis, 497 in dilatation of the heart, 798 in hypertrophy, 777 a symptom of aneurism of the aorta, 845 of atheroma of the aorta, 837 value of, as a sign of heart disease, 749 Papillary muscles, the, of the heart, arrangement of, 393, 394 relations of, 413, 414 action, 402 Paracentesis pericardii, in acute pericarditis, 604 in pericardial dropsy, 665 mode of performing the oper- ation, 606 precautions, 607 [Paracentesis pericardii, Pep- per's case, 606] Paracentesis thoracis, in pleu- risy, 354 in pneumothorax, 362 Patches, white, on the heart, origin of, 608 [Pepper's case of paracentesis pericardii, 606] Percussion, in cancer of the lung,147 in diagnosis of phthisis, 127 Pericardial friction, see Fric- tion. Pericardial sac, the average capacity of, 540, 664 Pericarditis, article on, 474 rheumatic pericarditis, 474 due to other causes, 534, 596 Pericarditis, chronic, simulat- ing mediastinal tumor, 832 Pericarditis, relative frequency of, in acute rheumatism, 474 relation of, to the severity of the joint affection, 488 a cause of aneurism of the heart, 454, 455 of carditis, 662 of fatty degeneration of the heart, 811 of fibroid disease of the heart, 470, 824 of adherent pericardium, 554 Pericarditis, rheumatic, arti- cle on, 474 etiology, 475 relation of, to other symp- toms of rheumatism, 487 to endocarditis, 494 pathological anatomy, 496 symptoms, pain, 500 changes in pulse, respiration, &c., 505 in expression and general ap- pearance, 510 symptoms affecting the nerv- ous system and hyperpy- rexia, 513 Pericarditis, rheumatic- physical signs, 539 percussion, 542 inspection and palpation, 547 auscultation, 556 diagnosis, 546, 556, 582 relapses, 571 treatment, 602 Pericarditis, secondary to pleu- risy, 346 Pericarditis, tubercular, 462 Pericardium, adherent, article on, 607 a cause of atrophy of the heart, 761 of dilatation of the heart, 788, 791 of hypertrophy, 368, 609, 612, 766 effect of, on the cardiac im- pulse, 554, 580 Pericardium, distension of the, a cause of dyspnoea, 507 of dysphagia, 508 of cardiac syncope, 506, 510 of lividity of the face, 513 Pericardium, dropsy of the, 663 Pericardium, effusion into the, physical signs of, 497, 542, 545, 556 process of absorption and cure, 578 diagnosis of, from dilatation of the heart, 799 from hypertrophy of the heart, 782 relation of, to joint affection in acute rheumatism, 489 amount of, in pericarditis from Bright's disease, 592 Peritonitis, in phthisis, 126 Perspiration, profuse, a symp- tom of rheumatic endocar- ditis, 628 suppression of, in rheumatic hyperpyrexia, 517,519, 522, 530 Pharynx, condition of, in croup, 54 Phlebectasis laryngea, 25 Phlebitis, pathology of, 880 etiology, 881 symptoms, 882 treatment, 883 a cause of thrombosis, 893 a result of thrombosis, 895 diagnosis of, from lymphan- gitis, 907 Phlebolithes, 883 origin of, 883 Phosphorus, use of, in the treatment of angina pec- toris, 704 chronic poisoning by, a cause of fatty degeneration of the heart, 810 Phthisis pulmonalis, article on, 107 definition of, 107 pathology of tubercular phthisis, 108 morbid anatomy, 111 causes, 115 [communicability of, late ob- servations upon,116] progress, 119 theory of production, 120 symptoms, 122 Phthisis pulmonalis- varieties, 123 diagnosis, 127 complications, 126 prognosis, 130 treatment, 132 statistics, 143 Phthisis, pulmonary, compli- cating emphysema, 88 Phthisis, pulmonary, effects of, on the size of the heart, 366 a cause of atrophy of the heart, 761 of hypertrophy, 768 of fatty degeneration of the heart, 8Q9 predisposes to phlebitis, 882 changes in the pulmonary artery caused by, 901 Physical signs, of acute bron- chitis, 325 of chronic bronchitis, 334, 338 of phthisis, 123 of pleurisy in the adult, 343 of pleurisy in children, 345 of acute primary pneumonia, 166 Piles, origin of, 886 Pleura, rupture of aortic an- eurism into, 851, 862 Pleurisy, article on, 340 definition, 340 history, 340 etiology, 341 clinical history, 342 complications and sequelae, 346 pathological anatomy, 347 diagnosis, 345 prognosis, 350 treatment, 351 [occasional venesection in, defended, 352 effusion in, treated with jaborandi, 353] Pleurisy, a cause of pericardi- tis, 600 relation of, to pericarditis in Bright's disease, 591 Pleuritic pain, occurrence of, in pericarditis, 500, 504 Pleurodynia, article on, 339 definition, 339 symptoms, 339 etiology and pathology, 339 diagnosis, 339 prognosis, 339 treatment, 340 Pneumogastric nerves, relation of the, to aneurism of the aorta, 843 Pneumonia, article on, 152 synonyms, 152 varieties, 152 acute pneumonia, 153 definition of, 153 history, 153 etiology, 154 symptoms, 162 complications, 184 varieties, 186 terminations, 183 diagnosis, 203 treatment, 208 Pneumonia, catarrhal, 217 Pneumonia, chronic, 244 definition of, 244 920 INDEX OF VOL. II. Pneumonia, chronic- synonyms, 244 history and etiology, 244 morbid anatomy and pa- thology, 252 pathology, 257 symptoms, 260 diagnosis, 264 diagnosis of, from mediasti- nal tumor, 832 prognosis, 265 treatment, 267 [Pneumonia, early bloodletting in, sometimes useful, 216, 243] Pneumonia, in croup, 55, 63 Pneumonia, interlobular, 243 Pneumonia, lobular, 218 etiology, 219 pathology, 223 complications, 223 diagnosis, 229 prognosis, 230 treatment, 231 Pneumonia potatorum, 173 treatment of, 214 Pneumonia, relation of, to pericarditis in Bright's dis- ease, 592 Pneumonia, secondary to Bright's disease, 233 to cancer of the lung, 146 to heart disease, 234 to pleurisy, 346 to typhoid fever, 234 Pneumo-pericardium, article on, 472 diagnosis of, 473 Pneumothorax, article on, 360 definition, 360 varieties, 360 clinical history, 360 diagnosis, 361 prognosis, 361 treatment, 362 Pneumothorax, a cause of dis- placement of the heart, 447 Polypi, in the heart, 470 Position of the patient, the, affects the position of the heart, 379 characteristic of pericardial effusion, 548 of chronic heart disease, 749, 798, 803 Potash, chlorate of, in croup, 65 Potash, citrate of, in croup, 65 Potassium, iodide of, useful in aneurism of the aorta, 853, 868 Pregnancy, a cause of hyper- trophy of the heart, 768 predisposes to ulcerative en- docarditis, 719 Pressure of stethoscope, effect of, on pericardial friction sound, 563, 564, 584 a cause of pulmonary mur- mur in children, 730 Presystolic murmurs, explana- tion of, 727 relation of, to first sound of the heart, 727 to second sound, 728 diagnosis of, 750, 751 variable character of, 752 Privation, see Food, insuffi- cient. Profession, influence of, as a predisposing cause in pneu- monia, 155 Prognosis, in rheumatic endo- carditis, as to mitral dis- ease, 632 as to aortic disease, 644 Pseudo-angina pectoris, 688, 691 Puerperal state, predisposes to phlebitis, 882 Pulmonary apoplexy, pa- thology of, 746, 748 a consequence of pericardial distension, 510 relation of, to embolism, 781 Pulmonary artery, diseases of the, article on, 898 atheroma, 898 dilatation and aneurism, 898 narrowing, 899 Pulmonary artery, orifice of the, size of, in health, 365 m disease, 366 congenital contraction of, 368 Pulmonary artery, relations of, 411, 416, 420 to vertebral column, 436 to the aorta, 874, 420 variations in position of, 373, 374, 382, 429 in the length of, 373 communication of, with the aorta, a rare cause of mur- mur, 734 hypertrophy of, a conse- quence of mitral stenosis, 746 Pulmonary artery, the, regur- gitant murmur in, 734 systolic murmur in, 570 characters of, 637, 729 causes of, 638 clinical significance of, 638 diagnosis of, from pericardial friction, 557 systolic murmur in, due to anaemia, 901 to aneurism of the aortic sinus, 838 Pulmonary artery, valves of the, anatomical relations of, 412 results of disease of, 747 Pulmonary collapse, 307 Pulmonary veins, anatomical relations of the, 419, 423 Pulsation, epigastric, see Epi- gastrium. Pulse, characters of the, in angina pectoris, 669 in aortic regurgitation, 741 in aortic stenosis, 741 in acute bronchitis, 322 in cancer of the lung, 147 in carditis, 663 in cirrhosis of the lung, 300 in croup, 53, 55 in dilated heart, 797 in fatty heart, 806, 816 in fibroid disease of the heart, 825 in hydrops pericardii, 664 in hypertrophy of the heart, 778, 780 in mitral regurgitation, 745 in mitral stenosis, 745 in phthisis, 122,123,132 Pulse, characters of the- in pleurisy, 342 in acute pneumonia, 164, 171, 214, 235 in chronic pneumonia, 261 in rheumatic endocarditis, 628 in rheumatic pericarditis, 509 Pulse, the radial, characters of, in aneurism of the aorta, 845, 846 in atheroma of the aorta, 837 in abdominal aneurism, 865 in lymphangitis, 907 inequality of the, a sign of intra-thoracic aneurism, 849, 850 an unsafe guide in the diag- nosis of cardiac murmurs, 751 carotid pulse useful, 726 Pulse respiration ratio, in acute pneumonia, 164 in acute bronchitis, 327 in plastic bronchitis, 338 Pupils, contraction of, in can- cer of the lung, 149 inequality of the, due to an- eurism of the aorta, 846, 847 to abdominal aneurism, 865 Purgatives, value of, in treat- ment of aneurism of the aorta, 852 in chronic valvular diseases of the heart, 758 in dilated heart, 803 Pyaemia, a cause of dilatation of the heart, 788 of simple endocarditis, 618, 654 of ulcerative endocarditis, 719 of pericarditis, 597 Pyrexia, in acute primary pneu- monia, 162 in chronic pneumonia, 263 QUININE, in treatment of chronic bronchitis, 335 of phthisis, 142 of acute pneumonia, 215 of chronic pneumonia, 267 RACE, influence of, as a cause of pneumonia, 154 Regurgitation, aortic, a cause of aneurism of the aorta, 840 a result of aneurism of the aortic sinus, 838 Relapses, in acute pneumonia, 178 in rheumatic pericarditis, 571 symptoms of, 572 effect of, on prognosis, 573 Respiration, character of, in abdominal aneurism, 865 in angina pectoris, 668 in apneumatosis, 314 in acute bronchitis, 323 in broncho-pneumonia, 220 in croup, 53, 55 in endocarditis complicating old valvular disease, 650 in acute laryngitis, 18 INDEX OF VOL. II. 921 Respiration, character of- in mediastinal tumor, 828,830 in morbid growths in larynx, 26 in pericarditis, 507, 586 in adherent pericardium, 617 in rheumatic endocarditis, 628, 640 in rheumatic hyperpyrexia, 523 see, also, Dyspnoea. Respiration, influence of, on the position of the heart, 404 on pericardial friction sound, 584 ratio of, to the pulse in rheu- matic pericarditis, 509 Respirators, use of, 139 Rest, importance of, in the after-treatment of endo- carditis, 622 in the treatment of aneu- risms, 879 of aneurism of the aorta, 852 of angina pectoris, 703 of dilated heart, 800 of endocarditis, 660, 755 of haemoptysis, 902 of hypertrophy of the heart, 784 of pericarditis, 603 of phlebitis, 883 Rheumatic endarteritis, 840 Rheumatism, acute articular, a cause of dilatation of the heartj 788 of chronic valvular disease, 716 relation of, to chorea, 651, 652 Rheumatism, predisposes to aneurism, 840 to aneurism of the abdomi- nal aorta, 862 to atheroma of the aorta, 836 Rhonchi, character of, in croup, 53 Rickets, pneumonia secondary to, 156. Rigors, in acute primary pneu- monia, 163 in acute bronchitis, 322 Risus sardonicus, occurrence of, in rheumatic pericarditis, 516, 518, 539 Roup, an old popular name for croup,46 Rupture, of aneurisms, various modes of, 877 of abdominal aneurism, 861 of aneurism of the heart, 459 of the heart, article on, 820 etiology and pathology, 821 symptoms and diagnosis, 822 treatment, 823 of intra-thoracic aneurism, 851 of the aortic valves, 367 of the valves of the heart, 721 spontaneous, of the aorta, 856 SACCULUS LARYNGIS,mor- bid anatomy of, in croup, 61 Sarcoma, in the mediastinum, 826 Scarification, in acute laryn- gitis, 21 Scarlatina, a cause of endocar- ditis, 720 diagnosis of, from croup, 59 Sclerosis, chronic, of the valves of the heart, 710 Season, influence of, on croup, 50 predisposing cause of pneu- monia, 155 Secondary pneumonia, 21 Sedatives, in treatment of chronic bronchitis, 336 Sedentary habits predispose to angina pectoris, 674 to fatty heart, 805, 808 Seneca, description of angina pectoris by, 676 Senega, value of, in aortic re- gurgitation, 756 in chronic bronchitis, 336 in croup,66 in aeute pneumonia, 216 Septicaemia, a cause of carditis, 662 of acute fatty degeneration of the heart, 809 see Pyaemia. Septum, the fibrous, of the heart, 386 the interventricular, 387, 388 Servants, domestic, very liable to rheumatic pericarditis, 476, 486 Sex, influence of on the occur- rence of asthma, 97 of cancer of lung, 145 of cirrhosis of lung, 296 of croup, 49 of laryngitis, 18 of chronic laryngitis, 22 of phthisis, 115 of chronic pneumonia, 248 in prognosis of acute pneu- monia, 205 Sex, influence of, on the size and weight of the heart, 365 on the position of the heart, 416 on the area of pericardial effusion, 547 Sex, predisposing to aneurism generally, 879 to aneurism of the aorta, 842 of the abdominal aorta, 862 of the heart, 459 of the pulmonary artery, 902 to angina pectoris, 673 to aortic stenosis, 857 to dilatation of the heart, 788 to fatty heart, 805, 808 to fibroid disease of the heart, 823 to hypertrophy of the heart, 764 to mediastinal tumor, 828 to rheumatic pericarditis, 475, 486 to tubercular pericarditis, 464 to rupture of the aorta, 857 to rupture of the heart, 821 to valvular disease of the heart, 719 Sinuses, the aortic, aneurism of, 838 Skin, state of, in croup, 53 Smallpox, diagnosis of, from croup, 59 Soldiers, liability of, to aneu- rism of the aorta, 841 Sound, of the heart, the first, prolongation of, an early symptom of endocarditis, 628 also a sequela of endocardi- tis, 639 diagnostic value of, 647 Sound, of the heart, the sec- ond, modification of, in aortic regurgitation, 645 accentuation of, in mitral regurgitation, 634 character of, a valuable guide in mitral disease, 636 reduplication of, a conse- quence of mitral disease, 637 Sounds, of the heart, the, re- lation of, to the move- ments of the heart in health and disease, 725 changes in, caused by dilata- tion of the heart, 797, 799 by fatty degeneration, 816 by fibroid disease, 824 by hypertrophy, 777, 780 by intra-thoracic aneurism, 846, 847 by pericarditis, 556 suggestive of aortic athero- ma, 837 Spasm, cardiac, a cause of the sudden death in angina pec- toris, 693 Spasm, of larynx, in croup, 53 Spasms, muscular, tetanic or choreic, occurrence of, in angina pectoris, 670 in rheumatism with pericar- ditis, 518, 528 with endocarditis, 519, 628 without heart affection, 522 with delirium or mania, 529, 532 in non-rheumatic prricardi- tis, 536 Sphygmograph, indications of the, in angina pectoris, 689 in aortic stenosis, 742 in aortic regurgitation, 742 in hypertrophy of the heart, 778 an aid to prognosis in valvu- lar disease, 743 Sphygmograph, value of the, in diagnosis of intra-thoracic aneurism, 849 Spinal canal, rupture of aortic aneurism into the, 862 Spinal nerves, pressure on the, by aneurism of the aorta, 861 Spine, angular curvature of the, a cause of endocarditis, 718 Spleen, embolic infarction of the, 895 multiple abscesses in, due to embolism, 895 Spleen, state of the, in acute ulcerative endocarditis, 737 922 INDEX OF VOL. II. Spleen, state of the- in chronic valvular disease of the heart, 748 Splenization of the lung, 226 Squills, in croup, 67 Steam, use of, in croup, 65 Stenocardia, syn. for angina pectoris, 688, 691 Stenosis of the heart, 824 Sternum, relation of the, to the arch of the aorta, 375 to the heart, 374, 377, 427 to the pulmonary artery, 374 to the vertebral column, 434 Stimulants, contra-indicated, in treatment of aneurism of the aorta, 852 of atheroma of the aorta, 837 Stimulants, value of, in the treatment of angina pec- toris, 697, 703 in broncho-pneumonia, 232 in dilated heart, 802 in fatty heart, 820 Stomach, collapse of the, a cause of displacement of the heart, 438 distension of the, also causes displacement, 440 Strain, prolonged muscular, a cause of atheroma of the aorta, 836, 839 of dilatation of the heart, 790 of hypertrophy of the heart, 768 of chronic valvular disease, 720 sudden muscular, a cause of abdominal aneurism, 859, 862 of inflammation of the lym- phatics, 906 Stramonium, in the treatment of asthma, 104 Stridor, with inspiration, in croup, 53 with inspiration and expira- tion, in croup, 55 Stridulous laryngitis, 70 Strychnine, in the treatment of emphysema, 90 of acute pneumonia, 216 Subclavian artery, ligature of the, for the cure of intra- thoracic aneurism, 853 Subclavian artery, the left, po- sition of, in the chest, 411 Sugar, in sputa of acute pneu- monia, 166 Suspirious respiration, the, characteristic of heart dis- ease, 676, 685 (note) Swallowing, difficulty in, caused by pericardial effu- sion, 508 Sweating, in phthisis, 122 Syncope, from fatty heart, 806, 816 from dilated heart, 798 in rheumatic endocarditis, 628 in pericarditis, 506 Syphilis, a cause of aneurism, 840, 862 of arteritis, 871 of atheroma of the aorta, 836 of general arterial atheroma, 874 Syphilis, a cause- of fibroid disease of the heart, 823 of valvular disease of the heart, 721 of thrombosis, 893 Syphilitic affections, of the heart, 468 of the lung, article on, 270 Systole, the, of the heart, de- scribed, 401, 419, 424 Systolic endocardial murmurs, causes of, 729 TANNIN, in the treatment of haemoptysis, 141 [Tartar emetic, a dangerous medicine for young children, 330] Tartar emetic, in treatment of acute bronchitis, 330 of acute pneumonia, 210, 214 Temperature, in apneumato- sis, 314 in acute bronchitis, 322, 323 in brown induration of the lung,276 in cancer of the lung, 125 in croup, 53 in mediastinal tumor, 827, 829 in phthisis, 130 in pleurisy, 343, 349 in acute pneumonia, 176 in prognosis of broncho- pneumonia, 231 elevation of, in carditis, 663 in acute ulcerative endocar- ditis, 737 in acute fatty degeneration of the heart, 818 see, also, Hyperpyrexia. Temperature of air, influence of, on croup, 50 Tension, arterial, increase of, during the anginal parox- ysm, 689, 700 in Bright's disease, 769 Tepid bath, in treatment of pneumonia, 212 Tetanus, a rare complication of pericarditis, 536, 538 Thickness of the parietes of the heart, 365, 366, 775 [Thoracic duct, occlusion of, in aneurism of aorta, 805] Thorax, shape of, in cancer of the lung,147 Thrill, characters of the, due to pericardial friction, 555, 594, 596 relative frequency of, 561 late appearance of, 571 causes of, in chronic valvular disease, 724 Thrill, a sign of intra-thoracic aneurism, 847 of abdominal aneurism, 864 Thrombosis and embolia, arti- cle on, 892 pathology, 892 etiology, 893 effects of, 895 Thrombosis of the coronary arteries, 903 of the cerebral, 895 of the pulmonary, 896 Thumb, deformity of, in laryn- gismus stridulus, 56 not present in eroup, 54 Thymic asthma, diagnosis of, from croup, 56 Tobacco, in the treatment of asthma, 103 Tongue, characters of, in acute bronchitis, 322, 323 in croup, 53, 54 in acute pneumonia, 172 in phthisis, 122, 123 Tonsils, state of, in croup, 54 Toxaemia, 30 Trachea, pathology of, in croup, 61 smallness of, in childhood, 60 [Tracheotomy in America, sta- tistics of, 68] Tracheotomy, in aortic aneu- rism, 844, 856 in croup, 67 mode of operating, 69 statistics of, 67 in acute laryngitis, 22 in tubercular laryngitis, 41 in spasm of glottis, 35 in tumors of the larynx, 29 Tremblotement, in croup, 55 Tricuspid orifice, the, relations of, 397, 413 circumference of, in health and disease, 365, 366 Tricuspid regurgitant murmur, characters of, 622, 624, 7^9 causes of, 623, 730 diagnosis of, from pericar- dial friction, 557, 625 clinical significance of, in cases of rheumatic endo- carditis, 639 Tricuspid stenosis, characters of murmur, 728 Tricuspid valve, the, descrip- tion of, 394 relations of, 413, 434, 436 variations in the position of, 397 action of, 403 incompetence of, a result of endocarditis, 494 not often thus diseased, 658 Trismus, in rheumatic pericar- ditis, 518, 539 Tubercle, in the heart. 462 in liver, 115 in spleen and kidneys, 115 Tubercle, microscopic charac- ters of, 108 chemical analysis of, 109 varieties, 110 Tufnell's plan of treating aortic aneurism, 852, 867 Tumors, abdominal, effect of, on the action of the heart, 443 cancerous, also causing dis- placement, 445 mediastinal, 826 mediastinal, a cause of dis- placement of the heart, 449 Turkish bath, in treatment of acute pneumonia, 329 Turpentine, in treatment of acute bronchitis, 330 of chronic laryngitis, 23 of acute pneumonia, 216 INDEX OF VOL. II. 923 Tympanitic distension of the abdomen, a cause of dis- placement of the heart, 370, 377 Typhus, a cause of acute fatty degeneration of the heart, 810 Tyrosine, in sputa of acute pneumonia, 166 TTLCERATION of larynx, in U secondary croup, 61 Urine, characters of, in acute bronchitis, 322 in croup, 53, 54 in dilated heart, 799 in emphysema, 84 in fatty heart, 818 in hypertrophy of the heart, 653 in phthisis, 126 in acute primary pneumonia, 174, 237 in rheumatic hyperpyrexia, 523 in chronic valvular disease, 748 Uvula, oedema of, in croup, 54 VALERIAN, in croup, 66 Valerianate of zinc, in treatment of spasm of the glottis, 35 Valves, of the heart, aneurism of, 460, 619, 709 atheroma of, 719 calcification of, 710 rupture of, 721 Valves of the heart, diseases of the, article on, 706 pathological anatomy, 707 etiology, 713 physical signs, 722 symptoms, 735 diagnosis, 749 prognosis, 752 treatment, 755 Valvular disease of the heart, chronic, a frequent compli- cation of cardiac aneurism, 457 predisposes to recurrent en- docarditis, 655, 710 to ulcerative endocarditis, 719 comparative frequency of, after acute rheumatism, 494 influence of, on prognosis in rheumatism, 495 predisposes to endocarditis, 648 to pericarditis, 599 effect of, on area of pericar- dial effusion, 547 on the position of the im- pulse, 549 relation of, to adherent peri- cardium, 512, 613 Valvular disease of the heart, chronic, guides to progno- sis of, 752 Valvular disease of heart- chronic, relative importance of the different forms, 753 Varicocele, 886 Varicose aneurism, 880 Varicose veins, pathology and etiology of, 884 symptoms and treatment, 885 Vegetations, on the cardiac valves, mode of origin of, 620, 707 Veins, diseases of the, article on, 880 inflammation, 880 degeneration, 883 concretions and adventitious growths, 883 dilatation, 884 occlusion, 886 Veins, the cervical, fulness of, due to intra-thoracic aneu- rism, 846 from chronic heart disease, 798 from pericardial effusion, 509, 513 pulsation of, from tricuspid regurgitation, 747 the superficial abdominal, state of, in abdominal an- eurism, 886 Vena cava, rupture of aneu- rism into the, 851, 862 inferior, relations of, in the chest, 425 superior, relations of, 412, 421, 427 dilatation of, a consequence of mitral disease, 747, 748 Venesection, in treatment of acute bronchitis, 330 of pneumonia, 238 see Bloodletting. Venous murmurs, in the neck, causes of, 723 varieties of, 725 Ventricle of the heart, the left, dimensions of, in health and disease, 365, 366 breadth of, 382 thickness of parietes, 775 relations of, in the chest, 419, 424 movements of, 410 Ventricle, the left, aneurism of the, article on, 452 nature and mode of origin, 453 seat of the disease, 456 form and size, 457 state of other parts of the heart, 457 of other organs of the body, 458 symptoms and cause of death, 458 Ventricle, the left, dilatation of, 797 hypertrophy of, 776 hypertrophy of, due to an- eurism of the aortic sinus, 838 Ventricle, left, hypertrophy of, due to aortic stenosis, 857 most liable to rupture, 821 changes in, caused by mitral stenosis, 744 simple dilatation of, may cause a murmur, 797 Ventricle, the right, dimensions > of, 365,366 \ breadth of, 380, 430 length of, 373, 376 thickness of wall, 774 position of, 410, 419 action of, described, 410 dilatation of, in aneurism of the aortic sinus, 838 not liable to aneurismal dila- tation, 452 signs of dilatation of, 798 of hypertrophy of, 780 changes in, caused by mitral stenosis, 746 Ventricles, the, systole of, 401, 419, 424 Veratria, in treatment of pneu- monia, 211 Veratrum viride, use of, in hy- pertrophy of the heart, 785 in chronic valvular disease, 758 Vertebrae, erosionof the, caused by aneurism of the aorta, 861, 878 Vertigo, a symptom of aortic regurgitation, 743 of dilated heart, 798 Vestibule, the aortic, 386 Virginian prune, bark of the, useful in dilated heart, 785, 802 Vision, defective, due to aneu- rism of the aorta, 845 Vocal cords, superior, swelling of, in croup, 61 Voice, character of, in croup, 53, 54, 55 Voice, loss of, in rheumatic pericarditis, 509 Vomiting, in acute bronchitis, 322 in cirrhosis of the lung, 299 in acute pneumonia, 216 in phthisis, 140 Vomiting, a symptom of rheu- matic endocarditis, 628 of rupture of the heart, 822 of dilated heart, 799 treatment, 803 rTITARMTH of atmosphere, L V V after tracheotomy, 69] Weight of the heart, normal, 364 alfected by general diseases, 866 by local diseases, 367 when atrophied, 761 when hypertrophied, 740, 774 general remarks on, 368 [Wild cherry, as an expecto- rant in phthisis, 140] LIST OF CHIEF AUTHORS REFERRED TO IN EACH ARTICLE. ADHERENT PERICARDIUM, Article on, by Francis Sibson, M.D., F.R.S., p. 607. AUTHORS REFERRED TO. Bouillaud, on the diagnosis of adherent peri- cardium, 611 Hope, on the physical signs of adherent peri- cardium, 610 Kennedy, on adherent pericardium as a cause of hypertrophy of the heart, 609, 613 Skoda, description of the physical signs of adherent pericardium by, 611 Stokes, on the effects of adherent pericardium on the heart, 613 ANEURISM OF THE HEART, LATERAL OR PARTIAL, Article on, by Thomas Bevill Peacock, M.D., F.R.C.P., p. 452. AUTHORS REFERRED TO. Breschet, on the origin of aneurisms of the left ventricle, 452, 453 ; on the situation of aneurisms of the left ventricle, 456 Cruveilhier, on fibroid degeneration as a cause of aneurism of the heart, 453 ; on the cure of aneurism of the left ventricle by calcifi- cation, 459 Hope, on aneurisms of the base of the left ventricle, 456 Rokitansky, on endocarditis as a cause of aneurism of the left ventricle, 452, 453, 454; on aneurism of the mitral valve, 461 Thurnani, on the pathology of aneurismal dilatations of the heart, 452, 453 ; on the size of aneurisms of the left ventricle, 457 ; on aneurisms of the left auricle, and of the mitral valve, 461 ANGINA PECTORIS AND ALLIED STATES, Article on, by Professor Gairdner, M.D., p. 665. AUTHORS REFERRED TO. Anstie, on the relation of angina pectoris to the neuralgise, 688; on the value of arse- nic in the treatment of angina, 704 Brinton, on gout at the heart, a form of an- gina, 673 Brunton, L., on the character of the pulse in angina, as indicated by the sphygmograph, 689 Forbes, Sir J., on the connection between an- gina pectoris and heart disease, 671; on the etiology of angina, 673 Heberden, angina pectoris first described by, 665, 666 ; on sudden death in angina, 680 ; his treatment, 698 Latham, on the pain of angina pectoris, 666 Parry, on the pathology of angina pectoris, 669, 681 Seneca, description of angina pectoris by, 675 Stokes, on the peculiarity of the respiration during the anginal paroxysm, 685 Trousseau, on thoracic aneurisms as a cause of anginal symptoms, 667, 671; on the re- lation between angina pectoris and epilepsy, 670 Walshe, on pseudo-angina, 688; on the influ- ence of evident disease of the heart on the prognosis of true angina, 696 ; on the dura- tion of angina pectoris, 696 AORTA, ANEURISM OF THE ABDOMINAL, Article on, by William Murray, M.D., F.R.C.P., p. 859. AUTHORS REFERRED TO. Balfour, on the value of iodide of potassium in the treatment of aortic aneurism, 868 Habershon, on the pathological anatomy of abdominal aneurism, 869 925 926 LIST OF CHIEF AUTHORS Holmes, on the cure of abdominal aneurism by pressure, 869 Stokes, on the diagnosis of aneurism of the abdominal aorta, 866 ; on hemorrhage from abdominal aneurism, 867 Sibson, on the pathological anatomy of aneu- rism of the aorta, 860; on the rupture of abdominal aneurism, 862 Tufnell, on the cure of aneurism of the aorta by means of rest and restricted diet, 867 Walshe, on the physical signs of aneurism of the abdominal aorta, 865 AORTA, ANEURISM OF THE THORACIC, Article on, by R. Douglas Powell, M.D., F.R.C.P., p. 838. AUTHORS REFERRED TO. Balfour, on the value of iodide of potassium in the treatment of aortic aneurism, 853 Moxon, on the influence of over-exertion and strain in the production of aneurism, 840 Myers, on the causes of the prevalence of heart-disease amongst soldiers, 841 Peacock, on congenital narrowing of the aorta, 857 Rokitansky, on rupture of the aorta, 856 Stokes, on the physical signs of aneurism of the aorta, 846, 847 Walshe, on the value of inequality of the pupils as a sign of intra-thoracic aneurism, 847 ; on the diagnosis of aortic aneurism, 851 AORTA, DISEASES OF THE, Article on, by R. Douglas Powell, M.D., F.R.C.P., p. 834. AUTHORS REFERRED TO. Allbutt, Clifford, on the causes of atheroma of the aorta, 836 Moxon, on the pathology of arterial atheroma, 836 Rindfleisch, on the rarity of acute aortitis, 834 Welch, on syphilis as a cause of disease of the aorta, 836 APNEUMATOSIS, Article on, by Graily Hewitt, M.D., F.R.C.P., p. 306. AUTHORS REFERRED TO. JSarthez and Rilliet, on the difference between lobar and lobular pneumonia, 306 Fuchs, description of changes which blood undergoes within the vessels, 313 ; on the theory of the production of apneumatosis, 311 Gairdner, Dr., on the mechanism of produc- tion of apneumatosis, 310 Jenner, Sir William, on the influence of rickets in the production of apneumatosis, 312 Legendre and Bailly, on lobular pneumonia, 306 Mendelssohn and Traube, experiments on the production of apneumatosis, 310 ARTERIES, DISEASES OF THE, Article on, by John Syer Bristowe, M.D., F.R.C.P., p. 870. AUTHORS REFERRED TO. Peacock, on the origin of dissecting aneu- risms, 879 Scarpa, classification of aneurisms by, 875 Virchow, on the changes produced by inflam- mation in arteries, 871; on the pathology of atheroma, 872, 873 BRONCHITIS, Article on, by Frederick T. Roberts, M.D. Lond., p. 318. AUTHORS REFERRED TO. Fuller, on the use of tartar emetic in plastic bronchitis, 338 Gairdner, Dr., on the coexistence of collapse with bronchitis, 329 Laycock, Dr., on the presence of butyric acid in sputa in chronic bronchitis, 333 Niemeyer, on the movements of the chest in mechanical bronchitis, 325 Reynolds, Dr., on the inhalation of chloro- form in hay-asthma, 332 Stokes, on rhonchal fremitus in acute bron- chitis, 325 Walshe, Dr., on pulse-respiration ratio in plastic bronchitis, 338 REFERRED TO IN EACH ARTICLE. 927 BROWN INDURATION OF THE LUNG, Article on, by Wilson Fox, M.D., F.R.C.P., p. 274. AUTHORS REFERRED TO. Bamberger, on the symptoms of brown indu- ration of the lung, 27 6 Buhl, on the conditions of the capillaries in brown induration of the lung, 275 Rokitansky, on the thickening of the alveolar walls in brown induration of the lung, 275 Virchow, on the appearance of the lung in brown induration, 275 CANCER OF THE LUNGS, Article on, by Hermann Beigel, M.D., M.R.C.P. Lond., p. 144. AUTHORS REFERRED TO. Andral, on a case of complete aphonia in cancer of the lung, 149 Bayle, on the comparative rarity of cancer of the lung, 144 Begbie, Dr., on a case of effusion into the pleura in cancer of the lung, 149 Cockle, Dr., on a case of cancer of lung press- ing on the par vagum and simulating laryn- geal phthisis, 146 ; on dysphagia in cancer of the lung, 148; on the change of voice in cancer of the lung, 149 ; on the difficulty of diagnosing cancer of the lung, 149 Day, Dr., on the frequent occurrence of cancer of the lung as a sequence of cancer of the bones, 144 Ebermann, on the influence of age in cancer of the lung, 145 Friedreich, on a case in which tubercle and cancer coexisted, 151 Gairdner, Dr., on contraction of the pupils in cancer of the lung, 149 Pemberton, on the occurrence of melanosis in the lung, 145 Rokitansky, on the occurrence of fungus haematodes only in secondary cancer of the lung, 145 ; on cancerous pneumonia, 146 Rogers, Dr., on the occurrence of fungus haematodes in primary cancer of the lung, 145. Walshe, Dr., on the frequent occurrence of cancer of the lung secondary to cancer of the testicle, 144 Williams, Dr., on the characters of the sputa in cancer of the lung, 149 Winterich, on the presence of vocal fremitus in cancer of the lung, 150 CARDIAC CONCRETIONS, Article on, by John Syer Bristowe, M.D., F.R.C.P., p. 887. AUTHORS REFERRED TO. Richardson, on the origin of cardiac concre- tions, 889 Rokitansky, on concretions in the left ven- tricle, 888 CIRRHOSIS OF THE LUNG, Article on, by Charlton Bastian, M.A., M.D., F.R.S., p. 277. AUTHORS REFERRED TO. Barth, on the relative increase of cirrhosis of the lung with age, 278 Corrigan, Sir D., on the characters of cirrhosis of the lung, 277 ; on the production of the enlarged bronchi in cirrhosis of the lung, 285, 290 Gairdner, Dr., on the production of enlarged bronchi in cirrhosis of the lung, 291 Grisolle, oh cirrhosis following acute pneu- monia, 295 Huss, on the liability of cirrhosis of the lung to occur in drunkards, 295 Jones, Dr. Handfield, on the frequency of oc- currence of cirrhosis in several organs of the same individual, 294; on the similarity of the indurating processes in various parts of the body, 289 Laennec, on the dilatation of the bronchi in cirrhosis of the lung, 285, 290 Lebert, on the relative increase of cirrhosis of the lung with age, 278 Stewart, Dr., on the production of enlarged bronchi in cirrhosis of the lung, 291 Stokes, Dr., theory of production of enlarged bronchi, 290 Sutton, Dr., on "fibroid degeneration" of the lung, 280 Williams, Dr. C. J. B., on the enlargement of bronchial tubes in pleuro-pneumonia, 285 928 LIST OF CHIEF AUTHORS CORONARY ARTERIES, DISEASES OF THE, Article on, by R. Douglas Powell, M.D., F.R.C.P., p. 903. AUTHORS REFERRED TO. Dickinson, on occlusion of the coronary arteries as a cause of angina pectoris, 903 Hayden, on thrombosis of the coronary arteries causing fatty degeneration of the heart, 903 Latham, on the causes of angina pectoris, 903 CROUP, Article on, by William Squire, L.R.C.P. Lond., p. 46. AUTHORS REFERRED TO. Albers, on croup in general, 48; on morbid anatomy of croup, 62 AndrS, M., on tracheotomy in croup, 67 Baillou, first notice of croup by, 46 Barthez and Rilliet, MM., on morbid anatomy of croup, 62 Blair, Dr. Patrick, on distinction between croup and hooping-cough, 46 Blaud, M., on distinction of croup from diph- theria, 48 Bricheteau, M., on distinction of croup from diphtheria, 48 Buchanan, Dr. George, on tracheotomy in croup, 67 Carmichael, Mr., on tracheotomy in croup, 68 Cheyne, J., M.D., on croup in general, 48 ; on hysteria simulating croup, 60 ; on mor- bid anatomy of croup, 61 Clarke, Dr. John, on laryngismus stridulus, 56 Cruickshank, Dr., on tracheotomy in croup, 67 Desruelles, on the distinction of croup from diphtheria, 48 Emangard, on distinction of croup from diph- theria, 48 Evans, Dr. Conway, on tracheotomy in croup, 69 Farr, Dr. W., on mortality from croup, 48 Franks, on thymic asthma, 56 Fuller, Dr., on tracheotomy in croup, 67 Gendron, De 1'Eure, M., on tracheotomy in croup, 68 Ghizi, on distinction of croup from other dis- eases, 47 Goelis, on the nature of croup, 48 Guersant, on false croup, 70 Hoffman, on the treatment of secondary croup, 70 Home, Dr. Francis, early description of croup by, 47 Huxham, confusion between croup and hoop- ing-cough by, 47 Johnstone, Dr., on recognition of croup, 47 Jurine, on mortality from croup, 63 ; on croup in general, 48 Kopp, on thymic asthma, 56 Meigs, Dr., on treatment of secondary croup, 70 Millar, early description of croup by, 47 Pancoast, Dr., on tracheotomy in croup, 68 Rumsey, Mr., on the identity of epidemic croup and diphtheria, 70 Rush, on the nature of croup, 47, 48 Russell, Dr. Richard, on the diagnosis of croup, 47 Smith, Mr. Henry, on tracheotomy in croup, 68 Smith, Mr. Thomas, on a new tracheotomy tube, 69 Spence, Mr. J., on tracheotomy in croup, 67 Trousseau, M., on tracheotomy in croup, 68 Vieusseux, on croup in general, 48 Watson, Sir Thomas, on the formation of false membrane in croup, 62 West, Dr. Charles, on morbid anatomy of croup, 61; on treatment of croup, 67 Wichmann, on the nature of croup, 48 Williams, Dr., on the use of the stethoscope in diagnosis of croup, 57 Wilson, Dr. Charles, on croup in general, 48 Wood, Dr., on mortality in croup, 63 DISEASES OF THE LARYNX, Article on, by Morell Mackenzie, M.D., p. 17. AUTHORS REFERRED TO. Bevan, Dr., on the treatment of acute laryn- gitis by leeches, 21 Clark, Dr. Andrew, on the microscopic ap- pearances of papillomata of the larynx, 27 Gerhardt, on a case of intermittent hyperes- thesia of the larynx, 35; on syphilitic laryngitis, 42 Green, Dr. Horace, on chronic glandular laryngitis, 24 Jenner, Sir W., on rickets as a cause of spasm of the larynx, 33 Johnson, Dr. George, on oedema of the larynx secondary to Bright's disease, 43 Jones, Dr. Handfield, reports of cases of hyperesthesia of the larynx, 35 Lederer, on rickets as a cause of spasm of the larynx, 33 Ley, Dr., on direct pressure on the recurrent or pneumogastric nerves as a cause of spasm of the glottis, 33 Lisfranc, on scarification in acute laryngitis, 21 REFERRED TO IN EACH ARTICLE. 929 Louis, on the frequency of occurrence of tubercular laryngitis in phthisis, 40 Marsh, on scrofula as a predisposing cause of laryngismus stridulus, 33 Marshall Hall, on disease of the cervical por- tion of the spinal cord as a cause of spasm of the larynx, 33 Niemeyer, on the more frequent occurrence of acute laryngitis in people residing in towns than country, 18 Paget, Mr., on the microscopical appearances of fibro-cellular tumors of the larynx, 28 Rokitansky, on erectile tumors of the larynx, 28 ; on tubercular deposit in the larynx, 40 Romberg, on the impaired sensibility of the larynx in cholera, 36 Ruble, on the valvular murmur in tumors in the larynx, 26 ; on the laryngitis secon- dary to smallpox, 36 ; on atrophy of the cartilages of the larynx, in tubercular laryngitis, 40 Ryland, on a case of hydatids in the ventricle of the larynx, 28 ; on cartilaginous tumors of larynx, 28 Turek, on the functional paralysis of the vocal cords in tumors in the larynx, 26 West, Dr., on the croupous form of laryngitis secondary to measles, 37 Wilkes, Dr., on laryngitis secondary to ty- phoid fever, 38 EMPHYSEMA OF THE LUNGS, Article on, by Sir William Jenner, Bart., M.D. Bond., D.C.L. Oxon, F.R.S., p. 71. AUTHORS REFERRED TO. Budd, Dr., on the influence of loss of elas- ticity of the lung in production of emphy- sema, 72 Freund, on the nutritive changes in the lung, and their results in emphysema, 76; on the effect of hypertrophy of rib-cartilages in old people in the production of emphy- sema, 73 Gairdner, Dr. W., on the inspiratory theory of the production of emphysema, 73 Laennec, on the division of pulmonary em- physema, 71 Lehmann, on the urine in emphysema, 85 Louis, on the coexistence of bronchitis and emphysema, 87 Mendelssohn, on expiratory theory of produc- tion of emphysema, 73 Niemeyer, on the hereditary nature of em- physema, 89 Parkes, Dr., on the urine in emphysema, 85 Rokitansky, on the changes in the texture of the lung resulting from congestion, 79 Villemin, on the changes in the air-vesicles, 76 Virchow, on fatty degeneration of the heart in emphysema, 84 Waters, on the constitutional nature of the severer forms of emphysema, 76 Ziemssen, on a case of local emphysema, caused by loss of muscular power in the upper intercostal spaces, 75 ENDOCARDITIS, Article on, by Francis Sibson, M.D., F.R.S., p. 618 AUTHORS REFERRED TO. Cheevers, Norman, on endocarditis in the foetus, 618 Hasse, on the pathological anatomy of endo- carditis, 618 Moxon, on the pathological anatomy of endo- carditis, 618, 620, 661; on endocarditis secondary to chronic valvular disease, 655 Payne, on the pathological anatomy of endo- carditis, 618, 657 Rindfleisch, on the pathological anatomy of endocarditis, 618, 619 Rokitansky, on the pathological anatomy of endocarditis, 618 [HAEMOPHILIA, Article on, by Henry Hartshorne, A.M., M.D., p. 904.] HEART, ADVENTITIOUS PRODUCTS IN THE, Article on, by Thomas Bevill Peacock, M.D., F.R.C.P., p. 462. AUTHORS REFERRED TO. Andral, on hydatid cysts in the heart, 467 Aran, on polypi of the heart, 470 Baillie, description of tubercular growths in the pericardium by, 462 Bouillaud, on tubercle in the heart, 462 Cobbold, on entozoa in the heart, 468 Corvisart, on tubercular pericarditis, 463 ; on syphilitic growths in heart, 468 ; on fibro- cartilaginous degeneration of the heart, 177 Cruveilhier, on tubercular pericarditis, 463; on fibro-cartilaginous degeneration of the heart, 469 Jenner, Sir Wm., on fibro-cartilaginous de- generation of the heart, 469, 470 Laennec, on tubercles of the heart, 462; on syphilitic disease of the heart, 468 Louis, on tubercle in the heart, 462 ; in the ericardium, 463 VOL. ii.-59 930 LIST OF CHIEF AUTHORS Rilliet and Barthez, on tubercular pericar- ditis in children, 463 Rokitansky, on the rarity of tubercle in the heart, 462 ; on hydatid cysts in the heart, 467 Virchow, on syphilitic degeneration of the heart, 469 Walshe, on tubercular pericarditis, 463 ; on cancer of the heart, 464 HEART, ATROPHY OF THE, Article on, by W. R. Gowers, M.D.,p. 759. AUTHORS REFERRED TO. Bouillaud, on the varieties of cardiac atrophy, 760 Burns, Allan, description of atrophy of the heart by, 761 Chomel, on atrophy of the heart, 760, 761 Hayden, on atrophy of the heart, 760 Quain, on atrophy of the heart in phthisis, 761 Rindfleisch, on the pathological anatomy of cardiac atrophy, 762 Senac, on phthisis of the heart, 760 Walshe, on the varieties of atrophy of the heart, 760 ; on the symptoms, 762 HEART, DILATATION OF THE, Article on, by W. R. Gowers, M.D., p. 786. AUTHORS REFERRED TO. Beau, on asystolia of the heart, 791 Bouillaud, on the pathology of dilatation of the heart, 786 Corvisart, on aneurism of the heart, 786 Gairdner, on adherent pericardium as a cause of dilatation of the heart, 788 ; on chronic pulmonary emphysema as a cause of dila- tation, 789 Hayden, on the varieties of cardiac dilata- tion, 789; on the influence of adherent pericardium on the production of dilata- tion, 788, 789 Laennec, description of the physical signs of dilatation by, 786 Niemeyer, on the pathology of cardiac dilata- tion, 788, 792, 793 Stokes, on the pathology of dilatation of the heart, 787; on adherent pericardium as a cause of dilatation, 788; on dilatation of the auricles, 794; on alterations of the heart sounds from dilatation, 797 Walshe, on the physical signs of dilatation of the heart, 797, 800 Wilks, on the pathology of cardiac dilatation, 787, 789 HEART, FATTY DISEASES OF THE, Article on, by W. R. Gowers, M.D., p. 804. AUTHORS REFERRED TO. Hayden, on predisposition to fatty hyper- trophy of the heart, 805 ; to fatty degene- ration of the heart, 808 Laennec, on the pathological anatomy of fatty hypertrophy of the heart, 806; of fatty degeneration, 807 Louis, on acute molecular degeneration of the heart, 809, 812 Ormerod, on wasting diseases as a cause of fatty degeneration of the heart, 809 Paget, Sir James, on the pathological anatomy of fatty degeneration of the heart, 808, 809 Quain, on the causes of fatty hypertrophy of the heart, 805 ; on the pathology of fatty degeneration of the heart, 808, 811, 813; on fatty degeneration as a cause of rupture of the heart, 787 Rindfleisch, on the pathological anatomy of fatty degeneration of the heart, 812, 814 Rokitansky, on the microscopical appear- ances of fatty degeneration of the heart, 808, 814 Stokes, on acute molecular degeneration of the heart, 809, 812; on the physical signs of fatty degeneration of the heart, 816 ; on peculiarities of the respiration during anginal paroxysms, 817 Walshe, on the symptoms of fatty degenera- tion of the heart, 816 ; on the use of digi- talis in treatment, 820 HEART, FIBROID DISEASE OF TIIE, Article on, by W. R. Gowers, M.D., p. 823. AUTHORS REFERRED TO. Corvisart, on the pathology of fibroid disease of the heart, 823, 824 Hilton Fagge, on the pathology of fibroid dis- ease of the heart, 824 Pelvet, on fibroid disease as a cause of dilata- tion of the heart, 823, 824 Quain, on connective tissue hypertrophy of the heart, 823, 824 REFERRED TO IN EACH ARTICLE. 931 HEART, HYPERTROPHY OF THE, Article on, by W. R. Gowers, M.D., p. 763. AUTHORS REFERRED TO. Birtin, on the pathology of cardiac hyper- trophy, 763, 773, 775 Bright, on chronic renal disease as a cause of hypertrophy of the heart, 769 Corvisart, on cardiac hypertrophy as a cause of aneurism of the aorta and of cerebral apoplexy, 767, 779 Cruveilhier, on the real nature of concentric hypertrophy, 773 Laennec, on the physical signs of cardiac hypertrophy, 764, 777 Quain, on hypertrophy of the heart in phthisis, 768 ; on hypertrophy of the heart as a cause of apoplexy, 779 Rindfleisch, on the pathological anatomy of cardiac hypertrophy, 775 Senac, on the connection between hyper- trophy of the heart and arterial degenera- tion, 779 ; on the importance of rest in treatment, 784 Walshe, on the physical signs of hypertrophy of the heart, 776, 777 HEART, MALPOSITIONS OF THE, Article on, by Francis Sibson, M.D., F.R.S., p. 437. AUTHORS REFERRED TO. Bennett, on displacement of the heart by intra-thoracic tumors, 440, 443, 449 Gairdner, on the displacement of the heart in pleurisy, 446 Hope, on displacement of the heart by aneu- rism of the aorta, 451 Stokes, on epigastric pulsation in bronchitis and emphysema, 437 ; on cancer of the lung without displacement of the heart, 449 Townshend, on displacement of the heart by empyema, 445, 446 Walshe, on displacement of the heart by pleuritic effusion, 443 Wintrich, on displacement of the heart by pleuritic effusion, 445, 446,452; in pneumo- thorax, 447 HEART AND GREAT VESSELS, Position and Form of the, Article on, by Francis Sibson, M.D., F.R.S., p. 370. AUTHORS REFERRED TO. Braun,'on the relative position of the thoracic viscera, 418, 427 Haller, on the valves of the heart, 383, 390 Heath, description of the aortic sinuses, 391 Le Gendre, on the anatomy of the thorax, 427 Pirogoff, on the anatomy of the heart, 391, 413; on the relative position of the thoracic vis- cera, 417, 427 Reid, on the anatomy of the heart, 389 Sibson, on the medical anatomy of the thorax, 392, 416, 417 Thurnam, on the aortic sinuses, 389 HEART, WEIGHT AND SIZE OF THE, Article on, by Thomas Bevill Peacock, M.D., F.R.C.P., p. 363. AUTHORS REFERRED TO. Bouillaud, on the variations in the weight of the heart, 363, 368 Bright, on hypertrophy of the heart from chronic renal disease, 367 Glendenning, on the weight of the heart, in health and disease, 363, 364, 366 Laennec, on the size of the heart, 363 Reid, on the weight and dimensions of the heart, 363, 364 Cases by Bristowe, Vanderbyl, Church, &c., in the Pathological Transactions. HYDROPERICARDIUM, Article on, by W. R. Gowers, M.D., p. 663. AUTHORS REFERRED TO. Corvisart, on the physical signs of pericardial dropsy, 664 Graves, on effusion into the pericardium with- out evidence of inflammation, 664, 665 Laennec, on the occurrence of pericardial effusion during the last hours of life, 663 Stokes, ou pericardial dropsy, 664, 665 Walshe, on the causes of hydropericardium, 663 932 LIST OF CHIEF AUTHORS MEDIASTINAL TUMORS, Article on, by R. Douglas Powell, M.D., F.R.C.P., p. 826. AUTHORS REFERRED TO. Bennett, on mediastinal tumors, 828 Murchison, on the distinctive characters of lymphadenoma, 827 Symes Thompson, on mediastinal tumors, 828 Virchow, on the histology of morbid growths, 826 Walshe, on the diagnosis of mediastinal tu- mors, 832, 833 PERICARDITIS, Article on, by Francis Sibson, M.D., F.R.S., p. 474. AUTHORS REFERRED TO. Allbutt, Clifford, on paracentesis pericardii, 605 Burdon Sanderson, on the distribution of the nerves of the heart, 506 ; on the influence £ of the sympathetic nerves on the circula- tion, 512 Bouillaud, on pericarditis with nervous com- plications, 531, 535 Fuller, on delirium in pericarditis, 534 Fox, Wilson, on the treatment of hyperpy- rexia, 515, 516, 518 Frerichs, on pericarditis from renal disease, 589 Laennec, on paracentesis pericardii, 604 Moxon, on pericarditis from pyaemia, 597 Trousseau, on delirium in rheumatism, 529 ; on paracentesis pericardii, 604 Watson, Sir Thomas, on nervous complica- tions of acute rheumatism, 529, 534 PHTHISIS PULMONALIS, Article on, by John Hughes Bennett, M.D., F.R.C.P., p. 107. AUTHORS REFERRED TO. Andral, on the curability of phthisis, 130 Baudelocque, on damp as a cause of phthisis, 118 Bayle, description of tubercle, 110 Buchanan, Dr., on the effect of damp in the production of phthisis, 118 Dobell, Dr., on the dyspepsia of phthisis, 121 Fenwick, on mode of examining sputa for fragments of lung tissue, 129 Fox, Dr. Wilson, on the production of tuber- cle by the inoculation of other morbid pro- ducts, 116 Louis, on the occurrence of tubercle in the lung if in the body at all, 111 ; on the occurrence of tubercle in the mucous mem- brane of the stomach, 114 Macrae and M'Coll, Drs., on the freedom from phthisis of the islands of Lewis and Mull, 116 Magendie, on the production of tubercle in rabbits by damp, 118 Ringer, Dr., on the temperature in phthisis, 130 Roger and Boudet, on the frequent occurrence of concretions in the lungs of old people, 131 Sanderson, Dr. B., on the artificial production of tubercle, 116 Smith, Dr. E., on the value of cod-liver oil in consumption, 134 Van der Kolk, the first to point out fragments of the lung-tissue in sputa of phthisis, 129 Villemin, on the production of tubercle by inoculation, 116 Williams, Dr., on the average duration of phthisis, 143 ; on the value of cod-liver oil in the treatment of consumption, 134 Wood, Dr., on the relative mortality of phthisis before and after the introduction of cod-liver oil, 143 PLEURISY, Article on, by Francis E. Anstie, M.D., p. 340. AUTHORS REFERRED TO. B6hier, Prof., on acetate of methylamine in pleurisy, 351 Bowditch, on paracentesis thoracis in pleurisy, 354 Hillier, Dr., on mercury in the treatment of pleurisy of children, 353 Murchison, Dr., on the amount of fluid that ought to be drawn off in paracentesis thora- cis, 356 Niemeyer, on the use of cold in the treatment of pleurisy, 354 Steiner and Neuretuer, on the comparative rarity of pleurisy with effusion in young children, 342 Trousseau, on paracentesis thoracis in pleu- risy, 354 Ziemssen, on the influence of cold in the pro- duction of pleurisy, 342; on the displace- ment of organs in pleurisy of young chil- dren, 345 REFERRED TO IN EACH ARTICLE. 933 PNEUMONIA (ACUTE), Article on, by Wilson Fox, M.D.,F.R.C.P., p. 152. AUTHORS REFERRED TO. Addison, on the cause of the granular ap- pearance of the lung in pneumonia, 237 ; on the frequent complication of phthisis with pneumonia, 162 Andral, on the prognosis of pneumonia, 204 ; on a case of pneumonia which recurred fif- teen times, 157 Anstie, Dr., on the pulse in acute pneumonia, 236 Balfour, Dr., on bleeding in acute pneumo- nia, 209 Barthez and Rilliet, on hemorrhage from the large intestine and stomach in acute pneu- monia, 200 ; on the occurrence of vomiting in the acute pneumonia of children, 172; on cerebral disturbance in the pneumonia of children, 173 Beale, Dr., on the presence of chloride of so- dium in the sputa in acute pneumonia, 236 Bennett, Dr. Hughes, on bleeding in acute pneumonia, 209 ; on the influence of the constitution in pneumonia, 156 ; on vene- section in the treatment of acute pneumo- nia, 241 Bichat, on the distinction between pleurisy and pneumonia, 153 Bouillaud, on ante-mortem polypoid concre- tions in acute pneumonia, 199 Bright, Dr., on the frequent occurrence of pneumonia in Bright's disease, 161 Chambers, Dr. King, on the complication of heart disease with pneumonia, 162 Cruveilhier, on the injurious effects of cold on the aged in producing pneumonia, 158 Dechambre, on the effect of cold in producing pneumonia, 158 Dietl, on tartar emetic in the treatment of acute pneumonia, 210 Erichsen, Mr., on pneumonia following surgi- cal operations, 161 Farre, Dr., on the influence of temperature on pneumonia, 154 Gendrin, on the increase of the specific grav- ity of the lung-tissue in acute pneumonia, 189 Graves, Dr., on the occasional appearance of a murmur over the heart during the height of acute pneumonia, 171 Griesinger, on the presence of tyrosine in sputa of acute pneumonia, 166 ; on the ten- dency of pneumonia to assume epidemic characters in malarial districts, 159 Grimshaw, Dr., on the difference in the tem- perature of pneumonia and continued fever, 203 Grisolle, on the exciting causes of pneumo- nia, 157; on the great frequency of pneu- monia in infancy, 156 ; on the more frequent occurrence of pneumonia in males than females, 156 ; on frequency of pneumonia in rickets, 156 ; on the greater liability of females to pneumonia at menstrual periods, 156; on the icterus occurring in acute pneumonia, 185 ; on parotitis secondary to pneumonia, 185 ; on the delirium of acute pneumonia, 172 ; on the use of tepid baths in pneumonia, 212 Hillier, Dr., on the occurrence of deafness in acute pneumonia, 174 Hippocrates, on the frequent occurrence of pneumonia in the vigorous, 156 Huss, on the influence of the seasons on the occurrence of pneumonia, 155 ; on influence of sex in pneumonia, 205; on the disap- pearance of the relative disproportion of pneumonia in the two sexes in advanced age, 156 ; on gangrene of the lung in acute pneumonia, 195 ; on mortality of pericardi- tis secondary to acute pneumonia, 184; on abscess of the lung in acute pneumonia, 216; on treatment of delirium in acute pneumonia, 214; on venesection in the treatment of acute pneumonia, 240 Huxham, on certain atmospheres producing certain kinds of pneumonias, 155 Jackson, Dr., on the more frequent occurrence of complications in pneumonia in a damp than dry atmosphere, 155 Kocher, on veratria in the treatment of pneu- monia, 211 Laennec, on the clinical separation of pneu- monia from pleurisy, 154 ; on the crisis in acute pneumonia, 180 ; on tartar emetic in the treatment of acute pneumonia, 210 Laserre, on the frequent occurrence of pneu- monia during an epidemic of influenza, 159 Lombard, on the relative mortality from pneumonia and other diseases at different ages, 156 Louis, on the frequent absence of cough and rusty sputa in pneumonia secondary to typhoid fever, 234; venesection in treat- ment of acute pneumonia, 238 Murchison, Dr., on the greater liability to pneumonia in typhoid than in typhus fever, 160 Nysten, on the coldness of the expired air in acute pneumonia, 167 Remak, on the cast of the air-cells and bron- chial tubes in acute pneumonia, 166 Skoda,on the treatment of gangrene of the lung when secondary to acute pneumonia, 217 Steffen, on the influence of dentition in the prognosis of acute pneumonia, 205 Stokes, Dr., on the arterial injection stage of acute pneumonia, 187 ; on retraction of the chest walls after pneumonia, 182 Sydenham, on venesection in acute pneumo- nia, 164 Taylor, Dr. John, on the frequency of pneu- monia in Bright's disease, 161 Thomas, Dr., on bleeding in acute pneumonia, 211 Todd, Dr., on bleeding in acute pneumonia, 209 Virchow, on changes in lung-tissue in acute pneumonia, 188 Wachsmuth, on rapid loss of weight during acute pneumonia, and rapid increase after- wards, 182 934 LIST OF CHIEF AUTHORS Walshe, Dr., on pulse respiration in pneu- monia, 164 ; on haemoptysis in acute pneu- monia, 165 ; on coldness of expired air in acute pneumonia, 167 ; on pneumonia of the middle lobe, 196; on amphoric percussion note over upper part of chest in acute pneumonia, 202; on the inhalation of chloroform in pneumonia, 211 Weber, F., on the pneumonia of intra-uterine life, 190, 191; on the external application of cold water in acute pneumonia, 212 Wunderlich, on the effect of excessive exer- tion in producing pneumonia, 158 ; on the treatment of pneumonia by venesection, 238 Ziemssen, on rusty sputa in children in acute pneumonia when vomiting has taken place, 166 ; on the difference between the tempe- rature in pneumonia and tubercular men- ingitis, 203 Zimmermann, on the sudden elevation of the temperature in pneumonia, 176 PNEUMONIA (CHRONIC), Article on, by Wilson Fox, M.D., F.R.C.P., p. 244. AUTHORS REFERRED TO. Addison, Dr., on the cause of induration of the lung in chronic pneumonia, 254 Broussais, on chronic ulcerative pneumonia, 259 Charcot, on dilatation of the bronchi in fibroid induration of the lung, 255 Chomel, on the parts most commonly affected in induration of the lung, 257 Corrigan, Sir D., on the cause of dilatation of the bronchi in chronic pneumonia, 256 Heschl, on the microscopical appearances of the lung in chronic pneumonia, 253 Stokes, Dr., on the difficulty of defining chronic pneumonia, 245 ; on contraction of the side in chronic pneumonia, 262 Traube, on the character of the sputa in chronic pneumonia, 262; on inflammation of indurated lung as a common cause of gangrene of the lung, 256 Ziemssen, on clubbing of the fingers in chronic pneumonia, 263 PNEUMO-PERICARDIUM, Article on, by J. Warburton Begbie, M.D., p. 472. AUTHORS REFERRED TO. Bouillaud, on thO diagnosis of pneumo-peri- cardium, 472 Laennec, on the frequency of pneumo-peri- cardium, 472 ; on the physical signs of, 473 Stokes, on a case of pneumo-pericardium, 472; physical signs of, 472 Walshe, on the diagnosis of pneumo-pericar- dium, 473 PNEUMOTHORAX, Article on, by Francis E. Anstie, M.D., p. 360. AUTHOR REFERRED TO. Walshe, Dr., on the large percentage of perforative cases from tubercular disease of the lung itself, 360 PULMONARY ARTERY, DISEASES OF THE, Article on, by R. Douglas Powell, M.D., F.R.C.P., p. 898. AUTHORS REFERRED TO. Peacock, on communication between the aorta and the pulmonary artery, 900 Quincke, on the physical signs of obstruction of the pulmonary artery, 900 Wilks and Moxon, on atheroma of the pul- monary artery, 898 SYPHILITIC AFFECTIONS OF THE LUNG, Article on, by Wilson Fox, M.D., F.R.C.P., p. 270. AUTHORS REFERRED TO. Morgagni, on the connection between syphilis and phthisis, 270 Wagner, on syphilitic gummata in the lung, 271 REFERRED TO IN EACH ARTICLE. 935 THROMBOSIS AND EMBOLIA, Article on, by John Syer Bristowe, M.D., F.R.C.P., p. 892. AUTHORS REFERRED TO. Kirkes, on embolism of the cerebral arteries, 895 Virchow, on the pathology of embolism, 894 VALVES OF THE HEART, DISEASES OF THE, Article on, by C. Hilton Fagge, M.D., F.R.C.P., p. 706. AUTHORS REFERRED TO. Allbutt, C., on overwork as a cause of valvu- lar disease, 720, 755 Bouillaud, on the rheumatic origin of valvu- lar disease of the heart, 716 Corrigan, Sir D., on the mode of production of cardiac murmurs, 722; on the peculiar pulse of aortic regurgitation, 741 Chauveau, on the cause of blood murmurs, 723, 730 Corvisart, on the pathological anatomy of valvular disease, 607 ; on rupture of the cardiac valves, 721 Friedreich, on endocarditis in infants, 714; on hepatic pulsation, 748 ; on the prognosis of valvular disease, 753 Gairdner, on auricular systolic murmurs, 727 Hayden, on the murmur of tricuspid stenosis, 728 Moxon, on endocarditis secondary to valvular disease, 708 Peacock, on congenital valvular disease, 714, 715 ; on rupture of cardiac valves, 721, 722 Rindfleisch, on the pathological anatomy of endocarditis, 708 Walshe, on the relative importance of the dif- ferent forms of cardiac disease, 754, 755 VEINS, DISEASES OF THE, Article on, by John Syer Bristowe, M.D., F.R.C.P., p. 880. AUTHORS REFERRED TO. Briquet, on the pathology of varicose veins, 885 Rokitansky, on the origin of phleboliths, 883 END OF VOLUME IL HENRY C. LEA'S SON & CO.'S (late henry c. lea) CLASSIFIED CAT ALO G-LTE OF MEDICAL AND SURGICAL PUBLICATIONS. In asking the attention of the profession to the works advertised in the following pages, the publishers would state that no pains are spared to secure a continuance of the confidence earned for the publications of the house by their careful selection and accuracy and finish of execution. . The large number of inquiries received from the profession for a finer class of bind- ings than is usually placed on medical books has induced us to put certain of our standard publications in half Russia, and that the growing taste may be encouraged, the prices have been fixed at so small an advance over the cost of sheep, as to place it within the means of all to possess a library that shall have attractions as well for the eye as for the mind of the reading practitioner. The printed prices are those at which books can generally be supplied by book- sellers throughout the United States, who can readily procure for their customers any works not kept in stock. Where access to bookstores is not convenient, books will be sent by mail post-paid on receipt of the price, and as the limit of mailable weight has been removed, no difficulty will be experienced in obtaining through the post-office any work in this catalogue. No risks, however, are assumed either on the money or on the books, and no publications but our own are supplied, so that gentlemen will in most cases find it more convenient to deal with the nearest bookseller. HENRY C. LEA'S SON & CO. Nos. 706 and 708 Sansom St., Philadelphia, July, 1881. INCREASED INDUCEMENT FOR SUBSCRIBERS TO THE AMERICAN JOURNAL 0E THE MEDICAL SCIENCES. TWO MEDICAL JOURNALS, containing nearly 2000 LARGE PAGES, Free of Postage, for FIVE DOLLARS Per Annum. TERMS FOR 1881. The American Journal of the Medical Sciences, published 1 Five Dollars quarterly (1150 pages per annum), with L per annum, The Medical News and Abstract, monthly (768 pp. per annum), J in advance. SEPARATE SV RSCRIPTIONS TO The American Journal of the Medical Sciences, when not paid for in advance, Five Dollars. The Medical News and Abstract, free of postage, in advance, Two Dollars and a Half. *** Advance paying subscribers can obtain at the close of the year cloth covers, gilt-lettered, for each volume of the Journal (two annually), and of the News and Abstract (one annually), free by mail, by remitting ten cents for each cover. It will thus be seen that for the moderate sum of Five Dollars in advance, the subscriber will receive, free of postage, the equivalent of four large octavo volumes, stored with the choicest matter, original and selected, that can be furnished by the medical literature of both hemispheres. Thus taken together, the "Journal" and the "News and Abstract" combine the advantages of the elaborate preparation that can be devoted to the Quarterly with the prompt conveyance of intelligence by the Monthly; while, the whole being under a single editorial supervision, the sub- scriber is secured against the duplication of matter inevitable when periodicals from different sources are taken together. The periodicals thus offered at this unprecedented rate are universally known for Henry C. Lea's Son & Co.'s Publications-{Am. Journ. Med. Sai..). 2 their high professional standing. I. THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES, Edited by I. MINIS HAYS, M.D., for more than half a century has maintained its position in the front rank of the medical literature of the world. Cordially supported by the profession of America, it circulates wherever the language is read, and is universally regarded as the national exponent of American medicine-a position to which it is entitled by the distinguished names from every section of the Union which are to be found among its collaborators.* It is issued quarterly, in January, April, July, and October, each number containing about three hundred octavo pages, appropriately illustrated wherever necessary. A large portion of this space \s devoted to Original Communications, embracing papers from the most eminent members of the profession throughout the country. k oilowing this is the Review Department, containing extended reviews by com- petent writers of prominent new works and topics of the day, together with numerous elaborate Analytical and Bibliographical Notices, giving a fairly complete survey of medical literature. Ihen follows the Quarterly Summary of Improvements and Discoveries in the Medical Sciences, classified and arranged under different heads, and furn- ishing a digest of medical progress, abroad and at home. Thus during the year 1880 the "Journal" contained 67 Original Communications, mostly elaborate in character, 170 Reviewsand Bibliographical Notices, and 147 articles in the Quarterly Summaries, illustrated with 47 wood engravings. That the efforts thus made to maintain the high reputation of the "Journal" are successful, is shown by the position accorded to it in both America and Europe as the leading organ of medical progress:- This is universally acknowledged as the leading , The Philadelphia Medical and Physical Journal American Journal, and has been conducted by Dr. j Issued its first number in 1820, and after a brilliant Hays alone until 18b9, when his son was associated i career, was succeeded in 1827 by the American with him. e quite agree with the critic, that this Journal ol the Medical Sciences \ periodical of a"rguage'!ndclieer' world-wide reputation; the ablest and one of the U11h a,tcord the.flrst P.lace, for nowhere shall oldest periodicals in the world-a journal which has we find moie able and more impartial criticism, and , an unsullied record.-Gross's History of American nowhere such a repertory of able original articles. I Med! Literature 1876 V f American Indeed, now that the British and Foreign Medico- 1 • , ... Chirurgical Review" has terminated its career the 1 be best medical journal ever published in Europe American Journal stands without a rival.-London Or Amerlca--Fa. Med. Monthly, May, 1879. Med. Times and Gazette, Nov. 24, 1877. ft is universally acknowledged to be the leading The best medical journal on the continent Bos- American medical journal, and, in our opinion, is ton Med. and Sura. Journal April 1879 second to none in the language.-Boston Med. and . .... . . Surg. Journal, Oct. 1877. The present number of the American Journal is , . , , an exceedingly good one, and gives every promise ,lnis 18 medical journal of our country to which of maintaining the well-earned reputation of the the Am®rlcan physician abroad will point with the review. Our venerable contemporary has our best &reate®t satisfaction, as reflecting the state of medi- wishes, and we can only express the hope that it fal cu"ure m his country. For a great many years may continue its work with as much vigor and ex- 11 .as n t"6 medium through which our ablest cellence for the next fifty years as it has exhibited 'Ynters have made known their discoveries and in the past.-London Lancet, Nov. 24 1877 observations.-Address of L. P. Tandell, M.D., be- ' fore International Med. Congress, Sept. 1876. And that it was specifically included in the award of a medal of merit to the Pub- lishers in the Vienna Exhibition in 1873. The subscription price of the "American Journal of the Medical Sciences" has never been raised during its long career. It is still Five Dollars per annum ; and when paid lor in advance, the subscriber receives in addition the "Medical News and Abstract," making in all nearly 2000 large octavo pages per annum, free of postage. II. THE MEDICAL NEWS AND ABSTRACT. Thirty-eight years ago the "Medical News" was commenced as a monthly to convey to the subscribers of the "American Journal" the clinical instruction and yj*<*Comin'?"vCati>?n8 ar® invited from gentlemen in all parts of the country. Articles inserted by the Editor are liberally paid for by the publishers. 7 Henry C. Lea's Son & Co.'s Publications-(Am. Journ. Med. Sei.}. current information which could not be accommodated in the Quarterly. It consisted of sixteen pages of such matter, together with sixteen more known as the Library Department and devoted to the publishing of books. With the increased progress of science, however, this was found insufficient, and some years since another periodical, known as the "Monthly Abstract," was started, and was furnished at a moderate price to subscribers to the "American Journal." These two monthlies have been consolidated, under the title of "The Medical News and Abstract," and are furnished free of charge in connection with the "American Journal." The "News and Abstract" consists of 64 pages monthly, in a neat cover. It contains a Clinical Department in which will be continued the series of Original American Clinical Lectures, by gentlemen of the highest reputation through- out the United States, together with a choice selection of foreign Lectures and Hospital Notes and Gleanings. Then follows the Monthly Abstract, systemati- cally arranged and classified, and presenting five or six hundred articles yearly ; and each number concludes with an Editorial and a News Department, giving cur- rent professional intelligence, domestic and foreign, the whole fully indexed at the close of each volume, rendering it of permanent value for reference. As stated above, the subscription price to the "News and Abstract" is Two Dollars and a Half per annum, invariably in advance, at which rate it ranks as one of the cheapest medical periodicals in the country. But it is also furnished, free of all charge, in commutation with the "American Journal of the Medical Sciences," to all who remit Five Dollars in advance, thus giving to the subscriber, for that very moderate sum, a complete record of medical progress throughout the world, in the compass of about two thousand large octavo pages. In this effort to furnish so large an amount of practical information at a price so un- precedentedly low, and thus place it within the reach of every member of the profes- sion, the publishers confidently anticipate the friendly aid of all who feel an interest in the dissemination of sound medical literature. They trust, especially, that the sub- scribers to the "American Medical Journal," will call the attention of their acquaintances to the advantages thus offered, and that they will be sustained in the endeavor to permanently establish medical periodical literature on a footing of cheap- ness never heretofore attempted. PREMIUM TOR OBTAINING NEW SUBSCRIBERS TO THE "JOURNAL." Any gentleman who will remit the amount for two subscriptions for 1881, one of which at least must be for a new subscriber, will receive as a premium, free by mail, a copy of any one of the following recent works :- "Seiler on the Throat" (see p. 19), " Barnes's Manual of Midwifery" (see p. 24), "Tilbury Fox's Epitome of Diseases of the Skin," new edition (see p. 19), "Browne on the Use of the Ophthalmoscope" (see p. 29), "Flint's Essays on Conservative Medicine" (see p. 15), " Sturges's Clinical Medicine" (see p. 15), " Swayne's Obstetric Aphorisms," new edition (see p. 21), "Tanner's Clinical Manual" (see p. 5), "West on Nervous Disorders of Children" (see p. 21). *** Gentlemen desiring to avail themselves of the advantages thus offered will do well to forward their subscriptions at an early day, in order to insure the receipt of complete sets for the year 1881. The safest mode of remittance is by bank check or postal money order, drawn to the order of the undersigned. Where these are not accessible, remittances for the "Journal" maybe made at the risk of the publishers, by forwarding in registered letters. Address, Henry C. Lea's Son & Co., Nos. 706 and 708 Sansom St., Phila., Pa. 3 4 Henry C. Lea's Son & Co.'s Publications-(Dictionaries). JJUNGLISON (ROBLEY), M.D., Late Professor of Institutes of Medicine in Jefferson Medical College, Philadelphia. MEDICAL LEXICON; A Dictionary of Medical Science: Con- taining a concise explanation of the various Subjects and Terms of Anatomy, Physiology, Pathology, Hygiene, Therapeutics. Pharmacology, Pharmacy, Surgery, Obstetrics, Medical Jurisprudence and Dentistry. Notices of Climate and of Mineral Waters; Formulae for Officinal, Empirical and Dietetic Preparations; with the Accentuation and Etymology of the Terms, and the trench and other Synonymes ; so as to constitute a French as well as English Medical Lexicon. A New Edition. Thoroughly Revised, and very greatly Mod- ified and Augmented. By Richard J. Dunglison, M.D. In one very large and hand- someroyal octavo volume of over 1100 pages. Cloth, $6 50 ; leather, raised bands, $7 50; half Russia, $8. (Just Issued.) The object of the author from the outset has not been to make the work a mere lexicon or dictionary of terms, but to afford, under each, a condensed view of its various medical relations, and thus to render the work an epitome of the existing condition of medical science. Starting with this view, the immense demand which has existed for the work has enabled him, in repeated revisions, to augment its completeness and usefulness, until at length it has attained the position of a recognized and standard authority wherever the language is spoken. Special pains have been taken in the preparation of the present edition to maintain this en- viable reputation During the ten years which have elapsed since the last revision, the additions to the n omen Mature ofthe medical sciences have been greater than perha ps in any simila r per io d of the past, and up to the time ofhis death the author la bored assiduously to i ncorpora te every- thing requiring the attention of the student or practitioner. Since then, the editor has been equally industrious, so that the additions to the vocabulary are more numerous than in any pre- vious revision. Especial attention has been bestowed on the accentuation, which will be found marked on every word. The typographical arrangement has been much improved, rendering reference much more easy, and every care has been taken with the-mechanical execution. The work has been printed on new type, small but exceedingly clear, with an enlarged page, so that the additions have been incorporated with an increase of but little over a hundred pages, and the volume now contains the matter of at least four ordinary octavos. A book well known to our readers, and of which may safely confirm the hope ventured by the editor every American ought to be proud. When the learned " that the work, which possesses for him a filial as well author of the work passed away, probably all of us as an individual interest, will be found worthy a con- feared lest the book should not maintain its place tinuance of the position so long accorded to it as a in the advancing science whose terms it defines. For- standard authority."-Cincinnati Clinic, Jan 10 1874 tunately, Dr. Richard J Dunglison having assisted his It has the raremerU that it certainly has no rival' father in the revision of several editions oi the work, „„ 1 and having been, therefore, trained in the methods and vi- i , yand extent of imbued with the spirit of the book, has been able to ^rences.-London Medteal Casette . edit it, not in the patchwork manner so dear to the . -^8 a standard work of reference, as one of the best, heart of book editors, so repulsive to the taste of intel- if not the very best, medical dictionary in the Eng- ligent book readers, but to edit it as a work of the kind Bsh language, Dunglison's work has been well known should be edited-to carry it on steadily, without jar f°r about forty years, and needs no words Of praise or interruption, along the grooves of thought it has 011 oar Part to recommend it to the members of the travelled during its lifetime. To show the magnitude medical, and, likewise, of the pharmaceutical pro- of the task which Dr. Dunglison has assumed and car- fession. The latter especially are in need of such a tied through, it is only necessary to state that more work, which gives ready and reliable information than six thousand new subjects have been added in the on thousands of subjects and terms which they are present edition.-Phtla. Med. Times, Jan. 3,1874. liable to encounter in pursuing their daily avoca- Aboutthe first book purchased by the medical stu- iPfT-Cann°f V? expect®d dent is the Medical Dictionary The lexicon explana- waJ-Am tory of technical terms is simply a sine qua non. Ina , J vwu. science so extensive, and with such collaterals as medi A valuable dictionary of the terms employed in cine, it is as much a necessity also to the practising medicine and the allied sciences, and of the rela- physician. To meet the wants of students and most tions of the subjects treated under each head. It re- physicians, the dictionary must be condensed while dects great credit on its able American author, and comprehensive, and practical while perspicacious. It well deserves the authority and popularity it has was because Dunglison's met these indications that it obtained.-British Med. Journ.,Oc\.. 31, 1874. became at once the dictionary of general use wherever Few works of this class exhibit a grander monu- medicine was studied in the English language. In no ment of patient research and of scientific lore. The former revision have thealterations and additions been extent of the sale of this lexicon is sufficient to tes- so great. Morethan six thousand new subjects and terms tify to its usefulness, and to the great service ccn- have been added.The chiefterms have been set in black ferred by Dr. Robley Dunglison on the profession letter, while the derivatives follow in small caps; an and indeed onothers, by its issue.-London Lancet arrangement which greatly facilitates reference. We May 13 1875. LIO BLYN (RICHARD D.), M.D 11A DICTIONARY OF THE TERMS USED IN MEDICINE AND THE COLLATERAL SCIENCES. Revised, with numerous additions, by Isaac Hays, M. D., Editor of the " American Journal of the Medical Sciences." In one large royal I2mo. volume of over 500 double-columned pages ; cloth, $1 50 ; leather, $2 00° It is the best book of definitions we have, and ought always to be upon the student's table.- Southern Med. and Surg. Journal. RODWELL (G. F.}, F.R.A.S., A DICTIONARY OF SCIENCE: Comprising Astronomy, Chem- istry, Dynamics, Electricity, Heat, Hydrodynamics, Hydrostatics, Light, Magnetism, Mechanics, Meteorology, Pneumatics, Sound and Statics. Preceded by an Essay on the History of the Physical Sciences. In one handsome octavo volume of 694 pages, with many illustrations: cloth, $5. A CENTURY OF AMERICAN MEDICINE, 1776-1876. By Doctors E. H. Clarke, H J. Bigelow, S. D. Gross, T. G. Thomas and J. S. Billings. Inone very hand- some 12mo. volume of about 350 pages : cloth, $2 25. {Lately Issued.) This work appeared in the pages of the American Journal of the Medical Sciences durino- the year 1876. As a detailed account of the development of medical science in America, by gentle- men of the highest authority in their respective departments, the profession will no doubt wel- come it in a form adapted for preservation and reference. ^EILL {JOHN), M.D., and gMITH {FRANCIS G.), M.D., Prof, of the Institutes of Medicine inthe Univ of Penna AN ANALYTICAL COMPENDIUM OF THE VAK1OUS BRANCHES OF MEDICAL SCIENCE ; for the Use and Examination of Students. A new edition, revised and improved. In one very large and handsomely printed royal 12mo. volume, of about one thousand pages, with 374 wood-cuts, cloth, $4 ; strongly bound in leather, with raised bands, $4 75. ^ARTSHORNE {HENRY), M.D., Professor of Hygiene in the University of Pennsylvania. A CONSPECTUS OF THE MEDICAL SCIENCES; containing Handbooks on Anatomy, Physiology, Chemistry, Materia Medica, Practical Medicine Surgery and Obstetrics. Second Edition, thoroughly revised and improved. In one large royal 12mo. volume of more than 1000 closely printed pages, with 477 illustrations on wood. Cloth, $4 25 ; leather, $5 00. {Lately Issued.) We can say with the strictest truth that it is the , worthy. If students must have a conspectus thev best work of the kind with which we areacqnainted. will he wise to procure that of Dr Hartshorne - It embodies in a condensed form all recent contribu- Detroit Rev. of Med. and Pharm. Aug 1874 tions to practical medicine, and is therefore useful > .. . i 6 . to every busy practitioner throughout our country, , as many redeeming features besides being admirably adapted to the use of stu- 1 D Hartshorne evMhn 18 th6nl,ev-iiW? have dents of medicine. The book is faithfully and ably oerHation it t« skill in con- executed.- Charleston Med. Journ., April, 1875 active nractw-p w) -> m a< Physician in , active practice, who can give but limited time to the The work is intended as an aid to the medical familiarizing of himself with the important changes student, and as such appears to admirably fulfil its which have been made since he attended lectures object by itsexcellent arrangement, the full compi- The manual of physiology has also been improved lation of facts, the perspicuity aud terseness of lan- and gives the most comprehensive view of the latest guage, and the clear and instructive illustrations advances in the science possible in the space devoted in some parts of the work.-American Journ. of to the subject. The mechanical execution of the Pharmacy, Philadelphia, July, 1874. book leaves nothing to be wished for.-Peninsular The volume will be found useful, not only to stu- Journal of Medicine, Sept. 1874. dents, bntto many otherswhomay desire torefresh After carefully looking through this conspectus their memories with the smallest possible expendi- we are constrained to say that it is the most com- ture of time.-N. Y. Med. Journal, Sept. 1874. plete work, especially in its illustrations, of its kind The student will find this the most convenient and that we have seen.-Cincinnati Lancet, Sept. 1874. useful book of the kind on which he can lay his The favor with which h fl hnnd.-Paeific Med. and burg. Journ., Aug. 1874. Compendium was received, was an evidence of its This is the best book of its kind that we have ever various excellences. The present edition bears evi- examined. It is an honest, accurate, and concise ■ deuce of a careful and thorough revision. Dr. Harts- compend of medical sciences, as fairly as possible home possesses a happy faculty of seizing upon the representing their present condition. The changes salient points of each subject, and of presenting them and the additions have been so judicious and tho- in a concise and yet perspicuous manner. Leaven- rough as to render it, so far as it goes, entirely trust- worth Med. Herald, Oct. 1874 TUDLOW {J. L.), M.D. A MANUAL OF EXAMINATIONS upon Anatomy, Physiology, Surgery, Practice of Medicine, Obstetrics, Materia Medica, Chemistry, Pharmacy and Therapeutics. To which is added a Medical Formulary. Third edition, thoroughly revised and greatly extended and enlarged. With 370 illustrations In one handsome royal 12mo. volume of 816 large pages. Cloth, $3 25 ; leather, $3 75. The arrangement of this volume in the form of question and answer renders it especially suit- able for the office examination of students, and for those preparing for graduation. WANNER {THOMAS HAWKES), M.D., ^c. 2 A MANUAL OF CLINICAL MEDICINE AND PHYSICAL DIAG- NOSIS. Third American from the Second London Edition. Revised and Enlarged by Tilbury Fox, M. D., Physician to the Skin Department in University College Hospital, L indon, ic. In one neat volume, small 12mo., ofabout 375 pages, cloth, $150. *** On page 3, it will be seen that this work is offered as a premium for procuring new subscribers to the "American Journal of the Medical Sciences.'' Henry C. Lea's Son & Co.'s Publications-{Manuals). 5 6 (HENRY), F.R.S., Lecturer on Anatomy at St. George's Hospital, London. ANATOMY, DESCRIPTIVE AND SURGICAL. The Drawings by H. V. Carter, M.D., and Dr. Westmacott. The Dissections jointly by the AuTHORand Dr. Carter. With an Introduction on General Anatomy and Development by T. Holmes, M.A., Surgeon to St. George's Hospital. A new American, from the Eighth enlarged and improved London edition. To which is added " Landmarks, Medical and Surgical," by Luther Holden, F.R.C.S., author of " Human Osteology," " A Manual of Dissections," etc. In one magnificent imperial octavo volume of 983 pages, with 522 large and elaborate engravings on wood. Cloth, $6 ; leather, raised bands, $7 ; half Russia, $7 50. (Now Ready.) The author has endeavored in this work to cover a more extended range ofsubjects than is cus- tomary in the ordinary text-books, by giving not only the details necessary for the student, but also the application of those details in the practice of medicine and surgery, thus rendering it both a guide for the Learner, and an admirable work of reference for the active practitioner. The en- gravings form a special feature in the work, many of them being the size of nature, nearly all original, and having the names of the various parts printed on the body of the cut, in place of figures of reference, with descriptions at the foot. They thus form a complete and splendid series, which will greatly assist the student in obtaining a clear idea of Anatomy, and will also serve to refresh the memory of those who may find in the exigencies of practice the necessity of recalling the details of the dissecting room ; while combining, as it does, a complete Atlas of Anatomy, with a thorough treatise on systematic, descriptive and applied Anatomy, the work will be found of essential use to all physicians who receive students in their offices, relieving both preceptor and pupil of much labor in laying the groundwork of a thorough medical education. Since the appearance of the last American Edition, the work has received three revisions at the hands of its accomplished editor, Mr. Holmes, who has sedulously introduced whatever has seemed requisite to maintain its reputation as a complete and authoritative standard text-book and work of reference. Still further to increase its usefulness, there has been appended to it the recent work by the distinguished anatomist, Mr. Luther Holden-"Landmarks, Medical and Surgical" which gives in a clear, condensed and systematic way, all the information by which the prac- titioner can determine from the external surface of the body the position of internal parts. Thus complete, the work, it is believed, will furnish all the assistance that can be rendered by type and illustration in anatomical study. No pains have been spared in the typographical execution of the volume, which will be found in all respects superior to former issues. Notwithstanding the increase of size, amounting to over 100 pages and 57 illustrations, it will be kept, as heretofore, at a price rendering it one of the cheapest works ever offered to the American profession. The recent work of Mr. Holden, which was no- to consult his books on anatomy. The work is ticed by us on p. 53 of this volume, has been added simply indispensable, especially this present Amer- as an appendix, so that, altogether, this is the moit ican edition.- Va. Med. Monthly, Sept. 1878. practical and complete anatomical treatise available ..... . . ,, „ , . to American students and physicians. The former The addlt'°" of 'he re^-t f Mr Holden finds In it the necessary guide in making dissec- as an appendix, renders this he most practical and tions; a very comprehensive chapter on minute comply treatise available to American students, anatomy ; and about all that can be taught him on flad a comprehensive chapter on minute general and special anatomy; while the latter, in anatomy, about all that can be taught on general its treatment of each region from a surgical point of and sP«c,al anatomy , while its treatmen of each view, and in the valuable addition of Mr. Holden, region, from a surgical point of view, in the valu- will find all that will be essential to him in his able section by Mr Hoiden.is all that will beessen- practice-AVm Remedies, Aug. 1878. V '^em 111 Practice-OAio Medical Recorder, This work is as near perfection as one could pos- ° sibly or reasonably expect any book intended as a It is difficult to speak in moderate terms of this text-book or a genera) reference book on anatomy new edition of "Gray." It seems to be as nearly to be. The American publisher deserves the thanks perfect as it is possible to make a book devoted to of the profession for appending the recent work of any branch of medical science. The labors of the Mr. Holden, "Landmarks, Medical and Surgical," eminent men who have successively revised the which has already been commended as a separate eight editions through which it has passed, would book. The latter work-treating of topographical seem to leave nothing for future editors to do. The anatomy-has become an essential to the library of addition of Holden's " Landmarks" will make it as every intelligent practitioner. We know of no indispensable to the practitioner of medicine and book that can take its place, written as it is by a surgery as it has been heretofore to the student. As most distinguished anatomist. It would be simply regards completeness, ease of reference, utility, a waste of words to say any thing further in praise beauty, and cheapness, it has no rival. No stu- of Gray's Anatomy, the text-book in almost every dent should enter a medical school without it; no medical college in this country, and the daily refer- physician can afford to have it absent from hig ence book of every practitioner who has occasion library.-St. Louis Clin. Record, Sept. 1878. Also for sale separate- TTOLDEN (LUTHER), F.R.C.S., A-J- Surgeon to St. Bartholomew's and the Foundling Hospitals. LANDMARKS, MEDICAL AND SURGICAL. Second American, from the Third and Revised English Edition. In one handsome 12mo. volume, of about 140 pages. (Preparing.) TJEATH (CHRISTOPHER), F.R.C.S., II Teacher of Operative. Surgery in University College, London. PRACTICAL ANATOMY: A Manual of Dissections. From the Second revised and improved London edition. Edited, with additions, by W. W. Keen, M. D., Lecturer on Pathological Anatomy in the Jefferson Medical College, Philadelphia. In one handsome royal 12mo.volume of 578 pages, with 247illustrations. Cloth, $3 50 ; leather, $4 00. Henry C. Lea's Son & Co.'s Publications-(Anatomy). A LLEN (HARRISON), M.D. Professor of Physiology in the Univ, of Pa. A SYSTEM OF HUMAN ANATOMY: INCLUDING ITS MEDICAL and Surgical Relations. For the Use of Practitioners and Studentsof Medicine. With an Introductory Chapter on Histology. By E. 0. Shakespeare, M D., Ophthalmologistto the Phila. Hosp. In one large and handsome quarto volume, with several hundred original illustrations on lithographic plates, and numerous wood-cuts in the text. (Shortly.) In this elaborate work, which has been in active preparation for several years, the author has sought to give, not only the details ofdescriptive anatomy in a clear a nd condensed form, but also the practical applications of the science to medicine and surgery. The workthus has claims upon the attention of the general practitioner, as well as of the student, enabling him not only to re- fresh his recollections of the dissecting room, but also to recognize the significance of allvaria- tions from normal conditions. The marked utility of the object thus sought by the author is self-evident, and his long experience and assiduous devotion to its thorough development are a sufficient guarantee of the manner in which his aims have been carried out. No pains have been spared with the illustrations. Those of normal anatomy are from original dissections, drawn on stone by Mr. Hermann Faber, with the name of every part clearly engraved upon the figure, after the manner of "Holden" and "Gray," and in every typographical detail it will be the effort of the publishers to render the volume worthy of the very distinguished position which is anticipated for it. TALLIS (GEORGE VINER)~ AJ Emeritus Professor of Anatomy in University College, London. DEMONSTRATIONS OF ANATOMY; Being a Guide to the Know- ledge of the Human Body by Dissection. By George Viner Ellis, Emeritus Professor of Anatomy in University College, London. From the Eighth and Revised London Edition. In one very handsome octavo volume of over 700 pages, with 256 illustrations. Cloth, $4.25 ; leather, $5.25. (Now Ready.) This work has long been known in England as the leading authority on practical anatomy, and the favorite guide in the dissecting-room, as is attested by the numerous editions through which it has passed. In the last revision, which has just appeared in London, the accomplished author has sought to bring it on a level with the most recent advances of science by making the necessary changes in his account of the microscopic structure of the different organs, as devel- oped by the latest researches in textural anatomy. Ellis's Demonstrations is the favorite text-book | its leadership over the English manuals upon dis- of the English student of anatomy. In passing I sec ting.-Phila. Med. Times, May 24, 1879. through eight editions it has been so revised and ' adapted to the needs of the student that it would | a dissector, or a work to have in hand and seem that it had almost reached perfection in this \ studied while one is engaged in dissecting, we re- special line. The descriptions are clear, and the - 8afd it as the very best work extant, which is cer- methods of pursuing anatomical investigations are ' tainly saying a very great deal. As a text-book to given with such detail that the book is honestly , be studied in the dissecting-room, it is superior to entitled to its name.-St. Louis Clinical Record, anX of the works upon anatomy.-Cincinnati Med. June, 1879. News> MaX 24> 1879- The success of this old manual seems to be as well [ We most unreservedly recommend it to every deserved in the present as in the past volumes. ) practitioner of medicine who can possibly get it. The book seems destined to maintain yet for years 1 Va. Med. Monthly, June, 1879. WILSON (ER ASM US), F. R.S. F A SYSTEM OF HUMAN ANATOMY, General and Special. Edited by W. H. Gobrecht, M.D., Professor of General and Surgical Anatomy in the Medical Col- lege of Ohio. Illustrated with three hundred and ninety-seven engravings on wood. In one large and handsome octavo volume, of over 600 pages ; cloth, $4 ; leather, $5. ^MITH (HENRY H.), M.D., and JJORNER ( WILLIAM E.), M.D., Prof, of Surgery in the Univ, of Penna., &e. Late Prof, of Anatomy in the Univ, of Penna. AN ANATOMICAL ATLAS ; Illustrative of the Structure of the Human Body. In one volume, large imperial octavo, cloth, with about six hundred and fifty beautiful figures. $4 50. SCHAFER (ED WARD ALBERT), M.D., U Assistant Professor of Physiology in University College, London. A COURSE OF PRACTICAL HISTOLOGY: Being an Introduction to the Use of the Microscope. In one handsome royal 12mo. volume of 304 pages, with numerous illustrations: cloth, $2 00. (Just Issued.) HORNER'S SPECIAL ANATOMY AND HISTOL- for their Pass Examination. With engravings on OGY. Eighth edition, extensively revised and wood. In one handsome royal 12mo. volume, modified. In 2 vols. 8vo., of over 1000 pages, Cloth, $225. with 320 wood-cuts : cloth, $6 00. CLELAND'S DIRECTORY FOR THE DISSECTION SHARPEY AND QUAIN'S HUMAN ANATOMY. OF THE HUMAN BODY. In one small volume Revised, by Joseph Lbidy, M.D., Prof of Anat. royal 12mo. of 182 pages: sloth $1 25. °f °°?avo v°l,s-a?0®1 HARTSHORNE'S HANDBOOK OF ANATOMY AND 1300 pages, with 511 illustrations Cloth, $6 00. PHYSIOLOGY. Second edition, revised. In one BELLAMY'S STUDENT'S GUIDE TO SURGICAL royal 12mo. vol., with 220 wood-cuts; cloth ANATOMY : A Text-book for Students preparing 7o. Henry C. Lea's Son & Co.'s Publications-(Anatomy). 7 8 Henry C. Lea's Son & Co.'s Publications-{Physiology'). DALTON (J. C.), M.D., Professor of Physiology in the College of Physicians and Surgeons, New York, Ac. A TREATISE ON HUMAN PHYSIOLOGY. Designed for the use of Students and Practitioners of Medicine. Sixth edit., thoroughly revised and enlarged, with three hundred and sixteen illustrations on wood. In one very beautiful octavo vol- ume, of over 800 pages. Cloth, $5 50 ; leather, $6 50 ; half Russia, $7. (Lately Issued.} During the past few years several new works on phy-, served intact, the work in the present edition has been Biology, and new editions of old works, have appeared, brought up fully abreast of the times. The new chemical competing for the favor of the medical student, but । notation and nomenclature have also been introduced none will rival this new edition of Dalton. As now en- into the present edition. Notwithstanding the multi- larged, it will be found also to be, in general, a satisfac-1 plicity of text-books on physiology,this will lose none tory work of reference for the practitioner.-Chicago of its old time popularity. The mechanical execution Meh. Journ. and Examiner, Jan. 1876. of the work is all that could be desired.-Peninsular Prof. Dalton has discussed conflicting theories and Journal of Medicine, Dec. 1875. conclusions regarding physiological questions with a This popular text-book on physiology comes to us in fairness, a fulness, and a conciseness which lend fresh- its sixth edition with the addition of about fifty percent, ness and vigor to the entire book. But his discussions of new matter, chiefly in the departments of patho- have been so guarded by a refusal of admission to those logical chemistry and the nervous system, where the speculative and theoretical explanations, which at best principal advances have been realized. With so tho- existin the mindsof observers themselves as only pro- rough revision and additions, that keepthe work well liabilities, that none of his readers need be led into upto the times, its continued popularity may beconfi- grave errors while making them a study.-The Medical dently predicted, notwithstanding the competition it Record, Feb. 19,1876. may encounter. The publisher's work is admirably For clearness and perspicuity, Dalton's Physiology done. St. Louis Med. and Surg. Journ.,Dec. 1875 commended itself to the student years ago, and was a The revision of this great work has,brought it forward pleasant relief from the verbose productions which it । with the physiological advances of the day. and renders supplanted. Physiology has, however, made many ad-1 it, as it has ever been, the finest work for students ex- vances since then-and while the style has been pre- ant.-Nashville Journ.of Med. and Surg., Jan. 1876. (CARPENTER ( WILLIAM B^M. D., F. R. S., F.G.S., F.L.S., Registrar to University of London, etc. PRINCIPLES OF HUMAN PH YSIOLOGY; Edited by Henry Power, M.B. Lond., F.R.C.S., Examiner in Natural Sciences, University of Oxford. A new American from the Eighth Revised and Enlarged English Edition, with Notes and Addi- tions, by Francis G. Smith, M.D., Professor of the Institutes if Medicine in the Univer- sity of Pennsylvania, etc. In one very large and handsome octavo volume, of 1083 pages, with two plates and 373 engravings on wood. Cloth, $5 50; leather, $6 50 ; half Russia, $7. (Just Issued.) We have been agreeably surprised to find the vol-1 new a year or two ago, looks now as if it had been a ume so complete in regard to the structure and func- received and established fact for years. In this ency- tions of the nervous system in all its relations, a I clopaedic way it is unrivalled. Here, as it seems to subject that, in many respects, is one of the most diffi- us, is the great value of the book: one is safe in sending cult of all, in the whole range of physiology, upon a student to it for information on almost any given which to produce a full and satisfactory treatise of subject, perfectly certain of the fulness of information the class to which the one before us belongs. The it will convey, and well satisfied of the accuracy with additions by the American editor give to the work as which it will there be found stated.-London Med. it is a considerable value beyond that of the last Times and Gazette, Feb. 17, 1877. English edition. In conclusion, we can give ourcor- The meritsof "Carpenter's Physiology" are so widely dial recommendation to the work as it now appears. ttnnwn and appreciated that we need only allude briefly The editors have, with their additions to the only to the fact that in thelatestedition will be found a com- work on physiology in our language that, i n the full- prehensive embodiment of the results of recent physio- est sense of the word, is the production of a philoso- i0,rjca] investigation. Care has been taken to preserve pher as well as a physiologist, brought ri up as fully tbe practical character of the original work. In fact as could be expected, if not desired, to the standard tbe entire work has been brought up to date, and bears of our knowledge of itssubjectat the present day. evidence of the amount of labor that has been bestowed It will deservedly maintain the place it has always UpOn it by its distinguished editor, Mr. Henry Power, had in the favor of the medical profession. Journ. The American editor has made the latest additions, in of Nervous and Mental Disease, April, 1877. order fully to cover the time that has elapsed since the Such enormousadvances haverecentlybeen madein last English edition.-N. Y. Med. Journal, Jan. 1877. our physiological knowledge, that what was perfectly ROSTER {MICHAEL), M.D., F.R.S., J- Prof, of Physiology in Cambridge Univ., England. TEXT-BOOK OF PHYSIOLOGY. Latest edition. In one hand- some 12mo. vol. of over 800 pages, with 72 illustrations. Cloth, $3 00. (Just Ready.) This is a valuable addition to medical literature, । to the general practitioner as well, feeling confident constituting one of the most lucid expositions of the that an examination will result in a just apprecia- science of physiology in its most modern aspect, tion of its merits.-Southern Practitioner, Aug. It is one of the best books for the student that we 1880. have seen. While not so voluminous as some of the Dr Fof,ter ha8 comblned in this work the conflict. text-books that have heretofore been placed betoie jng desiderata in all text-books-comprehensive- students of medicine, it is lull and comprehensive, ness> brevity, and clearness. After a careful and embraces a thorough and. complete inyestiga- perusai of the whole work we can confidently re- tion of the many intricate problems ot the science of C0Iumeud it, both to the student and the practitioner life, fully brought up to the most recent standpoint. a, being one of the best text-books on physiology ex- We cordially commend it, not only to students, but tant -The London Lancet. LEHMANN'S MANUAL OF CHEMICAL PHYSIOL- LEHMANN'S PHYSIOLOGICAL CHEMISTRY. Com- OGY. Translated from the German, with Notes plete in two large octavo volumes of 1200 pages, and Additions, by J. Cheston Morris, M.D. With with 200 illustrations; cloth, $6. Illustrations on wood. In one octavo volume of 336 pages. Cloth, $2 25, J TTFIELD (JOHN). Ph.D., Il Professor ofPractical Chemistry to the Pharmaceutical Society of Great Britain. Ac. CHEMISTRY, GENERAL, MEDICAL AND PHARMACEUTICAL; Including the Chemistry of the U. S. Pharmacopoeia. A Manual of the General Principles of the Science, and their Application to Medicine andPharmacy. Eighth edition,revised by the author. In one handsome royal 12mo. volume of 700 pages, with illustrations. Cloth, $2 50 ; leather, $3 00. (Noro Ready.) We have repeatedly expressed our favorable of chemistry in all the medical colleges in the opinion of this work, and on the appearance of a United States. The present edition contains such new edition of it, little remains for us to say, ex- alterations and additions as seemed necessary for ceps that we expect this eighth edition to be as the demonstration of the latest developments of indispensable to us as the seventh and previous chemical principles, and the latest applications of editions have been. While the general plan and chemistry to pharmacy. It is scarcely necessary arrangement have been adhered to, new matter for us to say that it exhibits chemistry in its pre- has been added covering the observations made sent advanced state.-Cincinnati Medical News, since the former edition The present differs from April, 1879. the preceding one chiefly in these alterations and The popnlarity which this work has enjoyed is in about ten pages of useful tables added in the owing to the original and clear disposition of the appendix -Am. Journ. of Pharmacy, May, 18/9. facts of the science, the accuracy of the details, and A standard work like Attfield's Chemistry need the omission of much which freights many treatises only be mentioned by its name, without further heavily without bringing corresponding instruction comments. The present edilion contains such al- to the reader. Dr. Attfield writes for students, and terations and additions as seemed necessary for primarily for medical students; he always has an the demonstration of the latest developments of eye to the pharmacopoeia and its officinal prepara- chemical principles, and the latest applications of tions; and he is continually putting the matter in chemistry to pharmacy. The author has bestowed the text so that it responds to the questions with arduous labor on the revision, and the extent of which each section is provided. Thus the student the information thus introduced may be estimated learns easily, and can always refresh and test his from the fact that the index contains three hun- knowledge.-Med. andSurg. Reporter, Aprill9,'79. dred new references relating to additional mater- We noticed only about two years and a half ago ial.-Druggists' Circular and Chemical Gazette, the publication of the preceding edition, and re- May, 1879. marked upon the exceptionally valuable character This very popular and meritorious work has of the work. The work now includes the whole of now reached its eighth edition, which fact speaks the chemistry of the pharmacopeia, of the United in the highest terms in commendation of its excel- States, Great Britain, and India.-New Remedies, lence. It has now become the principal text-book May, 1879. (J REE NE (WILLIAM H.), M.D., Demonstrator of Chemistry in Med. Dept , Univ, of Penna. A MANUAL OF MEDICAL CHEMISTRY. For the Use of Students. Based upon Bowman's Medical Chemistry. In one royal 12mo. volume of 312 pages. With illustrations. Cloth, $1 75. (Now Ready.) It is well written, and gives the latest views on I The little work before us is one which we think vital chemistry, a subject with which most physi- will be studied with pleasure and profit. The de- cians are not sufficiently familiar. To those who ■ scrintions, though brief, are clear, and in most cases may wish to improve their knowledge in that direc sufficient for the purpose This book will, in nearly tion, we can heartily recommend this work as being all cases, meet general approval.-Am. Journ. of worthy ofa carefulperusal.-Phila. Med. and Surg. ■ Pharmacy, April, 1880. Reporter, April 24, 1880. (JLASSEN (ALEXANDER). Professor in th?Royal Polytechnic School, Aix la-Chapelle. ELEMENTARY QUANTITATIVE ANALYSIS. Translated with notes and additions by Edgar F Smith, Ph. D.. Assistant Prof, of Chemistry in the Towne Scientific School, Univ, of Penna. In one handsome royal 12ino. volume, of 324 pages, with illustrations; cloth, $2 00. (Just Ready.) It is probably the best manual of an elementary advancing to the analysis of minerals and such pro- nature extant, insomuch as its methods are the best, ducts as are met with in applied chemistry. It is It teaches by examples, commencing with single an Indispensable book for students in chemistry.-< determinations, followed by separations, and then | Boston Journ. of Chemistry, Oct. 1878. fl ALLOWAY (ROBERT), F.C.S., Ua Prof of Applied Chemistry in the Royal College of Science for Ireland, etc. A MANUAL OF QUALITATIVE ANALYSIS. From the Fifth Lon- don Edition. In one neat royal 12mo. volume, with illustrations ; cloth, $2 75. (Lately Issued.) REMSEN (IRA), M.D., Ph.D., Professor of Chemistry in the Johns Hopkins University, Baltimore. PRINCIPLESOF THEORETICAL CHEMISTRY, with special reference to the Constitution of Chemical Compounds. In one handsome royal 12mo. vol. of over 232 pages: cloth, $1 50. (Just Issued.) BOWMAN'S INTRODUCTION TO PRACTICAL WOHLER AND FITTIG'S OUTLINES OF ORGANIC CHEMISTRY, INCLUDING ANALYSIS. Sixth CHEMISTRY Translated with additions from the American, from the sixth and revised London edi- Eighth German Edition By Ira Remsen. MD., tion. With numerous illustrations. In one neat Ph D., Prof. ofChemistry and Physics in Williams vol., royal 12mo., cloth, $2 25. College, Mass. In one volume, royal 12mo. of 550 pp., cloth, $3. Henry C. Lea's Son & Co.'s Publications-(Chemistry). 9 10 Henry C. Lea's Son & Co.'s Publications-(Chemistry'). mWNES (GEORGE), Ph.D. X A MANUAL OF ELEMENTARY CHEMISTRY; Theoretical and Practical. Revised and corrected by Henry Watts, B. A., F R.S., author of "A Diction- ary of Chemistry," etc. With a colored plate, and one hundred and seventy-seven illus- trations. A new American, from tht Twelfth and enlarged London edition. Edited by Robert Bridges, M.D. In one large royal 12mo. volume, of over 1000 pages ; cloth, $2 75; leather, $3 25. (Just Issued.) This work, Inorganic and organic, is complete in what formidable magnitude with its more than a one convenient volume. In its earliest editions it thousand pages, but with less than this no fair repre- was fully up to the latest advancements and theo- sentation of chemistry as it now is can be given. The ries of that time. In its present form, it presents, type is small but very clear, and the sections are very in a remarkably convenient and satisfactory man- lucidly arranged to facilitate study and reference.- nor, the principles and leading facts of thechemistry Med. and Surg. Reporter, Aug 3, 1878 of to-day. Concerning the manner in which the The work ig too well known to American gtudent8 various subjects are treated, much deserves to be to need any extended notice; suffice it to say that said, and mostly, too, in praise of the book. A re- the revision by the English editor has been faithfully view of such a work as Fownes s Chemistry within done and thal Profef8or Bridges hag added gome the 1 nuts of a book-notice for a medical weekly is fregh aQd valuabie matt especially in the inor- simply out otthe question.-Cincinnati Lancet and ganic chemistry. The book has always been a fa- Olmic, Dec. it, is/s. vorite in this country, and in its new shape bids When we state that, in our opinion, the present fair to retain all its former prestige.-Boston Jour. edition sustains in every respect the high reputation of Chemistry, Aug. 1878. which its predecessors have acquired and enjoyed, It will be entirely unnecessary for us to make any we express therewith our full belief in its intrinsic remarks relating to the general characterof Fownes' value as a text-book and work ot reference.-Rm. Manual. For over twenty years it has held the fore- Journ. of Pharm., Aug. 1878. most place as a text.bo'£ and the elaborate and The conscientious care which has been bestowed thorough revisions which have been made from time upon itby the American and English editors renders to time leave lit tie chance for any wide awake rival to i t still, perhaps, the best book for the student and the steP before it.-Canadian Pharm. Jour., Aug. 1878. practitioner who would keepalive the acquisitions As a manual of chemistry it is without a superior of his student days. It has,indeed, reached a some- in the language.-Md. Med. Jour., Aug. 1878. DLOXAM (C. L.), A-' Professor of Chemistry in King's College, London. CHEMISTRY, INORGANIC AND ORGANIC. From the Second Lon- don Edition. In one very handsome octavo volume, of 700 pages, with about 300 illus- trations. Cloth, $4 00; leather, $5 00. (Lately Issued.) We have in this work a completeand most excel-] It would be difficult for a practical chemist and lent text-book for the use of schools, and can heart- teacher to find any material fault with this most ad- ily recommend it as such.-Boston Med. and Surg. mirable treatise. The author has given us almost a J ourn., May 28, 1874. cj clopsedia within the limits of aeon venient volume, The above is the title of a work which we can most and has done so without penning the useless para- conscientiously recommend to students of chemis- graphs too commonly making up a great part of the try. It is as easy as a work on chemistry could be bulk of many cumbrous works. The progressive made, at thesarne time that it presentsa full account 8c*6ntist is not disappointed when he looks for the of th atscience as it now stands. We have spoken j"ecor(i o* new and valuable processes and discover- ofthe work as admirably adapted to the wants of >e«, while the cautious conservative does not find its students; it is quite as well suited to the require- Pa«eK monopolized by uncertain theories and specu- ments of practitioners who wish to review their a . A Peculiar pomt of excellence is the crys- chemistry, or have occasion to refresh their memo- lal'lzed of expression in which great truths are ries on any point relating to it. Ina word, it is a °,n8 book to be read by all who wish to know what is h r b important topic, and HiGnkAmLuw ahla4 • tv yet, after reading it, he feels that little, if any more S 1R7V should have been said. Altogether, it is seldom yoa ' ' ' see a text-book so nearly faultless. - Cincinnati Lancet, Nov. 1873. rtLOWES (FRANK), D.Sc., London. Senior Science- Master at the High School, Newcastle-under-Lyme, etc. AN ELEMENTARY TREATISE ON PRACTIC AL CHEMISTRY AND QUALITATIVE INORGANIC ANALYSIS. Specially adapted for Use in the Laboratories of Schools and Colleges and by Beginners. Second American from the Third and Revised English Edition. In one very handsome royal 12mo. volume of 372 pages, with 47 illustrations. Cloth, $2 50. (Just Ready.) This is a valuable work for those about to com- ference and instruction in his library. As a rule, mence chemistry, the more so as by its use they are such volumes are too technical and abstruse for simultaneously acquainted with the manipulation study without some didactic aid, but the volume of chemical analysis, a method which is the most piesented is easy of comprehension, and will be of valuable to impa i t a thorough knowledge of chemis- great value to college stud°nts and busy practition- try. It is a very good little book, and will make ers.-N. Y. Am. Med. Bi-Weekly, April9, 1881. for itself many warm friends and supoorters. It mi, „ „„ , - treats the subject well and the tables are very clear O-T j tab 88 Particularly demand praise, for they and valuable.-St. Louis Med. and Surg. Journ., ? rorn,ed-fbo'h for convenience of re- Mar. 1881. ference and tulness of information. In short, we ' ' do not remember to have met with a book which Ihis work is not only well adapted for use as a could better serve the stud- nt as a guide to the sys- text-book in medical colleges, but is also one of the tematic study of inorganic chemistry.-Louisville best that a practitioner can have for convenient re- Med. News, March 12, 1881. KNAPP'S TECHNOLOGY; or Chemistry Applied to t very ha ndsome octavo volumes, with 500 wood the Arts and to Manufactures. With American engravings,cloth, $6 00. additions by Prof. Walter R. Johnson. In two 1 Henry C. Lea's Son & Co.'s Publications-(Phar., Mat. Med., etc.). pARRISH (ED WARD), Late Professor of Materia Medica in the Philadelphia College of Pharmacy. A TREATISE ON PHARMACY. Designed as a Text-Book for the Student, and as a Guide for the Physician and Pharmaceutist. With many Formulae and Prescriptions. Fourth Edition, thoroughly revised, by Thomas S. Wiegand. In one handsome octavo volume of 977 pages, with 280 illustrations ; cloth, $5 50 ; leather, $6 50; half Russia, $7. (Lately Issued.} Of Dr Parrish's great work on pharmacy it only the work, not only to pharmacists, but also to the remains to be said that the editor has accomplished multitude of medical practitioners who are obliged his work so well as to maintain, in this fourth edi- to compound their own medicines It will ever hold tion, the high standard of excellence which it bad j an honored place on our own bookshelves.-Dublin attainedin previous editions, under the editorship of i Med. Press and Circular, Aug. 12, 1874. its accomplished author. This has not been accom ~ , . . , , plished without much labor.and many additions and , We expressed our opinion of a former edition in improvements, involving changes in the arrange- e""8 of unqualified praise, and we are in no mood mentof the several parts of the work, and the addi- t0 detract from that opinion in reference to the pre- tion of much new matter. With the modifications sent edition, the preparation of which has fallen in to thus effected it constitutes as now presented, a com competent hands. It is a book with which no pharma- pendium of the science and art indispensable to the cist can dispense, and from which no physician can pharmacist, and of the utmost value to every ; fal1 der^e much information of value to him in practitioner of medicine desirous of familiarizing; Practice. Pacific Med and Surg. Journ., June, 74. himself with the pharmaceutical preparation of the Perhaps one, if not the most important book upon articles which he prescribes for his patients. Chi-■ pharmacy which has appeared in the English lan- cago Med. Journ., July, 1874. guage has emanated from the transatlantic press. The work is eminently practical, and has the rare1 " Parrish's Pharmacy" is a well-known work on this merit of being readable a nd interesting, while it pre- side of the water and the fact shows us that a really serves astrictly scientificcharacter The whole work j useful work neverbecomes merely local in its fame, reflects the greatest credit on author,editor and pub I Thanks to the j udicious editing of Mr. Wiegand, the lisher It will convey so me idea of the liberality which I posthumous edition of " Parrish" has been saved to has been bestowed upon its production when we men- the public with all the mature experience of its au- tion that there are nolessthan 280 carefully executed thor, and perhaps none the worse for a dash of new illustrations. In conclusion, we heartily recommend blood.-Land. Pharm. Journal, Oct. 17, 1874. QR IFF I TH (ROBERT E.), M.D. A UNIVERSAL FORMULARY, Containing the Methods of Prepar- ing and Administering Officinal and other Medicines. The whole adapted to Physiciar s and Pharmaceutists. Third edition, thoroughly revised, with numerous additions, b; John M. Maisch, Professor of Materia Medicain the Philadelphia College of Pharmacy. In one large and handsome octavo volume of about800pp., cl., $450 ; leather, $5 50. (Lately Issued.) To the druggist a good formulary is simply indis-1 A more complete formulary than it is in its pres- pensable, and perhaps no formulary has been more i ent form the pharmacist or physician could hardly extensively used than the well-known work before desire. To the first some such work is indispensa- us. Many physicians have to officiate, also, as drug ble, anditis hardly less essential to the practitioner gists. This is true especially of the country physi- who compounds his own medicines. Much of what cian, and a work which shall teach him the means is contained in the introduction ought to be com- bv which to administer or combine his remedies in mitted to memory by every student of medicine, the most efficacious and pleasant manner, will al- * As a help to physicians it will be found invaluable, ways hold its place nponhisshelf A formulary of | and doubtless will make its way i nto libraries n ot this kind is of benefit also to the city physician in already supplied with a standard work ofthe kind, largest practice.-Cincinnati Clinic, Feb. 21. 1874.1 - The American Practitioner, Louisville, July, '74. TjIARQUHARSON (ROBERT). M.D., Lecturer on Materia Medica at St. Mary's Hospital Medical School. A GUIDE TO THERAPEUTICS AND MATERIA MEDICA. Se- cond American edition, revised by the Author. Enlarged and adapted to the U. S. Pharmacopoeia. By Frank Woodbury, M.D. In one neat roy al 12mo. volume of 498 pages: cloth, $2 25. (Just Ready.) The appearanee of a new edition of this conve- copious notes have been introduced, embodying the nient and handy book in less than two years may latest revision of the Pharmacopoeia, together wi'h certainly be taken as an indication of its useful- the antidotes to the more prominent poisons, and ness. Its convenient arrangement, and its terse- such of the newer remedial agents as seemed neces- ness, and, at the same time, comoletene»s of the sary to the completeness of the work. Tables of information given, make it a handy book of refer- weights and measures, and a good alphabetical in- ence.-Am. Journ. of Pharmacy, June, 1 879. dex end the volume.-Druggists' Circular and This work contains in moderate compass such Chemical Gazette, June, 1879. well-digested facts concerning the physiological It is a pleasure to think that the rapidity with and therapeutical action of remedies as are reason- which a second edition is demanded may be taken ably established up to the present time. By a con- as an indication that the sense of appreciation of the venient arrangement the eorrespondirg effects of value of reliable information regarding the use of each article in health and disease are presented in remedies i not entirely overwhelmed i n the cultiva- parallel c lumns, not only rendering reference tion of pathological studies, characteristic of the pre- easier but also impressing the facts more strongly sent day. This work certainly merits the success it noon the mind of the reader. The book has been has so quickly achieved.-New Remedies, July, '79. adapted to the wants of the American student, and CHRISTISON'S DISPENSATORY. With copious ad- CARPENTER'S PRIZE ESSAY ON THE USE OF ditions. and 213 large wood engravings By R. Alcoholic Liquors in Health and Disease. New Eolesfield Griffith, M.D. One vol. 8vo., pp. edition, with a Preface by D. F Condib. M.D., and 1000, cloth, $4 00. explanations of scientific words. In oneneatl2mo. volume, pp. 178, cloth, 60 cents. 11 12 SJTILLE {ALFRED), M.D., LL.D., and TfAJ^CH {JOHN M.). Ph.D., Prof, of Theory and Practice of Medicine -LU. Pr^f. of Mat. Med. and Hot in Phila. and of Clinical Med. in Univ, of Pa. Coll. Pharmacy, Secy, to the American Pharmaceutical Association. THE NATIONAL DISPENSATOBY: Containing the Natural History, Chemistry, Pharmacy, Actions and Uses of Medicines, including those recognized in the Pharmacopoeias of the United States, Great Britain and Germany, with numer- ous references to the French Codex. Second edition, thoroughly revised, with numerous additions. In one very handsome octavo volume of 1692 pages,with 239 illustrations. Extra cloth, $6 75 ; leather, raised bands, $7 50 ; half Russia, raised bands and open hack, $8 25. (Now Ready.) Preface to the Second Edition. The demand which has exhausted in a few months an unusually large edition of the National Dispensatory is doubly gratifying to the authors, as showing that they were correct in thinking that the want of such a work was felt by the medical and pharmaceutical professions, and that their efforts to supply that want have been acceptable. This appreciation of their labors has stimulated them in the revision to render the volume more worthy of the very marked favor with which it has been received. The first edition of a work of such magnitude must necessarily be more or less imperfect; and though but little that is new and important has been brought to light in the short interval since its publication, yet the length of time during which it was passing through the press rendered the earlier portions more in arrears than the la'er. The opportunity for a revision has enabled the authors to scrutinize the work as a whole, and t® introduce alterations and additions wherever there has seemed to be occasion for improve- ment or greater completeness. The principal changes to be noted are the introduction of seve- ral drugs under separate headings, and of a large number of drugs, chemicals and pharma- ceutical preparations classified as allied drugs and preparations under the heading of more important or better known articles: these additions comprise in part nearly the entire German Pharmacopoeia and numerous articles from the French Codex. All new investigations which came to the authors' notice up to the time of publication have received due consideration. The series of illustrations has undergone a corresponding thorough revision. A number have been added, and still more have been substituted for such as were deemed less satisfactory. The new matter embraced in the text is equal to nearly one hundred pages of the first edition. Considerable as are these changes as a whole, they have been accommodated by an enlargement of the page without increasing unduly the size of the volume. While numerous additions have been made to the sections which relate to the physiological action of medicines and their use in the treatment of disease, great care has been taken to make them as concise as was possible without rendering them incomplete or obscure. The doses have been expressed in the terms both of troy weight and of the metrical system, for the purpose of making those who employ the Dispensatory familiar with the latter, and paving the way for its introduction into general use. The Therapeutical Index has been extended by about 2250 new references, making the total number in the present edition about 6000. The articles there enumerated as remedies for particular diseases are not only those which, in the authors' opinion, are curative, or even beneficial, but those also which have at any time been employed on the ground of popular belief or professional authority. It is often of as much consequence to be acquainted with the worthlessness of certain medicines or with the narrow limits of their power, as to know the well attested virtues of others and the conditions under which they are displayed. An additional value possessed by such an Index is, that it contains the elements of a natural classification of medicines, founded upon an analysis of the results of experience, which is the only safe guide in the treatment of disease. This evidence of success, seldom paralleled, keep the work up to the time.-New Remedies, Nov. shows clearly how well the authors have met the 1879. existing needs of the pharmaceutical and medical This is a great work by twfi of the ablest writers on professions. Gratifying as it must be to them, they materia medica in America The authors have pro- have embraced the opportunity offered for a thor- ] (juce(j a WOrk which, for accuracy and comprehensive- ough revision of the whole work, striving to em- j negs, js unsurpassed by any work on the subject. There brace within it all that might have been omitted in js no book jn the English language -which contains so the former edition, and all that has newly appeared | mucb vaiuable information on the various articles of of sufficient importance during the time of its col- [be materia medica. The work has cost the authors laboration, and the short i nterva.1 elapsed since the , years of laborious study, but they have succeeded in previous publication. Alter having gone carefully producing a dispensatory which is not only national, through the volume we must admit that the authors but will be a lasting memorial of the learning and have labored faithfully, and with success, in main- ab,litv of the authors who produced it.-Edinburgh taining the high character of their work as a com- Medical Journal, Nov. 1879. pendium meeting the requirements of the day, to ' . .. , ■ , .. which one can safely turn in quest of the latest in- H 18 V faJ m°r8'"'^national or universal than formation concerning everything worthy of notice in any other book of the kind in our language, and connection with Pharmacy, Materia Medica, and more comprehensive in every sense.-Pacific Med. Therapeutics.-Am. Jour, of Pharmacy, Nov. 1879. and SurO- J^m., Oct. 1879. It is with great pleasure that we announce to our Th® National Dispensatory is beyond dispute the readers the appearance of a second edition of the very best authority. It is throughout complete in National Dispensatory. The total exhaustion of the al l the necessary details, clear and lucid in its ex- first edition in the short space of six months, is a planations, and replete with references o the most sufficient testimony to the value placed upon the further particulars can be work by the profession. It appears that the rapid obtained, if desired. Its value is greatly enhanced sale of the first edition must have induced both the }he extensive indmes-a general index of materia editors and the publisher to make preparations for medica, etc., and also an index of therapeutics It a new edition immediately after the first had been ™uld be a work of supererogation to say more about issued, for we find a large amount of new matter this well-known work No practising physician can added and a good deal of the previous text altered afford to be without the National Dispensatory, and improved, which proves that the authors do not Canada Med. and Surg. Journ., Feb. 1880. intend to let the grass grow under their feet, but to Henry C. Lea's Son & Co.'s Publications-(Mat. Med. and Therap.). Henry C. Lea's Son & Co.'s Publications-(Mat. Med., Therap., etc.). J^AISCH {JOHN M.), Phar. D., Prof, of Materia Medica and Botany in the Phil a. Coll. of Pharmacy. A MANUAL OF ORGANIC MATERIA MEDICA. Being a Guide to Materia Medica of the Vegetable and Animal Kingdoms. For the use of Students, Druggists, Pharmacists and Physicians. In one handsome 12mo. volume, with numer- ous illustrations on wood. (Preparing.) EXTRACT FROM THE AUTHOR'S PREFACE. When in 1866 the author was called to the chair of Materia Medica in the institution named (the Philadelphia College of Pharmacy), he seriously felt the need of a suitable text book which could be used in connection with his lectures, and made preparations for the publication of such a work at an early date. To elaborate a system of classification, which should be with- out difficulty comprehended and readily applied by those for whom it was intended, was by no means an easy task, and the author found occasion, almost every year, to either remodel that previously selected, or to make what in his opinion seemed to be desirable improvements. The publication of the " National Dispensatory" in a measure supplied the want felt, at least as far as a work of reference is corn-err ed, but owing to its local arrangement, it is not adapted to systematic instruction. However, its publication rendered a modification of the original plan for a treatise on Materia Medica desirable, and it is now presented in a form giving an outline of the substance of the lectures and embracing what are considered the essential physical, histo- logical, and chemical characters of the organic drug, so as to render the work also a useful and reliable guide in business transactions. Regarding the classification, the author is conscious of its imperfections, but he believes it to be convenient and capable of practical application. In reference to the scope of the work, the main aim has been to embrace all the drugs recog- nized by the U. S. Pharmacopoeia, together with the old, but now unofficinal ones, and such others, the use of which has been recently re rived or suggested, and which seem to deserve attention. The medical properties and doses of the various drugs are merely briefly stated as subjects of general important information ; the present work is not intended for giving instruc- tion in the therapeutic application of drugs. jgTILLE {ALFRED), M.D., Professor of Theory and Practice of Medicine in the University of Penna. THERAPEUTICS AND MATERIA MEDICA ; a Systematic Treatise on the Action and Uses of Medicinal Agents, including their Description and History. Fourth edition, revised and enlarged. In two large and handsome 8vo. vols. of about 2000 pages. Cloth, $10; leather, $12; half Russia, $13. (Lately Issued.) It is unnecessary to do much more than to an- of the present edition, a whole cyclopaedia of thera- nounce the appearance of the fourth edition of this peutics.-Chicago Medical Journal, Feb. 1875. well known and excellent work. Brit, and For. The rapid exhaustion of three editions and the uni- Med.-Chir. Review, Jet 187a. versal favor with which the work has been received For all who desire a complete work on therapeu- by the medical profession, are sufficient proof of its tics and materia medica for reference, in cases in- excellence as a repertory of practical and usefulin- volving medico-legal questions, as well as forin- formation for the physician. The edition before us formation concerning remedial agents, Dr. Stille's is fully sustains this verdict, as the work has been care- "-par excellence" the work. Being out of print, by fully revised and in some portions rewritten, bring- the exhaustion of former editions, theauthor has laid ing it up to the present time by the admission of the profession under renewed obligations, by the chloral and croton-chloral, nitrite of amyl, bichlo- careful revision, importantadditions, and timely re- ride of methylene, methylic ether, lithium com- issuing a work not exactly supplemented by any pounds, gelseminum, and other remedies.-Am. other in the English language, if in any language. Journ. of Pharmacy, Feb. 1875. The mechanical execution handsomely sustains the We can hardly admit that it has a rival in the well-known skill and good taste ot the publisher.- multitude of its citations and the fulness of its re- St. Louis Med. and Surg. Journal, Dec. 1874. search into clinical histories, and we must assign it From the publication of the first edition "Stilld's a place in the physician's library ; not, indeed, as Therapeutics" has been one of the classics; its ab- fully representing the present state of knowledge in sence from our libraries would create a vacuum pharmacodynamics, but as byfarthe most complete which could be filled by no other work in the lan- treatise upon the clinical and practical side of the guage.andits presence supplies, in the two volumes question.-Boston Med. and Surg. Journal, Nov. 5, 1874. (JORNIL (K), AND TJANVIER {L.), Prof, in the Faculty of Med , Paris. J- Prof in the College of France. MANUAL OF PATHOLOGICAL HISTOLOGY. Translated, with Notes and Additions, by E. 0. Shakespeare, M.D., Pathologist and Ophthalmic Surgeon to Pbilada. Hospital, Lecturer on Refraction and Operative Ophthalmic Surgery in Univ, of Penna., and by Henry C. Simes. MD., Demonstrator of Pathological Histology in the Uniy. of Pa. In one very handsome octavo volume of over 700 pages, with over 350 illustrations. Cloth, $5 50; leather, $6 50; half Russia, $7. (Just Ready.) We have nohesitation in cordially recommending the subject admits of definition, and this one chap- the English translation ofCornil & Ranvier's ''Pa- ter is worth the price of the bonk The illustra- thological Histology" as the best work of the kind tions are copious and well chosen. Without the in any language, and as giving to its readers a slightest hesitation, the translators deserve honest trustworthy guide in obtaining a broad and solid thanks for placing this indispensable work in the basis for the appreciation of the practical bearings hands of American students.-Phila. Med. Times, of pathological anatomy.-Am. Journ. of Med. April 24, 1880 Sciences, Aoril, 1880. This volume we cordially commend to tbeprofes- Tbis important work, in its American dress, is a sion. It will prove a valuable, almost necessary welcome offering to all students of the subjects addition to the libraries of students who are to be which it treats. The great mass of material is physicians, and to the libraries of students who are arranged naturally and comprehensively. The physicians.-American Practitioner, June, 1880. classification of tumors is clear and full, so far as 13 14 RENWICK (SAMUEL), M.D., J- Assistant Physician to the London Hospital, THE STUDENT'S GUIDE TO MEDICAL DIAGNOSIS. From the Third Revised and Enlarged English Edition. With eighty-four illustrations on wood. In one very handsome volume, royal 12mo., cloth, $2 25. {Just Issued.) (JREEN (T. HENRY),M.D., '-J Lecturer on Pathology and Morbid Anatomy at Charing-Cross Hospital Medical School, etc. PATHOLOGY AND MORBID ANATOMY. Fourth American.from the Fifth Enlarged and Revised English Edition. In one very handsome octavo volume of about 350 pages, with 138 fine engravings ; cloth, $2 25. {Just Ready.) Extract from the Author's Preface. In preparing the fifth edition of my Text-book on Pathology and Morbid Anatomy, I have again added much new matter, with the object of making the work a more complete guide for the student. All the chapters have been carefully revised, some alterations have been made in the arrangement of the work, and an addition has been made to the number of wood-cuts. The new wood cuts, as in previous editions, have been drawn by Mr. Collings from my own micro- scopical preparations; We have long considered this the best guide yet | been thoroughly revised, and much new matter presented to the student for the identification of va- 1 has been added. To the physician as a guide in rious morbid tissues. We h i ve found it moresaiis- i diagnosis, we recommend this volume.-Physician factory than any other. The present edition has I and Surgeon, May, 1881. 1DRISTO WE {JOHN SYER), M.D., FR.C.P., JU Physician and Joint Lecturer on Medicine, St Thomas's Hospital. A TREATISE ON THE PRACTICE OF MEDICINE. Second American edition, revised by the Author. Edited, with Additions, by James H. Hutch- inson, MD., Physician to the Penna. Hospital. In one handsome octavo volume ol nearly 1200 pages. With illustrations. Cloth, $5 00; leather, $6 00; half Russia, $6 50. (Noto Ready.) The second edition of this excellent work, like the i The views of the author are expressed with preci- first, has received the benefit of Dr. Hutchinson's sion and sufficient promptness toimpressthe student annotations, by which the phases of disease which i with the weight of his authority ; and should the are peculiar to this country are indicated, and thus | medical professor differ on any subject from his doc- a treatise which was intended for British practi- trine, hewill need to find strong arguments to carry tioners and students is made more practically nstful i his class to the opposite conclusion.-N. 0. Med. and on this side of the water. We see no reason to Surg. Journ , Feb. 1880. modify the high opinion previously expressed with The readsr wU1 find every conceivable subject regard to Dr. Bristowe s work, except by adding connected with the practice of medicine ably pre- our appreciation of the careful labors of the author seHted, in a stvle at once clear interesting, and con- in following the lateral growth of medical science. cj8e The additions mide by Dr. Hutchinson are Boston Medical and Surgical Journal, February, approptiate and practical, and greatly add to its 1880. usefulness to American readers. - Buffalo Med. and What we said of the first edition, we can, with Surg. Journ., March, 1880. increased emphasis, repeat concerning I his: ''Every We rega,dit as an excellent work forstudentsiand page is cha racterized by the utterances of a thought- for practitioners. It is clearly written, the author's ful man. W iat has been said, has been well said, -tyje attractive, and it is especially to be com- and the book is a fair reflex of all that is certainly meaded foritg excellent exposition of the pathology known on the subjects considered. Ohio Med and clinical phenomena of disease.-St. Louis Clin. Recorder, Jan. 7, 1880. Record, Feb. 1880. LJABERSHON (S. O.). M.D. J-J- Senior Physician to, and late Lecturer on the Principles and Practice of Medicine at, Guy's Hospital, etc. ON THE DISEASES OF THE ABDOMEN, COMPRISING THOSE of the Stomach, and other parts of the Alimentary Canal, (Esophagus, Caecum, Intes- tines and Peritoneum. Second American, from the Third enlarged and revised Eng- lish edition. With illustrations. In one handsome octavo volume of over 500 pages. Cloth, $3 50. {Now Ready.) This valuable treatise on diseases of the stomach amended by the author. Several new chapters have and abdomen has been out of print for several years, been added, bringing the work t'nlly up to the times, and is therefore not so well known to the profession and making it a volume of interest to the practi- as it deserves to be. It will be found a cyclopaedia tioner in every field of medicine and surgery. Per- of information, systematically arranged, on all dis- verted nutrition is in some form associated with all eases of the alimentary tract, from the mo ith to the diseases we have to combat, and we need all the rectum A fair proportion of each chapter is devoted light that can he obtained on a subject so broad and to symptoms pathology, and therapeutics. The general. Dr Habershon's work is one that every present edition is fuller than former ones in many practitioner ah mid read and study for himself.- particulars, and has been thoroughly revised and -V. K Med. Journ , April, 1879. GLUGE'S ATLAS of PATHOLOGICAL HISTOLOGY. PAVY'S TREATISE ON THE FUNCTION OF DI- Translated, with Notes and Additions, by Joseph GESTION: its Disorders and their Treatment. Lewy, M. D. In one volume, very large imperia) From the Second London edition In one hand- quarto, with 320 copper-plate figures, plain and some volume, small octavo, cloth, $2 00. colored, cloth. $4 00 HOLLAND'S MEDICAL NOTES AND REFLEC- LA ROCHE ON YELLOW FEVER.considered in its TIONS. 1 vol 8vo., pp. 500, cloth. $3 50 Historical, Pathological, Etiological and Thera BARLOW'S MANUAL OF THE PRACTICE OF peutlcal Relations. In two large and handsome . MEDICINE. With Additions by D. F.Condie, octavo volumes of nearly 1500 pp , cloth $7 00. yj n 1 vol 8vo., pp. 600. cloth. 4:2.50. STOKES' LECTURES ON FEVER Edited by John tODD'SCLINICAL LECTURESonCERTAIN ACUTE WilliAm Moore, M. D., Assistant Physician to the Diseases. In one neat octavo volume, of 320 pp. Cork Street Fever Hospital. In one neat 8vo cloth $2 50 volume cloth, $2 00. Henry C. Lea's Son & Co.'s Publications-(Pathology, etc.). Henry C. Lea's Son & Co.'s Publications-(Practice of Medicine}. JjTLINT (A USTIN), M.D., Professor of the Principles and Practice of Medicine in Bellevue Med. College, N. Y. A TREATISE ON THE PRINCIPLES AND PRACTICE OF MEDICINE ; designed for the use of Students and Practitioners of Medicine. Fifth edition, entirely rewritten and much improved. In one large and closely printed octavo volume of 1153 pp. Cloth, $5 50; leather, $6 50; very handsome half Russia, raised bands, $7. (Just Ready.) Practically, this edition is a new work; for so The style and character of this work are too well many additions and changes have been made that known to the profession to require an introduction, one well acquainted with previous editions would For a number of years this volume has occupied a hardly recognize this as an old friend The size of leading position as a text-book in the majority of the volume is somewhat increased. An entire new medical schools, and the high position accorded to section and several new chapters have been added, it in the past is a guarantee of a hearty welcome in It is universally conceded that no text book upon this new edition The book may be said to represent this subject was ever published in this country the present state of the science of medicine as now that can at all compare with it. It has long been understood and taught. It is a safe guide to students at the very head of American text-book literature, and practitioners of medicine.-Maryland Medical and there can be no doubt but that it will be many Journal, March 1, 1881. years before it yields the place to others.-Wa«4- A marked feature of valu0 in the n0w 0dition of ville Journ. of Med. and Surg , Feb. 1881. Fliat is th0 condpn^ed ,.ection on morbid anatomy "Flint's Practice'' is recognized to be a standard prefacing each subject discussed, and the very good treatise of high rank upon the principles and the prefix on general pathology, chapters all of them practice of medicine wherever the English language written, as the author states in hi' preface, by Ur. is read. The opinions everywhere reveal the man Wm. H. Welch, lecturer on pathological histology of extensive experience, diligent study, calm judg- in Bellevue Hospital Medical College. Dr. Welch ment, and unbiassed criticism. The work should has done his part of the work to all acceptation.- be in the hands of every practitioner.-New York Cincinnati Lancet and Clinic March 12 1881. Me.d. Record, Feb. 26, 1881. The aulbor has, in this edition, revised and re- This edition differs so much from all previous written a great part and made it accord with the editions, on account of the revisions eliminations, more advanced ideas which have been developed amplifications, and additions, so conspicuously ma within the past few years. He is the more fitted to nifest, that no one can be said to possess toe actual do so, as he is actively engaged in his profession, viewsof the author on the practice of medicine, un- and can make deductions, not from the work of less he becomes the possessor of this volume It is others, but from his own labors. It is a treatise certainly the only American work on this subject wnich every American physician should have upon which can be unreservedly recommended, and the his table, and which he should consult on occasions only one which does justice to American authors, when his leisure permits him to do so.-St. Louis observers, and practitioners. - Gaillard's Medical Med. and Surg. Journal, March, 1881. Journal, Feb. 1881. J^Y THE SAME AUTHOR. CLINICAL MEDICINE; a Systematic Treatise on the Diagnosis and Treatment of Diseases. Designed for Students and Practitioners of Medicine. In one large and handsome octavo volume of 795 pages; cloth, $4 50 ; leather, $5 50; half Russia, $6. (Now Ready.) The eminent teacher who has written the volume in this country as that of the author of two works under consiieration has recognized the needs of of great merit on special subjects, and of numerous the American profession, and the result is all that papers, exhibiting much originality and extensive we could wish. The style in which it i written is research. - The Dublin Journal, Dec. 1879. KKJrh a"th7'8; " is. C'ear aad 'o™ble, ^d There ls ev reafion to beliere that tM book f " W s'® be weH received. The active practitioner is denredZ the best writers and teachers this frequently in n0ed of 80me work thlat win enable «bn" 7 bas ever produced We have not space for him4 to /btain iaforniation in the diagnosis and t^deration of this remarkable work as treatment of cases with comparatively little labor. we would d^rc.-St. Lome Clm. Record, Oct. 1879. Dr Flint bas the faculty 'of expre4ing bimgelf It is here that the skill and learning of the great clearly, and at the same time so concisely as to clinician are displayed He has given us a store- enable the searcher to traverse the entire ground house of medical knowledge, excellent for the stu- of his search, and at the same time obtain all that dent, convenient for the practitioner, the result of a is essential, without plodding through an intermi- long life of the most faithful clinical work, collect- nab'e space.-N. Y. Med. Jour.. Nov. 1879 Sy8teraaJie as,un- The great object is to place before the reader the tr> h e£bed by a ju gment no less clear ial0!d observations a nd experience in diagnosis atid ctne D e £70' '°n 18 elose-~^chives of Medu tr0at neQt. Such a w .rk is especially valuable to ' ec' ' y students. It is complete in its special design, and To give an adequate and useful conspectus of the yet so condensed, that he can by its aid, keep up extensive field of modern clinical medicine is a task with the lectures on practice without neglecting of no ordinary difficulty; but to accomplish this o'her branches. It will not escrpe the notice of the consistently, with brevity and clearness, the diff'rent practitioner that such a work is most valuable in subjects and their several parts receiving the atten- culling points in diagnosis and treatment in the in- tion which, relatively to their importance, medical tervals between the daily rounds of visits since he opinion claims for them, is still more difficult. This can in a few minutes refresh his memory, or learn task we feel bound to say has been executed wi»h the latest ad vance in the treatment of diseases which more than partial success by Dr Flint, whose name demand his instant a'tention.-Cincinnati Lancet is already familiar to students of ad vanced medicine I and Clinic, Oct. 25, 1879. ^Y THE SAME AUTHOR. ESSAYS ON CONSERVATIVE MEDICINE AND KINDRED TOPICS. In one very handsome royal 12mo. volume. Cloth, $1 38. (Just Issued.) DAVIS'S CLINICAL LECTURES ON VARIOUS eases of Women and Children, Medical Jnrispru- IMPO RTAN T DISEASES ; being a collection of the dence, etc. etc. By Dunolisox, Forbes, Tweedie, Clinical L'ctnres delivered in the Medical Wards and Conolly. In four large super-royal octavo of Mercy H ispi al, Chicago. Edited by Frank H volumes, of 3254 double-columned pages, strongly Davis, M.D. Second edition, enlarged. In one ' and handsomely hound in leather. $15; cloth. $11 handsome royal 12mo. volume. Cloth, $1 75. STUROES'S INTRODUCTION TO THE STUDY OF THE CYCLOPEDIA OF PRACTICAL MEDICINE: CLINIC AL ME DICI N E. Bei ng a Guide to the In- eomprising Treatises on the Nature and Treatment vestigation of Disease. In one handsome 12mo of Diseases, Materia Medica and Therapeutics, Dis- volume, cloth, $1 25. (Lately Issued.) 15 16 RICHARDSON (BENJ. >.), M.D., F.R.S., M.A., LL.D., F.S.A., -Al Fellow of the Royal College of Physicians, London. PREVENTIVE MEDICINE. In one octavo volume of about 500 pages. (In Press.) The immerse strides taken by medical science during the last quarter of a century have had no more conspicuous field of progress than the causation of disease. Not only has this led to marked advance in therapeutics, but it has given rise to a virtually new department of medi- cine-the prevention of disease-more important, perhaps, in its ultimate results than even the investigation of curative processes Yet there has been no attempt to gather into a systematic and intelligible shape the accumulation of knowledge thus far acquired on this most interesting subject. Fortunately, the task h s been at last undertaken by a writer who of all others is, perhaps, best qualified for its performance, and the result of his labors can hardly fail to mark an epoch in the history of medical science. The plan adopted for the execution of this novel design can best be explained in his own words :- "With the object here expressed I write this volume. I have nothing to say in it that has any relation to the cure of disease, but I base it nevertheless on the curative side of medical learning In other words, I trace the diseases from their actual representation as they exist before us, in their natural progress after their birth, as far as I am able, back to their origins, and try to seek the conditions out of which they spring. Thereupon I endeavor further to analyze those conditions, to see how far they are removable and how far they are avoidable." [Y700DBURY (FRANK), M.D., ' ' Physician to the German Hospital, Philadelphia, late Chief Assist, to Med. Clinic, Jeff. College Hospital, etc. A HANDBOOK OF THE PRINCIPLES AND PRACTICE OF Medicine ; for the use of Students and Practitioners. Based upon Husband's Handbook of Practice. In one neat volume, royal 12mo. (In Press.) T^OTHERGILL (J. MILNER), M.D. Edin., M.R.C.P. Lond., -I Asst. Phys, to the West Lond Hosp. ; Asst. Phys, to the City of Lond. Hosp.,etc. THE PRACTITIONER'S HANDBOOK OF TREATMENT; Or,the Principles of Therapeutics. Second edition, revised and enlarged. In one very neat octavo volume of about 650 pages. Cloth, $4 00; very handsome half Russia, $5 50. (Just Ready.) The junior members of the profession will find in to the thoughtful reader all the charms and beau- it a work that should not only be read, but care- ties of a well-written novel. No physician can fully studied. It will assist them in the proper well afford to be without this valuable work, for Its selection and combination of therapeutical agents originality makes it fill a niche in medical litera- best adapted to each case and condition, and enable ture hitherto vacant.-Nashville Journ. of Med. them to prescribe intelligently and successfully, and Surg., Oct. 1880. To do full justice to a work of this scope and char- Throughout the work, while room is left for dif- acter will be impossible in a review ol this kind. fereHCe of opinion in matters of detail, the main The book itself must be read to be fully appreciated. | courses of treatment are so carefully founded on -St. Louis Courier of Medicine, Nov. 1880. well-established principles, that no e.-sential dif- The author merits the thanks of every well-edu- ference is felt to be possible. The closing chapter cated physician for his efforts toward rationalizing : contains much concentrated worldly wisdom ; and, the treatment of diseases upon the scientific basis if carefully read, digested, and assimilated, will, in of physiology. Every chapter, every line, has the many an emergency, stand the young medical man impress of a master hand, and while the work is in good stead.-Lond. Med. Record, Oct. 12, 1880. thoroughly scientific in every particular, it presents I FINLAYSON (JAMES), M.D., ■A- Physician ar d Lecturer on Clinical Medicine in the Glasgow Western Infirmary, etc. CLINiCAL DIAGNOSIS; A Handbook for Students and Prac- titioners of Medicine. In one handsome 12mo. volume, of 546 pages, with 85 illustra- tions. Cloth, $2 63. (Just Issued.) The book is an excellent one, clear, concise, conve- tive from preface to the final page, and ought to be nient, practical It is replete with the very know- gi ven a place on every office table, because it contains ledge the student needs when he quits the lecture- in a condensed form all that is valuable in semeiology room and the laboratory for the ward and sick-room, and diagnostics to be found in bulkier volumes, and and does not lack in information that will meet the because in its arrangement and complete index, it is wants of experienced and older men.-Phila. Med. unusually convenient for quick reference in any Times, Jan. 4, 1879. emergency that may come upon the busy practitioner. This is one of the really useful books. It is attrac- ~N- Med- Jan. 1879. U7A TSON (THOMAS), M.D., ^c. LECTURES ON THE PRINCIPLES AND PRACTICE OF PHYSIC. Delivered at King's College, London. A new American, from the Fifth re- vised and'enlarged English edition. Edited, with additions, and several hundred illustra- tions, by Henry Hartshorne, M.D., Professor of Hygiene in the University of Penn- sylvania. In two large and handsome 8vo. vols. Cloth, $9 00 ; leather, $11 00. (Lately Published.) fJA R TSHORNE (HENR Y), M.D., A-A. Professor of Hygiene in the University of ■ Pennsylvania ESSENTIALS OF THE PRINCIPLES AND PRACTICE OF MEDI- CINE. A handy book for Students and Practitioners Fifth edition, thoroughly re- vised and rewritten. With over one hundred illustrations. In one handsome royal 12mo. volume, of about 600 pages. (In Press.) Henry C. Lea's Son & Co.'s Publications-(Practice of Medicine}. REYNOLDS (J. RUSSELL). M.D., Prof. of the Principle# and Practice of Medicine in Univ. College. London. A SYSTEM OF MBDIUJNE with Notes and Additions by H^nry Habts- horne, M.D., late Professor of Hygiene in the University of Penna. In three large and handsome octavo volumes, containing 3052 closely printed double-columned pages, with numerous illustrations. Sold only by subscription. Price per vol., in cloth, $5 00; in sheep, $6.00: half Russia, raised bands, $6.50. Per set in cloth, $15; sheep, $18; half Russia, $19.50 Volume I. (just ready) contains General Diseases and Diseases of the Nervous System. Volume II. (just ready) contains Diseases of Respiratory and Circulatory Systems. Volume III. (just ready) contains Diseases of the Digestive and Blood Glandular Systems, of the Urinary Organs, of the Female Reproductive System, and of the Cutaneous System. Reynolds's System of Medicine, recently completed, has acquired, since the first appearance of the first volume, the well-deserved reputation of being the work in which modern British medicine is presented in its fullest and most practical form. This could scarce be otherwise in view of the fact that it is the result of the collaboration of the leading minds of the profession, each subject being treated by some gentleman who is regarded as its highest authority-as for instance, Diseases of the Bladder by Sir Henry Thompson, Malpositions of the Uterus by Graily Hewitt, Insanity by Henry Maudsley, Consumption by J. Hughes Bennet, Dis- eases of the Spine by Charms Bland Radcliffe, Pericarditis by Francis Sibson, Alcoholism by Francis E. Anstie, Renal Affections by William Roberts, Asthma by Hyde Salter, Cerebral Affections by H Charlton Bastian, Gout and Rheumatism by Alfred Baring Gar- rod, Constitutional Syphilis by Jonathan Hutchinson, Diseases of the Stomach by Wilson Fox, Diseases of the Skin by Balmanno Squire, Affections of the Larynx by Morell Mac- kenzie, Diseases of the Rectum by Blizard Curling, Diabetes by Lauder Brunton, Intes- tinal Diseases by John Syer Bristowe, Catalepsy and Somnambulism by Thomas King Cham- bers, Apoplexy by J. Hughlings Jackson, Angina Pectoris by Professor Gairdner, Emphy- sema of the Lungs by Sir William Jenner, etc. etc. All the leading schools in Great Britain have contributed their best men in generous rivalry, to build up this monument of medical sci- ence. St. Bartholomew's, Guy's, St Thomas's, University College, St. Mary's, in London, while the Edinburgh, Glasgow, and Manchester schools are equally well represented, the Army Medical School at Netley, the military and naval services, and the public health boards. That a work conceived in such a spiri', and carried out under such auspices should prove an indispensable treasury of facts and experience, suited to the daily wants of the practitioner, was inevitable, and the success which it has enjoyed in England, and the reputation which it has acquired on this side of the Atlantic, have sealed it with the approbation of the two pre-eminently practical nations. Its large size and high price having keptit beyond the reach of many practitioners in this country who desire to possess it, a demand has arisen for an edition at a price which shall ren- der it accessible to all. To meet this demand the present edition has been undertaken. The five volumes and five thousand pages of the original have, by tne use of a smaller type and double columns, been compressed into three volumes of over three thousand pages, clearly and hand- somely printed, and offered at a price which renders it one of the cheapest works ever presented to the American profession. But not only is the American edition more convenient and lower priced than the English; it is also better and more complete. Some years having elapsed since the appearance of a portion of the work, additions are required to bripg up the subjects to the existing condition of science. Some diseases, also, which are comparatively unimportant in England, require more elaborate treatment to adapt the articles devoted to them to the wants of the American physi- cian ; and there are points on which the received practice in this country differs from that adopted abroad. The supplying of these deficiencies has been undertaken by Henry Harts- horne, M.D.,late Professor of Hygiene in the University of Pennsylvania, who has endeavored to render the work fully up to the day, and as useful to the American physician as it has proved to be to his English brethren. The number of illustrations has also been largely increased, and no effort spared to render the typographical execution unexceptionable in every respect. Really too much praise can scarcely be given to subjects with which he should be familiar.-Gail* this noble book. It is a cyclopaedia of medicine lard's Med. Journ., Feb. 1880. written by some of the best men of Europe. It is . ... . ... full of useful information such as one finds frequent There is no medical work which we have in times need of in one's daily work As a book of reference Past more frequently and fully consulted when per- il is invaluable. It is up with the times. It is clear ploxed by doubts as to treatment, or by having un- and concentrated in style, and its form is worthy usual or apparently inexplicable symptoms pro- of its famous publisher. - Louisville Med. News, sented to us than "Reynolds' System of Medicine." Jan. 31 1880. Among its contributors are gentlemen who are as well known by reputation upon this side of the "Reynolds' System of Medicine" is justly con- Atlantic as in Great Britain, and whose right to sidered the most popular work on the principles and speak with authority upon the subjects about practice of medicine in the English language The which they have written, is recognized the world contributors to this work are gentlemen of well- over. They have evidently striven to make their known reputation on both sides of the Atlantic, essays as practical as possible, and while these are Each gentleman lias siriven to make his part of the । sufficiently full to entitle them to the name of work as practical as possible, and the information ■ monographs, they are not loaded down with such contained is such as is needed by the busy practi- i an amount of detail as to render them wearisome tioner. - St. Louis Med. and Surg. Journ.,3&n. '8Q. to the general reader. In a word, they contain just that kind of i nformation which the busy practitioner Dr. Hartshorne has made ample additions and frequently finds himself in need of. In order that revisions, all of which give increased value to the I any deficiencies may be supplied, Ihe publishers volume, and render it more useful to the Ameri- have committed the preparation of the book for the can practitioner. There is no volume in English press to Dr. Henry Hartshorne, whose judicious medical literature more valuable, and every pur- notesdistributed throughout the volume afford abun- chaser will, on becoming familiar with it, eongrat- l dant evidence of the thoroughness of the revision to ulafe himself on the possession of this vast store- which he has subjected it.-Am. Jour. Med. Sciences, house of information, in regard to so many of the [ Jan. 1880. Henry C. Lea's Son & Co.'s Publications-(Practice of Medicine}. 17 18 RARTHOLOW {ROBERTS), AM., M.D., LL.D. AJ Prof, of Materia Medico. and General Therapeutics in the Jeff. Med. Coll, of Phila., etc. A PRACTICAL TREATISE ON ELECTRICITY IN ITS APPLI- CATION TO MEDICINE. In one very handsome 8vo. volume of about 270 pages, with 98 illustrations. (Just ready.) EXTRACT FROM THE AUTHOR'S PREFACE. I have attempted in the preparation of this work to avoid these errors; to prepare one so simple in statement that a student without previous acquaintance with the subject, may read- ily master the essentials; so complete as to embrace the whole subject of medical electricity, and so condensed as to be complete in a moderate compass. I have endeavored to keep con- stantly in view the needs of the two classes for whom the work is prepared-students and prac- titioners. I have asfumed an entire unacquaintance with the elements of the subject as the point of departure-for I am addressing those who have either failed to acquire this prelimi- nary knowledge, or having acquired it, find that after the lapse of years, it has become misty and confused. In the accounts of electrical phenomena I have adhered to the modes of expres- sion with which the medical electrical text-books have made us familiar. This book, then, must be regarded as the exposition of electricity as a remedial agent, made by a medical practitioner for the use of medical practitioners. No claim is made on the ground of pure science. It is believed, however, that the work makes an adequate presentation of the subject, regarding electricity as a remedial agent-as one of the means employed for the treat- ment and cure of disease. So tar as we know, the need of a clear, simple, practitioners. From this standpoint the work is untechnical, reliable, concise, and modern treatise worthy of the careful study of all who desire to in- upon the subject of medical electricity is only snp- vestigate this subject for purely practical purposes, plied by the volume under consideration. It is not Tim work meets a want of very many students and too much to say that, if availed of, it will render medical practitioners. We greatly err if it be not accessible to a vast number of members of the pro- gladly welcomed by them. The author, from his fession a therapeutic agent of the greatest value, but long experience as a practitioner, is ad mirably fitted which has heretofore been practically of no use to perform the task of writing a work of this kind whatever to them.-Maryland Med. Journal, June for this special class of men.-Detroit Lancet, June, 1, 1881. 1881. We have not yet come across a book that can com- This hook is expressive of careful research and a pare.W1^ this in clearness and simplicity of state- nice di8crilniDation in the selection of such matter ment. We have for a long timtf needed a text-book from that at the author-g command as is best adapted on medical electricity, condensed and yet complete, for tbe guidance and instruction of the physician and this wan* has been well supplied by the dIstin- wboge intere8t ln electricity is proportionate to its guished author. Ihe illustrations are elegant, and practical bearing on diagnosis and treatment. It is the book as a whole is a valuable addition to the thorough, it is accurate, it is readable, and above collection of any student or practitioner.-Buffalo ttn is essentially utilizable, if we may use the word, Med. and. Surg. Journal, June, 1881. and renderg eagy of access to the general practitioner As a whole, the book must be looked upon as an the modus operandi of employing this very valu- exposition of electricity for remedial purposes, writ- able therapeutic agent.-W. Y. Medical Gat., June ten by a medical practitioner for the use of medical 11, 1881. J^ITCHELL {S. WEIR}, M.D^~ Phys, to Orthopaedic Hospital and the Infirmary for Dis. of the Nervous System, Phila., etc. etc. LECTURES ON DISEASES OF THE NERVOUS SYSTEM, ESPECIALLY IN WOMEN. In one very handsome 12mo. volume of about 250 pages, with five lithographic plates. Cloth, $1 75 (Just Ready.) The life-long devotion of the author to the subjects discussed in this volume has rendered it eminently desirable that the results of his labors should be embodied for the benefit of those who may experience the difficulties connected with the treatment of this class of disease. Many of these lectures are fresh studies of hysterical affections; others treat of the modifica- tions his views have undergone in regard to certain forms of treatment, while, throughout the whole work, he has been careful to keep in view the practical lessons of his cases. It is a record of a number of very remarkable > ordinarily rich in acute observation and sound in- cases, with acute analyses and discussions, clinical, struction. The reputation of the author is a guar- physiological, and therapeutical It is a book to | antee of that, and no reacer will be disappointed, which the physician meeting with a new hysterical ! Nor can too much be said in praise of the admirable experience, or in doubt whether his new experience style of his m-dical writings, and each of these leo- is hysterical, may well turn with a well-grounded tures reads with the finished grace of a polished hope of finding a parallelism ; it will be a new ex- essay. Indeed, the book throughout is so fascinating perience, indeed, if no similar one is here recorded a one that it could not fail to be read entire by every -Phila. Med. Times, June 4, 1881. one who begins its pages. -Phila. Med. and Surg. The name of the author is sufficient guarantee that Reporter, May 7, 1881. these topics are ably and appreciatively discussed ; Tbe book throughont ig not only intenfiely enter- sufllce it to say that ihe principles of treatment, both tainlDK. butlt contains a large amount of rare and hygienic and therapeutic are clearly indicated. valaab]e inforn)ation. Dr Mitchell has recorded The articles being in the form of clinical lectures, Eot on|y the results of his most, careful observation, abound in illustrative cases, and are much easier , butbagadded to the knowledge of the subjects treat- reading than a systematic treatise on the same l ed by bis original investigation and practical study. to^.-College and Clinical Record, May 15,1 81. | Th/book is one we can commend to all of our read- It is needless to say that these lectures are extra- । ers -Maryland Med. Journal, May 1, 1881. TJA MIL TON (AL LA N McLA NE^lf. D~ A A Attending Physician at the Hospital for Epileptics and Paralytics, Blackwell's Island, N. Y., and at the Out-Patients' Department of the New York Hospital. NERVOUSDISEASES;THEIR DESCRIPTION AND TREATMENT. Second edition, thoroughly revis°d and rewritten. In one handsome octavo volume of about 600 pages, with numerous illustrations. (In Press.) Henry C. Lea's Son & Co.'s Publications-(Nerv. Dis, &c.). Henry C. Lea's Son & Co.'s Publications-(Dis.of the Skin, MORRIS {MALCOLM), M.D., d-'-*- Joint Lecturer on Dermatology, St. Mary's Hospital Med. School. SKIN DISEASES, Including their Definitions, Symptoms, Diagnosis, Prognosis, Morbid Anatomy and Treatment. A Manual for Students and Practitioners. In one 12mo. volume of over 300 pages. With illustrations. Cloth, $1 75. (NowReady.) To physicians who would like to know something beginner.-St. Louis Courier of Medicine, April, about skin diseases, so that when a patient presents 1880. himself for relief they can make a correct diagnosis The author of this mannai has evidently a full and and prescribe a rational treatment we unhesitatingly intimate acquaintance with the literature of derma- recommend this little book of Dr. Morris. The affec tol and with the m08t recent deveiopraeats and °f??u •klU are a.terse' appliances of cutaneous medicine. He has produced ner and their several characteristics so plainly sei a lai practicai book, by aid of which, who so forth that diagnosis will be easy. The treatment chooses may triin his eye to the recognition of in each case is such as the experience of the most H ht bnt sigaifloant differences. The descriptions eminent dermatologists advise.-CTncinnaH Medl- are aelther t00 vaene nor over.refined . the direc- cat News, April, 1880. tions for treatment are clear and succinct.-London This is emphatically a learner's book ; for we can Brain, April, 1880 safely say, so far as our judgment goes, that in the The author's task has been well done and has pro- whole range of medical literature of a like scope dnced one of the best recent works upon the difficult there is no book which for clearness of expression subject of which it treats ; there is no work published and methodical arrangement is better adapted to which gives a better view of the elementary facts promote a rational conception of dermatology, a and nri iciples of dermatology.- New 0, leans Medi- branch confessedly difficult and perplexing to the cal and Surgical,Journal, April, 1880. mX ( T2LBURF), M.D., F.R.C.P., and T. C. FOX, B.A., M.R.C.S., Physician to the Department for Skin Diseases, University College Hospital. EPITOME OF SKIN DISEASES. WITH FORMULAE. ForStu- dentsand Practitioners. Second edition, thoroughly revised and greatly enl urged. In one very handsome 12mo. volume of 216 pages. Cloth, $1 38. (Just Issued.) FLINT {AUSTIN), M.D., Professor of the Principles and Practice of Medicine in Bellevue Hospital Med. College, N. T. A MANUAL OF PERCUSSION AND AUSCULTATION; of the Physical Diagnosis of Diseases of the Lungs and Heart, and of Thoracic Aneurism. Second edition. In one handsome royal 12mo. volume: cloth, $1 63. (Just Ready.) The little work before us has already become a I author has for mmy years given, in connection with standard one. and has become extensively adopted | practical instruction in auscultation and percussion, as a text-book. There is certainly none better. It I to private classes, composed of medical students ana contains the substance of the lessons which the | practitioners.-Cincinnati Med. News, Feb. 1880. ^Y THE SAME AUTHOR. PHTHISIS: ITS MORBID ANATOMY, ETIOLOGY, SYMPTOM- ATIC EVENTS AND COMPLICATIONS, FATALITY AND PROGNOSIS, TREAT- MENT AND PHYSICAL DIAGNOSIS; in a series of Clinical Studies. By Austin Flint, M.D., Prof, of the Principles and Practice of Medicine in Bellevue Hospital Med. College, New York. In one handsome octavo volume : $3 50. (Lately Issued.) JDY THE SAME AUTHOR. A PRACTICAL TREATISE ON THE DIAGNOSIS, PATHOLOGY, AND TREATMENT OF DISEASES OF THE HEART. Second revised and enlarged edition. In one octavo volume of 550 pages, with a plate, cloth, $4. T>Y THE SAME AUTHOR. A PRACTICAL TREATISE ON THE PHYSICAL EXPLORA- TION OF THE CHEST AND THE DIAGNOSIS OF DISEASES AFFECTING THE RESPIRATORY ORGANS. Second and revised edition. In one handsome octavo volume of 595 pages, cloth, $4 50. THROWN {LENNOX), F.R.C.S. Ed., ■J-J Senior Surgeon to the Central London Throat and Ear Hospital, etc. THE THROAT AND ITS DISEASES. Second American, from the Second English Edition, thoroughly revised. With one hundred Typical Illustrations in colors, and fifty wood engravings, designed and executed by the author. In one very handsome imperial octavo volume of over 350 pages. (Preparing.') (JE1LER (CARL), M.D., u Lecturer on Laryngoscopy at the Univ, of Penna., Chief of the Throat Dispensary at the Univ. Hospital, Phila., etc. HANDBOOK OF DIAGNOSIS AND TREATMENT OF DISEASES OF THE THROAT AND NAS\L CAVITIES. In one handsome royal 12mo. volume, of 156 pages, with 35 illustrations; cloth, $1. (Just Ready.) We most heartily commend this book as showing . A convenient little handbook, clear, concise, and sound judgment i n practice, and perfect farniliarby accurate in its method, and admirably fulfilling its with the literature of the specialty it so ably epi- ! purpose of bringing the subject of which it treats tomizes.- Philada. Med. Times, July 5, 1879. ■ within the comprehension of the general practi- I tioner.-N C. Med. Jour., June. 1879. CLINICAL OBSERVATIONS ON FUNCTIONAL HILLIER'S HANDBOOK OF SKIN DISEASES, for NERVOUS DISORDERS Bv C. H andfield Jones Studentsand Practitioners. Second Am Ed. In M.D., Physician to St. Mary's Hospital, &c. Sec- one royal 12mo. vol. of 358 pp. With illustrations, ond America n Edition. In one handsome octave Cloth, $2 25. ▼olumeof 348 pages,cloth, $3 25. 19 Henry C. Lea's Son & Co.'s Publications-(Venereal Diseases, RUMSTEAD {FREEMAN J.), M.D., LL.D., Late Professor of Venereal Diseases at the Col. of Phys, and Surg., New York, &c. THE PATHOLOGY AND TREATMENT OF VENEREAL DIS- EASES. Including the results of recent investigations upon the subject. Fourth Edition, revised and largely rewritten with the co-operation of R. W. Taylor, M.D., of New York, Prof, of Dermatology in the Univ, of Vt. In one large and handsome octavo volume of 835 pages, with 138 illustrations. Cloth, $4 75; leather, $5 75; half Russia, $6 25. (Now Ready.) We have to congratulate our countrymen upon ' will more than repay him for the outlay.-Archives the truly valuable addition which they have made | of Medicine, April, 18q0. to American literature. The careful estimate of the Thlg now cla8gical work on venereal disease comes value of the volume, which we have made, justifies I t0 „g in ltg fonrth edltil)n rewritt enlarged, and us in declaring that this is the best treatise on ; materially improved in every way. Dr. Taylor, as venereal diseases in the English language, and we we had e reason to 'ct h' perfornfed t'hig might add if there is a better in any other tongue . t of big work wlth unusl\a] Silence. We feel cannot name it ; there are certainly no books in | that wbat hag been wrjtten bag donft but gca jug. which the student or the general practitioner can tice to the raeritg of this trul t treatig/2St find such an excellent risumi of the literature of Louis Oouri,r of Medicine, Feb. 18S0 any topic, and such practical suggestions regarding the treatment of the various complications of every ;Ye ", that we have here practically a new book venereal disease. We take pleasure in repeating -that the statement of the title page, as to the fact that we believe this to be the best treatise on vene- 'hat it has been largely rewritten, is a sufficiently real disease in the English language, and we con- modest announcement for th* important changes in gratulate the authors upon their brilliant addition the text. After a thorough examination of the pre- to American medical literature.-Chicago Med. Jour- i seQt edition, we can assert confidently that the enor- nal and Examiner, February, 1880. ' ™0"® '"h01- have described has been here most T. . ... , x . ,, . , faithfully and conscientiously performed.-Amer. It is, without exception, the most valuable single Journ. Med. Sci Jan 1880 work on all branches of the subject of which it treats j „' ' in any language. The pathology is sound, the work ,.Tt 18 one of the best general treatises on venereal is, at the same time, in the highest degree practical, diseases with which we are acquainted, and is espe- and the hints that he will get from it for the man- c^a^y to be recommended as a guide to the treatment agement of any one case, at all obscure or obstinate, | syphilis. London Practitioner, March, 1880. QROSS {SAMUEL W.), A.M., M.D., Lecturer on Genito-Urinary and Venereal Diseases in the Jefferson Medical College, Phila. A PRACTICAL TREATISE ON IMPOTENCE, STERILITY, AND ALLIED DISORDERS OF THE MALE SEXUAL ORGANS. In one very hand- some octavo volume of 174 pages, with 16 illustrations. Cloth, $1 50. (Just Ready.) (JUL LERIER (J.), and J J UM STEA D (FR EEM AN J.). rS Surgeon to the Hdpital du Miidi. Professor of Venerea l Diseases in the College of Physicians and Surgeons. N. Y AN ATLAS OF VENEREAL DISEASES. Translated and Edited by Freeman J. Bumstead. In one large imperial 4to. volume of 328 pages, double-columns, with 26 plates, containing about 150 figures, beautifully colored, many of them the size of life; strongly bound in cloth, $17 00 ; also, in five parts, stout wrappers, at $3 per part. Anticipating a very large sale for this work, it is offered at the very low price of Three Dol - LARS a Part, thus placing it within the reach of all who.are interested in this department of practice. Gentlemen desiring early impressions of the plates would do well tb order it without delay. A specimen of the plates and text sent free by mail, on receipt of 25 cents. LEE'S LECTURES ON SYPHILIS AND SOME CHAMBERS'S MANUAL OF DIET AND REGIMEN FORMS OF LOCAL DISEASE AFFECTING PR1N- IN HEALTH AND SICKNESS. In one handsome CIPALLY THE ORGANS OF GENERATION. lu octavo volume. Cloth, $2 75. one handsome octavo volume; cloth, $2 25. FULLER ON DISEASES OF THE LUNGS AND AIR- CONDIE'S PRACTICAL TREATISE ON THE DIS PASSAGES. Their Pathology, Physical Diagnosis, EASES OF CHILDREN. Sixth edition, revised Symptoms and Treatment. From the second and and augmented. In one large octavo volume oi revised English edition. In one handsome octavo nearly 8C0 closely-printed pages, cloth, $5 26; volume of about 500 pages : cloth, $3 50. leather $6 25. BASHAM ON REN AL DISEASES : a Clinical Guide WILLIAMS'S PULMONARY CONSUMPTION; its to their Diagnosis and Treatment. With Illustra- Nature, Varieties, and Treatment. With an An- tions. In onel2mo. vol. of 304 pages, cloth, $2 00. alysis of One Thousand Cases to exemplify its LECTURES ON THE STUDY OF FEVER. By A. duration. In one neat octavo volume of about Hudson, M.D., M.R.I.A., Physician to the Meath 350 pages ; cloth, $2 ;>0. Hospital In one vol. 8vo., cloth, $2 50. SLADE ON DIPHTHERIA ; its Nature and Treat- A TREATISE ON FEVER. By Robert D. Lyons, ment, with an account of the History of its Pre- K CC I n one octavo volume of 362 pages, clot h valence in various Countries. Second and revised $2 25 edition. In one neatroyal 12mo. volume, cloth, HJLL 0N SYPHILIS AND LOCAL CONTAGIOUS WAL8HE ON THE DISEASES OF TH^ HEART AND U handsome octavo v°lume I GREAT VESSELS. Third American Edition. In ' 1 vol. Svo„ 420 pp„ cloth, $3 00. SMITH'S PRACTICAL TREATISE ON THE WAST- SMITH ON CONSUMPTION ; ITS EARLY AND RE America f^om^hTs^ond MEDIABLE STAGES. 1 vol. 8vo„ pp. 254 $2 26 WILSON'S STUDENT'S BOOK OF CUTANEOUS vo volume, cloth. $2 50. MEDICINE and Diseases of the Skin. In one LA ROCHE ON PNEUMONIA. 1 vol.8vo., cloth, very handsome royal 12mo. volume. $3 50. of 500 pages. Price, $3 00. 20 Henry C. Lea's Son & Co.'s Publications-(Dis. of Children, &c.). gMITH (J. LEWIS), M.D., Clinical Professor of Diseases of Children in the Bellevue Hospital Med. College, N. Y. A COMPLETE PRACTICAL TREATISE ON THE DISEASES OF CHILDREN. Fifth Edition, thoroughly revised and rewritten. In one handsome oc- tavo volume of about 800 pages, with illustrations. (In Press.) The very marked favor with which this work has been received wherever the English lan- guage is spoken, has stimulated the author, in the preparation of the Fifth Edition, to spare no pains in the endeavor to render it worthy in every respect of a continuance of professional confidence. Many portions of the volume have been rewritten, and much new matter intro- duced, but by an earnest effort at condensation, the size of the work will not be materially increased. ^EATING {JOHN M.), M.D., Lecturer on the Diseases of Children at the University of Pennsylvania, etc. THE MOTHER'S GUIDE IN THE MANAGEMENT AND FEED- ING OF INFANTS. In one handsome 12mo vol. of about 100 pages. (Nearly Ready.) JJIEST {CHARLES'), M.D., Physician to the Hospital for Sick Children, London, Ac. LECTURES ON THE DISEASES OF INFANCY AND CHILD- HOOD. Fifth American from the Sixth revised and enlarged English edition. In one large aftd handsome octavo volume of 678 pages. Cloth, $4 50 ; leather, $5 50. (Lately Issued.) ^Y THE SAME AUTHOR. (Lately Issued.) ON SOME DISORDERS OF THE NERVOUS SYSTEM IN CHILD- HOOD ; being the Lumleian Lectures delivered at the Royal College of Physicians of London, in March, 1871. In one volume small 12mo., cloth, $1 00. ^Y THE SAME AUTHOR. LECTURES ON THE DISEASES OF WOMEN. Third American, from the Third London edition. In one neat octavo volume of about 550 pages, cloth, $3 75; leather, $4 75. ^WAYNE {JOSEPH GRIFFITHS), M.D., Physician-Accoucheur to the British General Hospital, Ac. OBSTETRIC APHORISMS FOR THE USE OF STUDENTS COM- MENCING MIDWIFERY PRACTICE. Second American, from the Fifth and Revised London Edition with Additions by E. R. Hutchins, M.D. With Illustrations. In one neat 12mo. volume. Cloth, $1 25. (Lately Issued.) *** See p. 3 of this Catalogue for the terms on which this work is offered as a premium to subscribers to the American Journal of the Medical Sciences. CHURCHILL ON THE PUERPERAL FEVER AND MEIGS ON THE NATURE, SIGNS AND TREAT- OTHER DISEASES PECULIAR TO WOMEN. 1vol. MENT OF CHILDBED FEVER. 1 vol. 8vo., pp. 8vo., pp. 450, cloth. $2 5 0. 365, cloth. $2 00. DEWEES'S TREATISE ON THE DISEASES OF FE- ASHWELL'S PRACTICAL TREATISE ON THE DIS- MALES. With illustrations. Eleventh Edition. EASES PECULIAR TO WOMEN. Third American, with the Author's lastimprovementsahd correc- from the Third andrevised Londonedition. 1 vol. tions. In one octavo volume of 536 pages, with 8vo., pp. 528, cloth. $3 50. plates, cloth. $3 00. flHURCHILL {FLEETWOOD), M.D., M.R.I.A. ON THE THEORY AND PRACTICE OF MIDWIFERY. A new American from the Fourth revised and enlarged London edition. With notes and additions by D. Francis Condie, M.D., author of a Practical Treatise on the Diseases of Chil- dren, &c. With one hundred and ninety-four illustrations. In one very handsome octavo volume of nearly 700 large pages. Cloth, $4 00 ; leather, $5 00. WINCKEL {F.), ' ' Professor and Director of the Gynaecological Clinic in the University of Rostock. A COMPLETE TREATISE ON THE PATHOLOGY AND TREAT- MENT OF CHILDBED, for Students and Practitioners. Translated, with the consent of the author, from the Second German Edition, by James Read Chadwick, M.D. In one octavo volume. Cloth, $4 00. (Lately Issued.) MONTGOMERY'S EXPOSITION OF THE SIGNS RIGBY'S SYSTEM OF MIDWIFERY. With notes AND SYMPTOMS OF PREGNANCY. With two and Additionallllustrations. Second American exquisitecolored plates, andnumerous wood-cuts edition. One volume octavo, cloth, 422 pages. Ini vol. 8vo., of nearly 600 pp., cloth, $3 75. $2 50. 21 22 STROMAS (T. GAILLARD), M.D., A- Professor of Obstetrics, Ac., in the College of Physicians and Surgeons, N. K, Ac A PRACTICAL TRE ATISE ON THE DISEASES OF WOMEN. Fifth Edition, thoroughly revised and rewritten. Tn one large and handsome octavo volume of over 800 pages, with 266 illustrations. Cloth, $5 ; leather, $6 ; very handsome half Russia, raised bands, $6 50. (Just Ready.) The author has taken advantage of the opportunity afforded by the call for a new edition of this work to render it worthy a continuance of the very remarkable favor with which it has been received. Every portion of the work has been carefully revised, very much of it has been rewritten, and additions and alterations introduced wherever the advance of science and the increased experience of the author have shown them desirable. At the same time special care has been exercised to avoid undue increase in the size of the volume. To accommodate the numerous additions a more condensed but v ry clear letter has been used, notwithstanding which, the number of pages has been increased by more than fifty. The series of illustrations has been extensively changed ; many which seemed to be superfluous have been omitted, and a large number of new and superior drawings have been inserted. In its improved form, there- fore, it is hoped that the volume will maintain the character it has acquired of a standard authority on every detail of its important subject. An examination of the work will satisfy that it is its author's large experience, but reflects his care- one of great merit. It is not a mere compilation ful study among other authorities in his branch, from other works, but is the fruit of the ripe both at home and abroad Dr. Thomas is an able thought, sound judgment, and critical observations and conscientious teacher.. His wri ings convey of a le rned, scientific man. It is a treasury of his meaning in the same practical and instructive knowledge of the department of medicine to which manner. The last edition of this work is fresh from it is devoted In its present revised state it cer- his pen, with decided changes and improvements tainly hold-a foremost position as a gynaecological over former editions. His book presents generally work, and will continue to be regarded as a stan- accep'ed facts, and as a guide to the student is more dard authority -Cincinnati Med. News, Dec. 1880, useful and reliable ihan any work in the language This work needs no introduction to any of the on diseases of women. This last edition will add civilized nations of the world. The edition before "e* laurels to those already won. - Md. Med. us adds to the streng b of former volumes. With Journ., Nov. 15, 1880. the wisdom of a master teacher he here gives the It has been enlarged and carefully revised. The results that, in his judgment, are most trustworthy author has brought it fully abreast with the times, at the present time. In its own place it has no and as the wave of gynaecological progression has rival because the author is the best teacher on this been widespread aud rapid during the twelve years subject to the masses of the profession As hitherto that have elapsed since the issue of the first edition, this work will be the text-book on diseases of wo- one can conceive of the great improvement this edi- men We only wish that in other branches of medi- tion must be upon the earlier. It is a condensed en- cine a* capable teachers could be found to write our cyclopedia of gynaecological medi'ine. The style of text-books.-Detroit Lancet, Jan 1881. arrangement, the maiterly manner in which each Since its first appearance, twelve years ago, until 8.»bjec' is treated and the honest convictions de- the pre-ent day, it has held a poshion of high re- from Pr;'bably the largest clinical experience gard, and is generally conceded to be one of the" in that specialty of any in this country, all serve to most practi al and trustworthy volumes ye- pre co"m®n? " ,he h'g?^7ermJ o T' seated to the physician aud student in the depart- -Nashville Journ. of Med. and Sury., Jan. 1881. meut of gynaecology. The woik embodies not only DARNES (ROBERT), M.D., F.R.C.P., A-' Obstetric Physician to St. Thomas's Hospital, Ac. A CLINICAL EXPOSITION OF THE MEDICAL AND SURGI- CAL DISEASES OF WOMEN. Second American, from the Second Enlarged and Revised English Edition. In one handsome octavo volume, of 784 pages, with 181 illustrations. Cloth, $4 50 ; leather, $5 50 ; half Russia, $6. (Just Issued.) Dr Barnes stands at the head of his profession in i country, is shown by the second edition following the old country, and it requires but scant scrutiny so soon upon the first.-Am. Practitioner, Nov. of his hook to show that it has been sketched by a 1878. master It is plain, practical common sense ; shows Dr Barnes-s work ig one of a practical character, very deep research without being pedantic, is emi- largely illustrated from cases in his own experience, nently calculated to inspire enthusiasm without in- but by no means confined to such, as will be learned culcating ra-huess; points out the dangers to be from the fact that he quotes from no less than 628 avoided as well as the success to be achieved in the medical authors in numerous countries. Coming various operations connected with this branch of Rnch an author 1t is not necessarv to say that medicine; and will do much to smooth the rugged work jg a valuable one, and should be largely path of the young gynaecologist and relieve the per- con<ulted by tbe profession.-Am. Sapp Obstetrical plexity of the man of mature years. - Canadian Journ Gt. Britain and Breland, Oct. 1S78. Journ. of Med. Science, Nov. 1878. „ , , , , . ,. ,. . No other gynaecological work holds a higher posi- We pitv the doctor who, having any consider- tion, having become an authority everywhere in able practice in diseases of women, has no copy of I diseases of women. The work has been brought " Barnes" for dailv consultation aud instruction. It fully abreast of present knowledge. Every practi- is at once a book of great learning, research, and tioner of medicine should have it upon the shelves individual experience, and at the same time emi- of his library, and the student will find it a superior nently practical. That it has been appreciated by | text-book.-Cincinnati Med. News, Oct. 1878. the profession, both in Great Britain and in this I TJODGE (HUGH L.), M.D., Emeritus Professor of Obstetrics, Ac., in the University of Pennsylvania. ON DISEASES PECULIAR TO WOMEN; including Displacements of the Uterus. With original illustrations. Second edition, revised and enlarged. In one beautifully printed octavo volume of 531 pages, cloth, $4 50. Henry C. Lea's Son & Co.'s Publications-(Dis. of Women). PMMET (THOMAS ADDIS). M.D., Surgeon to the Woman's Hospital, New York, etc. THE PRINCIPLESAND PRACTICE OF GYNAECOLOGY, for the use of Students and Practitioners of Medicine. Second Edition. Thorougly Revised. In one large and very handsome octavo volume of 875 pages, with 133 illustrations. Cloth, $5; leather, $6; half Russia, raised bands, $6 50. {Just Ready.) Preface to the Second Edition. The unusually rapid exhaustion of a large edition of this work, while flattering to the author as an evidence that his labors have proved acceptable, has in a great measure heightened his sense of responsibility. He has therefore endeavored to take full advantage of the opportunity afforded to him for its revision. Every page has received his earnest scrutiny; the criticisms of his reviewers have been carefully weighed; and while no marked increase has been made in the size of the volume, several portions have been rewritten, and much new matter has been added. In this minute and thorough revision, the labor involved has been much greater than is perhaps apparent in the results, but it has been cheerfully expended in the hope of rendering the work more worthy of the favor which has been accorded to it by the profession. In no country of the world has gynaecology re- not careless reading but profound study. Its value celved more attention than in America. It is, then, as a contribution ro gynaecology is, perhaps,greater with a feeling of pleasure that we welcome a work than that of all previous literature on the subject on diseases of women from so eminent a gynsecolo- combined.-Chicago Med Gaz., April 6,18S0 gist as Dr. Emmet, and the work is essentially cliai- The wide repntation of the author makes Itspnb- cal, and eaves a strong impress of the author's in- Hcation an eveDt iu the gynecological world ; and dividnality. To criticize, with the care it merits, a lance thro h its 7bhows that it is a work the book throughout, would demand far more space to be studied wsith care.8 . . It mQst always be a than is at our command In parting, we can say work to be carefully 8tudied and frequently con- that the work teems with original ideas, fresh and sulted b tboge who practise this branch of our pro- valuable methods of practice, and is written in a feS8ion._Lonti. Med_ Timesand Gaz., Jan. 10, I860, clear and elegant style, worthy of the literary repu- m, , « , . ,, , tation of the country of Longfellow and Oliver Wen- The character of the work is too well known to dell Holmes.- Brit. Med. Journ. Feb. 21, 1880. require extended notice-suffice it to say that no recent work upon any subject has attained such No gynaecological treatise has appeared which great popularity so rapidly. As a work of general contains an equal amount of original and useful reference upon the subject of Diseases of Women it matter; nor does the medical and surgical history is invaluable. As a record of the largest clinical of America include a book more novel and useful, experience and observation it has no equal. No The tabular and statistical information which it physician who pretends to keep up with the ad- contains is marvellous, both in quantity and accu- vances of this department of medicine can afford to racy, and cannot be otherwise than invaluable to be without it.-Nashville Journ. of Medicine and future investigators. It is a work which demands Surgery, May, 1880. nUNCAN (J. MATTHEWS), M.D., LL.D., F.R.S.E., etc. CLINICAL LECTURES ON THE DISEASES OF WOMEN, Delivered in Saint Bartholomew's Hospital. In one very neat octavo volume of 173 pages. Cloth, $1 50. (Just Ready.) They are in every way worthy of their author ; The author is a remarkably clear lecturer, and indeed, we look upon them as among the most valu- his discussion of symptoms and treatment is full able of his contributions They are all upon mat- and suggestive. It v'H be a work which will not ters of great interest to the general practitioner, fail to be read with benefit by practitioners as well Some of them deal wi h subjects that are not, as a as by students. - Phila. Med. and Surg. Reporter, rule, adequately handled in the text-books; others \ Feb. 7,1880. \ of them, while bearing upon topics that are usually We have read this book with a great deal of treated of at length in such works, yet bear snch a pleasure. It is full of good things. The hints on stamp of individuality that, if widely read, as they pathology and treat men t scattered through the book certainly deserve to be, they cannot tail to exert a are sound, trustworthy, and of great value. A wholesome restraint upon the undue eagerness with healthy scepticism, a large expetience, and a clear which many young physicians seem bent upon fol- jndgment are everywhere manifest. Instead of lowing the wild teachings which so infest the gyuse- bristling with advice of doubtful value and un- cology of the present day. N. Y. Med. Journ., SoaQd character, the book is in every respect a safe March, 1880. guide.-The London Lancet, Jan. 21, 1880. f)AMSBOTHAM (FRANCIS H.), M.D. ^THE PRINCIPLES AND PRACTICE OF OBSTETRIC MEDI- CINE AND SURGERY, in reference to the Process of Parturition. A new and enlarged edition, thoroughly revised by the author. With additions by W. V. Keating, M. D., Professor of Obstetrics, <fcc., in the Jefferson Medical College, Philadelphia. In one lirge and handsome imperial octavo volume of 650 pages, strongly bound in leather, with raised hands ; with sixty-four beautiful plates, and numerous wood-cuts in the text, containing in all nearly 200 large and beautiful figures. $7 00 JDARRY (JOHN S.), M.D., Obstetrician to the Philadelphia Hospital, Vice-Prest. of the Ohstet. Society of Philadelphia. EXTRA-UTERINE PREGNANCY: ITS CLINICAL HISTORY, DIAGNOSIS, PROGNOSIS AND TREATMENT. In one handsome octavo volume. Cloth, $2 50. (Lately Issued.) BANNER (THOMAS H.), M.D. 2 ON THE SIGNS AND DISEASES OF PREGNANCY. First American from the Second and Enlarged English Edition. With four colored plates and illustra- tions on wood. In one handsome octavo volume of about 500 pages, cloth, $4 25. Henry C. Lea's Son & Co.'s Publications-{Dis. of Women). 23 24 TEISHMAA (WILLIAM), M.D., Regius Professor of Midwifery in the University of Glasgow, Ac. A SYSTEM OF MIDWIFERY, INCLUDING THE DISEASES OF PREGNANCY AND THE PUERPERAL STATE. Third American edition, revised by the Author, with additions by John S. Parry, M.D., Obstetrician to the Philadelphia Hospital, &c. In one large and very handsome octavo volume, of 733 pages, with over two hundred illustrations. Cloth, $4 50; leather, $5 50 ; half Russia, $6. (Just Ready ) Few works on this subject have met with as great i seems to require, and we canuot but admire the a demand as this one appears to have. To judge ability with whica the task has been performed, by the frequency with which its author's views are • We consider it an admirable text-book for students quoted, and its statements referred to in obstetrical (during their attendance upon lectures, and have literature, one would judge that there are fewphy- I great pleasure in recommending it. As an exponent sicians devrting much attention to obstetrics who ( of the midwifery of the present day it has no snpe- are without it. The author is evidently a man of . rior in the English language.-Canada Lancet, Jan. ripe experience and conservative views, and in no 1880. branch of medicine are these more valuable than in >p0 fbe American student the work before us must this. New Remedies, Jan. 1880. prove admirably adapted, complete in all its parts, We gladly welcome the new edition of this excel- essentially modern in its teachings and with dem- lent text-book of midwifery. The former editions onstrations noted for clearness and precision, it will have been most favorably received by the protes- gain in favor and be recognized as a work of stand- sion on both sides of the Atlantic In the prepara- ard merit. The work cannot fail to be popular, and tion of the present edition the author has made such is cordially recommended.-N. 0. Med. and Surg. alterations as the progress of obstetrical science Journ., March, 1880. pLAYFAIR ( W. S), M.D., F.R.C.P., -A- Professor of Obstetric Medicine in King's College, etc. etc. A TREATISE ON THE SCIENCE AND PRACTICE OF MIDWIFERY. Third American edition, revised by the author. Edited, with additions, by Robert P. Harris, M.D. In one handsome octavo volume of about 700 pages, with nearly 2C0 illustrations. Cloth, $4 ; leather, $5 ; half Russia, $5 50. (Just Ready.) The medical profession has now the opportunity . a very intelligent idea of them, yet all details not of adding to their stock of standard medical works I necessary for i full understanding of the subject are one of the best volumes on midwifery ever published, omitted.-Cincinnati Med. News, Jan. 1880. The subject is taken up with a master hand. The The i-apiditv with which one edition of this work part devoted to laborin all its various presentations, follows another is proof alike of its excellence and the management and results, is admirably arranged, of the e8tlmate that the profeRSion has formed of it. and the views entertained will be found essentially [t jg indeed so well known and so highly valued modern, and the opinions expressed trustworthy that nothing need be said of it as a whole. All The work abounds with plates, illustrating various things considered, we regard this treatise as the very obstetrical positions; they are admirably wrought, best on Midwifery in the English language.-Al Y. and afford great assistance to the student.-N. O. Medical Journal'May 1880 Med. and Surg. Journ., March, 1880. T, . . , . ' ' ' ... . „ „ " , It certainly is an admirable exposition of the If inquired of by a medical student what work on Science and Practice of Midwifery. Of course the obstetrics we should recommend for him, as par additions made by the American editor, Dr. R. P. excellence, we would undoubtedly advise him to Harris, who never utters an idle word, and whose choose Playfair s. It is of convenient size, but what studious researches in some special departments of is of chief importance, its treatment of the various obstetrics are so well known to the profession, are subjects is concise and plain. WJiile the discussions of great value.-The American Practitioner, April, and descriptions are sufficiently elaborate to render 1880. JJARAES (FA ACO UR T), M. D., -LJ Physician to the General Lying-in Hospital, London. A MANUAL OF MIDWIFERY FOR MIDWIVES AND MEDICAL STUDENTS. With 50 illustrations. In one neat royal 12mo. volume of 200 pages ; cloth, $1 25. (Now Ready.) pAR VIA (THEO PHIL US), M.D., Prof, of Obstetrics and of the Med and Surg. Diseases of Women in the Med. Coll, of Indiana. A TREATISE ON MIDWIFERY. In one very handsome octavo volume of about 550 pages, with numerous illustrations. (Preparing.) pODGE {HUGH L.), M.D., Emeritus Professor of Midwifery, &c., in the University of Pennsylvania, Ac. THE PRINCIPLES AND PRACTICE OF OBSTETRICS. Illus- trated with large lithographic plates containing one hundred and fifty-nine figures from original photographs, and with numerous wood-cuts. In one large and beautifully printed quarto volume of 550 double-columned pages, strongly bound in cloth, $14. The work of Dr. Hodge is something more than body in a single volume the whole science and art of a simple presentation of his particular views in the Obstetrics. An elaborate text is combined with ac- dejartment of Obstetrics; it is something more curate and varied pictorial illustrations, so that no than an irdinarytreatise on midwifery; it is, in fact, fact or principle Is left unsta ted or unexplained, a cyclopaedia of midwifery. He has aimed to em- -Am. Med. Times, Sept. 3, 1864. *** Specimens of the plates and letter-press will be forwarded to any address, free by mail, on receipt of six cents in postage stamps. ^HADWICK {JAMES R.), A AL,M.D. VA MANUAL OF THE DISEASES PECULIAR, TO WOMEN. In one neat volume, royal 12mo., with illustrations. (Preparing.) Henry C. Lea's Son & Co.'s Publications-(Midwifery). HAMILTON (FRANK H.) M.D., LL.D., Surgeon to the, Bellevue Hospital. New York. A PRACTICAL TREATISE ON FRACTURES AND DISLOCA- TIONS Sixth Edition, thoroughly revised, and much improved. In one very handsome octavo volume of over 900 pages, with 352 illustrations. Cloth, $5 50; leather, £6 50; half Russia, raised bands, $7 00. So many kind expressions of welcome have been Dr Hamilton has devoted great labor to the study showered upon each successive edition of this val- of these subjects. His large experience, extended uable treatise, that scarcely anything remains for research, and patient investigation have made him us to do but to extend the customary cordial greet- one of the highest authorities among living writers ing. It is the only complete work on the subject in this branch of surgery. This work is systematic of Fractures in the English language. We con- and practical in its arrangement, and presents its gratulate the accomplished author on the deserred subject matter clearly and forcibly to the reader success of his work, and hope that he may live to or student.-Maryland Medical Journal, Nov. 15, have many succeeding editions pas- under hisskill- 1880. ed supervision. -Phila. Coll, and Clin. Record, The only complete work on its subject in the Eng" Nov 15, 1880. lish tongue, and, indeed, may now be said to be Universal verdict has pronounced it, humanly the only work of its kind in any tongue. It would speaking, a perfect treatise upon this subject. As require an exceedingly critical examination to de- it is the only complet and illustrated work in any tect in it any particulars in which it might be im- language treating of fracture.- and dislocations, it proved. The work is a monument to American is safe to ufflrm that every wide-awake surgeon and surgery, and will long serve to keep green the general practitioner will regard it as indispensable memory of its venerable author.- Michigan Med. to the safe and pleasant conduct of their profes- News, Nov. 10, 1881. sional work.-Detroit Lancet, Nov. 18, 1SS0. A SHHURST (JOHN, Jr.), M.D., Prof, of Clinical Surgery, Univ, of Pa., Surgeon to the Episcopal Hospital, Philadelphia. THE PRINCIPLES AND PRACTICE OF SURGERY. Second Edition, enlarged and revised. In one very large and handsome octavo volume of over 1000 pages, with 542 illustrations. Cloth, $6; leather, $7; half Russia, $7 50. {Just Ready.) Conscientiousness and thoroughness are two very language all that is necessary to be learned by the marked traits of character in the author of this student of surgery whilst in attendance upon lec- book. Out of these traits largely has grown the tures, or the general practitioner in his daily routine success of his mental fruit in the past, and the pre- practice.-Md. Med. Journal, Jan. 1879. sent offer seems in no wise an exception to what has gone before. The general arrangement of the vol- Th® 7act that this work has reached a second edi- ume is the same as in the first edition, but every part ti°n so very soon after the publication of the first has been carefully revised, and much new matter °ne, speaks more highly of its merits than anything added.-Phila. Med. Times, Feb. 1, 1879. might say in the way of commendation. It , , .. . „ . .... , seems to have immediately gained the favor of stu- The favorable reception of the first edition is a deuts and physicians.-CinAn. Med. News,!^.'^. guarantee of the popularity of this t dition, winch is fresh from the editor's hands with many enlarge- We have previously spoken of Dr. Ashhurst's ments and improvements. The author of this work work in terms of praise We wish to reiterate those is deservedly popular as an editor and writer, and terms here, and to add that no more satisfactory his contributions to the literature of surgery have representation of modern surgery has yet fallen gained for him wide reputation. The volume now from the press. In point of judicial fairness, of offered the profession will add new laurels to those power of condensation, of accuracy and conciseness already won by previous contributions. We can of expression and thoroughly good English, Prof, only add that the work is well arrang'd, filled with Ashhurst has no superior among the surgical writers practical matter, and contains in brief and clear I in America.-Am. Practitioner, Jan. 1879. QTIMSON (LEWIS A.), A.M., M.D., Rj Surgeon to the Presbyterian Hospital. A MANUAL OF OPERATIVE SURGERY. In one very handsome royal 12mo. volume of about 500pages, with 332 illustrations ; cloth, $2 50. {Just Issued.) The work before us is a well printed, profusely performing them. The. work is handsomely illus- illustrated manual of overfour hundred and seventy trated, and the deecriptions are clear and well drawn, pages. The novice, by a perusal of the work, will It is a clever and useful volume; every student gain a good idea of the general domain of operative i should possess one. The preparation of this work surgery, while the practical surgeon has presented does away with the necessity of pondering over to him within a very concise and intelligible form larger works on surgery for descriptions of opera- the latest and most approved selections of operative lions, as it presents in a nut-shell just whatis wanted procedure. Theprecision and conciseness with which I by the surgeon without an elaborate search to find the different operations are described enable the it.-Md. Med Journal, Aug. 1878. author to compress an immense amount ot practical The author's conciseness and the repleteness of information in a very small compass. N. Y. Medical the ^Ork with valuable illustrations entitle it to be Record, Aug. 3,1878. i classed with the text-books for students of operative This volume is devoted entirely to operative sur- i surgery, and as one of reference to the practitioner, gery, and is intended to familiarize the student with i -Cincinnati Lancet and Clinic, July 27, 18/8. the details of operationsand the different modes of SKEY'S OPERATIVE SURGERY. In 1 vol. 8vo. N eit.l, M. D., Professor of Surgery in the Penna, cl of 650 pages ; with about 100 wood-outs $3 25 Medical College, Surg'n to the Pennsylvania Hos- pital, &c. In one very handsome octavo vol. of COOPER'S LECTURES ON THE PRINCIPLESAND 739 pages, with 316 illustrations, cloth, $3 75. Practiceof Surgery. Ini vol. 8vo. cl'h. 750p. $2. milleu»sprinc1PLESOF SURGERY. Fourth Arne- GIBSON'SINSTITUTES AND PRACTICE OF BUR- rican, from the Third Edinburgh Edition. In one gery. Eighth edit'n, improved and altered. With large 8vo. vol. of 700 pages, with 340 illustrations, thirty-four plates. In two handsome octavo vol- cloth, $3 75. umes.aboutlOOOpp..leather. raised bandr. $6 50. MILLER'S PRACTICE OF SURGERY. Fourth Arne- THE PRINCIPLES AND PRACTICE OF SURGERY. rican, from the last Edinburgh Edition Revised by By Willi am PikriEjF.R S.E., Profes'rof Surgery the American editor. In onelarge 8vo. vol. of nearly in the University of Aberdeen. Edited by John 700 pages, with 364 illustrations: cloth, $3 75. Henry C. Lea's Son & Co.'s Publications-(Surgery). 25 26 fl ROSS (SAMUEL D.), M.D., Professor of Surgery in the Jefferson Medical College of Philadelphia. A SYSTEM OF SURGERY: Pathological, Diagnostic, Therapeutic and Operative. Illustrated by upwards of Fourteen Hundred Engravings. Fifth edition, carefully revised and improved. In two large and beautifully printed imperial octavo vol- umes of about 2300 pp., strongly bound in leather, with raised bands, $15; half Russia, raised bands, $16. We have seldom read a work with the practical " Primus inter Pares.'' It Is learned, scholar-like, me- value of which we have been moreimpressed. Every thodical, precise, and exhaustive. We scarcely think chapter is-io concisely put together, that the busy any living man could write socompleteand faultless a practitioner, when in difficulty, can at once find the treatise, or comprehend more solid, instructive matter information he requires. Uis work is cosmopolitan, in the given number of pages. The labor must have the surgery of the world being fully represented in it. been immense, and the work gives evidence of great The work, in fact, is so historically unprejudiced, and powers of mind, and the highest order of intellectual so eminently practical, that it is almost a false compli- discipline and methodical disposition and arrangement ment to say that we believe it to be destined to occupy of acquired knowledge and personal experience.-A.K. a foremost place as awork ofreference, while a system Med. Journ., Feb. 1873. of surgery like the present system of surgery is the As a whole, we regard the work as the representative practice of surgeons. Ihe pnntingand bindingof the "System of Surgery" in the English language.-St. work is unexceptionable; indeed it contrasts, in the Louis Medical and Surg. Journ., Oct. 1872. latter respect, remarkably with English medical and , ' surgical cloth-bound publications, which are generally The two magnificent volumes before us afford a very so wretchedly stitched as to require re-binding before complete view of the surgical knowledge of the day. they are any time in use.-Dub. Journ. of Med. Sci., Some ??ars ha,d pleasure of presenting the March 1874 first edition of Gross's Surgery to the profession as a . . , . .... work of unrivalled excellence; and now we have the Dr. Gross s Surgery, a great work, has become still regun of years of experience, labor, and study, all con- greater, both in size and merit, in its mostrecent form. | densed upon the great work before us. And to students The difference in actual number of pagesis not more or practjtioners desirousofenriching theirlibrary with than 130, but. the size of the page having been in- a treagure of reference, we can simply commend the creased to what we behove is technically termed ele- pUrchase of these two volumes of immense research.- phant,''there has been roomforconsiderableadditions, 'Gincinnati Lancetand Observer, Sept. 1872. which, together with the alterations, are improve- , , x . . . . . . mental-Lond. Lancet, Nov. 16,1872. A complete system of surgery-not a mere text-book of operations, but ascientific accountof surgical theory It combines, as perfectly as possible, the qualities of and practice in all its departments.-Brit, and For. a text-book and work of reference. We think this last Med. Chir. Rev., Jan. 1873. edition of Gross's "Surgery," will confirm his title of T)Y THE SAME AUTHOR. A PRACTICAL TREATISE ON THE DISEASES, INJURIES and Malformations of the Urinary Bladder, the Prostate Gland and the Urethra. Third Edition, thoroughly Revised and Condensed, by Samuel W. Gross, M.D., Surgeon to the Philadelphia Hospital. In one handsome octavo volume of 574 pages, with 170 illus- trations: cloth, $4 50. (Just Issued.) For reference and general information, the physician eases of the urinary organs.-Atlanta Med. Journ.,Oct. orsurgeoncan find no work that meets their necessities 1876. more thoroughly than this, a revised edition of an ex- jg wjth pleasure we now again take up this old cellent treatise, and no medical library should be with- worj( jn a decidedly new dress. Indeed, it must be re- out it. Replete with handsome illustrations and good garded as a new book in very many of its parts. The ideas, it has the unusual advantage of being easily chapters on "Diseases of the Bladder," "Prostate comprehended,by the reasonableand practical manner Body;>> and "Lithotomy," are splendid specimens of in which the various subjects are systematized and descriptive writing; while the chapter on "Stricture" arranged We heartily recommend it to the profession is one of the most concise and clear that we have ever as a valuable addition to the importanthterature of dis- read.-New York Med. Journ., Nov .1876. UK THE SAME AUTHOR. A PRACTICAL TREATISE ON FOREIGN BODIES IN THE AIR-PASSAGES. In 1 vol. 8vo., with illustrations, pp. 468, cloth, $2 75. TAR UITT (ROBERT), M.R. C.S., ^THE PRINCIPLES AND PRACTICE OF MODERN SURGERY. A new and revised American, from the Eighth enlarged and improved London edition. Illus- trated with four hundred and thirty-two wood engravings. In one very handsome octavo volume, of ndhrly 700 large and closely printed pages, cloth, $4 00 ; leather, $5 00. All that the surgi^Al student or practitioner eould practice of surgery are treated, and so clearly and desire.-Dublin Quarterly Journal. perspicuously, as to elucidateevery important topic. It is a most admirable book. We do not know We have examinedthebook most thoroughly, and when we have examined one with more pleasure.- can say that this successis well merited. His book, Boston Med and Surg. Journal. moreover, possesses the inestimable advantages of having the subjects perfectly well arranged and In Mr. Druitt's book, though containing only some classified and of being written in a style at once seven hundred pages, both the principles and the clear and succinct.-Am. Journal of Med. Sciences. ASHTON ONTHE DISEASES, INJURIES, and MAL- SARGENT ON BANDAGING AND OTHER OPERA- FORMATIONS OF THE RECTUM AND ANUS; TIONS OF MINOR SURGERY. New edition, with with remarks on Habitual Constipation. Second an additional chapter on Military Surgery. One American, from the Fourthand enlarged London 12mo. vol. of 383pages withl84 wood-cuts Cloth, Edition. With illustrations. In one 8vo. vol. of $1 76. 287 pages, cloth,$3 26. Henry C. Lea's Son & Co.'s Publications-(Surgery'). JJOLMES {TIMOTHY}, M.A., Surgeon and Lecturer on Surgery at St. George's Hospital, London. A SYSTEM OF SURGERY; THEORETICAL AND PRACTICAL. In Treatises by various authors. American Edition, Thoroughly revised and rewritten bv John H Packard, M.D., Surgeon to the Episcopal and St. Joseph's Hospi- tals, Philadelphia, assisted by a large corps of the most eminent American surgeons. In three large and very handsome imperial octavo volumes of about 1000 pages each, with over 1000 illustrations on wood and thirteen lithographic plates, beautifully colored. (Sold only by subscription.} Price per volume, in cloth, $6 00; in leather, $7 00; in half Russia, $7 50. Per set, in cloth, $18 00 ; in leather, $21 00 ; in half Russia, $22 50. Volume I. (nearly ready} contains General Pathology, Morbid Processes, Injuries in General, Complications of Injuries and Injuries of Regions. Volume II. (shortly) contains Diseases of Organs of Special Sense, Circulatory Sys- tem, Digestive Tract and Genito-urinary Organs. Volume III. (shortly) contains Diseases of the Respiratory Organs, Joints, Bones, and Muscles, Operative and Minor Surgery, Gunshot Wounds, Hospitals and Miscel- laneous Subjects. This great work, issued some years since in England, has won such universal confidence wherever the language is spoken, that its republication' here, in a form more thoroughly adapted to the wants of the American practitioner, has seemed to be a duty owing to the pro- fession. To accomplish this, the aid has been invited of over thirty of the most distinguished gentle- men, in every part of the country, and for more than a year they have been assiduously engaged upon the task. Though the original work presents the combined labor of the most eminent members of all the most^jarominent schools of England, yet the lapse of time since the appear- ance of the last edition, the progress of science, and the peculiarities of American practice, have rendered necessary a most careful, thorough, and searching revision. Each article has been placed in the hands of a gentleman specially competent to treat its subject, and no labor has been spared to bring each one up to the foremost level of the times, and to adapt it thor oughly to the practice of the country. In certain cases, this has rendered necessary the sub- stitution of an entirely new essay for the original, as in the case of the articles on Skin Diseases, and on Diseases of the Absorbent Systrm, where the views of the authors have been superseded by the advance of medical science, and new articles have therefore been prepared by Drs. Arthur Van Harlingen and S. C. Busey, respectively. So also in the case of Anaesthetics, in the use of which American practice differs from that of England, the original has been supplemented with a new essay by J. C. Reeve, M.D., treating not only of the employment of ether and chloroform, but of the other anaesthetic agents of more recent discovery. The same careful and conscientious revision has been pursued throughout, leading to an increase of nearly one- fourth in matter, while the series of illustrations has been more than doubled, and the whole is presented as a complete exponent of British and American Surgery, adapted to the daily needs of the working practitioner. In order to bring it within the reach of every member of the profession, the five volumes of the original have been compressed into three, by employing a douole-columned imperial octavo page, and in this improved form it is offered at less than one half the price of the original. It is beautifully printed on handsome laid paper and forms a worthy companion to Reynolds's " System of Medicine," which has met with so much favor in every section of the country. The work will be sold by subscription only, and in due time every member of the profession will be called upon and offered an opportunity to subscribe. The few notices appended will serve to indicate the hearty approval accorded to the unrevised edition on its appearance some years since:- There is so much that is instructive, even to the library of the surgeon.-Edinburgh Medical Jour- experienced practitioner, in their practical and dis- nal. criminating manner of dealing with mooted ques- It lg a cyciopa.aia of gurgery of the most complete tions none cf which seem to be neglected; their and extensive character; and we may justly state abundant illustrations drawn at once from an un that lt8 design and execution do great honor to those limited field of hospital experience, and their candid concerned, and that the large number and high and sensible mode ot handling the whole snbject, gtandiDg the aulbors selected for the various that these particular portions ot the work possess a lnonographg render this " System" what it no doubt value winch places them far above any publication wag jntended to be, representative of the actual state on the same topics yet issued in the language.-Am. of surgical Bcience and art in th^conntry.-London Journ. Mt a. Sciences. Lancet The enumeration of the treatises, and the names In conclusion, we will add thatVe can most con- of the surgical writers from whose pens they pro- sciencionsly recommend the book to every medical eeed, suffice to show that this is no ordinary book, practitioner. In recommending the " System of Sur- and that in the thousand pages of this goodly volume gery" to our friends who have to deal in surgical lies a store of information such as no other surgical cases, we by no means wish to confine our recom- work in the language can pretend to offer. Those who meudation to them alone. Every practitioner of are acquainted with the special researches and pub- medicine may cull r jmething worthy of note from a lications of the respective authors will not fail to perusal of this volume.- The British Med. Journal. notice that by a judicious exercise of editorial dis- Tbe four volumes remain a monument to the sur- cretion, each subject has been entrusted, as far as gjcai geniug of Our day. The great majority of me- possible, to a surgeon ot the hospitals who is known tropolitan surgeons of eminence and proved ability to have given especial attention to it, and to possess are repregented in them: and for many years to facilities tor summingup with authority the accepted tomg whoever wishes to know the moat anthori- opinions of the day, and adding original matter to tative words of English Surgical science on most Hie stock. London Lancet. subjects in the domain of surgery, must turn to these The work must be considered a very complete ac- pages to read what there is set forth. But taken as count of everything connected with the science and a whole it is the most important surgical work which practice of surgery. In conclusion we can cordially l'as ever issued from the English press. Loudon leeommend this work as a valuable addition to the Lancet. Henry C. Lea's Son & Co.'s Publications-(Surgery). 27 28 I) RY ANT (THOMAS), F.R.C.S., AA Surgeon to Guy's Hospital. THE PRACTICE OF SURGERY. Third American, from the Sec- ond and Revised English Edition. Thoroughly revised and much improved, by John B. Roberts, M.D. In one large and very handsome imperial octavo volume of over 1000 pages, with 672 illustrations. Cloth, $6 50; leather, $7 50 ; very handsome half Russia, raised bands, $8 00. (Just Ready.) Btr. Bryant's work has long been a favorite one the whole work has been carefully revised, much with surgeons. As its name indicates, it is of a tho- of it has been rewritten, imports nt additions hai e roughly practical character. It is distinctly indi- been made to almost every chapter.-Cincinnati vidual in that it gives the results of the author's Med. News, Jan. 1881. large and varied experience as an operator and cli- The English edition, from which this is printed, nical teacher, and is on that account prized deserv- bag been carefully revised an.l rewritten; almost edly high as an original work. I he sty Ie is neces- every chapter has received additions and nearly ganly condensed, the descriptions of surgical dis- one hundred new cuts int oduced. The labors of eases brief and to the point The illustrations are tbe Atnerjcan editOr, Dr John B. Roberts, have well chosen, and the typical cases of the author s very much increased the value of the book. He experience are full of interest, and are of more i han baK introduced many new illustrations and much ordinary value to the working surgeon. A. 1. new material not found in the English edition. Medical Record, March 5, 1881. He bag wrjtten too with great conciseness, which It is a work especially adapted to the wants of is a rare virtue in an American editor of an English students and practitioners. While not prolix, it work. If one could procure or wished only one affords instruction in sufficient detail for a full un- surgery, this volume would certainly be selected, derstanding of surgical principles and the treat- If he desired two, Erichfen's Surgery would be ment of surgical diseases. It embraces in its scope added, and if he wished a third, Gross's Surgery all the diseases that are recognized as belonging to would justly be the work selected. As the great surgery, and all traumatic injuries. In discussing work of Gross is amply sufficient for the waits of these it has seemed to be the aim of the author any surgeon, the priority given to Erichsen, and rather to present the student with practical infor- above all others, to th* work of Bryant, is no mation, and that alone, than to burden his memory labored eulogy of the last volume, but a simple and with the views of different writers, however dis j u*t statement of its demonstrable and pre-eminent tinguished they might have been. In this edition merits.-Am. Med. Bi-Weekly, Feb. 26, 1881. P RICH SEN (JOHN E.), AJ Professor of Surgery in University College, London, etc. THE SCIENCE AND ART OF SURGERY; being a Treatise on Sur- gical Injuries, Diseases and Operations. Carefully revised by the Author from the Seventh and enlarged English Edition. Illustrated by eight hundred and sixty two en- gravings on wood. In two large and beautiful octavo volumes of nearly 2000 pages : cloth, $8 50 ; leather, $10 50; half Russia, $11 50. (Now Ready.) Of the many treatises on Surgery which it has been The seventh edition is before the world as the last our task to study, or our pleasure to read, there is none word ot surgical science. There may be monographs which in all points has satisfied us so well as the classic which excel it upon certain points, but as a con- treatise of Erichsen. His polished, clear style, his free- spectns upon surgical principles and practice it is dom from prejudice and hobbies, hisunsurpassed grasj unrivalled. It-will well reward practitioners to of his subject, and vast clinical experience, qualify him read it, for it has been a peculiar province of Mr. admirably to write a model text-book. When we wish, Erichsen to demonstrate the absolute interdepend- at the least cost of time, to learn the most of a topic in ence of medical and surgical science We need surgery, we turn, by preference, to his work. It is a scarcely add, in conclusion, that we heartily com- pleasure, therefore, to see that the appreciation of it is mend the work to students that they may be general, and has led to theappearance of anoiher edi grounded in a sound faith, and to practitioners as tion.-Med. and Surg. Reporter, Feb. 2,1878. an invaluable guide at the bedside.-Am Practi- Notwithstanding the increase in size, we observe that tioner, April, 1878. much old matter has been omitted. The entire work For the past twenty years Erichsen's Surgery has has been thoroughly written up, and not merely amend maintained itsplace as the leading text-book, not only ed by a few extra chapters A great improvement has in this country, but in Great Britain. Thatitisable been made in the illustrations. One hundred and fifty to hold its ground, is abundantly proven by the tho- new ones have been added, and many of the old ones roughness with which the present edition has been have been redrawn. The author highly appreciates the revised, and by the large amount of valuable mate- favor with which his work has been received by Ameri- rial that has been added. Aside from this, cne hun- can surgeons, and has endeavored to render his latest dred and fifty new illustrations have been inserted, edition more than ever worthy of their approval. That including quite a number of microscopical appear- he has succeeded admirably, must, we think, be the ances of pathological processes. So marked is this general opinion. We heartily recommend the book to change for the better, that the work almost appears both student and practitioner.-N. Y.Med. Journal, as an entirely new one.-Med. Record, Feb. 23,1878 Feb. 1878. T1OLMES (TIMOTHY), M. Jr, AA Surgeon to St. George's Hospital, London. SURGERY, ITS PRINCIPLES AND PRACTICE. In one hand- some octavo volume of nearly 1060 pages, with 411 illustrations. Cloth, $6; leather, $7 ; half Russia, $7 50. (Just Issued.) This is a work which has been looked for on both its force and distinctness.-N. Y. Med. Record, April sides ofthe Atlantic with much interest. Mr. Holmes 14 1876. is a surgeon of large and varied experience and one It wlll be found a mo8t exceUent epitome of sur- of the best known, and perhaps the most brilliant b the ral practilioner wh^ has not the writer upon surgical subjects in England. It is a *ln/e J Mention to more minute and extended book for students-and an admirab e one-and for work *nd tothe medical student. In fact, weknow the busy general practitioner. It will give a student of no ine we can more cordially recomm nd. The all the knowledge needed to pass a rigid examina- author bag succeeded well in giving a plain and tion The book fairly justifiesthe high expectations practical accouut of each surgical injury and dis- that were formed of it. Its style is clear and forcible £ and of the treatment which is most com- even brilliant at times, and the conciseness needed m0Diy advigabie. It will no doubt become a pop"- to bring it within its proper limits has not impairea larwGrkin the profession, and especially as a text- book.- Cincinnati Med. News, April, 1876. Henry C. Lea's Son & Co.'s Publications-(Surgery). Henry C. Lea's Son & Co.'s Publications-(Ophthalmology'). 29 AWT ELLS ( J. SO EL BERG}, • ' Professor of Ophthalmology in King's College Hospital, &c. A TREATISE ON DISEASES OF THE EYE. Third American, from the Third London Edition. Thoroughly revised, with copious additions, by Chas. 8. Bull, M D., Surgeon and Pathologist to the New York Eye and Ear Infirmary. Illus- trated with about 250 engravings on wood, and six colored plates Together with selec- tions from the Test-types of Jaeger and Snellen. In one large and very handsome octavo volume of 900 pages. Cloth, $5; leather, $6 ; half Russia, raised bands, $6 50. (Just Ready.) The long-continued illness of the author, with its fatal termination, has kept this work for some time out of print, and has deprived it of the advantage of the revision which he sought to give it during the last years of hi- life. This edition has therefore been placed under the editorial supervision of Dr. Bull, who has labored earnestly to introduce in it all the advances which observation and experience have acquired for the theory and practice of ophthalmology since the appearance of the last revision. To accomplish this, considerable additions have been required, and the work is now presented in the confidence that it will fully deserve a continu- ance of the very marked favor with which it has hitherto been greeted as a complete, but con- cise, exposition of the principles and facts of its important department of medical science. The additions made in the previous American editions by Dr. Hays have been retained, including the very full series of illustrations and the test-types of Jaeger and Snellen. This new edition of Dr. Wells's great work on the guage. In the second edition, the author showed eye will be welcomed by the profession at large as industrious research in adding new material from well as by the oculist. It contains much new matter every quarter, and his spirit was eminently candid, relating to treatment and pathology, and is brought A work thus built up by honest effort should not be thoroughly up with the pre-ent status of ophthal- suffered to die, and we are pleased to receive this mology. Its chapter on refraction and accommo- third edition from the hands of Dr. Bull. His labor dation-a subject much discussed of late years, and his been arduous, as the very great number of addi- of great importance-is exceedingly complete.- tions bracketed with his initial testify. Under Louisville Med. News, Nov. 13, I860. the editorship which the third edition has enjoyed, The merits of Wells's treatise on diseases of the work ?s ?ure sustain its good reputation, and eye have been so universally acknowledged, and are maintain its usefulness. N. 1. Med. Journ., Jan. so familiar to all who profess to have given any at- 1881. tention to ophthalmic surgery, that any discussion There is really no work which approaches it in of them at this late day will be a work of superero- adaptation to the wants of the general practitioner, gation. Very little that is practically useful in re- while the most advanced specialist cannot rise from cent ophthalmic literature has escaped the editor, a perusal of its ample pages without having added and the third American edition is well up to the to his knowledge. The American editor, Dr. Bull, times. As a text-book on ophthalmic surgery for the won his spurs in ophthalmology some time back. English-speaking practitioner, it is without a rival. His additions to the work of the lamented Wells are -Am. Journ. of Med. Sei., Jan. 1881. many, judicious, and timely, and in just so much The work has justly held a high place in English have added to its value.-Am. Practitioner, Jan. ophthalmic literature, and at the time of its first ap- 1881. pearance was the best treatise of its kind in the lan- KTETTLESHIP {EDWARD}, F.R.C.S., ■J' Ophthalmic Surg. and Leet. on Ophth. Surg. at St. Thomas' Hospital, London. MANUAL OF OPHTHALMIC MEDICINE. In one royal 12mo volume of over 350 pages, with 89 illustrations. Cloth, $2. (Just Ready.) The author is to be congratulated upon the very information they contain. We do not hesitate to successful manner in which he has accomplished his pronounce Mr Nettleship's book the best manual on task; he has succeeded in being concise without ophthalmic surgery for the use of students and sacrificing clearness, and, including tbe whole " busy practitioners" with which we are acquain- ground covered by more voluminous text-books, ted.-Am. Jour. Med. Sciences, April, 1880. has given an excellent risvmi of all the practical (BARTER {R. BRUDENELL}, F.R.C.S., Ophthalmic Surgeon to St. George's Hospital, etc. A PRACTICAL TREATISE ON DISEASES OF THE EYE. Edit- ed, with test-types and Additions, by John Green, M.D. (of St. Louis, Mo.). In one handsome octavo volume of about 500 pages, and 124 illustrations. Cloth, $3 75. (Just Issued.) It is with great pleasure that we can endorse the work [chapter is devoted to a discussion of the uses a nd selec- as a most valuable contribution to practical ophthal-1 tion ofspectacles, and is admirably compact, plain, and mology. Mr. Carter never deviates from the end he has j useful, especially the paragraphson the treatment of in view, and presents the subjectin a clear and concist presbyopia and myopia. In conclusion, our thanks are manner, easy of comprehension, and hence the more due the author for many useful hintsin the great sub- valuable. We would especially commend, however, as jeet of ophthalmic surgery and therapeutics, afield worthy of high praise, the manner in which the th era- where of late years we glean but a few grains of sound peutics of disease of the eye is elaborated, for here the I wheat from amass ofchaff.-New York Medical Decor d, author is particularly clear and practical, where other : Oct. 23,1875. writers are unfortunately too often deficient. The final DRO WNE {EDGAR A.}, Surgeon co the Liverpool Eye and Ear Infirmary, andtothe Dispensary for Skin Diseases. HOW TO USE THE OPHTHALMOSCOPE. Being Elementary In- structionsin Ophthalmoscopy, arranged for the Use of Students. With thirty-five illustra- tions. In one small volume royal 12mo. of 120 pages : cloth, $1. (Now Ready.) LAURENCE'S HAND7-BOOK OF OPHTHALMIC LAWSON'S INJURIES TO THE EYE, ORBIT SURGERY, for the use of Practitioners. Second AND EYELIDS: their Immediate and Remote edition, revised and enlarged With numerous Effects. With about one hundred illustrations, illustrations. In one very handsome octavo vol- In one very handsome octavo volume, cloth ume, cloth, $2 75. $3 50. 30 RURNETT (CHARLES H.), M.A , M.D J Aural Surg to the Presb. Hosp., Surgeon-in-charge of the Infir. for Dis. of the Ear, Phila. THE EAR, ITS ANATOMY, PHYSIOLOGY AND DISEASES. A Practical Treatise for the Use of Medical Students and Practitioners. In one hand- some octavo volume of 615 pages, with eighty-seven illustrations : cloth, $4 50 ; leather, $5 50 ; half Russia, $6 00. {Now Ready.) Foremost among the numerous recent contribu- the observations and discoveries of others, has pro- tions to aural literature will be ranked this work duced a work which, as a text-book, stands facile of Dr. Burnett. It is impossible to do justice to princeps in our language. We had marked several this volume of over 600 pages in a necessarily brief pa-sages as well wor.hy of quotation and the atten- notice. It must suffice to add that the book is pro- tion of the general practitioner, but their number and fusely and accurately illustrated, the references are the space at our command forbid. Perhaps it is bet- conscientiously acknowledged, while the result has ter, as the book ought to be in the hands of every been to produce a treatise which will henceforth medical student, and its study will well repay the rank with the classic writings of Wilde and Von busy practitioner in the pleasure he will derive from Trdltsch. - The Land. Practitioner, May, 1879. the agreeable style in which many otherwise dry On account of the great advances which have been and mostly unknown subjects are treated. 'Io the made of late years in otology, aud of the increased specialist the work is of the highest value, and his interest manifested in it, the medical profession will sense °f gratitude to Dr. Burnett will, we hope, be welcome this new work, which presents clearly and proportionate to the amount of benefit he can obtain concisely its present aspect, whilst clearly indi- fl'om the caretui study of the book, and a constant eating the direction in which further researches can r^eIellce t0 lt8 trustworthy pages. Edinburgh be most profitably carried on. Dr. Burnett from his Jour., Aug. 18/8. own matured experience, and availing himself of JTAYLOR (ALFRED S.),M.D., J- Lecturer on Med. Jurisp. and Ohemistry in Quy's Hospital. A MANUAL OF MEDICAL JURISPRUDENCE. Eighth Ameri- can edition. Thoroughly revised and rewritten. Edited by John J. Reese, M.D., Pref, of Med. Jurisp. and Toxicology in the Univ, of Penn. In one large octavo volume of ;933 pages, with 70 illustrations. Cloth, $5; leather, $6; half Russia, raised bands, $6 50. {Just Ready ) The American editions of this standard manual is to announce, not criticize the completed task. The have for a Ion/ time laid claim to the attention of value of the gem is too well known to require more the profession in this country; and that the profes- than the telling that the master-hand has rebright- sion has recognized this claim with favor is proven eued its facets and polished its angles before leaving by the call for frequent new editions of the work, it as his legacy to his brethren in the profession.- This one, the eighth, comes before us as embodying Phila Med. Times, Dec. 4, 1880. the latest thoughts and emendations of Dr Tayl.r, It win guffi,e t0 remark that this new edition upon the subject to winch he devoed his life, with stows the signs of judicious revision A great num- an assiduity and success which made him facile ter of illustrative medico-legal cases which have prin'eps among English wnters on medical juris- occurred since the last edition was published are prudence. Both tne author and the book have cjted jn teir proper connection, and add much to made a mark too deep to be affected by criticism, the interest and value of the work; they comprise whether it be censure or piaise. In this case, how- tte bulk of the additions to the text. As an indica- ever, we should only have to seek for laudatory tion of the reshnes<of the work, we notice numev- teims.-Arn. Journ. of Med. Ser., Jan. 1881. ous references to medici-legal experience that has It is not very often that a msdical book reaches its transpired during the year just ended ; among these tenth edition, or that the last earthly labor is per- is a comment by the American editor upon that formed by ihe author in retouching the work that midsummer madness, the Tanner fasting exploit of first came from his hand thirty-five years before, last Augast. In these features and in others there All this, however, has happened in the case of Dr. is ample evidence that this admirable book will Taylor and his classical treatise. The pen dropped maintain its high place as a standard authority con- from the grasp only when the shadows of old age cerniug the matters of which it treats.- Boston were rapidly deepening into the darkness of death. Med. and Surg. Journal, Jan. 13, 1881. Under the circumstances, all the journalist has to do Df THE SAME AUTHOR. THE PRINCIPLESAND PRACTICE OF MEDICAL JURISPRU- DENCE. Second Edition, Revised, with numerous Illustrations. In two large octavo volumes, cloth, $10 00 ; leather, $12 00. This great work isnow recognized in England as the fullest and mostauthoritativetreatise on every departmentof its important subject. In laying it, in its improved form, before the Amer- ican profession, the publishers trust that it will assume the same position in this country. T>Y THE SAME AUTHOR. n POISONS IN RELATION TO MEDICAL JURISPRUDENCE AND MEDICINE. Third American, from the Third and Revised English Edition. In one large octavo volume of 850 pages; cloth, $5 50 ; leather, $6 50. (Just Issued.) The present Is based upon the two previous edi- being described which give rise to legal investiga- tions; "but the completerevision rendered necessary tions. - The Clinic, Nov. 6, 1875. by time has converted it into a new work." This. Dr. Taylor has brought to bear on the compilation statement from the preface contains all that it is de- Of this volume, stores of learning, experience, and sired to know in reference to the new edition. Ihe practical acquaintance with his subject, probably far works of this author are already in the library of beyond what any other living authority on toxicol- every physician who is liable to be called upon for Ogy couid have amassed or utilized. He has fully medico-legal testimony (and whatoneis not?), sothat sugtained his reputation by the consummate skill all that is required to be known about the present an(j iegaj acumen be has displayed in the arrange- book is that the author has kept it abreast with the ment of n18 subject-matter, and the result is a work times. What makes it now, as always, especially on Poisons which willbelndispensable to every stu- valuable to the practitioner is its conciseness ana dent or practitioner in law and medicine.-The Dub- practical character, only those poisonous substances lin journ, of Med Ser., Oct. 1875. Henry C. Lea's Son & Co.'s Publications-(Med. Jurisprudence). Henry C. Lea's Son & Co.'s Publications-(Jhtb. ROBERTS ( WILLIAM}, M.D., A-* Lecturer on Medicine in the Manchester School of Medicine, etc. A PRACTICAL TREATISE ON URINARY AND RENAL DIS- EASES, including Urinary Deposits. Illustrated by numerous cases and engravings. Third American, from the Third Revised and Enlarged London Edition. In one large and handsome octavo volume of over 600 pages. Cloth, $4. (Just Ready.) THOMPSON {SIR HENRY}, Surgeon and Professor of Clinical Surgery to University College Hospital. LECTURES ON DISEASES OF THE URINARY ORGANS. With illustrations on wood. Second American from the Third English Edition. In one neat octavo volume. Cloth, $2 25. (Just Issued.) JOY THE SAME AUTHOR. ON THE PATHOLOGY AND TREATMENT OF STRICTURE OF THE URETHRA AND URINARY FISTULAS. With plates and wood-cuts. From the third and revised English edition. In one very handsome octavo volume, cloth, $3 50. (Lately Published.) rrUKE {DANIEL HACK}, M.D., A- Joint author of The Manual of Psychological Medicine, &c. ILLUSTRATIONS OF THE INFLUENCE OF THE MIND UPON THE BODY IN HEALTH AND DISEASE. Designed to illustrate the Action of the Imagination. In one handsome octavo volume of 416 pages, cloth, $3 25. (Lately Issued.) -DLANDFORD {G. FIELDING}, M.D., F.R.C.P., J-' Lecturer on Psychological Medicine at the School of St. George's Hospital, &e. INSANITY AND ITS TREATMENT: Lectures on the Treatment, Medical and Legal, of Insane Patients. With a Summary of the Laws in force in the United States on the Confinement of the Insane. By Isaac Ray, M. D. In one very handsome octavo volume of 471 pages; cloth, $3 25. It satisfies a want which must have been sorely actually seen in practice and the appropriate treat- feltbythebusygeneralpractidonersofthiscountry. ment for them, we find in Dr. Blandford's work a It takes the form of a manual ofclinicaldescription considerable advanceover previous writings on the of the various forms of insanity, with a description subject. His pictures of the various forms of mental of the mode of examining persons suspected of in- disease are so clear and good that no reader can fail sanity. We call particular attention to this feature to be struck with their superiority to those given in of the book, as giving it a unique value to the gene- oidinary manuals in the English language or (so far ral practitioner. If we pass from theoretical conside- as our own reading extends) in any other.-London rations to descriptions of the varietiesof insanity as Practitioner, Feb. 1871. f EA {HENRY C.}. ^SUPERSTITION AND FORCE: ESSAYS ON THE WAGER OF LAW, THE WAGER OF BATTLE, THE ORDEAL AND TORTURE. Third Revised and Enlarged Edition. In one handsome royal 12mo. volume of 552 pages. Cloth, $2 50. (Just Ready.) This valuable work is in reality a history of civi- more accurate than either of the preceding, but lization as interpreted by the progress of jurispru- from the thorough elaboration, is more like a har- dence. . . . In " Superstition and Force" we have monious concert and less like a batch of studies.- a philosophic survey of the long period intervening The Nation, Aug. 1, 1878. between primitive barbarity and civilized enlight- Many will ba tempted to say that this, like the R6™ * "Ot % Cn aptfel7n/ e that "Declineand Fall,"isone of the uncriticizable books should not be most carefully studied and however Its fact8 ftre innumerable, its deductions simple and well versed the reader may be tn the science of inevitable, and its chevaux-de-frise of references jurisprudence he will find much in;Mr. Lea's vol- bristlingand dense enough to make the keenest ume of which he was previously ignorant. The stouteKt and best eoninned assailant thlnfc book is a valuable addition to the literature of Se advancing TorT theT^ soma! science.- Westminster Review, Jan. 1880. vergial init t0 pgrovoke as8Rult. The author is no The appearance of a new edition of Mr. Henry C. polemic. Though he obviously feels and thinks Lea's "Superstition and Force" is a sign that our strongly, he succeeds in attaining impartiality highest scholarship is not without honor in its na Whether looked on as a picture or a mirror, a work tive country. Mr. Lea has met every fresh demand such as this has a lasting value.-Lippincott's for his work with a careful revision of it, and the Magazine, Oct. 1878. present edition is not only fuller and, if possible, ^Y THE SAME AUTHOR. STUDIES IN CHURCH HISTORY. THE RISE OF THE TEM- PORAL POWER-BENEFIT OF CLERGY-EXCOMMUNICATION. In one large royal 12mo. volume of 516 pp.; cloth, $2 75. (Lately Published.) The story was never told more calmly or with hasapeculiarimportancefortheEnglishstudent,and greater learning or wiser thought. Wedoubt, indeed, is a chapter on Ancient Lawlikely tobe regarded as if any other study ofthis field can be compared with final. Wecan hardly pass from our mention ofsuch this for clearness, accuracy, and power. - Chicago works as these-with which that on "Sacerdotal Examiner, Dec. 1870. Celibacy'' should be included-without noting th e Mr. Lea's latest work, " Studiesin Church History," literary phenomenon that the head of one of the first fully sustains the promise of the first. It deals with American housesisalso the writer of someofitsmost three subjects-the Temporal Power, Benefit of original books.-London Athenaeum, Jan. 7,1871. Clergy, and Excommunication, the record of which ^±enry C. Lea's Son & Co.'s Publications. INDEX TO CATALOGUE. PAGE American Journal of the Medical Science# . 1 Allen's Anatomy 7 Anatomical Atlas, by Smith and Horner . . 7 Ashton on the Rectum and Anus . . .26 Attfield's Chemistry .9 Ashwell on Diseases of Females . . .21 * Ashhurst's Surgery 25 Browne on Ophthalmoscope 29 Browne on the Throat 19 ♦Burnett on the Ear 30 *3arnes on Diseases of Women . . . .22 Barnes' Midwifery 24 Bellamy's Surgical Anatomy .... 7 *Bryant'sPractice of Surgery .... 28 Bloxam's Chemistry 10 Blandford on Insanity 31 Basham on Renal Diseases 20 Bartholow on Electricity ..... 18 Barlow's Practice oi Medicine . . . . 14 Bowman's (John E.)Practical Chemistry. . 9 *Bristowe's Practice 14 ♦ Bumstead on Venereal 20 Bumstead and Cullerier's Atlas of Venereal . 20 ♦Carpenter's Human Physiology . . 8 Carpenter on the Use and Abuse of Alcohol . 11 ♦Cornil and Ranvier 13 Carter on the Eye 29 Cleland's Dissector 7 Classen's Chemistry 9 Clowes' Chemistry 10 Century of American Medicine .... 5 Chadwick on Diseases of Women . . .24 Chambers on Diet and Regimen . . . .20 Christison and Griffith's Dispensatory . . 11 Churchill's Practice of Midwifery . . . 21 Churchill on Puerperal Fever . . . .21 Condie on Diseases of Children . . . .20 Cooper's (B. B.) Lectures on Surgery . . 25 Cullerier's Atlas of Venereal Diseases . . 20 Cycloptedia of Practical Medicine • .15 Duncan on Diseases of Women . . . .23 ♦Dalton's Human Physiology .... 8 Davis's Clinical Lectures 15 Dewees on Diseases of Females . . . .21 Druitt.'s ModernSurgery 26 ♦Dungiison's Medical Dictionary ... 4 Ellis's Demonstrations in Anatomy ... 7 ♦Erichsen's System of Surgery . . .28 ♦Emmet on Diseases of Women . . . .23 Farquharson's Therapeutics .... 11 Foster's Physiology 8 Fenwick's Diagnosis 14 Finlayson's Clinical Diagnosis .... 16 Flint on Respiratory Organs . . . . 19 Flint on the Heart 19 ♦Flint's Practice of Medicine .15 Flint's Essays 15 ♦Flint's Clinical Medicine 15 Flint on Phthisis 19 Flint on Percussion 19 ♦Fothergill's Handbook of Treatment . . 16 Fownes's Elementary Chemistry . • . 10 Fox on Diseases of the Skin .... 19 Fuller on the Lungs, &c. . . . . .20 Green's Pathology and Morbid Anatomy . . 14 Greene's Medical Chemistry .... 9 Gibson's Surgery . • • • • .25 Gluge's Pathological Histology, by Leidy . . 14 ♦Gray's Anatomy.. 6 Galloway's Analysis . . . . . . 9 Griffith's (R. E.) Universal Formulary . . 11 Gross on Sterility 20 Gross on Urinary Organs 26 Gross on Foreign Bodies in Air-Passages . . 26 ♦Gross's System of Surgery . ... 26 Habershon on the Abdomen 14 ♦Hamilton on Dislocations and Fractures . . 25 Hartshorne's Essentials of Medicine . . .16 Hartshorne's Conspectus of t h e Medical Sciences 6 Hartshorne's Anatomy and Physiology . . 7 Hamilton on Nervous Diseases . . . .18 Heath's Practical Anatomy .... 6 Hoblyn's Medical Dictionary . . . . 4 Hodge on Women 22 PAGB Hodge's Obstetrics ... ' . . 24 Holland's Medical Notes and Reflections . . 14 ♦Holmes's Surgery 28 Holden's Landmarks 6 Horner's Anatomy and Histology . . . 7 Hudson on Fever 20 Hill on Venereal Diseases 20 Hillier's Handbook of Skin Diseases . . 19 Jones (C. Handheld) on Nervous Disorders . 19 Knapp's Chemical Technology . . . 19 Keating on Infauts 21 Lea's Superstition and Force . • • 31 Lea's Studies in Church History . . . 31 Lee on Syphilis 20 ♦Leishman's Midwifery 24 La Roche on Yellow Fever 14 La Roche on Pneumonia, &c 20 Laurence and Moon's Ophthalmic Surgery . 29 Lawson on the Eye ... ... 29 Lehmann's Physiological Chemistry, 2 vols. . 8 Lehmann's Chemical Physiology . . 8 Ludlow's Manual of Examinations ... 5 Lyons on Fever 20 Maisch's Materia Medica 13 Mitchell's Nervous Diseases of Women . . 18 Medical News and Abstract ... 2 Morris on Skin Diseases 19 Meigs on Puerperal Fever 21 Miller's Practice of Surgery . . . . 25 Miller's Principles of Surgery . . . .25 Montgomery on Pregnancy . ... 21 Nettleship's Ophthalmic Medicine . . .29 Neill and Smith's Compendium ol Med Science 5 Parvin's Midwifery 24 Parry on Extra-Uterine Pregnancy . . .23 Pavy on Digestion . . .14 ♦Parrish's Practical Pharmacy . . .11 Pirrie's System of Surgery .... 25 ♦Playfair's Midwifery 24 Quain and Sharpey's Anatomy, by Leidy . . 7 ♦Reynolds' System of Medicine . . . .17 Richardson's Preventive Medicine . . .16 Roberts on Urinary Diseases . . • .31 Ramsbotham on Parturition ... 23 Remsen's Principles of Chemistry ... 9 Rigby's Midwifery 21 Rodwell's Dictionary of Science . ... 4 Stimson's Operative Surgery ... .25 Swayne's Obstetric Aphorisms . . . .21 Seiler on the Throat 19 Sargent's Minor Surgery 26 Sharpey and Quain's Anatomy, by Leidy . . 7 Skey's Operative Surgery 25 Slade on Diphtheria 20 Schafer's Histology 7 ♦Smith (J. L.) on Children 21 Smith (H. H.) and Hemer's Anatomical Atlas 7 Smith (Edward) on Consumption . . 20 Smith (Eust ) on Wasting Diseases in Children 20 ♦Stille's Therapeutics 13 *Still6 & Maisch's Dispensatory . . . .12 Sturges on Clinical Medicine . • . .15 Stokes on Fever 14 Tanner's Manual of Clinical Medicine . . 5 Tanner on Pregnancy . .... 23 ♦Taylor's Medica] Jurisprudence . .30 Taylor's Principles and Practice of Med Jurisp 30 Taylor on Poisons . • .30 Tuke on the Influence of the Mind . . .31 ♦Thomas on Diseases of Females . . . 22 Thompson on Urinary Organs . . . .31 Thompson on Stricture 31 Todd on Acute Diseases 14 Woodbury's Practice 16 Walshe on the Heart 20 Watson's Practice of Physic .... 16 ♦Wells on the Eye 29 West on Diseases of Females .... 21 West on Diseases of Children .... 21 Weston Nervous Disorders of Children . . 21 Williams on Consumption . ... 20 Wilson's Human Anatomy 7 Wilson's Handbook of Cutaneous Medicine . 20 Wiihler's Organic Chemistry .... 9 Winckel on Childbed 21 Books marked * are also bound in half Russia. HENBY C. LEA'S SON & CO.-Philadelphia.