tMtMto&tMiW*- /.vtH K %&x ::,/\ /;//;/»&///. NLM 051107140 7 NATIONAL LIBRARY OF MEDICINE Surgeon General's Office Gt t & ^section,.......................................... ....... n.....U%/ 3 I, J& NLM051107407 ON DISEASES OF THE LUNGS AND PLEURAE INCLUDING CONSUMPTION R. DOUGLAS POWELL, M.D., Lond. Fellow of the Royal College of Physicians ; Physician to the Middlesex Hospital and Joint-Lecturer on Practical Medicine at the Medical School; Physician to the Hospital for Consumption and Diseases of the Chest at Brompton ; Late Assistant Physician and Lecturer on Materia Medica at the Charing Cross Hospital. CbirO EDition RE-WRITTEN AND ENLARGED, WITH ILLUSTRATIONS. NEW YOEK: WILLIAM WOOD & COMPANY 56 & 58 Lafayette Place 1886 ^f \ 8 ' • *. The Publishers Book Composition and Electrotyping Co. 157 and 159 William Street New York XLo LIOXEL SMITH BEALE, M.B., F.R.C.P., F.R.S., professor op medicine at king's college, physician to king's college hospital, THIS BOOK IS INSCRIBED WITH THE AFFECTION AND GREAT RESPECT OF Gbe Butbor. PREFACE. The present volume is an amplified edition of the work on Consumption and on certain Diseases of the Lungs and Pleural, which was published in 1878. The entire work has been re- considered, and for the most part rewritten ; and new chapters have been added on the Physical Examination of the Chest; on Asthma ; on the Etiology of Phthisis ; on the Complications of Phthisis ; on the Surgical Treatment of Pulmonary Cavities ; on Hydatid of the Lungs, and on Mediastinal Tumors. The prophy- laxis and treatment of Consumption has, contrary to the general plan of the book, and with the view of avoiding repetitions, been dealt with in chapters apart from those in which the varieties of the disease are described. The author trusts that no apology is needed for the compara- tively large portion of the work which has been devoted to treat- ment. Only those measures of treatment, however, have been advocated of the value of which the author has been practically convinced, and many remedial measures have on this account been omitted or only barely alluded to. In thus exercising his discretion, the author has felt the double responsibility of, on the one hand, avoiding a multiplicity of remedies that would only prove an embarrassment to the earnest practitioner, and, on the other, of omitting nothing of real value in treatment. The author is conscious of some failing in both these directions, especially in the section dealing with the climatic treatment of Phthisis ; all that he can plead is that he has written up to the y[ PREFACE. limits of his present convictions and experience ; his responsibil- ity is lightened by the knowledge of the recent works written by those able climatologists to whom he has alluded in the text. The very friendly reception which his former work met with by his professional brethren, encourages the author to hope that some of the short-comings of the present book will be indulgently attributed to the increasing cares and interruptions under which it has been written. The sincere thanks of the author are due to many friends who have helped him by suggestions and information in the course of his work, and acknowledgments are also due to his friend, Mr. J. Bland Sutton, for careful revision of proofs and preparation of Index. 62 Wimpole Street. CONTENTS. CHAPTER I. On some Essential Points in the Anatomy and Functions of the Lungs. PAGE The anatomy of the lungs. Pulmonary circulation. Respiratory func- tion and mechanism. Respiration in the new-born child. The con- tractile powers of the lung, their residual tension and elastic resilience. Schema for demonstrating the respiratory movements. The statics of respiration. Lymphatics and nerves of the lung. CHAPTER II. The Physical Examination of the Chest. The chest, its shape and measurements. The cyrtometer. Pneuma- tometry. Spirometry. Vital capacity ; influence of body weight on. Topography of the chest. Physical exploration, inspection, move- ments, etc. Methods of percussion. Table of terms. Auscultation. Breath-sounds, healthy and morbid; their probable mechanism and significance. Microscopical examination of the sputum. . . .16 CHAPTER III. Diseases and Deformities of the Chest Walls.' Pleurodynia. Aponeurotic rheumatism. Myalgia. Intercostal neural- gia. Herpes zoster. Perichonditis and periostitis of ribs. Fascial creaking. The rickety thorax. Alar thorax. .... 47 CHAPTER IV. Diseases of the Pleura. Classification of pleurisies. Simple pleurisy; pathology; symptoms; dull- ness ; displacement of heart; absence of vocal fremitus ; supplemen- tary signs ; pressure signs ; diagnosis ; treatment. Local pleurisy from extension ; treatment. Secondary pleurisy ; septic. Suppura- tive pleurisy ; symptoms ; physical signs ; pectoriloquie aphonique ; putrid effusions ; treatment..........51 CHAPTER V. On Pleuritic Effusions, considered especially with regard to Operative Treatment. Classification of pleuritic effusions :—Simple inflammatory and chronic pleuritic effusion. Paracentesis thoracis in serous effusions ; local Vlll CONTENTS. anaesthesia ; requisites for operating ; Potain's aspirator ; Empyema ; thoracentesis ; mode of operating. Single opening and injection of pleura ; double opening...........' 0 CHAPTER VI. Pneumo-thorax, Hydro- and Pyo-Pneumo-thorax. Causation of pneumo-thorax ; symptoms ; physical signs ; displacement of heart; diagnosis; prognosis ; treatment. Hsemo-thorax. . . 88 CHAPTER VII. Bronchitis—Bronchial Catarrh. Definition of the disease ; etiology ; symptoms ; diagnosis; prognosis and treatment. Dust bronchitis, case in illustration. Plastic bronchitis : pathology ; physical signs ; prognosis and treatment. 98 CHAPTER VIII. On Pulmonary Vesicular Emphysema. Pathology of the disease. Compensatory changes. Etiology. Discussion of the views of Sir William Jenner, Rindfleisch, Gairdner, and Freund. Failure of nutrition a possible factor in its causation. Clinical vari- eties of the disease. Local pulmonary emphysema. General emphy- sema ; large lunged, small lunged ©r senile emphysema. Illustrative case, tracings of thoracic movement. Treatment. . . .111 CHAPTER IX. (Edema of the Lungs. Varieties of the condition ; inflammatory ; mechanical. Morbid anato- my; symptomatology; prognosis and treatment. . . . 12:3 CHAPTER X. Pneumonia. Definition of the disease; etiology ; individual predisposition ; previous diseases ; climatic influences ; epidemic influences ; exciting causes ; septic causes ; infectious 'pneumonia. Pneumonococci, observations of Friedlander, Giles, Klein, Ziehl. Salvioli, Zaslein, and Dreschfeld. Pathology and morbid anatomy ; various stages of the diseases, symp- toms in the various stages of hepatization, crisis and resolution. Comparison of the temperature of pneumonia and idiopathic ery- sipelas. Pythogenic pneumonia; illustrative case; termination of ■ pneumonia; diffuse suppuration; abscess; gangrene and oedema. Prognosis ; exceptional symptoms ; convulsions ; jaundice ; delirium ; exalted temperature ; haemoptysis. Treatment, in the stage of hy- peraemia, consolidation, crisis period, and resolution ; in sphacelus, purulent infiltration, and in abscess. . . . . .125 CHAPTER XI. Broncho-Pneumonia. Definition of the disease. Etiology ; symptoms ; varieties ; disseminated broncho-pneumonia and the confluent form ; physical signs, course and treatment . . . . . . . .144 CONTENTS. ix CHAPTER XII. Narrowing and Dilatation of the Bronchi. Narrowing of the bronchi; etiology ; varieties ; symptoms of bronchial narrowing and its treatment. Dilatation of the bronchi—bronchi-ec- tasis—cylindrical and sacculated. Causes of bronchial dilatation. Symptomatology and treatment ...... 148 CHAPTER XIII. Abscess and Gangrene of the Lung. Etiology and varieties of suppuration of pulmonary tissue. Symptoms and treatment. Gangrene of the lung ; circumscribed ; diffuse eti- ology, symptoms, physical signs, and treatment .... 155 CHAPTER XIV. The Surgical Treatment of Pulmonary Cavities. The kinds of cavities for surgical treatment. Distinction of pulmonary from pleural cavities. Methods for defining the outlines of a cavity. Surgical exploration. Various steps in the surgical procedures . . 158 CHAPTER XV. Asthma. Definition of the disease ; its relation to bronchial spasm ; clinical facts and arguments in support of the view. Etiology of asthma ; various exciting causes ; direct irritation ; reflex and centric irritation ; erup- tive affections of the bronchial tract. Symptomatology ; mode of attack; physical signs; prognosis; clinical varieties of asthma. Idio- pathic or true catarrhal asthma, peptic, cardiac, eruptive, ursemic and other toxasmic forms. Treatment; climatic ; medicated airs and baths ; regulation of the digestive function ; treatment of the par- oxysm .......... 164 CHAPTER XVI. On the Pathology of Phthisis. Nature of the morbid processes which lead to phthisis. Characters of tubercle; the initial processes ; broncho-alveolitis ; pulmonary fi- brosis. The giant-cell; views of Burdon Sanderson, Wilson Fox, and others, on the primary seat of tubercle. The influence of the respir- atory movement upon the lesions of phthisis .... 178 CHAPTER XVII. Etiology of Phthisis. Causative conditions. Predisposition and the tubercle bacillus. Descrip- tion of the bacillus, and discussion as to its relationship with phthisis. Contagious nature of phthisis considered; climatic causes; dusty occupations; social conditions, and constitutional liability. Inher- ited tendencies ......... 18(i X CONTENTS. CHAPTER XVIII. On the Varieties of Phthisis. PAGE Pneumonic phthisis and its varieties. Alveolar catarrh. Catarrhal phthi- sis ; cases in illustration. Acute pneumonic phthisis ; confluent form; case in illustration of the disseminated variety . . . .197 CHAPTER XIX. Chronic Pneumonic Phthisis—Fibroid Phthisis. Illustrative case of the chronic pneumonic form. Fibroid phthisis ; its secondary nature ; case in illustration. Diagnosis and prognosis . 209 CHAPTER XX. Tubercular Phthisis. Acute tuberculo-pneumonic phthisis, the characteristic phenomena illustrated by typical clinical examples. Chronic tubercular phthisis; pulmonary tuberculisation ; clinical symptoms.....219 CHAPTER XXI. On the Cavity Stage of Phthisis. Stages in the formation of cavities; varieties of cavities, recent, quies- cent, secreting and ulcerous. Signs of cavities. Elastic tissue in sputum ; its significance. Extension of cavities. Cicatrisation. Ulcer- ous cavities ; their septic nature.........225 CHAPTER XXII. On Haemoptysis. Causes of haemoptysis classified. Hemorrhage from pulmonary artery or its capillaries ; from bronchial artery or capillaries ; from the aorta or one of its great branches. Symptoms, diagnosis, prognosis, and treatment. 233 CHAPTER XXIII. On Hemorrhagic Phthisis and Recurrent Hemoptysis. Hemorrhage, its causative relation to phthisis. Recurrent hemoptysis. Illustrative case. Pathology .... .239 CHAPTER XXIV. On False or Spurious H.emoptysis. Various sources of hemorrhage, apparent and real. Means of distin- guishing spurious haemoptysis. Treatment......245 CHAPTER XXV. Laryngeal Phthisis-Ulceration of the Bowels in Phthisis. Laryngeal phthisis; primary and secondary; morbid anatomy and symp- toms of the disease ; methods of physical examination and diagnosis. Ulceration of the bowel ; seat of the disease ; symptoms . . .250 CONTENTS. XI CHAPTER XXVI. Bronchi-ectatic Phthisis—Dust Phthisis—Diabetic Phthisis. PAGE Bronchi-ectatic phthisis ; general account. Dust phthisis; etiology of the disease. Phthisis occurring in diabetic patients .... 260 CHAPTER XXVII. Syphilitic Disease of the Lung—Sytphilitic Phthisis. Syphilitic ulceration of the bronchial tubes; modes of affection ; congen- ital ; acquired ; symptoms ; physical signs. Syphilitic phthisis. . 264 CHAPTER XXVIII. On other important Complications of Phthisis. Tubercular meningitis ; illustrative case. Analysis of symptoms. Dura- tion of the disease. Lardaceous disease. Albuminuria as a compli- cation of phthisis. Fistula..........268 CHAPTER XXIX. General Remarks on the Prophylaxis and Treatment of Phthisis. Threatened and incipient phthisis ; General remarks on the treatment of phthisis ; hygiene of the sick room ; Koumiss in phthisis . . . 277 CHAPTER XXX. Remarks on Climatic Change and Treatment for Early Stage cases of Phthisis. Climatic resorts. Marine, maritime, and inland climates. Autumn re- sorts. Sea voyages. Winter resorts. Spring stations. Summer . 287 CHAPTER XXXI. Treatment of Phthisis (continued). Acute first stage cases. The uses and administration of cod-liver oil in phthisis. Substitutes for the oil. Acute pneumonic phthisis. Py- rexia. Topical medication of the lung. Night-sweats. General sum- mary...............300 CHAPTER XXXII. Treatment of Phthisis {continued). Quiescent, secreting and ulcerous cavities ; surgical treatment in ulcer- ous cavities. Chronic and fibroid stages of phthisis. Tubercular phthisis. Bronchi-ectatic phthisis. Syphilitic phthisis. . . . 312 CHAPTER XXXIII. Treatment of Phthisis (continued). Ulceration of the bowel in phthisis ; acute ulceration ; chronic ulceration. Laryngeal phthisis. Haemoptysis ; primary haemoptysis ; recurrent haemoptysis ; intercurrent haemoptysis. Vomiting with cough. In- tercurrent pleurisy, pneumonia, and bronchitis.....318 xn CONTENTS. CHAPTER XXXIV. On Abscess and Growth in the Mediastinum. PAGE Abscess ; its symptoms ; diagnosis and treatment. Mediastinal growths. Pathology ; etiology ; symptoms ; physical signs ; and diagnosis . 327 CHAPTER XXXV. Hydatid of the Ling. Symptoms ; before rupture ; after rupture of the cysts ; treatment . . 333 APPENDIX. Note on International Nomenclature........338 LIST OF ILLUSTRATIONS. PLATES I. AND II. Microscopical Preparations of Tubercle-bacilli. Fig. 1. An instrument for estimating thoracic resilience 2. An apparatus for demonstrating the respiratory movements . 3. An apparatus for demonstrating the respiratory movements . 4. A figure to illustrate the regional anatomy of the chest 5. A figure to illustrate the regional anatomy of the chest 6. Diagram of percussion signs in cases of moderate effusion. (Front view). . . . . *. . 7. Diagram of percussion signs in cases of moderate effusion. (Back view) ......... 11. A trochar for performing paracentesis .... 12. The fittings of Potain's aspirator ..... 13. Tracing of thoracic movement in emphysema 14. Tracing to show recession of the parieties during inspiration in em physema ........ 15, 16. Temperature charts of pneumonia and idiopathic erysipelas com pared ......... 17. Temperature chart in a case of pythogenic pneumonia. 18. Elastic tissue and fragment of a small vessel in sputum. 19. Temperature chart, fluctuating hectic in acute pneumonic phthisis Case of Annie T. ...... . 20. Temperature chart, hectic type. Lucy B. 21. Outline oiVchest dullness in George S. . . . 22. Elastic tissue in sputum . . ,-#*-*T"r~"f;; . 23. Temperature chart in hectic. . /^ W'. X/i 9 13 21 54 55 76 77 118 118 132 135 204 205 207 213 228 305 ^fen u\. » DESCRIPTION OF PLATE I. Fig. l— Acute miliary tuberculosis. Lung : two alveoli which have be- come fused together. Alveoli filled with large epitheloid cells. Tubercle- bacilli in large numbers between the cells, and in a few instances within the cells (a a). x 400 Fig. 2.—Phthisis. Lung : section from wall of minute cavity. Inner mar- gin of cavity teeming with bacilli. No bacilli elsewhere. a. Cavity. b. Bacillary margin. c. Surrounding caseous tissue. X 75 Drawings made by Mr. Edgar Thurston, from specimens prepared by Dr. Percy Kidd. (This plate appears also in the volume of the " Medico-Chirurgical Transac- tions " for 1885). DESCRIPTION OF PLATE II. Fig. 1.—Sputum from a phthisical patient showing bacilli. X 400 Fig. 2.—Pus removed from the interior of the pleura in a case of empyema of tubercular origin, showing abundance of bacilli. X 400 Drawings by Mr. E. Thurston, from preparations by Mr. Taylor. Fig. 3.—Naked-eye appearance of a cover-glass on which secretion from a pulmonary cavity was spread and treated by Ehrlich's method of staining. The tubercle-bacilli are grouped together so thickly as to be visible to the naked eye as red points. Preparation and drawing by Dr. Percy Kidd. PowbII on. Lungs PI I . & i C () \ f, ^w S\ -) \ - N •A - I s X 400. lENCKE, LITH \\ \ s\' / / ,V \ / \ \ y -,v ' \ / •** *.^ / / . \ \ ^ N ' k , DISEASES OF THE LUNGS AND PLEURA. CHAPTER I. ON SOME ESSENTIAL POINTS IN THE ANATOMY AND FUNCTIONS OF THE LUNGS. Before proceeding to discuss the pathology, detection and treatment of chest diseases, it will be well perhaps to recall to the recollection of the reader, certain essential features in the anatomy and configuration of the lungs, which are very practically concerned in the phenomena they present. Unfortunately, physiology is so widely separated from practical medicine in our schools, that the student has to relearn the one in its application to the other. Who for instance can rightly understand the phenomena of asthma, emphysema, pleuritic effusion, or pneumo-thorax, without a working knowledge of the statical and dynamical conditions of respiration in health. It was on the other hand complained by Addison, that morbid anatomy had not been sufficiently used to cast light upon the structure and function of parts in health, and it may perhaps be assumed, that the link between physiology and pathology is not so clearly observed nor so firmly maintained in our minds as it might well be. Let this re- flection be my apology for devoting a chapter to certain physiological and anatomical considerations. Anatomy. —Perhaps one could not better summarize the rough anatomy of the lung than by quoting the first four aphorisms of Addison respect- ing it, viz.: "1. That the aerial cellular tissue of the lungs is made up of well-defined, rounded, or oval lobules united to each other by interlobular cellular membrane, each lobule constituting a sort of distinct lung in miniature, having its own separate artery and vein; 2, that these lobules do not communicate directly with each other; 3, that they do not consist of the globular extremities of as many bronchial tubes, but are made up of a collection of cells in which, by a common opening, a minute filiform bronchial tube abruptly terminates; 4, that the pulmonary artery accom- panies the bronchi, branch for branch, to the minutest divisions of the latter."1 1 Observations on the Anatomy of the Lungs. Medico-Chimrgical Transac- tions, vol. xxiv., p. 146. Also New Sydenham Society's collection of Addison's Works, p. 2. 2 DISEASES OF THE LUNGS AND PLEURAE. If we trace the bronchial tubes from the trachea into the recesses of the lungs, we find that in the course of subdivision they present certain important changes of structure. They divide in a peculiar way: 1, from the main bronchi down to the calibre of -§- in. they divide symmetrically or dichotomously; 2, beyond £ in. the bronchi proceed in straight lines, gradually diminishing in size and giving off lateral branches alternately at an angle of 45°; 3, the lateral branches again divide dichotomously until they reach a diameter of about yfg- in., when they terminate in the alveo- lar canals or passages, the lobules referred to by Addison. Down to a diameter of ^ in. (1 mm.), the bronchial divisions are possessed of cartilages and muscular coat, are lined by a ciliated epithe- lium and are furnished with mucous glands. Their arterial supply is thus far derived from the bronchial artery, the capillaries of which ter- minate in the bronchial veins, forming a part therefore of the systemic circulation. Below the diameter of ^V m« 0- mm.), the bronchioles have neither cartilages, mucous glands, nor any continuous muscular coat; circular and longitudinal elastic fibres replace the muscular coat and the epithelium lining them is flattened. Their arterial supply is still derived from the bronchial artery, terminating however in the pulmonary venous capillaries and forming therefore a part of the pulmonary circulation. The alveolar canals or passages, into which the ultimate bronchioles enter, are relatively large and immediately subdivide dichotomously two or three times, then terminate in somewhat bulbous ends—the infundibula. The first divisions of the alveolar canals are each somewhat larger than the ultimate bronchioles. The distance from the termination of the bronchiole to that of the infundibula, i.e., to the extreme periphery of the lung, is from -^ to ^ of an inch. The entire inner surface of the alveolar passages and their infundibular terminations is pitted by little secondary recesses, the alveoli, ^fa in. to y^-j- in. diameter. The alveolar passages and infundibula consist mainly of a framework of elastic fibrous tissue with a few unstriated muscular fibres; the alveoli or recesses within them are lined by a single layer of capillaries supported by a delicate membrane with elastic fibres, the elastic fibres forming bun- dles arranged round the openings of the alveolar recesses into the common infundibular passages; here the smooth muscular fibres are also found in greatest abundance. A delicate epithelium lines the alveoli. Each lobule of the lung is thus made up of the branched alveolar passages and the alveoli opening into them, connected with one terminal bronchiole; it measures from about T1g- to i in. in diameter. With regard to the blood vessels of the lungs, it should be borne in mind that the pulmonary artery carrying dark blood, subdivides with the bronchial tubes and finally furnishes a capillary layer to each alveolus, ANATOMY AND FUNCTIONS OF THE LUNGS. 3 each branch proceeding to its capillary distribution without communi- cating with any other branch. A. junction between the pulmonary and systemic vessels is, however, effected at the pulmonary lobules by the dis- charge of the capillaries of the bronchial artery into those of the pulmonary vein as aforesaid. The veins have no valves, and for the most part take a separate course to the root of the lung in the interlobular or pulmonary fissures. They anastomose freely. Respiratory function and mechanism.—In the recesses of the lungs within the alveoli and alveolar passages is effected that interchange of gases by means of which oxygen is on the one hand absorbed, and carbon dioxide (CO2) exhaled, although no doubt the minutest bronchi allow of a certain oxygenation of blood through their fine membrane. The laws under which this interchange is carried on are those which regulate the diffusion of gases and their passage through moist membranes, but some physico-chemical processes are also involved which are probably somewhat complex. This is, so to speak, the nucleus or basis of the respiratory function, but in order that this function may go on uninterruptedly, it is obvious that special provisions must be made for a regulated renewal of the blood operated upon, and a thorough and sustained ventilation of the minute air chambers in which the process takes place. The rhythmic contractions of the right ventricle of the heart ensure a continuous cur- rent of blood through the alveolar capillaries, and the rhythmic respira- tory movements secure, under conditions to be immediately stated, a thorough ventilation of the lungs. Let us now glance at the mechanism by which these respiratory move- ments are effected. It need scarcely be observed that in the foetus at the full term the lungs are in a state of complete and airless collapse, that the diaphragm is in a position of extreme convexity upwards, and the thorax in the position of utmost contraction, the respiratory function being effected by the interchange of gases between the foetal capillary tufts of the placenta and the maternal blood in which they are steeped. In the new-born child, however, on the placental circulation being interrupted, carbon dioxide accumulates in the blood and stimulates the respiratory nervous centres, thus exciting acts of inspiration. This central nervous stimulation would probably not alone be sufficient, but it is sup- plemented on the first exposure of the child to the external air, by a general excitation of the cutaneous nerves causing strong inspiratory movements. In the Gulstonian Lectures for 1872, Dr. Hensley conjec- tured that the first expansion or unfolding of the air cells of the lungs in the infant, was caused by the penetration of the blood through their capillaries: and this view was supported by some experiments made in the same year by Liebermann, who roughly imitated the structure of an air- sac by taking two ox-bladders, placing one within the other, and between them a layer of india-rubber tubing. On injecting oil through the tubing, 4 DISEASES OF THE LUNGS AND PLEURAE. the bag, previously collapsed, expanded, drawing in air with a perceptible sound.1 Probably all these forces come into operation nearly simultane- ously, and we thus get successive inspiratory expansions of the chest, in obedience to which the air penetrates the lungs, and is never again fully expelled. It is not at all curious that the lungs, thus once inflated, should remain more or less permanently expanded, retaining in their interior a certain amount of air. They, like any ordinary elastic air bags, would do this, whether in or out of the body. But in the body, whether during life (within the limits of ordinary respiration), or after death the lungs are expanded beyond the point to which they would, from their mere elasticity, revert. This is a fact admitted by modern physiologists, but not, so far as I am aware, explained by them, nor is its importance in clinical medi- cine sufficiently recognized. I am, therefore, the more desirous to draw attention to it here. We have no difficulty in understanding how, after the separation of the placenta, the gradual accumulation of carbon dioxide should excite the medullary centre to initiate respiratory movements, and how further ex- citation should be conveyed to this centre from the peripheral nerves, on the sudden contact of cool air with the surface of the body. Moreover, we may well believe that the physical effect of a diversion of the blood through the lungs would be to unfold the air vesicles, and thus enable them to become permeated with air. In order to account, however, for the maintenance of the lung in the semi-expanded state we must further assume that when the muscles of respiration, which are for the most part inspiratory muscles, have once been excited to action, they remain perma- nently shortened by virtue of their vital contractility or tonus. And in the course of tissue growth, the ribs and cartilages become moulded to that wider arc which they have thus been brought to assume. The contractile power of the lungs derived from their residual tension, has been measured by different observers with somewhat different results. Dr. Carson, in 1820,2 demonstrated the existence of this reserve tension, and estimated it in different animals as equivalent to from six to twenty, or more, inches of water, according to the size of the animal. He fully perceived the importance of this elastic force, both in the respiratory mechanism and as an aid to the circulation. Dr. Carson indeed regarded the respiratory movements as due to an antagonism between the elastic resilience of the lungs, and the muscular action of the diaphragm. He maintained that the traction of the lungs upon the diaphragm gave rise to a sense of uneasiness, to overcome which the muscle contracted but 1 Wien. Med. Zeit. No. 5, 1872. I am indebted to Dr. Lauder Brunton for the reference to this experiment. Hensley's lecture is briefly alluded to in the Brit Med. Journal, June 22, 1872. 2 Philosophical Transactions, 1820, pt. i., p. 29. ANATOMY AND FUNCTIONS OF THE LUNGS. 5 that the enduring lung-elasticity on the cessation of the muscular effort again drew up the diaphragm. This view, although erroneous, was based upon an accurate observation of phenomena which were for a long time afterwards ignored. Donders, in 1853,1 made some experiments on the human subject. By connecting a manometer with the trachea, and then carefully opening the thorax, he was able to ascertain the residual elastic tension of the lungs, and concluded that in the healthy person it was equal to 80 milli- meters (about three inches) of water. He further added 20 mm. for the tonicity of contractile elements in the lung. Dr. Salter, in 1865,2 found the residual tension in the dog equal to four inches of water. Dr. M. Perls, in 1869,3 gives the result of one hundred experiments, conducted in the same manner as those of Donders, upon persons who had died of different diseases: out of these, in 25 cases death had been caused by diseases remote from the lungs, although in most instances the lungs were in some degree affected. The highest degree of residual tension registered by Dr. Perls' manometer from these 25 cases was 60 mm. of water, the lowest 5 mm.: mean 35.3 mm. It is very possible that the experiments of both Donders and Perls give results somewhat short of those of perfect health. It is, at all events, singular that the highest elastic pressure obtained by Perls from one of the 25 cases in which the lungs were presumably healthy, does not equal that (63 mm.) obtained from cases of bronchitis and phthisis respectively. The amount of muscular tissue in the human lung is at most but very scanty. Donders added 20 mm. to his estimate of residual lung con- tractility on account of muscular tonicity. Strieker admits that here and there in the free margins of the alveolar passages nearest the bron- chial terminations from which they are prolonged, delicate bands of smooth muscular fibre are to be found " which often consist of merely an isolated fibre imbedded in a delicate connective tissue. The mem- braneous walls of the alveoli themselves are entirely destitute of muscular tissue, nor have I been able to discover any muscular fibres in the more compact borders of the individual alveolar septa."4 It seems that this tissue is more abundant in the lungs of animals. Muller found the lung of a dog contract on the application of iced water.6 Although in the human subject we may conclude that so far as the 1 Zeitschrift fur Eationelle Medicin, N.F., bd. iii. (1853), p. 290. 2 Lectures at the College of Physicians, Lancet, 1865, vol. ii., p. 142. 3 Deutches Archiv fur Klinische Medicin, bd. vi. (1869), p. 1. 4Human and Comparative Histology, New Syd. Soc. Edit., vol. ii., p. 60. • 6Ludwig's Arbeiten, 1869, p. 64. Dr. Brunton informs me that this contract- ility was found to continue for two days if the lungs were supplied with blood by artificial circulation. 6 DISEASES OF THE LUNGS AND PLEURAE. lung proper is concerned, muscular action takes no direct part in the respiratory mechanism, it is yet impossible not to see that the muscle- containing bronchial tubes which ramify throughout the lungs with whose texture they are in intimate union, must indirectly add to their contrac- tility. We are more concerned now, however, with the purely elastic elements of the breathing apparatus. It is curious that whilst the residual tension of the lungs had been thus so carefully tested and measured, the thoracic tension necessarily equal and opposite to it should have almost escaped observation, or rather should have been deliberately misplaced as an expiratory force. It was maintained by Hutchinson nearly forty years ago, in an able and elaborate paper read before the Koyal Medical and Chirurgical Society of London,1 that inspiration is a wholly muscular act; the muscles in expanding the thorax having to contend against, (1) the elastic resistance of the lungs; (2) the inertia and elastic resistance of the chest walls. Ex- piration on the other hand being effected by the elastic recoil of the lungs and chest walls. This view of the mechanism of healthy breathing has been accepted without question by the authors of most of our physiologi- cal text-books. Hutchinson estimated the resistance to each inspiration arising from the chest walls alone, at more than 100 lbs., and in deep inspiration at from 400 to 1000 lbs. There are certain facts, however, many of which have been long known, which clearly show that in quiet inspiration there is no inertia or elastic resistance of the chest walls to be overcome, but that on the contrary the thoracic elasticity is a reserve force of appreciable power constantly tend- ing to enlarge the thorax, and therefore acting in favor of inspiration. That this must be so, would follow as a matter of reasoning from what has been observed above respecting the state of tension in which the lungs are maintained, so long as they remain healthy, throughout life; but more fully to demonstrate my proposition, I will briefly refer to some observations and experiments of other authors as well as my own. The late Dr. Salter3 was, I believe, the first to point out that at the commencement of breathing, the elasticity of the chest walls should be placed as an inspiratory force. By a simple experiment he showed that in the dead subject, the thorax, when relieved from the traction of the lungs by making an opening into the pleura, expanded to the extent of Tfa inch. Paul Bert3 (1870) in some ingenious experiments, recorded simultaneously the elastic pressure of the lungs, and the expansion of the chest wall, at the moment of opening the pleura of a recently killed doo- Traube4 in 1871, found that in the living dog the chest walls on being 1 Vide Transactions of the Society, vol. xxix., 1846.. 2 Loc. cit. 3 Lecons sur la Respiration, 1870, p. 359. 4 Gesammelte Beitrage, bd. i. ; Experimentelle Untersuchun°-en 1871 n 141 ANATOMY AND FUNCTIONS OF THE LUNGS. 7 relieved from the traction of the lungs, expanded in the manner indicated by Salter; but Traube does not seem to have been aware either of Salter's or of Bert's experiments, and he erroneously asserts that the expansion which he attributes to muscular action, is not obtained in the dead ani- mal. The table on page 8 contains the details of ten post-mortem exam- inations made by myself in 1876,1 to estimate the extent to which the chest wall would expand of its own resilience, when relieved from the traction of the lungs. The difficulty of finding the thoracic organs per- fectly healthy in the dead subject is well-known, and out of the ten cases operated upon in only four instances were they approximately so. The experiments were performed after the manner of Salter by taking a fine Fig. 1. tube, A, expanded below and having stretched across its expanded ex- tremity, B, a piece of caoutchouc provided with a projecting button, C. The instrument having been filled with colored fluid, was so adjusted that the button was accurately applied to the third cartilage, the integuments having been previously reflected from the front of the chest. The level of the fluid having been noted on the scale D attached to the stem, the thorax was cautiously opened and an immediate rise of the colored fluid was observed. A simple calculation enabled one to ascertain the actual 1 " On some effects of Lung Elasticity in Health and Disease." Medico-Chirur- gical Transactions, vol. lix. Table giving Observations on Thoracic Resilience in Ten Cares post-mortem. All observations were made with the co-operation of Dr. Coupland at the Middlesex Hospital. CO p co-rn > P.M. 1 M. 33 24 hrs. 2 F. 38 21 hrs. 3 M. 58 27 hrs. 4 F. 44 20 hrs. 5 M. 27 23 hrs. 6 F. 36 7 M. 60 8 M. 64 9 M. 41 12 hrs. 10 F. 56 40 hrs. Case. Amputation. Tumor of jaw. Epithelioma of penis. Carcinoma of uterus Delirium tre- mens Comp. fract., bruised strum. Fractured ribs, left side Strangulated hernia Fractured skull. Carcinoma of uterus Point of application of bulb. 3rd L. cart. 3rd mid. st. 4th mid. st. 5th mid. st. 4th mid. st. 5th mid. st. 4th mid. st. 4th mid. st. 4th mid. st. 5th mid. st. Pleura opened. a—2nd L. space b—2nd R. space a—3rd space b—3rd space a—3rd R. space b—3rd R. space c—3rd L. space a—2nd R. space b—2nd L. space a—3rd R. space b—2nd L. space a—2nd R. space b—2nd L. space a—2nd R. space b—2nd L. space a—2nd R. space b—2nd L. space a—2nd R. space b—2nd L. space a—3 I'd L. space b—3rd R. space Rise of fluid in stem. Centim. 3.15 0 0 0 2.4 2.3 2.3 —0.3 0 -0. 0 0 0 0 0.3 0 0 0 0 -0.4 Total. Equivalent expansion of Chest. Millim. 3.15 3.5 2.4 H 4.6 0.3 0 0 0.3 0 -0.4 2.143 2.39 1.63 3.19 0 0 Remarks. Right lung adherent, emphysematous; left free, slightly emphysematous; abdomen flaccid. Slight further rise on making two fresh openings at 5th space; slight bronchitis. Right lung adherent, side more prominent; some emphysema of both lungs, mostly of the right. Lungs quite healthy, no adhesions; col- lapsed to about ^th of bulk; rigor mortis, no decomposition; abdomen flaccid. (Edema of both lungs, recent pleural adhe- sions both sides. Bronchitis; adhesions both sides. Cartilages ossified; right lung emphysema- tous; three pints of serum in left pleura. Lungs emphysematous and oedematous. Lungs highly oedematous; dynanometer connected with trachea registered no pressure. Rigor mortis passing off; abdomen distend- ed, chest-walls rigid, lungs emphysema- tous, but collapsed half an inch. ANATOMY AND FUNCTIONS OF THE LUNGS. 9 expansion registered. The results of the experiments will be seen in the table. In the four comparatively healthy cases the expansions measured were 1.63 mm., 2.143 mm., 2.39 mm., and 3.19 mm. respectively.1 These figures, small though they are, indicate pretty well the limits of expansion of the ribs during calm breathing. Thus Hutchinson calcu- lated the costal movement in health at -^ to £ line=l to 2 mm.; Sander- son gives 1.6 mm. My own measurements would give rather a higher figure, viz., 2 to 3 mm. But from some careful tape measurements I have found the total circumferential expansion in health (in quiet breathino-) not to exceed -J to \ in. (4 to 8 mm.), in some exceptional cases £ to •£ in. Age, sex, and many other conditions influence the mobility of the thorax. It would appear then—and this is the point to which I wish especially to direct attention—that in health throughout ordinary inspiration, the limit of thoracic recoil, ichich we may call the reserve capacity of the thorax, is barely reached; and therefore that the sole resistance to be overcome by the inspiratory muscles is that of the lungs. In order more clearly to show the main physical conditions present in the chest and how they are modified, (a) during normal respiratory move- ments, and (b) in certain diseases, the subjoined schema or diagram-model of the chest was designed. Fig. 2. The schema consists of a cylinder of glass, closed at each end by a metal plate screwed on and perforated for the admission of certain tubes. 1 For fuller details respecting these and other experiments see the original paper, " On some effects of Lung Elasticity in Health and Disease," by the author in the Medico-Chirurgical Transactions, vol. lix. 10 DISEASES OF THE LUNGS AND PLEUR.E. A central partition, EF, made of sheet india-rubber, divides the cylinder into two air-tight compartments, each of which, as will be presently seen, represents one half of the thorax. Tube D represents the trachea, and is connected with an elastic bag, (c) representing the (left) lung. Tube G- communicates with the space between the lung and the wall of the chamber, which space, therefore, corresponds to the pleural cavity. This tube is connected with a mercurial manometer, the free end of which, L, is open to the normal atmospheric pressure. Tube B also communicates with the same (pleural) space, and is provided with a stop-cock and a mouthpiece. Exactly the same parts are repeated on the opposite side of the par- tition, EF, which therefore represents the mediastinum. The apparatus must be ascertained to be thoroughly, air-tight. Then by partially exhausting the air from chamber A through tube B (trachea tubes D and D' remaining open) we cause the bag c to expand to C, the mercury in the manometer, HKI, to rise towards the chamber, and the mediastinum, EF, to become convex, as indicated by the dotted line. By closing the stop-cock B we maintain all the parts in this position. If, next, we repeat the same process on the opposite side—partially exhausting chamber A' through B' until the mercury I' is at the same level as I—the bag c' will expand to C, the mediastinum, EF, will again become vertical, and by closing stop-cock B' the parts will be maintained in this position of equilibrium on the two sides. In the schema thus arranged, we have the conditions of the healthy chest rudely but accurately imitated. The two chambers represent the two sides of the chest, each containing a semi-expanded lung, C, C, sur- rounded by a pleural cavity, A, A', (here greatly exaggerated,2 the cavity being rather potential than real in the healthy chest), each cavity being separated from that on the opposite side by the mediastinum EF, which is common to both and equipoised between them. The walls of the natural thorax are, however, elastic or resilient in every part, although much more stiffly so than the lungs. We cannot exactly represent this resilience of the thoracic walls in our schema. The only parts of our apparatus which are at liberty to yield to the excess of external atmospheric pressure over that within the pleurae, are the small surfaces of mercury at H,H'. Hence the elevation of the mercury HI, H'l', towards the chamber on each side, multiplied by the area of aper- tures G,G', and divided by that of the whole surface of the chamber, would represent in millimeters the amount of recession of each portion of the thorax, provided each portion were equally resilient. 1 This is unavoidable, since the walls of the schema are rigid, and if the ba°-s fitted accurately, their further expansion in inspiration could not be represented No fallacy is hereby introduced, however. ANATOMY AXD FUNCTIONS OF THE LUNGS. 11 Although in the natural chest, the diaphragm yields far more than any other portion of the chest wall to the traction of the lungs; this is chiefly because its resistance is weaker, so that a recession of an inch on the part of the diaphragm is only equivalent to the recession of one or two millimeters on the part of the ribs or cartilages. For it must be further remembered, that the diaphragm is not elastic, and that the limits of its tension are therefore very narrow; and indeed, the elastic recoil of the diaphragm depends mainly upon the spring of the cartilages to which it is attached. Our mercurial columns therefore, after all, very conveniently and fairly represent the whole thoracic resilience in a lump sum. Having thus with the aid of our schema rehearsed the statical condi- tions of the chest, the dynamics of respiration may be easily demonstrated. In order to imitate an inspiration, aspiration must be made simultane- ously through the tubes L and I/, thus representing the contraction of the diaphragm and inspiratory muscles on the two sides. This can be conveniently done by means of a syringe attached to a branched caout- chouc tube affixed to the extremities L 1/ of the manometers. As the mercurial columns rise up the limbs L L' of the manometers, representing the expansion of the thorax, the lung C C enlarge by the entry of air through trachea tubes D and D'. It will be observed that, during the first part at least of inspiration, the weight of the two columns of mercury H I, H' I" tells in favor of the inspiration. This weight of mercury corresponds as before said to the outward resilience of the thoracic walls, and counter-balances the elastic traction of the lungs. This is a fact, well shown in the schema, and which has been already stated in the proposition, that in health the resili- ence of the ehest wall is in favor of inspiration. Moreover, from the ob- servations on the dead subject to which I have already referred, it would appear that this elastic aid to inspiration obtains throughout the act in calm breathing. Respiration is thus rendered smoother and less labori- ous, elasticity entering as an important item into the inspiratory, as it has been long known to do into the expiratory, act. The conditions present in the chest as shown by the schema must be further examined in their effects upon the heart and circulation. The disposition to the formation of a vacuum in the intra-pleural space A, equal to the weight of the column of mercury H I, causes an aspira- tion towards that cavity which was at first shown by the convexity of the mediastinum E F (dotted line): and there being a similar and equal as- piration towards the pleural cavity on the opposite side of the mediastinum, it follows that there is a constant determination of blood towards the cavi- ties and walls of the heart—a hollow organ situated within the mediasti- num, and communicating by a system of tubes with parts outside the thorax, (see fig. 2). This central attraction is forcibly overcome by the 12 DISEASES OF THE LUNGS AND PLEURJE. muscular contraction of the heart, but resumes its sway at the termination of systole, aiding the return of blood to the flaccid heart cavities, and encouraging the flow through the coronary vessels. This aspiration towards the heart is, be it remembered, in health a constant force, in- creased during inspiration, held in momentary abeyance during the more forcible muscular contraction of the heart, but not wholly extinguished even at the end of ordinary expiration. In the drawing on page 13, which depicts a somewhat more elaborate diagram-model of the chest (but essentially corresponding with that illus- trated by fig. 2), the mediastinum is represented by a double layer of caoutchouc enclosing a space, connected with which the manometer, D, shows at a glance the negative pressure to which the heart is constantly subjected through the traction of the lungs from either side. In discussing, however, what has been called the statics of respiration, we must not leave the diaphragm out of account. It is obrious that this muscular membrane must be drawn upwards and held in a state of ten- sion by the lungs during the respiratory pause. Mr. Le Gros Clark, in a paper read before the Royal Society in May, 1871/ demonstrated what he termed the passive tension of the diaphragm, and the observations of Traube,2 and more recently those of G. M. Garland of New York,3 show how this elastic traction upon the diaphragm importantly modifies the physical signs of pleuritic effusions. The capacity and willingness (if I may so say) of the thorax to enlarge within certain limits, without muscular effort from without or pressure from within, is a most valuable safeguard in some diseases, serving to protect the lungs from pressure during temporary conditions of inflam- mation or engorgement. If we look at a case of pneumonia, we find that, whereas on the healthy side the play of the chest-wall is natural or increased, on the other side it is annulled. There is no retreat with expiration, and in- spiration is checked by pain. On post-mortem inspection, we find the fine granulations of lymph evenly spread upon the pleural surfaces, show- ing no sign of pressure. The patient suffers little pain, except when he coughs or attempts to draw a deep breath. In fact, as the inflamed lung increases in bulk, the thoracic wall retreats to the position of inspiration • and this reserve capacity of the thorax is rarely exhausted in pneumonia,' so that the swollen and tender lung as a rule escapes compression. In temporary engorgement and oedema of the lungs, the consequences would be much more serious were it not for the reserve capacity of the thorax, which protects the organs from compression, save in extreme 1 Proceedings of the Royal Society, vol. xx., p. 122. s Gesammelte Beitrage, ii., p. 857, referred to by Fi ipsedia, English translation, vol. iv., p. 653. 3 Pneumono-Dynamics, by G. M. Garland, M.D., New York 1878 p. 51 2 Gesammelte Beitrage, ii., p. 857, referred to by Fraentzel in Ziemssen's Cv- clopsedia, English translation, vol. iv., p. 653. ^ Fig. 3.—A A. Lungs in position of moderate expiration within pleural cavities. B. Mediastinal space (pericardium). C C. Manometers showing elastic traction of lungs upon chest walls. D. Manometer showing negative pressure corresponding with traction of lungs within pericardium as CC show negative pressure within pleural sacs. E E. Tubes with stop-cock (shut) communicating with pleurae. F F Bronchial tubes uniting in U. Trachea. H. Tube communicating with separate bag placed in pleural cavity A, for convenience in representing pleuritic effusions, The instrument is represented as arranged by exhausting the air equally in the two chambers A and A to show the condition of respiratory statics in the position of respiratory pause. This is effected either by exhausting the air equally in the two chambers A and A until the bladders representing the lungs become partially inflated, or (what amounts to the same thing) by inflating the two lungs through the trachea, whilst stop-cocks EE are open, then closing these cocks and allowing the lungs to collapse to the point of equilibrium. 99999�6 14 DISEASES OF THE LUNGS AND PLEURAE. cases. Again, it is only in very extreme cases of emphysema that the eccentric thoracic resilience is entirely neutralized. I have directed my attention especially to this point in many cases, and I believe that the lungs are never enlarged so as to be compressed by the ribs. With regard to emphysema, the loss of the elastic spring of the chest- wall is one of the first important features of the disease. In the normal chest, a deep breath is drawn by first making a deep expiration, and then a deep inspiration. In emphysema, the power of making a deep expira- tion is partially or entirely lost; the whole reserve capacity of the thorax is taken up, and it is in this direction that the trouble of emphysematous people lies. Kegarding emphysema as in many cases essentially a disease of the lungs of a degenerative kind, we must observe in the constant traction of the thorax upon the lungs a determining cause of their en- largement. If, as is often the case in early life, the chest-walls be soft and feeble, they cannot properly expand, and we get a small, narrow, or distorted chest. On the other hand, if the elasticity of the lungs be re- laxed by disease, the chest expands gradually to the limits of its reserve capacity. Lymphatics.—I have preferred to pass on from the consideration of the general structure of the lungs to a discussion of the mechanism of the respiratory function, and even by way of illustration to refer to some morbid states of perverted respiratory mechanism, before completing our anatomical description of the lungs, by speaking of their lymphatic and nerve supply. I have done this with the view of bringing together these points of anatomy and function which are most concerned in the produc- tion of physical signs and symptoms. In the lymphatic and nervous ap- paratus of the lungs we have, so to speak, the drainage and function regulating systems, whose workings are hidden from us for the most part, to be brought to light mainly through the manifestations of disease. In truth, however, the important part played in pathology by the complex lymphatic system of the lung as disclosed to us by the researches of Sanderson1 and Klein,2 is becoming daily more clearly discerned as we become better acquainted with the origin of pulmonary diseases and their extension by infective processes. If we commence our scrutiny in the walls of the pulmonary alveoli, we find that the spaces of the capillary vascular network contain, indeed _ constitute, lacunae or lymph spaces which are lined or loosely occupied with protoplasmic connective-tissue cells: the lacuna? intercommunicate by fine processes and discharge into lymphatic vessels which, in the depth of the lung, accompany the minutest subcapillary blood-vessels (peri- vascular lymphatics), but which, on the surface of the lung, occupy the grooves between the lobules (sub-pleural lymphatics). The connective- 1 Tenth and Eleventh Reports, Medical Officer of Privy Council. 2 The Anatomy of the Lymphatic System, part ii.—The Lun°\ ANATOMY AND FUNCTIONS OF THE LUNGS. 15 tissue cells lining the lacunae in the alveolar walls, send fine protoplasmic processes, which insinuate between the epithelial cells of the alveolar sur- face (pseudo-stomata), and thus maintain the lymphatic system in living contact with the air spaces. Dr. Hamilton' describes and figures some granular polygonal cells lying singly or in groups upon depressions of the alveolar surface, but denies their resemblance to pseudo-stomatous cells. "Although (remarks Dr. Hamilton, p. 106), there seems to be little evi- dence that these young granular embryonic cells are of a connective-tissue tyPe> yef that they have a pseudo-stomatous action in transferring foreign bodies from the alveolar cavity to an underlying lymphatic, as claimed by Klein and others, can be verified." The sub-pleural lymphatics inosculate by deep branches with the peri- vascular lymphatics, and further communicate directly with the pleura by means of fine canals which open upon its surface (stomata). Both these sets of lymphatics course respectively onwards to the bronchial glands. The bronchial tubes also give rise to lymphatics (peri-bronchial), which have their rootlets in fine canals and intercommunicating spaces in the mucosa, in direct communication with the mucous surface by pro- toplasmic processes of connective tissue cells projected between the col- umnar epithelial cells. These bronchial rootlets discharge into the larger lymphatic vessels of the adventitia, which, like the rest, course onward towards the bronchial glands at the root of the lung. The peri-vascular and peri-bronchial lymphatics, being adjacent, freely inosculate, especially at their finer divisions in the depth of the lung. Connected with the peribronchial lymphatics distinct acini or rudimentary glands have been discovered by Prof. Burdon Sanderson in the lung of the guinea pig, and it is reasonable to suppose that they are also represented in the human lung, although their existence has not as yet been demonstrated. The whole lung is thus pervaded in every crevice of its structure by lymphatic tissue, consisting of branched protoplasmic cells communicating with fine tubes and interstitial spaces occupied or lined with endothelial cells. Xerves.—The nerve supply to the lungs is derived from the anterior and posterior pulmonary plexuses, which are formed by the interlacement of branches from the vagi, joined by others from the sympathetic, chiefly from the second, third, and fourth thoracic ganglia. The nerves from these plexuses accompany the bronchi, but their exact mode of termina- tion is as yet undetermined. It seems, however, probable from the re- searches of Kemak, Stirling3 and others, that they terminate in the muscular fibres of the walls of the minute bronchi, and in their course pre- sent ganglia singly and in groups. One may with tolerable safety infer further that twigs are communicated to the ultimate lobules of the lungs. 'Pathology of Bronchitis, etc., 1883, p. 104. 2Quain's Anatomy, 9th edit., vol. ii., p. 521. CHAPTER II. THE PHYSICAL EXAMINATION OF THE CHEST. Befoke proceeding to physical examination, preliminary inquiries have to be made into the health history of the patient, the circumstances which have led up to his present illness and the chief symptoms which give him distress. In the course of these inquiries the appearance and manner of the patient may be noticed; and the experienced physician, practically skilled in the physiognomy of disease, will thus gain information of great value, as a clue to the often confused story of the patient, and in suggest- ing to him further questions. It would be folly to attempt to learn from a book the physiognomy of disease: clinical study, an habitually careful scrutiny of the features and postures of actual sufferers will alone impart it. The student will early recognize the aspect of turgid lividity and labored breathing of chronic bronchitis with dilated heart, from the pallor, anxiety, throbbing vessels, and dyspnoea with restlessness of advanced aortic regurgitant disease. The hectic look of phthisis, the grave drawn lineaments of asthma, the swollen features and cyanosed mucous membranes in heart disease, the puffy pallor of albuminuria, may in their more marked degrees be soon recognized even by the beginner. The finer traits and markings of dis- ease, however, require more experience for their detection, and are of even more value in suggesting inquiries and often in leading one to suspect the presence of disease before sufficient signs can be found to justify a posi- tive diagnosis. Incipient tuberculosis and obscure aneurysm may be named as two instances in which the features of illness sometimes suggest a more guarded diagnosis than the actually discoverable signs would warrant. The relationship between physical signs and the diagnosis of pulmonary disease is again of a strictly practical kind, although of course depending upon acoustic principles, and he who A^ould become a successful ausculta- tor, i.e., a good diagnostician, must study auscultation in association with morbid anatomy. Thus will the stethoscope reveal to him at the bed- side, in most cases, an accurate picture of the lung, heart or pleura under examination, as though the organ were exposed to his view. This inti- mate association in the mind between physical signs and the lesions which give rise to them is only to be acquired by genuine clinical and post-mortem observation; no amount of reading or clinical work alone will suffice for its attainment. It is the object of a text-book, however, to supply certain data for comparison and to lay down principles and methods upon which a satis- factory exploration of the chest is best founded. PHYSICAL EXAMINATION OF THE CHEST. 17 Shape of the Chest.—It is impossible in a word to describe the shape of the chest, but it may be said in the adult to be conical from above downwards, flattened in front and grooved in the posterior median line, so that the antero-posterior diameter is about one-third less than the transverse. In the child these two diameters are more nearly equal. The shape of the upper portion of the chest is obscured by the pectoral muscles, extending from the upper arm to the clavicle and ribs, giving it a some- what square outline. In the female the apparent form of the thorax is still further altered by the mammary development. Measurements of the Chest.—Two instruments are of value for clinical use in the measurement of the chest, viz., the double tapes1 consisting of tapes connected by a central piece for adaptation to the spine, from which point each tape is graduated. The back piece being carefully held over the spinous processes and a mark being made exactly in the median line of the sternum, the two tapes are brought round the chest at the same level and with moderate firmness of application, to overlap one another at the front line. A comparative measurement of the two sides is thus at once read off, the sum of the two measurements giving the total circumference. By holding the tapes lightly the expansion of the chest can be meas- ured during calm breathing, and by making the patient take a deep breath followed by a full expiration the total expansibility is ascertained, also, what is equally of value, the contractility of the chest beyond the point of ordinary expiration. Finally, a comparison in all these respects can be made between the two sides. By means of the cyrtometer2 a tracing of the circumferential outline of the chest is obtained. This instrument consists of two pieces of thin lead piping connected by a hinge of rubber tubing. The hinge is care- fully applied over the spinous process at the level required, and the piping moulded round the chest until the two ends cross one another in the median line in front; a mark is then made and the instrument allowed to fall away from the chest, held by the flexible joint; it is subsequently ad- justed in position on a sheet of paper, and " sternum " and " spine " being marked, the pencil is carried round the inner circumference, and an exact outline of the shape of the chest is thus obtained, any comparative or general alteration in shape being readily observed.3 The circumference of the chest varies much in different individuals and within the range of health. Thus, Walshe4 has noted in adult males of medium height, measurements ranging between 27 inches and 44 inches 4 First introduced into clinical use by Dr. Charles J. Hare. 2 First used clinically in the form of jointed whalebone by M. Woillez. (Walshe's Diseases of Lungs, 4th edit., p. 33). 3 The use of callipers for taking comparative antero-posterior measurements is attended with so many practical difficulties as to be of little value for clinical purposes. 4 Diseases of the Lungs, 4th edit., p. 30. 2 18 DISEASES OF THE LUNGS AND PLEURAE. in the circumference, taken opposite the sixth rib. He would regard 33 inches as a fair average in the adult. Dr. Sieveking,' on the other hand, places the average measurement above the nipples as 38 inches. The minimum chest measurement for a recruit in this country is 34 inches, except he be under twenty years of age, and a growing lad, when an inch less is accepted. •For clinical purposes these absolute measurements do not teach us much. Relative measurements of the two sides are of value in certain diseases attended with enlargement or diminution of the chest on one side. Cyrtometer tracings are of most value since they give exact in- formation as to shape. The mobility of the chest is of more importance than its mere size, as it affords a better indication of vital capacity. In the healthy adult the difference between extreme inspiration and extreme expiration should not be less than 2£ inches, as measured by the tapes at or about the level of the nipples. It may amount to as much as five inches. (Walshe.) The difference should be nearly equally divided between the two sides, a slight excess in favor of the right side being of no account. In calm breathing, however, the actual movement of the chest is very small, averaging in the healthy male (according to Walshe) ^ inch: the movement upwards of any one spot of the chest surface not exceeding two to four millimetres.2 Pneumatometry.—The power ordinarily employed by the inspiratory and expiratory forces during calm breathing, and that which they are capable of exercising during extremest effort, have been carefully esti- mated by various authors, and most recently by Waldenburg." The instrument employed by Waldenburg for this purpose consists of a manometer provided with a- naso-oral mask so padded as to fit with ac- curacy, each.limb of the manometer measuring about twelve inches (270 mm.), and being half filled with mercury. For calm breathing the mercurial surface would indicate a difference of from one to two millimeters. With forced inspiratory effort the mer- cury could be maintained at a minus pressure of 2^ inches (60 mm.), nearly double this pressure being momentarily attainable. The expiratory force exceeded this inspiratory by twenty to thirty mm., i.e., with forced expiratory effort 3| inches (90 mm.), of positive mer- curial pressure might be maintained and, momentarily, as much again. Marked variations from the healthy standard are met with in disease, and in two directions:— 1 Medical Adviser in Life Assurance, p. 140. 2 Medico-Chirurgical Transactions, vol. lix., p. 169. The whole subject of mensuration will be found fully discussed in Walshe's treatise. For detailed re- searches respecting the movements of individual ribs consult Dr. Eansome's ad- mirable work on Stethometry. 3 The subject of pneumatometry and spirometry is most fully and ably dis- cussed by Waldenburg in his work, Die pneumatische Behandlung der Respir- ations- und Circulations-krankheiten. Berlin, 1880. PHYSICAL EXAMINATION OF THE CHEST. 19 (1.) The inspiratory power is diminished whilst the expiratory {except in extreme cases) remains normal. This type is observed in phthisis, even in the earliest stages of that disease. It is found also in laryngeal, trach- eal and bronchial obstructions, and to a less extent in pneumonia or in pleuritic effusion. (2.) The expiratory pressure is lowered, the inspiratory remaining normal or being even increased, or sub-normal, but in all cases remaining relatively higher than the expiiatory. This type obtains in emphysema, bronchitis and asthma, also in diseases of the abdominal organs which impede the play of the expiratory muscles. Spirometry.—In the healthy adult at rest the respirations number from sixteen to twenty per minute, they are somewhat slower during sleep than when awake, and are readily accelerated by movements, effort, or excitement of any kind. There is an influx and efflux of about 30 cubic inches (500 cc), of air (tidal) with each act of calm breathing, about 100 cubic inches (1,600 cc), remaining in the lungs as reserve and residual air. By the deepest ex- piration following a full inspiration, a healthy man of average build can expel from 200 to 250 cubic inches (3000 to 4000 cc), which represents the " vital capacity of the individual," leaving still behind in the lungs a certain amount of "residual" air which cannot be removed by any ex- piratory effort. These facts were originally worked out by Hutchinson * by means of an instrument called the spirometer, which consisted essentially of a graduated gasometer nicely balanced and provided Avith a mouth piece, through which the patient could breathe into the meter previously set at zero. By a series of very elabofate investigations Hutchinson arrived at the following important conclusions which have not been altered or materially added to since his original paper. Hutchinson found that the vital capacity varied with the height in a very definite manner as will be seen by the subjoined table. Height. Vital Capacity Hutchinson. Weight. Circumference From observation. From calculation. of Chest. Allen.2 ft. in. ft. in. cub. in. cub. in. 5 0 to 5 1 174 174 120 lbs. 34.06 in. 5 1 " 5 2 177 182 126 " 35.13 " 5 2 " 5 3 189 190 133 " 35.70 " 5 3 " 5 4 193 198 136 " 36.26 " 5 4 " 5 5 201 206 142 " 36.83 " 5 5 " 5 6 214 214 145 " 37.50 " 5 6 " 5 7 229 222 148 " 38.16 " 5 7 " 5 8 228 230 155 " 38.53 " 5 8 " 5 9 237 238 162 " 39.10 " 5 9 " 5 10 246 246 169 " 39.66 " 5 10 " 5 11 247 254 • 174 " 40.23 " 5 11 " 6 0 259 262 178 " 40.80 " 1 Medico-Chirurgical Transactions, vol. xxix., 1846. 2 Med. Exam, for Life Ins. N.Y., 1872. Quotedby Dr. Sieveking, loc. cit., p. 141. 20 DISEASES OF THE LUNGS AND PLEURAE. In the preceding table the two columns of vital capacity, one taken from a number of observations, the other from calculation, are so nearly identical that we may take it that every inch in stature above five feet should add eight inches to the vital capacity. The last column has been added to show the corresponding circumferential measurements of the chest. The body weight also iufluences the vital capacity; for example, at the height of five feet six inches the vital capacity decreases one cubic inch per lb., from 161 lbs. (an excessive weight as will be seen for the height) to 196 lbs. After thirty and up to sixty years of age there is a decrease of nearly 1-j c. in., per year of age. In disease the vital capacity decreases from ten to seventy per cent. This diminution is dependent upon, but not directly proportional to, the extent of breathing surface encroached upon, since the lung or portion of lung remaining healthy may take a compen- satory action. (Waldenburg). Topography of the Chest.—For convenience in clinical examination and description the chest is mapped out into certain regions; these are suffic- iently indicated by the terms employed, viz:— Anteriorly, the supra-clavicular, clavicular, infra-clavicular, mammary and infra-mammary regions on the right and left sides respectively. In the median line, the supra-sternal, upper sternal and lower sternal regions. Laterally, the axillary and infra-axillary regions. Posteriorly the upper scapular (supra-spinous), the lower scapular (infra-spinous), the inter-scapular and the basic regions on each side. For the purpose of more accurately noting for future reference, the locality of any particular physical signs, there is no better or simpler plan than that of employing imaginary lines and levels drawn upon the chest surface. Thus the chest can be mapped out in latitude and longitude by parallel vertical lines drawn from summit to base through the mid-sternal, para-sternal,sterno-nipple,nipple, anterior axillary, mid-axillary, posterior axillary, mid-scapular, interscapular and vertebral lines, intersected by parallel lines drawn horizontally at the levels of the several rib cartilages in front and the several spinous processes behind, with the addition of nipple level, ensiform level, etc A careful observation of the adjoining diagrams will impress upon the memory, the main features in the topography of the chest organs and of those abdominal viscera in immediate relation with the chest. Marginal references are made at certain levels to facts of topography, which it is of some importance to bear in mind in clinical work. It will be observed that the upper or anterior lobes of the lungs occupy most of the front aspect of the chest, whereas posteriorly the lower or posterior lobes correspond with nearly the whole surface. The division between PHYSICAL EXAMINATION OF THE CHEST. 21 the two lobes takes place on either side close to the spine at the level of the spinous process of the third dorsal vertebra, and the line of separation slants downwards and outwards, across the junction of the middle and lower thirds of the scapula and the sixth rib in the axillary line. On the left side it courses along this rib to terminate at its upper border in the nipple line; on the right side, having reached the sixth rib in the axilla, the line of separation continues downwards to the eighth rib, a second Fig 4 (from Guam's AnatomyV-X 7th cervical spine = apex of lung. A. Division between the lobes = tip of spine of 3rd vertebra, i.e., 3 inches below summit of lung. B. Division of bronchi = 4th dorsal spine. C Long axis of spleen = 10th rib. . E. Base of right lung = 10th dorsal spine. Base of left lung - 11th spine (base of this lung in diagram represented too high). ...... , D. Upper end of left kidney = 11th dorsal spine, the right being ] X. = 1st lumbar spine. , inch lower. cleft passing almost transversely forward opposite the fourth space, to terminate in the median line at the junction of the sixth cartilage with the sternum; thus marking off the third lobe, which is interpolated in front between the upper or anterior, and the lower or posterior, lobe. In physically exploring the chest, inspection, palpation, percussion, and auscultation are successively employed. 22 DISEASES OF THE LUNGS AND PLEURJE. Inspection.—-The chest should always, if possible, be uncovered, so that a general view of its conformation can be obtained, whether it be the broad, well-formed chest of robust health; or the small, narrow, long chest —with antero-posterior and lateral diameters diminished, costal angle narrowed, and ribs unduly oblique and approximated—adapted to small lungs; or whether the thorax be unduly expanded with widened intercos- tal spaces, straightened ribs, increased costal angle, and deepened antero- posterior diameter—making up the round-shouldered barrel-shaped chest adapted to the accommodation of enlarged lungs. Again, the thorax Fig. 5 (from Quain's Anatomy).—A. Upper margin of sternum = lower border of 2nd dorsal B. 2nd costal cartilage = 5th dorsal vertebra. C. Infra-sternal depression (xiphi sternal articulation) = lower part of 9th dorsal vertebra. may be distorted by various kinds of spinal curvature, by rickets in early life, or by continued pressure in any particular direction. Finally, there may be local flattenings or bulgings of the chest walls, due to alterations in the subjacent viscera, and giving rise to a want of symmetry on the two sides. The movements of the chest are of great importance in diagnosis. The free and equable expansion of the chest implies the free entry of air into the lungs; on the other hand, relative immobility or recession of any 999� PHYSICAL EXAMINATION OF THE CHEST. 23 portion of the chest during inspiration, signifies that the entry of air to the corresponding portion of lung is, from some cause, retarded or im- peded. In cases of general obstruction to the entry of air, whether by impediment at the main air-passage or in its entire distribution, there is universal recession of all the soft parts—the supra-clavicular regions sink downwards, the hypochondria recede, and the intercostal spaces deepen during the effort to expand the chest against atmospheric pressure. On the other hand, when the difficulty of expansion, whether from intrinsic disease of the lung or pleura, or from obstruction of air-passages, is re- stricted to one side of the chest or to a portion of one lung, the restrained expansion during inspiration is limited to that portion. Thus from in- spection alone we may often form an opinion as to the seat, and even surmise the nature, of the disease present. Various instruments which have already been referred to—callipers, cyrtometer, double tapes—are valuable for the purpose of recording differ- ences in shape and measurement, but the information which they are useful in recording is at once obtained by the eye of the trained observer. By inspection we thus learn: 1, whether a patient be large-chested or small-chested; 2, whether the shape of the chest be good and symmetri- cal, deformed, flattened, or bulged in any of its parts; 3, whether its movements be free and equable, or irregular and restricted, generally or locally; 4, any surface markings, enlarged veins, tumors, abnormal pulsa- tions, etc., will at once attract the eye and be duly noted. Palpation is employed in aid both of inspection and percussion. (a) During preliminary inspection of the chest, the position of the heart's apex beat should be invariably, and as a matter of habit, ascer- tained, and any deviation from its normal position, viz., the fifth inter- costal space one inch to the sternal side of the left nipple line, should be noted. (b) Any local bulging or tumor will naturally be manipulated to as- certain its relation with bone or soft structure, whether it be solid, fluc- tuating or pulsating. (c) In connection with percussion the observer should notice differ- ences of resistance as well as of tone. (d) Increase or diminution of vocal vibration or fremitus will be noted over any spot of altered resonance by applying the hand and making the patient utter some resonant words, such as " ninety nine." Vocal fremitus is increased by consolidation of lung, provided the bronchi be not occluded; diminished by much thickening of the pleura, by obstruction of the main bronchus, or by air in the pleura; annulled by fluid in the pleura. It must be observed, however, that in some cases of fluid in the pleura a certain degree of vocal vibration may be com- municated, probably from lung adherent to the chest wall above the fluid, possibly conveyed by some long bands of adhesions. The loudness or 24 DISEASES OF THE LUNGS AND PLEURAE. feebleness of the voice, as well as height or depth of pitch, must of course be taken into account in judging of fremitus, and corresponding part on two sides should always be compared. (e) Loud coarse bronchial rales may cause the chest walls to percep- tibly vibrate producing rhonchal fremitus; sometimes cavernous or large crackling rales will do the same. Pleuritic friction may likewise be per- ceptible to the hand—friction fremitus. In cases of effusion into the pleural cavity, or in hydatid cysts near the surface, fluctuation may some- times be elicited. Percussion is the method by which we test the resonance of various parts of the thorax and compare it with that which experience has found to obtain in health. The theory of percussion sounds is of course ulti- mately based upon acoustic principles; but in the multiple conditions, quoad percussion, present in the healthy and diseased chest, it would be impossible to give an intelligible explanation of the observed results in any moderate space, and moreover quite beyond the ability of the writer. It must suffice, then, to point out that by percussion we detect the various degrees of resonance yielded by different parts of the chest surface, which depend upon the relative amount of air and solid structure subjacent, and upon other minor causes to be incidentally noticed. Method of Percussing.—It is best to use the fingers only for percus- sing. One finger of the left hand should be placed firmly upon the chest, so that the two last phalanges be accurately applied to the part percussed. With one or two of the fingers of the right hand, semi-flexed, the per- cussion should be made, so that the stroke fall vertically upon the applied or pleximeter finger. Be it observed:— 1. That the pleximeter finger be applied accurately and with sufficient firmness. 2. That it be applied precisely in the same manner and to the same spot pn the corresponding sides of the chest in comparing them, e.g., the finger must not be applied along the intercostal space on one side, and across the ribs on the other. 3. The percussion stroke must be made from the wrist, quite vertical to the surface percussed, and in comparing two spots the force of per- cussion stroke must be the same. These conditions cannot be nearly so wrell preserved if percussion be made from the elbow. 4. As a rule the percussion stroke should be light. The precise limits of dullness, whether in chest or abdomen, cannot be obtained by hard percussion, since the vibrations of collateral parts are too strongly elicited. It is laid down in most text-books that percussion should be made " staccato," the percussion finger not being allowed to rest upon the plexi- meter. This I am convinced is an error, which is avoided by non- observance by nine out of ten of the best manipulators in actual prac- tice. It is sometimes, of course, advisable to employ the lightest possible PHYSICAL EXAMINATION OF THE CHEST. 25 staccato percussion. It is also sometimes necessary to employ hard per- cussion to elicit dullness or resonance of deep-seated parts. 5. The sense of touch must be used equally with that of hearing in percussion. The degrees of resistance appreciated by the pleximeter finger are to be carefully noted. Dullness, and particularly the hardness and want of resilience over thickened and adherent pleura, may thus readily be felt by the pleximeter finger. Various pleximeters and plessors are used by some observers, modifica- tions of those designed by Piorry. The simplest pleximeter consists of a piece of ivory some two inches long and half an inch broad, the plessor being a small hammer with an india-rubber tip to the striking surface. These instruments may possibly be of value in demonstrating to a class, but their employment by students should not be encouraged for three reasons:— 1. We may rely upon having our fingers with us, but are apt to leave detached instruments behind. 2. Patients when very ill are frightened or annoyed by instruments, and may be readily hurt by them. 3. The important reason is, however, that in using such instruments we deprive ourselves altogether of the information gained by the sense of resistance. Some physicians are inclined of late to take to the pleximeter, still using the fingers as the plessor; but inasmuch as it is the plexi- meter finger with which we appreciate resistance chiefly, the objection in greatest measure still holds good. The position of the patient during physical examination of the chest by percussion and auscultation is of importance. If not in bed the sitting posture, with the back supported by a cushioned chair is the best for ex- amining the front of the chest; if in bed, the semi-reclining posture with the back firmly supported. Whilst the back is being examined the patient should be directed to lean slightly.forward and to let the arms fall looselv down between the knees, in which position the supra-scapular regions, at which the very summits of the lungs are situated, are best ex- posed. If the patient stoops forward too much with folded arms and bent back, the respiratory movements are impeded, and a very considerable amount of dullness may be developed at the right base by the thrusting backwards of the postero-upper surface of the liver. Each region of the chest surface should be systematically tested by percussion, the two sides of the chest being at all points compared. Not only, however, must the two sides of the chest be thus compared from above downwards, but percussion should be employed from side to side across the sternum, so as to define the limits of the anterior margins of the lungs from either side. By this means valuable information is often elicited in cases of consumption, cancer, pleuritic effusions, etc. 26 DISEASES OF THE LUNGS AND PLEURE. Terms. palpation. Vocal fremitus normal__... increased.. diminished. absent..... Rhonchal fremitus... Friction fremitus... PERCUSSION. Normal resonance. Increased resonance. . tympanitic resonance skodaic resonance Impaired resonance .. amphoric resonance. absence of resonance. Transmission of the vibration of rhonchus to the hand applied to the chest. Transmission of the vi- brations of pleuritic friction. AUSCULTATION. Breath-sounds. Definition. The transmission of laryngeal vibrations to the chest wall, ap- preciable by the hand. An arbitrary term sig- nifying the varying degrees of resonance of the different parts of the chest, within the range of health. Drum-like note . A peculiar form of tym panitic resonance of high pitch and great clearness. The modified resonance sometimes elicited over a cavity, and often accompanied by " cracked pot sound" (bruit de- pot fel6). Vesicular. Exaggerated. Synonyms. Consolidation of lung. Bronchial obstruction or separa- tion of lung from parietes by thickened pleura. Effusion of fluid or air in the pleura. Partial obstruction of larger bronchi. Bronchitis. Pleuritic roughening. Hyper-resonance. Relaxed lung note. Dullness of different degrees; hardness wooden percussion. Tubular note.......... Absolute dullness Tonelessness. Flat ness................. Significance. Health—needs confirmation by other signs. Air in the pleura. Lung in contact with surface relaxed, but not compressed by a moderate effusion into the pleura. Central consolida- tion in pneumonia will some- times produce this note. Incomplete consolidation: co- existing increased resistance may often be appreciated dur- ing percussion. Pulmonary excavation near the surface and freely communi- cating with the bronchi. Normally obtained on percus- sing the trachea with the; glottis open. Consolidation or lung displaced by fluid or tumour. Inspiratory sound soft and breezy, expira- tory sound shorter, weaker or even ab- sent. There should be no perceptible pause between the inspiratory and expi- ratory sounds. Intensified normal breath-sound due to increased movement of tidal air. Normal breath-sounds. Puerile. Compensa tory. Supplement- ary.............. Healthy lung. Increased function. When heard oyer a portion of one lung, signifies compensatory action to make up for deficiency or disease elsewhere. Normal in young children and in adults during violent exercise of the lungs. PHYSICAL EXAMINATION OF THE CHEST. 27 Terms. Definition. Synonyms. Significance. auscultation. Breath-sounds (continued). Weak......... Deficient movement of Feeble. Partial sup- Diminished function. tidal air. pression ............ Suppressed... Absence of breath- Lung distant from surface or bronchus obstructed. Interrupted... Inspiratory sound par- Jerking. Wavy. Cog- Irregular expansion, partial con- tially or completely divided into two or solidation about small bronchi. May be of purely nervous origin through irregular con- three sounds. traction of muscles. Prolonged expiration.. Expiration lengthened Partial consolidation of lung or to or beyond duration partial obstruction of bronchi. of inspiration. Vesiculo- The vesicular part of Harsh. Coarse. Sub- Commencing consolidation. the breath-sound be- tubular, Indetermin- Some authors use the term as ing partially or com-pletely annulled, the descriptive of the roughened breath-sound of dry catarrh tubular or glottic of the larger bronchi. (Heard portion of that sound heard with greater dis normally in neighborhood of bronchi). tinctness especially during expiration, which is prolonged. A blowing breath- Bronchial. Blowing. Hepatization or consolidation of sound the inspiration Tracheal. the lung. (Heard typically and expiration being May be high pitched or over trachea.) about equal in pitch whiffing, medium or and duration and distinctly divided. Placing mouth in position to pronounce word commencing with guttural ch (y) and drawing breath to and fro imitates the sound with exact- ness (Skoda). Carvernous... A blowing breath. Pulmonary excavation or con- sound of hollow qual- densed lung with dilated ity, most so in the bronchus. expiratory portion, which is usually of lower pitch than the inspiratory. Similar to the above, but with blowing Large pulmonary cavity. characterand hollow- ness intensified. Adventitious sounds. Musical sounds gene- Rale (rale and rhonchus rated by partial ob- being indifferently struction in a bron- used by many au- chial tube imparting thors). vibrations to the air currents. Sonorous rhonchi... Low pitched, loud snoring. Bronchitis of the larger tubes. High pitched, whis-tling Bronchitis or spasmodic narrow- ing of the medium or fine tubes. 28 DISEASES OF THE LUNGS AND PLEUR.E. Terms. Adventitious sounds. (continued) Stridor. Rales. Small crackling Medium crackling. Large crackling. Gurgling. Small bub- bling..... Medium and large bub- bling...... Clicking sounds Crepitation... Metallic tink- ling......... Definition. Synonyms. A coarse vibrating rhonchus, generated at the larynx or by pressure on the main bronchi. Moist sounds or rattles produced by the bub- bling of air through fluid in the lung or bronchi. A fine rale produced in the minute bronchio- les and alveoli of con- solidatedlungconsist ing of numerous small sharply defined crackles chiefly au- dible during inspira- tion, but in less de gree with expiration Similar to above of larger size. Stridulous rhonchus or rale............... ■ Rhonchi "and" rales" are used indifferently by many authors. Subcrepitant rales Moist crepitations... Significance. Crackles of larger size and fewer in number produced in minute pulmonary cavities. Larger and more liquid ra'es produced in cavities of medium and large size. A rale produced by the bubbling of air through mucus in the finer bronchi, and more or less muffled by transmission through spongy lung Similar rales generated in larger tubes. Crepitant rales. Moist crackling. Cavernous rale... Sub-mucous or muco- crepitant rale........ Single sounds, or few in number, mostly lim- ited to inspiration and of sticky, semi fluid character. A minute dry crackling sound in which the crackles are infinitely small and even, and occupy chiefly the latter part of inspira- tions. The metallic resonance sometimes imparted to a moist sound by a large pulmonary or other cavity. The sound may be gene- rated in the cavity or resonated from a bronchus in connec- tion with it. Pressure of a malignant or aneurysmal tumor upon a main bronchus or the trachea, Sometimes produced by laryn- geal paralysis. Thin fluid in minute bronchial tubes with consolidation of the lung. Resolving pneumonia. Resolving pneumonia. Broncho- pneumonia. Rapid caseous pneumonic softening. Softening pneumonia or tubercle. Mucous rales. Tracheal rattles.......... Dry crackle. Fine dry crepitation, Pneumonic crepita tion. Cavity in the lung. Capillary bronchitis. Pulmon- ary oedema Bronchitis of larger tubes. Secretion collecting in the tra- chea during last moments of life. Commencing softening of tuber- cular deposits in the lung. Early stage of pneumonia. The sound is sometimes heard in a certain degree of pulmonary cedema, and during the first two or three deep inspirations over a portion of lung not used (e.g. the extreme bases in bed- ridden patients). A large dense walled pulmonary cavity or a pleuritic cavity. PHYSICAL EXAMINATION OF THE CHEST. 20 Terms. Adventitious sounds (contin ued). Splash___ Bell sound.... Friction. Dry Friction . Moist friction. VOICE SOUNDS Normal..... Increased or di- minished. Annulled or ab- sent........... Bronchophony. Pectoriliquy. -Egophony. Definition. The succussion of air and fluid produced by the shock of cough in a large cavity or by shaking a patient. with the ear applied over a hydro-pneu- mo-thorax. A metallic ring heard on sharp percussion over a pneumo-tho- rax, commonly eli- cited by the use of coins. A rubbing sound pro duced by the move- ments of two sur- faces of the pleura that are in contact. and inflamed roughened. A sound often closely imitating moist ere pitation produced by attrition of surfaces covered by soft moist lymph. The sound of the voice transmitted through the healthy lung. The loud transmission of the laryngeal vibrations, apart from articulation. The clear transmission of articulate sounds Heard best during whispering, when bronchophony (which usually, Dut not al- ways accompanies it) is excluded. High pitched, trem ulous modification of the voice, due to the transmission of the upper tones or harmo- nics. Synonyms. Hippoeratic succussion sound. Cough splash. Bruit d'airain. Significance. A large cavity containing air and fluid. Hydro or pyopneumo- thorax. Pneumo-thorax. Pleurisy. Leathery or creaking Heard at commencement and at, friction. Dry rub. termination of pleuritic attack. Spongy friction. Fric tion crepitus, etc..... Sometimes heard over upper confines of recedent effusion and in other conditions of thick moist pleuritic exudations. Lung separated from chest watt by fluid or growth. Pulmonary consolidation. Cavity in the lung. A close imi- tation of this sound pectorilo- quie aphonique may be some- times heard through a pleuritic effusion (sero-fibrinous) on making the patient whisper roughly. Pleuritic effusion. 30 DISEASES OF THE LUNGS AND PLEUR.E. The foregoing table includes all the terms used in a technical sense, which are necessary for describing the sounds met with in chest diseases. They are—with one or two unimportant additions—those which were carefully selected by my friend Dr. Mahomed and myself, as English members of a committee nominated at the International Medical Congress held in London in 1881, to endeavor to simplify the terminology of aus- cultation for international use. The list has at least the advantage of not including any new or unknown terms, and as it only differs on the side of greater simplicity from the terminology in the last edition of my work, and in my more recent article on physical signs in Quain's Dictionary of Medicine, I venture to introduce it here pending the final report of the committee above mentioned. A few observations are still necessary upon the mechanism of chest signs. The results of clinical observation will not bear out the views cur- rent since the time of Laennecwith regard to many points in the mechan- ism of auscultatory phenomena—views, however, which have not escaped the criticism and opposition of such able observers as Beau, Spittal, Skoda, Bondet, Chauveau, and others. Our difficulty indeed lies in arriving at a true judgment amidst the conflicting and ably maintained opinions of many authors, in gathering and knitting together the frag- ments of truth which lie scattered over their extended battle ground. I will endeavor as briefly as possible, and in the way of comment upon some of the headings of the above table, to give the rationale of the physical signs there mentioned. Percussion.—The explanation of the sounds elicited by percussion is comparatively simple. The degrees of resonance and impaired resonance are dependent upon (1) the proportion of air and solid under percussion, (2) the tension of the air within the chest cavity, (3) the range of vibra- tion of the chest wall. In the well-formed chest of the young adult, and within the range of normal conditions of quiet breathing, we obtain over the pulmonary regions that degree of resonance or clearness of percussion which is typi- cal of health. At any stage of the inspiratory act, however, the percus- sion note is somewhat deadened by closure of the glottis and compression of the chest by the expiratory muscles, the tension of the confined air being increased and its vibratility and that of the chest wall diminished. It is said that the chest resonance is increased at the end of deep inspira- tion. This is only true about the confines of normal resonance. On trial it will be found that the clearest percussion note is elicited within the range of calm breathing. In pneumo-thorax, with free communica- tion with a bronchus, i.e., when the air has approximately the normal atmospheric tension, we get the most deep-toned percussion resonance (tympanitic resonance). If, however, the communication with the lung be only by a valvular opening admitting of entry, but not of escape of air, PHYSICAL EXAMINATION OF THE CHEST. 31 we get increased tension and correspondingly deadened note, as the air accumulates with distension of the chest wall. Dr. C. J. B. AVilliams' and more recently Dr. Bristowea both regard the percussion note as pri- marily due to the vibration of the chest wall and as modified by the con- ditions of the underlying cavities or viscera, so far as they afford varying degrees of impediment to the chest-wall vibration. In the above-described circumstances it is true we cannot separate increased tension of air from increased tension or rigidity of solids, and there are many states in dis- ease, and even within the range of health, in which the resilience of the chest walls is impaired, and an impairment of resonance thereby accounted for. Thus many robust people, soldiers especially, have rigid resisting chest walls, and percussion in such persons yields a diminished sound. On the other hand in children, and in delicate persons with thin elastic ribs, we may get an amount of resonance which may even mask a certain degree of underlying disease. Mere adhesion of the pleural surface, i.e., the delicate spongy adhesion without appreciable thickening, is not suffi- cient to alter percussion note, since it does not of itself impair mobility. A thickened adherent pleura gives rise to a dead, hard percussion note. Underlying cavities or dilated bronchi will give certain degrees of tubular or amphoric resonance, especially whilst the glottis is open, but the reso- nance in such cases is always less full than, as well as different in quality from, that of healthy lung. In percussion, it must be borne in mind that over a surface where, from the underlying conditions, we should expect complete dullness, we may yet elicit a considerable degree of reso- nance conducted from adjacent parts containing air. This lateral con- duction from resonant areas, modifying the percussion note over areas of consolidation, is more noticeable on hard than on light percussion, and it is only by gentle percussion that the limits of dullness can be accurately defined. In the healthy chest we obtain, during moderate expiration, super- ficial cardiac dullness, corresponding with that small area marked off by a horizontal line drawn from the apex beat to the mid sternum, and from the same point (the apex beat) to the lower margin of the fourth cartilage at its junction with the sternum. On firm percussion, the deep heart's dullness may be elicited as high as the third cartilage, mid-way between the nipple and the sternum, and to the right margin of the ster- num at the nipple level. Stomach note is obtained at the sixth cartilage in the left mid sterno-nipple line; in the left posterior axillary line a small area of dullness, extending upwards from the margin of the ribs for a couple of inches, marks the situation of the spleen. On the right front of the chest in the nipple line, liver dullness is obtained below the level of 1 Diseases of the Chest, 4th edition, p. 13. 2 Practice of Medicine, 5th edition, p. 372. 32 DISEASES OF THE LUNGS AND PLEURAE. the sixth rib, and on deep percussion for a rib higher; posteriorly, about two fingers' breadth of dullness at the extreme right base marks the situ- ation of the liver in contact with the thorax. Lung resonance is obtained anteriorly over the supra-clavicular fossa, and posteriorly extends upwards to the level of the seventh cervical spine, i.e., about 1-J- in. above the level of the clavicle. It is in these highest regions of the chest, corresponding with the extreme summits of the lungs, that the first evidence of phthisi- cal disease is often obtained. Auscultation.—With regard to respiratory murmurs or breath- sounds it may be broadly stated that all breath-sounds, whether healthy or morbid, with the exception of normal vesicular inspiration are generated in the larynx, and modified in their transmission through the different media normally, or abnormally, intervening between the larynx and the point of observation. The following propositions express, I believe, the exact truths respect- ing the nature of breath-sounds (excluding rales and adventitious sounds). 1. The vesicular respiratory murmur is a sound having a double mech- anism being made up of (a) a bruit produced by the passage of air to and fro through the glottis, and reverberated downwards through the bron- chial tubes, (b) an infinite number of minor bruits similarly produced at the openings of the pulmonary lobuli. 2. All other breath-sounds (excluding adventitious sounds) are due to the conduction of the glottic sound above mentioned through media of different kinds, forms, and densities; any local currents of air being only so far operative in as much as they serve to assist conduction. '3. It may be observed that, although in cavernous and amphoric breath- ing the breath-sounds may be generated locally by the air currents enter- ing and issuing from the cavity, yet this local mechanism is not essential to the sounds, and is often wanting. Vesicular murmurs.—It would seem a simple thing to demonstrate once for all the production of vesicular murmur. Yet in truth the con- ditions of its mechanism are most difficult to reproduce. If the lungs, re- maining in the chest, or placed upon the table, be auscultated, whilst air is injected through the trachea, sounds are doubtless heard more or less closely resembling those of vesicular breathing, but in such an experiment the whole mechanism of respiration is inverted. In natural breathing, the air is not injected into the lungs—it enters to fill the space that would otherwise be left vacant by their expansion; the important difference being, that in inspiration there is no period at which any air tension beyond that normal to the atmosphere exists. The lungs are never in- flated, nor are they ever even approximately emptied of air, so that in truth the function of respiration proceeds by interchange of gases within an area of comparative calm, only so far disturbed by tidal and secondary currents as to effect its thorough ventilation. But at the narrow isthmus PHYSICAL EXAMINATION OF THE CHEST. 33 of the glottis through which the air—small in amount compared with the lung capacity—has to pass and repass sixteen or seventeen times a minute, the current is rapid, and the air necessarily cast into audible vibrations, producing a blowing sound which, carried along the bronchial channels, becomes infinitely divided, hushed and broken up, to form part of the rustling murmur of normal inspiration. M. Beau,1 in 1834, first sought to prove that tracheal, vesicular, bronchial and cavernous breath-sounds were not due, as Laennec had thought, to the friction of the air against the parietes of the trachea, alveoli and caverns, but that they resulted in the manner above mentioned, from the reverberation in these parts of a single sound which was produced in the superior air passages. MM. Barth and Roger observe, however, that the inspiration loses nothing in force at the base of the lung, and maintain that the vesicular murmur ought consequently to have its origin in part, at least, in the lungs themselves. And indeed my own observation goes to the support of their opinion—viz., that the respiratory murmur in the majority of instances, does not lose intensity towards the base of the lung. Even if it be so, however, I do not see how the fact should invalidate M. Beau's view, for the propagation of a sound in the bronchial tubes—which remain open through the traction exercised upon them by the elastic lungs—is too perfect to suffer any diminution in a distance so small as that which separates the summit from the base of the lung. On the other hand, M. Beau repeats the observation of Laennec that, in animals with long necks, such as the ruminants, the respiratory mur- mur is much more feeble than in the carnivora, as evidence in favor of the glottic production of the respiratory bruit. One has possibly in such case, however, to deal with differences of structure and of functional activity. Dr. Spittal,2 writing but a few years after Beau's views were first pub- lished, brought forward some additional experiments in support of them, in which by eliminating the respiratory movement of the lungs as a fac- tor, he sought to show how far the respiratory sounds were really con- ducted laryngeal sounds. Skoda also believes the respiratory murmur to be due to a double cause, viz., the conduction of the glottic bruit through the bronchial tubes, and a sound produced in the air-cells and small bronchi. During expiration, the air passing from a large space, the air-cells, into a smaller, the bronchi, becomes compressed, and hence the expiratory murmur of the larynx, trachea and large bronchi is as a rule louder than the inspira- tory. Dr. Blakiston/ who attributes the pulmonary sound to the air 'Archives general es de m6decine, 1834, 2me se'rie, torn, v., p. 557. 3 On the cause of the sounds of Respiration. Edinburgh Medical and Surgical Journal, vol. Ii., 1839. 3 Diseases of the Chest, p. 18. 3 34 DISEASES OF THE LUNGS AND PLEURAE. rushing through the smaller bronchial tubes, well points out that there is no contractile resistance within the lung to be overcome by the enter- ing air, the lungs being expanded not by the injection into them of air, but by the enlargement of the thorax by the inspiratory muscles. And it is curious to note that Skoda himself when criticising a statement of Fournet's, implying a dilating power of the air entering the lungs, remarks, "Air enters only when a vacuum is formed, and does not strug- gle against obstacles, except when a vacuum exists beyond these. I must not conclude the review of the chief opinions that have been held respecting the mechanism of the respiratory murmurs without refer- ring to a most important, and to my mind the only conclusive experi- ment that has been recorded, correcting the too exclusive theory of Beau. The experiment was conducted by MM. Bondet and Chauveau' upon a horse suffering from pneumonia affecting the lower half of the left lung. On auscultating the animal, exaggerated breathing was heard over the right lung and over the upper half of the left, tubular breath-sound being distinct over the lower or affected half of the left lung. These prelimin- ary observations made, the trachea was opened by an incision twenty centimeters in length, and the following phenomena were noted:— (1) On auscultation over the trachea below the incision, the wound being held widely open, the inspiratory bruit was almost completely lost, and the expiratory sound but faintly audible. (2) On auscultation over the consolidated lung, whilst the wound in the trachea was held widely open, no tubular sound could be heard during inspiration, and only a faint, brief and abortive sound during expiration. Over the rest of the lung and over the opposite (sound) lung, however, the normal respiratory sounds were clearly heard with quite normal dis- tinctness. (3) A tube supplied with a musical reed being introduced into the trachea, the artificial voice-sound was heard very distinctly over the con- solidation, but was inaudible over the rest of the lung. This experiment at first sight appears almost conclusively to show that the whole of the respiratory murmur is generated within the lung, since it was not notably impaired by eliminating the glottic element. The artificial voice-sounds, on the other hand, audible over the consoli- dation, showed that a possible fallacy, viz., the blocking of the left lower bronchi by blood clot, did not exist. The glottic bruit is, however, a fact which cannot be denied, and that the sound is propagated downwards to the lung is equally certain from the experiments of Beau, Spittal, Barth and Roger, some of which I have myself repeated; nor is it possible as a matter of reasoning to con- ceive, but that a sound, loud in the trachea and traceable down the bronchi 1 Revue mensuelle de m^decine et de chirurgie, tome i., 1877, p. 161. PHYSICAL EXAMINATION OF THE CHEST. 35 so far as they can be reached, should enter as an element at least into deeper sounds. I have also already directed attention to the tense con- dition of patency, in which the walls of the bronchi, the minute bronchi especially, are held by the elastic tissue of the lung in which they are imbedded, as being highly favorable to the reverberation of sound through them. I must confess to great doubts whether the movement of the air in the bronchi gives rise to any appreciable sound, and whether even the angles of subdivision of these tubes would suffice to throw the tidal air into audible vibrations. It can scarcely be doubted that the intra-pul- monary portion of the inspiratory murmur is generated, as suggested by Bondet and Chauveau, at the junction of the bronchioles with their in- fundibula. Here are repeated on a minute scale, but at innumerable points, the conditions of a vibratile aperture terminating with considerable abruptness in an expanded chamber, conditions which are favorable to the production of veines fluides whose sum total amounts to a consid- erable sound of such a kind as that of vesicular inspiration. All experiments seem to show that the expiratory murmur is of extra- pulmonary, i.e., glottic, origin. Weak, harsh (vesiculo-tubular), and exaggerated breathing.—Weak- ness of breath-sound may simply arise from feebleness of the muscular chest movements; it is then better spoken of as partially suppressed breath- ing. When the weakness of breath-sound arises from defect in the lungs it is always accompanied by some harshness, the true vesicular sound of the lung being more or less completely wanting and the glottic sounds faintly audible, their conduction being partially obscured by occlusion of some of the finer bronchi. In harsh breathing the glottic sounds are better conveyed to the ear by the partially consolidated lung. In this form of breath-sound the expiration is always more audible and prolonged than natural, and the inspiratory and expiratory sounds are distinctly divided by a very brief interval, this breath-sound being in fact the tracheal sounds conducted from some distance. There is a kind of " harsh " breathing which would, however, be better styled rough or coarse dry vesicular breathing, which is commonly heard in the neighborhood of small and cicatricial deposits. This sound is probably a true pulmo- nary sound, it resembles coarse and exaggerated inspiration of very dry character; which features are not distinct in the expiration. Exaggerated breath-sound is heard in the healthy young child. More rapid breathing, more rapid passage of air through the glottis and into the lungs, are the conditions upon which this enhanced breath-sound depends. The expiration is generally rather prolonged, and both sounds are coarser than ordinary. Exaggerated breath-sound is usually, in health, limited to children of tender years, and hence its synonym " puerile breathing," but some persons preserve this quality through adult life. This variety of breathing is heard over the sound side in cases in which 3G DISEASES OF THE LUNGS AND PLEURAE. the respiratory function of one lung is in abeyance from any cause. It maybe similarly heard over one portion of a lung, the rest being diseased. Hence another synonym, compensatory breath-sound. It indicates res- piratory vigor and is so far of good augury, inasmuch as it shows that an enlarged lung, or portion of a lung, is not merely dilated but also func- tionally more active, a most important fact to ascertain in cases of one- sided chest disease. When a lung is separated from the surface by an interval of fluid or has its bronchus occluded from any cause, we get suppression of the breath- sounds over it. In order for this suppression to be complete in pleuritic effusion, the effusion must be sufficient to compress the lung; otherwise feeble bronchial breath-sound is conducted through the fluid. Even in cases of considerable effusion, however, a certain amount of breath-sound is heard over the upper part of the chest, although it is obvious that the collapsed lung can take no part in producing the sound. When the lung is separated from the thoracic wall by greatly thickened adhesions, and —as is usually the case—is itself indurated and collapsed by interstitial growth, the breath-sound is partially suppressed, the glottic bruits being only very imperfectly conducted. Jerking or ivavy and cogged breathing are varieties to which different authors attach very different importance. In jerking or wavy breathing the inspiration, instead of being a continuous sound, is two or three times interrupted. The expiration is rarely affected in this way, and may be normal or simply harsh and somewhat prolonged. One so frequently meets with jerking respiration in nervous people, that when unaccom- panied by other morbid sounds but little importance is to be attached to it. It may be due to, (a) irregular action of the respiratory muscles under conditions of pain, as in pleuro-dynia pleurisy, myalgia, and also in hysteria and other nerve disorders; (b) (when on the left side) to cardiac pulsation, it being then of strictly cardiac rhythm; or (c) it is possible that in nervous people during excitement of the heart's action, the im- pulsion of blood through the pulmonary small vessels and capillaries may cause some sensible modification of the respiratory rhythm; (d) certain textural diseases of the lung itself, causing a want of uniformity in elas- ticity and expansile power, may account for some cases of local waviness of breath-sound (Dr. Walshe considers that pleuritic adhesions may do so); (e) waviness of breathing caused by any of the above circumstances may be superadded to other more definite signs of lung disease. Thus pulsa- tile waviness of cardiac rhythm is often combined with well-marked cav- ernous respiration. A remarkable instance of wavy, cavernous breathing was witnessed by the author in a case in which the entering bronchus to a large cavity was partially occluded by a small pulmonary aneurysm pro- jecting into its calibre close to the cavity, and thus alternately stopping and permitting the cavernous sound. The death of the patient from PHYSICAL EXAMINATION OF THE CITEST. 37 sudden haemoptysis within a few hours verified and explained this obser- vation.1 Cogged wheel rhythm is a character of the respiration to which much importance is attributed by some authors. It is attributed to minute obstruction in the finer bronchial tubes, probably by glutinous and ad- herent mucus (Walshe), which the current of air succeeds in forcing at intervals without producing any distinct bubbling. Dr. Walshe believes that this sound is due to the same cause as liquid rales, into which it is finally converted. This sound has some affinities with wavy respiration, and, like it, is commonly limited to inspiration, but the inspiratory sound is more subdivided. Prolonged expiration.—Prolongation of expiration is perhaps the most important, as it certainly is the earliest of the signs of commencing con- solidation of the lung. It marks the transition between vesicular and bronchial breath-sound, and it indicates that over a certain extent of lung the vesicular element of breath-sound is diminished or lost, glottic sounds becoming predominant, or alone heard, with their distinctive characters and proportion. Thus with prolonged expiration we get division between inspiration and expiration (divided respiration), a characteristic of the glottic type. The vesicular quality of the inspiration is gradually lost as the expiration becomes more distinct, i.e., harshness is always combined with prolonged expiration. The expiration instead of being inaudible, or occupying but a fractional part of the duration of inspiration, comes to equal it or even slightly to exceed it in duration. These are par ex- cellence the characteristics of the glottic breath-sound, and as, on the one hand, prolongation of the expiration-sound is associated with harshness, i.e., want of vesicularity of the respiration, so, on the other, it passes into true bronchial breathing, in which the glottic sounds are conducted in all their intensity.. I may here remark that in listening for charac- teristic moist sounds or rales, our attention will be attracted mainly to the inspiratory portion of respiration, during which most of the morbid sounds are heard; whilst modified breath-sounds are most characteristically heard during expiration. Bronchial respiration.—This variety 01 respiratory murmur is heard normally at the lower part of the trachea, and in less degree at the inter- scapular region at the level of the spinous process of the fourth dorsal vertebra; as a morbid sign it is best heard over a lung consolidated by acute pneumonia. Skoda pointed out that this breath-sound could be best imitated by placing the tongue in the position to form the consonant ch (hard), j, and drawing the breath to and fro. Bronchial breathing varies in intensity according to the degree of con- solidation, the proximity to the main bronchial channels, and the condi- tion of the secondary and tertiary bronchial divisions. Most auscultators 1 Path. Hoc. Trans., vol. xxii., p. 48. 38 DISEASES OF THE LUNGS AND PLEURAE. think with Laennec that the sounds are originated in the affected lung; but on reflection one is compelled to regard it as a sound conducted from the larynx for the following reasons: 1. In pneumonia, in which it is best heard, the lung is injected by a coagulated substance which fills it, and maintains it in the state of per- manent inspiration, a condition which forbids the entry of air. There no longer exist the currents of air in the bronchi of the affected lung. MM. Barth and Roger maintain, and with them my friend and colleague Dr. R, Thompson agrees, that the inspiratory air-current passing to in- flate the sound lung secures the entry also of air to the diseased side. Any air so obtaining entrance, however, could scarcely produce a respira- tory sound. 2. It is not certain that the air moving in the bronchial tubes of itself produces any sound. Probably such air currents serve but to facilitate the propagation of vibrations which originate elsewhere. 3. The experiment of Bondet and Chauveau upon the hepatized lung of the horse already given (p. 34), appears to me to settle the question. These observers on holding widely open the wound in the trachea caused the respiratory bruit heard over the hepatized lung to disappear, whilst over the sound lung the respiratory murmur was scarcely at all modified. It is probable that the bronchial tubes vibrate in unison with the air which they contain, and thus augment the sounds which they convey. It would appear then, that the two conditions for the production of bron- chial breath-sound are consolidation of lung and patency of bronchi. Any obstruction of the main bronchus will obscure the sound, and the separa- tion of the lung from the parietes, whether by fluid or by thickened pleura, renders it less distinct. In some rare cases of pneumonia the breath-sound is suppressed, I presume from the small bronchi being oc- cupied by exudation overflowing into them "from the alveoli. Bronchial breath-sound may be produced by other than lung conditions. A medi- astinal tumor, aneurysmal or cancerous, situated between the thoracic wall and a bronchus will yield the sound. The expressions blowing, tubular and tracheal, merely have reference to extent and intensity of bronchial breathing, blowing referring rather to extension than intensity, this degree of bronchial breathing being heard when the lung is incompletely consolidated; tubular breathing being the most characteristic quality of bronchial breathing, tracheal respiration still more intense, being heard over consolidation in the neighborhood of the main bronchi or their primary divisions. Cavernous breath-sound.—This consist of a hollow inspiratory and ex- piratory sound, which has been compared to the sound produced by blow- ing into the cavity formed by the two hands. The expiration must be especially attended to in listening for cavernous breath-sound- it is wavering, hollow and prolonged. Drs. Flint and R. Thompson, both PHYSICAL EXAMINATION OF THE CHEST. 39 attach much importance to the fact that the expiration is of lower pitch than the inspiration, as serving to distinguish cavernous respiration from bronchial, where the inspiratory and expiratory murmurs are of similar pitch. Cavernous respiration is heard over pulmonary cavities, (1) which are of a certain size (larger than a filbert), (2) which are in part at least empty, (3) which communicate freely with one or more bronchi. As to the mechanism of this sound, one cannot deny that it may be imitated by breathing into the hollow of the two hands, but it is questionable whether this mechanism suffices to explain the cavernous respiration heard over the lungs. 1. In the first place, the cavernous sounds are heard during the whole period of inspiration and of expiration. Now I doubt the possibility— but no one would deny the rarity—of the existence of a cavity in the lung capable of contracting and expanding with such completeness as to gen- erate the sounds: for the air will only enter such a cavity (except when impelled there by the act of coughing) in accordance with precedent expansion. 2. One again and again meets with cases in which very well-marked cavernous breathing may be heard over large cavities whose powers of expansion are almost nil. 3. The observations of Beau, Spittal and" Skoda lead them to adopt this view respecting cavernous sounds in preference to that of Laennec more usually accepted. It is doubtful, however, how far "consonance" in the right sense of that term is concerned, as Skoda maintains, with the production or reinforcement of the cavernous sounds. For there can be no definite relationship between the bronchial and cavern spaces and their walls which would enable them to attune to one another save in a very haphazard way. Amphoric breathing.—This is really a variety of cavernous breathing, the cavity being large, superficial and thin walled. There can be no doubt, however, that in some cases, in which the cavity is large and the thickened tuberculous lung textures so removed as no longer to restrain the chest movements, direct influx and efflux of air through the bronchial tubes communicating with the cavity will cause the sound. In cases of pneumo-thorax, in which the opening is free, amphoric breath-sound is heard to perfection; if the communication be valvular the sound is not heard at all, or very imperfectly so. Rales.—With regard to the different rhonchi and rales, some are of such obviously simple mechanism as to require but little explanatory comment. The rhonchi, for instance, are but musical notes of higher or lower pitch, depending upon vibrations of air set up in tubes, partially obstructed by local thickenings of their lining membranes, by mucous collections or pellets adhering to their sides so as partially to obstruct them, or finally by spasmodic narrowing of the tubes. It will be ob- 40 DISEASES OF THE LUNGS AND PLEURAE. served that all these causes of sibilant and sonorous rhonchi within the chest are of a temporary or transient nature, and accordingly these sounds are very inconstant, appearing and disappearing, or shifting from one spot to another, even whilst the patient is under examination. A vigorous cough, clearing the tubes of mucous collections, will com- monly for a time remove a sonorous rhonchus, and the sibilant sounds in asthma or bronchitis with spasm, will be partially or wholly removed by the inhalation of chloroform or ether. It must further be noted that in all cases the true respiratory murmur is obscured and enfeebled by the presence of these rhonchi, to return on their removal. Stridor is a variety of the sonorous rhonchus in which the vibrations are very coarse, and the sound produced very hoarse and low pitched. It may be occasioned by some paralytic affection of the glottis, which prevents the cords from being drawn apart during inspiration, and allows them partially to flap together, and thus to vibrate. It is in other cases produced by the pressure of a tumor directly upon a main tube, as the trachea or main bronchus. The vibrations which produce stridor, and those of the stronger forms of rhonchus, are so coarse as to be perceptible to the hand applied to the surface of the chest, thus producing one kind of rhonchal fremitis. It may be noted that the sounds under considera- tion are chiefly, but by no'means solely, heard during inspiration, the coarser forms and especially stridor being more particularly limited to that portion of the breath-sound. Great difference of opinion has prevailed respecting the nature and mechanism of crepitant rdle or fine crepitation. All observers agree that it is most typically heard in the first stage of pneumonia, and some regard it as the pathognomonic sign of that disease. This sound is defined by Walshe as composed of a variable, sometimes immense, number of sharp crackling sounds of minute size, all perfectly similar to each other, and rapidly evolved in puffs more or less prolonged. The sounds are dry in quality and co-exist exclusively, except in rare cases, with inspiration; and once established remain a persistent condition, until superseded by other phenomena. Williams's description of the sound, as resembling that produced by slowly and firmly rubbing a lock of hair between the finger and thumb close to the ear, has been generally accepted as an accurate one. The fine crepitation of pneumonia is very exactly imitated by other conditions: pulmonary collapse from disease, certain degrees of pulmonary oedema, oedematous pleura, and the first stage of pulmonary apoplexy, may be instanced as several circumstances in which the sound may be pro- duced, and the only condition common to all cases is the expansion of a moist and heterogeneous tissue. The application of the term dry to the sound, although acoustically correct, is peculiarly misleading, for moisture of tissue is probably one of the conditions essential to its production. Thus the sound may sometimes be most typically heard over a pleura, the two PHYSICAL EXAMINATION OF THE CHEST. 41 layers of which are separated by oedematous cellular tissue, a condition commonly found over old contractile lung consolidations. Again, in oedema of the lung, as for instance in some forms of heart disease and albuminuria, the fine crepitation may be well heard. In saying however, that fine crepitation may be well heard under these several conditions, I am bound to confess that there is to the fine crepitation of pneumonia an element superadded, a peculiar quality of the breath-sound, due to the consolidation of the lung, something short of the typical bronchial quality, and yet far beyond mere harshness, which gives a special character to the crepitant rale, and increases its loudness and definition. The fine crepi- tation under other conditions is, as a rule, unattended with any breath- sound. The actual state of lung in pneumonia which gives rise to the crepitation may, I think, safely be assumed to be one of oedematous exu- dation from congestion. When the exudation into the air cells is com- plete and consolidated, the crepitation ceases. Sub-crepitant rale is a small bubbling rale audible during both inspira- tion and expiration, but chiefly so with inspiration, generally occupying the beginning only of the expiratory sound. It is typically heard in the resolution stage of pneumonia, at the period when the sputa are becoming opaque and more or less purulent. This rale is more commonly heard than the dry crepitation in the moist catarrhal pneumonia which com- plicates phthisis. In oedema of lung beyond mere wetness of tissue, in which the fine bronchial tubes at the bases become partially occupied by thin fluid, although still permeable to air, the rale is also heard. Its mechanism consists simply in the presence of this fluid in the fine bron- chial tubes, and it is most typically heard in those cases in which, as in pneumonia, the bronchial tubes are surrounded by consolidated lung. The transitions between sub-crepitant and sub-mucous, and mucous rale are very fine, and, minutely regarded, are of no practical importance. We have often to appeal to other signs, the character of the respiration and the presence of percussion resonance or dullness, to help us in the inter- pretation of these rales. Thus, in capillary bronchitis of the adult, we have a fine bubbling rale of comparatively muffled character, which is attributable to secretion in the small bronchial tubes, but the same condi- tion in the infant—capillary bronchitis without any lung involvement— will give rise to a very sharply defined, almost metallic sub-crepitant rale, not to be distinguished from that of broncho-pneumonia or pneumonia undergoing resolution. The absence of bronchial breathing or of dullness will in some cases help us in the diagnosis, in others we must rely upon the general features of the case. Dry crackling is a sound comparatively rarely heard. It consists of a few, usually two or three only, sharply defined clicks heard during the latter portion of a deep inspiration; the inspiratory murmur being en- feebled or absent, and the expiratory sound prolonged, and more or less 42 DISEASES OF THE LUNGS AND PLEURAE. bronchial. The sound is said to be significant of commencing softening of "tubercular" deposits. It is also heard over centres of inspissating morbid products. In the former case a crepitant rale, and in the latter a moist and more abundant crackling rale, is delevoped by cough in many instances. Humid crackling, moist crackling, humid clicking, or by whatever other synonymous phrase we designate it, is a sound very frequently heard in the so-called second or softening stage of phthisis, and in the adult the sound is very significant of pulmonary softening; indeed the true humid clicking means commencing destruction of lung, and is usually associated with pulmonary tissue in the sputa, a sharply defined, moist or bubbling sound consisting of two or three inspiratory and one or two expiratory elements. The respiratory murmur is masked or replaced by the crackles, and does not return until, by enlargement or coalescence of the minute cavities giving rise to them, the rales have become enlarged to cavernous rales, or gurgling, and the breath-sound has become blowing or cavernous in quality. The humid crackle varies much in degree or sharp- ness of definition according to the condition of the pulmonary tissue situ- ated between the centres to whose softening it is due. If these centres are but necrotizing islets scattered through a large tract of lung, all of which is consolidated by catarrhal pneumonia (or mixed catarrhal and croupous pneumonia), as in the acutest form of pneumonic phthisis, the clicks are very strongly conducted, very metallic, and mingled with other coarse crepitant sounds. But in other cases the softening nodules are more or less widely separated by spongy and tolerably healthy lung tissue, when the humid clicks are muffled and more or less obscured. Over portions of lung which whilst undergoing softening are, owing to fibroid change or pleural thickening, functionally inactive under ordinary cir- cumstances of respiration, no moist sounds may be heard until a sharp cough has forced air into the softening tissues and developed the sounds. This is a most important point to remember in auscultation. Cavernous rale—gurgling rale. With enlargement or coalescence of small cavities to the size of, or exceeding a walnut, a second possible mechanism is to be taken into calculation as accounting for the large liquid rales produced. Of course fluid bubbling in a cavity will account for the sounds heard, as we may perceive on listening over a secreting cavity whilst the patient coughs, when we hear the splashing and gurgling sounds from forcible commingling of air and fluid. But in large and comparatively dry cavi- ties we can hardly imagine any such commingling of air and fluid to take place, during ordinary or deep breathing; even supposing, as I have en- deavored to show is not necessarily the case, air to pass to and fro into the cavity with any appreciable current. Any mucous rales produced in the associated bronchi, will, however, be heard with exaggerated intensity PHYSICAL EXAMINATION OF THE CHEST. 43 over the cavity, and if the cavity be of sufficient dimensions will give rise to metallic tinkling sounds. It is entirely erroneous to suppose—as may be demonstrated frequently on post-mortem inspections—that metallic tink- ling is significant of pneumo-thorax only: it may be most typically heard over a large cavity, and its mechanism is probably the same in both instances, viz.: the reverberation through a large thin-walled and empty cavity of a moist rale produced in the bronchus, or fistulous canal leading to the cavity. Voice-sounds.—Enough has beeen said in the earlier part of this chapter respecting the mechanism of breath-sounds to make it clear, that, to my mind at least, there can be no good reason for any mystery, as to the way in which voice-sounds are intensified or annulled under different morbid conditions of the lungs and pleurae. There can, at all events, be no doubt that voice-sounds are conducted from the larynx, and the more the expiratory sound is broken up into articulate sounds the more favor- able are the conditions for transmission backwards through the bronchial channels. These channels in the normal state are, as already stated, held patent by the elastic traction upon them of the surrounding lung, and they serve therefore as so many speaking tubes, although the direction of the current of air during articulation is not favorable to the best possible conduction. The rapid subdivisions of the tube and their being imbedded in an ill- conducting material, is, however, highly unfavorable to conduction of sound, and were it not for the shortness of distance the voice sounds would not be audible at all. Up to the point of subdivision of the main bron- chi, a few inches more or less of tubing would make but little difference in intensity of conduction; hence it is that mere linear distance from the glottis does not tell much upon the conduction of voice-sounds. They are in health pretty nearly as well or as badly heard at the base as at the apex or middle of the lung. If the glottis be destroyed by tubercular or syphilitic disease the voice-sound is of course annulled, and even the whis- per sound is impaired, showing that the glottis is to some extent concerned in the production of the whisper, probably being held open during that process. If the main bronchus on one side be compressed or occluded, the voice-sounds are annulled on that side, and vocal vibrations, which are merely palpable sounds, are similarly obscured. If on the other hand the termination of the tubes be surrounded by a better conducting material, as in pneumonia, or if the tissue normally surrounding them be con- densed upon them, as in that portion of a lung near the surface immedi- ately above an effusion, the voice-sounds will become loud and sharply defined. Vocal resonance may be and is, no doubt, reinforced by a cer- tain amount of reverberation or echo produced within the tubes, adding to its loudness but taking from it clearness and definition, for the condi- tions of true consonance can hardly obtain in an apparatus of which con- 44 DISEASES OF THE LUNGS AND PLEURAE. duction of sound is in no sense a function. If a large bronchus, instead of being subdivided into innumerable smaller and diminishing branches, abruptly terminate in an empty cavity occupying the area of its former distribution, it is obvious that the voice and whisper sounds transmitted down it will be loudly heard over the cavity. sEgophony is a voice-sound concerning the mechanism of which there has been much dispute. I have myself nothing to add respecting it, except that the sound appears to be the bronchophonic sound conducted through a thin layer of fluid. One may here notice a peculiar sign, to which attention has been drawn by Dr. Bacelli of Rome, whose observa- tions have been noticed and confirmed by Dr. Gueneau de Mussy, now of Paris. The sound, pectoriloquie aphonique, is described as heard over the base of the chest in patients with pleuritic effusion, provided the effusion be of an homogeneous serous kind. On placing the ear over the back of the affected side, and making the patient repeat in a whisper some rough words, as " trente-trois," or "one," "two," "three," the sound is con- ducted through the fluid and up the stethoscope to the ear with great distinctness, the articulation being perfectly recognized. In cases of purulent effusions, on the other hand, no such conduction is to be ob- tained. Dr. Bacelli and M. Gueneau de Mussy regard this sign therefore as an important aid in distinguishing between cases of serous and puru- lent effusion. In my own experience it has sometimes proved useful and sometimes failed. Although a sign of a certain value it is not to be im- plicitly relied on. Amphoric Resonance or metallic echo is a sound which is often heard in cases of pneumo-thorax. It is probably to be regarded as a reflected sound due to the impingement of vibrations against the walls of a large echoing cavity. The voice-sounds are not conducted through a pleura distended with air much more readily than through fluid, but a lung cavity in relation with such an air sac will transmit vocal vibration to it which may produce an echo. It is in cases in which the communication with the pleura is very small that this sound is best heard. The cough sounds and laryngeal sounds heard in disease are of such obvious mechanism as to require no special comment. The Microscopical Examination of the Sputum. Valuable information may sometimes be obtained from a careful ex- amination of the sputum, and in doubtful cases this aid to diagnosis ought not to be neglected; at the present time, when the intimate relation of micro-organisms to disease is a subject of such pressing interest, the help of the microscope becomes more and more imperative. In examining sputum it is only necessary to spread a small portion on a glass slide and cover it with a thin cover-glass. If the specimen be simply mucus, such as is secreted in health, a thin EXAMINATION OF THE SPUTUM. 45 film will be observed, entangling air-bubbles, leucocytes, and occasionally a few ciliated epithelial cells derived from the air passages. By running a drop of acetic acid under the cover glass the nuclei of the cells become more conspicuous. Beginners are very apt to mistake particles of dust, cotton fibres, pieces of feathers and foreign bodies of various kinds, which accidentally contaminate the fluid, for objects of graver import. In bronchitis the sputum, which in the early stages is very frothy, becomes of a yellowish tint as the disease progresses. This change is due to the presence of a greater number of leucocytes, granular matter and oil globules. Blood corpuscles may occasionally be observed. If the disease be the result of irritant particles, as soot, dust, etc., pigment par- ticles may be detected. The sputum of pneumonia is characterized under the microscope by the presence of blood corpuscles uniformly diffused throughout the mucus. In phthisis, when the lung is actually breaking down, shreds of pul- monary tissue may by careful manipulation be detected in the expectora- tion. For this purpose the expectoration should be collected for twenty- four hours, then boiled with an equal quantity of solution of caustic soda, (20 grains to the 1 oz.) and frequently stirred; the boiling fluid should then be poured into a conical glass vessel and freely diluted with distilled water. A more or less copious sediment deposits, numerous specimens from which should be diligently searched with the microscope for the boldly curved loops and fragments of pulmonary elastic tissue. (See Plate I, fig. 1). Micro-organisms.—For the satisfactory detection of these minute bodies it is necessary to resort to special methods in the preparation of the sputum, and to employ powers magnifying at least 300 times. The examination may be conducted on unstained specimens, but it is far more reliable to stain the specimen, which may be readily done by means of the aniline dyes sold for this purpose. A method known as the AVeigert-Koch method consists in spreading out a thin film of sputum on a slide or cover-glass, and drying by passing it rapidly several times through the flame of a spirit lamp. Several drops of the stain ] are then poured on the speci men and allowed to remain for about fifteen minutes or more. The stain is then washed off with dis- tilled water and afterwards with alcohol, and allowed to dry. It may then be mounted in Canada balsam. For staining tubercle-bacilli Dr. Heneage Gibbes's method gives very good results. (Full directions for preparing the stain will be found in the IMncet, May 5th, 1883, but it may be obtained ready for use from Messrs. R. and J. Beck, 68 Cornhill, 1 A i or one per cent, solution of either Gentian violet or Spiller's purple, in water, is recommended by Dr. Gibbes. Practical Histology and Pathology, 2nd edit., p. 135. 46 DISEASES OF THE LUNGS AND PLEURAE. E.C.) It is used as follows:—The sputum in a very thin layer is dried on a cover-glass; a few drops of stain are next to be gently warmed in a test-tube until the steam rises and then poured into a watch-glass, and the cover-glass with the sputum placed upon the stain and allowed to re- main four or five minutes. The specimen is then well washed in methy- lated spirit until no more stain comes away, then dried and mounted in Canada balsam as usual.' If time be not important it is better still to dis- pense with warming the stain, and to allow the cover-glass to remain in the cold fluid for thirty minutes or longer. The peculiarities of the various bacilli will be found described under the diseases to which they particularly refer. Besides pus cells, leucocytes, blood corpuscles, and foreign bodies of various kinds, pieces of morbid growth, hydatids, echinococcus booklets, and even mould, as penicillium, may be coughed up. Mould when pres- ent-usually comes from the interior of phthisical cavities. CHAPTER III. DISEASES AND DEFORMITIES OF THE CHEST WALLS. The diseases of the chest-walls are of importance chiefly from the fre- quency with which they simulate more deeply seated lesions. Pleurodynia, nXavpa the side, odvvrj pain, may be due to rheuma- tism, myalgia or intercostal neuralgia. The symptoms are very similar in all these conditions, but more particu- larly in the two first named, and there can be no doubt that aponeurotic rheumatism and myalgia are conditions frequently associated and difficult to separate. Pleurodynia commonly begins quite suddenly with severe pain of a tingling or burning character, much aggravated by respiratory movements, especially those of deep inspiration or tussive expiration. The pain may be situated at any part of the chest. A common seat is over the centre, at and about the insertion of the pectoralis muscle on either or both sides, or at the margin or sides of the chest where the recti and serrati muscles are inserted. When the pain is lateral it is almost always limited to one side. The breathing of the patient is ham- pered and may even be greatly distressed by the severity of the pain. Aponeurotic rheumatism is not common before thirty, although it may occur in young people of distinctly rheumatic diathesis. It is fre- quently attributable directly to exposure to cold, e.g., coming out from heated rooms and walking or driving in evening-dress. Middle-aged and elderly people, who are the subjects of gout and allied rheumatic affec- tions, lumbago, sciatica, etc., are specially liable to this affection. Myalgia is, except so far as muscular tenderness is inevitably more or less associated with the preceding 'condition, generally traceable to some strain. It sometimes occurs in whooping cough and very commonly in the course of phthisis. Unquestionably the disease has in most instances a definite pathology in the rupture of some minute muscular fibres. Intercostal neuralgia is a more definite ailment than either of the above, and occurs more especially at two periods of life, and in two forms. 1. It is very common in young females in the form of infra-mammary neu- ralgia, in which the pain is referred to the surface of the chest below the left breast. This affection is most generally associated with anaemia, at- tended with leucorrhoea, amenorrhcea, or other form of menstrual disturb- ance. The disease is very rarely seen in the male sex. 2. Intercostal neuralgia occurs also on either side of the chest in persons of middle or advanced middle life, and is more common in females. The pain is of a 48 DISEASES OF THE LUNGS AND PLEURAE. very severe stinging or burning character, along the course of the periph- eral distribution of one or more of the intercostal nerves. It may last for days or even weeks before the appearance of the very characteristic lesion, herpes zoster, after the appearance of which the pain is soon miti- gated or subsides altogether. This disease appears also to be commonly associated with the rheumatic or gouty diathesis. Although most com- mon in middle-aged adult females, it is by no means limited to them, and may sometimes be observed in quite young people. The pain attendant upon herpes zoster in the young, however, is rarely severe, and I believe never precedes the appearance of the eruption by any considerable time. The physical signs of pleurodynia, when carefully considered, are quite sufficient for diagnosis:— 1. The disease per se does not raise the temperature, in which fact we have one very important element in the diagnosis from pleurisy. 2. There is usually decided tenderness on pressure over the seat of pain. In intercostal neuralgia this tenderness is very superficial, and is best elicited by gently pinching up the skin; the tenderness may be ob- served, too, not only over the point most complained of, but also in the lateral spinal region corresponding with the distribution of the posterior cutaneous* branches of the affected nerves. In these cases the situation is almost always below the left breast, and the patient presents the other physical signs of anaemia. In myalgia the pain is markedly elicited by bringing the muscles affected into action, e.g., causing the patient to grasp the back of a chair, and to bring the pectoral muscles into action, or to raise himself in bed or turn on one side so as to involve other mus- cles. In aponeurotic rheumatism and in myalgia there is also tenderness on firm pressure over the muscles in the intercostal spaces, etc. 3. The respiratory movements are restrained by the pain, and respira- tion on the affected side is correspondingly weak, but it is of vesicular character and unattended with any rubbing sounds; one may sometimes hear, however, muscular rumbling sounds due to the voluntary restraint exercised upon this side by the patient. The percussion resonance is un- altered. Pleurisy and pericarditis are the two conditions most simulated by pleurodynia. In phthisical subjects, where there is perhaps already ex- isting pyrexia, it is often difficult to be sure that there is not some dry pleurisy, and here the diagnosis is not very important. Aponeurotic rheumatism of the front of the chest is distinguished from pericarditis by the absence of the physical signs proper to the latter complaint. Treatment.—Intercostal neuralgia in young anamiic subjects requires general treatment by iron, quinine, arsenic, and fresh air, with generous diet; and local treatment, by soothing applications such as belladonna plasters, or chloroform liniment three parts with belladonna liniment one part, sprinkled on lint or flannel backed by oiled silk. Belladonna or DISEASES OF THE CHEST WALLS. 49 aconite may also be efficaciously applied in the form of the solid liniments suggested by Dr. Sansom and prepared by Messrs. Savory and Moore. Menthol alone, or in combination with chloral hydrate or croton chloral hydrate, as suggested by Mr. W. Martindale,' is a valuable application in the herpes zoster form of intercostal neuralgia, before the eruption has appeared; afterwards the local remedies must be used with caution. In this latter form of neuralgia; however, the pain is often very severe and intractable, and sub-cutaneous morphia and atropine medication may be necessary. Local depletion by leeches will always give temporary relief, but in the anaemic form of neuralgia at least, it is inadmissible. The myalgic forms of pleurodynia are best treated by keeping the affected side of the chest at rest by strapping, as for dry pleurisy. Aponeurotic rheu- matism may often at once be cured by the application of a well-made mustard poultice kept on for twenty minutes. In the case of any rheu- matic diathesis, general remedies, especially iodide of potassium with qui- nine, will be required. Perichondritis or periostitis of the rib is a disease sometimes giving rise to some perplexity in diagnosis. It is commonly due to syphilis, when the other manifestations of that disease may be observed. Direct injury is another frequent cause of this malady. A short time ago I had for some months under my observation, a lady in whom a thickening of the covering of the first two ribs in the left infra-clavicular region, was traceable to an attack of typhoid fever four or five months previously; local prominence, obscured breath-sound, some venous enlargement, and great tenderness were to be noted. In this case the thickening probably involved the fascial tissues between the ribs also, and there was much hesitation in diagnosis from local abscess or empyema, not only on my own part, but also by two very able surgeons, to whom I submitted the case. The lady ultimately, but very slowly, got well, under repeated and prolonged change of air and other remedies. In some instances the first piece of the sternum is involved in perios- titis, and when the periosteal thickening is intra-thoracic, as well as on the external surface, the symptoms and signs of thoracic tumor may be developed. Amongst the thoracic parietal conditions that should be here noted is the very remarkable fascial creaking, that may not very uncommonly be heard especially over the supra-spinous and scapular regions. This phe- nomenon is attended with a certain amount of pain. I have met with more than one case of this kind which has been treated by very able practitioners, with great perseverance and activity by blisters and iodine counter-irritants for many weeks, under the impression that the case was one of chronic pleurisy. The condition is, however, so far as I have been able to observe, a permanent one, and is only important in diagnosis. If 1 Extra Pharmacopoeia. 50 DISEASES OF THE LUNGS AND PLEURiE. the attention be once awakened to the possibility of the sounds being extra-thoracic, the diagnosis can be confirmed by making the patient stop breathing and by listening whilst the shoulder is shifted about. Amongst the deformities of the chest, I would mention a deficiency of the clavicular portion of the pectoralis muscle, on one side of which I have seen two examples. A remarkable flattening or rather hollowing below the clavicle is thus occasioned, suggestive of grave internal lesion, the true cause of which is, however, at once rendered obvious by making the patient grasp the back of a chair with both hands and attempt to lift it, when the existing muscular fibres start into action and the defect is declared. The shape of the chest is nicely conformed as a rule to the condition of the lungs. Thus we have the small long thorax, with oblique approxi- mated ribs, associated with small lungs, the large expanded barrel-shaped chest with emphysematous lungs, the local flattening or enlargement with pulmonary or pleuritic diseases. Such conditions require no comment here. Nor, again, need we do more than make reference to the promi- nent upper chest of dorsal caries, the distortions corresponding to lateral curvatures of the spine, or the results of occupational pressure, e.g., the hollowed lower sternum of shoemakers. An area of the chest surface in the infra-mammary region on each side, having the fifth space in the nipple line for its centre, is unsup- ported by muscles, being an interval between the insertion of the pecto- ralis, the serratus and the rectus muscles. Thus in any obstruction to the entry of air into the lungs telling upon their general surface the atmospheric pressure is least supported by muscular action at these por- tions. Thus in young children, in whom the ribs and cartilages readily yield in any condition of general dyspnoea, as from croup, bronchitis, etc., this part of the chest on each side becomes depressed and the ster- num tilted outwards. Repeated bronchial attacks thus give rise to the prominent sternum and depressed inferior and lateral thorax which persist and constitute the pigeon-breast. In the rickety thorax a more or less deep groove corresponds on each side with the junction of the ribs and their cartilages, there being here a knuckling in, so to speak, of the ribs, causing the-sternum to come for- ward with undue prominence. The alar thorax of phthisis is produced by the small narrow thorax affording but insufficient breadth of support for the scapula, the superior extremities of which are tilted forwards and inwards by the weight of the arms and the inferior angle of the scapula thrown outwards, the effect on a thin subject being to produce a winged appearance when viewed from behind. CHAPTER IV. DISEASES OF THE PLEURA. The pleura on each side of the chest is a closed serous cavity or sac intimately applied to, and in organic union by its outer surface with the lung and the costal parietes. The internal surface of the sac is lined with endothelium. The costal and parietal portions of the internal surface are in close contact, lubricated merely by some moist serous secretion. This contact or apposition is maintained by atmospheric pressure bearing upon the interior of the lung and the exterior of the chest-wall, which more than counter-balances the constant tendency for the two surfaces of the sac to spring apart from the opposite elastic tractions of the lung and thoracic wall. In the cellular tissue subjacent to the pleura is a layer of lymphatics, which in the visceral portion freely inosculates with the pul- monary lymphatics, and communicates by open mouths (stomata) with the pleural sac. These lymphatics run their course towards the root of the lung. When we regard the position and connections of the pleura, its exten- sive endothelial surface, the conditions of negative pressure in which that extended surface is ever maintained, its richness in lymphatics (indeed the pleural have, with other sacs of the kind, been regarded as lymphatic spaces), we cannot wonder that it should frequently become the seat of disease, nor that it should be one of the chosen sites for the manifestation of lesions from blood contamination. Few are the autopsies after adult age in which one fails to find some imperfections in the pleura—few are the cases of septic or pyaemic poisoning in which the membrane is not actively involved. The diseases of the pleura are:— (a) Inflammatory.—(1) Primary or simple (general or local), (2) sec- ondary and septic, (3) suppurative. (b) Effusive. — Hydro-thorax, pyo-thorax, pneumo-thorax, haemo- thorax. (c) Growths and thickenings.—Fibrous, tubercular, malignant. 1. Simple Pleurisy.—Amongst the common causes of simple pleu- risy, exposure to cold is the most frequent. The depression of tempera- ture may be general, in persons insufficiently clothed, or whilst vital re- sistance is lessened from mental shock or insufficient food. Or the patient may receive a chill from exposure to draught or sudden change of tem- perature whilst over-heated. Certain diathetic states favor the occur- 52 DISEASES OF THE LUNGS AND PLEURAE. rence of such pleurisies, e.g., the rheumatic diathesis or albuminuria. But prior to the attack the patient may have been in good health. Pathology.—-The pathology of the disease may be briefly summed up as consisting in the first place of hyperaemia of the pleura, its vessels be- coming minutely injected; in a very few hours the normal glistening ap- pearance of the pleural surface is lost, it becomes cloudy as though breathed upon, and gradually covered with a layer of lymph. Both the costal and visceral layers are thus affected, and the effect of the move- ment of the two surfaces, covered with sticky lymph, upon one another is to roughen them, causing the effused lymph to present numerous little elevations and pittings. New vessels rapidly extend into the lymph from the pleural vessels, forming loops which, unless the opposed surfaces be speedily separated by effusion, meet and inosculate, and thus organic union takes place between them. But most commonly in simple pleurisy an effusion of liquor sanguinis takes place from the vessels, and collects in the pleura, thus separating, more or less widely from below upwards, the pleural surfaces. In due time, and in ordinary cases, the acuteness of the disease passes away, the fluid effusion is again absorbed, the lymph- covered surfaces come again in contact and rapidly adhere, the originally effused lymph becoming in course of time degenerated and absorbed. Symptomatology.—The symptoms and signs of pleurisy are in accord- ance with its pathology, and are divided into three stages, viz:—1. The stage of hyperaemia and commencing exudation. 2. The stage of effu- sion. 3. The period of absorption and convalescence. Pain in the side and rigors are the two symptoms which usher in an attack of pleurisy, and either may precede the other by a few hours. The pain is that of an acute " stitch" in the side, usually felt in the lower axillary or infra-mammary region, but not uncommonly referred, and es- pecially so with children, to a much lower point in the abdominal wall, to which the terminal cutaneous twigs of the affected intercostal nerves are distributed. The pain interferes Avith the respiratory movements, which are restrained and shallow, the patient inclining to the affected side so as to lessen its movement. The rigors are of variable severity, sometimes very sharp and decided, at other times amounting only to recurring chills. It is stated that the rigors of pleurisy are repeated, whilst in pneumonia one severe shivering occurs at the commencement of the disease: on neither hand, however, is this statement more than generally speaking correct. There is occasional dry interrupted cough. The temperature is elevated usually to about 102° or 103°, the face anxious, pale, the pulse small and moderately frequent. The fever has never the marked character of that of pneumonia, and the flushed cheek so characteristic of the latter disease is rarely present. In a word the patient with acute pleurisy is not so ill as one with pneumonia, although he may be in more suffering. DISEASES OF THE PLEURA. 53 In the first stage of the disease there is no percussion dullness. On listening to the chest the respiratory murmur will be found to be uneven and partially suppressed on the affected side, and more or less distinct friction sound, usually of a grating character, is heard most distinctly at the end of inspiration and the beginning of expiration, over the seat of pain, usually in the mammary or infra-mammary region or over the base of the lung. In left-sided cases friction, of cardiac rhythm, may be heard over the precordial region. Friction-fremitus is occasionally to be felt. In some cases which present all the symptoms and febrile phenom- ena characteristic of pleurisy no friction sound can be heard; this may be explained by the manner in which the affected side of the chest is held fixed by the patient, or by the pleuritic exudation commencing on the diaphragmatic or mediastinal aspect of the pleura, and thus being beyond the reach of appreciation by the stethoscope. In a certain number of instances the disease stops short at the dry or plastic stage, and the patient is said to have had a dry pleurisy; this however,- though common enough in secondary and especially in tubercu- lar pleurisies, is rarely observed in cases which have presented in any marked degree the features of acute illness characteristic of an attack of simple pleurisy. Within a short time, it may be but a few hours, fluid commences to be effused, and dullness may be detected at the extreme base posteriorly, gradually extending upwards towards the apex. With the occurrence of effusion the pain becomes less, the breathing easier and less catching, although quicker than natural. The movements of the affected side are notably lessened, whilst in marked contrast to the effacement of respira- tory sounds on the affected side is their exaggerated intensity on the sound side. In moderate degrees of effusion the dullness varies slightly with the position of the patient; whilst lying down, for instance, the reso- nance may be good to just below the nipple, whereas on sitting up there is dullness up to this point, and it may be higher. Over the lower portion of the dull area the respiratory murmur is absent, and the friction is no longer to be detected; but as the upper limits of dullness are approached in the scapular region, distant tubular breathing may be heard, and fric- tion sound of a moister character is audible, especially in front. As the effusion advances ihe breathing becomes increasingly distressed until apncea is threatened. The signs of pleuritic effusion may be divided into three groups.—(a) The cardinal signs of pleuritic effusion, the presence of which is alone essential for diagnosis, viz:—(1) Percussion dullness. (2) Displacement of the heart. (3) Annulled vocal fremitus. (4) Diminished and altered or absent breath-sound. These signs are common to both serous and purulent effusions. (b) Subordinate or supplementary signs, viz:—(1) Increased semi- 54 DISEASES OF THE LUNGS AND PLEUR/E. circumference of chest. (2) Intercostal bulging, elasticity or fluctuation. (3) Skodaic resonance. (4) Altered voice-sound. (5) Displacement of ' abdominal viscera. (6) Signs in the other lung. (7) Cardiac displace- ment bruits. These signs are none of them essential for diagnosis; any or all of them may be wanting. (c) Signs indicative of nature of fluid, viz:—(1) Pectoriloquie aphon- ique (Bacelli). (2) Temperature signs. (3) Other pyrexial or septic phenomena. These are of especial importance with regard to the diag- nosis of empyema, and will be discussed under suppurative pleurisy. 1. The dullness of effusion is absolute and toneless. It is distin- guished by our American confreres ' from more ordinary degrees of dull- ness by the term "flatness." It is the dullness of a brick wall rather than that of a table. In ascertaining the limits of dullness in cases of effusion, very light percussion should be employed, or the resonance of neighboring parts will be elicited. Fig. 6.—Percussion signs in case of moderate effusion. A, area of complete dullness ("flatness"); B, area of t3Tmpanitic (Skodaic) resonance; C, inferior curved line of tympanitic (stomach) reso- nance. In cases of moderate effusion, the lung being texturally healthy, the upper margin of dullness in front is not a level line, but slants downwards and inwards in such a manner as to leave a somewhat triangular space of resonance (B, Fig. 6), the apex of the triangle being at the sterno-clavicu- lar articulation. The resonance within this area is of a peculiar tympan- itic quality, termed Skodaic resonance, to which I will again refer. The line of dullness (flatness) is highest in the axilla, and extends round the scapular region until in the interscapular region it again slants down- wards, a tongue of comparative resonance (B, Fig. 7) protruding down- wards in the postero-median line, which has been described by Dr. Gar- land as the " dull triangle,"2 in contrast with the flatness or absolute dull- 1 Austin Flint, " On Percussion and Auscultation.'1 8 "Pneumono-Dynamics," by G. M. Garland, M.D., New York, 1878, page 15. DISEASES OF THE PLEURA. 55 ness of the percussion-note external to it. Even in cases in which the effusion is very considerable and of old standing, the triangular area of comparative resonance (but now somewhat tubular in quality) can still be made out at the sterno-clavicular angle, and also in the upper inter- scapular region. The curved line marking the upper limit of dullness posteriorly, is sometimes spoken of as the letter S curve of Dr„ Ellis,1 and Dr. Garland maintains that the curve invariably commences at a lower level behind than in front. I have not found this to hold ^ood, however, in all cases. The line of dullness does not very notably shift (although in this respect cases vary within narrow limits) with the position of the patient. In cases of extreme effusion, the "flatness" of the percussion- note extends throughout the utmost limits of the thorax, and, of course, in such cases these triangles of resonance are not to be found. In other cases, again, oedema or consolidation of the lung may obscure the signs over the areas referred to. Fig. 7.—Percussion signs in case of moderate effusion. A, area of complete dullness (" flat- ness "); B, pulmonary note usually impaired; C, more or less tympanitic high-pitched resonance. Thus the upper margin of the effusion, in typical cases, is not a water- level, but presents a curve, having its convexity upwards and in the lateral region, contrasting in this respect with the upper limit of dullness in cases of hydro-pneumo-thorax. As the fluid increases the dullness encroaches upon the median line, extending farthest across at the third and fourth cartilages, but being continued further outwards below this level by the outline of the displaced heart (D, Fig. 6). The lower limit of dullness in typical cases of effusion is again peculiar (C, Fig. 6), the arch of the diaphragm being still preserved, even when the effusion is very considerable—so long, indeed, as Skodaic resonance 1 Boston Medical and Surgical Journal, January 1st, 1874, p. 13, and December 14th, 1876, p. 689; quoted by Garland. 56 DISEASES OF THE LUNGS AND PLEURJE. is manifested. This can be best observed in left-sided cases, and to it I will again allude immediately. 2. Displacement of heart towards the sound side is the second cardinal sign of pleuritic effusion. The absence of this sign would negative the diagnosis of unilateral effusion, unless it were explained by some special circumstances, e.g., retention of the pericardium by old adhesions, the result of some former disease, or consolidation of the opposite lung. But these and other causes of fixity of heart are rarely met with; the medias- tinal folds are ready to shift to one side or the other, instantly or slowly, in obedience to the rapidity or slowness with which the pleura on one side is occupied, and the lung on that side collapsed, leaving the traction of the other lung upon the mediastinum unopposed. I venture to lay much emphasis upon the displacement of the heart, rather than on dis- placement of other organs, as a sign of pleuritic effusion, because it takes place immediately and pari passu with the effusion. In this respect it strikingly differs from displacement of the diaphragm and abdominal viscera. The diaphragm is held up in the arched position until the effu- sion has mounted to a considerable height, and when the heart has already markedly retreated towards the opposite side. In fact, displacement of abdominal viscera is no essential sign of pleuritic effusion, and is only present in extreme cases; whereas displacement of heart is an essential sign, and (unless prevented by countervailing causes) is present from the first in all cases of unilateral effusion. Although the exact position of the heart is often somewhat difficult to make out, the trouble taken is well rewarded by the importance of the sign. The position of the apex beat should be carefully felt for by the hand, and, if necessary, by the ear through the medium of the stethoscope. Percussion may also be usefully employed to trace from the sound side the line of cardiac dullness.1 The axis of the heart is not greatly changed in direction by any common degree of effusion; it becomes a little more vertical, and in very extreme cases it may become slightly twisted. I have never seen, nor have I been able to produce by experiment, anything ap- proaching to the complete turnover of the heart represented in some books as occurring in effusion.2 In cases in which the heart is greatly displaced, a systolic murmur is developed over its base, which disappears 1 There is one fallacy with reference to cardiac displacement in the earlier stages of effusion that may be here noted—viz., that as the base of the lung re- tracts, the right or left margin of the heart (as the case may be right or left-sided) becomes uncovered : this may lead to an apparent delay in the displacement of the organ, the more extreme left or right boundary thus being within reach of palpation. 2 Notes on Displacements of the Heart. By the Author. British Medical Journal, July 17th, 1869. DISEASES OF THE PLEURA. 57 on removal of a portion of the fluid, and is presumably due to straighten- ing or slight tension of the great vessels from pressure of the fluid. 3. Absence of vocal fremitus is a third very important sign of pleuritic effusion; it is obviously due to the intervention of a bad conductor of such vibrations between the vibrating media and the chest walls. If these two latter be united at any point by a cord of adhesion, the fremitus may there be felt. Just as light percussion is needed to define the exact limits of dullness, so light palpation is necessary, employing the finger-tips rather than the whole hand, in order better to exclude vibrations from above as the confines of the effusion are approached. It will thus be observed that the three most essential signs of pleuritic effusion are elicited by palpation and percussion. 4. The stethoscopic signs in pleuritic effusion are sometimes mislead- ing. A certain value is justly attached to the absence of breath-sounds, and (except towards the upper confines of the effusion) of voice-sounds in the diagnosis of pleuritic effusion; but in some of the most typical cases of this disease the breath-sounds are audible over the whole side, well de- fined, tubular, and not easily distinguished from the breath-sounds of pneumonia. The voice-sounds may also be well conducted over the whole side, and the whisper exaggerated even to pectoriloquy. In September, 1881, a boy, aged eleven years, was admitted into my ward at Middlesex Hospital, with acute pleurisy and effusion on the right side of four days' duration. On the fifth day after admission, the dullness had extended to the clavicle and well over the median line. The vocal fremitus was annulled, the heart was beating considerably outside the left nipple line, and the cyrtometer tracing showed enlargement of affected side, but tubu- lar breath-sound and whispering pectoriloquy could be well heard pos- teriorly to the base, and somewhat more feebly over the lower two-thirds anteriorly. It was difficult to believe that one was listening over an im- movably compressed lung, separated from the ear by some inches of fluid. Twenty-six ounces of clear serum were, however, readily removed the next day, with great relief to the little patient. This is no isolated case, and I am inclined to believe that the not infrequent presence of these auscultatory phenomena leads to the somewhat common diagnosis of " pleuro-pneumonia," a combination—I mean in the sense now employed of pneumonia with effusive pleurisy—in my experience of rare occurrence. The reasons why we should have absence of breath-sound in pleuritic effusion seem so ready to hand, that an exaggerated importance has per- haps on this account been attached to this negative sign—for (1) a certain thickness of fluid separating the lung from the parietes, and (2) the lung being collapsed and immovable, how should it yield any respiratory sounds? Although the first explanation is a valid reason why the respira- tory sounds should be weakened and distant, yet it must be remembered that fluid is by no means a bad conductor of sound, and particularly the 58 DISEASES OF THE LUNGS AND PLEURvE. more homogeneous kinds of fluid.1 The second suggestion well illustrates the falseness of the still prevalent views as to the production of breath- sounds. It is impossible, with a due regard to clinical observations of such cases, to hold that the breath-sounds (with the single exception of the vesicular portion of the normal respiratory murmur) are generated within the lungs or bronchi. They are really laryngeal (glottic) sounds conducted down the tubes and through a certain thickness of residual (tidal) air. Over the sound side in the boy just referred to, the laryngeal breath-sound was heard together with the vesicular sound as the soft (but exaggerated) respiratory murmur, but over the effusion the tubular sound was alone heard, imperfectly conducted through solid and fluid media. Supplementary signs of effusion.—Much importance has always been attached to increased semi-circumference as a sign of effusion. On in- spection there is generally an apparent enlargement of the affected side, whilst to actual measurement there may be little or no difference. Any relative enlargement that may be present is more obvious during deep expiration. The total circumference of the chest is, however, always in- creased in effusion. In any case in which we obtain any decidedly increased measurement on the affected side, we may be sure that the effu- sion is a large one. The shape of. the affected side is altered in effusion, being more rounded. This is well shown by a cyrtometer tracing, and arises from the fact that the outspring of the ribs is entirely relaxed on the affected side (even if there be no positive intra-thoracic pressure), whilst on the sound side it is only partially so. When we bear in mind that the capacity of a globe is greater than that of any other shaped figure, and further remember that, in pleuritic effusion, the heart is displaced to the sound side, it is clear that in all cases of effusion, and quite apart from any relative increase in circumferential measurement, there is in- creased capacity on the affected side of the thorax. Cyrtometer tracings thus give us more information than tape measure- ments, since they also take into account altered shape. Intercostal dullness or fluctuation is a sign of inconstant and rather exceptional occurrence in cases of effusion, intra-thoracic pressure alone being insufficient to cause it. It is more commonly present in children than adults, and especially in weakly children with wasted muscles. Ataxy of intercostal muscles, and a certain degree of laxity or softening of thoracic pleura, are needed for the presence of this sign, which, in my 11 have had recently at Brompton Hospital a case of pleuritic effusion on the left side, in which an endocardial mitral murmur was well heard through the fluid below the angle of the scapula—as well conducted as it would be through lung. It is a question whether the complete absence of breath-sound in some cases of pleuritic effusion is not attributable to partial or complete occlusion of the bronchus by accumulation of mucus. DISEASES OF THE PLEURA. 59 experience, has been more often associated with purulent than with sim- ple effusion.' jEgophony is a sign commonly met with in pleuritic effusions, and is of some value in the diagnosis of localized effusions from consolidation. It will often be observed on listening for aegophony in cases of acute effu- sion that a certain lisp attends the voice-sound, which lisp is more sharply conducted than the aegophonic sound. In such cases, if the whispered voice be listened to, it will be found to be very distinctly heard through the fluid. ( Vide p. 64, Bacelli's sign). Pressure signs.—The presence or absence of pressure signs in pleu- ritic effusions is a matter of importance in determining whether or not interference by removal of the fluid is called for. It has been already pointed out (page 82) that whereas cardiac displacement is an essential sign of effusion, it is no evidence of intra-thoracic pressure. Displace- ment downwards of the diaphragm is on the other hand always a sign of intra-pleural pressure. The relationship of the diaphragm to the cavities above and below it, is quite a different one to that which the mediastinum bears to the pleura on either side. We have on the thoracic side of the diaphragm, under normal conditions, a negative pressure; on the ab- dominal side the prevailing pressure is positive, although there may at times possibly be a negative pressure, which can never, under any cir- cumstances, contend against the elastic traction of the lungs.2 The nega- tive pressure is maintained within the pleura until the lung has com- pletely contracted before the advancing fluid; and after this point any further accumulation compresses the lung, and by its weight and pressure forces down the diaphragm. Hence displacement downwards of the • abdominal viscera is a late phenomenon in pleuritic effusion. It also varies according as the patient has been keeping about or in bed. Fur- ther, it is more often met with in purulent than in serous cases; and possibly this may (if it be the fact, as my observations would lead me to think) be explained by the nutrition and elasticity of the lung becoming damaged by the more severe fever attendant upon suppuration. It is obvious that mere loss of tone in the diaphragm would not, as in the case of the intercostals, account for the difference. I have found the intra- thoracic pressure to vary from a negative pressure to £ in. and 1-| in. posi- tive pressure of mercury at the commencement, and at the termination 1 Dr. Stokes draws attention to the fact that intra-thoracic pressure alone is in- sufficient to cause bulging of the intercostal spaces, which he considers as rather due to inflammatory paralysis, and as significant of seventy of lesion, and as therefore of value in prognosis. Vide Stokes, "On Diseases of the Chest," New Sydenham Society's edition, 1882, pp. 485, 512. 2 The outspring of the lower ribs tends, through the diaphragm, to act as a counterpoise to the upward traction of the lungs. 60 DISEASES OF THE LUNGS AND PLEURAE, of paracentesis from ■£ in. to % in. and even 1 in. negative pressure, there being in all cases a more or less considerable amount of fluid still remain- ing in the pleura. The clinical outcome of these observations upon the displacement of the diaphragm is of very great practical importance—viz., that, as was first pointed out by Traube, and more fully explained in an admirable monograph by Garland of Boston, stomach-note may be obtained at the sixth rib in the nipple line in the presence of a large effusion on that side. Similarly, on the opposite side, under the same conditions, the liver- dullness may not be appreciably lowered. These facts are to be borne in mind in choosing the spot for paracentesis, otherwise awkward accidents may happen. My observations would lead me to assert that, in recent cases, the period of effusion at which the intra-thoracic pressure is converted from a nega- tive pressure or zero to a positive pressure upon the lung and heart is marked clinically (1) by the dullness mounting up above the third carti- lage (patient in sitting posture), and (2) by the Skodaic resonance becoming changed from the full note to a more tubular quality, and finally becom- ing extinguished. Skodaic resonance is thus of some clinical value in guiding us to a judg- ment as to the presence or absence of pressure within the thorax, and the advisability or urgency of interference by paracentesis. Different views have been held respecting the mechanism of Skodaic resonance in pleuritic effusion. Skoda himself regarded it as the relaxed lung note, due to the lung contracting upward towards its root as the fluid advances, and, when in contact with the parietes, yielding a note on percussion similar to that given out by a healthy lung on the post-mortem table. My colleague, Dr. E. Thompson,1 regards the note as significant of a lung still in con- tact with the parietes at the upper part of the chest, but slightly on the stretch, its periphery being adapted to the somewhat wider arc assumed by the ribs when released from the lung traction below. Whichever of these explanations we adopt (and they are probably both accurate at dif- ferent stages of the effusion), it is obvious that a slightly negative or at least a zero pressure is essential for the Skodaic resonance of this mechan- ism—the full-toned Skoda note. On the other hand, we often meet with cases of effusion in which at, and near, the sterno-clavicular angle a tubular quality of resonance is obtained, resembling the percussion note over a considerable lung-cavity, or over the cheek held on the stretch with the mouth slightly open. This resonance corresponds, I believe, with that explained by Hudson2 as produced by the lung being collapsed upon its root, and thus yielding the tracheo-bronchial resonance. This 1 " Physical Examination of the Chest," p. 49. 2 Quoted by Walshe, " Diseases of the Lungs," fourth edition p 74 DISEASES OF THE PLEURA. 61 note clinically signifies a higher degree of effusion than the other; it means that the lung is not simply contracted, but collapsed by the pressure of the advancing fluid. In the next degree of effusion all resonance of whatever kind is everywhere lost. In addition to the displacement murmur over the heart already alluded to, another sign of intra-pleural pressure, of more importance, is the occurrence of crepitant sounds over variable portions of the sound lung. These congestion rales give evidence of great stress of circulation in the sound lung, and are associated with a congestive cough, and a blood- streaked viscid sputum. AVith the development of such signs the dyspnoea becomes increasingly urgent, the surface dusky, and the patient is in imminent danger from syncope. It is not usual, however, for the effusion to attain such dangerous proportions; in a large number of cases the area of Skodaic resonance is not encroached upon, when the tide turns and absorption of the fluid commences. The fever of acute pleurisy subsides in from a few days to a week or a fortnight, according to the severity of the attack; the tongue cleans, the appetite returns, and the patient has only to gain strength and to await recovery from the results of the local inflammation and effusion. In favorable cases, as the fluid becomes absorbed, the lung expands from above downwards, the pleura friction-sound returns, and with it usually some pleuritic pain, although of not nearly so intense a character as in the first instance. Dr. Gee, in his work on Auscultation, has very minutely and accurately described the physical signs and other phenomena attendant upon rece- dent effusiens; suffice it here to say that the respiratory murmur slowly returns, at first in the upper portion of the chest, and the heart gradually resumes its normal position. The absorption of the last portion of fluid is often considerably delayed, and dullness and weak respiration may long persist at the posterior bases. In some cases the effusion may show no signs of becoming absorbed, in others again complications may arise. But in the great majority of instances the prognosis, in cases of simple acute pleurisy, is decidedly good. The diagnosis of pleurisy is not attended with any great difficulty. As regards pain it may be simulated by pleurodynia, or intercostal myal- gia, neither of which affections is, however, attended with febrile phenom- ena, nor with friction sounds nor the signs of effusion. Pneumonia is the disease with which pleurisy is more often confounded, and we must ob- serve that the two may co-exist. The absence of rapidly supervening bronchial respiration with bronchophony and fine crepitation, the free- dom from blood-stained sputa, and the gradual effacement of respiratory sounds and of vocal fremitus, with increasing displacement of heart as dull- ness on percussion increases in extent, render the diagnosis of pleurisy with effusion certain. 62 DISEASES OF THE LUNGS AND PLEURAE. The chief difficulty in diagnosis is, however, to ascertain the prob- able nature of the pleurisy, whether simple with serous, or suppurative with purulent, effusion. I will postpone the discussion of this point until the consideration of the graver malady. The treatment of acute pleurisy of ordinary severity does not call for any very energetic measures. In the first stage of the disease our object is to reduce arterial pressure within the vessels of the diseased pleura—vessels which are temporarily paretic and in a state of acute turgescence. One or two doses of aperients, and action upon the skin and kidneys by saline dia- phoretics and diuretics, are useful general measures to this end. At the first onset of this disease small doses of aconite may sometimes be given with advantage, with the view of reducing arterial pressure, but with the commencement of effusion this remedy should be stopped. The pyrexia of pleurisy never of itself causes anxiety. Rest in bed must be absolutely enjoined, even in the least severe cases, and the diet restricted to nutri- tious fluids. There is no object to be gained by restraining the patient from taking bland drinks to ease thirst. The application of leeches to the side is often of great value in lessening the intensity of the local lesion as judged of by pain and pyrexia. Hot poultices, frequently changed, are also valuable, serving by the dilatation of superficial capil- laries to ease pressure upon the deep distribution of the intercostal arteries. A blister applied under the poultice is sometimes useful. A fair amount of sleep must be produced by the judicious administration of opiates, which may be given in the form of Dover's powder, or in adults, if the pain be very severe, by subcutaneous injection. The temperature of the patient and the signs of effusion must be carefully watched. Stage.of effusion.—Whilst the inflammatory fever is at its •height, the less Ave meddle with any effusion present—unless it become of itself a danger—the better. We must bear in mind that a certain amount of effusion is as much to be looked for in acute pleurisy as exudation into the air-vesicles in pneumonia, or " running at the nose " in nasal catarrh; and the products in the three cases do not, cceteris paribus, essentially differ. The pulmonary exudation consolidates in situ; the nasal product stiffens the handkerchief; and the exudation into the closed pleural sac remains limpid and liquid only until exposure to air or the presence of a foreign body (or perhaps intrinsic change from lapse of time) determines - a certain variable amount of coagulation, a thin layer of which covers the roughened surface of the pleura and protects it, and ■ flakes of which sometimes float in the fluid. Again, given acute inflammation of the coverings of the lungs, a certain amount of effusion is useful in separating and bathing in a bland fluid the tender and inflamed surfaces, and fur- ther, in keeping at rest the affected portion of lung. It is too often for- gotten that the lung is in health exercising a constant traction upon the pleural sac, the vessels of which have therefore to sustain a negative or aspiratory pressure; this being so, it is but natural and physiological that, DISEASES OF THE PLEURA. 63 if these vessels become temporarily weakened and congested by the in- flammatory process, increased exudation should proceed from them. The effect of this exudation is to neutralize lung traction, and therefore to lessen afflux of blood to the weakened vessels. It is, moreover, the surest and most natural means of giving that rest to the inflamed surfaces which they need for recovery. The effusion reaches its acme, the fever subsides, and in a few days the tide turns, re-absorption being effected in a few weeks. Fluid effusion being thus both natural and salutary in acute pleurisy, we must be watchful, but not meddlesome, in our treatment of its earlier stages. Up to the end of a week or ten days we need not, in ordinary cases, consider how to promote its removal; and, in the majority of cases, after this period the fluid will gradually subside by spontaneous absorp- tion. Counter-irritation is of undoubted value at this stage, and small doses of iodide of potassium may be added to the prescription. As the absorption is being effected, and when pain arises from the pleural sur- faces again coming together, the firm application of a broad band of adhesive plaster round the affected side, or of several bands in the man- ner suggested by Dr. Roberts,1 extending well beyond the median line in front and behind will relieve pain, and facilitate adhesion. Mineral acid tonics, usually with iron, are now required, and change of air will hasten the complete re-absorption of fluid, and the restoration of the function of the lung. Towards the end of the second or third week of illness, if absorption be not in fair progress, the question arises whether it be advisable to interfere and remove a portion of~the fluid by paracentesis. Thanks to the labors of Hamilton Roe, Trousseau, Bowditch, Dieulafoy and others, this operation has been rendered safe and easy of performance, so that we may consider the advisability of artificially removing the fluid from the chest, without being harassed in our judgment by the fear of so doing. The extent of the effusion, the condition and family history of the patient, and the nature of the fluid effused, are the points which determine for or against the operation, and the following propositions seem to me to be best justified by experience. 1. With good Skodaic resonance down to the third rib, and with no material enlargement of the side, we may assume, as I have already pointed out, that, although much fluid be present, the lung is only held in the position of physiological rest, and that therefore operative interference is not called for. 2. The continuance of pyrexia would, at the end of the second week, at all events, dispose us to wait longer. If no progress in absorption has been made, however, by the end of the third week, we may with propri- ety remove a portion with the aspirator. 1 Theory and Practice of Medicine, 5th edit., p. 453. 64 DISEASES OF THE LUNGS AND PLEURAE. 3. If the family history of the patient be unfavorable, our inclination would be to early interference, lest interstitial changes occur in the lung unfavorable to its re-expansion. [In cases, however, in which the effu- sion has occurred on the side on which there is already existing lung-dis- ease of a phthisical nature, we should be loath to interfere, as experience certainly shows that an effusion checks, and sometimes arrests, the tuber- cular process. ] 4. In cases in which the effusion mounts up to the second rib, or higher, extinguishing Skodaic resonance, and causing decidedly increased measurement of the side, we may be sure that there is positive intra-tho- racic pressure, impeding the heart's action, and compressing the lung so as to retard circulation through it. In such a case the pressure may amount to one inch or one inch and a half of mercury. Under these circumstances the patient is in danger of syncope. The signs especially indicative of danger, viz: straining, retching cough, with frothy, viscid sputa, sometimes streaked with a speck or two of blood, and the presence on the healthy side of rather fine crepitant rale, have been already pointed out. In the presence of such signs, no matter what the stage of the dis- ease, immediate interference is called for. The removal of two or three pints of fluid by the aspirator or syphon will give the patient immediate relief, and no further operation may be necessary. It has been well pointed out by Dr. B. Foster, that the symptoms of danger, livid ity, pal- pitation, etc., are often in abeyance whilst the patient is perfectly still. 5. In cases in which there is any reason to suspect that the fluid may be purulent—quite apart from any question as to its amount—the needle of a fine subcutaneous syringe must be inserted at about the sixth space mid-axillary line, and a sample removed for inspection. Should it be pus of healthy character and sweet, steps must be taken for its thorough evacuation within a few days. Provided the pus be perfectly sweet, it is, I think, best not at once to operate upon a large effusion by making a free opening. The lung is compressed, and it is better in the first in- stance to remove a portion of the fluid by means of the syphon, for the double purpose of re-expanding the lung-texture, and diminishing the cavity of the abscess to be subsequently (within a short time, however) dealt with. Dr. Foster has also insisted upon the advantage of thus pro- ceeding. : Local Pleukisy, Pleukisy from Extension.—Although local pleurisy sometimes occurs as a primary disease from exposure to cold, it is much more commonly determined by neighboring disease; and con- versely, pleurisy from extension is in most instances of localized and re- 1 " On the Treatment of Pleurisy and Pleuritic Effusion." Address to the North Wales Branch of the British Medical Association, by G. Balthazar Foster, M.D., F.R.C.P. DISEASES OF THE PLEURA. 65 stricted area. Local pleurisy may arise from injury or disease of the chest- wall, e.g., a blow on the chest, fractured rib, syphilitic periostitis, cancer of the breast, or from subjacent disease of the lung, haemorrhagic infarct, gangrene, pneumonia, tubercle or cancer. The pathology of local pleurisy is, except for any associated lesions, the same as that of simple pleuritis, but it does not usually proceed to fluid effusion. As a rule the two opposed surfaces pass through the stages of injection, of lymph exudation and then either adhere and enter into organic union, or become smoothed down to present hereafter localized thickened opacities. A local pleurisy, however arising, may extend and involve the whole pleural sac. The course of local pleurisy is generally favorable. Treatment.—In nine cases out of ten immediate relief is given by firmly strapping the affected side, so as to restrain movements, and in simple cases this may suffice for the cure. In some other cases, however, the pressure of strapping cannot be borne, either on account of its increas- ing the pain, or from the fact that the pleurisy has supervened on the side most available for respiration, as in certain cases of phthisis. Under such circumstances the application of a small blister, with or without a hot linseed poultice superposed, will give relief, or if the pain be very severe a couple of leeches may be applied. A very useful clinical test as to the amount of relief that may be expected from strapping in any given case, is obtained by observing the effect of steady and firm pressure upon the side by the hand. An opiate, or morphia subcutaneously, may be employed in association with local remedies, but it is much better practice to arrest a lesion, than merely to lessen pain from it. 2. Secondary Pleurisy, Septic Pleurisy.—Many pleurisies which are spoken of as simple are really secondary to some morbid constitu- tional conditions, e.g., the rheumatic diathesis; some pleurisies are so dis- tinctly rheumatic as to require special treatment. Pleurisy, like other serous inflammations, frequently arises in association with albuminuria. These two pleurisies, the rheumatic and the albuminuric, are generally attended with copious effusions, sero-fibrinous, rarely purulent, rich in fibrin in the former, and in this variety the disease is also attended with profuse sweatings. It is not uncommon to get pleurisy, sero-fibrinous, as a complication in jaundice. The pleurae are frequently involved in general outbreaks of miliary tuberculosis. In septicaemia and pyaemia pleurisy is commonly present, and under these conditions the lymph and fluid exuded are highly charged with pus elements. 3. Suppurative Pleurisy.—Suppurative inflammation of the pleura is a far graver malady than any we have yet considered in this chapter. Whereas in acute simple pleuritis the inflammatory products consist of simple fibrinous exudation, which coagulates in a thin layer upon the 5 66 DISEASES OF THE LUNGS AND PLEUR.E. pleural surfaces, and of liquor sanguinis, which exudes through the weak- ened vessels and collects in the pleura; in suppurative pleurisy, on the other hand, we have a more intense and a less sthenic process, accom- panied by the exudation of a more corpuscular and less coagulable lymph, and of liquor sanguinis rich in leucocytes. The one case—simple exu- dative pleurisy, is perfectly analogous with sthenic exudative pneumonia, the other—suppurative pleurisy, with the corresponding disease occasion- ally met with under greatly depressed conditions of system, whether from intemperance or other causes, viz., purulent infiltration of the lung; and just as in pneumonia, the simple may pass into the suppurative inflamma- tion, so it is not unknown in pleurisy for a hydro-thorax to become an empjrema. Fraentzel,1 indeed, denies the occurrence, save on very rare occasions, of an effusion purulent from the first. " In almost every case the effusion is at first fibrino-serous" becoming subsequently purulent. Unquestionably serum is more easily effused than pus, and purulent effu- sions are at first thin and diluted, but the pus element is from the first largely present and active in acute empyemata. What the conditions are that determine suppurative rather than sim- ple pleurisy we do not precisely know, and we have to speak of " depressed conditions of the system," "morbid constitutional states," and the like; expressions which, nevertheless, are in keeping with our knowledge and are generally understood. We may, indeed, with some plausibility main- tain that some septic agent present in the blood renders the inflammation purulent rather than serous, as in the joint affections in pyaemia, although the pus-producing quality in the blood is very difficult to estimate, and would seem to be of varied sorts. In such diseases as pyaemia, scarlatina, typhoid fever, and in the puerperal state, pleurisy, when it arises, is most generally suppurative; in rheumatism, gout, albuminuria, and delirium tremens, it is, on the other hand, as a rule, simply serous. Empyema is again very apt to occur in cases in which disease of the lung is also present. Perforation of the pleura in phthisis almost always leads to pyo-thorax, no doubt principally from the escape of purulent matter into the sac. Bacilli have been found in tubercular purulent effusions, and MM. Ohauffard and Gombault2 have found that the fluid of sero- fibrin- ous pleurisy in tubercular subjects when introduced into subcutaneous tissues of guinea pigs will, in a certain proportion of cases, lead to tuber- culosis. The symptoms of suppurative pleurisy do not very strikingly differ from those of serous effusion; in many cases from symptoms and signs alone it is impossible to make a certain diagnosis. The symptoms are commonly less acute but more adynamic in character than in ordinary pleurisy. The rigors or chills are more persistently recurrent, the daily 1 Ziemssen's Cyclopaedia, vol. iv., p. 611. 2 Bull, et Mems. Soc. Med. des Hop. de Paris, 3me sene, I., 1884, p. 309. DISEASES OF THE PLEURA. 67 fever continuing week after week; the pulse is from the first more fre- quent than in serous pleurisy, and keeps up its frequency throughout the disease. The tongue is more furred, with a greater tendency to become dry and brownish in the centre. The general condition of the patient is more depressed and anxious, and emaciation is much more rapid than in ordinary pleurisy. But perhaps the most important sign of the effusion being purulent (although not absolutely characteristic), is the occurrence of hectic sweats breaking out whenever the patient falls asleep. The physical signs must necessarily be for the most part the same, whether the case be one of simple or suppurative pleurisy. Are there any physical signs, however, which are characteristic of pus in the pleura? (Edema of the chest-wall when it occurs, is, I believe, an absolute sign of the presence of pus. An erysipelatous blush over a portion of the chest, or still more evident pointing, are also sure signs of the effusion being puru- lent. But these are late signs, and therefore of greatly mitigated value. It is maintained by Dr. Bacelli of Rome,1 that by the mode of transmis- sion of vocal vibrations, the diagnosis between empyema and hydro-thorax may be made with certainty, whilst all other evidence of duration of dis- ease, oedema, emaciation, intermittent fever, and anaemia, are insufficient for the purpose. In order to appreciate this sign, the unaided ear must be applied to some convenient point of the affected side, e.g., over the dull region posteriorly, below the angle of the scapula, and the patient directed to whisper some rough word; this will be well conducted to the ear if the fluid be serous, not so if it be purulent. Dr. Bacelli's theory to account for the difference of conduction in the two cases is, that in serous effusions, the fluid, being thin and homogeneous, transmits vibra- tions with facility, but the more the fluid departs from the homogeneous nature of serum, the thicker it is, and the more clouded by the presence of amorphous protein bodies and formed or corpuscular elements, the less complete the conduction of sound through it. This physical sign is totally different from that of cegophony, which is a compressed lung- sound modified by transmission through a thin layer of fluid. ^ Unfortunately, although of undoubted usefulness as an additional sign, it cannot be allowed that this sign has the crucial value attributed to it by its distinguished advocate. Pectoriloquie aphonique is heard in perfection in some cases of pure sero-fibrinous effusion, but I have also heard it very well marked in some cases of purulent effusion, and per- fectly in cases of foetid sero-purulent effusion. At the International Medical Congress, 1881, I reported ten cases bearing upon this point. " In six of these, in which the fluid was clear, five yielded the sign, the sixth did not. In two cases, also acute, the fluid was purulent; yet in 1 Archivio di Medicina, Roma, 1875. See a critical reference to Dr. Bacelli's paper by Dr. Gueneau de Mussy.—Union Medicale. Jan. 4th, and Feb. 17th, 1876. 68 DISEASES OF THE LUNGS AND PLEURAE. both cases Bacelli's sign was present when one would not have expected it. In two cases, both of old standing, the fluid was serous, containing effete pus elements; in one of these cases the sign was wholly absent, in the other it was present in a modified degree."' There is, indeed, only one criterion in these cases, and that is the ex- ploring puncture made with a grooved needle or fine trochar, and this method may be employed without danger or inconvenience at any period at which absolute certainty of diagnosis becomes of importance. Pulsation is sometimes communicated to the fluid by the heart's action, and in some cases this pulsation strongly simulates that of aneu- rysm. Dr. Walshe has referred to this point, and similar cases have been observed by others, in all of which, according to Fraentzel,2 the fluid has been purulent. In each of the two cases observed by Traube, and also in the one that came under Fraentzel's notice, pericarditis with effusion into the pericardium was present. Traube considers the occurrence of pulsation as due in part to suppurative softening with increased extensi- bility of the pleura costalis, and in part to the presence of pericardial effusion favoring the transmission of the heart's impulse. Some few years ago Prof. Maclean was kind enough to allow me to examine, at Netley, a soldier who had a very excessive effusion into the left pleura, and who had so marked a pulsation in the left supra-mammary region as to cause some hesitation in performing paracentesis, lest there should be a large aneurysm in addition to the hydro-thorax. A right judgment was, however, without much difficulty arrived at, and a large quantity of serous fluid was removed, and with it the doubtful sign of aneurysm dis- appeared. There was no pericarditis suspected in this case (and the heart was of course carefully auscultated). Another case of effusion, right- sided and of older standing, came under my notice at the Brompton Hos- pital some months ago, in which a rhythmic impulse conveyed through the fluid suggested aneurysm as a complication. The fluid was, how- ever, removed by several tappings; it was somewhat opaque and at first slightly blood-stained. No aneurysm was present. It is thus clear that neither suppuration in the sac nor pericarditis is necessarily associated with pulsation, and probably nothing more is needed to account for the phenomenon in question than an amount of fluid which shall exercise a certain degree of pressure (neither too much not too little) upon the beating heart. Two or three other instances have come under my obser- vation in which the diagnosis of mere fluid in the pleura has been much shaken by another unusual pressure effect, viz., altered quality of voice and cough. A husky voice, and a laryngeal quality of cough, undistin- guishable from that so often heard in cases of mediastinal tumor or aneu- 1 " Transactions of the International Medical Congress," 1881, vol. ii., page 146. 2 Ziemssen's Cyclopaedia, vol. iv., p. 638. DISEASES OF THE PLEURA 69 rysm, have given rise to great doubts as to the diagnosis, yet both phe- nomena have disappeared after paracentesis. Putrid effusions.—Two cases1 have come under my observation, which lead me to think that sometimes the fluid in sero-fibrinous effusions un- dergoes spontaneous decomposition, and becomes converted info a foetid sero-purulent matter, a discolored stinking fluid being removed on para- centesis. On this point a remark of Professor Marshall's is interesting. He observes:—" The sero-fibrinous effusion appears to have a greater ten- dency to quick decomposition, when air is admitted into the pleural sac, than the sero-purulent or purulent product. Pus is more stable and less inclined to rapid putrefaction than the sero-fibrinous fluid."2 In the cases referred to, however, there had been no opportunity for contamination from without. In such cases septic phenomena of the more virulent kind present themselves, of which continued rapidity of pulse, a red tongue, smooth and denuded of epithelium, sometimes aphthous or thinly coated, com- plete anorexia and vomiting or diarrhoea, are the most characteristic. In the presence of such symptoms we may be sure that an effusion is puru- lent, aud has probably undergone decomposition, and only with its free evacuation and disinfection will they vanish. In all cases of doubt, then, I would still counsel the timely use of the needle-syringe, by means of which a sample of the fluid can be obtained with little or no pain to the patient, and absolutely without danger of doing mischief. In suppurative pleurisy the only efficient treatment is by evacuation of the pus, and the progress is, generally speaking, favorable in accordance with the promptness with which the pus is recognized, and its removal effected. 1 Viz., Case 7, Trans, international Congress, vol. ii., Medical Section, p. 143, seen with Dr. Stamford of Tunbridge Wells, and a case more recently seen with my colleague, Dr. Finlay, at Middlesex Hospital. 2 Lancet, vol. i., 1882, p. 300. CHAPTER V". ON PLEURITIC EFFUSIONS CONSIDERED ESPECIALLY WITH REGARD TO OPERATIVE TREATMENT. Pleuritic effusions, whatever be their original source or nature, have so much in common with regard to treatment, that they may be conveniently brought together for consideration in this point of view. Much progress has been made in the treatment of these effusions within the last few years, and so much has been written and said upon the sub- ject, that it would take up many chapters, and be quite beyond the prac- tical scope of this work to review the literature in any formal manner. I shall therefore, for the most part, content myself with relating those methods of treatment which have proved most successful within my own observation and experience. Pleuritic effusions are naturally grouped into:— (1) Simple inflammatory effusions, in which the fluid is sero-fibrinous and which may be acute or chronic. (2) Suppurative effusions, in which the fluid is purulent, and of recent or old date. (3) Hydro-thorax or dropsy of the pleura. (4) Haemo-thorax. (5) Pneumo-thorax. 1. Simple Inflammatory Effusion into the Pleura.—Acute effu- sion. The general grounds upon which operative interference should be adopted, withheld or delayed, were fully laid down in the preceding chapter. The tendency at the present time is perhaps rather towards too great an anxiety with regard to the presence of fluid effusion, and to a corresponding impatience for its removal. One might, indeed, feel some misgivings as to whether Nature ought ever to be burdened by ha ring to remove so vast an accumulation, did not experience show that she is fully equal to the task; and when we con- sider how, throughout the body, effusion and absorption are perpetually going on, constituting an extra-vascular circulation amounting in the aggregate to many pints, we cease to have any real difficulty in under- standing this ready removal of fluid collections. If at the end of a week or ten days from the time when the pleuritic effusion has reached its height, appropriate remedies having been used, there be no signs of any material abatement of the fluid, it will be judi- cious to draw off a portion of it. Doubtless the employment of purga- PLEURITIC EFFUSIONS. 71 tives, and diuretics or mercurials would still, in most cases, ultimately effect the withdrawal of the fluid though the natural channels. I have known an acute serous effusion require six months' treatment by tonics and diuretic remedies for its final removal. In another case, after many months of fruitless treatment by ordinary methods, mercury, pushed to salivation, rapidly removed the effusion.' But this protracted or severe medicinal treatment is not always successful, and is at least attended with great risk of permanent damage to the lung, and of complication with other diseases. The better course in such cases surely is to adopt the timely removal of a portion at least of the fluid by paracentesis; but the worst course of all is to leave such cases alone or to treat them with in- different drugs. Dr. Bowditch observes: " I cannot see any valid reason for continuing any active treatment more than one, two or three weeks without puncturing."2 In those cases in which there is an indisposition on the part of the vessels and lymphatics to reabsorb the fluid, the effusion is commonly very great, and the intra-thoracic pressure considerable, perhaps equivalent to an inch or an inch and a half of mercury.s Now although, during the inflammatory fever, fluid can, even up to this degree of pressure, be effused, owing to the high tension of the general circulation, and the relaxed condition of the vessels locally, yet when the fever has passed, more or less general exhaustion and anaemia prevail, the pressure of the circula- tion falls, and the effect of the high pressure upon the pleural surface is necessarily to render it especially anaemic, and, by the powerful com- pression of the lung, to hinder absorption by the lymphatics. The fact, frequently noticed, that after removal of even a small portion of the fluid the rest is rapidly absorbed, almost demonstrates the correctness of this view. Trousseau observes "this greater slowness in the absorption is, perhaps, as much dependent on the pressure exerted by the excessive quantity of fluid upon the serous membrane by which absorption has to be performed, as by the mere greatness of the quantity."4 It is probable that absorption of pleuritic effusions takes place largely through the lymphatics, otherwise one would expect to find some albu- men in the urine whilst so large a quantity of albuminous fluid was being taken up by the systemic veins. This I have not found, and Dr. Dickinson remarks in his recent work on Albuminuria, " It has been said that the same result (temporary albuminuria) has followed the rapid absorption of serous fluid from the pleura, a sequence, which, to say the least, must be rare." 1 Dr. Hope—Medico-Chirurgical Review, 1841—strongly recommended the treatment of pleuritic effusions by mercury. 2 "Thoracentesis," by Henry J. Bowditch, M.D., 1870, p. 13. 8 " Observations on Paracentesis," Clin. Soc. Trans., vol. hi., 1870, p. 240, Med. Chir. Trans., vol. lix., p. 187. ■•Clinical Medicine, New Syd. Soc. Trans, of 3rd edit., 1868, vol. hi., p. 229. 72 DISEASES OF THE LUNGS AND PLEURAE. In other cases, on the subsidence of acute symptoms, absorption goes on well enough up to a certain point, beyond which, however, the patient remains at a standstill, his chest being perhaps half full of fluid. In these cases there is usually considerable depression of general health, and iron tonics, good diet, and iodine embrocations or blistering, with change of air, will generally effect complete absorption. If sure that the fluid were not purulent, one would be loth to interfere at this stage. Chronic pleuritic effusion.—Patients may live for a long time, and with surprisingly little discomfort, with very large effusion into the pleura. Not a few cases are still from time to time met with in which one side of the chest is distended with fluid, the effusion dating from an attack of pleurisy months or even a year or two previously, and which, on removal, proves to be perfectly limpid and serous. The inflammatory attack lead- ing to such an effusion is sometimes only marked by slight symptoms, rapid effusion no doubt relieving the inflammatory condition and cer- tainly removing the pleuritic pains. Trousseau remarks that these patients are frequently quite unconscious of having anything seriously the matter, although the pleura may contain a large quantity of fluid. I have still under my occasional observation a policeman, stalwart-looking enough to frighten thieves, who for four or five years has had his left pleura completely full of slightly turbid serum. After a few partial tappings it became evident that no expansion of the lung could be looked for, and in the absence of any urgent symptoms it has not been thought prudent to submit him to any radical measures of treatment involving long illness and, probably, a permanent thoracic fistula. I think, with Dr. Wilson Fox,1 that the fear lest the effusion should become purulent from mere lapse of time, urged by Trousseau as a reason for early operation, is not well grounded; there is very little disposition for such a transformation to take place, unless the patient have a fresh inflammatory attack. But perfect recovery in these old-standing cases is well nigh impossible, the lung having become bound down and thickened by long-continued com- pression, and it is to be hoped that the reproach of their not very infre- quent occurrence will soon be removed from us. I am bound to confess, however, to holding very strongly the belief that there will always be a certain small number of cases in which the lung is from the first coated by an exudative layer of unusual thickness and uniformity, which, as pointed out by Walshe,2 contracts forcibly and aids the fluid in bringing about a collapse of lung. Such a membranous layer affords a serious impediment to absorption, and is apt to undergo a degree of organization which renders the constriction of the lung a per- manent condition. Under these circumstances, and especially in strongly built adult chests (as in the case of the policeman above quoted), a large 1 Brit. Med. Jour., Dec, 1877, p. 752. 2 Diseases of Lungs, 4th edit., p. 252. PLEURITIC EFFUSIONS. 73 pleural space remains which it is almost impossible to obliterate, and which must be occupied by some kind of effusion. Paracentesis thoracis in serous effusions.—Choice of spot for puncture. —Supposing paracentesis to be necessary, the first step to be taken is to select the best position for puncture. The physician is responsible in choosing the site for puncture, and must not share the responsibility with others. In choosing the spot he has to be sure (1) that it is out of reach of diaphragm and heart; (2) that there is no adherent lung there. The sixth space in the mid-axillary line is the best point for puncture, and should be selected if, when tested by percussion, palpation, and ausculta- tion, it prove satisfactory. This spot is most convenient because (1) most accessible whilst the patient is reclining in an easy posture; (2) the parietes are here moderately thin, and the intercostal space sufficiently roomy; (3) the mamma in the female is out of the way; (4) we are suffi- ciently high up to be free from danger of perforating the diaphragm; (5) this point has the advantage over that most commonly chosen, below the angle of the scapula, in there being less probability of the canula becoming blocked by the flocculi, which tend, from the position of the patient, to gravitate towards the back of the chest (most of the dry tappings I have observed have occurred with the posterior puncture); (6) this point has the advantage over one chosen more anteriorly in being more central with regard to the effusion. Some authors prefer other sites for puncture. The matter is not one of any great importance. Prof. Marshall would choose the anterior weak spot in the chest wall in the fifth space nipple line. Another so-called weak spot, preferred by some operators, is in the line of the angle of the scapula; my point is between them. Of course, in special cases of limited effusion the point for puncture must be selected accordingly, it being re- membered, however, that a central rather than the lowest point of the effu- sion should be chosen for puncture. Vertical and horizontal marks should be made upon the chest point- ing to the precise spot chosen. Local anaesthesia, puncture.—The patient reclining near the edge of the bed, with the head and shoulders slightly raised and leaning towards the diseased side, a piece of ice with a flat surface, an inch or two square, dipped in salt, should be applied with firm pressure to the spot marked for puncture. In twenty or thirty seconds the spot will be frozen; it should then be rapidly wiped, a small incision made through the skin, and the trochar, previously steeped in carbolic solution (1 in 40), smartly thrust into the pleura. The canula will have been previously connected with three or four feet of tubing filled with water and leading to a vessel containing a certain quantity of water, which must be two or three feet below the level of the patient; or the tubing may be connected with a bottle which can be gradually exhausted of air by a suitable syringe. The 74 DISEASES OF THE LUNGS AND PLEURAE. operation having been completed, the canula must be withdrawn rapidly, the edges of the wound being compressed between the finger and thumb and a fold of lint soaked in collodion applied. A band of strapping three or four inches broad and of sufficient length, should then be firmly ap- plied round the affected side, so as to extend a couple of inches beyond the median line in front and behind. The following list includes all the apparatus needed for the perform- ance of paracentesis in a case of serous effusion, and suggests some further remarks respecting the performance of the operation. 1. A lump of ice and some salt. 2. A small scalpel or lancet. 3. Carbolic solution (1 in 40). 4. Trochar and canula connected with three feet of tubing; the whole having been previously filled with water. 5. Basin containing one pint of water. 6. Lint. Collodion. 7. Piece of strapping plaster four inches by twenty. 1. The plan named in the text of cutting a plane surface upon a lump of ice, dipping it into some salt, and then applying it firmly to the surface of the skin, is by far the best means of obtaining local anaesthesia for paracentesis thoracis. If no ice be obtainable, the ether spray may be used, or the operation performed without the aid of any anaesthetic. 2. It is always best to make a small incision through the skin (except perhaps when quite capillary instruments are used). The clean-cut wound heals much more readily than the bayonet thrust, and less pain is felt by the patient because the skin is not stretched by the trochar. 3. It would seem needless to add a word of warning on the importance of seeing* to the scrupulous cleanness of trochars or aspiration needles used in paracentesis. Cases have, however, come under my own observation, in which-carelessness in this respect. apparently led to decomposition of the fluid, suppurative pleurisy, and ultimately to the death of the patient. If an instrument be not fresh from the makers, its purity should be insured by submitting it to the flame of a spirit lamp. If rubbed over first with a little oil, the metal will not be tarnished by the heat.1 4. The best instrument for tapping the chest is the simplest one possible which will effect the object required, viz., to remove fluid without admitting air from a cavity with walls more or less elastic, and which is contracting and expanding alternately, the contraction and expansion movements increasing in depth and force as the fluid is withdrawn. If a simple hydrocele trochar be used, it is inevitable that before any considera- ble quantity of fluid has been withdrawn, air will be sucked into the chest. With regard to the question as to the expediency, I should rather say the imperative importance, of avoiding the admission of air during para- 1 For this last practical hint I am indebted to Mr. E. A. Fardon, Resident Medical Officer at Middlesex Hospital. PLEURITIC EFFUSIONS. 75 centesis in the cases now under consideration, I fail to see the usefulness of any further discussion. True it is that, in some cases, air has been admitted into the pleura without any harmful result, but these cases are exceptional, and against them must be brought other cases far more numerous, in which renewed fever, fresh pleurisy, and the conversion of the serous into purulent effusion has followed.1 And, apart from these directly evil consequences, let us remember that air is more foreign to the pleural cavity than serum; that whilst air is present it is quite as impossible for the lung to expand, or for the heart to return to its normal position as though fluid were there, nor is the absorption of air by the pleura when altered by recent or old inflammation more easy than that of serous fluid. Why then allow this, at best foreign, and in most cases noxious, element to enter at all? The only plausible answer is, that unless we do so, all the fluid cannot be removed. This is true as a state- ment, but is no answer, because we do not wish, in any case of simple effusion into the pleura, to withdraw all, or nearly all, the fluid, but only a sufficient quantity to relieve pressure and to encourage the absorption of the remainder. Hence, then, we must have some addition to the ordinary canula by which, whilst the fluid is allowed to flow from the chest, air is absolutely excluded from entering it. The simplest contrivance for this purpose is perhaps that ingeniously suggested by M. Reybard, viz., to tie on to the neck of the canula a piece of gold beater's skin rolled into a tube. When wet, this acts as a perfect valve, allowing of the free exit of fluid but collapsing over the ori- fice of the canula on the slightest aspiration towards the pleura. An ordinary hydrocele trochar can be readily fitted with this form of valve. But a piece of india-rubber tubing attached to the canula, and having its other extremity under water at a lower level than the chest, is the most complete means of excluding air, and we can in this way, moreover, employ whatever degree of syphon power we wish to aid the removal of the fluid. The trochar which will be found most generally useful for this purpose, is one which I brought before the notice of the Clinical Society in 1870,2 in the paper already referred to, and I have not since found anything to improve in its con- struction. This trochar is, as I was not then aware, essentially the same as that designed by Mr. Charles Thompson, and described in the Medical Times in March, 1858. The padding in the cap of the canula through which the stem of the trochar works seems an improvement; it was suggested by Mr. Hawksley, the maker of the in- strument. 1 The late Dr. Fuller, in an otherwise admirable clinical lecture, was I believe the last clinical teacher who regarded with indifference the admission of air dur- ing paracentesis for serous effusions. Brit. Med. Jour., Feb. 3rd, 1872. 2Z,oc. cit. 76 diseases of the lungs and pleurae. The canula (fig. 11) has a calibre of about & of an inch, (4mm.), and is provided with a lateral branch (a) furnished with a leather collar on to which the tube piece (d) screws. The trochar has only a small and light handle, and works through the cap of the canula ; this cap (c) is so padded with leather that, when forcibly screwed down, the stem of the trochar is grasped by the padding in an air-tight manner. The tubing attached to d should be about three feet long, and should be interrupted, near the canula, by a piece of glass tubing let in so that the nature of the fluid, etc., may be observed. It is a very good plan to fill the tubing, ready attached to the canula, with water before making the puncture. As soon as the instrument has been introduced, and the stilette (b) withdrawn, the fluid flows through a and no admission of air is possible. The trochar should be dip- ped in carbolic solution before being used, and the receiving basin lowered so as to allow a syphon column of between two and three feet of tubing. ~l ~° > a It Fig. 11. It is often convenient, and if properly managed is quite harmless, to withdraw the fluid into a bottle by aspiration. For the purpose now indicated, the fittings of Potain's aspirator are the best. A cork (c, fig. 12) made of india-rubber, and of such dimensions as to accurately fit any ordinary wine or seltzer-water bottle, is perforated by two tubes, one of which (a) fits on the basin end of the exit tube attached to the canula already described. The second tube b, is adapted to an exhausting syringe. Each of these tubes is supplied with a stop-cock, and the tube d in connection with the canula should extend somewhat further into the bottle than b'. Now the ordinary " aspiration" method is as follows :—Having fitted the ap- paratus, to exhaust the air from the bottle, and then having connected the canula- tubing, to open stop-cock a when the fluid rapidly fills the bottle. The stop-cock a is then again closed, the bottle detached and emptied, and the process repeated. By adopting this method of practice, however, we are employing quite an un- known suction power, which may amount to anything short of 15 lbs. to the square inch, and which is not only quite unnecessary but, if incautiously used, extremely dangerous, and especially so towards the latter part of the operation when there is already negative pressure within the pleura. A very safe and useful way of using this apparatus is that which I sometimes employ, viz., to open the stop-cock a, and just to keep the syringe in sufficient action to permit or encourage the flow of fluid through the exit tube d into the bottle. When the bottle is filled, the stop-cock, a, must be closed before the cork is withdrawn, otherwise there will be a rush of air into the chest. I cannot say that this plan has any advantage over the syphon, both methods are very con- venient and safe for removing fluid from the chest, the syphon excelling the other PLEURITIC effusions. 77 in the uniformity and measurability of the power employed, and also in simplicity and freedom from extra fittings. If a soft plug of fibrine block the canula it may be impelled through the tube by a momentarily increased aspiration power, or it may be dislodged by reversing the syphon or cautiously thrusting back the trochar. In cases in which fine capillary trochars are used aspiration is necessary, and the usual method of employing this agency does not remove the fluid with the same dangerous rapidity as through larger instruments, but there is the same un- certainty as to the amount of negative pressure induced within the thorax. In some cases, however, in which there is doubt respecting the diagnosis, a fine exploratory trochar, previously passed through the flame of a spirit-lamp, should be first employed.1 Fig. 12. The usual plan of applying a bandage round the chest after paracentesis is not a good one; it hampers the movements of the healthy side and distresses the pa- tient. It may be a question whether any application of the kind is necessary, but I have always preferred to keep the affected side at rest by the firm application of a band of strapping round the lower ribs to beyond the median line in front and behind, thus leaving the healthy side free. In acute pleuritic effusions the operation of paracentesis has rarely to be repeated, the remaining fluid being absorbed without much difficulty. In cases, however, of what may be called chronic hydro-thorax (cases which will become more rare as acute pleuritic effusion is more efficiently treated), in which the lung is bound down by adhesions more or less strong, repeated tappings are necessary, and they should be performed in the way above described and with the same scrupulous care to avoid ad- mitting air. The syphon power employed may sometimes, in these cases, be increased with the view of aiding lung expansion. In most cases the 1 It would be very easy of course by a pressure guage fitted into the bottle to know at any moment what degree of aspiration is being used, but this arrangement would require a special bottle, whereas a great advantage of Potain's cork adjust- ment is that it renders any ordinary bottle available. 78 DISEASES OF THE LUNGS AND PLEUR.E. lung partially expands, and is partly met by some flattening of the chest wall, attraction of the heart, and enlargement of the opposite lung. Meanwhile no symptoms arise from the operation, and after a rest of a day or two it is better to allow the patient to be about and to enjoy the fresh air. Tonics and iodine frictions may be employed in the intervals, and a pad of spongio-piline may be inserted underneath the strapping in the infra-mammary region, so as to keep up some pressure at this portion of the chest where flattening first commences. 2. Empyema.—Cases of suppurative pleurisy resulting in pyo-thorax are necessarily of far graver character than those we have just been con- sidering, and present many more points of difficulty in their treatment. There is good reason to believe that in some rare instances, especially in children, the purulent fluid has been absorbed, the pus #ells having first undergone fatty degeneration.' Dr. Fox regards M. Moutard-Martin (De la Pleuresie purulente) as having placed this question beyond dispute. I have myself seen one case which has satisfied my mind as to the pos- sibility of a local empyema becoming absorbed, but I know not the ulti- mate fate of the patient, a child aged about five years. Dr. Edebohlsa has recently related an instance in a child, in which, after proof by needle puncture of the effusion being purulent further operative treat- ment was not allowed. Some months later, the child was again examined and its chest was found free from fluid. Twelve months after, however, the signs of decided phthisis were present. In some other cases the fluid portion of the effusion is absorbed, and the remainder thus inspissated is deposited in a thick layer on the pleura. The spontaneous disappear- ance of such effusions is, however, too uncommon to be expected; and the process of reabsorption is one too full of peril to be anticipated with anything but dread. It is indeed an attempt at such absorption that occasions the most characteristic hectic symptoms in the second stage of suppurative empyema. In the event of the more liquid portions becom- ing absorbed and inspissated pus left behind, although for a time the patient may do well, yet at any future period pleuritic abscess or second- ary tuberculosis may ensue upon the softening of the caseous deposit. If left to run its natural course, a case of purulent effusion will in the infinite majority of instances either (1) prove fatal from exhaustion or syncope; or (2) after a few weeks of hectic, the empyema may sud- _ denly burst through the lung with perhaps immediately disastrous results. More commonly, however, this sudden outburst is followed by long- continued profuse expectoration of decomposing purulent matter with symptoms of chronic septic poisoning, and gradual exhaustion with secondary disease of the lung. Cases have occurred in which an em- 'Dr. Wilson Fox, Brit. Med. Jour., Vol. 2, 1877, p. 752; Dr. Clifford Allbutt, idem p. 726, and Dr. Goodhart, p. 795. 2 New York Medical Record, Jan. 26th, 1884. PLEURITIC EFFUSIONS. 79 pyema has burst into the peritoneal cavity, or the sheath of the psoas muscle, in other cases it may simulate peri-nephritic abscess; or (3) the pus may point and discharge by a fistulous opening through an intercos- tal space. It is contrary to all the principles of enlightened treatment passively to allow either of these phenomena to occur, and we can never do so without taking great blame to ourselves when it is too late. In no other situation in the body would a large collectio.n of pus be allowed to remain after it had been fairly recognized, and we should not depart from one of the best-established of all rules in medicine because statistics bring out the fact that the results of paracentesis in empyema are still far from satisfactor}7'.1 It is perfectly clear, then, that we must adopt some surgical measures for the treatment of all cases of empyema, or take upon ourselves the re- sponsibility for a large mortality; fortunately our hands have been greatly strengthened in this matter by the advance in surgery within the last few years. It is still more true with suppurative than with serous effusions, that the greater the duration of the effusion, the more difficult is its ultimate removal, because in the former cases we must evacuate all the pus from the pleura, and the more complete the power retained by the surrounding walls of closing in and obliterating the cavity left behind, the better. Hence, in active cases, as soon as it is ascertained that there is pus in the pleural cavity, the question of its removal should be at once considered. I have already referred to the signs upon which the diagnosis of sup- purative as distinguished from serous pleurisy may be made, (see page 65). The association of the attack with pyaemia, scarlatina, the puerperal state, typhoid fever, the scrofulous diathesis, or already existing pulmonary dis- ease, renders it much more probable that the fluid effused will be purulent. A typhoid character of symptoms, with great rapidity of pulse; daily elevations of temperature, continued beyond the period at which in simple pleurisy it should subside; continued rapidity of pulse; the occurrence of hectic sweats and of secondary chills; marked emaciation; anorexia and furred tongue are all signs which strongly point to pus in the pleura. Oedema of the side sometimes appears as a later sign, and when it occurs is of great importance. It is impossible to lay down any hard and fast rule as to the exact time at which all such cases should be interfered with. No two cases are precisely alike, and each must therefore be dealt with on its own merits and in the discretion of the observer. But the general rule laid down by Dr. Hamilton Roe, who (with Hughes and Cock of Guy's Hospital and Trousseau in Paris) practically revived the operation of paracentesis thoracis, should be acted upon, viz., "that as soon as it is clear that 1 See cases related by Dr. Goodhart in Guy's Hospital Reports, 1877, p. 183. 80 DISEASES OF THE LUNGS AND PLEURAE. pleurisy is subdued, and that a large quantity of fluid remains in the chest, we should proceed at once to ascertain its quality, by introducing the exploring needle' (invented by Sir B. Brodie), and if it is found to be purulent, the operation should forthwith be performed."' The period for exploration here referred to by Dr. Roe would be from about the second to the third week of the disease. The next question is as to the best method of removing the fluid. It may be convenient, and particularly so in cases in which symptoms of asphyxia or syncope are threatening, to remove in the first instance a portion of the pus by means of the syphon or aspirator; and some authors prefer, in children at all events, to try one or two aspirations before having resort to the more radical operation. Although by this means temporary relief is obtained from any pressure-symptoms that may be urgent, the effusion will certainly re-accumulate, and we cannot be said to have yet dealt with the case until the pus has been thoroughly evacuated. Dr. Clifford Allbutt's objections to incomplete tappings or partial aspirations in purulent effusions, seem to me to be very valid ones. He remarks,3 " My two objections, and these complete ones, to repeated aspirations are: —1. Aspiration does not prevent the formation of a pulmonary fistula. 2. It does not prevent absorption, but rather favors it. By the pressure of a full cavity, absorption is often prevented and fever absent; draw off some of the pus, you relieve pressure, and absorption begins." These objections hold good in acute purulent effusions. In chronic empyema of old standing the conditions present are different. There is this very important difference then, with regard to treatment, between serous and purulent effusions, thai a serous effusion, not being in itself hurtful, need only be partially evacuated when circumstances require it; a purulent effusion on the other hand is of itself highly poison- ous, and, although it may be convenient for the moment to remove a portion only, yet no real progress will have been made in the treatment of the case until the whole of the pus has been evacuated, and free exit, provided to prevent any further accumulation. The objects in view in paracentesis for serous and for purulent fluids are very different. In empyema we desire completely to evacuate the pus, to allow as little subsequent suppuration as possible, and to provide free drainage for such pus as may form. It is clear that we cannot empty the pleura, even in recent cases, with- out admitting air in place of the fluid. Hence we must adopt one of th;ee measures. 1. Either to disinfect the air admitted into the pleura, 1 The ordinary subcutaneous injection syringe (I think first recommended for this purpose by Dr. Ringer) or the needle of an aspirator would now be substitu- ted for the old-fashioned grooved needle. 2 Medico-Chirurgical Transactions, vol. xxvii., p. 198. 3 British Medical Journal, Nov. 24, 1877, p. 727. PLEURITIC EFFUSIONS. 81 and having inserted a drainage tube, to close the wound with antiseptic dressings, to be renewed with the same precautions every three or four days. 2. To make a single free opening and insert a tube through which the pleura can be daily washed out with some disinfecting fluid. 3. To make a double opening and introduce a drainage tube, so as to permit of the escape of pus as rapidly as it is formed. The point to be chosen for incision in cases of purulent effusion is a different one from that to be preferred in serous effusion. A moderately low opening is desirable, in the seventh or eighth intercostal space, and in the posterior axillary line, due precautions being taken with regard to position of heart, lung and diaphragm. My reason for recommending a lower and more posterior point for puncture in these cases is, that in acute empyema we wish to empty the pleural cavity of pus, and we look for obliteration of the abscess-sac by the descent of the lung as it re- expands, and by the return of the heart to its normal position: these processes converge towards the lower and postero-lateral position of the ciiest. Professor MarshallJ would lay down the rule never to perform open paracentesis lower than the sixth or seventh interspace at the sides of the chest, and in the adult, he recommends in preference the fifth space in the nipple line over the "weak spot" of the chest wall. Further ob- servations are needed to determine the relative advantages of different positions of opening in cases of acute empyema, and probably the results will show that there is room for differences of opinion. If there be any doubt at the time of operating as to the eligibility of the spot selected for puncture, an exploratory trochar should be first introduced. Antiseptic operation.—Of the three above-named methods, the first is to be preferred, and it is on the whole the least troublesome, since, al- though there are several points of detail needing attention during the operation and at the subsequent dressings, these dressings require to be removed at less frequent intervals, and all injections of the pleura are dispensed with. I will briefly give the headings of this method, which the practitioner will have no difficulty in supplementing as soon as the principal objects in view are clearly discerned. (a) The apparatus required, consists of—1. A Lister's hand-ball spray producer or small steam-spray apparatus charged with carbolic acid solu- tion (1-40), and having pieces of linen wrapped round the submerged ends of the tubes so as to prevent them from becoming blocked by any foreign particles. 2. A tray containing a solution of carbolic acid (1-20) in which to 1 Lecture on Diseases of the Chest Cavity, delivered at the Bromptou Hospital. Lancet, March 4th, 1882. 6 82 DISEASES OF THE LUNGS AND PLEURAE. place all instruments to be used, which instruments must of course be thoroughly clean. 3. The instruments that should be at hand consist of a bistoury, a full-sized trochar and a fine exploring trochar, drainage tubing (well soaked in antiseptic), scissors, dressing and torsion forceps, and in case of removal of rib, raspatory, bone-clippers, etc. 4. An anaesthetic must be administered or local anaesthesia employed. It is most convenient to give chloroform and ether, and these anaesthetics are as a rule remarkably well borne by empyema patients. 5. The hands of the operator and assistants must be carefully washed and rinsed in carbolic acid solution, and the nails cleansed; the same pre- cautions being observed each time the case is subsequently dressed. The surface of the patient's chest must be well sponged over with carbolic lotion 1 in 40. 6. Boracic or carbolized charpie. Antiseptic gauze, not less than eight layers thick, and about 12 by 16 inches area. Under the outermost layer of the gauze, a piece of thin prepared mackintosh must be inserted, care being taken that it does not reach beyond the edges of the gauze in any direction. Some rollers for bandaging made of the same antiseptic gauze material must be ready to keep the application in place. And a turn or two of elastic bandage for the purpose of finally maintaining in close apposition the free margins of the dressings. After a preliminary incision, which should be sufficiently free (not a mere nick, as for the trochar in serous effusion), down to the intercostal membrane, either a large trochar should be inserted or the incision con- tinued with the knife. An incision is apt to get occluded by false membrane, and in this re- spect the trochar is preferable; but circumstances at the time, such as the amount of intercostal space, will determine the employment of one or other instrument. Some surgeons prefer, even in acute cases, to resect an inch or so of a rib, with the view of getting more room. I would not recommend this procedure, at least in the first instance. In a case in which difficulties have arisen at the first tapping, and in which there is reason to suspect loculation of the empyema, it is a great advantage to resect a rib, and thus get room for the free introduction of the finger, to break down adhesion cysts. The escape of fluid through an incision may be facilitated by introducing through the incision the blades of a Trous- seau's dilator, or of clean ordinary dressing forceps, and opening them out so as to stretch the wound. As much of the fluid having escaped as will do so, a piece of drainage tube three to five inches long, is introduced, through which probably more fluid will at once escape. The side having been washed, a piece of protective is placed round the tube, which, unless provided with a broad rim, must be retained by being transfixed by a silk suture secured round strips of plaster to the side of the chest. A broad PLEURITIC EFFUSIONS. 83 rim to the tube is safer however. A soft thick pad of charpie is then to be placed over the orifice of the tube, and the broad eight-layer thick- ness of antiseptic gauze superposed and kept firmly in place by many turns of carbolized bandage extending above and below, so as to envelope the whole chest. Some arrangement of shoulder straps will prevent the bandages from slipping down, and a few turns of elastic bandage are very useful to preserve the free edges of the dressing in close contact with the chest. The air, except that first introduced under the spray, and what may filter through the thickness of the dressings is thus excluded. It is often necessary to dress the wound again, with precisely the same precautions, a few hours later, the dressings having become soaked with discharges; one full day may then elapse, and subsequently perhaps two or three days. The tube should be removed and washed on the third, and subsequent, dressings of the wound. The patient must be kept in bed, and the strength well supported by nutritious and digestible food. The temperature must be carefully watched, and will be found, if all has gone well, to fall to the normal. It is very important before commencing each dressing to see that the spray producer is properly charged, and in good working order; any care- lessness in detail will neutralize the results of all former trouble. The discharges upon the removed dressings should be perfectly free from odor, and after the first two or three changes, become very small in amount. Thus, the pleural sac is kept practically empty, and the entry of air being more ready into the lung, than through the dressings, the gradual expansion of the lung is encouraged. The drainage tube will require shortening as the cavity contracts, and the lung expands, and will by degrees be removed altogether. The above is undoubtedly the most successful method of treating cases of acute and subacute empyema, and although it seems more troublesome than less thorough methods, yet it takes really very little more time, and the occasions for changing the dressings are less frequent.1 The fact that under this system, the dressings after the first few days may be left undisturbed for two or three days together, is of obvious advantage to the patient by keeping the cavity for these intervals practically closed, and thus affording the lung the very best opportunity of re-expanding. I am far, however, from contending that the antiseptic method is the only one that can with safety be adopted. I say that it is the best and most favor- able to the rapid recovery of the patient. Single opening and injection of pleura. — Supposing the antiseptic treatment not to be strictly followed, all instruments and tubes used should still be steeped in carbolic lotion. The lighter and simpler the 1 The materials are sold by Gardiner of Edinburgh, Mayer and Meltzer of Great Portland Street, and Krohne and Sesemann of Duke Street, London. 84 DISEASES OF THE LUNGS AND PLEURAE. dressings used, the better. A large piece of absorbent cotton-wool should be first laid over the tube for the discharge to soak into, and a pad of oakum applied over that, the whole being kept in place by a few turns of elastic bandage round the chest. For the first two or three days the dressings will have to be changed twice daily; then, if the drainage be perfectly free, the discharge will readily diminish and remain sweet, and one dressing daily will be sufficient. The drainage-tube must be removed at least once every two or three days, and thoroughly cleansed or renewed. The temperature of the patient must be carefully observed; it is an im- portant test of the efficiency of the treatment. If there be any decided rise of temperature we may fear that some accumulation of pus is present. Unless the contents of the pleura be foetid, antiseptic injections are best avoided, since they tend to retard the expansion of the lung. In those cases in which they are necessary they should be used with care. The pleura should never be syringed out, but an irrigator should in all cases be used. A tin pot or glass vessel, provided with a hole near the bottom, to which tubing is fitted, the tubing being supplied with a nozzle or pipe for insertion into the wound is the simplest and best irrigator, or a syphon arrangement may be extemporized. The vessel, having been filled with the lotion required, is simply raised a foot or two above the patient, when the fluid flows into the chest equably, and with a uniform and measurable pressure. As it escapes from the chest the fluid is caught by a tray or other suitable receiver. The irrigator and syphon have the advantage over the syringe, inasmuch as with them we know exactly how much force we are using, and this force is used equably and slowly. Amongst the sudden deaths that have occurred alter paracentesis, not a few have happened whilst the pleura was being washed out. Syncope and cerebral embolism are the most common causes of such deaths; the one likely to be induced by any sudden increase or removal of intra-thoracic pressure, the other by such similar disturbance of pressure as may loosen any clots which have formed in the veins of the compressed lung. Amongst the best disinfecting lotions may be mentioned—iodine, one drachm of the tincture to the pint of warm water; carbolic acid, two per cent.; Condy and water; quinine solution, two or three grains to the ounce; boro- glyceride has recently been used in watery solution, one to forty. In the case of very young children, who are terrified at injections, immersion in a warm bath colored with Condy's fluid is an ingenious plan suggested by Dr. Barlow and Mr. Parker. It is a question likely to be more fully debated, whether, in acute cases of empyema, resection of a portion of a rib be desirable. The operation is a very simple one, and has been advocated at this stage of the disease by Mr. Godlee.' Should the tube become nipped this operation may at 'Proceedings of the Roy. Med. and Chir. Society, N.S., vol. i., p. 255. PLEURITIC EFFUSIONS. 85 any time be performed, but in the first instance, in acute cases, it is rarely necessary or advantageous. Drainage by double opening.— This method of treatment, which consists in making two openings, and passing a drainage tube through the chest cavity from one to the other, is but very rarely practised now for cases of acute, or indeed in chronic, empyema. It would be quite unjustifiable to adopt the method as a primary measure. For cases treated antiseptically one opening is quite sufficient as a rule. This plan of drainage may, however, be resorted to on the failure of one of the other methods. A long probe, or curved steel sound provided with a bulb at one end, is inserted either into the opening already pre- sent, or through a fresh incision made at one of the anterior interspaces, and passed directly backwards and downwards so as to impinge posteriorly opposite an interspace. The surgeon then cuts down upon the bulbous end of the sound, and having secured to it an india-rubber drainage tube, withdraws the sound, carrying the tubing with it through the chest. The two ends of the tube are then secured outside the chest in the usual way. By this means, as fast as fluid forms in the pleural cavity it is drained off. In some cases in which we cannot hope for, or do not desire, the lung to expand, this is one of the best methods of treatment; but in all toler- ably recent cases the expansion of the lung is one of the main objects of our solicitude, and other methods are therefore preferable. In an em- pyema which proves to be loculated, this plan of treatment is especially suggested, but probably the more modern method of resecting portions of one or two ribs, and with the finger or a sound freely breaking down the adhesions, is far more efficient. The treatment of chronic empyema of old standing is a question of great difficulty, the cases which occur being so various in their nature and ori- gin, and also in their duration and in the degree of expansibility of the lung. They may be divided into— 1. Cases of simple chronic empyema. 2. Cases in which the empyema is secondary to some lung disease, most commonly phthisis. 3. Cases in which the empyema has supervened upon pneumo-thorax. 4. Cases in which the empyema is associated with bronchial fistula or external sinus. It is to be hoped that, as time goes on, and effusions into the pleura are more promptly treated in the acute stages, cases of simple chronic empyema will be less frequently met with. The degree in which the fluid is purulent varies very much. In some cases it is greenish and opalescent, in others opaque and creamy looking. In very few cases of old standing can the pus be regarded as active, the corpuscles being as a rule dead and more or less fattily changed. It is, 86 DISEASES OF THE LUNGS AND PLEUR.E. however, much more difficult to deal with this purulent fluid than with serum, and active suppuration is also more readily set up in a pleura which has already yielded pus. In these old-standing cases, we can no longer hope to gain more than a very partial re-expansion of the compressed lung. Our treatment is directed to secure the removal of the fluid, and obliteration of the pleural cavity, the imperfect expansion of the lung being met by flattening of the chest-wall and enlargement of the opposite lung. Enlargement and increased function of the healthy lung is indeed the final aim of our treatment. These results can only be obtained by prolonged and steady treatment. Two or three successive tappings with the trochar and syphon may be employed, with the object of withdrawing sufficient fluid to induce a negative pressure within the thorax, and thus to encourage expansion of lung, flattening of chest-wall, and encroachment of neighboring organs. In the intervals of the tappings, the chest should be strapped round its. lower part, and a compress applied to the infra-mammary region, the part where flattening first commences. AVe may, by this means, cause the lung at its upper part to contract adhesions to the chest wall, the gradual growth downward of which obliterates inch by inch the pleural cavity. The resonance of the opposite lung meanwhile gradually extends across the sternum, and the heart is drawn over with it. Our degree of success in these cases depends mainly upon their dura- tion. If, after a fair trial, we do not seem to be making further progress, a double opening and the insertion of a drainage tube is one plan left to us. Another is a free incision and complete evacuation of the purulent fluid under the carbolized spray, and the subsequent antiseptic treatment of the wound. A third is the resection of three or four ribs, in conjunc- tion with a free opening, by which means the contraction of the chest wall is facilitated. Professor Marshall has suggested the division sub- cutaneously of the cartilages of some of the ribs with the same view.1 The spot to be chosen for incision in cases of chronic empyema in which the lung is presumably firmly bound down, should be at a higher point than in recent cases, since the cavity will be closed, less perhaps by the descent of the lung than byt the sinking in of the chest Wall, the coming over of the heart and the raising of the diaphragm. Prof. Mar- shall well points out that if a low interspace be chosen the tube will soon be deflected upwards, and interfere with the apposition of the diaphragm and thoracic wall. Should this inconvenience arise at any period of the treatment it will be best to make a second opening higher and allow the lower one to close. I have just sufficiently alluded to the methods of dealing with simple 1 Lancet, March 11th, 1882, p. 381. PLEURITIC EFFUSIONS. 87 chronic empyema, and looking to the great difficulties that are in the way of effecting a cure in these cases, the long illness their treatment involves, and their frequent termination in chronic thoracic fistula, and finally lardaceous degeneration of organs, we may well pause in cases which present no active symptoms, and consider whether they are not best left alone. Each case must be judged of on its own merits, the presence of hectic or of undue pressure upon the heart or the opposite lung being symptoms especially calling for interference. In cases of empyema secondary to lung disease, and especially in those that have resulted from pneumo-thorax, and in which the air has been gradually replaced by fluid, the rules of treatment would be somewhat different from those guiding us in simple chronic empyema. In the first place we should be in no hurry to interfere. One may not infrequently note an amelioration of symptoms, sometimes even a cessation of cough and expectoration in cases of phthisis, in which pneumo-thorax has oc- curred on the side of advanced disease; and in such cases it is well to leave the lung compressed for a while by fluid, to give time for the activity of disease to subside, and for the perforation of the lung to close, which does happen in a fair number of cases. The time probably comes sooner or later when interference is necessary, on account of the supervention either of important pressure signs or of septic phenomena. The point now is to evacuate the pleura without bringing to bear any negative pressure upon the lung, which we desire still to keep collapsed and at rest. A free opening, with irrigation of the pleura, is therefore indicated. In a third class of cases in which we have to deal with an empyema that has burst through the lung, and established a bronchial fistula, free external incision is also to be advocated, but even although the expec- toration be foetid it is well to attempt antiseptic treatment; for the lung may not be materially diseased, and provided the pleura be kept drained, there is good reason to hope that the perforation may granulate and be- come closed, and the lung again expand. Hence it is better, if possible, to get the discharges sweet by efficient drainage and antiseptic measures, rather than by injections; this can in some cases be effected. Cases of local empyema require incision, and, as for more general col- lections, the seat of incision should be as nearly as possible opposite the centre of the empyema. CHAPTEK VI. PNEUMO-THORAX—HYDRO- AND PYO-PNEUMO-THORAX. Pneumo-thorax has since the time of Laennec,1 who first rendered it clinically recognizable, attracted considerable attention, especially amongst French and English writers. Laennec described pneumo-thorax as of three kinds, viz., (1) simple, (2) associated with fluid effusion into the pleura, and (3) with fluid effusion and a fistulous opening communicating with a bronchus. In the first two non-perforative varieties of pneumo- thorax, the gas found in the pleura was, Laennec affirmed, effused there by simple exhalation from the pleura (or the fluid it contained), or it was the product of decomposition. In the third or perforative variety the air gained access to the pleura through the fistulous opening in the lung. In an able article in the Gazette Hebdomadaire for 1864, M. Jaccoud main- tains that there is no sufficient proof of the occurrence of simple pneumo- thorax, and expresses serious doubts as to the occurrence of air ill the pleura at all, save occasionally perhaps from the decomposition of liquid effusion. M. Jaccoud contends that the cases of so-called simple or essential pneumo-thorax, have probably been cases in which minute per- foration of the pleura has occurred, the aperture having soon closed, and, in some instances, the air subsequently undergone absorption. There can be little doubt that M. Jaceoud's criticism is just, and that although in gangrenous and some allied conditions of the lungs or pleurae, some gaseous products of decomposition may collect in the pleural cavity, or the air may, as suggested by Dr. Gairdner, transude through the more or less devitalized membrane, yet such cases are uncommon, and are moreover rendered unworthy of notice beside the gravity of the lesions which have given rise to them. The causes of pneumo-thorax may, therefore, be thus enumerated. (1) Perforation of the pleura by the breaking down of sub-pleural nodules in the course of phthisis. (2) The rupture of air vesicles in emphysema or during great expiratory efforts; the separation of sloughs in gangrene, or the breaking through the pleura of an hydatid cyst or a pulmonary hemorrhage. (3) The discharge of an empyema through the lung or the thoracic wall. (4) Gunshot and other wounds of the thorax. Excluding gunshot wounds, the discharge of empyemata and gangrene of the lung, it is infinitely rare for pneumo-thorax to occur from any other cause than the breaking down of sub-pleural consolidations in phthisis. 1 Traite de 1'Auscultation, t. ii., p. 240 et seq. PNEUMO-THORAX. 89 About five per cent, of cases of phthisis die with pneumo-thorax.1 The constant breaking down of tubercular and pneumonic infiltration in the course of this disease tends, by undermining the pleura and interrupt- ing its vascular supply at certain points, to cause it to soften and to give way during some trifling increase of air pressure from cough or effoi t. The perfoiation may occur at any period of phthisis: even at the very commencement of the disease a small sub-pleural tubercle may soften and break through the pleura, but such an occurrence is much more common in the more advanced stages. In the majority of cases of phthisis, as already pointed out, pleurisy of a dry and adhesive kind accompanies and keeps pace with the progressing lung consolidation. But it may be observed post mortem in some cases which are marked by acuteness of process, and by the pneumonic char- acter of the consolidations, that no adhesion between the pleural surfaces has taken place; each pleural surface, the visceral pleura more especially, being covered by a thin, finely granular, semi-transparent layer of lymph, which may readily be scraped off with the knife, leaving the shining, almost healthy-looking pleura denuded. At certain points of the surface thus affected will be seen opaque yellow spots, some close under the pleura, others more dimly seen through it, varying in size from that of a pin's head to a split bean, on making a vertical section through any of which, we divide a more or less softened caseous nodule, having its centre perhaps already excavated. It is at some one or more of these points that the pleura most commonly gives way. Pneumo-thorax is thus most likely to happen in the more acute pneu- monic forms of phthisis. It is least apt to occur in the more chronic fibroid forms of the disease. In these latter varieties of phthisis, however, the complication is sometimes met with. In some papers on this subject contributed to the Medical Times and Gazette, for January and February, 1869, I pointed out that sinuses, in no respect differing from those one sees extending from chronic abscesses, or carious bone, may sometimes be found extending from old cavities towards the surface. Such sinuses may penetrate both layers of the pleura and open into the subcutaneous cellular tissue of the thoracic wall; or if, as is rarely the case, the pleura be not firmly adherent, a communication with the pleural cavity is es- tablished. In one remarkable case described in the paper referred to, a sinus had opened from an old cavity through the posterior mediastinum into the opposite pleural cavity. When a communication is thus effected between a more or less deep-seated cavity and the pleural surface, the perforation is so oblique or sinuous as to be always practically valvular. Pneumo-thorax occurs somewhat more frequently on the left than on 1 A contribution to the pathology of pneumo-thorax, by Samuel West, M.D., Lancet, vol. i., 1884, p. 791. 90 DISEASES OF THE LUNGS AND PLEUR.E. the right side, although the experience of different authors varies on this point.' The gas effused into the cavity of the pleura approximates in composi- tion to that of expired air. Dr. Davy * found 100 parts to consist of carbonic acid 8 parts, and of nitrogen 92 parts. In five examinations of the gas from a case of pyo-pneumo-thorax at different periods, he found it to vary in composition, the highest proportion of carbonic acid being 16, oxygen 1.5, and nitrogen 82.5, the lowest, carbonic acid 6.0, oxygen 5.5, nitrogen 88.5. Dr. Duncan3 estimated the foetid gas from a case of pneumo-thorax secondary to empyema to contain 26 parts of sulphuretted hydrogen and carbonic acid, and 74 nitrogen. Whether the communication with the pleura be patent or valvular is a matter of some importance as regards both symptoms and treatment. (a) If the opening be direct and patent, there can be no positive air- pressure within the pleura since no air can be pent up there. By means of a trochar fitted by tubing to a water-pressure guage, I have ascertained post mortem the degree of intra-pleural pressure present in 16 cases of pneumo-thorax. In 4 out of these cases the pressure was nil. (b) If the opening be oblique or valvular, although during inspiration air may enter the pleura, yet the moment the air is compressed in expiration the sides. of the oblique opening close, or the tongue of the valve is depressed and the air cannot escape at all, or only with more or less difficulty according to the perfectness of the valve. In 12 cases out of the 16 above mentioned, there was more or less intra-pleural pressure present varying in degree from If inch to 7 inches of water.4 The first effect of perforation of the pleura is effusion of air, and, perhaps, the escape of some purulent fluid from the ruptured lung into the pleural cavity; the second effect is more or less intense pleuritis; and thirdly, if the patient survive, we usually get more or less effusion, generally purulent in character. The principal symptoms of pneumo-thorax are—sudden acute pain m the side, followed, or rather attended, by great dyspnoea and shock. The pulse becomes frequent, feeble, small, the respirations relatively more frequent than the pulse, and the voice feeble or suppressed. There is 1 Louis, eight cases, seven left-sided ; Walshe (collected) eighty-five cases, fifty-five left-sided ; the author, thirty-nine cases, twenty-three left-sided (Dis- eases of Lungs, &c, 1878, pp. 125 and 142); Samuel West, eighty-three cases, forty-two left-sided. Wintrich, Regnaud, Lebert and Weil observe left-sided cases to be twice as frequent as right. Laennec regards the right side as most frequently affected (quoted by Samuel West, Lancet, vol. i., 1884, p. 791). The point is of little practical importance. 2 Philosophical Trans., 1823-24. 3Edin. Med. and Surg. Journ., vol. xxviii., p. 827. 4 Medico-Chir. Trans., vol. lix., 1876, p. 179. PNEUMO-THORAX. 91 occasionally great hyper-sesthesia of the affected side. The position of the patient is frequently changed, he may sit up or recline, with the head raised and an inclination to the sound side, (after fluid effusion to the affected side); the sitting posture with slight inclination forwards, and with the elbows resting upon the knees, is the one most commonly chosen. There, is nothing absolutely characteristic about these symptoms, except, perhaps, the suddenness with which they may supervene. The patient is sometimes conscious of " something having given away," and feels a peculiar trickling, cold sensation, associated with the pain in the affected side. All the symptoms of pneumo-thorax may be most closely simulated in an attack of acute pulmonary congestion supervening upon already advanced disease. On the other hand, there may be an almost entire absence of any special symptoms to mark the onset of the attack. In cases in which the pneumo-thorax supervenes in an advanced stage of the disease, "palpitation" may be the chief complaint of the patient. The physical signs, however, of pneumo-thorax are very positive, and can rarely be mistaken for those of any other disease. The alarmed, anxious and distressed countenance, the evident urgency of the dyspnoea usually amounting to orthopncea, and the small, whispering voice are in themselves, in marked cases, strikingly characteristic. I will enumerate the chief physcial signs, and will dwell only upon those which are most essentially important.—The affected side is enlarged, the shoulder raised, the intercostal spaces effaced, and little or no movement is perceptible with respiration, whilst the opposite side labors with the rapid breathing, its soft parts receding with each inspiration. The heart is displaced towards the sound side, and the abdominal organs are depressed. The percussion note is greatly hyper-resonant or truly tympanitic, where it had perhaps before been dull. Respiratory murmur is either absent, or very feeble; and at one or two points more or less distant amphoric breathing may be heard with metallic whisper and echo on coughing. Pectoriloquy is scarcely ever present. Metallic tinkling may be heard, especially after cough. Vocal fremitus is either absent or much dim- inished. On applying the stethoscope over one point of the area affected, whilst at another point percussion is made, using coins or other hard sub- stances for the purpose, a peculiar ringing sound is heard (bruit dy airain) very characteristic of pneumo-thorax. Later, when effusion of fluid has occurred, there is dullness at the lower, and hyper-resonance at the upper, part of the affected side, the distribution of dullness and resonance shifting with the altered position of the patient. On placing the ear down upon the chest, and giving the patient a somewhat abrupt shake, a splashing sound may be distinctly heard, perfectly characteristic of hydro-pneumo-thorax. This "succus- sion " sign may be observed in cases in which we can find no other evi- dence of the presence of fluid in the pleura. The explanation of this is 92 DISEASES OF THE LUNGS AND PLEURAE. simple enough; the moment pneumo-thorax occurs, the diaphragm on the affected side becomes flaccid and more or less concave, drawn downwards by the weight of the abdominal organs, and in its concavity a certain quantity of fluid may collect without yielding percussion dullness. In cases in which there is a considerable quantity of fluid present, intercostal fluctuation may be made out; or, on sharply percussing immediately below the line of contact of resonance and dullness, a thrill may sometimes be detected by the finger, significant of fluid vibrations. Hyper-resonance, absent, feeble, or amphoric respiration sounds, and displacement of heart are, however, the signs of pneumo-thorax of central importance about which the other signs of less value may be grouped. These three signs alone are sufficient to render the diagnosis certain, and their presence can be ascertained by a physical examination which will not add to the distress of the patient. The degree and extent of the hyper-resonance depend upon the quan- tity and tension of the air that has escaped into the pleural cavity. In some cases adhesions are so strong and extensive as to limit the pneumo- thorax to a small portion only, usually the base, of the pleural cavity. In such cases the symptoms are rarely urgent, and their cause may escape notice. But as a rule the whole lung is collapsed save, perhaps, at the summit, where there are frequently some old adhesions. The hyper- resonance has a drum-like quality which is usually characteristic, but in cases in which the tension of the air is very great, the vibrations of the chest-walJ are less free and the tympanitic note somewhat deadened. The boundaries of hyper-resonance include the sternum, and may extend be- yond it towards the healthy side, and if the left side be affected the normal cardiac dullness is altogether effaced. The character of the breath-sounds varies according to the nature of the opening; over the greater portion of the affected side the respiratory sounds are as a rule annulled, and in those cases in which the opening is small and quite valvular no auscultatory sounds may be detected at any point, although very often, even in these cases, at one spot a faint and distant hollow inspiratory sound may be heard on careful auscultation. In cases, however, in which the opening through the pleura is free, the entry and exit of the air to and from the pleural cavity gives rise to a variety of amphoric breathing, not loud, but peculiarly large and of metallic quality, which can rarely be mistaken. This amphoric breathing is most audible at some one portion of the chest nearest to the seat of perforation; it is commonly best heard at the mammary, or upper or lower scapular region, and is conducted more or less distinctly to a distance from this point. The expiratory portion of the amphoric sound is pecu- liarly indicative of a free and patent opening. In these latter cases, with free opening, the voice sounds may be attended with a metallic echo quite peculiar, whereas in the more valvular cases the voice sounds are not con- PNEUMO-THORAX. 93 ducted at all. Metallic tinkling may sometimes be present and is a use- ful additional sign; a sign, however, which I have heard very typically yielded by large pulmonary cavities* Feeble, and more or less modified breath-sounds may be heard at the apex where there are still adhesions, and, immediately after the occurrence of perforation, friction sounds may sometimes be heard over portions of lung as yet in contact with the thoracic wall. Displacement of the Heart—M. Gaide1 was the first to describe dis- placement of the heart as an important sign of pneumo-thorax. It is indeed a constant and, save in exceptional cases in which the base of the opposite lung is consolidated, an essential sign of perforation of the pleura, and it is singular that it should have escaped the notice of such acute clinical observers as Laennec and Louis. Its occurrence simultaneously with that of the perforation, already noticed but not explained by M. Gaide, is a fact that would of itself cast suspicion upon the usual accept- ance of the sign as being necessarily one of pressure. The cardiac dis- placement may be observed within a few minutes of the perforation, and is due in the first instance to the sudden removal from the mediastinum of the elastic traction of the lung which has collapsed, and the consequent unopposed traction upon it of the other lung. And, if the opposite lung be not solidified, the heart may from this cause alone be carried beyond the median line. Thus, I have recorded two cases, and have seen several others, in which the heart was displaced to the right«of the sternum, yet in which, as proved by experiment post mortem, no intra-thoracic pressure existed.2 Progress.—If the patient survive the dyspnoea and shock of the first attack—and he usually does so, provided the opposite lung be not exten- sively diseased—after the lapse of some thirty-six hours or two days, signs of reaction fever, and hectic, announce the supervention of acute pleuritis and commencing empyema. The cause of the suppurative pleu- ritis which generally follows upon perforation of the lung is, partly the irritation of the air admitted into the pleura, and partly the tearing of adhesions, but the most potent cause is the escape of some of the con- tents of a cavity into the pleural sac. The signs of fluid in the pleura soon become apparent, and in some cases the pleura becomes rapidly filled with fluid, what air remains being compressed into such a small compass at the summit of the thorax as to be very difficult to detect. A large portion of the air in these cases is either absorbed, or as suggested by Dr. Duncan,3 it may be expressed through the opening in the pleura. Dr. Duncan doubts whether the diseased pleura in pneumo-thorax can absorb 1 " Observations de pneumo-thorax." Archives gen. de medicine, t. xvii., 1828. 2 Medical Times and Gazette, Aug. 21, 1869. 3 Ed in. Med. and Surg. Joum. vol. 28, 1827. 94 DISEASES OF THE LUNGS AND PLEURAE. air, but it must be remembered that such absorption is encouraged by the gradual pressure of accumulating fluid. Moreover, the aperture is fre- quently much too low down to permit of expression of any large portion of the air through it. Another effect of the pleurisy is, sometimes, to completely close the original perforation. The case may thus in the course of time be completely transformed from one of pneumo to one of pyo-thorax. In other instances very little effusion takes place and the signs of pneumo-thorax remain marked to the end. Diagnosis.—There can be but little difficulty in distinguishing a case of pneumo-thorax in which the effusion of air is extensive from any other disease. Emphysema is the only other disease in which we get hyper- resonance 2 and enfeebled breathing combined, but emphysema is a disease which affects both lungs; the respiration is never quite suppressed nor of amphoric quality, nor is the heart ever displaced as in pneumo-thorax. The diagnosis is sometimes difficult, indeed impossible, between localized pneumo-thorax and a large, thin-walled pulmonary cavity. Such cavities may yield almost tympanitic resonance, and very typical metallic tinkling rhonchus. Localized pneumo-thorax is most commonly situated, how- ever, at the lower portion of the thorax, and in this situation such a large cavity as could be confounded with pneumo-thorax is of most rare occur- rence, unless it be continuous from the apex downwards, in which case the heart's beat would be felt over an extended area on the affected side. The cases which I have most often seen mistaken for pneumo-thorax, however, have been cases of advanced phthisis, in which acute congestion has rapidly supervened at the base of the comparatively sound lung. Pain limits the movements and lessens the sounds over the newly affected part, there is considerable high-pitched resonance on percussion, and the symp- toms may be precisely those of pneumo-thorax. Breath-sound and rhon- chus can be heard, however, on careful auscultation, the heart is not displaced, nor is the percussion note truly tympanitic. Sometimes at first sight the dyspnoea of asthma nearly resembles that of pneumo-thorax, and, with general hyper-resonance, we may have in asthma an absence of respiration over portions of the chest; but the portions of lung so affected will vary in position, perhaps, even while we are listening, and the general wheezing rales present elsewhere, together with the history of the case and the effect of treatment, will prevent any real difficulty -in diagnosis. _ I have seen more than one case of hysterical dyspncea closely simulating pneumo-thorax, but the expression of countenance cannot be simulated, and a moderately careful physical examination will lead to a right diag- nosis. The diagnosis of hydro or rather of pyo-pneumo-thorax from simple empyema is not difficult, the succussion splash, and the marked 1 The resonance of emphysema also lacks the drum-like note found in pneu-' mo-thorax. PNEUMO-THORAX. 95 shifting of the dullness and resonance with change of position, being quite characteristic of the former disease. But, as already observed, some cases of apparently pure empyema have their origin in perforation of the lung. The diagnosis in pneumo-thorax, however, does not consist merely in separating it from other diseases, but also in distinguishing the kind of perforation that has taken place, and the probable existence, or not, of air-pressure within the thorax. The discovery of amphoric (to and fro) breathing renders it pretty certain that the opening is a free one, admit- ting the ready passage of air both ways, and that consequently no air- pressure is present. The complete absence of all breath-sound, with increasingly urgent dyspnoea, distended side and greatly displaced and oppressed heart, are equally significant of a valvular opening and of increasing intra-thoracic pressure. In a third set of cases hollow inspi- ration and obstructed rhonchoid expiration suggest a partially valvular opening. Prognosis.—In the majority of instances, pneumo-thorax occurs to- wards the close of the disease, when the patient is already dying from ex- tensive pulmonary lesions. Hence it is as a rule of speedily fatal augury. If in less advanced cases it occur on the side already most diseased, pneumo- thorax does not always shorten life. I have indeed seen several cases in which by arresting for a time the activity of the pulmonary lesions, its occurrence has considerably prolonged life. Of thirty-nine cases collected from the post-mortem records of the Brompton Hospital, the greatest dura- tion of life was twelve mouths, four and a half, and four months in three cases respectively. The least duration ten minutes, fifteen minutes and six hours. The mean duration of the thirty-nine cases was about twenty- seven days.1 Cases in which a valvular opening is detected, are by no means neces- sarily the worst for prognosis, provided that they are promptly treated. The condition of the other lung is the point to ascertain in calculating the prognosis; if tolerably sound one may hope for arrest of the pulmon- ary disease and conversion of the case into one of chronic empyema. A tendency to the accumulation of fluid may be generally observed, and it is possible that not a few of the cases of empyema that come before us in which after paracentesis we find evidence of apex disease, the em- pyema has originated in pneumo-thorax; the effect of the pneumo-thorax and subsequent effusion having been to arrest the pulmonary disease. I have met with two or three cases that would be best explained in this way:—In one instance, the patient left the Hospital " cured" after the removal of six pints of a sero-purulent effusion by paracentesis. He had 1 On Consumption, etc. By R. D. Powell. Table of cases of Pneumo-thorax, p. 142. 96 DISEASES OF THE LUNGS AND PLEURAE. presented, however, signs of early (or old ?) disease at the apex of the lung soon after the tapping, and although he resumed his work for a time after leaving the Hospital, he again came under observation twelve months later with pneumo-thorax on that side, and died in three weeks. Treatment.—Life is threatened on the occurrence of pneumo-thorax by shock, asphyxia and exhaustion, and these are special indications for treat- ment. The shock—which is due to the sudden lesion of a vital organ, and to the sudden dislocation and impediment to the action of the heart— must be treated by the administration of a stimulant, but above all things by an opiate. Opium is most valuable in calming the nervous system and in lessening the sense of dyspnoea. It is best given in the form of pill with camphor; in other cases divided doses of chlorodyne, or morphia eubcutaneously may be administered. When the immediate shock has been relieved, the patient must be carefully examined and watched for signs of increasing pressure within the chest, to be treated by the timely introduction of a fine trochar. This trifling operation gives great,- and curiously, sometimes lasting, relief. It can be repeated, however, if nec- essary, or a fine trochar guarded with gold beater's skin may be left in the side. If we bear in mind that the chief way in which positive pres- sure is brought about within the pleura, is by the thoracic wall on the affected side being expanded to the position of extreme inspiration and then recoiling upon the air pent up in the pleura, the advantage in these cases, when the excess of air has been removed, of strapping the affected side so as to control inspiratory movement, becomes obvious. A broad band of strapping firmly applied over the lower ribs, and reaching some two or three inches beyond the median line in front and behind, is suffi- cient to restrain the movement of the affected side. As a rule pneumo-thorax occurs in persons already reduced in flesh and blood by previous illness; if the accident should occur at an earlier period of the disease, the venous engorgement, lividity, and general circulatory distress will be correspondingly marked. In such eases free dry cupping will give great relief. The portal system being the great reservoir for re- tarded blood, an occasional saline aperient is of value in pneumo-thorax, and also serves to correct the constipating effects of opium, the adminis- tration of which latter drug in repeated small doses, is on other grounds. desirable for the first few days. . The intensity of the secondary pleurisy must be moderated by fomen- tations or poultices, and the associated fever, pain, and hectic, treated by occasional doses of quinine and opium, with salines or mineral acid as the case may require. The occurrence of effusion may be regarded rather with satisfaction than otherwise, provided the opposite lung be tolerably sound; some cases of one-sided phthisis have undoubtedly been arrested by the occurrence of pneumo-thorax and consequent empyema, the com- pression of the lung checking all active" disease. Hence we should not be, PNEUMO-THORAX. 97 too hasty to remove the fluid by paracentesis, since, notwithstanding the presence of air, it has little tendency to become offensive, and the dys- pnoea is lessened and the perforation more likely to become closed, by the substitution of steady for elastic compression of the lung. Paracentesis performed too soon, or with too great an anxiety to remove all the fluid, will lead to a recurrence of the pneumo-thorax by re-opening the old per- foration. At a later period paracentesis may be necessary. The frequent administration of food in small quantities with sufficient stimulant to steady but not to excite the heart's action, is needed to pre- vent increased suffering from exhaustion. HvEMO-THORAX. H^emo-thorax, or hemorrhage into the pleural cavity, may result from injury, or be secondary to certain forms of chest disease. When traumatic in origin, the amount of blood poured out varies ac- cording to the vessel injured and the extent of the wound, be it heart, lung, aorta, intercostal or internal mammary artery. Such cases as these belong to the surgeon. The diseases which may be complicated by haemo-thorax are pleurisy (usually secondary to carcinoma or sarcoma), malignant disease of the oesophagus, pleurae or thoracic parietes. It may arise from an apoplexy of the lung breaking through the pleura, or be due to the bursting of an aneurism. The quantity of blood poured out may be just sufficient to impart a ruddy tinge to the fluid effused in an ordinary pleurisy, or so abundant as to fill the pleura and compress the lung. The symptoms of haemo-thorax do not differ from those presented in other cases of pleuritic effusion, except the hemorrhage be profuse, when those indicative of internal hemorrhage are superadded. The physical signs are similarly those of fluid effusion into the pleura. The use of the fine needle syringe or aspirator is needed to make the diagnosis certain. Treatment.—Observing the fluid of an effusion to be blood-stained, one would be unwilling to advise its removal except to an extent sufficient to relieve pressure symptoms. OHAPTEE VII. BRONCHITIS—BRONCHIAL CATARRH. Acute bronchitis is an active catarrhal inflammation of the mucous membrane of some portion of the bronchial tract Etiology.—Bronchitis is a disease especially prevalent in Northern latitudes, in exposed and elevated situations, and in districts where moist- ure of atmosphere as well as a low temperature and cold winds prevail. In our British climate these conditions are but too well fulfilled, and bronchitis is endemic amongst us. January, our coldest month, is that in which it is most prevalent. From the variable temperature and cold winds which characterize our spring weather, bronchitis is then also of common occurrence. In our autumn it is less prevalent, although per- sons with recurrent bronchitis get fresh attacks each year with the com- ing round of the cold weather. The occurrence of bronchitis is influenced by age, sex, occupation and condition of life, chiefly in so far as these circumstances favor exposure to the known exciting causes of the disease, or render the individual less able to resist the action of such causes. From the period of dentition onwards through childhood bronchitis is common. This is to be accounted for partly on grounds of lessened power of resistance, partly, as will be presently pointed out, in consequence of dentition itself, and in part also from the imperfect nasal development, and frequently obstructed nasal passages of children necessitating oral breathing. This abnormal method of breathing not infrequently remains a habit through life, and is a fertile source of chest troubles by the direct manner in which air is thus permitted to enter the bronchi and lungs, unwarmed by the nasal passages. Old people have but feeble powers of resistance to the causes of bron- chitis, and the disease is very prevalent and fatal amongst them. The male sex is more exposed to the causes of bronchitis than the fe- male, and suffers more accordingly. Recurrent bronchial catarrh, associated with asthmatic symptoms, and with more or less emphysema, is well known to be an hereditary affection, and may occur very early in life. The winter bronchitis to which many individuals become subject at certain periods of life is also very markedly hereditary, and is no doubt really a phenomenon of senility. It cannot with these exceptions be said that bronchitis is hereditary. With regard BRONCHITIS. 99 to children my own observations would lead me to the opinion that the predisposition running through families is very often connected rather with the imperfect development of the nasal passages, already alluded to, sometimes also associated with enlarged tonsils, necessitating oral breathing, than due to any inherited delicacy of the bronchial mem- brane. Cachexia of various kinds, gout, syphilis, phthisis, alcoholism, Bright's disease, must be ranked amongst the predisposing causes of bron- chitis. Of all the exciting causes of bronchitis, depression of temperature is the most important. The attack commonly supervenes upon ex- posure to sudden changes of temperature, or to wet, cold winds, especially in depressed conditions of the system, as after being over-heated by exertion, or exhausted by mental fatigue or shock. Dr. Sturges finds, from his careful analysis of the Registrar General's Returns for a series of years, that cold is a far more potent cause of bronchitis than of pneumonia. A large rainfall again, Dr. Sturges observes, increases the mortality from bronchitis, but does not affect the pneumonia rate. Bronchial catarrh is very prevalent in low-lying marshy districts, cold, wet weather with variable winds being most favorable to its occurrence.1 " Catching cold " has been explained by Riegel in accordance with the experiments of Ro- senthal, who found that the superficial vessels of animals exposed to a high temperature became dilated and partially paralyzed. Such animals on being removed to a cold room lose heat rapidly, their temperature be- coming quickly reduced to below the normal by the rapid radiation of heat from the blood coursing through the surface vessels. Whether the cold be "caught" in the head, or in the bronchi or lungs, or in some other internal organ is, in part at least, a matter of constitutional predisposition. As examples of the effects of local applica- tion of cold in determining renal congestion, I mav allude to the following cases:— On the 20th of May, 1882, a youth aged twenty was admitted into Middlesex Hospital under my care with suppression of urine of thirty-six hours' duration, the suppression persisting up to the time of death on the evening of the 25th from uraemic coma. Post mortem, the kidneys pre- sented the intensely injected blood-dripping appearance of acute nephritis. The boy had had scarlet fever when fourteen years of age, but there was no history of any renal complication. He had been for twenty-one months the subject of lymphomatous tumors involving the glands of the right side of the neck and pectoral region. For this intumescence more or less continuous cold had been applied by means of Leiter's tubes for 1 " The Natural History and Relations of Pneumonia," Octavius Sturges,M.D., F.R.C.P., 1876, p. 152. 100 DISEASES OF THE LUNGS AND PLEURAE. five weeks, when the symptoms of suppression presented themselves. I had in my ward at this time another patient, a youth with exophthal- mic goitre for whom I was employing the cold treatment, by means of the same useful apparatus. Frequent examinations of the urine were made, however, and after ten days slight albuminuria appeared, and the treat- ment was immediately suspended. The effect of prolonged chill to the feet in producing tonsillitis, and nasal or bronchial catarrh or pulmonary congestion, according to the nat- ural predisposition of the subject, might be quoted as parallel examples with those related above. The influence of ice applications to the head, in reducing pyrexial temperatures, and the still more certain effects of the cold bath, may be likewise referred to in the same category, but on careful scrutiny of such effects of cold, whether under physiological or pathological conditions, one cannot feel satisfied with the mere blood-cool- ing hypothesis suggested by Rosenthal, but must invoke the more indirect action of the nervous system, to account for the phenomena. Dusty employments lead to chronic catarrh of the proximal air pas- sages, and if long continued, such catarrh may extend more deeply into the lungs. It is very instructive to note, however, how out of those who are exposed to obviously mechanical influences of this kind, many escape unharmed. In noting the history of patients who have been suffering from irritative bronchitis, I have found instances in which the fathers of the patients had passed their lives at the same occupation without com- plaint. Hirt has observed that the inhalation of injurious gases, and even of dust, may after a time fail to excite catarrh, the workmen becoming as it were acclimatized to such conditions.1 The second or third generation seems to become more vulnerable to such given influences. Many a fresh catarrh, in cases of confirmed pulmonary disease, may be traced to dusty winds, or to the irritating fogs which occasionally pre- vail in this metropolis. Blood inhaled to distant bronchial tubes during an attack of haemoptysis, or from hemorrhage during tracheotomy, may set up bronchitis. A very virulent bronchitis, attended with profuse ex- pectoration, is occasioned by the passage of acrid septic matters from foetid pulmonary or pleural cavities over the bronchial surfaces. Acute bronchial catarrh, commonly supervenes upon, or forms a part of, the epidemic disease influenza. Perhaps in this category hay asthma should be included as a specific catarrh, due more distinctly than influenza to the reception of a particulate poison. Many of the specific fevers, measles, whooping cough, enteric fever, small-pox, are attended usually in the early or eruptive periods with bronchial catarrh; the bronchial mucous membrane in measles and small-pox, being often involved in the 1 "Krankheiten der Arbeiter," Breslau, 1873, quoted at length by Rie°-el i Ziemssen's Cyclopoedia, vol. iv., p. 312. BRONCHITIS. 101 exanthematous eruption. During the first dentition some children have repeated attacks of bronchial catarrh, coincident with the eruption of each tooth; just as other children suffer at these times from nasal catarrh, or others again from intestinal catarrh. It may be urged that, during this period, children are frequently the subjects of irregular febrile disturb- ance which renders them more liable to chills, and that this period is usually chosen too for the change from long clothes to naked legs and chest; but for the most part the catarrhal affections prevalent at this age cannot be explained otherwise than as being of reflex nervous origin, and the fact that under the same circumstances we may get convulsions in the place of either of the above occurrences, is strongly confirmatory of the truth of this view. Certain heart diseases, mitral regurgitation, and in a still greater de- gree mitral stenosis (a disease, I am persuaded, often congenital,) predis- pose to bronchial catarrh by obstructing the return of blood from the lungs, thus causing mechanical congestion of these organs and of the small bronchi. Finally, it is very important to remember that one attack of bronchitis predisposes to future attacks. The morbid appearances of acute catarrh are but rarely to be observed post mortem, but they may sometimes be seen in perfection in the trachea by means of the laryngoscope during life. (1) In the first stage there is hyperaemia of the mucous membrane with oedema of the basement layer. Upon hyperaemic swelling of the mucous follicles in part depends the temporary check to secretion, and probably the ducts of the follicles are also for a time occluded by the swollen condition of the membrane they traverse. In this stage the affected membrane is minutely injected, swollen, and unduly lacerable, present- ing in some severe cases, especially in young children, minute hemor- rhages. (2) The mucous flow is soon increased, however, and is mingled with sanious exudation from the basement layer, and sheddings of columnar epithelium, and of mucous cells derived from multiplication of the deeper cells of the epithelial layer. Thus is constituted the muco-purulent " secretion," of bronchitis, thin and glairy at first, thicker and more opaque after a few days. To the naked eye the appearance of the mucous mem- brane is more slaty in hue, covered with secretion, sanious or thick, ac- cording to the stages referred to. (3) The tissues of the bronchial tubes beneath the basement mem- brane do not remain passive whilst these active processes are going on in the layers above them. The connective tissue cells multiply, and the endothelium of the lymphatic spaces of inner and outer fibrous* layer pro- liferates; the products of such proliferation do not, however, find their way to the surface, being unable to penetrate the basement membrane, but collect in the interstices of the cellular tissue, and fill up the lymph 102 DISEASES OF THE LUNGS AND PLEURAE. paths along which they slowly course towards the sub-pleural lym- phatics. 1 By these processes, thickening of the bronchial membrane is effected, together with that thickening of lung texture spreading from the bron- chial sheaths, which forms a part of the pathology of hypertrophous em- physema. Acute bronchitis may be conveniently divided according to Walshe into:— (a) Bronchitis of the larger and medium sized tubes. (b) General and capillary bronchitis. To these should be added— (c) The acute asthenic bronchitis of the young and aged. a. The symptoms of acute catarrh affecting the large bronchial tubes are commonly, in the first instance, those of an ordinary cold in the head; chills of a creeping character, never amounting to a rigor, occur from time to time on the first day, and are attended with a feeling of malaise, a somewhat hurried pulse, slight soreness of the throat, sneezing, and coryza. The temperature is raised a degree or so above the normal, but although there is thirst, aching, perhaps pains in the limbs, and a consid- erable sense of feverishness, the febrile phenomena are really very slight in adults, more decided in young children. After some twenty-four or forty- eight hours the patient complains of a soreness, or rawness as it is usually more accurately described, felt behind the upper sternum, accompanied by a sense of constriction or oppression in this region. The cough is fre- quent, dry, and is attended with more or less pain of a rending character. The voice is deepened and sometimes husky or suppressed, and the breath- ing is perceptibly quickened. On the second or third day secretion takes place, and with the expectoration of a thin aerated mucus the patient soon experiences a marked sense of relief. In fact the pyrexial stage has already passed, the pulse is quiet, the cough loose, and expectoration easy, the mucus expelled becoming more opaque and semi-purulent. The secretion subsides, and the cough gradually lessens, and usually disap- pears in a week or ten days, but in the morning, after his first sleep,- the patient still feels some oppression in the chest, and is not relieved until he has brought up some purulent mucus. As regards physical signs we may hear a few dry, sonorous rhonchi vibrating through the chest, obviously produced in the larger tubes; and if only the largest bronchi be affected, no rales of any kind are heard. When the secretion is more established the rhonchi are looser, modified or for the moment removed by cough, and accompanied, especially over the base of the lungs, by scattered, muffled, bubbling rales. The per- cussion over the chest is unaltered, and the rales are symmetrically dis- 1 Hamilton. "Pathology of Bronchitis," p. 33, et. seq. Dr. Hamilton goes very minutely into this important part of the pathology of bronchitis. BRONCHITIS 103 tributed over the two sides, but more abundant over the bases of the lungs. b. When the acute catarrh affects the smaller and capillary bronchial tubes the dyspnoea becomes marked, with lividity of lips and an anxious, distressed expression of face, the nares expanding with each respiration. In feeble and old people, there may be considerable systemic shock with general prostration, reduced temperature, and rapid, feeble pulse. In more robust persons the febrile action is at first decided, although the temperature rarely mounts above 101° or 102°; the pulse is full and not very quick, between 80 and 100 in the minute, the respirations being rapid out of proportion to the pulse. The cough is frequent, and is very soon accompanied by the expectoration of a viscid adhesive mucus, diffi- cult to get rid of. The digestive functions are impaired, the tongue furred, the bowels usually confined, and the urine loaded with lithates. On inspecting the chest, the thoracic movements are observed to be increased both in frequency and depth, the diaphragm partaking but little in the respiratory efforts. The explanation of this is soon found, for it is with the front and upper parts of the lungs that the patient is principally breathing. The resonance on percussion is everywhere unimpaired, it may be even increased. Fine bubbling rales are audible over both posterior bases: to a much less extent, or not at all over the upper and anterior por- tion of the chest, where, however, sibilant and sonorous rhonchi prevail. This distribution of the rales in bronchitis is mainly a question of gravi- tation. Dr. Walshe has well observed that even in bronchitis of mild type and not involving the capillary tubes, we may still get fine bubbling rales at the posterior bases from gravitation of the secretion to the minute tubes. The diagnosis of bronchitis of this degree depends upon the symmet- rical distribution of fine bubbling rales not associated with any percussion dullness, or bronchial quality of breath-sound, and with but a moderate rise of temperature. The diseases which may be confounded with it, are pulmonary oedema, tuberculosis and acute phthisis. If oedema be limited to the lungs, how- ever, it must be dependent upon cardiac defect, the history and signs of which must be looked for. Tuberculosis is the disease most readily to be mistaken for bronchitis, for the signs of acute pulmonary tuberculosis are almost identical with those of capillary bronchitis. If the tuberculosis of the lungs be only a part of a general distribution of tubercle, the special adynamic symptoms of that disease will be apparent. When restricted, or mainly so, to the lungs, the excessive dyspnoea and great prostration occurring in a patient in early adult or middle life are suspicious signs. The temperature may not help us at all, for in some cases of pulmonary tuberculosis it is not high. But, if present, a high temperature, especially when accompanied by profuse sweatings, always means something more than simple bronchitis. The distribution of physical signs is, however, 104 DISEASES OF THE LUNGS AND PLEURAE. in tuberculosis somewhat different, and their characters are not quite the same. With urgent dyspnoea we may have comparatively few moist sounds, and these are quite as marked at the apex as at the base, and sometimes more so. There may be at one apex some evidence of previous pulmonary disease. With only scattered sonorous or sibilant rales over the chest, or these accompanied with a short inspiratory crepitus, we have, in tuberculosis, quite a disproportionate amount of dyspnoea, with marked recession of soft parts. The history of attack and other features of the case, however, exclude asthma. Acute phthisis cannot, after attentive auscultation and percussion,well be confounded with bronchitis. More or less pneumonic crepitation,with patchy tubular breathing and larger clicks, are superadded to the catarrhal bronchial rales, and the signs are distinctly more advanced at some one portion of the chest, whether this be the apex or base. The fever again is characteristically high and remittent. c. Acute asthenic bronchitis (suffocative catarrh) is a malady com- monly met with at both extremes of life, and in the aged, especially, it is one of the most fatal of diseases. A fairly typical example may be thus related in illustration of the salient features of the disease. Mrs. M., a widow, aged 76, of thin, spare build and of previous good health, was dining out with friends on the evening of December 27th, feeling in her usual good health and spirits. She had never before suf- fered from any chest illness, but, it was believed, that on her way home she became chilled. Mrs. M. appeared, however, well the following morning, but towards the latter part of the day (28th) felt drowsy and somewhat chilly; she became more obviously ill in the course of the even- ing, the breathing being quickened and oppressed, and towards midnight her symptoms became so aggravated that the doctor was sent for. Mrs. M. was now found to be in a state of profound collapse with small, feeble pulse, cold extremities, low temperature and sweating surface. The res- pirations were quick and shallow, the countenance anxious, with some lividity of mucous membranes. No morbid sounds save a few wheezing rhonchi were to be heard over the chest. A free recourse to brandy and other stimulating remedies rallied the patient so notably, that the friends became hopeful, and the doctor plied his remedies and planned out food, physic and stimulants with a cheery exactness. By mid-day or evening the chest signs had become more marked, short inspirations being followed by prolonged wheezing expira- tions, the pulse keeping steady at about 90 beats a minute. The cough and expectoration were now troublesome and difficult, preventing, as the night advanced, more than brief snatches of sleep. The body temperature rose to about 100°, and it was observed that the patient wandered in slight delirium, from which, however, she could readily rouse herself. Fine, bubbling rales were now, at the close of the second or third day, BRONCHITIS. 105 audible over the chest, most abundantly and most definedly at the pos- terior bases, where but very little air could be heard to penetrate. The respiratory movements were peculiar. The chest lifted quickly by the action of the superior auxiliary muscles, whilst the bases of the thorax receded. The long wheezing expiration which followed was apparently produced by the downward recoil of the chest upon the diaphragm pushed upwards to meet it by the contraction of the abdominal muscles. Tracheal rattles soon became developed, removable at first temporarily by cough, but soon to return. The pulse quickened, the patient became more exhausted, with muttering delirium or incoherence, and death closed the scene at about the 70th hour. Such is a sketch of the phenomena presented by a typical case of this fatal malady, the characteristic features being, (1) the first shock of the disease, causing almost fatal collapse at about the twelfth hour of attack; (2) the rallying of the patient, and the oncoming of the signs of general bronchitis, attended with slight febrile reaction; (3) at about the third day the appearance of signs (labored ineffectual thoracico-abdominal movements, with filling of lower bronchi) of bronchial paralysis and of the circulation of venous blood through the nerve-centres. No doubt this later circumstance accounts for the forcible respiratory efforts, far beyond the strength of the patient, that come on at this third fatal period, and continue to the very end. It is rare, indeed, for recovery to ensue in any case in which this character of breathing has once been observed. Young children not unfrequently succumb to the first shock of bron- chitis, being overwhelmed before their illness seriously attracts the at- tention of their parents. A considerable proportion of the infants brought to our hospitals dead, or in a dying condition from sudden illness, are found post mortem, to present no other lesions beyond the signs, very slightly marked, of early bronchitis. A few petechial spots in the medi- astinum, pericardium or pleura, may testify to the brief struggle of the little patients. The prognosis in bronchitis of whatever degree, is, in adults, generally speaking, favorable. Capillary bronchitis in very young and in old peo- ple is, on the other hand, very frequently fatal, yet there is perhaps no disease whose mortality is more influenced by treatment than that we are now speaking of. Taking the capillary bronchitis in the adult as our type in regard to treatment, the first thing to be seen to is the warmth of the room; a fire and a steam-kettle are the first things to procure, so as to raise the tem- perature of the room to between 65° and 67° F., and immense relief is given to the patient by this means alone. Due care must be taken, how- ever, to ensure a proper supply of air as well as to preserve a uniform temperature. The use of the steam-kettle is not only to moisten the air of the room, but in most bed-rooms it is the only possible means of rais- 106 DISEASES OF THE LUNGS AND PLEURiE. ing and maintaining the temperature at the desired height. A large mustard or mustard and linseed poultice should be applied to the front of the chest, or to the back, and followed up by hot linseed applications or cotton-wool to the chest. In children a jacket poultice is often very useful, but one must not forget that both in young or weakly children, and in old people, a linseed poultice wrapped round the chest may be a very serious impediment to free thoracic movements, and in such cases it is often more judicious to have recourse to cotton-wool covered with oil silk and an occasional mustard, or mustard and linseed poultice, to keep the blood determined to the surface. As regards drugs, a saline mixture with ipecacuanha is the best to be- gin with. In strong adults antimony wine is very useful, especially in the dry stage of the catarrh, and should be given in small doses at fre- quent intervals. In old people, on the other hand, we must usually add ammonia to our prescription. The special danger in infants arises from the possible occurrence of pulmonary collapse and secondary broncho- pneumonia. The collapse arises from want of power of expectorating, and the resulting broncho-pneumonia is just as mechanical in its origin, being dependent upon the determination of blood, during the thoracic efforts at expansion, to those parts of the lung which cannot expand on account of their bronchi being plugged. The timely administration of ipecacuanha emetics, if the secretion be abundant, will avert this danger. Friction, with stimulating liniments, such as the ammonia or acetic tur- pentine liniments of the Pharmacopoeia, if necessary further diluted, is of great service in young children after the first stage has passed. In old people danger arises principally from exhaustion or paralysis of the bronchial tubes, the latter, perhaps, being but another evidence of exhaustion. To avert these dangers, we must, from the first, support the patient by the frequent administration of nutritious liquids, and by the timely employment of stimulants in carefully regulated doses. Of all alcoholic stimlants, brandy is certainly the best for this purpose. The administration of opiate remedies in bronchitis should, as a rule, bo avoided, and absolutely so in cases in which lividity of lips shows already defective aeration of blood. In young children and old people opium must be used for bronchitis with the utmost caution. As a sedative at night, bromide of ammonia with aromatic spirits of ammonia is one of the best we can choose. Chloral is not very suitable in acute cases, but a small dose combined with bromide of ammonia will suffice to give rest without risk of depressing the heart's action too much. When the heart fails, and symptoms of over-loading of the right ventricle present them- selves, digitalis may be usefully given, stimulants persevered with, and dry cupping may be tried with advantage. In a few cases, I have cer- tainly seen good results from the substitution of belladonna for digitalis. In certain cases, in which there is marked venous plethora, with a weak BRONCHITIS. 107 and failing heart's action, from an over-burdened right ventricle, venesec- tion is attended with manifest relief. Next to avoiding a fatal issue, our efforts should be directed to pre- venting the case going on to chronic bronchitis, especially in those who have had previous attacks. When the acute stage is past, some patients at once convalesce without any special treatment. In other cases the se- cretion continues abundant and more purulent. The saline mixture must now be given less frequently, or changed for a more stimulating expector- ant containing senega and ammonia, and some mineral acid with calumba or quinine, ordered to be taken twice a day. The turpentine acetic lini- ment is of great value in this stage, its usefulness being partly, I suspect, due to inhalation of turpentine vapor. In chronic cases, with profuse muco-purulent expectoration, much ad- vantage is gained by the use of tar, which may be taken in the form of pills (British Pharmacopoeia) or in Guyot's or Jozeau's capsules. The resinous preparations are also sometimes useful in this stage. In many cases it is best, however, to leave the bronchial mucous membrane »alone, and to direct treatment towards improving digestion and appetite. In all cases of secondary bronchitis we must direct our treatment with due regard to the removal or amelioration of the more general disease which underlies the bronchial affection. Cases of secondary bronchitis are, as a rule, chronic, with acute exacerbations. With bronchitis secondary to gout or kidney disease, to alcoholism, to heart disease, and to already existing diseases of the lungs, I will not further deal. The affection of the bronchial mucous membrane is, in such cases, most commonly a part of a much wider affection. It is the primary disease that we should especially treat, and to direct too much attention to the pulmonary condition would apparently sanction an erro- neous view of such cases. Dust Bronchitis.—In certain cases of exposure to dusty employments, the whole effect of the irritant falls upon the bronchi. Habitual cough with recurring bronchitis and subsequent emphysema, paroxysms of asthma, etc., are the leading phenomena in these cases, and are commonly met with amongst potters, miners, flax-dressers, millers, plasterers, ma- sons and others. The following case is not an unusual one of bronchitis and asthma induced by the inhalation of dust. William C----, aged 38, residing in London, admitted into the Brompton Hospital under my care January 23rd, 1877. # Patient was a man of temperate habits, married, one child living: his wife had had one miscarriage, but there was no history of syphilis. He had been for twenty years employed as a fret-cutter. Four years previous to admission, he had had an attack of bronchitis, and since that time he had suffered constantly from cough, with suffocative attacks nearly every night. 108 DISEASES OF THE LUNGS AND PLEURAE. Patient had never had haemoptysis but had lost flesh considerably. His father died of rheumatic gout, and his mother of dropsy. There was no phthisis in the family. On admission, patient complained of cough, which became worse and was attended with severe attacks of dyspnoea at night. Expectoration moderate. Occasional night-sweats. Appetite poor, bowels constipated. He was a tall and fairly well-built man, with a somewhat suffused countenance and breathless look. The chest was well formed, but expan- sion with inspiration impaired. Right semi-circumference, an inch and a half above the nipple level, 15£ inches, left 15f inches. Right ditto, two inches below nipple level, 16 inches, left 16^ inches. Percussion note over the front of the chest was hyper-resonant, the resonance ex- tending on the right side a hand's breadth beloAv the nipple, on the left side, over the normal area of heart's dullness, and interiorly to the costal margin. Diffused sibilant rales were audible front and back, and at the posterior bases some mucous rales were heard. At the time of my visit on the" 26th of January, the patient had been in Hospital three days, and was suffering, as before admission, from nightly attacks of dyspnoea, and from troublesome cough. He was on the ordinary full diet of the Hos- pital. The Mistura Potassii Iodidi cum Stramonio of the Hospital Phar- macopoeia, containing three grains of iodide of potassium, ^ gr. of extract of stramonium to each dose, was now ordered to be taken at 12 noon, 4 p. m., 8 p.m., and 12 midnight, the diet remaining the same, and from the next night he had no serious dyspnoea. On January 31st, a note is entered. " Patient feels much better, and dyspnoea almost gone, cough easier." February 3rd, "has not felt suffocating sensation for the last six nights." He continued the mixture, however, for a month, and then took it in half doses for another fortnight. On February 8th, respira- tions were free and unaccompanied by rale, and by the end of the month the cough had disappeared. March 1st. Right semi-circumference above nipple, 15£ in., left, 15£. Right semi-circumference below nipple 16-J, left 16^. Expansion above nipple level, ordinary inspiration £ inch; deep inspi- ration 1£ to 1-J inch. Below nipple level no movements on ordinary in- spiration, one inch expansion on deep inspiration. Weight on admission, 8st. 91bs.; on leaving Hospital, 9st. 2 lbs. Unfortunately I did not, in this case, measure the mobility of the chest on admission. But my observation of " expansion with inspiration impaired " refers to total mobility of chest, and the circumferential meas- urements at that date may be taken as those of a chest fixed by the em- physematous condition of the lungs. The later measurements, however which were similarly taken in the position of repose are almost identically the same; but at this period the mobility of the chest, its capability not only of expansion but also of contraction, was nearly equal to that of BRONCHITIS. 109 health, and bore valuable testimony to the recovery of the lungs in vital capacity, a point not to be estimated by reference to chest expansion alone. Again, it may be observed in this case as in many others, that mere rest from his dusty occupation did not suffice for the patient's recovery; although doubtless had he remained in pure air a sufficient length of time, he might have recovered without treatment. His attacks had the parox- ysmal character peculiar to asthma, coming on towards the small hours of the morning, i.e., after a certain period of repose, whilst the breath - lessness and cough of the bronchitis and attendant emphysema were con- stant through the day. The effect of the stramonium and iodide of potassium mixture was very striking and immediate. Having regard to the period at which the dyspnoea became distressing, the mixture, was so ordered that by midnight he had taken in the course of twelve hours a grain of stramonium extract, and twelve grains of the iodide. To which of these two drugs, both active in the relief of asthma, the amelioration of symptoms was due I am unable confidently to say. The mixture was not prescribed experimentally, but as a well-tried and trusted remedy in similar cases. The mechanism of the dyspnoea, however, was pretty obvious; the man had an unduly secreting, and probably a somewhat thickened, bron- chial tract, with great irritability of the bronchial muscular apparatus, and constant tendency to spasm of the tubes. At a certain time after repose, secretion would accumulate and give rise to spasm. The hyper- sensitiveness upon which the bronchial spasm depended was at once les- sened by the stramonium, whilst the iodide had a more permanently alterative action upon the mucous membrane and its secretion. This ex- planation would be perhaps generally accepted, but abundant experience with regard to iodide of potassium assures me that it alone frequently suffices very rapidly to relieve asthma. In what way the drug does this is, so far as I know, entirely unexplained. The patient left the Hospital well, but after a time, failing to find other work, was reduced to the necessity of recommencing his old employment, and soon had a return of all the old symptoms for which he was treated elsewhere by ordinary remedies (ether and expectorants) without avail. In the trade of fret-cutting the operator has constantly, with his mouth, to blow away the fine wood dust that collects upon his work, and thus necessarily inhales much of the dust. The patient above referred to, stated that he could distinguish by the taste the different kinds of wood, and he found rosewood (the taste of which he compared to cayenne pepper) to be the most irritating. Walnut wood iras more astringent and bitter, but less irritating. I have since seen this patient in fairly good health, having for some time abandoned his former work. There does not seem to be any reason, however, why a respirator perforated with a 110 DISEASES OF THE LUNGS AND PLEURAE. tube, should not be so adapted as to enable such patients to carry on their occupations without injury to health. Plastic Bronchitis. Apart from croup and diphtheritic conditions, plastic exudation into the bronchial tubes is of rare occurrence. It is said to be more common in females than in males. It may occur at any age from infancy to advanced life, and is not nec- essarily associated with any obvious derangement of the general health. Pathology.—The morbid lesions resulting in the production of fib- rinous casts of the bronchial tubes are:—1. Inflammation of the bronchial membrane in hyperinotic subjects. 2. Hemorrhage into the bronchial tubes. The casts are found in the smaller and medium, rarely in the larger, tubes, and never extend to the trachea. They are fibrinous in character, usually laminated, solid or tubular, and often speckled with blood. Symptoms.—Troublesome straining cough coming on in paroxysms, with great dyspnoea, also of a paroxysmal character, and the expectoration of gelatino-fibrinous looking masses which, on floating out in water, are found to present moulds of the bronchial tubes, constitute the essential symptoms of plastic bronchitis; and, until the latter phenomena of actual expectoration of casts is presented, there is nothing that can be said to be truly characteristic, in the symptoms of this malady. The bronchial casts are expectorated frequently in small pieces, Avith the interposition occasionally of larger and more characteristic moulds. The smaller frag- ments clothed in mucus may readily escape observation (Walshe). Haemoptysis in streaks may occur, or a decided haemoptysis may precede the appearance of the casts. A noticeable feature of the disease, in most cases, is its chronicity, or, rather, the long period, weeks, months, or even years, during which the patient may suffer recurrences of the plastic attacks; each attack being attended with the symptoms above described. A mild degree of pyrexia may be associated with each attack. Physical Signs.—The signs of this malady are very indefinite, being those of bronchitis affecting one base, or of broncho-pneumonia. In some cases a certain degree of dullness, with very feeble respiration, may be present. It cannot be said that there are any physical signs proper to this malady. Prognosis.—As a rule these patients recover, but the disease may ul- timately terminate in phthisis, or any particular attack may proceed to broncho-pneumonia. Treatment.—The treatment of this disease is that of bronchitis, salines and alkalies being indicated, and hot moist inhalations calculated to give relief. CHAPTER VIII. ON PULMONARY VESICULAR EMPHYSEMA. Pulmonary vesicular emphysema may be defined as a dilatation of the air-cells of the lungs with antecedent or associated atrophic changes, or, more briefly still, as a dilatation of the lung proper with textural atrophy. This disease may in its acute form affect persons of any age; in its chronic and more permanent form it affects, most commonly, persons in middle or advanced middle life. Atrophous or senile emphysema, which scarcely merits consideration as a variety of the disease, affects only aged people, and is indeed but a part of the senile state. Pathology.—The perfectness of the function of respiration consists quite as much in the power of contracting as in that of filling the chest, and it is this power of contracting the chest that is lost in emphysema. The lungs having lost their reserve elasticity, no longer tend further to contract at the completion of expiration: nay, expiration is never com- pleted, the thoracic parietes and diaphragm instead of being drawn in- wards by the traction of the lungs recoil simply to their position of repose, and oppose their dead wreight to the inspiratory muscles instead of aiding the action of these muscles by their elastic rebound. Hence in extreme emphysema the inspiratory act, commencing at the point where in health calm inspiration would end, has to overcome, (1) what remains of the elastic resistance of the lungs, (2) the inertia of the parietes, and (3) the elastic resistance of the parietes: instead of, as in health, having to deal with the elastic resistance of the lungs alone, and being in this work aided by the outward spring of the ribs. (See p. 6). Consequently, in marked cases the breathing is always forced and more or less difficult. Let me now briefly recount the conditions present in emphysema, making such addi- tional comments as seem called for. (1) The lungs in all cases of emphysema are permanently expanded to about the position of ordinary inspiration, their elasticity being, so to speak, relaxed to this point. The individual air-cells are correspondingly enlarged and the pulmonary vascular system lengthened. The enlargement of the air-cells commences, as pointed out by Rind- fleisch,1 in the central infundibular cavities which, normally about one- third larger than the alveoli opening into them, become proportionately 'Pathological Histology, vol. ii., p. 7. (New Syd. Soc. Edition). 112 DISEASES OF THE LUNGS AND PLEURAE. much larger. The alveoli themselves next enlarge, their septa become withered, and the lung conformation is thus simplified. (2) The texture of the lung is impaired more or less. In acute emphysema loss of tone from repeated over-distension, e.g., during paroxysms of coughing, is the chief defect present, and, in young persons especially, is speedily recovered from. In cases of long-standing emphysema, resulting from repeated attacks of asthma or bronchitis, what may be regarded as the second stage of the disease is entered upon; the nutrition of the lung suffers, many of the small vessels become obliterated, withering backwards from their capil- laries, the alveoli atrophy, the partitions between adjacent infundibula or alveolar spaces become thinned and finally give way, and the spaces here and there coalesce to form blebs or small cavitations, with thread-like remnants of vessels crossing them, resembling in miniature the trabeculae of tubercular cavities. Where the disease has resulted from oft recurrent catarrhs, commonly with a history of a distinct attack of bronchitis at the commencement, ill-developed fibrous tissue, the result of repeated and long-continued congestion, toughens the lung texture, assists in impair- ing elasticity, and partakes in the subsequent degeneration. In cases of constitutional or hereditary origin, the atrophic changes originating in fatty degeneration of the epithelium and vessels of the lungs, precede or accompany the catarrhal phenomena. This impairment of the texture of the lung renders any dilatation, however induced, more or less permanent. In these cases of primarily impaired lung texture, en- largement of the chest to the limits of thoracic resilience takes place quite insidiously, and the chest thus assumes permanently, by imperceptible degrees, the position of moderate inspiration. It must not be forgotten, too, that the ribs themselves, and especially their cartilages, often prema- turely undergo textural changes of a degenerative kind, the result of which is an increased rigidity and a straightening of the rib arch, and thus an enlargement of the thorax. The chief results of the above pathological processes are loss of elas- ticity of lung and obliteration of vessels, the latter result being in part. due to primary atrophic changes in the capillaries extending back to larger vessels, in part to secondary atrophic changes from narrowing of the blood-current as the vessels become lengthened, thus causing them to wither from deprivation of proper blood-supply. (3) In consequence of the relaxed elasticity of the enlarged lungs they no longer exercise any traction upon the mediastinum except during in- spiration. Hence an important, because constant, aid to the return of blood to the heart is lost. Many authors go further than this, and hold that the large lungs in emphysema are, so to speak, pent up in the chest, and exercise pressure upon the heart between them, and upon the ribs and diaphragm which PULMONARY VESICULAR EMPHYSEMA. 113 enclose them. A little reflection and clinical observation will, however, render it clear to anyone that this supposed pressure of the lungs upon the surrounding parts is, if not impossible, of infinitely rare occurrence and minute degree. The enlarged thorax, flattened diaphragm, and lowered heart, are all phenomena due to defective recoil of the lungs, not to their forcible distension: and are to be observed in health on the lungs being inflated during deep inspiration, which position is retained in em- physema. (4) In addition to the negative impediment to the circulation referred to in the preceding proposition, there is a positive impediment in the stretched, and in part obliterated, capillaries of the lungs. (5) In consequence of the two last-mentioned conditions the venous system is over-full and the over-worked right heart thickens. The in- creased power of right ventricle at length becomes, however, inadequate to contend against the ever present, and from time to time (during bron- chitis or asthma) increased, resistance to the pulmonary circulation. The whole venous system becomes engorged, especially the hepatic and portal systems; the circulation is carried on at a heightened pressure, venous hemorrhages occur, and oedema, commencing at the legs, sooner or later sets in. (6) Another effect of the relaxed state of the lung as regards elasticity in emphysema, is to interfere with that condition of permanent patency, in which the small bronchi are normally held by the constant traction upon them of the elastic lung from all sides. In emphysema this traction becomes, in expiration at first, entirely neutralized, and in marked cases collapse of the bronchioles must occur during expiration, thus accounting for the labored and obstructed character of that portion of the respiratory act. (7) Compensatory changes in emphysema.—Amongst the consequences of emphysema those which are of the nature of compensation must not be forgotten. So ready are the adaptations of our economy to altered circumstances, that it may be said that emphysema alone does not kill. (a) As the capillaries become partially obliterated, fresh communications are opened up between the neighboring vessels corresponding to them, by the formation of fresh anastomotic loops, or by the widening of commun- ications already existing. The pulmonary and systemic veins communi- cate normally on the walls of the smaller bronchi. With the formation of pleuritic adhesions, so common in this disease, new loops of vessels connect the pulmonary with the systemic circulation, and along the in- sertion of the diaphragm especially, and margins of the sternum, fringes of enlarged vessels mark the connection between the two circulations. Thus, in some measure the pressure of the pulmonary circulation is eased. (b) The hypertrophy of the right ventricle of the heart above alluded to, is up to a certain point of a strictly compensatory nature, serving to over- 8 114 DISEASES OF THE LUNGS AND PLEURAE. come by increased power the increasing impediment to the pulmonary circulation. Thus, for a time at least, equilibrium is maintained, to be disbalanced again and again, however, in most cases by intercurrent at- tacks of bronchitis or other cause of over-strain, until at last the limits of compensatory recuperation are passed. Etiology.—When we come to inquire how this over-expansion of the air-vesicles is produced, we are met by various explanations, none of which alone is sufficient to explain all cases. Sir William Jenner has shown that expiratory effort—during straining or coughing, particularly the latter—is an efficient cause of general emphysema, those portions of lung which are least supported, viz., the apices and anterior margins, and also the parts corresponding with the comparatively yielding intercostal spaces, becoming first affected. But with the production of emphysema in these portions of the lungs a shifting of the relationship between the lung and the thoracic surface takes place, and parts which were originally in apposition with the ribs come to be opposed to interspaces, and in their turn yield before the distending force of air pent up and compressed dur- ing cough.1 Again, in the production of local emphysema, inspiratory pressure is undoubtedly an important agent. Thus, if one lung be dis- abled or bound down by some inflammatory process (as old pleurisy or chronic pneumonia) the other lung perforce becomes more capacious; whether this extra capacity shall be derived from true hypertrophy or mere dilatation (emphysema) depends upon the nutritive vigor of the pa- tient. During bronchitis certain of the air-tubes may become occluded by mucus, and the inspiratory force then operates as a distending power upon the remaining portions of the lung until the deficiency in air-space is com- pensated for. Professor Rindfleisch, who adopts Dr. Gairdner's inspira- tory theory in regard to the production of emphysema, further holds that " during the antecedent bronchitis, first one, then, another bronchial tube is plugged with secretion, and so first one, then another segment of the lung is subjected to an abnormal degree of (inspiratory) distension."2 In the histories of the majority of cases of pulmonary emphysema, however, facts are wanting which would justify our accepting the inspira- tory cause as effective in their production. When secondary to repeated attacks of bronchitis, the tussive expiration is a much more powerful cause of over-distension of lung than any inspiratory efforts (short of that 'Sir William Jenner (Reynold's Syst. of Med., vol. hi., p.* 478) refers to Men- delssohn as having in a paper, Der Mechanismus der Respiration und Circula- tion, in 1845, anticipated him in this view respecting emphysema. The author- ship and advocacy of the view in this country rests, however, with Sir W. Jenner. * Manual of Pathological Histology, vol. ii., p. 6. (New Syd. Soc. Edit.) In an interesting paper read before the Belfast meeting of the British Medical Association, Dr. McVail of Glasgow also advocates the inspiratory theory of em- physema. Brit. Med. Jour., Nov. 15, 1884. PULMONARY vesicular emphysema. 115 prolonged and urgent dyspnoea, which is not met with in these cases) could be. Moreover, both the expiratory and inspiratory theories imply the presence of some pre-existing bronchitis, or some local lesion dis- abling a portion of the lung, or the pursuance of some occupations re- quiring repeated efforts, during which the glottis is closed and the chest compressed, all of which are wanting in a considerable proportion of cases. In truth, the emphysema frequently precedes the bronchial affection, although it is subsequently aggravated by the first attack of bronchitis; and, admitting with Drs. Jackson,1 Greenhow," AYaters3 and others, that a failure of nutrition is in a large proportion of cases the predisposing , cause of emphysema, we need go but little further to explain the occur- rence of that disease in its earlier grades. The effect of damaged textural nutrition of the lungs is to relax them by impairing their elasticity, and, as I have elsewhere shown, the thoracic elasticity or resilience tends to expand the chest to the degree of from one to four millimeters in each direction. As the lungs relax their elasticity, they yield to this traction exercised upon them by the thoracic wall, and to the weight of the ab- dominal organs dragging upon the diaphragm, and thus we get expansion of lung to such a degree that any extension will suffice to cause symptoms of dyspnoea. Impairment of a degenerative kind in the elasticity of the ribs and cartilages, referred to by Freund, may take place jx^ri passu with, or may even precede, this change, but this increased rigidity of cartilages would not operate in any other way than by increasing and rendering more fixed the enlargement of the chest. It is from this latter view of the mechanism of emphysema that one can appreciate with increased force the fact that it is in the lessened power of contracting the chest and emptying the lungs that the great defect lies in emphysema. The act of expiration is never completed; there is too much residual air constantly in the lungs, and inspiration is short and jerking from the act being commenced where it should end. The force of expiration as estimated by the manometer is remarkably lessened in emphysema, whilst that of inspiration remains normal, or it may be even increased (Waldenburg);4 the relationship between inspira- tion and expiration being thus, in this respect, the reverse of that obtain- ing in health. The vital capacity of persons with emphysema is, as might be supposed, greatly curtailed. Clinical Varieties of Pulmonary Vksicular Emphysema.— Whilst pulmonary vesicular emphysema has but one essential pathology, 1 Dr. Jackson of Boston, quoted by Greenhow and Jenner. 2 Chronic Bronchitis, etc., pp. 121-122, 1869. 3 Quain's Dictionary, 1882. 4 Die Pneumatometrie und Spirometrie, von Dr. L. Waldenburg, 1880, p. 56. 116 DISEASES OF THE LUNGS AND PLEURAE. its distribution may be local or general, and as above shown, it may vary in degree beWeen wide limits. Local pulmonary vesicular emphysema.—(1) A dilatation of the lung, accompanied by more or less atrophic changes, which takes place around old cicatrizing nodules of disease, contracting cavities, and points of pul- monary collapse from any cause. The site of the emphysema is here de- termined by that of the primary lesion, on which its presence is mechan- ically dependent. Whilst the effect of the emphysema is clinically to mask the physical signs proper to the consolidation; it brings no compensatory advantage to the patient, since the emphysematous portions of the lung , are deficient in respiratory function. (2) It often happens that a whole lung is disabled by destructive disease, by permanent collapse from long- continued fluid pressure, or interstitial fibrous growth. In these cases it is inevitable that the opposite and originally unaffected lung shall enlarge, and fortunately in many instances this enlargement is really of the nature of compensatory hypertrophy, i.e., there is greatly increased mobility of the side, the respiratory murmur is loud and puerile over the whole ex- tended area of the lung, and the patient's breathing powers are fairly maintained; we may safely assume in such cases increased function cor- responding with increased size, Avhich is at least the clinical definition of true hypertrophy. It is not easy to obtain opportunities for the minute examination which is, however, I believe, only required to find a corres- ponding development of lung texture, with increased blood supply, and an absence of the atrophic changes of emphysema. In other cases, how- ever, in which the lung disablement has occurred in a subject of broken constitution, whether from hereditary tendency, prolonged fever, faulty habits, or comparatively advanced age at the time of attack, the " sound" lung whilst enlarging to the clinical outline and pattern of hypertrophy, does not yield to auscultation the sounds of vigorous breathing, but a feeble diluted breath-sound wanting in concentrated vesicular quality. The expanded side lacks mobility; rustling crepitant sounds may be heard at different points, especially near its anterior margin. The patient has not the signs of improved aeration; he presents a livid tinge about the peripheral parts and extremities, and his enlarged lung has brought no corresponding relief to his breathless condition. Here we have a dila- tation of the lung mechanically induced, and attended with atrophic changes, which constitutes emphysema. General pulmonary vesicular emphysema.—A. Large lunged emphy- sema. This is the condition of typical, symmetrical emphysema, to the description of which this chapter has been chiefly devoted. It is only necessary further to say or rather to repeat, that there are really two groups of. cases included in the variety, viz., (1) that in which the disease is distinctly secondary to recurrent bronchitis, or to chronic lung over- strain, and in which the degenerative changes supervene, and render the pulmonary vesicular emphysema. 117 lesion permanent and irrecoverable. (2) That in which the atrophic changes are primary, and the bronchitis and other phenomena are secon- dary. Such cases are either hereditary or are induced by intemperate living, or acquired cachexia, gout, syphilis, etc. B. Small-lunged or senile emphysema. This resembles the second group of the last variety in being an emphysema of essentially atrophic origin. It is, however, but the atrophy of old age most obvious at the lungs, but present everywhere. The pathology of this disease, if such it can fairly be called, is identical with that of the preceding, save that it supervenes in lungs already small and shrunken with the general atrophy of the body. Such people are prone to bronchial attacks, their heat-sus- taining powers are very feeble, but under good conditions of warmth and clothing, with careful living, and a moderate amount of stimulants, they may enjoy life to even beyond the average age. The clinical phenomena presented, by cases of marked emphysema are only in comparatively small part significant of the emphysematous lung alone, being largely due to attendant and for the most part secondary lesions. The physical signs of emphysema will be sufficiently indicated in the description of the following extreme case of the disease: George D----, oil and tallow warehouseman, admitted into the Bromp- ton Hospital under my care in December, 1875. The patient was a tall man with no hereditary tendency to phthisis, but of gouty parentage on the father's side. He had up to three years before admission never been laid by with any illness. At that time he had an attack of bronchitis, and since then had complained of shortness of breath and cough, constant in the winter, attended with frothy and viscid expectoration and with a sense of constriction felt below the ribs. He had never spat blood nor suffered from hectic; lost and gained flesh rapidly. His principal symptoms on admission were, great shortness and diffi- culty of breathing; the head and face becoming congested, almost cyan- osed at times, during attacks of dyspnoea and cough. No pain, but great sense of constriction below the ribs. Appetite bad, digestion tolerably good, boAvels irregular at present but relaxed by medicine. Sleep fairly good. Physical signs.—Pulse 80. Respiration slow and forced. Tempera- ture normal. Great oedema of lower extremities and scrotum. Chest greatly expanded: extraordinary muscles of respiration prominently em- ployed, respiratory movements mainly thoracic. Intercostal spaces above nipple level slightly depressed during inspiration, becoming quite level with the ribs on expiration. Below nipple level intercostals greatly de- pressed during inspiration, becoming level with ribs or even slightly puffed outwards during expiration; seventh and eighth ribs yield inwards with inspiration. Heart's impulse most perceptible at left costal margin at the level of the tip of ensiform cartilage. 118 DISEASES OF THE LUNGS AND PLEURA. Girth of chest on each side above nipple level, 18 inches. At level of base of ensiform cartilage right side, 18J-, left 18^ inches, \ inch extreme expansion with inspiration in both these situations. The whole chest resonant down to the margin of the ribs both in front and behind; at posterior bases on both sides fine, bubbling rales heard principally with inspiration. Similar rales heard over lower two-thirds of the right and left fronts. Apices clear, cardiac sounds unattended with bruit. Abdomen somewhat distended, and contains a small quantity of fluid. Liver depressed. The subjoined tracings show very well the nature of the respiratory movements in this case. They were taken by a very simple apparatus con- sisting of a straight rod connected by a flexible joint with an expanded button to apply to the chest, the other end scratching upon a horizontal sphygmograph plate previously smoked. Fig. 13.—Tracing of respiratory movement showing total forward thrust at third mid-sternum. Fig. 14.—Tracing, showing recession, C, C, C, during inspiration, seventh rib, axillary line. Tracing Fig. 13 represents the movement of the sternum at the level of the third cartilage. (The man was sitting in a chair, with bis back resting against a flat board). It is equivalent to exaggerated thoracic breathing, although the patient was inspiring in the degree natural and necessary for him. Tracing Fig. 14 was taken at the 7 th rib in the lat- eral region, right side, and shows a distinct recession c, c, c, during each inspiration.' This was perhaps due to the bases of the lungs being in some measure disabled by secretion, but the disablement and collection of secretion were undoubtedly in the greatest measure owing to the in- action of the diaphragm in consequence of the flattening of its arch. The thoracic movement was certainly somewhat in excess in this case from the same cause, but in most cases of emphysema the respiration becomes thoracic rather than abdominal. 1 The right lung was found post mortem to be more highly emphysematous than the left. PULMONARY VESICULAR EMPHYSEMA. 119 The patient died, after he had been in the hospital three weeks, from general dropsy and cyanosis. The post-mortem examination revealed the usual phenomena of large, dilated heart, the right side most affected, the tricuspid orifice measuring 6^ inches in circumference; large emphysematous lungs, the emphysema most marked at the anterior and upper parts and in the right lung, there being oedema and slight congestion at both bases; there were no signs of active bronchitis; the bronchial tubes contained a frothy thin fluid; spleen hardened, kidneys mechanically congested, liver enlarged and fatty. Treatment.—It will be obvious from what has preceded that the treatment of emphysema is mainly palliative, consisting of the prevention of fresh catarrhs, asthma and bronchitis, the avoidance of over-exertion and straining occupations, the escape from dusty, irritating atmospheres, and, when possible, the timely migration to more genial climates during the winter or early spring months. We cannot cure emphysema, but we may by judicious measures arrest textural decay, and prevent fresh over-strain. Emphysema, let me again remark, is never, within the normal period of human life, fatal, save in its complications, but it is the factor which endangers recovery from many diseases. In the dietetic treatment of emphysema, we must so far restrict ingoings as to adapt the resulting products:— 1. To the needs of a necessarily limited muscular activity, a lessened tissue metamorphosis. 2. To a somewhat retarded circulation through the lungs from capil- lary obliteration. 3. To a lessened oxygenation and a corresponding tendency to plethora of venous blood. A restricted, well-assorted dietary, and the maintenance in fair activity of the eliminatory functions of the skin, kidneys and bowels, will fulfill the double indication of avoiding surcharge of the economy by waste ma- terials, and diminishing the tendency to venous plethora, visceral conges- tion, and over-work of heart. With regard to the treatment of emphysema by drugs, there are cer- tain very clear indications to be followed. Measures for the regulation of secretions have been alluded to, and require no further detailed descrip- tion; they will from time to time be called for by the disordered condition of these secretions. Intercurrent attacks of bronchitis, asthma, etc., will require their ap- propriate treatment, but except at such times one should—so to speak— forget the lungs in the medicinal treatment of this complaint. Dyspnoea is not always to be regarded as an indication for ether nor a bronchial wheeze for squills. We must rather have careful regard to the general condition of the patient, and especially to vessels and heart tonicity. 120 DISEASES OF THE LUNGS AND PLEURAE. Iron, arsenic, and strychnia are the best general tonics, and should be given in small doses for lengthened periods, say for a month at a time with intervals of rest from drugs. The arseniate of iron is an excellent preparation for our purpose, e.g., in TV to £ gr. doses with \ gr. of nux vomica, and a little pepsin twice a day after food. A little aloes may be added if necessary, or the occasional morning use of aperient waters with more rarely a mercurial, with the view of maintaining equilibrium in the portal system. Five drop doses of tincture of iron with a little strychnia, twice a day, will often prove of value in restoring muscular tone to the heart and to the bronchi, after any fresh attack of bronchitis or asthma, involving renewed strain upon the right ventricle; and occa- sionally at these times it is desirable to give digitalis in moderate doses for a few weeks, five minims three times in the day is usually quite sufficient for the purpose. In the advanced stages of emphysema and its concomitant affections, when the limbs become dropsical, the abdomen full, the viscera engorged, and with—what is the key to the whole situation—the right ventricle fluttering at the epigastrium, the pulse small, irregular and intermitting, and the jugulars distended and filling from below; in these cases abso- lute rest in bed, the free administration of digitalis, with diuretics and diffusible stimulants, will sometimes still serve to rescue such patients from impending death. The flow of urine freely returns, the pulse steadies, and the dropsy subsides under this treatment. Albuminuria, usually more or less present under these conditions, is no contra-indication to the use of blue pill, which, given in combination with squill and digi- talis for three or four successive nights, will frequently give a start in the direction of improvement. The heart is the failing link in the phenomena present, and digitalis is the remedy, but it sometimes taxes our ingenuity and resolution to give the drug in a combination in which it can be borne. Convallarin may be tried as an alternative sometimes, but is by no means equal to digitalis, in influencing heart and vessels. The true value of the employment of compressed or rarefied air in the treatment of emphysema, has not yet been fully ascertained. But in en- deavoring, so far as is possible, to form a judgment upon the subject, we must carefully distinguish between condensed or rarefied air climates or baths, and the same modifications of air pressure brought to bear upon the interior of the lungs only, not upon the whole body. If a man, him- self surrounded by the ordinary atmosphere, inhales from a compressed air chamber, his lungs become forcibly expanded by an air rich in oxygen on account of its concentration. Such a treatment may be useful in cer- tain cases of collapse from long-continued compression of the lung by fluid or from inflammatory thickening, but it is not adapted for a patient whose chest is already over-expanded from impaired, power of expiration. PULMONARY VESICULAR EMPHYSEMA. 121 The effect, too, of inhaling compressed air in this way is to render the lungs more anaemic, whereas, in emphysema, they are already defectively supplied with blood; and the only advantage, on the other hand, to be gained is the doubtful one of displacing the stagnant residual air by one highly charged with oxygen. If, however, the emphysematous patient be immersed in an atmos- phere compressed, say, to half again the density of ordinary air, his res- piratory mechanism is neither helped nor impeded by the new conditions, for the atmospheric pressure is not only increased on the inner surface of the lungs, but also, and similarly, over the whole body. He is simply breathing a concentrated air, but as the vital capacity of his lungs is con- siderably diminished, some advantage may be thus obtained from the air inhaled being (bulk for bulk) richer in oxygen. Be it remembered, how- ever, that with increased density we get diminished mobility of the air particles, so that the osmotic interchange of gases on which respiration truly depends, is more slowly effected. Again, the heart's action is somewhat impeded by the increased pressure upon the vessels; still it is true that emphysematous people do well at the sea-level, and I have found at the Brompton Hospital, where a compressed air-bath has recently been fitted, that patients with.emphysema experience in the bath decided comfort, and are perhaps somewhat benefited by its use. These baths cannot in any sense be regarded as curative in emphysema.' It is generally held that elevated climates are unsuitable for patients with emphysema, inasmuch as such patients must breathe more deeply to obtain the same amount of oxygen from a rarefied atmosphere. Respira- tion in a rarefied air would thus tend rather to increase the evils already present in an over-expanded chest with deficient power of expiration. But there are some considerations from which it would appear that such an atmosphere is much less unsuitable to emphysematous patients than one might at first assume.2 (a) In the first place it must be remembered that, with an abundant air supply, we use only a very small proportion of the oxygen present in the air for our respiratory purposes—in other words, expired air is not nearly exhausted of its oxygen; (b) secondly, although the air of elevated regions is rarefied, its particles are more actively mobile, and oxygenation is rela- 1 Vide Walshe, Diseases of the Lungs, 4th edit., p. 333. Brawn, The Curative Effects of Baths and Waters, edited by H. Weber, M.D., p. 53. Cohen, Inhalation in the Treatment of Disease, Philadelphia, 2nd edit., p. 41. The simplest com- pressed air-bath consists of an iron chamber, into which air is gradually pumped to an excess of half an atmosphere or more. The bath is in daily use at the Ben Rhydding Sanatorium. 2 It has been proposed to use rarefied air-baths, but I need scarcely say that the above remarks refer exclusively to the rarefied air of elevated regions, inas- much as one would hardly with seriousness suggest placing any patients under an air pump! 122 DISEASES OF THE LUNGS AND PLEURAE. tively quickened. Thus Tyndall and Frankland' have shown that the loss of weight of a candle burning on Mont Blanc at an elevation of 1200 feet, is identically the same as that of another candle of similar dimen- sions, burning in the valley of Chamouni below; (c) thirdly, the circula- tion through the lungs, as elsewhere, is carried on at less pressure in elevated regions, and the heart, tuned originally to lower latitudes, finds relief in this way. There are many other features, besides the mere elevation, with which we are now only concerned, which would of course have to be taken into consideration in coming to a decision as to the relative advantages of high or low climates in the treatment of emphysema. No statistics upon the subject have, so far as I know, been published. But, inasmuch as it is the expiration which is at fault in emphysema, and since, from the defective lung recoil, there is an undue amount of residual air retained in the lungs, the most decided treatment, indeed the only real treatment of the physical kind under consideration, is that of causing the patient to expire into a partially exhausted chamber. This method of treatment has been tried by several good observers, especially by Waldenburg, Schnitzler2 and Berkart.3 Dr. Waldenburg 4 relates sev- eral cases in which marked benefit has ensued upon the employment of this treatment; and although most of his results are complicated by the simultaneous use of turpentine, saline spray or other inhalations, yet the relief of symptoms and gain in vital capacity cannot by these other means be accounted for. In most of his cases, Dr. AValdenburg caused the patient to inspire compressed air and to expire into rarefied air.5 These mechanical methods of treatment are attended with many practical difficulties, and the results obtained are only as yet sufficiently encouraging to warrant fresh investigation. And further, it must always be carefully remembered, that we have in emphysema to deal with a more or less advanced degenerative disease of the lung texture. 'Quoted byBraun, loc. cit., p. 59. 2 Wiener Klinik, 1875, Heft 6. See abstract of Dr. Schnitzler's views in Dr. Dobell's Reports, vol. ii., p. 114. 3 Lancet, Nov. 25th, 1871. 4 Die Pneumatische Behandlung der Respirations-und Circulations-Krankhei- ten. Berlin, 1875, pp. 385-411. 5 Waldenburg's apparatus is an adaptation of Hutchinson's spirometer, with weights so adjusted as to exercise positive or negative pressure upon the contain- ed air as may be required. It is described and figured in his work (p. 128), and also in Cohen's work (p. 45). CHAPTER IX. (EDEMA OF THE LUNGS. (Edema of the lungs consists of an escape of serum from the vessels into the interstices of the organ, and into the alveolar and bronchial spaces. There are many causes of this condition, but they range themselves naturally under two heads. 1. Disturbance of circulation. 2. Morbid conditions of blood. Thus, we may have inflammatory oedema from active congestion, and mechanical oedema from retarded circulation, which may be due to mere feebleness of heart, or obstruction to the passage of blood through the lungs, as in emphysema, mitral stenosis, mitral regurgitation, or pressure from tumors on the pulmonary veins. A certain amount of oedema, due to impaired vascular tonicity, commonly remains for some time after acute inflammation of the lung has passed. The powerful inspiratory efforts to draw air into the lungs through the constricted passages in croup and asthma, and other extended bronchial obstructions, cause an afflux of blood resulting, in some cases, in more or less oedema of the lung tex- tures. In all those conditions of blood which favor the escape of serum from the vessels we may have pulmonary oedema. Of these conditions albu- minuria is the most important; scurvy, purpura, anaemia, hydraemia, come a long way afterwards as possible causes. Morbid Anatomy.—(Edematous lungs are large, heavy, wet, inden- ted by the ribs, pitting on pressure, and on section exuding from their texture and tubes an abundant, frothy serosity, sometimes blood-stained. All these characters are especially marked at the bases, or most de- pendent parts of the organs, and indeed, may only be apparent there un- less otherwise locally determined. (Edema affects both lungs, but most commonly one side is more affected than the other, owing to the posture adopted by the patient. It is very usual to find the pleura on one or both sides containing an undue amount of serum. Except at the extreme bases, and when very thoroughly water-logged by old standing oedema, the lungs are more or less crepitant, and portions cut off will float in water. Under the microscope some epithelial shedding may be observed in the al- veoli; otherwise the texture of the organs is unchanged by oedema alone. Symptomatology.—The symptoms of oedema of the lungs are mingled with those of the other diseases of which this condition is but a conse- 124 DISEASES OF THE LUNGS AND PLEURAE. quence. Dyspnoea, straining cough, with thin, watery, mucoid sputa, are the chief symptoms. The patient sits up supported in bed, the respira- tory movements are thoracic, "lifting" in character, the bases of the chest receding with inspiration. The front of the chest is hyper-resonant, the posterior bases more or less dull. Over the posterior aspect of the lungs, extending from the base upwards, the respiratory sounds are enfeebled or annulled, and fine, bubbling rales are heard chiefly with inspiration. Emphysema crackle, pneumonic crepitation, and the crepitation of air penetrating a collapsed lung, are of almost identically similar characters so far as the rale is concerned, with that of oedema. The distinctions must be drawn from associated percussion and auscultatory phenomena. Prognosis.—(Edema of the lungs is usually of grave significance. In chronic Bright's disease, and in cardiac dropsy it is one of the later phe- nomena. In those forms of heart disease, however, telling directly upon the circulation through the lung, a certain degree of pulmonary oedema may precede general dropsy, and may long persist without further conse- quences. It is very common in old people with feeble hearts and emphy- sematous lungs, to have a certain amount of pulmonary oedema as a per- manent condition, and I have met with several people in Avhom slight oedema sounds have for years persisted on one side, probably the result of a past inflammatory attack. No doubt some of these cases are better explained by an oedematous condition of the connective tissue uniting the pleural surfaces over a lung that has been the seat of a former inflam- matory attack. The supervention of oedema of the lungs in acute bron- chitis, or in pneumonia, is of very fatal augury, being due to failure of heart. Treatment.—The treatment of acute oedema from failing heart is referred to in the chapter on pneumonia. In cases of local oedema from loss of tone of vessels after inflammation, iron, mineral acids, and some- times small doses of digitalis are of great value. In all other serious cases of pulmonary oedema, derivative treatment is called for. Dry cupping gives much relief, especially in obstructive cardiac disease, and in emphysema with dilated heart. The vegetable diuretics, juniper, scoparium with digitalis, and moder- ate doses of the iodide and neutral salts of potash, are valuable; watery purgatives and diaphoretics are to be used in turn. The exact nature of the case, whether renal or cardiac, will determine us in selecting our rem- edies. In cardiac cases we rely more upon diuretics and digitalis, with occasional small doses of mercurial and saline aperients. In renal cases our derivative treatment is rather effected through the bowels and skin, by brisk, watery aperients and sudorifics, including air-baths. In all cases we must fairly support the patient. CHAPTER X. PNEUMONIA. Pneumonia may be defined as an acute febrile disease, characterized by inflammatory consolidation of some portion of one or both lungs. It is true in a sense that pneumonia and inflammation of the lungs are synonymous terms, but the latter expression by no means covers the whole pathology of the disease, indeed a careful examination of the eti- ology and clinical features of pneumonia, would suggest its being placed in our nosology amongst such diseases as acute rheumatism, erysipelas, quinsy, influenza, the inflammatory phenomena in each of these diseases being but the local expressions of a general state, and only exceptionally proceeding beyond hyperaemia and simple exudation. Etiology.—(a) Individual predisposition. No age is exempt from pneumonia, but the disease occurs most at the period of life between twenty and forty, when persons are most exposed in the active struggle of life. The male sex is more frequently attacked than the female in proportion of three to two, and at the period of life referred to, the prevalence is twice as great amongst males.1 Depressed vitality, arising from debauch- ery, intemperance, over-fatigue, anxiety, insufficient food, over-crowding, renders the individual more prone to attack. (b) Previous diseases. Chronic disease of any kind, but especially alcoholism, albuminuria, and gout, are liable to engender pneumonia. A plethoric state of body seems also to favor its occurrence, and to add much to the severity of attack. (c) Climatic influences. Cold seasons, great variations of temperature, rough, cold winds, bring about pneumonia, and account in many instances for its epidemic prevalence. Dr. Hjaltelin considered a highly ozonized condition of atmosphere, which he observed to exist coincidently with the Iceland epidemic described by him, to have had something to do with its occurrence.5 (d) Epidemic influences. An epidemic of influenza has in some in- stances preceded a similar occurrence of pneumonia.3 1 Memoi-andum on the incidence of Fatal Pneumonia, by G. B. Longstaff, M. B-, Oxon., F.S.S., drawn from the Registrar General's returns for the decade 1871-80. Collect. Invest. Record, vol. ii., July, 1884. 2 Epidemic pneumonia in Iceland in the year 1863, by John Hjaltelin, M.D., Inspecting Medical Officer of Iceland. Edin. Med. Jour., vol. ix., 1864, page 969. 3 Hjaltelin, loc. cit. 126 DISEASES OF THE LUNGS AND PLEURJE. Ziemssen,1 on a careful consideration of the-occurrences of pneumonia, which have been tabulated for Europe, Northern America and Africa be- tween the years 1836 and 1856, finds that the curve of pneumonia fluctu- ations is not concentric with that of other inflammatory diseases, whilst it remarkably coincides with the curve of typhus. Exciting causes of Pneumonia.—Cold, either in the form of absolute depression of external temperature, or chills from undue exposure to cold draughts, insufficient clothing, damp beds and the like, is by far the m st common exciting cause, of pneumonia. Not only are most cases of spo- radic pneumonia to be thus accounted for, but a considerable proportion of the epidemic occurrences of the disease in modern times are attributed to lowness of temperature and cold winds; individual susceptibility and special exposure being the predisposing circumstances. Thus, the epi- demic in Iceland in the winter of 1863, was prepared for, by a previous occurrence of influenza, presumably rendering the respiratory organs vul- nerable, and was attended with rough and cold weather, and winds highly ozonized. The epidemic related by Dr. Welch,2 as affecting the 22nd Regiment stationed at New Brunswick, was similarly explained. From a strength of 652 men, £2 were attacked; 12 cases occurred in January, the coldest month; 32 in February and March, the months of greatest tem- perature fluctuations; 320 of the men were housed in the " exhibition building," a large, cold, draughty, wooden structure, freely exposed on all sides; of these 38 were attacked. Of the whole 52 cases, Dr. Welch at- tributes 27 to lowness of temperature and cold draughts, 7 cases to sleep- ing on mattresses carelessly stuffed with damp, snowed straw, 5 to expos- ure to great cold at night, 6 to chilling of body whilst perspiring from strong exercise, and in 7 cases the exciting cause was obscure. Dr. AVelch does not consider that climatic conditions were operative, save in the one factor of low temperature. Intemperance seems to have been present as a predisposing cause in many instances, and it is further stated that the men had had a previous six years' service in Malta. Out of 152 women and children, who had in this latter respect been under the same conditions, however, only two cases of pneumonia occurred—a remarkable circumstance, attributable no doubt to less exposure, and superior shelter in the warmer barracks and married quarters. It is to be observed that merely a low external temperature may not be so favorable to the occur- - rence of pneumonia as exposure to great variations. It frequently hap- pens that workmen getting warm at their work in the sunshine of a May- day throw off coverings, and get chilled by a N. or N.E. wind, of which they were before unconscious. 1 On the fluctuations in frequency to which pneumonia is liable, with special reference to those occurring during the two decimal periods, 1836-1856, Prater VierteJjahrschrift, 1858, Bd. ii., and Edin. Med. Jour., vol. iv., 1858. 2 Army Medical Reports, 1867, Appendix ix. Remarks on Pneumonia. PNEUMONIA. 127 Septic causes.—Comparatively recent etiolegical researches, and es- pecially the evidence brought together by the Committee of Collective Investigations, leave no room for doubt that cases and groups of cases of pneumonia are occasionally met with, which are attributable to bad san- itary conditions, and especially exposure to sewer gas emanations.1 The disease Avhen thus arising is of somewhat different type from the inflam- matory form, and merits the name " pythogenic "2 that has been used to distinguish it. Other cases occur which may be classified under this heading, and which are more distinctly secondary to septic poisoning, such as the pneumonias which complicate general septicaemia, induced by foetid ab- sorption from unhealthy wounds. Infectious pneumonia.—There is also evidence to show that, under cer- tain circumstances not completely known, pneumonia may be communi- cated by one person to another. The Collective Investigation Committee, in answer to a special request for information as to the etiology of pneu- monia, received about 100 replies, in eighty of which no other cause than exposure to cold could be assigned for the attack. The twenty remaining replies are abstracted in the Record,3 and amongst them nine observa- tions are included, in which there was apparent transmission of the dis- ease from one member of a family to others, in at least one of which the evidence is very strong. The difficulty is of course the usual one, of sep- arating cases of several persons being attacked in consequence of exposure to a common cause, from those in which the first attacked has transmitted the disease to others. It is probably the pythogenic form of the disease, in which infection is most to be met with, but not exclusively so. In the epidemics at Iceland and New Brunswick, already referred to, no suspicion of communication of the disease by infection is mentioned, and similarly with one of the two epidemics described by Surgeon-Major Maunsell4 in N.W. India (Mooltan and Bunnoo), in 1882 and 1883, both of which were apparently due to conditions of temperature. In the second epidemic, however, twenty of the attendants were attacked. Pneumonococci.—Any statement with regard to the etiology of pneu- monia would be far from complete without careful reference to certain micro-organisms which are held by some observers to be the originators and propagators of the disease. 1 The admirable reports on Epidemics of Pneumonia, British and Foreign, by Dr. Sturges and Dr. Coupland .in the second (1884) volume of the Collective Investigation Record, part i., are the most recent, and contain full literary ref- erences on this subject. 2 A term first suggested by the late Dr. Murchison for typhoid fever, Med. Chir. Trans., vol. xli., p, 221, and first applied to pneumonia by Drs Grimshaw and Moore, Dublin Journal of Medical Science, 3rd series, vol. lix., 1875. 3 Vol. ii., page 60, et seq. 4 Collective Investigation Record, 1884, pp. 77 and 93. % 128 DISEASES of the lungs and pleurae. Friedliinder (Virchow's Archiv, Bd. 87) was the first to recognize the constant occurrence of masses of micrococci in lungs affected with acute croupous pneumonia. They are oval in shape, about 0.001 mm. long, and may occur singly or as diplococci (dumb-bells) or in chains. One observer, Ziehl, attributes the characteristic brown sputum to the presence of numbers of these micro-organisms. Dr. Giles, writing in the British Medical Journal, July 7th, 1883, found the micrococci both in the blood and sputum m cases of \ neumonia occurring in India. This observer produced pneumonia by injecting the cultivated organism into the subcutaneous tissue of rabbits.1 Dr. Klein2 mentions that Friedlander and Frobenius, also Salvioli and Ziislein have produced pneumonia in mice, rats, and rabbits by inoc- ulation from cultures. Klein has investigated the matter, and finds besides bacilli other species. of micrococci present. In the lungs of patients dying of pneumonia he found the organisms, but in many of the alveoli he found fibrin and blood corpuscles but no micrococci. He regards the dependence of the disease on these micrococci as questionable, for he found injection of the cultivated micrococci into rabbits and mice produced septicaemia but not pneumonia. The peculiar hyaline capsule, which Friedlander maintains is characteristic. of this form of pneumonococcus, Klein has seen round the micrococci in pyaemia of rabbits produced by inoculation from swine plague (schweine- suche). Some years must yet elapse before the exact position of micro-organ- isms with regard to disease can be finally determined; and, before this particular micro-organism can be accepted as the spore of pneumonia, i.e., as the only means by which that disease can be originated or propa- gated, there are many difficulties to be surmounted. The climatic con- ditions in which the disease most occurs, its common origin in exposure to surface chill, the rareness with which infective propagation is observed, and the not yet ascertained constancy of the presence of the coccus, nor of its virulence under cultivation, are circumstances requiring to be ex- plained by the exclusive germ theorists of pneumonia. It is a point worthy of note that the diseases already enumerated as those with which 1 Dr. Dreschfeld in a paper communicated to the Medical Society at Manches- ter, 1884, describes a peculiar form of pneumonia which had been recently pre- valent there, intermediate in character between ordinary pneumonia and the septic or "epidemic" form of the disease. Micrococci were abundantly found post mortem in the exudations, pericardial effusions and blood. Dr. Dreschfeld regards the different forms of pneumonia as varieties of one disease, due most probably in all cases to a specific infective agent, the pneumonococcus. British Medical Journal, May 10th, 1884. See also Ueber Wanderpneumonie und ihre Bezichung zur epidemischen Pneumonie, von Prof. J. Dreschfeld. Fortschritte der Medicin, Bd. hi., 1885. 2 Ein Beitrag zer Kenntniss des Pneumonokokkus, in Centr-alblatt fur die Med. Wiss., Berlin, no. 30, July, 1884. » PNEUMONIA. 129 pneumonia may be best compared, are equally remarkable for their ap- parently double mode of origin, viz., from exposure to chill, and from exposure to poison influences. One might be tempted to say that each of the two diseases, ordinary and pythogenic pneumonia, or idiopathic and wound erysipelas, or influenza and virulent catarrh, is quite as distinct from the other as typhus is from enteric fever, but clinical experience does not favor this view. To take a simple instance, a slight dampness of feet will with almost unerring certainty give to many persons a severe catarrh with the usual symptoms of malaise, chilliness, coryza, etc. The catarrh thus acquired is virulent, and will run through the household. The composite organic " splinters" from the first subject who acquired the catarrh, may demonstrably contain micro-organisms to account for their contagiousness, yet the onset of the disease can scarcely be attribu- table to the reception of such organisms, but must rather be regarded as some form of vaso-motor disturbance bringing about changes, possibly favorable to the habitation of ever-present germs. In considering these difficult but interesting and important problems, one must not confound what may be the carriers of the disease with the disease itself, nor look upon what may be only epiphytes as genuine disease-spores. Pathology and Morbid Anatomy.—The morbid anatomy of pneu- monia consists of an acute hyperaemia of the affected lung, resulting in a fibrino-corpuscular exudation into the alveoli, perhaps including the smaller bronchioles, and forming a film upon the pleural surface. This exudation coagulating in situ, fixes the lung in a state of immoveable expansion more densely solidified than it could be by any artificial injection with coagulable fluid. In the accomplishment of this second stage of " hepatization," all the severity of the disease is manifested, and with its attainment the disease proper is at an end. The local consequences of the disease do not thus terminate, however. With the first consequence of extraneous influences—coagulation of the exuded products—a chain of secondary phenomena commences, partly chemical, partly vital, attending their liquefaction and re-absorption. Thus, after a usually very short, but sometimes more prolonged period of malaise, the malady is ushered in abruptly with rigors, rapidly mounting and maintained high temperature, on the second to the fifth day of which the local signs present themselves; on the seventh to the tenth day the temperature falls, but the local lesion has yet to be removed. Pneumonia is thus artificially divisible into three stages. The first stage begins with the rigor and ends with the appearance of definite signs of consolidation. It may be termed the stage of initial fever with pulmonary engorgement, and it lasts from two to five days. If death should occur at this stage, the affected lung is found to be in a condition of inflammatory oedema, heavy, engorged with florid blood, pit- ting on pressure, and still crepitating; on section, exuding abundant, 9 130 diseases of the lungs and plkur.e. blood-stained, frothy serosity. Pulmonary hyperaemia and fluid exudation are the conditions present. When the pneumonia occurs in very cachec- tic subjects, or in its more intensely pythogenic forms, scattered pulmon- ary hemorrhages may be found. A mere out-burst from engorged ves- sels at some one time, however, is not necessarily associated with disease of a specially low type. It must be observed that throughout the febrile period of pneumonia there is an advancing area of lung thus affected. The second stage, that of pulmonary hepatization, emerges from the former and terminates in from forty-eight hours to five or six days. It is characterized by continued high temperature and by increasing signs of consolidation of lung. In this stage of red hepatization the affected portion of lung is bulky, heavy, and solid to the feel. The pleural surface is covered with a thin layer of soft, finely granular, lymph, which can be readily scraped off, exposing the glistening pleura beneath. On section the lung is firm and dry, presenting a red granular surface which is readily broken by the pressure of the finger. There may be a little frothy secretion in the bronchial tubes, the mucous membrane of which is injected. A portion cut from the consolidated lung sinks at once in water. A thin section of a portion of the consolidation when microscopically examined shows the alveoli, alveolar passages, and sometimes the smallest divisions of the bronchi, to be occupied by closely packed red blood discs and leucocytes entangled in the meshes of coagulated fibrin. The alveolar' wall is not changed beyond sometimes slight swelling of its epithelium, a few cells of which may be shed. Towards the latter portion of this stage there is more or less emigration of leucocytes from the alveolar walls. In cases in which the pulmonary inflammation supervenes upon hypostatic conges- tion in continued fever, the consolidation is softer, darker, and more spleen-like in appearance and has been called " splenification of lung." Third stage.—That of resolution. The commencement of this stage is characterized in normal cases by a remarkably rapid fall of temperature attended with profuse sweatings or other critical phenomena, and the signs of commencing liquefaction of the elements of the lung consolida- tion. This stage of pneumonia is also termed that of grey hepatization in its earlier period, and sometimes by the more erroneous term purulent infiltration at its later period. The exuded products now rapidly undergo molecular degeneration, the fibrinous element becoming completely emul- sified,- and the corpuscles more or less broken down by fatty changes. As a rule the alveolar walls remain intact, beyond perhaps slight swelling of their epithelial lining, and the emulsified products are more or less read- ily removed, chiefly by absorption, but, in part, also, by expectoration. In some cases, however, the texture of the lung is involved in the in- flammatory change, the alveolar walls become infiltrated with leucocytes, and the reparative stage of grey hepatization is changed for that of ad- PNEUMONIA. 131 vancement to suppurative disintegration of the lung itself. This un- toward event must be regarded as a complication rather than as a feature of pneumonia. It is again not difficult to understand how, in course of the dangerous processes above described, thrombosis of larger branches of the pulmon- ary artery may take place, or such extensive capillary stagnation as shall lead to necrosis and abscess or gangrene of a portion of the lung. The portion of lung affected in pneumonia is most commonly the base on one side, the right being more frequently affected than the left. Both bases are rarely simultaneously attacked, but it is not very uncommon for the second base to become more or less involved in the course of the disease. Perhaps the frequency with which this happens has been exag- gerated from the fact that both tubular breath-sound and crepitant rale may be audible at one base by reflection from a corresponding point of the other.x The upper lobe is attacked in a goodly proportion of cases, more especially so in children than adults; although, amongst the latter especially, apex pneumonia includes the more cachectic cases, from alco- hol and other causes, yet the disease in this situation otherwise runs a normal course. Symptomatology.—The general aspect and symptoms of pneumonia on the third day of attack are usually such as to leave but little room for doubt as to the nature of the case. The flushed look and burning skin, the hurried noiseless breathing, and rapid but regular pulse, the frequent short cough half-stifled from pain, the dryish thickly-coated tongue, and the singular prostration of the patient, are a group of signs which, super- vening speedily upon a well-marked attack of shivering, cannot be other- wise interpreted than as being those characteristic of an attack of ordin- ary acute basic pneumonia in full intensity. On closer examination the respirations are found to number about 40 in the minute: they are not obstructed nor attended with such marked action of the nares as in capillary bronchitis. The pulse 120; the tem- perature 104°. Fig. 15. On inspecting the chest its movements are found to be chiefly one-sided, but there is no apparent difference in size on the two sides, and the heart is found beating in its normal position. The movements of the affected side are voluntarily restrained by the patient, and a severe pain referred to this part often cuts short the cough or any attempt to draw a full breath. The percussion signs in front are not materially altered; on auscultation the respiratory murmur is found here to be weakened on the affected, exaggerated on the healthy side. Posteriorly, over the base of the affected side the percussion note is dull, but not without some wooden quality of tone quite distinct from the dead, flat note of effusion. The dullness extends upwards to a variable height, and over the dull portion the respiration is characteristically bronchial ' Vide previous edition On Consumption, etc., 1878, p. 208. 132 DISEASES OF THE LUNGS AND PLEURAE. or tubular, the voice-sounds well-conducted, broncho-phonic, and the peculiarly explosive, fine, inspiratory crepitation of pneumonia is heard, especially towards the upper limits of dullness. If there be any expec- toration it is scanty, viscid, frothy, and more or less rust-colored from blood staining; it contains an excess of chlorides, and is deficient m phosphate of soda. The urine is scanty and concentrated, deficient in chlorides and sometimes yields a thin cloud of albumen. I have for convenience of description taken the symptoms and signs of a typical pneumonia at its most striking period, (the second or third day after the rigor), that at which the practitioner is most commonly called upon to see such a case. There is no doubt that the general Dmo/Dit 3 ! <-l jf 6 7 a 7 M) sr /z. /j Km*. ME WE- »it ME ME \ E ME HEME Hi lt;L 106" 105" TOP-|t05° 1 . |K2° \.m' 100* 99° sari 98-97* JMm. —*-- ¥ i^ t ■f' z\": .4.. zz "."5" -i: _J._. "f .4.. _f- _4-_ 4"_; :.■;::.• t -Tr. :±: :t: L'l~.' '.'.\t- "i" . ;.- t ..!.... • • ■:"*N '■'"■ it:. +- -4-' "T" .-J— —«. :tT- V* -1 \- :i: X- 4- ~i—1 ■-f— -t- :1~ 'X' ■]■- _.{.! )••• -*- =t -t- i Tf :.T~ zji -t\ .'...i.. ■:1: . + t- 3- '.".!",- Ex: 3?. ::K ~rv rj: A 1: ~zl~z -4." .-...- -iv: .._!_ fe? .4... ..4. ..... —f- ..i... ...;.. r: ;.iu w.~ .--I.-. 4- 4: fe $ 4 ..i... ■.:.!:: ....i. .....* - "T -t .-t- -+•• .....'■■ i '-: ....... "■.r "i" '."'. J... :.":'" ... j... /1U /to //z so u Fig. 15. Fig. 16. Fig. 15—The chart illustrates temperature record of a case of pneumonia (left lung), arising from exposure to chill in a child aged seven years. The physicial signs developed at the left poster- ior base and anterior apex on the third day. The early temperature was somewhat moderated by tepid spongings (s), and a dose or two quinine (Qx). (Middlesex Hospital Records, No. 1 02, 3882). Fig. 16.—Temperature chart from case of idiopathic erysipelas, a man aged 32 admitted on third day of attack. The chart is introduced merely for comparison with that of pneumonia. symptoms may precede the appearance of physical signs by a very percep- tible interval of time, during which, on examining the chest, no dullness is as yet to be found. The breath-sound at one base has, however, at a very early period a peculiar, rough, harsh quality, very like that of exag- gerated breathing, and slight crepitus may be audible. A few hours later the characteristic pneumonic crepitus is abundantly evident, whilst the percussion note, although shortened and heightened in pitch, is, as yet, PNEUMONIA. 133 by no means dull. In other cases, again, the physical signs of complete consolidation may develop so rapidly as to render no previous stage notice- able. And here it is well to remark that there may be observed in dif- ferent cases some diversity in the general symptoms which precede the pulmonary lesion. The rigors may be strongly marked and speedily followed by severe headache, and even somewhat violent delirium, such as to suggest meningeal inflammation. But the hurried regular breathing must not escape notice. In other cases, a marked icteric tinge of skin with gastric disturbance suggests the oncoming of jaundice, but the fever runs too high for simple jaundice, and the^ breathing and pulse also be- token a more acute disease. Finally, the local symptoms, severe pain and dyspnoea, may be those which chiefly attract attention, and these are not infrequently cases of the worst augury as regards the lungs—cases in which the disease is in the smallest sense idiopathic, and has rather been, so to speak, forced upon the patient by exposure to cold. To follow our assumed case of pneumonia further onwards:—the temperature rising after the onset with rigor to 104° hovers thereabouts with but little variation (unless influenced by treatment) for four, five> six, or seven days, and then rapidly falls within forty-eight hours to nor- mal. This abrupt fall of temperature, which marks the crisis in pneu- monia, is often attended with very profuse sweats, a copious discharge of urine, depositing abundant lithates, and more rarely with diarrhoea. More or less exhaustion is always present, and sometimes tffe collapse is very marked. After this brief period of shock has passed, the patient who has been suffering throughout from complete anorexia, thirst, restlessness, and increasing weakness, with dyspnoea, troublesome cough, and blood-stained expectoration, is now rapidly relieved from many of these symptoms. The sense of dypsncea is greatly lessened, although the breathing is still double-quick. The pulse becomes quiet, the skin moist, and the tongue begins to clean at the tip and edges. Appetite does not yet return, but the sleep is quiet and refreshing. On examination, however, the physical signs will be found to have but little changed, dullness and bronchial breathing being as distinct as ever. At the upper boundaries of the consolidation, the crepitation if present, or when it returns (for it often is but little marked or disappears for a few days), is found to have altered in character. It is larger, moister, less explosive, and is heard during expiration as well as inspiration, although still most abundantly with inspiration. This sub-crepitant rale marks the commencing resolution of the hepatized lung, and extends downwards as the consolidation slowly melts away. The sputa now become more or less opaque, although usually still scanty. In some cases the expectora- tion at this stage is muco-purulent, amounting to several ounces during the day. But it yields no lung-tissue to microscopic examination after boiling in caustic soda solution. Sometimes, again, from first to last there is no expectoration in pneumonia. 134 DISEASES OF THE LUNGS AND PLEURAE. After the period of crisis there is in some cases a slight return of fever, but of a different character to that of the original disease. The temper- ature assumes a hectic type, with a moderate daily rise to 101° or even 102°, and in these cases slight daily chills are complained of. These symptoms are somewhat alarming, and suggest the possibility of some caseation or softening of lung-tissue proceeding, or of purulent effusion, into the pleura. But they do not-either of them necessarily bear such untoward meanings. I have observed such symptoms now in several cases in which the pulmonary lesions entirely cleared up. Their rationale is to be sought undoubtedly in the too rapid absorption of inflammatory products resulting in an overdose of material not alto- gether aseptic and inert. In some cases it is possible that more pro- nounced local or general results may ensue. Parkes observed, " the ex- udation . . . may contaminate the blood during softening to such an ex- tent as to lead to renewal or increase of the fever and inflammation of other parts; or to coagulation of the blood in the heart or great vessels." * Other authors, so far as I am aware, are silent on this point. Pythogenic pneumonia.—The following case is introduced as an ex- ample of a fairly typical case of this variety of pneumonia. Minnie L----, aged nineteen, a nursemaid living in London, a light- haired, well-nourished girl, was admitted into my ward, Nov. 27th, 1882. She had a family history of chest delicacy, but had herself had no previous illnesses. Severaf persons in the house where she resided, however, were stated to have suffered from feverish and abdominal symptoms. The water, of which patient drank freely, was regarded with suspicion, and directions had been given that it should be boiled before being used for drinking purposes. Patient had returned from Folkestone to town at the end of October, and had been in her usual health, except for slight headache during a fortnight, until November 23rd, when she was taken ill with shivering, frontal headache, pains in back and limbs, giddiness, nausea, and cough without expectoration. The shivering was repeated several times in the four days' interval between date of attack and admis- sion. On the fourth day of illness, the skin was hot and dry, the lips parched, cracked, the tongue coated, and bowels confined. No physical signs could be discovered except some splenic enlargement. On the 8th day, imperfect dullness and patchy crepitations were observed at the left base, with bronchial breathing. On the 10th day, some tubular breath- sound was also heard at left sub-clavicular region. On 13th day, there was patchy dullness and crepitation over the left back and front of the chest. Exaggerated breathing in right sub-clavicular region, but crepi- tation also scattered over the axillary region and posterior base. Eusty sputa. Delirium. 1 Clinical Lecture on a case of Acute Pneumonia. Medical Times and Gazette, Feb. 25, 1860. PNEUMONIA. 135 On the 14th day, the note was as follows:—Right side, considerable tubular resonance over 10th and 11th ribs posteriorly: dullness above, to include scapula. Coarse rales at extreme base, inspiratory crepitation over scapula. In front exaggerated respiration; in lower axilla sub-crep- itant rales. Left side, posteriorly, patchy dullness, coarse, scattered liquid rales. Anteriorly, dull in sub-clavicular region, with moist rales and some larger clicks. One doubtful spot suggestive of typhoid fever was observed on the abdomen. Death occurred on the morning of 16th day. The ap- pended chart, Fig. 17, gives the temperature of this case and illustrates Fig. 17.—Dlustrates case of pythogenic pneumonia. B = Cool bath. Qx = Quinine, 10 grs. *= Salicylate of soda, 20 grs. every four hours. fairly well the more prolonged and fluctuating course of the fever, which characterizes typical cases of this variety from the more ordinary form of pneumonia. Post mortem, no lesions of enteric fever present. The upper part of the right lung was solid, except the extreme apex and anterior edge. Several wedge-shaped, dark patches were seen on section (recent hemor- rhagic infarcts). In the neighborhood of these infarcts there were thrombi in the vessels. This was the case with the infarcts in the other lobes; the general appearance of the section was that of red hepatization, the central portions of a lighter color than the rest, and inclining to grey. Right middle lobe. Soft and crepitant. Right lower lobe. Quite solid, in appearance similar to the upper, also containing some infarcts. 136 DISEASES OF THE LUNGS AND PLEURAE. Left upper lobe. Same as right upper lobe as regards area of consoli- dation. Color rather dark. Considerable oedema with some infarcts. Left lower lobe. Fairly crepitant, except a patch of consolidation at its upper, and one at its lower edge. Heart. Ante and post-mortem coagula in cavities of both sides. Muscular tissue firm. The diagnosis in this case was at first very uncertain, and even when pulmonary signs made their appearance, they were of that scattered de- scription not incompatible with their being a part of the manifestations of enteric fever. The enlargement of the spleen, again, pointed in the same direction, and although there were, with one doubtful exception, no spots present, one or two relaxed pale motions were passed. The extent of the pulmonary lesions, however, led to the diagnosis of typhoid or pythogenic pneumonia, which proved correct. Unfortunately no search was made for micrococci either before or after death. The character of the lesions described, however, is highly suggestive of their septic origin. Tekminations of Pneumonia.—Although as a rule the consolidation of pneumonia clears up pretty uniformly in the inverse order of its for- mation, it certainly does not do so in all cases, and detached islets of re- solving exudation sometimes give rise to physical signs—largish clicks and circumscribed blowing sounds, which it may be almost impossible to distinguish from those of pulmonary disintegration. A careful examina- tion of the sputa in the manner already explained will help us much to a right view of such cases. As already stated, the third stage of pneumonia, that of grey hepati- zation, may be altered for that of diffuse suppuration of the lung. The symptoms which attend this fatal change are of a typhoid type, the fever continuing shows a fluctuating range, the tongue becomes dry, brown and tremulous, the prostration is marked and attended with muttering deli- rium, sweating and sudamina may be present. The redux crepitations normal to the period of disease are replaced by coarse liquid rales; the respirations become increasingly rapid, and attended with rattling; the pulse rapid, compressible. Death soon terminates the scene. Abscess, i. e., circumscribed suppuration of the lung, is, like the pre- ceding condition, of uncommon occurrence in pneumonia. The symp- toms attending its formation may be very slight. Eigors followed bv sweatings towards the latter period of the disease would suggest suppura- tion. It not infrequently happens, however, that the first sign which enables us to recognize pulmonary abscess as a complication of pneumonia, is its discharge through the bronchus, and the sudden expectoration of a large quantity of pus. This having occurred, cavernous breath-sound and gurgling rales may be heard over a portion of the consolidation where the breath-sounds were perhaps before suppressed. Gangrene of the lung is a condition not of uncommon occurrence iii the PNEUMONIA. 137 later stages of pneumonia in cachectic subjects, and particularly in the intemperate. It more frequently met with in apex pneumonia in adult persons. The symptom which characterizes the onset of gangrene is foetor of breath. There may be no other sign of the complication present, for the sphacelus need not be large, and until it has been evacuated no ap- preciable cavity may exist. The disintegration of the sphacelus is, how- ever, attended with darkened foetid sputa, which, on microscopical exam- ination, will be found to contain fragments of lung-tissue. Acute pneumonia may terminate in the chronic form of the disease. (Edema of the lung may long persist after pneumonia in persons past middle life; it remains not infrequently a permanent condition. Prognosis.—More than 24,000 persons die annually in England and Wales of pneumonia, a mortality sufficiently great to place the disease in the front rank of those dangerous to life. Advanced age and alcoholism are the most important states unfavorable to recovery from pneumonia; pre-ex- isting chronic disease, e. g., Bright's disease or diabetes, are likewise very unfavorable elements in prognosis. The severity of attack varies much in individual cases, and in the pneumonias prevalent in different years. Hence the extent and type of the disease must in each case be taken into account. It will be obvious that double pneumonia is much more serious than single. The prognosis is probably far more serious in the pytho- genic forms of pneumonia, but such cases differ greatly, and we have no statistics by which their mortality can be exactly compared with that of ordinary pneumonia. The danger in these cases arises more from the general state than from extent of lung involved. In children pneumo- nia runs generally a favorable course, and the consolidation melts away sometimes with astonishing rapidity. Apex pneumonia, excluding cach- ectic (especially phthisical and alcoholic) cases is not more dangerous than basic pneumonia, and recovery may be quite as complete in the one as in the other. Pneumonia is a relatively fatal malady in those whose nervous systems have been " used up " by previous mental anxiety or over- strain. For an admirable discussion of the effects of different methods of treatment upon the mortality I must refer the reader to Dr. Sturges' work.' The two conclusions that prominently arise out of a careful con- sideration of the subject are: (1) That pneumonia will ever claim a cer- tain proportion of victims, all our efforts to the contrary notwithstanding. (2) That above this certain small percentage of fatal cases, there is a highly fluctuating margin, in which elevation or depression of the death-rate is greatly dependent upon treatment. That we have not yet arrived at the lowest possible mortality from pneumonia the most recent statistics, if we may trust them, show. Of 1,065 cases collected by the Investigation Committee, the mortality was about I in 5-J, and subtracting from the gross total the intemperate, 1 On Pneumonia, 1884, p. 200. 138 DISEASES OF THE LUNGS AND PLEURAE. the mentally or physically depressed, the infectious cases, and those occur- ring in aged people (above 65 years)—withdrawing, that is to say, all the principal causes of fatality—the death-rate is still 1 in 8:1 a rate not greatly less than that of all cases admitted to five of our large London hospitals.9 The subjoined table gives a brief analysis of the cases, 42 in number, which have come under my own observation at the Middlesex Hospital, with an average of 30 beds, between July, 1880, and December, 1883. Cases. Age. Death. Remarks. 7 under 10 0 13 between 10-20 1 Pythogenic case, see chart, p. 135. 17 20-40 5 Two intemperate, both complicated with delirium tremens, one of them dying on forty-eighth day of gangrene of the lung. One case complicated with heart disease. 3 " 40-60 0 2 60-80 1 Aged 75. 42 7 Of the 42 cases 7 died, of which 5 would come under the category of special causes, viz., advanced age, intemperance, and blood poisoning. Exceptional symptoms in pneumonia and their bearing on prognosis.— In children and very rarely in adults of unstable, nervous systems, convul- sions may replace rigors at the onset of pneumonia. Jaundice is not in- frequently observed in slight degree in the early stages: it is sometimes well-marked. Delirium is occasionally a marked feature of the disease, and is always a grave symptom. In intemperate subjects delirium tre- mens is very apt to complicate pneumonia. The temperature sometimes mounts above 105°, also in cases of great gravity. Decided haemoptysis is rare in pneumonia, and is regarded by Walshe as significant of tubercle. I have seen several examples, however, in which rather sharp haemoptysis has attended pneumonia, which has never- theless run otherwise the usual favorable course. A brick-dust rustiness of sputa is the usual degree of sanguineous tinge, in the first days of pneumonia: a darker and more prune juice color is, however, sometimes observed in old people, and in them it is not necessarily of unfavorable augury. The absence of any coloration of sputa, in otherwise well-marked pneumonia, would lead me, from experi- ence, to fear a tardy or incomplete convalescence. I have observed two well-marked examples of dense consolidation of lung from pneumonia, involving the whole lung, in which breath-sound was inaudible, and vocal fremitus correspondingly diminished. The diagnosis was arrived at prin- cipally from the very slight cardiac displacement being quite inadequate, 1 Collective Investigation Record, vol. ii. Report on Acute Pneumonia, p. 66. 2Loc. cit., p. 51. PNEUMONIA. 139 as the result of so extended an effusion into the pleura. In both cases redux crepitation was subsequently developed, and the consolidation cleared up. Doubtless the absent breath-sound was due to an unusually large overflow of exudation into the small bronchi.1 Treatment.—Before speaking of treatment it is important again to observe, that pneumonia differs greatly with regard to severity and type in different epidemics, and that the subjects of pneumonia are individuals differing, perhaps even widely, in constitution and powers of resistance. Eence, while there may be a general plan of treatment best adapted to steer the patient through the dangers of this disease, there is room for much diversity in detail, and no one system of treatment can be accepted for all cases. The difficulties and dangers which arise in the course of the disease, are grouped about its four consecutive periods of hyperoem ia, consolida- tion, crisis and resolution. Absolute confinement to bed in a good, airy room, warmed to a tem- perature between 62° and 65°, with the air slightly moistened, and a careful, obedient nurse, are of the first importance in the treatment of all cases of pneumonia. « (1) Stage of hyperaemia.—In the first stage of the disease (a) shock; (b) pyrexia; (c) pulmonary congestion; (d) pain; chiefly attract our atten- tion with regard to treatment. The shock at the commencement of the disease, immediately after the rigor, is often considerable, especially in old people and young children, although it is rarely so marked as in acute bronchitis. Alcoholic stimu- lants may be needed at this period, but quietude in bed and nutritious soup are the best restoratives; a few doses of bromide with aromatic am- monia may be required. We can frequently only conjecture the cause of the pyrexia in the early hours of pneumonia, and considering the nature and peculiar dan- gers in the later stages of pneumonia, perhaps the worst treatment of this symptom is that very generally adopted, viz., the administration of aconite. The favorable issue of the disease usually turns upon the maintenance of heart power and vessel tonicity, both of which are lowered by aconite at the very outset, sometimes beyond recall, as has happened in cases that have come within my experience. The pyrexia of pneumonia is of brief duration, and if the temperature, which should in all cases be carefully watched and recorded, do not mount above 104°, it per se requires no energetic interference. Tepid 1 Dr. Petrone, Lo Sperimentale, Nov., 1882, records six cases of what he speci- fies as solid pneumonia; one occurring in his own practice, and the others related by MM. Grancher, Brissaud, Beurmann and Leroux, in which the dullness, absence of fremitus, and breath-sounds resembled the signs of effusion, and were accoun- ted for post mortem by fibrinous exudation extending into the small tubes. 140 DISEASES OF THE LUNGS AND PLEURAE. sponging will slightly moderate it and be comforting to the patient; cool drinks and saline medicines will be similarly useful. If the temperature mount to 105°, five-grain doses of quinine, repeated every three hours, with perhaps a ten-grain dose to begin with, should be given to the adult. In children, who can be lifted about with great ease, the temperature may be kept under by the warm bath at 90°, employed as often as may be necessary, with smaller doses of quinine. In adults this measure is, in private practice, more difficult and disturbing to carry out. Supposing the temperature, however, to show a tendency to rise in spite of quinine and sponging, the cold pack or the cool bath, i.e., at 80° or 70°, must be had recourse to. Ice bags to the head or Leiter's tubes are very useful in adults in aid of anti-pyretic measures. Kairin is too prostrating a drug for employment in the early stages of pneumonia. Anti-pyrin is less so, but I cannot from present experience confidently re- commend it. In this pyrexial stage of pneumonia the bowels should be well cleared by a few grains of calomel, and a saline aperient. Liquor ammonise ace- tatis, and citrate of potash, are most useful remedies, having, with the help of a saline purge, the effect of relieving blood-pressure by natural elimination from skin, kidneys, and bowels, instead of emptying the arterial into the venous system, as is the effect of drugs of the aconite class when given in efficient doses. Eest and saline medicines diminish hyperaemia, and the measures for the relief of pain have the same tendency. In old people and children poultices are sometimes found to be op- pressive, and will then be better exchanged for cotton-wool applications covered with oiled silk. It is very important in all cases to avoid ham- pering the movements of the sound side of the chest. The pain of pneumonia, which indicates the seat of lesion and aggra- vates dyspnoea, should be treated by local rather than general measures. Opium, or the subcutaneous use of morphia, may be necessary in excep- tional cases, but they are not desirable means of combating this symptom. Hot poultices frequently renewed, due care being taken to apply them with as little disturbance of the patient as possible, are valuable in pneu- monia in relieving pain by lessening arterial tension in the pleura. This they effect by dilating the superficial capillary distribution of the intercos- tal vessels concerned. When the pain is severe, from four to a dozen leeches may be employed with great relief, and it is sometimes well to encourage the bleeding by the immediate renewal of poultices or fomen- tations. The condition of the patient, and especially the evidence of ve- nous plethora under existing circumstances, e.g, amount of lividity and hardness of pulse, will guide us with regard to the number of leeches. In country or colonial practice cases may very possibly be met with in which a venesection to eight or twelve ounces may be most useful at the first PNEUMONIA. 141 onset of pneumonia. I have not met with cases as yet in which more than local depletion has been indicated, but from local depletion I have often seen good results. In cases of severe pain, where leeches are not desirable, a blister 3x3 applied underneath the poultice is often valuable. Cold applications are recommended by many physicians; I cannot say that I have been at all impressed with their utility. As a rule, stimulants are not needed in the treatment of this stage of pneumonia, but in cases of typhoid type with high fever, delirium, tremulous tongue, and rapid, com- pressible pulse, they must be had recourse to in sufficient and properly regulated doses, the alcohol being given alternately with a mixture con- taining carbonate of ammonia. The habits of the patient must be borne in mind in estimating the quantity of stimulants required. In cases of low type, in which the features of the disease remind one of idiopathic erysipelas, it may be good practice to place the patient at once on 20 or 30 minim doses of tincture of iron, with half-ounce doses of liquor am- moniae acetatis, and this plan in alcoholic cases will sometimes answer without the aid of alcohol. The diet of the patient must consist of nutritious fluids, milk, strong beef tea, mutton or chicken broths, with perhaps some farinaceous thick- ening. The milk may be diluted with effervescing water or flavored with tea or coffee. Cream is sometimes a useful addition to the dietary. The food and stimulants should be given at reasonable intervals of about two hours, and in reasonable quantity, adapted to the exigencies of the case. It has occurred to me sometimes to see a patient overdone with food, his circulation overloaded, and the abdomen distended from many pints of fluid, much of which is waste, at a time when the respiratory functions are almost in abeyance, the right heart is already embarrassed, and elimin- ation of unused material is difficult. (2) Stage of consolidation.—The next period for treatment is that of consolidation of the lung. Continued pyrexia and pain, with still extend- ing disease, and possible invasion of the opposite lung, attend this period. And thus far, the treatment is but a continuance of that already laid down. At this period of the disease, from the 4th or 5th day to the crisis, life is most usually threatened in severe cases by, (1), failure of heart; (2) hy- peraemia (not truly inflammatory, but as a consequence of heart failure and vessel paralysis) of the sound lung. In severe cases stimulants are necessary, and they may be often use- fully combined with quinine. Two to five grains of quinine should be given in milk, so that the patient gets from ten to twenty grains in the twenty-four hours, and as much brandy or wine as his symptoms demand. If symptoms of failure of heart be observed, and often in anticipation of such arising, small doses of digitalis (five to ten drops of the tincture) should be added, either to the stimulant or to the mixture. 142 DISEASES OF THE LUNGS AND PLEURAE. It is sometimes advisable to substitute for the salines ammonia and bark, in other cases iron and acetate of ammonia. Excessive pyrexial symptoms must be met as before. With regard to the usefulness of mod- erate doses of digitalis in this period of pneumonia, whilst speaking from convincing experience of the fact, I would point out that this use of the drug is consistent with the most rational aim in the treatment of this disease. Salines, poultices, leeches, and possibly venesection, have the common object of lessening pulmonary congestion, easing arterial tension, and depleting the venous side of the circulation; supporting foods, and, when necessary, alcohol, quinine and digitalis, again pull together in maintaining heart power and tonicity of vessels at the period when these tend to fail. There are many cases of pneumonia, however, in which the simplest possible treatment with the fewest drugs is the best. It is a small detail to notice, but one by which much comfort may be given to the patient, especially at this stage, when the respiratory passages are dry, hot, and often sore, viz., to direct the nurse to anoint the aper- ture of the nostril with a little sweet oil, which, by trickling into the pas- sages, keeps them lubricated. At the stage of the disease now under consideration the symptoms and signs reach their acme, and the strength of the patient its ebb: the crisis is anxiously waited for, and is not unattended with dangers of its own. (3) Period of crisis.—The rapid fall of temperature that occurs where crisis is well marked in pneumonia, and the copious sweating or other phenomena attending it, are frequently associated with considerable shock and exhaustion. Failure of heart and pulmonary oedema are the special sources of danger. These must be met by carefully supporting the patient, temporarily increasing the stimulants to any necessary amount, and by giving moderate, three grain, doses of quinine, in combination, perhaps, with small doses of digitalis. Port wine may often at this period be substituted for brandy. The dangerous symptoms associated with crisis pass in a few hours, although sometimes for a day or two the temperature remains sub-normal. At the termination of crisis it is often wise to suspend medicinal treat- ment altogether for a time, continuing the poultices, and regulating the diet to longer intervals. Until critical discharges have ceased, no impor- tant alteration should be made in the dietary. No active measures should . be taken to arrest such discharges. (4) Resolution stage.—During the early part at least of this fourth period of pneumonia (as we have artificially divided the phases of that disease), the same recuperative measures should be continued, strict rest in bed being still enjoined, the dietary being gradually improved some solids allowed, and the stimulants (if any used) cautiously curtailed and changed to port wine or malt liquors. The condition of the tongue will be the guide on these points. PNEUMONIA. 143 The kidney and bowel secretions must be looked to, for it must be borne in mind that inflammatory products are being absorbed and elimin- ated. After a few days, simple quinine or quinine and iron tonics, or a little mineral acid twice daily, may be usefully employed. The resolution as a rule proceeds steadily and satisfactorily. In some cases, however, as already pointed out, a secondary and recurrent rise of temperature, with slight chills and sweatings, attend the resolution process; quinine must then be steadily continued, or if this drug disagree, then arsenic may be tried, the patient being very strictly kept at rest. After a consolidation has cleared up it is not uncommon for there to be some return of crepitation over the seat of past pneumonia. This, which is doubtless due to local atonicity of vessels favoring a passive congestion, is best treated by the employment of tincture of iron internally. A very analogous condition is not infrequently met with in acute nephritis, in the course of convalescence from which we may get increased albumin, and some return of blood in the urine, without any associated rise of temperature. Counter-irritants are occasionally useful in resolving pneumonia, and two or three grains of iodide of potassium, in combination with citrate of iron and quinine, will sometimes hasten convalescence in indolent cases. Change of air is needed to complete convalescence after pneumonia, and in no disease is it more important that convalescence should be com- plete. The only conditions that need be specially observed with regard to such change, are the avoidance of damp, low-lying, ill-drained locali- ties, and the choice of places where the patient can get out on level ground. Lymphatic and scrofulous persons will recover best at the sea- side, the nervous and bilious subjects inland. Sphacelus of the Lung.—In rare instances it happens that the expec- toration in pneumonia becomes foetid, or distinctly gangrenous. In slight cases such symptoms will yield to the frequent use of respirators charged with eucalyptus, ten drops with an equal part of spirit to be in- haled for half an hour every two or three hours, or Eobson's dry eucalyp- tus or pine-oil spray may be kept in more or less constant use about the bed, the patient occasionally inhaling the spray more directly. When the sloughing of the lung is extensive, and a gangrenous cavity is formed, it may be necessary to call in surgical assistance. (See Chap. XV.) In purulent infiltration of the lung we cannot do more than try to support the patient by bark and ammonia, wine and food. In circumscribed abscess we must endeavor to keep the abscess cavity as empty and disinfected as possible; helping expectoration by change of posture, employing disinfectant inhalations as for sphacelus, and keeping up the patient's strength. Surgical interference may again in these cases be necessary, but it should not be too hastily had recourse to, the abscess frequently contracting under ordinary treatment. CHAPTEE XI. BRONCHO-PNEUMONIA. Broncho-pneumonia or lobular inflammation of the lung is an affec- tion partly exudative, partly catarrhal, of certain lobules of the lung and of their associated bronchioles. The inflammatory lesion is, however, not always strictly confined to separate lobules or groups of lobules, for in some cases and especially in those originating in blood conditions, more diffused areas of lung are affected, being less restricted by lobular divis- ions; in other cases again the inflamed patches are not terminal to bron- chi but extend laterally from them. Etiology. — Broncho-pneumonia is most commonly met with as a primary disease in infancy and childhood. It may occur at any age as a disease secondary to capillary bronchitis, whooping-cough, measles, tra- cheotomy, diphtheria, pyaemia and allied conditions, and phthisis, but is nevertheless most common in childhood. The mode of origin of the disease may be:—(1) By extension from bronchitis. (2) By congestion and stasis consequent upon lobular col- lapse of lung, a condition of frequent occurrence in children with weak walled or rickety chests, in the course of bronchitis and whooping-cough. After tracheotomy, when the mechanism of cough or rather of expectora- tion is spoiled, lobular collapse and consequent pneumonia is very common. (3) By inhalation of inflammatory or septic products. In capillary bron- chitis the inhalation of the bronchial products into the alveoli will set up alveolitis. In cases of tracheotomy again, there is a tendency for changed blood, purulent secretions and septic matters to become inhaled into the lungs and to set up lobular pneumonia. In diphtheria, during the period of softening of the membranes, there is, apart from tracheotomy, a dis- position to septic involvement of the lobuli. In phthisis the inhalation of blood or sputa in course of expectoration frequently sets up new centres of lobular inflammation. The inhalation of dust or acrid vapors may possibly cause broncho-pneumonia. (4) By conveyance of morbific septic agencies through the vessels as in pyaemia, septicaemia and tuberculosis. Here the lesions, as before said, may not be strictly lobular, but affect vascular rather than bronchial territories. (5) By extension from deposits in the lung, chiefly tubercular. Symptomatology.—In describing the clinical features of broncho- pneumonia, cases of infantile form such as those arising primarily, or in association with bronchitis or whooping-cough, will be especially in mind.. BRONCHO-PNEUMONIA. 145 Clinically, broncho-pneumonia is met with in the disseminated and the confluent form. Disseminated broncho-pneumonia.—In this form of the disease the symptoms are those of capillary bronchitis, with which it is invariably as- sociated. In young children the distinction between the two diseases is often impossible, and is practically of but little importance. When the disease supervenes, however, upon a less urgent bronchitis, its access is marked by a rise of temperature, an increased urgency of dyspnoea and a greater rapidity of pulse. Shivering is rarely to be noted in young chil- dren, and its analogue convulsions are, so far as my experience goes, un- common in this form of pneumonia. The rise of temperature is generally above 102°, but although the range or average of temperatures is above that of bronchitis, it is less maintained and more fluctuating in character than in croupous .pneumonia. The dyspcena, at first urgent, with flushed face, and working aloe nasi, becomes less apparent as the strength of the" little patient fails, and his nervous- centres become less sensitive in the struggle. Pallor of countenance, with perhaps a faint tinge of lividity appears, and the skin becomes moister, even perspiring. The rapidity, of breathing continues, however, or in- creases, and on uncovering the chest and abdomen, recession of soft parts with inspiration is observed. The pulse becomes more frequent and of lessened force. The tongue is from the first thickly coated, the lips dry, the urine scanty and depositing lithates, and the bowels disordered, con- stipated, or it may be relaxed. The physical signs characteristic of this disseminated form of the disease are of very uncertain value. The percussion note is either un- altered or is somewhat raised and of semi-tympanitic quality. Ausculta- tion reveals fine sub-crepitant (small bubbling) rales scattered over both lungs, most abundant at the posterior bases. Over other parts of the lungs a patchy distribution of the rules may sometimes be recognized, and is then of value in diagnosis. The rales are persistent, not being in any degree cleared by cough, and are often better heard immediately after cough. The breath-sounds are notably enfeebled and masked. Patches of tubular breathing may sometimes be discovered. Should recovery take place the pyrexia gradually subsides with con- siderable fluctuations, the physical signs clear up, the tongue cleans, appetite returns, but strength is only slowly recovered. This form of broncho-pneumonia is, however, of a very grave character, very often proving fatal, and in all cases leaving behind pulmonary delicacy. Indeed the disease may be said rarely to occur in children who are of good stock, and in good previous health. Confluent bronchopneumonia.—This form of the disease does not in its pathology essentially differ from the preceding, but the adjacent lobules of a large portion of lung, not infrequently involving the whole 10 14G DISEASES OF THE LUNGS AND PLEURAE. lobe are affected, and by their juxtaposition the lung is more or less densely consolidated. Confluent broncho-pneumonia may be associated with ordinary bron- chitis of catarrhal origin, and very often arises in the course of whooping- cough. It comparatively rarely arises from the other causes of broncho- pneumonia. The symptoms of the disease are identical with those of the preceding variety, except that pleuritic pain is more commonly experienced on the affected side. The physical signs are somewhat different. The pulse and respirations are similarly quickened, and the signs of obstructed inspiration are ob- served but not symmetrically, the deficient expansion on one side being, in cases where the disease is at all extensive, notably greater than on the other. Most commonly the posterior and lower portion of one lung is affected, and over .this region the percussion note is distinctly impaired, in the earlier stages having a somewhat tympanitic quality, but as the lobules coalesce becoming more toneless. Vocal fremitus in young chil- dren is of no value, but on auscultation the cry of the child is broncho- phonic in character with a tendency toward aegophony. Children, how- ever, who are seriously ill with broncho-pneumonia rarely cry. The breath-sound over the consolidated area is weak and bronchial, being considerably masked by abundant sub-crepitant rales of very sharply de- fined or metallic character. The disease may affect both sides, but as a rule the opposite lung is affected with bronchitis only, or it may be with a few centres of disseminated pneumonia. The temperature and other phenomena in this form of the disease are the same as in the preceding. There is a greater tendency for this form of broncho-pneumonia to become chronic and to run a long course of perhaps many months, terminating in pulmonary fibrosis with bronchi- ectasis or in a form of phthisis. In other cases the disease proceeds immediately to suppurative destruc- tion of lung and to the death of the patient, and in yet other cases the mere extent of the disease in the early stage proves fatal. The signs of suppurative destruction are, increased adynamia, main- tained rapidity of pulse, fluctuating temperature, and hectic sweatings with rapid loss of flesh. The rales become larger, more bubbling, even gurgling in character, and although children rarely expectorate, it is obvious that much secretion comes up to the throat, and irritative diar- rhoea with slimy stools frequently supervene. The prognosis in the confluent form of broncho-pneumonia is, how- ever, in a given number of cases more favorable than in the disseminated form. The bronchitis of the opposite lung may clear up, and time is thus allowed for reparative changes to take place in the affected lung. These changes sometimes go on with great rapidity, but never so quickly as may occasionally be observed in the lobar pneumonia of children. BRONCHO-PNEUMONIA. 147 Treatment of Broncho-pneumonia.—The treatment of broncho- pneumonia is mainly that of bronchitis with careful support of the patient. In the disseminated form of the disease it is doubtful if poultices are of any service, and it is most important that the respiratory movements be allowed as free play as possible. In the more localized confluent form of the disease poulticing is sometimes useful. The timely use of emetics in whooping-cough will sometimes avert the occurrence of broncho-pneu- monia, but it must be allowed that the disease is often started by the imprudent exposure of children with whooping-cough to the external air, under the delusion that in this disease such exposure is harmless or bene- ficial. A careful nurse or mother who understands how to hold a child during the paroxysms of whooping cough, so as to permit the fullest play to the respiratory muscles, may help much in averting pulmonary collapse and subsequent pneumonia. The room should be kept at a temperature between 62° and 65°, the air moistened, and in some cases the addition of a little tar water to the bronchitis kettle is useful. The temperature of the patient if high can be kept within bounds by the occasional use of the warm bath 90° to 95°, and the head may be sponged with water, cooler than this but not cold. The secretions must be kept clear, the patient well supported by beef tea, chicken broth, veal tea, milk, cream, and when stimulants seem requisite they should be liberally given. In all septic cases they are re- quired in full doses. Port wine is an excellent stimulant, and may be combined with a few minims of Battley's cinchona, or with small doses of quinine; or brandy may be added to the milk or broth. Careful support of the patient and good nursing are of infinitely more importance than medicine, but sometimes a little ammonia and ipecacu- anha seem useful. In the convalescent stage of both varieties of this disease, the practi- tioner must bear in mind the frequent presence of rickets, of a delicate family history, and the decided tendency to remnants of disease being left behind in the lungs or bronchial glands. Cod-liver oil with steel wine, containing a few minims of syrup of the iodide of iron, are now valuable, and a change of air, to a warm seaside place if possible, is very important. CHAPTER XII. NARROWING AND DILATATION OF THE BRONCHI. Narrowing of the Bronchi.—General narrowing of the bronchi is practically only met with as a consequence of swelling of mucous mem- brane in catarrhal affections, or of exudation in croupous and diphtheritic maladies. Doubtless cases may occur in which there is some general diminution in the calibre of the bronchial system, but they are not recog- nizable during life. In association with atrophic and contractile changes in the lung, whether congenital as atelectasis, or from disease, the tubes traversing the affected part are widened, never contracted. Localized narrowing of a bronchus may arise:—1. From cicatricial contraction of an ulcerated surface within the bronchus. 2. From con- tractile sclerosis of the bronchial sheath at one or more points. 3. From invasion of the calibre of the bronchus by malignant growths. 4. From pressure upon the bronchus by enlarged glands, growths, hydatid, or aneurismal tumor. 1. The cicatricial changes ensuing upon ulceration are amongst the very rare cases of bronchial narrowing and are always of syphilitic origin. 2. In association with the more chronic indurative form of phthisis, it is not uncommon to find bronchial tubes narrowed or even obliterated by what may be regarded as cicatricial growths involving the sheath of the bronchus, (a) at points adjacent to tuberculo-fibroid nodules: (b) at the entrance to cavities which have undergone considerable or complete con- traction, and are surrounded by a zone of cicatricial induration in which the entering bronchus is involved. In this way partially contracted cavi- ties are not infrequently closed. 3 and 4. The invasion of malignant growths and the pressure of tumors are amongst the most common causes of obstruction to the main bronchi; and are of too obvious a mechanism to require further exposition. The necessary consequence of narrowing of a bronchus at any point is more or less complete retention of secretion behind, and changes of a destructive but variable kind in the lung. Sometimes a cavity becomes thus shut off by occlusion' of its communicating bronchus. Its purulent contents may then collect, and subsequently inspissate into a creamy debris which may at a later period become cretaceous. In other cases the puru- lent secretions increase, become pent up, causing elevation of tempera- ture and other signs of abscess, and finally when they attain to a certain NARROWING OF THE BRONCHI. 149 degree of pressure the narrowed bronchus yields, and a discharge takes place, after which accumulation again commences. In cases, however, in which the secretion is derived from the bronchial mucous membrane, the lung not being primarily involved, it is thick, viscid, and more purulent, and collects in such quantities as to distend the bronchi behind the obstruction. When sufficient distension has taken place a paroxysmal cough will expel through the narrowed orifice a certain portion, the overflow so to speak, of the collection, in the form of thick viscid and more or less nummulated sputa, generally not offensive. The condition of lung that attends narrowing of a bronchus is in the later stages one of airless collapse. Dr. Pearson Irvine contended in an able series of papers in the Pathological Transactions, for 1877 and 1878, that emphysema was the primary consequence of bronchial pressure, since the effect of the narrowing would be to impede expiration, whilst inspi- ratory effort tending to widen the narrowing would be successful. It is obvious, however, that so soon as secretion begins to collect behind the obstruction, the air cells can no longer be penetrated by air, whilst that which remains in them must slowly be expelled. Secondary changes of a destructive character not infrequently ensue in a lung whose main bron- chus is occluded by pressure, changes which are regarded by many as arising from disturbed innervation through pressure upon the pulmon- ary plexuses,1 but although this pathology may hold good in some cases, it is probable that as a rule the pulmonary destruction is the result of the retention of pent-up secretions, and is analogous in origin to similar conditions of kidney ensuing upon hydro or pyo-nephrosis.2 The symptoms and signs of bronchial narrowing need only be con- sidered with regard to those cases in which the constriction is situated at one or other main bronchus. In these cases the signs of narrowing of the bronchus sometimes present themselves, before the cause of that nar- rowing can be precisely made out. Relatively feeble breath-sound of harsh or blowing quality over one lung, and particularly over the upper interscapular region of the affected side are the first signs to be observed. The percussion note, at first un- altered, becomes of higher tone, the vocal fremitus and resonance being lessened on the affected side. The more or less exaggerated vesicular breath-sound over the unaffected side, is in marked contrast with the feebleness of breathing, and want of vascularity on the affected side. As the case proceeds, the feebleness of the breath-sound becomes in- creased to final extinction; low-toned sonorous rhonchus is heard through- out the affected side, and with increasing loudness and roughness as the 1 Sir William Gull, Guy's Hospital Reports, 3rd series, vol. v., p. 309, 1859. 2 See article on Mediastinal Tumors by the Author, Reynolds' System of Med- icine, vol, v., in which this mattei1 is more fully discussed. 150 DISEASES OF THE LUNGS AND PLEURAE. interscapular region is approached. Impairment in the mobility of the affected side comes to be observed, then most usually some shrinking of the side and percussion dullness over the affected lung. From the first there is cough, which may be of laryngeal type from involvement of the nerves of the larynx, coincidently with the bronchial compression. The cough is, however, generally spasmodic in type, the passage of the thick sputa through the stricture giving rise always to more or less, sometimes to very severe, paroxysms of dyspnoea. As pulmonary collapse proceeds, pleuritic pains and the signs of dry pleurisy present themselves, and, with advancing dullness, may lead the observer away from the right diagnosis. The heart is uncovered and shifted towards the affected side, unless its position be otherwise determined by the pres- sure of a tumor. In the most common class of cases, those in which the narrowing is due to the pressure of an aneurism or malignant growth, the signs of tumor will be developed at an early stage of the iisease. In cases of syphilitic narrowing there will be the history of syphilis, the signs of narrowing and the absence of those of tumor. In an interest- ing case that has recently come under my notice, in which the left bron- chus was almost obliterated, and the lower portion of the trachea narrowed by syphilitic cicatrices, in addition to an absence of the signs of aneurism, it was observed that the patient's distress was greatly increased by an attempt to lie in the prone position, and that he felt most easy when erect and walking about the room. In aneurism the patient's troubles are much increased by movement. From the profuseness of the expectoration in the later stages of bron- chial narrowing in association with consolidation of the lung, these cases are sometimes mistaken for phthisis, at other times for pleuro-pneumonia or empyema. A careful consideration of all the signs present will be necessary to establish the diagnosis, for these are undoubtedly among the most difficult cases in chest diagnosis. Treatment.—Much may be done in the way of giving ease in most cases. The cause of the constriction, be it aneurism or syphilis, must be appropriately treated. Small, regulated doses of chloroform for inhalation are valuable, in giv- ing relief to spasmodic cough and in aiding expectoration. In cases in which paroxysmal dyspnoea arises from compression of the bronchus by aneurism, nitro-glycerine (1 minim of 1 p.c. solution) will give relief by lessening tension within the sac. Expectorant remedies are worse than useless. Chloral and paraldehyde give more promise for usefulness than opiates. When the main bronchus is involved the prognosis is of the gravest character. Dilatation of the Bronchi—Bronchi-ectasis.—Chronic bronchi- tis and emphysema commonly entail some general enlargement of the NARROWING OF THE BRONCHI. 151 bronchial tubes, the widening being most apparent in the smaller divisions of the tubes. At portions of the lungs, as the apices, which are but im- perfectly supported externally, the bronchial dilatation may be so consider- able, and attended with such changes in the surrounding tissue, as to merit the term bronchi-ectasis. Bronchi-ectasis consists of a manifest widening of a more or less limited portion of the bronchial tubes. There are two forms of bronchi-ectasis, the cylindrical and the sacculated. In cylindrical or fusiform bronchi-ectasis, the dilatation involves some length of the tubes, varying from a few inches to a system of tubes rami- fying through an entire lobe. The enlargement is uniform throughout the length of tubes affected. In sacculated bronchi-ectasis a restricted portion of a tube is enlarged to a globular form, from half an inch to an inch in diameter. The whole calibre of the tube is as a rule involved, and the ectasia may be solitary or there may be many scattered through the lung. As a rule this form of bronchi-ectasis is situated at the peripheral portions of the lung, corresponding with the smaller bronchi, and small openings lead from the rounded and apparently closed distal side of the sacs, to fine tubes, the branchlets of the widened bronchus. Bronchi-ectasis is never a primary disease, but is dependent upon either increased pressure within the tubes, or traction upon their walls. The following may be enumerated as the causes of bronchi-ectasis:— 1. Increased air-pressure during cough, acting principally at those portions of the lungs where there is least support, notably the apices. This cause becomes operative in the course of chronic bronchitis and emphysema, and assists the action of those causes which bring about damage to the texture of the bronchi. 2. Obstruction of a bronchus, whether from intrinsic cicatricial changes or growth from the lodgment of foreign bodies, or from the external pres- sure of an aneurism or other tumor (see Narrowing of the Bronchi, p. 148). The bronchial tubes behind the obstruction become distended by accumu- lation of mucous secretion, and the lung surrounding them condensed and airless. The dilatation of the tubes in this form of the disease is of the cylindrical kind, affecting most notably the tertiary branches, which are less firmly supported by cartilaginous plates, but the minutest bron- chioles, and even the infundibula, become more or less occupied with muco-purulent secretion. 3. When the vesicular texture of a lung is obliterated by permanent collapse or contractile growth, the tendency of the inspiratory force is to widen the bronchial tubes traversing that lung; and any. further contrac- tion of the condensed tissue in which the tubes are imbedded will further widen them. (a) Secondary to a pneumonia or a dry pleurisy, a portion of a lung, or perhaps a whole lobe, will in certain cases become condensed by con- 152 DISEASES OF THE LUNGS AND PLEURAE. nective tissue growth, extending to its interstices from the pleura along the interlobular septa, and from the sheaths of bronchi and vessels pene- trating it. The result of such fibrous over-growth—which may be termed chronic interstitial pneumonia, leading to cirrhosis of the lung—is neces- sarily a contraction of the lung from collapse of its vesicular structure. The pleural surfaces of such a lung are invariably adherent. It is obvious that any inspiratory effort telling upon such a lung must tend to widen the elastic bronchial tubes with which it is penetrated. (b) Such a lung being held attached at its circumference by the pleu- ritic adhesions, and its bronchial tubes branching to the periphery from the root, it is clear that when the thoracic wall has receded, and the sur- rounding organs, thoracic and abdominal, have approximated as far as possible, any further contraction of the lung must drag upon the bron- chial tubes and extend their calibre in all directions. The medium and sub-capillary tubes imbedded in the depth of the lung are most affected, and become widened out into fusiform and globular cavities, the finest tubes become extensively obliterated in the course of the contractile dis- ease. The secretions of the widened tubes tend to collect from the shape of the tubes, and the hardened tissue by which they are surrrounded, rendering effectual expulsion with cough impossible; decomposition of the stagnant secretions follows, resulting in irritative inflammation of the cavities and adjacent parts. Neighboring bronchi-ectatic cavities may coalesce from atrophy and softening of their adjacent walls, and extensive irregular lobulated excavations of the lung may thus arise. The bronchial cavities just spoken of often closely resemble true pul- monary vomicae. The distinction is made post mortem by finding on the cavity .walls remnants of bronchial membrane, with its characteristic columnar epithelium. (c) In cases of thoracentesis for old standing empyemata, bronchi-ecta- sis amounting to complete loculation of lung may arise in a manner not essentially different from that just described. In such cases obliteration of the pleural cavity is finally affected from above downwards, by the gradual growth of adhesions agglutinating the approximated pleural surfaces. The parenchyma of the lung is, however, in these cases, irretrievably condensed, so that the degree of enlargement of the organ necessary to fill the remaining thoracic space is only to be obtained by widening out the bronchial tubes, and further contraction of the fibrous lung must continue to have the same effect. Thus, the lung in some cases comes to be a mere shell enfolding bulbous bronchial cavities. It is noticeable that in these cases, unlike those just considered pro- fuse and foetid secretions rarely collect in the bronchial cavities. This difference arises from the fact that the thoracic space is mainly filled by the expansion of the upper part of the bronchial system, the base of the narrowing of the bronchi. 153 lung remaining collapsed. Hence drainage is better secured, and the cavities not being irritated by stagnant secretions, become comparatively dry and inert. (d) In congenital collapse of any portion of the lungs, atelectasis pul- monum, the bronchial tubes ramifying through that portion are widened. Symptomatology.—It is obviously impossible to separate the symp- toms and signs of bronchi-ectasis from those of the pulmonary lesions with which this condition of tubes is associated. The expectoration is profuse, muco-purulent, nummulated, with a tendency to diffluence, often very foetid, and yielding on examination neither elastic tissue nor tubercle bacilli. It is expelled with violent paroxysmal cough, often terminating in vomiting. In cases in which the bronchial dilatation is secondary to pressure or contraction of the bronchus, the expectoration is most viscid and mucoid, is not as a rule foetid, and is expelled with considerable difficulty in suc- cessive thick, viscid masses at such times as there shall have been sufficient accumulation to force the narrowed passage. In these cases, as soon as the bronchi become distended with secretion, all breath-sound is extin- guished, the affected portion of lung being at first imperfectly tympanitic, and latterly dull on percussion, and the affected side motionless and more or less retracted. In bronchi-ectasis ensuing upon cirrhosis of the lung from any of the causes considered, we have together with the signs of such cirrhosis, pro- fuse expectoration coming on at intervals with severe paroxysms of cough, the matter expelled being horribly foetid, thin, and purulent, and often containing small curdy-looking masses: whiffs of foetid gas precede and attend the expectorations. Yet in spite of these distressing symptoms the patient may, for a long time at least, suffer comparatively little in general health, nutrition and appetite being fairly maintained, and hectic but little marked. The physical signs vary according as the bronchi are filled or emptv. After a severe cough with profuse outflow of sputa, diffused tubular breath-sound with mucous rattles may be heard over the affected side, to be obscured later on with fresh accumulation; dullness of percussion and more or less retraction of side are proper to the cirrhosis. In cases in which neighboring bronchiectasis have broken into one another, a considerable area of excavation may be produced, usually in the supra-scapular region, over which cavernous breath-sound and gurgling rales with pectoriloquy may be distinctly heard, and the percussion note may have a perceptibly tubular character. In such cases the symptoms are more severe, hectic is more marked, nutrition suffers, and diarrhoea with red tongue are commonly observed. Elastic tissue is to be found in the sputa, but not the bacilli of tubercle. The diagnosis is often extremely difficult between bronchi-ectasis and 154 DISEASES OF THE LUNGS AND PLEURAE. localized empyema, and especially so where the bronchi-ectasis is secondary to partial or complete occulsion of a bronchus. Treatment.—In compression of the bronchus by aneurism or growth we can effect little by treatment. We may relieve whatever spasm there may be in association with the organic stricture, by small regulated in- halations of chloroform, a few drops at a time put on absorbent wool in a small bottle to be sniffed. I have known a pungent vapor, e.g., of strong peppermint essence in hot water, sniffed through the nostrils, give relief to the spasmodic cough and aid expectoration. In aneurismal and syphilitic cases, large doses of iodide may be given. In foetid bronchi- ectasis we are often but too helpless in effectual treatment. Tar, creosote, carbolic acid and eucalyptus may be given internally, and used as inhala- tions. In cases where the patient is getting exhausted, and in which any definite area of excavation can be defined, exploration should be made by cutting cautiously down to the pleura, inserting a fine exploring trochar, and if the cavity be struck introducing a drainage tube. If no definite cavity be struck, it is well to insert the fine trochar in several directions, with the hope of setting up adhesive or cicatricial inflammation along its tracks. A very guarded opinion as to the ultimate good that will be effected by these measures, and their tentative nature, must in all cases be given, however, to friends. CHAPTER XIII ABSCESS AND GANGRENE OF THE LUNG. Circumscribed suppuration of the pulmonary tissues may arise from a variety of causes, the most important of which are, acute primary in- flammation, wounds of the thorax, lodgment of foreign bodies, acute pneumonia in broken constitutions, circumscribed gangrene, abscesses secondary to pyaemia, and infective emboli. Abscesses of primary origin are usually single. The most frequent causes of multiple abscesses are infective emboli and pyaemia. The col- lections of pus may vary in size from a pin's-head to that of a walnut. Those which form in association with acute pneumonia are of small size, numerous and irregular in shape. Abscesses occurring in connection with lobular pneumonia involve the terminations of the bronchi and assume a dendritic form. Symptoms.—The formation of pus in the lungs as in other organs, is usually attended with severe rigors and pyrexia, and in broken or debili- tated constitutions often leads to great prostration. The first evident symptom of an abscess may be the sudden discharge of pus with frag- ments of lung tissue. Physical signs.—If the abscess be of any size the signs would be dullness on percussion, with gurgling rales and the other signs of cavity. Treatment.—The treatment of abscess of the lung consists gener- ally in the pursuance of the remedies for the diseases that may have led up to it. Quinine or bark and mineral acids are useful. Disinfectant inhalations are also of service, and the patient should be encouraged to evacuate the contents of the abscess cavity from time to time. Under these ordinary measures of treatment with good ventilation, and change of air at the earliest moment, abscess of the lung not infrequently heals. In some cases operative treatment is called for. (See Chapter XV.) Gangrene of the Lung. Death of a portion of the substance of the lung may occur under two forms; (a) circumscribed, (b) diffuse. (a) The circumscribed form is that usually seen, the gangrenous area is distinctly defined, and may vary in size from that of a nut to a con- siderable patch involving the greater part of one lobe. The lower lobes and superficial parts of the lungs are those most frequently affected. The 156 DISEASES OF THE LUNGS AND PLEURAE. necrosed portions of the pulmonary tissue become moist, soft, pulpy, present a bluish-green color, and evolve a peculiar and highly offensive odor. The limits of the dead tissue are indicated by a zone of hyperaemia and consolidation. The dead tissue may slough and be discharged through a bronchus, leaving a ragged cavity behind. Occasionally the pleura is involved and the foetid material finds its way into the pleural cavity, but this is rare, as adhesions usually form between the pulmonary and parietal layers of the pleura. (b) In the diffuse form there is no line of demarcation between the dead and healthy tissue, but inflamed, congested and gangrenous lung tissue are all mixed up together. The greater portion of one lobe, or of an entire lung, may be affected, or perhaps both lungs may be affected at several points. Etiology.—Gangrene may arise as a result of acute pneumonia, or from the inhalation of noxious gases. Pressure interfering with the circulation through the lungs, caused by mediastinal growths, and aneurism; foreign bodies in the air-passages or lodged in the lungs from without, e.g., bullets, pieces of cloth, etc., may cause gangrene. It also occurs in drunkards and in the insane. It may complicate the asthenic fever left after such debilitating constitutional disturbances as small-pox, measles, typhus and the like. Pyaemic emboli, or the inhalation of foetid discharges from cancer of the mouth or cancrum oris, or the bursting of a neighboring abscess into a bronchus, may lead to gangrene of the lung. Symptoms.—The most characteristic symptoms of gangrene of the lungs are the peculiarly offensive odor of the breath, associated with the expectoration of gangrenous material containing lung-tissue. The only condition likely to be mistaken for it, is old standing bronchi-ectasis sud- denly becoming foetid from necrosis of portions of mucous membrane, f torn which it is to be distinguished by the presence in the sputa of elastic fibres, and the previous history of the case. The general symptoms are usually those of extreme depression, asthenia, and collapse, death soon ending the scene. Hectic may be present in some cases. Physical signs.—In the early stages the auscultatory signs are in- distinct and not to be relied upon, but later, if the gangrene be circum- scribed, the physical signs are dullness over the affected area, with gurg- ling rales accompanied by an amphoric quality of breath-sound. The distinctness of physical signs, however, varies according to the degree of freedom of the cavity from the shreddy gangrenous tissue. Treatment.—This should be nourishing and stimulating, alcohol being freely given. Antiseptic inhalations of creosote, carbolic acid or eucalyptus should be used. Antiseptics internally are of little use. In cases of circumscribed gangrene with marked hectic or septicaemic symp- GANGRENE OF THE LUNG. 157 toms, and in which the locality of the gangrenous part can be fairly defined, paracentesis should be performed and an attempt made to drain the cavity; this proceeding is still further urged if there be reason to believe that the pleura is adherent and the surrounding lung consolidated. (See Chapter XV.) CHAPTER XIV. THE SURGICAL TREATMENT OF PULMONARY CAVITIES. The cavities of the lung in which artificial drainage may be sought to be effected by the aid of the surgeon, have their origin in:— (1) Abscess of the lung, (a) Suppurative. (b) Gangrenous. . (c) Hydatid. (2) Bronchi-ectatic excavation of the lung. (3) Tubercular or phthisical cavities. There are certain principles common to the surgical treatment of all these forms of cavity, and there are certain precautions which should be borne in mind with regard to each. The proper method of procedure in all—even the apparently most obvious and straightforward—cases is to divide the operation into two stages, viz:—1. That of exploratory puncture. 2. That for establishing drainage. In simpler words the surgeon must find the cavity before he can tap it, and present experience teaches that it is not easy to define a cavity with the stethoscope, and still more difficult to strike it with the trochar. It must be said, too, that accurate auscultation with a view to strictly defining the outline of cavities for the purposes of surgery, requires a closer study on the part of physicians. • Distinction of pulmonary from pleural cavities.—It is often a very difficult matter to distinguish a pulmonary from a pleural cavity. The mistake of confounding an empyema with a lung cavity is chiefly of im- portance at the apices of the lungs, where it is most apt to be made, since there is less temptation to interfere with a lung cavity in this situa- tion than in any other. Sometimes pleuritic cavities are here discovered post mortem which, had they been recognized during life, might have been dealt with and the patient saved. Having determined on operative - treatment, however, the discovery that a supposed pulmonary cavity was really a local empyema, would be a matter for congratulation rather than otherwise. The clinical features most characteristic of a pulmonary cavity are as follows:— Distinctness of breath-sounds, their hollow quality, and the presence of gurgling rales and cavernous splash on coughing. Whispering pecto- riloquy is another essential sign of much importance in association with the other signs in distinguishing a pulmonary from a pleural cavity. It TREATMENT OF PULMONARY CAVITIES. 159 must be borne in mind, however, that one observation is often not suffi- cient for diagnosis, for if the cavity be filled with secretion, or its bron- chus from any cause temporarily occluded, none of the signs may be obtained. In the case of cavities near the surfaee, a distinctly tubular percussion-note may be elicited, most clearly when the patient's mouth is open, contrasting with the dullness over a more or less extended area of the surrounding lung. To define the outline of a cavity.—In investigating an area of excava- tion with a view to surgical treatment, a circle should be drawn to include the centre of greatest intensity of physical signs. Then using a stetho- scope with a small chest piece, this centre should be gradually approached from all sides, and a mark made at each point where pectoriloquy and cavernous breath-sound are first distinctly recognizable. In this way an outer circle is drawn, marking off a larger area. Further, the limits of dullness should be defined, and the position of other organs, the heart and diaphragm especially, taken into careful account. Surgical Exploration.—The physician having thus marked out the area for exploration as accurately as possible, I believe it to be the best practice for the surgeon to make an incision along the lower margin of the intercostal space, which crosses the centre of the area marked. Having stopped all bleeding and fairly exposed the intercostal space, a puncture should be made with a fine silver canula through the central part of the inner circle, pushing the trochar boldly in, and quite vertically to the surface at the spot chosen. Several points may be thus explored should the first puncture not be successful. The sign of success is the escape of some purulent secretion through the canula, showing that the cavity has been struck; the secretion may slowly well up, or be shot out with a rush of foetid gas. The instrument should be introduced for an inch and a half or two inches in the first place, and the stilette then withdrawn for a few minutes; if no matter appear the instrument should be pushed in further, and then slowly and cau- tiously withdrawn, the surgeon testing each depth from the surface and endeavoring to ascertain by lateral movements the resistance of tissues and degree of fixity of the instrument. The length of the canula should be known beforehand, so that its depth of penetration may at anytime be calculated. A small syringe or aspirator should be at hand, which may at any time be fitted to the canula. Having failed to strike the cavity it is probably best to desist from further measures, but a fearless and thorough exploration should be made at several points before accepting failure. A silver canula is useful since it becomes readily discolored on meeting with gangrenous tissues or the foetid contents of a cavity. The advantages of incising first the chest wall down to the pleura are great. The depth of the external tissues 160 DISEASES OF THE LUNGS AND PLEURAE. to be otherwise traversed by the trochar, unless this precaution be adopted, is considerable and uncertain, and the tightness with which the instru- ment is grasped by the skin renders it difficult or impossible to gain information with regard to resistance or otherwise within the chest. Only a rough guess can even be made as to the extent to which the lung has been penetrated. Further steps in the operation.—If the escape of a few drops of dis- colored fluid or pus show that the cavity has been reached, the canula must be most jealously maintained in situ by an assistant, and used as a guide in further steps.' The next point to decide is whether there is room for the drainage tube, and if there be any doubts on this point it will be best at once to remove an inch of rib before opening the pleura. The costal pleura having next been divided for an inch, it will be at once seen whether the visceral pleura be adherent. In most cases it is so, and a narrow-bladed bistoury can be guided along the exploratory canula, so as to divide the inner pleural layer, and at the discretion of the surgeon to pass onwards until the cavity is reached. Only a slight. incision need be made with this instrument, however, and it can then be withdrawn, to be replaced by the narrow probe-pointed forceps of Lister, passed along the directing canula until the cavity is reached, then opened out and withdrawn, so as to rend open the cavity with the least risk of serious hemorrhage.2 The finger can now be inserted, the cavity thor- oughly explored, its dimensions in different directions ascertained, and a large drainage tube introduced. After the remarks already made in connection with empyema, it is scarcely necessary for me again to insist upon the importance of all in- struments used, of whatever kind, being thoroughly clean and steeped in 1 in 20 solution of carbolic acid. The hands of the operator and of all those who have to do with the case must be carefully rinsed and all sponges wrung out of a similar solution of strength 1-40. The spray should also be used during the operation. If this should not be deemed necessary on account of foetor being already present, it is well, as recom- mended by my colleague, Mr. Godlee, to thoroughly mop out the wound with a 1 in 40 solution of chloride of zinc, which has the additional ad- vantage of arresting capillary hemorrhage. The usual charpie and car- 1 In the discussion on Dr. Cayley's case of gangrenous cavity of the lung cured by external drainage, Mr. Godlee suggested the use of a canula devised by Sit' J. Fayrer for exploring abscess of the liver, and provided with a groove for the purpose of acting as a director to guide any instrument to the cavity. Proceed- ings of the Roy. Med. Chir. Soc, N. S., vol. i., No. 6, 1884. 2 Prof. Mosler of Greifswald, Ueber locale Behandlung von Lungenkaver- nen, Berl. Klin. Wochenschrift, Oct., 1873, was the first I believe to advocate the method of opening pulmonary cavities by the use of dressing forceps. TREATMENT OF PULMONARY CAVITIES. 161 bolic gauze dressing is further requisite, allowing a sufficient thickness for the discharges to drain into. Smart hemorrhage will sometimes occur during this operation, as might be expected, but on air being freely admitted it usually soon ceases, if not, the wound must be for a short time plugged. I have not yet seen more than enough to cause momentary anxiety. Still it is most desirable to avoid as much as possible the use of cutting instruments in dealing with the lung. In some cases, although the fine trochar gives evidence of having reached the cavity, it cannot at the time be found with the coarser in- struments, the guiding canula having perhaps become displaced. Under these circumstances it is best to leave in a drainage tube, in the hope that the cavity may finally discharge through it. This happened in a most successful case of Dr. Cayley's, operated upon by Mr. Gould.J The treatment subsequent to the operation must be carried on in the same carefully antiseptic manner, and in accordance with ordinary prin- ciples, and the special circumstances of each case. In cases in which, on cutting through the parietal pleura, the lung is found not to be adherent, it is best to postpone the further steps of the operation for a few days, by which time adhesions will have become suffi- ciently established. The danger of finding no adhesions is naturally much greater in recent than in chronic cases, and if the operation be persisted in, there is much risk of a virulent pleurisy being set up by the escape of some of the foetid contents of the cavity into the pleura. It is best therefore, if possible, to wait a few days before proceeding further. I have elsewhere' pointed out the importance of making the puncture over the point which the physical signs indicate tp be the central part of the cavity, otherwise risk is run of missing it altogether, or of opening up some outlying loculus, which retracts and interrupts free drainage. I have already intimated under their several headings, that neither suppurative nor gangrenous cavities require as a matter of course imme- diate interference; the abscess may discharge or the sphacelus escape through the bronchial tubes, and the patient make a good recovery. * The physician must judge by the general principles already laid down, as to the necessity of interference. In diffuse gangrene, but little could be hoped for from surgical treatment. The surgical treatment of bronchi-ectatic cavitation of the lung has hitherto, it must bo confessed, been only partially successful, but where the area of disease is definable, and the patient's health is becoming un- dermined in spite of all the resources of medicinal and climatic treatment, 1 Med. Cliir. Trans.,vol. lxvii., also discussion in Proceedings, N. S.,vol. i., No. 6. 8 Med. Chir. Trans., vol. lxiii., p. 351, 1880. 11 162 DISEASES OF THE LUNGS AND PLEURAE. operative measures may be advised, and I believe good may be effected, although the cavity or rather area of excavation be not thoroughly drained, by setting up contractile changes in the track of the drainage tube. In a case which occurred in my practice at the Middlesex Hospital in 1879, the first I believe of the kind in which the operation was performed, I was much struck by the extraordinary effect draining the cavity had upon the cough and expectoration. Although the amount of discharge though the drainage tube did not exceed two ounces, the expectoration, which had previously amounted to sixteen or twenty ounces per diem, was reduced to almost nothing.' The surgical treatment of phthisical cavities offers less prospect of advantage than in other cases, and chiefly for these reasons. Firstly, the cavities are usually situated at the apex, and their drainage per vias naturales is therefore fairly maintained, so that the reason for interfer- ence is in the majority of cases not present. Secondly, the cavities are rarely single when associated with any activ- ity of symptoms, there being usually other smaller cavities in process of formation and coalescence at lower portions of the same or in the opposite lung. Thirdly, experience teaches that completed excavation in phthisis is often the prelude to changes of a healing kind, resulting in more or less contraction of the cavity, drying of its secretion, and amendment of all symptoms. In fact, excavation in phthisis is a conservative process in so far as it results in the removal of morbid materials that are far more in- jurious than vacuity: half the history of phthisis is made up of this elimination process with which the hectic phenomena are identified, and with the accomplishment of which they cease if the perfected elimination be not overlapped by activity of process in other centres. Hence pulmonary surgery with regard to phthisis has not I fear a hopeful future. Apex cavities have, however, been tapped and aspirated, and iodized solutions injected into them,2 and although the results have hitherto not been encouraging, the operative measures have been gener- ally well borne. Cases now and again present themselves in which the extent of excavation, superficialness of cavity, restriction of disease to one side, and large amount of secretion, strongly suggest external drainage, and I have seen indications after death of an attempt of such cavities to find an external vent by perforation of the chest wall. An interesting case was recorded by Dr. Hastings as long ago as 1844, in which a large apex cavity on the left side was incised through the 1 On a case of basic cavity of the lung treated by paracentesis, by R. Douglas Powell, M.D., and R. W. Lyell, F.R.C.S., Med. Chir. Trans., 1880. 2 F. Mosler, Ueber locale Behandlung von Lungenkavernen, Berl. Klin. Wochenschrift, October, 1873. Pepper, Philadelphia Medical Times, March, 1874. TREATMENT OF PULMONARY CAVITIES. 163 second intercostal space, and a drainage tube inserted, with immediate relief to cough and expectoration.' Sir Spencer Wells, in a letter to the Lancet, shortly after the recent discussion on the surgical treatment of lung cavities at the Medico- Chirurgical Society, alluded to the case of an old man still living, in whom in 1843 a pulmonary cavity opened naturally by perforating the chest wall in the axillary region." The proposed operation of extirpating diseased portions of lung in phthisis and other affections, cannot yet be considered as fairly within the range of practical surgery. 1 This case was under the care of Dr. Hastings and Mr. Storks, and was com- mented upon by Dr. Hocken, Lond. Med. Gazette, December, 1844. 2 See Lancet, 1884. CHAPTER XT. ASTHMA. On more closely regarding the several varieties into which asthma is divisible for clinical convenience, it will be observed that they represent merely etiological sub-divisions of a disease which consists essentially of a paroxysmal dyspnoea from disturbed innervation of the bronchi. To discuss again the numerous theories that have been held respecting the true nature of this disease would occupy too much space. These theories have been well related in Salter's ' standard work. The essentially spasmodic nature of asthma was recognized by Laennec, in consequence of the want of physical signs indicative of chest disease in the earlier periods of the malady, and from the fact that Andral had made some post-mortem examinations without finding anything in the lungs to account for the paroxysms. The character and seat of the spasm were more precisely ascertained by Dr. C. J. B. Williams2 from his care- fully devised experiments showing the contractility of the bronchial tubes under various kinds of excitation. The anatomical and physiological facts upon which the bronchial spasm theory—now generally, but not universally, accepted—is based, are beyond dispute, viz.:—1. That the bronchial tubes are more or less muscular down to their terminations in the infundibula or alveolar passages (Schultze).3 2. That the bronchial tubes are capable of contrac- tions, even to closure, in their smaller divisions, under electrical and mechanical stimuli (Williams). 3. That the nerve supply of the bron- chial membrane is derived from the vagus and sympathetic, through the medium of the pulmonary plexuses and of ganglia distributed, to an un- defined extent, along the course of the bronchi. (See page 15). The clinical facts and arguments from which this view finds support may thus be summarized:— 1. The fact that an attack of asthma may supervene in the course of a few minutes, or even seconds, in a person in whom there can be found no evidence of chest disease. 1 On Asthma, its Pathology and Treatment, by Henry Hyde Salter, M.D., F.R. S., 1868. 2,Experiments on the contractility and sensibility of the lungs and air tubes, 1840, see Diseases of the Chest, by C. J. B. Williams, M.D., 4th edit., p. 320. 3 Strieker's Human and Comparative Histology, (New Syd. Soc. Edit.), vol. ii., p. 60, 1872. ASTHMA. 165 2. Of the organic lesions which can be said in different cases of asthma to have led up to the spasmodic seizures, there are none which singly or combined are proper to that disease. 3. Asthma leads on to certain pathological conditions recognizable during life, notably emphysema, chest deformity, cardiac disease, and visceral congestions; but these lesions are distinct mechanical conse- quences after long continuance of the disease, and in their earlier stages are totally inadequate to account for the asthmatic phenomena. 4. In view of the fact, which cannot be gainsaid, that asthma often occupies that period in the morbid history of cases, which intervenes between the occurrence of some inflammatory chest lesion and the super- vention of marked emphysema and its associated phenomena, it has been maintained that asthma is a mere symptom, and its antecedents and sequelae form one continuous though protracted pathological process.1 The oc- casional occurrence, however, of asthma, without any pre-existing lesion, the frequent subsidence of the dyspnceic phenomena whilst the lesions remain, and the total inadequacy of any one or any combination of these lesions to give rise to the asthma paroxysm, compel us still to look beyond the pulmonary system for the pathology of the disease. 5. The family histories and mental proclivities of many asthma patients, the capriciousness and intermittent character of their attacks, recall to mind such affections as neuralgia, migraine, epilepsy. To how many causes may an attack of neuralgia be traced !—dental irritation, loaded rectum, fatigue, mental exhaustion, exposure to chill, disordered stomach, may be enumerated amongst them, yet the neuralgia is inde- pendent of them all, having its pathology apart; nay more, it may in turn produce certain peripheral affections, of which urticaria, herpetic eruptions, and local sweatings are examples. It will similarly be found that although many pathological states may be associated with asthma, the discovery of which may be of great value in directing treatment, yet the disease is a thing apart from them all, a disorder of the nervous system. Etiology.—A considerable number of cases of asthma are attributa- ble to inherited predisposition, and in many instances what is termed a neurotic family history obtains, although direct inheritance of asthma may be wanting. Epilepsy, insanity, neuralgia, chorea, hysteria, and asthma, being diseases all within the range of interchangeability in families. Asthma is said to be much more common in males than in females. This does not happen to be in accord with my own experience. The disease is again stated by Dr. Salter and others to occur most frequently in the first decade of life, a period during which the maladies commonly calling it forth, prevails, e.g., measles, bronchitis, whooping cough.2 Be- 1 Berkart, On Asthma, 1878, p. 111. All that can be said in favor of the.organic as against the nervous theory of asthma, is ably adduced and argued in this vol- ume. 2 Berkart, p. 127. 166 DISEASES OF THE LUNGS AND PLEURAE. tween puberty and early middle life, and in females about the menopause, the disease is not uncommonly first manifested. A depressed state of the general health predisposes to the occurrence, perhaps one might better say to the recurrence of asthma; but there are many individual exceptions to this rule. The exciting causes of asthma are:—(a) Direct. (1) Irritants of all kinds, in the form of organic and inorganic dust or irritating vapors; (2) climatic influences of most varied kinds, those most distinctly potent being associated with dampness, excess of ozone, insufficient ventilation; (3) inflammatory chest affections, especially bronchitis, chronic pneu- monia, pulmonary fibrosis; (4) pressure upon a main bronchus. In this group it will be observed that the irritation which occasions the spasm, is applied to the mucous membrane in the form of dust parti- cles, irritating atmospheric conditions, inflammatory excitation, direct pressure, or, as in the chronic fibrous affections of the lung, from mucus collecting in the bronchial tubes. (b) Reflex excitation. (1) Gastro-intestinal disturbance, especially flat- ulent distension of stomach or bowels, and loaded colon; (2) intestinal parasites; (3) excitation at some higher point of the naso-bronchial tract;' (4) uterine disturbances, menstrual and climacteric; (5) excitation of cutaneous nerves. In these cases the broncho-pulmonary distribution of the pneumo-gastric and sympathetic nerves, is affected reflexly by irrita- tion applied at some distant distribution of the same or of other nerves. (c) Centric excitation. (1) Pressure of tumors upon the pulmonary plexus or disease affecting the pneumo-gastric centre; (2) emotional causes; (3) morbid conditions of blood circulating through the nervous centres (" humoral" asthma). The production of asthma in association with morbid conditions of blood is probably of very complex mechanism. It is said that in those subject to asthma the circulation of blood tainted by the products of in- complete secondary digestion, causes the attack through direct irritation of the broncho-pulmonary nerves. Flatulent dyspepsia and irritating intestinal secretions are, however, inseparable concomitants of probably greater potency. Again, the asthma frequently observed in uraemic con- 1 Attention has recently been especially drawn to the fact that some cases of asthma are due to the presence of nasal polypi, and to a peculiar turgid condi- tion of the turbinate bones, in fact to irritation of the sensory fibres of the fifth nerve, distributed to the nasal membrane. Hay asthma is probably in a great measure due to this reflex irritation. Dr. Semon refers to the observations of Dr. Hack of Freiburg with commendable caution in the Year-book of Treatment, 1884, p. 284. From Dr. Semon's observations it appears that the turbinates are by no means the bodies especially concerned in the production of the numerous reflex maladies, asthma, cough, vertigo, epilepsy, etc., attributed to them by this author. ASTHMA. 167 ditions is associated with pulmonary oedema, perhaps bronchial oedema also, and cardiac disturbance or disease. (d) Eruptive affections of the bronchial tract. Asthma has been fre- quently observed to be associated with cutaneous affections, especially eczema and psoriasis. Sir Andrew Clark ' has recently pointed out its fre- quent concurrence with urticaria, and contended that the phenomena of asthma were mainly due to urticarial-like swellings of the bronchial mucous membrane, such as occur in hay fever, with which the asthma often alternates, and out of which it often comes. I am convinced that a certain proportion of the cases of asthma I have met with may be thus explained. It is to be observed, however, that urticaria is itself a nervous lesion usually of reflex origin. Symptomatology.—The subjects of asthma present in the advanced periods of their malady a characteristic physiognomy:—thin, of nervous temperament, grave-featured, with slightly depressed angles of the mouth, high-shouldered and round-backed, they carry the impress of suffer- ing in feature and build, and one is sometimes surprised at the power of work, keenness of wit and capacity for enjoyment with which these persons are gifted. It requires many severe attacks, however, to bring about these characteristic appearances, and in the intervals between the earlier seizures, there may be nothing in the physiognomy of the patient symptomatic of asthma. In the latter periods of the disease, and at an earlier date, after having recently passed through an attack, there may be quickened breathing accompanied by slight wheezing, very perceptible to the observer although the patient would consider himself quite free from dyspnoea. There is another type of asthmatic, which may perhaps be distinguished as the gouty type, in which the patient is full-fleshed with excess of adi- pose tissue, especially about the abdomen, the general build being rather of the short-necked apoplectic type, than of the thin stork-like look of the victim of the neurotic form of the disease. The distinction is one of considerable practical importance. Attack.—Patients with true spasmodic asthma may be seized at any time of the day or night, but more frequently the attack comes on at night after the first sleep. A certain feeling of oppression about the chest attended perhaps with some wheezing may give warning of the ap- proaching seizure. More rarely the attack comes on almost instantane- ously, and without warning. The sense of oppression may partially awaken the patient or give rise to some disturbing dream, and he either starts up in a fright with the fit of dyspnoea full upon him, or more gradually awakens to the increasing difficulty of respiration. A severe attack of asthma is to the inexperienced truly alarming to witness; the expression of face, pale, staring, anxious and distressed, the 1 Paper read before the Bath Meeting of the British Medical Association, 1882. 168 DISEASES OF THE LUNGS AND PLEURAE. mouth slightly opened, its corners twitched downwards with each brief effort at inspiration, whilst the neck muscles start forward in violent con- vulsive action. The shoulders are rounded, the body inclined forwards, and the hands rigidly grasp some firm object to fix the scapular and humeral attachments of the chest muscles. With the powerful inspira- tory jerk thus effected the thorax is lifted en masse, but the deepening of the supra-clavicular hollows and depressed lower thorax, sternum, and epigastrium, bear witness to the small penetration of air to the lungs in response to all this effort. Expiration is still more difficult, for the ex- piratory force is, so to speak, beaten in detail. The air current in in- spiration starts towards points of obstruction with a force proportional to expansion. In expiration, however, each infundibular current is ob- structed whilst yet a feeble stream, the expiration is thus prolonged, labored, and but feebly and gradually effected, when, without a moment's pause, the quick, short, powerful, inspiratory jerk again takes place. The actual number of respirations per minute may not be increased, the pulse is, however, invariably quick, small, and often irregular and vacillating. In earlier attacks, more especially, there is great restlessness and fre- quent change of posture, with a disposition to lose self control in the desperation of air hunger. But the experienced asthmatic assumes and maintains some favorite attitude. The severity of attack may last from a few minutes to many hours, but it will be observed that even in the most urgent cases there are intervals of partial relaxation, during which the breathing becomes more easy, to be followed shortly by full intensity of spasm. Towards the close of the attack cough comes on, and with the expec- toration of some viscid mucous pellets, the dyspnoea is greatly mitigated. The body temperature during the seizure is depressed, cold sweats break out over the forehead, and the features become dusky, and partially cyanosed. In very severe cases capillary hemorrhages into the conjunctiva have been noticed (Walshe). The mind rarely becomes even for a moment clouded, however, and only in early cases does the patient sometimes lose that self-control which is of so much service to him in the struggle. The urine is generally abundant, pale, and of low specific gravity, and the solid ingredients are lessened (Ringer). The subsidence of the attack is generally gradual but sometimes almost sudden, with more or less expec- toration, and the exhausted sufferer falls into a troubled sleep. Physical signs.—During the'attack the thorax is semi-expanded, with but little movement in response to the respiratory efforts, the percussion- note is resonant, and more or less of the emphysema type. Careful per- cussion is, however, impossible and useless. Auscultation reveals but little or no breath-sound, beyond a short wheezing in response to the sharp inspiratory jerk, whilst the expiratory murmur is wholly obscured by the prolonged cooing sibilus of varying note. The heart's impulse ASTHMA. 169 ■can be best felt, and sometimes strongly so, at or below the ensiform car- tilage. The amount of expectoration varies with the intensity and duration of the attack. The most characteristic expectoration consists of little pellets about the size of a pea, and '' of the consistence of jelly or thick arrowroot, of a pale grey color, of an opalescent transparency, and a saltish taste " (Salter). These pellets are constituted of a viscid homogeneous matter, containing peculiar spheroidal or elongated cell-like bodies, of the size of large pus cells, but without nuclei, and with no distinct mem- brane. More or less numerous pigmented granular cells are also to be seen. Slight haemoptysis is occasionally, but rarely, observed in severe cases of asthma. Where pulmonary oedema or congestion follows upon severe attacks of asthma, the expectoration is more abundant, consisting of a frothy sometimes slightly blood-stained mucus. Fibrinous casts of tubes may be found in asthma sputum, but are not constantly present. After a severe attack of asthma, much prostration and fatigue is ex- perienced from the severity and duration of the struggle, and from want of food and sleep. These symptoms will be soon recovered from, how- ever, but renewed attacks commonly ensue at short intervals, until at the end of a certain series the malady appears to be for a time exhausted. More or less wheezing rhonchi generally persist for some hours or days, and in severe cases it is usual to find at the bases some fine bubbling rales. The percussion signs and chest conformation at this period are those of acute pulmonary emphysema, varying in degree according to the severity of the attack. After a succession of attacks there is an amount of acute emphysema of the lungs with oedema of their bases, and over- strain of the right ventricle of the heart, requiring some time and treat- ment to remove. From single attacks, even although very severe, the patient after a night's rest may feel quite restored. In other cases again, the attacks are brief, but return each night; these are cases usually in which the paroxysm is controlled by some remedy, and although jaded by disturbance of rest, such patients are able to pursue their daily work or pleasures. Periodicity of seizure is usually a marked feature of asthma. The seizures maybe daily, weekly, monthly, yearly, or at other tolerably regular intervals. A patient may suffer a series of daily seizures, and then enjoy a certain interval of freedom. It will be observed, however, with asthma as with epilepsy, that as time advances the attacks, unless influenced other- wise by treatment, tend to become more frequent although less severe, a number of minor seizures being interpolated between the more regular attacks, the gradually increasing emphysema rendering the intervals less and less defined. In the earlier years of true spasmodic asthma, patients are able in the intervals of attack to take part in sports and exercises, which make large 170 DISEASES OF THE LUNGS AND PLEURAE. demands upon the respiratory powers. As the disease continues from year to year, however, it gradually entails other symptoms significant of definite pulmonary lesions; shortness of breath, and more or less wheezing continue through the intervals: the physical signs of emphysema remain permanently, and visceral congestion and associated dyspeptic symptoms- become manifested. The heart especially suffers, its right ventricle be- comes dilated, systemic venous fullness ensues, and, finally, oedema of extermities, abdominal dropsy with enlarged and hardened liver, and albuminous urine supervene, (see Emphysema, p. 119). In a certain number of cases of asthma, on the other hand, the lungs give way, an atrophous form of emphysema appearing, which proceeds to coalescence of vesicles with adjacent pulmonary thickening, bronchi-ectasis and a spurious kind of phthisis at one or both apices. In yet other cases, in young sub- jects, the asthma is superseded by catarrhal phthisis, with the onset of which the paroxysms of asthma may wholly cease. The prognosis of asthma proper is estimated by ascertaining the amount of physical damage the patient has as yet sustained to lung and heart. Asthma per se never kills, nor is the asthmatic prone to some of the diseases, e.g., tubercle, cancer, Bright's disease, which shorten life. His own peculiar malady is enough for him to contend with, and it enforces upon him a comparatively sheltered life. Asthma is in fact compatable with a life of medium length and of much usefulness, but of much suffering and self-denial. Family longevity should be inquired into in regard to prognosis. For purposes of clinical classification asthma may be conveniently divided into:— 1. Idiopathic or true spasmodic asthma. 2. Catarrhal asthma':— Simple. Dust. Bronchitic. Hay. 3. Peptic asthma:— Gastro-intestinal. Humoral or metabolic. 4. Cardiac asthma. 5. Eruptive asthma. 6. Uraemic asthma and other toxaemic forms. 1. Idiopathic or true spasmodic asthma includes those cases of true neurosis in which no lesion can be found and in which the exciting cause of the attack, if any can be found, is either some mental or emotional dis- turbance, e.g., mental shock, violent emotion, severe anxiety, or if ma- terial, is of so slight and ephemeral a kind as, e.g., a brilliant light, a transient odor, the momentary application of cold to the surface, and the like. This form of asthma, as already said, can be best compared to neu- ralgia, epilepsy, migraine, perhaps also mania. The neurosis is inherited ASTHMA. 171 either directly or through some of the allied forms mentioned. The attacks are more distinctly periodic than in any of the other forms of asthma, and with the completion of each attack the peculiar neurosis often seems to be for a time worn out. 2. Catarrhal asthma.—In this variety catarrhal symptoms precede and attend those characteristic of asthma, the dyspnceic phenomena being- due to direct catarrhal irritation of the bronchial nerves, to reflex excita- tion of them through branches more highly distributed to the main bron- chi or larynx, or lastly to similar excitation through the medium of the fifth nerve distributed to the nasal mucous membrane. Bronchitic asthma is but a catarrhal affection of the bronchial tubes in a subject predisposed to asthma; the special character of the disease being derived from the individual peculiarity, not from the catarrhal affec- tion, which commonly arises in the ordinary way. In this affection during the acute stage the dyspnoea is more or less continuous. Subsequently, with the greater freedom of secretion and expectoration, the dyspnoea occurs chiefly in the early morning after a few hours' sleep, and is due to accumulation of mucus in the tubes, with the expulsion of which the spasm ceases. In many of these cases there is some evidence to be found of a former inflammatory chest attack. In cases of old standing emphysema fresh bronchial catarrh is often attended with dyspnceal seizures of an asthmatic type, which are due to obstruction of the tubes by mucus disturbing the, at all times, unstable respiratory equilibrium of the subject of emphysema. Only in popular parlance can such cases be called asthma. Of dust asthma I have detailed a well-marked example arising from the inhalation of wood dust; other mechanical irritants have similar effects upon a certain proportion of those exposed to them (see page 107). Hay asthma is a disease in which catarrh of a very intense kind is set up in the nasal and upper bronchial passages by the inspiration of pollen dust from graminaceous plants (anthoxanthum odoratum, species of Poa and other varieties). The perfumes of various flowers and the powder of ipecacuanha are said to affect sensitive persons in a similar manner. Only a small proportion of those who suffer from "hay fever" or summer catarrh are afflicted with asthmatic paroxysms; and it is probable that the hay or other specific emanations produce asthma in a person predisposed to that malady after the manner of other irritants. 3. Peptic asthma is placed by Salter as a sub-variety of excito-motory or reflex asthma, in which the asthma is occasioned by " irritation of the gastric filaments of the pneumo-gastric nerve propagated reflexly to the pulmonary filaments, and producing through them motor phenomena, i.e., bronchial contractions" (loc. cit., p. 124). It is not to be doubted that 172 DISEASES OF THE LUNGS AND PLEURAE. many cases of asthma are to be met with which are manifestations of dyspepsia, in the sense of some form of gastro-intestinal irritation. This class of peptic asthma may, however, with great practical utility be enlarged to include cases in which faulty secondary digestion appears answerable for the incitement of the paroxysms. Dr. Salter expressed the belief that the introduction of food frequently gave rise to asthma, not by irritation of the alimentary canal, but by absorption into the veins of materials .perfectly normal to the stage of the digestive process, but which in the asthmatic stimulated the unduly sensitive pulmonary nervous system to produce spasm (p. 32). Certain articles of diet, especially saccharine and carbonaceous matters, prove especially irritating to some asthmatics. In the incomplete metabolism that is a notable phenomenon in the gouty subject, the blood circulating through the lungs is also charged with imperfectly changed and effete materials. It may well be believed, too, that in cases of loaded colon, asthma is sometimes set up by the reabsorption of putrefactive matters. Whilst it is possible that in this "humoral" form of peptic asthma, the offending material affects the periphery of the pulmonary nervous system, it seems to me much more probable that the central portion of that system takes cognizance of such matters, and is unduly irritated by them. 4. Cardiac asthma is a consequence of heart failure. In heart dis- eases of various kinds, fatty and senile degenerations, valve disease with incomplete or damaged compensation, paroxysms of dyspnoea are met with. Most commonly the attacks occur during sleep or towards the morning, when the blood pressure is naturally low. Signs of passive congestion of the bases of the lungs, and more especially on one side, may generally be detected, and some blood-staining of sputa is not infre- quently observed to follow the attack. 5. In uraemic asthma, oedema of the lungs is generally present. I have seen cases, however, in which the morbid material in the blood seemed to be more directly the excitant. 6. Eruptive asthma.—Under this heading may be included those cases in which asthma is associated with cutaneous eruptions (especially urti- caria) in which there is reason to suspect that the bronchial mucous membrane is involved. Treatment.—There is no disease which is so extensively " quacked" as asthma. Persons who are the victims of the pure neurosis are amongst the most restless of mankind. Their temperaments are often of the highly- strung nervous type, and whilst they are gifted with much courage, en- durance and determination, they possess little faith, many friends, and much credulity. The practitioner who would guide these sufferers, must himself have clear opinions respecting the salient points in treatment, and must be patient in hearing and endeavoring to understand the in- dividual experience of the patient himself. ASTHMA. 173 The treatment of asthma must be divided into climatic, anti-spasmodic and remedial. Climatic treatment consists, firstly, in the removal of the patient from those external surroundings which appear to have led up to his attack, to more favorable conditions of residence, e.g., from a dusty to a pure atmosphere, from a cold, damp house oi locality to a dry soil and a well- ventilated and cellared house with no trees, unless they be of the pine tribe, in near proximity. Secondly, to tell with precision what locality will suit a given individual with asthma is very difficult; there are idiosyncracies in each case, and no asthmatic should burden himself with a house until he has first tested the locality by residence there for some time. There are, however, certain climates which are most likely to prove beneficial for asthma patients. (1) Bournemouth, the St. George's Hill neighborhood of Weybridge, Farnborough, and Bagshot districts, may be named amongst English localities, and Arcachon for the winter and spring abroad, as places which are under all circumstances preferable to cold, damp neighborhoods, but as being best adapted for the purest forms of asthma in which the neurosis is most marked. (2) Torquay, St. Mary Church, Pau, Cimiez, Hyeres, Algiers, are varied resorts adapted for winter residence for the mixed catarrhal forms of asthma. (3) Experience teaches a certain number of asthmatics that a sea voyage does most for them, and in such cases the cure may best be thus started. Cases of dust and hay asthma are especially suited for this plan, as also are cases in which the first seizure has been traceable to a nervous system broken down by anxiety, overwork or excesses. (4) In young subjects with as yet no marked emphysema, the rarefied airs of St. Moritz, Davos, Wiesen, yield good results, and in the hot months they may be resorted to with advantage by some older subjects. Ilkley, Ben Rhydding, and Dartmoor, are very suitable situations for convalescent asthmatics in the summer season. (5) A considerable number of asthma patients do best in towns, being chiefly cases of those who have removed from more or less damp localities surrounded by trees. As a rule asthmatics (and indeed all chest invalids) should repair to large towns or sea-side resorts in the late autumn, and perhaps the late spring. Medicated airs and baths.—In cases of catarrhal asthma and in those in which a gouty element, or an association with eczematous eruptions or urticaria, can be observed, a short, two or three weeks' summer course at Mont Dore, Aix les Bains, Allevard les Bains, or Dax, will be attended with long-continued benefit, the course at one of these bathing resorts being followed up by a further sojourn at some bracing place, e.g., Eaux Bonnes, Cauteret, Spa, or the Swiss mountains, or returning home to 174 DISEASES OF THE LUNGS AND PLEURAE. Ilkley, Ben Rhydding, Braemar, or other moorland districts of Yorkshire or Scotland. A course of Turkish baths in London, Ramsgate, or Ben Rhydding, for those who cannot get abroad, sometimes proves of great service. I have in some cases seen much benefit from the use of the compressed air baths at Ben Rhydding, but I can only mention this as an empirical fact. Minute traces of arsenic mingled with the vapors at the Mont Dore baths, are regarded as answerable for their good effects, and at Allevard the sprayed air of the inhalation chambers is decidedly charged with sulphuretted hydrogen. This latter treatment is most adapted for the chronic bronchitic forms of the disease; at the other places probably the sweating of the skin and bronchial membranes constitutes the chief remedial factor. Regulation of the digestive function.—Not less important than the selection of a suitable climate, is the careful regulation of the digestive functions of the asthmatic. In a large proportion of cases the exciting cause of the attack is some error in digestion, whilst in all cases the diges- tive function ultimately suffers, and reacts unfavorably upon the spas- modic troubles. In cases in which there is excess of uric acid or urates, and a disposition to flatulent dyspepsia, cutaneous eruptions, etc., sweet wines, raw fruits, sugar, cooked butters, pastry, should be excluded from the dietary. Very slow eating should be strictly enjoined, and the staple food, including a moderate supply of meat, should be taken by the mid- day meal, only the lightest possible diet being allowed later in the day. An alkaline bitter may often be taken twice a day with great advantage when the tongue is red and coated, bismuth being added when there is gastro-dynia. The liver and bowels require careful attention, very small doses of mercurial being useful from time to time, whilst in these, as in all neurotic subjects, large doses of this drug are positively harmful. A sulphate of soda saline should be taken in hot fluid in the morning after each dose of mercurial. If the rectum be loaded, relief should be effected by enemata rather than by violent aperients. When the tongue is fairly clean, or at all events when the practitioner is satisfied that the primae viae are efficiently acting, a course of arsenic is often of the greatest service. Treatment of the paroxysm.—Most commonly the practitioner makes _ his first acquaintance with the asthmatic patient when the paroxysm is at its height. A few questions as to duration of attack, preceding attacks, and circumstances and symptoms immediately antecedent to present seiz- ure, will suffice to direct a rational and safe treatment. When irritating matter is present in the stomach, whether in the shape of undigested food or irritant catarrhal mucus, an emetic of twenty grains of ipecacuanha, or a subcutaneous injection of ^ to £ grain of apomor- phia, will give prompt relief by its removal. Warm water, with a little ASTHMA. 175 carbonate of soda, should be given to encourage a thorough clearance of the stomach. In cases of catarrhal asthma during the paroxysm ten minims of ipecacuanha wine, with fifteen or twenty minims of ethereal tincture of lobelia, given every half hour for two or three doses, then every hour or two hours, will often prove serviceable. The fluid extract of Grindelia Robusta (U. S. P.) in fiftesn minim doses, maybe sometimes substituted for the ether. In the choice of sedative remedies, a careful judgment must first be arrived at as to the amount of tubal catarrh and secretion present. The well-known " cures " of asthma, appear to owe their efficacy partly to an evacuant, partly to a sedative action. The fumes of the " Himrod," " Green Mountain," "Chester," and similar powders first excite more or less cough, after which, and especially if expectoration be effected, the spasm yields. A powder containing four drachms of powdered stramo- nium, two drachms of each of powdered nitre and aniseed, and five grains of tobacco is a very efficacious combination, much used at the Brompton Hospital. A teaspoonf ul of this powder should be made into a conical heap on a plate, lighted at the summit, and the fumes inhaled through a large inverted funnel. In the more purely nervous forms of asthma, when as yet there is no secretion present, more purely sedative remedies must be used. By closely shutting the room and filling it with the fumes of nitre,1 the asthmatic sufferer will sometimes gain relief and rest. Salter con- sidered nitre thus used a powerful sedative; but it must be confessed that its mode of action is obscure; its efficacy in certain cases is, however, un- questionable. A little chlorate of potash may sometimes be combined usefully with the nitre (about one drachm to the ounce). In the full height and intensity of attack, iodide of ethyl, nitrite of amyl2 or chloro- form may be inhaled with temporary advantage, and the true spasmodic nature of the affection will be well demonstrated by the complete subsi- dence of the sibilus under the influence of chloroform. The effect of these drugs is as a rule very evanescent, however, and their use is only desirable to mitigate extreme symptoms. Nitro-glycerine and nitrite of sodium have been recommended. Joy's cigarettes and Savory and Moore's datura tatula cigarettes will, provided the patient can inhale the smoke into the lungs, in many cases give great relief to the urgent symptoms, their efficacy being due to stra- monium and, probably, some opium combined. In severe cases an almost unfailing remedy is morphia used subcutane- 1 Four ounces of nitrate of potash dissolved in half a pint of boiling water, pour out into a soup plate, and draw through thick blotting paper, dry and cut in squares of four inches. 2 Convenient five-drop capsules of these last two drugs enclosed in silk are made by Martindale of New Cavendish Street, W. 176 DISEASES OF THE LUNGS AND PLEUR/E. ously in doses of from | to | a grain. Morphia is a remedy which, from the immediate relief it affords, is apt to be given somewhat recklessly, and to be called for by the patient peremptorily without counting the cost in after consequences. The drug, however, should be used with caution, for not a few casualties have arisen from its employment. In catarrhal cases it should not be employed, and in the most purely neurotic cases, for the relief of which it is best adapted, it is a demoralizing remedy. In fact the employment of morphia in asthma is exactly comparable to its. use in neuralgia; prompt in relieving, it lowers nerve tone, hampers secretion and increases liability to recurrence. The tendency of the patient is increasingly to fly to the use of the drug for trivial attacks, until custom renders a large and dangerous dose necessary. In certain cases the drug is necessary; they are exceptional, however, and in such cases the most strenuous efforts should be made by the practitioner to remove his patient out of the conditions to which the asthma appears attributable. Hypodermic injections of atropine ToT"sV gr- are some- times useful, and are not open to the same objections as morphia. Chloral in full doses of fifteen or twenty grains every four or six hours is also efficacious in pure asthma, and it may be used also in the catarrhal forms; its administration, however, requires strict medical supervision and very precise directions.' In hay asthma Salter recommends tobacco smoking continued to the development of symptoms of collapse. The remedy is only serviceable to those unaccustomed to smoking. In cases of catarrhal asthma especially, and in some other less-defined cases, one of the most valuable remedies is iodide of potassium, in com- bination with stramonium. The iodide is especially indicated in those cases in which there is a nightly paroxysm, but in which there is a per- ceptible dyspnoea and wheezing throughout the day. Three to five grains of iodide of potassium, with \ grain of extract of stramonium, should be given every three or four hours during the day, e.g., 8 a.m., 12 noon, 3 p.m., 6 p.m., 9 p.m., so as to administer some twelve to thirty grains of the salt, and two to three of the extract, by bed- time. After a day or two, when the patient suffers slight iodism and the physiological effect of the stramonium upon pupil and throat becomes apparent, the remedy may be continued in half doses. In the many cases in which this remedy proves valuable, it should be commenced on the first approach of asthma phenomena. In some cases in which asthma has been contracted in malarious climates, or in which a neuralgic ele- ment is traceable, quinine may be usefully given in combination with iodide of potassium. Five grains of salicylate of quinine in pill (with 'No doubt "Bromidia," consisting of chloral, gr. xv. ; pot. bromid. gr. xv. ; ext. cannabis ind., gr. \ ; ext hyoscyami, gr. \, in each fl. 3 j., will become much used in asthma. ASTHMA. 177 citric acid) may be taken three times a day, either at separate times or with each dose of iodide. Alcoholic stimulants should only be given in asthma when necessary as a restorative and in small doses. Strong coffee is of great value as a restorative after a severe paroxysm, and in some cases it distinctly relieves spasm; or caffeine, of which two or three pills of 2£ grains each, made with glycerine of tragacanth, may be taken for the same purposes. After an attack of asthma, especially if it has been severe and has left any pul- monary oedema behind, it is good practice to give small doses of digitalis (five to ten minims, three times a day) to restore tone to the heart and small vessels. The digestive system requires careful looking to; the secretions will necessarily have become disordered by the drugs used for the relief of the paroxysms, and by the venous conjection of viscera necessarily attendant upon the impeded pulmonary circulation. It is probable, too, that the function of the pneumo-gastric nerve becomes seriously enfeebled for a time by the attack and the remedies. A little pepsine and hydro-chloric acid after food, in combination with nux vomica or quinine given an hour or two before food, prove very serviceable. The most careful considera- tion must immediately be given, however, as to whether the patient cannot be moved to a more suitable locality, and this may in some cases be wisely effected, even in the midst of an attack. 12 CHAPTEE XVI. ON THE PATHOLOGY OF PHTHISIS. On inspecting the lungs of one who has died of phthisis, we meet with a very great variety of appearances, which may, nevertheless, be recognized as the results of a comparatively few morbid processes; we see consolida- tion of the lung in every stage of formation, decay, and removal; and, glancing at the emaciated form before us, we have a very practical defini- tion of Phthisis Pulmonalis, viz.:—progressive consolidation and decay of the lung with progressive wasting of the body. The exact nature of the morbid processes which lead to this destruc- tion of lung and waste of body, whatever their etiological origin may be, are of two kinds. 1. Inflammation affecting with different degrees of intensity the different tissues of the lung, and running an acute, chronic, or chequered course. 2. A new growth—Tubercle—with its characteris- tic granulations disseminated through the lungs, or collected into nodular groups, or mingled with inflammatory changes, developing into fibroid tissue, or immediately undergoing necrotic change. We may meet with either of these processes in the acute or chronic form without any admix- ture of the other, but it is comparatively rare to meet with chronic tuber- cle unmixed with inflammatory changes. It may be here recollected that fatty degeneration is one of the conse- quences of inflammation, and is the means by which the products of inflammation become eliminated or absorbed, or for a time sequestered by caseation.* The tendency of all new growth is also sooner or later to fatty decay, and in tubercle we find a special aptitude in this direction, it being a cellular neoplasm devoid of vessels. There are furthermore two conditions so inseparable from phthisis as to constitute a part of its pathology, viz.:—3. The respiratory movements of the chest cavity with their attendant mechanical effects upon the lungs and pleura under in- fluences of disease. 4. The penetration of the lungs by specific and putrefactive organisms. 1. The inflammatory process takes the largest and most important share in the production of the various appearances met with in phthisical 1 It has been recently held that there is something specific in caseous change; indeed, that this change is at least in great part brought about by the action of minute organisms, or their germs, the bacilli of tubercle. I have failed in the en- deavor to find anything tangible in this hypothesis. PATHOLOGY OF PHTHISIS. 179 lungs; it is the destroying element in this disease, as was long ago pointed out by Addison.' It may, therefore, be appropriately spoken of first. With that form of inflammation of the lung—acute sthenic pneu- monia—agreeing in many of its characters with an acute specific disease (e.g., idiopathic erysipelas), we have but little to do in dealing with cases of phthisis; we only meet with it as an exceptional complication. A person affected with acute basic pneumonia who is already cachectic, or rendered so by neglect during the disease, may become phthisical; some cases of basic phthisis have this origin. But the pneumonia which is the most constant element of true phthisis, and which will indeed, as already hinted, be found the main factor in the more chronic and cachectic forms of- basic lung disease, is of a very different kind; its onset is usually in- sidious, and its origin appears to be generally by extension of a catarrhal process from the finer bronchial tubes to the interior of the alveoli; hence its name—catarrhal pneumonia, or as it might be termed, broncho- alveolitis. This form of pneumonia is essentially lobular, although the coalescence of many adjacent lobules may cause the consolidation of a whole lobe. The alveoli are affected by this inflammation with all degrees of intensity, from mere superficial catarrh causing slight epithelial des- quamation to the most deeply destructive involvement of their walls. In the simplest alveolar catarrh the cellular products may escape with the expectoration, leaving the alveolar wall undamaged. In the next degree of intensity, the alveoli and minute bronchi become blocked with the large granular cells, which are produced in great abundance, and which may perchance be mingled with a few leucocytes. These cells, thus stuffing the alveoli, almost immediately begin to undergo fatty de- generation—the process by which resolution is naturally affected. They may liquefy, and be partially absorbed, partially expectorated; but the alveolar walls have been damaged, and permanent local collapse remains behind from their agglutination. This is the natural cure of the disease in this degree, the slightest degree that can be called phthisis. More commonly the cellular products, after having undergone com- plete fatty degeneration, become inspissated by absorption of fluid matter, and remain for a long time—perhaps for the lifetime of the patient—in the cheesy condition, or subsequently become cretaceous. This may be called natural arrest by obsolescence, and these cheesy masses are com- monly looked upon as " old tubercle." In the still more intense degree of the process—catarrhal alveolitis— now under consideration, the alveolar wall is deeply involved in the in- flammation, so that it subsequently undergoes fatty degeneration together with its cellular contents to an extent which varies with the intensity of the process, and breaks down in the subsequent liouefaction, gradually or rapidly according to circumstances. 1 Collected writings published by New Sydenham Society, p. 56. 180 DISEASES OF THE LUNGS AND PLEURAE. The elastic tissue of the lung takes no active part in any of its inflam- matory processes; it escapes but little altered when the alveoli break down, and thus, on being recognized in the sputa, affords certain evidence of pulmonary destruction. It will, of course, be understood that there is no real line of demarcation between the degrees of severity above de- scribed separately. The intensity of the first attack may at once deter- mine the depth of injury, or the lighter may gradually pass into the graver degree. But in addition to the parenchyma proper of the lung, which, with its epithelium, is the special seat of catarrhal pneumonia, there is the fibrous stroma, if one may so style it, formed by the interlobular areolar tissue, supplying sheaths to the vessels and bronchi, contributing also to the formation of the alveoli, and intimately connected at the surface of the lung with the investing pleura. It could not be expected that an inflam- mation of the lung of any great severity would leave this widely spread tissue untouched; and it might also be anticipated, on reflection, that a tissue thus, comparatively speaking, deeply placed would, as a very general rule, only be affected secondarily to disease of the parenchyma or pleura. From this interstitial tissue under conditions of inflammatory irritation are derived, in great part, the tough, fibrous, pus-secreting walls of cavi- ties, and the trabecular which for a long time resist the most severely destructive processes. The inflammatory process in this tissue is, as a rule, a much more deliberate one; even when in a state of active ulcera- tion, as in the walls of some cavities, the destruction is molecular, spha- celus is rare. Inflammatory reaction in this tissue, indeed, more gener- ally partakes of the character of growth under irritation, producing a more or less general condition of fibrosis of the lung. Decay, however, in most instances, finally sets in; the fibrous tissue, at first merely hyper- plastic, loses its characters as such; its nuclei, at first very abundant, gradually fade; its fibres fuse into tough homogeneous bands, and in their turn become granular and fatty, and finally crumble away. The various primary diseases—catarrhal pneumonia, croupous pneu- monia, chronic tubercle, pleurisy, etc.,—upon which pulmonary fibrosis supervenes, are thereby marked by clinical features of great interest and of significance for prognosis. But sometimes the fibrosis is so extensive as to become, whatever its origin may have been, the essential disease. Such cases have been very conveniently classified separately by Sir Andrew Clark under the term " fibroid phthisis." He regards the disease as sometimes of idiopathic origin, or—what amounts to nearly the same thing—as a disease which progressively invades and destroys the lung from some one point of origin, as a local pleurisy or bronchitis. 2. In order to apprehend the nature of tubercle, its relationship to other products of pulmonary phthisis, and some of the most important ways in which it extends and is disseminated, we must recall to mind that PATHOLOGY OF PHTHISIS. 181 the whole lung is pervaded in every crevice of its structure by lymphatic tissue, consisting of branched protoplasmic cells communicating with fine tubes and interstitial spaces occupied or lined with endothelial cells,1 The characteristic form of tubercle is the grey granulation, a hard, semi- transparent, cartilaginous-looking nodule of about the size of a pin-head, intimately connected with the surrounding tissue. Each granulation consists essentially of a collection of small, rounded, lymphoid cells with a delicate reticulated stroma, the cells being derived by multiplication prin- cipally from the lymphatic elements of the lung; no vessels are present in tubercle, although a vascular zone sometimes surrounds young granu- lations.5 From their close contiguity to vessels, however, the nutritive supply of the granulations is assured until from the dense multiplication of cells their central portions suffer deprivation. In the centre of the small collection is usually to be found one or more " giant cells," irregu- lar masses of protoplasm enclosing many nuclei, with a more or less branched outline, which blends with the stroma of the tubercle. Hamil- ton s regards the giant cell as an essential part of tubercle, and maintains that the peculiar fibro-cellular texture of the granulation is evolved by development of the periphery at the expense of the central protoplasm of the " cell." Ziegler' and others 5 are of opinion that there is nothing in the shape, size, or characters of the cells, absolutely significant of tuber- cle, the giant cells being found in many other morbid products (a fact which Hamilton admits), and not being necessarily present in the tuber- cular granulation. The grouping of the cells to form a definite nodule of a certain size which is avascular, and tends to necrotise in the centre, constitute the features peculiar to this neoplasm. Moreover, when sub- jected to proper staining processes, one or more tubercle-bacilli will probably be detected in the nodule, particularly within the giant cells. Whilst Dr. Burdon Sanderson has especially observed the sheaths of the minute bronchi as favorite sites for the origin of the tubercular granula- tions (there being, in the guinea pig at all events, minute gland acini in these situations), Dr. Wilson Fox has, on the other hand, pointed out a remarkable obstruction to the minute vessels of the lung as most charac- teristic of the tuberculizing process. Dr. Klein has also shown that the ultimate branches of the pulmonary artery become both invaded by the growing adenoid tissue from without, and thickened and obstructed at 1 For the development and further organization of this lymphatic, new growth is required " no more than the presence, at the seat of the irritation, of a pre-ex-' isting element of the group of connective-tissue corpuscles and endothelium.'' Buhl, quoted by Klein, op. cit., part ii., p. 69. 2 Vide plate v., fig. xxiii. of Klein's work. 3 Hamilton, Pathology of Bronchitis, Catarrhal Pneumonia and Tubercle, pp. 172-177, 1883. 4 Ziegler, Pathological Anatomy, part i., p. 166, 1883. BProf. See, Phtisie Bacillaire, p. 42, 1884. 182 DISEASES OF THE LUNGS AND PLEURAE. points by proliferation of the endothelial lining of their own inner coat. The alveolar walls, the peri-bronchial, peri-vascular and sub-pleural tissues, are then the seats of tubercular growths; but under special circumstances of irritation tubercle may be developed upon the surface of the pleura from the endothelial cells of the stomata; this growth may similarly in- trude into the alveolar spaces from one point of the alveolar wall, as de- scribed and figured by Hamilton, p. 181, fig. 57, or possibly by outgrowth from the pseudo-stomatous processes which normally penetrate to the alveolar surface. It would seem then, that, broadly speaking, the seat of tubercle is the interstitial connective tissue of the lung. Under favorable circumstances' tubercle undergoes development into a peculiar form of fibroid tissue, at first very recognizable from ordinary hyperplastic fibrous tissue, but which subsequently becomes converted into bands or tracts of uniform homogeneous texture, and finally degen- erates and is removed. This development of tubercle, before its final decay, has hardly been sufficiently insisted upon as an essential character always observable if circumstances permit the attainment of the necessary stage. It is, however, in strict accordance with the lymphatic gland type of this morbid growth, and it is of some. importance as affecting the clinical characters of chronic tuberculosis. In acute tuberculosis, the patient does not often live long enough for any process of the kind to take place. In chronic pulmonary tuberculization, however, and when tubercle attacks a lung rendered quiescent by previous disease, the stages of development of tubercle into fibroid tissue may be seen. The anatomical relationship of tubercle to phthisis and to tuberculosis respectively is a question upon which very conflicting opinions have been expressed. Until the time of Addison, and indeed up to the researches of Virchow upon tubercle, Laennec's views held good, and the tendency is now to return to them and to regard tubercle as the anatomical lesion of phthisis, and its caseation and softening as'the cause of the lung de- struction in that disease.2 It was not long after Bayle's and Laennec's teachings became known before the " tubercle corpuscle " was discovered, and the revival of the views of the great French pathologist received sup- port from the discovery of the " giant cell," still regarded by some as the criterion of tubercle. But unquestionably the pathological observations of Buhl, and the experimental inquiries of Villemin and his many fol- lowers, and finally the discovery by Koch of the tubercle bacillus have far 1 The death and removal of tubercle may be greatly hastened by associated in- flammatory processes. 2 "L'unite de la phtisie comprenant toutes ces manifestations aigues et chro- niques; il n'existe plus de dualisme entre le tubercule et la pneumonie cas£eusp ni de distinction entre la phtisie turberculeuse et la phtisie inflammatoire la pneumonie caseeuse ayant elle-meme le bacille comme t6moin constant comme origine certaine ; la pathologie experimentale en fournira la preuve." PATHOLOGY OF PHTHISIS. 183 outweighed all histological considerations towards resuscitating the doctrine of Laennec with regard to the essential unity of the lesions of phthisis. The difference histologically between tubercle and catarrhal pneumonia is, however, enormous, and it is to me inconceivable how the two can be jumbled together as one product, even though they are often found in close association under apparently similar etiological conditions. If we regard the lymphatic elements which everywhere pervade the lung as the histological source of tubercle, it is easy to conceive that we may have tubercle not only in the form of isolated nodules (miliary tuber- cle), but also in a more diffused form thickening alveoli and consolidating the lung by more or less extensive tracts of adenoid tissue (diffused tubercle). It is impossible on anatomical grounds logically to refuse this admis- sion, and it is in this more liberal acceptation of the term tubercle by Dr. Wilson Fox, that one step on the return to Laennec's view may be regarded as having been taken. Let us, however, in this connection carefully note the difference between the terms tubercle and tuberculosis. Tuberculosis is a disease-process of the definite nature of which we are daily becoming better informed, tubercle is a disease-product. The pro- cess tuberculosis may be said to consist in the more or less wide or uni- versal dissemination through the body of a poison-influence which results in an outbreak through the infected region of innumerable tubercle growths. But tubercle may arise locally by direct infective irritation, and may thence occur not in isolated granulations but in the more diffused form. Hence there need be no ambiguity about the term tuberculosis, which signifies an acute and more or less general outbreak of miliary tubercle, whilst tubercle itself, which in the form of the miliary granulations is the essential lesion of tuberculosis, may yet arise locally, outside, as it were, the general system. 3. The respiratory movements of the chest cavity take part in the pathology of phthisis as of other chest diseases, but in a more marked degree. The real explanation of the recurring pleuritic pains and adhesions in cases of phthisis is, that when a portion of lung becomes damaged in tex- ture by disease it ceases to follow accurately the expansile movements of the chest-wall; a certain gliding or rubbing motion takes place between the two normally corresponding pleural layers at this point;' friction, 1 Most authors state that a gliding movement naturally takes place between the two pleural surfaces. I am myself inclined to think that in perfect health no such motion occurs, but that the expanding lung accurately follows the expan- sion of the chest. Whether this correspondence in expansion be perfectly accu- rate or no, the gliding and friction must be greatly exaggerated over the region of a diseased portion of lung, and the explanation of adhesions in the text remains good. 184 DISEASES OF THE LUNGS AND PLEURA. local pleuritis, and adhesion result. We can readily understand, there- fore, how it is that a friction sound is often the first evidence we get of local pulmonary disease, and that a new friction sound generally means more than mere dry pleurisy; it means, in fact, an accession of lung disease. When the lung disease is of a very chronic, indurative, contractile character, the effect of the continued inspiratory, efforts to expand the toughened lung is to stretch out the adhesions and to separate the pleural layers to a certain extent; the further contraction of the lung continues the process, so that the parietal and visceral pleurae may become separated by a considerable interval of half or three-quarters of an inch. This space is at first filled by serous fluid effused into the meshes of the areolar tissue of the stretched adhesions. We thus get the oedematous pleura. At a subsequent stage, however, of the disease, by the continued growth of the areolar tissue, the whole space becomes occupied by tough fibrous tissue, and the two layers become completely welded together into one uniform fibrous thickness. That this is the real history of the enormous thickening of the pleura in many cases of chronic phthisis I have satisfied myself by repeated observation.' It has seemed to me that thickening of the pleura has been regarded too much in the light of a dangerous pathological process, liable to extend into, and by its contractile power to compress, the proper lung, tissue, whereas it will be found on careful examination to be most generally a condition secondary and quite subsidiary to the lung disease. In primary pleuritis the thickened pleura is produced in a different way. After absorption of the fluid a certain thickness of lymph often remains between the two layers of the pleura, into which the granulations from each surface penetrate, and finally unite, completing the adhesion. There are many cases of phthisis of the pneumonic kind of tolerably acute progress, and attended with little contraction, in which, though the pleural surfaces are inflamed and covered with finely granular lymph, they do not become united. It is in these cases that pneumo-thorax is especially likely to occur. The constant movement of the lungs no doubt goes far to modify and hasten the progress of morbid processes going on within them. Let us think of the lung roughly as an intricately infolded membranous surface, closely allied to, and continuous with, the bronchial mucous membrane, but peculiarly rich in blood vessels and lymphatics. The products of a catarrh affecting the larger bronchial tubes can be readily expelled with- out difficulty or danger, but a much greater difficulty attends the removal of the products of a similar affection of the alveoli. Indeed, it is accom- plished only in small part by expectoration; those portions which are not 1 Vide Trans. Path. Soc, vol. xx., pp. 59-61. PATHOLOGY OF PHTHISIS. 185 readily liquefied and absorbed are apt to accumulate, and by their subse- quent decay to irritate the alveolar wall and to set up in it those prolifera- tive and inflammatory changes which constitute local "tubercle"—just as the retained secretions of a sebaceous follicle may give rise to the acne pustule. The thickened alveolar walls in their turn degenerate and soften or suppurate, and in these few changes occurring in numerous centres corresponding to the lobular groups of alveoli, we find the very basis and foundation of the chief morbid results of phthisis. Add to this group of changes the definite growth, miliary tubercle, which may arise in the neighborhood infected from the caseous foci, or which may spread throughout the system from such centres;—in a word, add a description of what we understand by the term tuberculosis to the phthisical changes we have enumerated, and all the active processes which produce pul- monary destruction in nine out of ten cases of consumption are summed up. The ceaseless movements of the lungs and the constant access of air to the diseased surfaces, keep up the suppuration and maintain the ten- dency to the absorption of septic matters, and by the inhalation of por- tions of sputa, laden with acrid and specific poison to distant parts of the lungs, the lesions of phthisis are further propagated and disseminated. 4. The penetration of the lung by specific and putrefactive organisms thus brought about results in changes of two kinds, each very decidedly influencing the clinical features of the disease. (a) In the excavation stages of phthisis the morbid secretions are nec- essarily invaded by putrefactive bacteria. (b) A special organism regarded as peculiar to phthisis, finds its way chiefly by inhalation, sometimes also by other routes to the lung. It is held by some observers to be primary to the lesions of phthisis, to be indeed the germ of that disease, others again regard it as an epiphyte to the generation of which the phthisical soil is specially favorable. CHAPTEE XVII. ETIOLOGY OF PHTHISIS. The tendency of modern inquiry is to range all the conditions which have been hitherto regarded as causative of phthisis on the side of pre- disposition, i.e., as conditions which bring about a state of receptivity, if I may say so—a capacity on the part of the tissues to receive and harbor with hospitality a certain organism, and on the other hand to regard the exciting cause as one and single—that organism, the tubercle bacillus. That there are difficulties in the way of accepting this view I shall point out, but it is based upon the results of careful observation and re- searches extending over many years. It is impossible at the present time to discuss the etiology of phthisis without first facing this question which is at the root of the matter, viz.: —The relationship of the bacillus tuberculosis to the disease. The specific nature of tubercle which was believed in by Laennec and by others long before his time, may be said to have been first demon- strated pathologically by Buhl in 1857, when he pointed out that an out- break of tuberculosis was almost always attributable to the previous existence of caseous matter somewhere in the body. Villemin advanced the question a step further in 1865, by showing that caseous matter intro- duced into a healthy animal, produced tuberculosis, and that therefore the tubercular virus dwelt in caseated products. The announcement of Villemin's discovery by Mr. Simon from the chair of the Pathological Society of London, was followed by numerous experiments, confirmatory and otherwise, by competent observers in this country; the general result being that Villemin's conclusions were substantiated. Some further ex- periments suggested that matters other than tubercular, when introduced into animals predisposed to tubercle, set up at first local, and then more diffused tubercle, but quite recent researches point to the probability of there having been some fallacy in these experiments; for due precautions being taken to use perfectly clean instruments and vessels, and to exclude all tubercular animals from the neighborhood of those under operation, inoculation with materials other than tubercular failed to produce tuber- culosis. ' Fresh point and precision were given to the conclusions of Villemin by Koch's discovery in 1882, of the presumed morbific agent in 1 For original experiments bearing upon this point, and for an admirable resume of the recent literature of the subject, see paper by Dawson Williams M.D., in the Pathological Transactions, vol. xxxv., p. 413. ETIOLOGY OF PHTHISIS. 187 the transmission of tubercle, viz., the bacillus tuberculosis. In this bacillus, in the opinion of Koch and his followers, dwell the virus and potentialities of tubercle. The main facts with regard to the life history and potentialities of the tubercle-bacillus may be stated as follows:— (1) The tubercle-bacillus is a minute rod-shaped fungus, measuring from 0'003 to 0*0035 millimeter in length, and about one-third that measurement in thickness. The rods are straight or slightly curved with rounded ends, and often enclose bright, spherical, spore-like granules of uniform size, arranged in linear series, and separated from one another by hyaline intervals. After having been stained with methyl blue, fuchsin or magenta, and then washed in nitric acid ten per cent., they retain the original dye, and are thus distinguished from any putrefactive or other bacilli.' (2) This organism is only caparble of growth and multiplication under culture in blood serum, or animal broth, at a constant temperature of 30° centigrade. It is of comparatively (to other bacteria) slow growth, and is unable to continue its development in decomposing fluids in the presence of more rapidly growing putrefactive bacteria. (Koch.) (3) All the conditions essential for the development of the bacillus, are, so far as its life history is known, alone to be found naturally in the animal body. (4) The bacillus is however, of very tenacious vitality, and will preserve its virulence and capacity for development, for six weeks or longer in decomposing sputum, for six months or longer in the dry state. (5) If a minute portion of bacillus-containing matter be placed upon a neutral culture-surface, and allowed to germinate, and if a fragment of the product of germination be similarly cultivated on a fresh surface, and so on for many generations, all foreign germs being excluded, the last product, if inoculated into an animal, will be as potent in producing tuberculosis as the first. (6) The bacilli, whether derived from free cultivation or from tuber- cle, if intimately diffused in water, and scattered in the form of spray through an atmosphere in which animals are placed so that they inhale it, will produce tuberculosis in them. The following is a summary of our knowledge respecting the distribu- tion of the bacilli in the lesions of phthisis. (Tj In the sputa of all cases of well-marked phthisis, the bacilli are to be found. (Plate II., fig. 2.) (8) In cavities in the lungs of tubercular or caseous pneumonic, i.e., 1 Klein and Gibbes on the relation of tubercle-bacilli to artificial tubercu- losis. Supplement to the 13th Annual Report of the Local Government Board, 1883-84, p. 177. 188 DISEASES OF THE LUNGS AND PLEURAE. of phthisical origin, whether large or minute, bacilli are invariably to be found. (Plate I., fig. 2.) (9) In caseous and catarrhal pneumonic consolidations of the lung, excepting in the immediate neighborhood of cavities, large or minute, bacilli are sparse and rather difficult to find, large fields of sections may be traversed without discovering them; yet this material is virulent in producing tubercle when inoculated.' (10) In the granulations of miliary tuberculosis, bacilli are very gen- erally but not invariably to be found, and often only in small numbers.2 In their most recent researches upon the artificial inoculation of guinea- pigs with tuberculous (bacilli-containing) sputum, Drs. Klein and Gibbes found that the tubercular lesions contained but few and in many instances no bacilli.3 (11) The results of inoculations made with dry bacillus culture by Koch and many others with the most minute precautions, have with much reason been accepted as proving the organism to be per se the virus of tubercle. These results have not altogether escaped challenge, how- ever, and another yet possible fallacy is indicated by the fate of the very analogous cultivation experiments of Sattler with the jequirity bacillus. Dr. Sattler observed that in an infusion of the seeds of the abrus preca- toi ius or jequirity plant—which when applied to the eye produces severe conjunctivitis—after a certain time bacilli appeared, which after cultiva- tion on meat-serum, gelatine, etc., for many generations would produce in a rabbit severe ophthalmia, yielding secretions containing the bacillus. Klein confirmed these experiments in every particular, but he observed further that if the infusions of jequirity containing the specific bacilli were heated to the boiling point for half or one minute, the bacilli were not killed but could be cultivated on meat jelly as before. This short process of boiling had, however, rendered the jequirity infusion inert, and the bacilli although their vitality was unimpaired, had lost their virulent properties. It was obvious that a portion of chemical poison from jequirity adhered to the organisms of Sattler's dry culture experi- ments.4 This poisonous principle had indeed, prior to Dr. Klein's 1 The most extended examination into the distribution of bacilli in the lesions of phthisis, is recorded in Dr. Percy Kidd's paper, read before the Medico-Chirur- gical Society this year, see Transactions, vol. lxviii. 2 In bovine tuberculosis the tubercle invariably contains bacilli in considerable numbers; the bacilli are smaller than those of human tubercle, and are much more generally contained within the cells of the textures affected. Klein and Gibbes, loc. cit., p. 178. 3Loc. cit., p. 182-183. Dr. Gibbes has been kind enough to show me some of his specimens from these animals of typical early stage tuberculosis of liver and lung, in which no bacilli are to be found. See also Kidd, loc. cit., p. 107. 4 Pathological researches, by Dr. Klein, 13th Report Local Government Board, p. 147. ETIOLOGY' OF PHTHISIS. 189 experiments, been discovered, and separated as an amorphous solid, "abrin," by Drs. Warden and Waddell in Calcutta.1 In the recent dis- cussion on Dr. Kidd's paper, Dr. Creighton expressed himself as not entirely satisfied that dry culture experiments were free from fallacy of this kind.2 It cannot, then, be said that the position of the tubercle-bacillus with regard to the etiology of phthisis is as yet established, although so inti- mate and exclusive is its association with the lesions of that disease that by its recognition in excreta or expectoration, we obtain a valuable crite- rion for diagnosis in obscure cases. The etiological question at issue is of the Avidest possible importance. The doubtful position of the bacillus does not affect established facts with regard to the infectiousness of tubercle and its contagiousness under arti- ficial and possibly under certain natural conditions, but it essentially affects our views as to whether phthisis is or is not a zymotic disease, and darkens counsel with regard to preventive measures. We cannot say with phthisis as with the more definite zymotic diseases that we have health on the one hand and a specific organism on the other; that when we observe a man sickening with phthisis, the tubercle parasite is already in possession of him; and that we might hope by exterminating the bacillus to eliminate phthisis from our list of diseases. The charac- teristic lesions of phthisis are brought about by many causes, and furnish a soil upon which the tubercle-bacillus will readily grow. Epiphytic in nature, concomitant in time, neither the seed nor the fruit of the disease, it must nevertheless be allowed that the tubercle-bacillus takes an im- portant part in the extension and conveyance of tubercular lesions. Notwithstanding the apparently insurmountable antagonism between those who adhere to the essentially bacillous nature of phthisis and those who do not, there is a neutral ground where the two views meet, and where they may perhaps ultimately agree. Even Koch himself believes that certain pathological changes are, if not necessary, at least highly favorable to the reception of the germ. " We have no doubt," observes Dr. AVeber,3 " that the bacillus is intimately associated with phthisis, but the exact relations appear to require still further elucidation. It is, for instance, not quite clear why the tubercle-bacillus thrives in some persons and not in others; or why, in some persons, it thrives at' one time and not at another. It seems to be an acknowledged fact that some micro- organisms do not grow in living tissues of a living animal. Dr. Klein states this with regard to the septic and zymogenic organisms properly so- ' The non-bat illar nature of abrus poison, by C. J. H. Warden and L. A. Wad- dell, Calcutta, 1884. 2 See remarks, Proceedings Royal Medico-Chirurgical Society, N. S., vol. i., p. 303. 3 Croonian Lectures, 1885, Lect. I. 190 DISEASES OF THE LUNGS AND PLEURe- called; and explains their occurrence in diseased tissues during the life of the subject, by assuming that these tissues had become practically dead before the organisms could grow in them. By analogy, the question arises whether the tubercle-bacillus settles and grows in healthy living tissues of the body or only in pathologically altered tissues. We know that it thrives in the bodies of most warm-blooded animals when inocu- lated, but this does not prove that it will find a nidus in a healthy tissue when merely brought into contact with it by the surrounding air." It is our duty to consider what are the conditions which bring about this "aptitude for the reception of the bacillus"—to use the language of the contagionists, an aptitude which in the opinion of others constitutes incipient phthisis. Experimental observations have abundantly shown that tuberculosis may be produced by inoculation of phthisical products in animals. Clini- cal experience and post-mortem observation furnish evidence of the con- veyance of tubercular matter from one part of a lung to another, setting up fresh grafts of disease; also of a more subtle conveyance of the tuber- cle poison from centres of disease through the medium of vessels and lymphatics to neighboring or distant parts of the lung or other organs. Nor are cases wholly wanting in which inoculation from one human being to another has proved effective. Contagion.—There is much in the nature of phthisis, and in the bent of the recent researches above alluded to, to encourage a belief in the contagious nature of the malady, a belief that was strongly held in the last century, and which in quite recent times has again in some measure returned. My own personal experience and observation convince me, that apart from artificial conditions—such as those brought about by experiment— and in the ordinary circumstances of life, phthisis is not an infectious malady.1 Nevertheless cases have even been recorded which are sufficient to convince others to the contrary, and " it would be rash to say that in no conditions of human association, can the degree of concentration be reached which might induce tuberculosis in a healthy person."s Climatic causes.—The only positive climatic influence made out in relation to phthisis is that dependent upon insufficient surface drainage. Towns, villages, hamlets, and houses situated at or near undrained locali- 1 Consult on this subject Dr. Bowditch, Is consumption ever contagious? Boston, 1864; Villemin, Etudes sur la Tuberculose, 1868; Budd, Lancet, Oct. 12th, 1867 ; Thomson, On Phthisis in Victoria ; Burney Yeo, Contagiousness of Pulmonary Consumption, 1882 ; C. T. Williams, British Medical Journal, Sept. 30, 1882 ; R. D. Powell, loc. inf. cit. ; Andrew, Lumleian Lectures, 1884 ; Collec- tive Investigation Record, vol. i. - On the Causative Relations of Phthisis, by the Author, British Medical Journal, Oct. 11th, 1884. ETIOLOGY OF PHTHISIS. 191 ties, on heavy, impermeable soils, or on low-lying ground, and whose sites are consequently kept damp, have a much larger number and proportion of cases of consumption than those which are situated on dry or rocky ground, or on light, porous soils, where the redundant moisture can easily escape.1 " Phthisis is invariably present in low and damp countries (Lan- cereaux),2 Buchanan,3 Bowditch,4 and Middleton/ have established the relationship in this country and in America between phthisis mortality and wetness of soil, Buchanan, especially, having observed the converse, viz., the diminished prevalence of the disease as one of the results of im- proved surface drainage." Phthisis most abounds in sub-tropical and temperate climates and within the lower ranges of elevation. M. Jourdanet maintains that the disease almost ceases to appear at the half distance between the sea-level and the snow-line for any given latitude.6 Whilst these statements are generally speaking true with regard to the climatic distribution of phthisis they are by no means absolutely so, nor can it yet be said how far the prevalence of the disease within certain limits is due to climatic influ- ences, for it must be observed that the regions of the earth included are those in which the insanitary social and commercial conditions of civilized life most prevail. It has been suggested that the prevalence of phthisis in low-lying and ill-drained situations may be explained by the presence of conditions favorable to the preservation of the tubercle-bacillus; but it must be recalled to mind on the one hand that the bacillus flourishes nowhere outside the living body, and on the other that its vitality is not destroyed within ordinary limits by external conditions.7 The experi- ments of Miguel and Emmerich have demonstrated what would necessarily be inferred, viz., that the proportion of bacteria in the atmosphere bears a numerical relationship to density of population and to barometric states, being most abundant in crowded cities (55,000 in 10 cubic metres in Paris), but absent in high latitudes and comparative solitudes (at 4000 metres elevation). M. Miguel attributes the absence of bacteria in ele- vated regions (1) to lessened dust, (2) to lessened power of the diluted air 1 Seventh Annual Report of the Registrar-General for Scotland, p. xlviii. 2 Distribution Geographique de la Phthisie Pulmonaire. 3 Simon's Reports to the Privy Council, 1867, 1877. 4 Bowditch. Consumption in New England and elsewhere, 2nd edit., Boston, 1868. 5 Paper read before the British Association at Bath, 1864. Mr. Middleton ap- pears to have regarded the foulness as well as humidity of atmosphere as effec- tive in augmenting the phthisis rate, whilst Buchanan more strictly refers to wetness of soil. 6 Quoted by Lancereaux, p. 30. ' De la Phthisie Bacillaire, Prof. See, 1884, pp. 19, 20, 74. 192 DISEASES OF THE LUNGS AND PLEURAE. to hold particles in suspension, (3) to lessened centres for production of bacteria. * These observations are valuable in precisely demonstrating the relative freedom of different localities from putrefactive products. Tubercle- bacilli have as yet been but rarely observed in atmospheric examination, so rarely as to render their presence apart from the question of direct contagion, which involves close proximity and the association of other ele- ments of the disease, of little importance. "A fruitful source of phthisis is the tendency 10 catarrh of the res- piratory mucous membrane," observes Dr. Hermann Weber,2 and further on he points out how these catarrhs may lead to phthisis, viz:—(1) By producing numerous mucous abrasions upon which the bacillus can settle; (2) by weakening epithelial cells and their ciliary action, in favor of the parasite; (3) by rendering respirations more shallow to the same effect; (4) " by weakening the nutrition and energy of the whole system." Amongst the more disputed conditions in connection with climate, it cannot escape observation that phthisis is nourished under those influ- ences favorable to the prevalence of catarrhal and inflammatory affections of the air-passages—more especially bronchitis and pleurisy—that is. on cold and damp soils, with variable temperature; and, as we know, at those seasons of the year, the spring and autumn, when these conditions pre- vail. In high and especially in dry situations, catarrhs are much less prevalent, respiratory conditions are more robust and active, and the processes of nutrition go on more vigorously in those to. whom such climates are favorable. Dusty employments.—The effect of dust inhaled in the pursuit of various employments has been exhaustively shown by Dr. Greenhow in the Public Health Reports for 1860 and 1861. Mining, flax-industries, pottery work, tool grinding, lace-work, etc., were all examined into, and, all allowances being made for social causes above alluded to, that the inhalation of dust remained as the positive cause of the undue prevalence of phthisis in the industrial localities, was shown by the fact " that the high death-rate from lung-disease belonged, according to the occupation, to men or to women of the district; that it sometimes was nearly twice as high for the employed sex as for the unemployed sex; and that it only extended to both sexes when both were engaged in the occupation."3 It is a remarkable fact that in those cases which are most typical of such mechanical origin the disease is very generally and strikingly one- sided, nor is the right side very notably more prone to attack than the left. Where on the other hand the fibroid characters of the disease are 1 Quoted in Prof. SeVs work, p. 80. 2 Croonian Lectures, 1885, Lecture I. 3 Simon, Third Report Med. Off. Privy Council, 1860, 1861, p. 34. ETIOLOGY OF PHTHISIS. 193 less marked, and the constitutional proclivity more definite, the two lungs are from an early period involved. Social conditio?is.—An examination of both climatic and industrial conditions predisposing to phthisis, cannot fail to convince any one how largely they are mixed up with conditions that fall under the heading of social relations. Phthisis is essentially a scourge of what we call civiliza- tion. Its rarity amongst nomadic tribes and savage populations in all climates, its prevalence in littoral districts, in river sites, and in industrial as compared with agricultural localities, in townships and cities—all point to social rather than to climatic influences, as predominant in the cultiva- tion of the disease. All the depressing conditions of life—anxiety, mental strain, disappointments, bad sanitation, over-crowding, debauchery—are concentrated at the centres of civilization. The weakly are helped to live; rickets, scrofula, syphilis, catarrhs prevail; the general tone of health is depressed; recovery from acute specific disease—measles, whooping-cough, and from inflammatory chest-diseases—is less complete; germs, putrefac- tive and other, are so rife, that special precautions against them are nec- essary to secure the healing of wounds. All that we know about phthisis would lead us to expect its prevalence under such conditions. And it is comforting to find statistical evidence that with improved sanitation, there has been an appreciable decline in the death-rates from phthisis.1 Constitutional liability.—Apart from all other etiological considera- tions of phthisis, the constitutional liability to the disease must be taken into account, this constitutional proclivity being most purely and strik- ingly manifested in hereditary liability, more complexly so in acquired liabilit}\ I do not maintain the first, and it would be absurd to argue the second, as being independent of the surrounding climatic and social conditions which I have already discussed; but it is of the utmost im- portance in order to gain a clear insight into these etiological factors, with a view to measures of prevention, that they should be considered separately. I have elsewhere defined the constitution of a man as " his build, the integrity or otherwise of the tissues of which each part of his body is 1 The death-rate has declined at every age with some insignificant exceptions in both sexes ; the decline being for males 14, for females 22, per cent. For both sexes the decline was greatest (28 per cent.) between the ages of 15 and 20, when deaths may be considered, in an economic sense, the greatest loss......The de- cline has been not much less considerable among both males and females at all other ages below 25, varying from 18 to 26 per cent. The mortality of males above 35 has diminished very little, but that of females has fallen between 14 and 24 per cent, until the age of 75, after which there is a trifling rise. The lives saved amounted to 3,966 males, 6,806 females ; not less than 2,885 of the former. and 4,233 of the latter, were of ages 15-35, that is, were among the most useful of the community.—Longstail', " On the Decline in the English Death-rate." Jour- nal of Statistical Society, June, 1884, p. 226. 13 194 DISEASES OF THE LUNGS AND PLEURAE. made up, and the wholesomeness or otherwise of the juices with which they are bathed; the sum of his vital force, his cell-quickening power which shall bear the call of judicious expenditure, for a long or but a brief period of time."1 This material and dynamic constitution is born with the infant, developed during the period of growth, and maintained with waning completeness during the wear and tear of subsequent life. Hereditary constitutional defect means unsoundness of original construc- tion with regard to some organ or tissue at birth. Acquired constitu- tional defect means that some part of the human mechanism has suffered deterioration from deficient supply of the needs of growth and function, through willful or involuntary exhaustion of vital powers, or from imper- fect recovery from acute disease. Inherited tendency to phthisis.—It is generally agreed that family pre- disposition obtains in 48 per cent, of cases of phthisis, and that the hereditary influence preponderates in females in the proportion of 59 per cent, to 37 per cent, males. It has, however, been well pointed out by my colleague, Dr. E. Thompson, to whose able work2 founded upon the Brompton Hospital Records, we owe the most recent information on the heredity of phthisis, that the discrepancy in this particular between the sexes is due not to the working of any law respecting heredity, but to the greater exposure of males, and the consequent increase in the prevalence of acquired cases amongst them. When the hereditary influ ence is watched through the offspring of consumptive parentage, it is seen that the numbers of the two sexes affected become nearly equal. Dr. Thompson comes to the same conclusion from another kind of calcu- lation.3 Thus out of 3000 male cases taken consecutively from the Brompton Hospital Records, he finds that 36 per cent, have a family history of phthisis, out of the same number of female cases 58 per cent, have such a family history. But taking the mean of the three estimates of the relative liability of males and females respectively to phthisis, given in the first Brompton Hospital Report, and by Dr. Pollock and Dr. Williams in their works he finds it to be in the proportion of 62 for the males, and 38 for the females, and there is a near equality between 36x62, and 58X38. Attempts have been made to throw some doubt upon the reality of hereditary influence in the etiology of phthisis.4 The reality of this influence, however, is only too certainly a matter of experience, and did it need demonstration, such may be found in the account of 80 families of 1 Etiological Relations of Phthisis. 2 The different aspects of family phthisis in relation especially to heredity and life assurance, by Reginald Thompson, M. D., 1884, p. 37. 3 Loc. cit., p. 40. 4 See Walshe, last edit, p. 461, and the same author in the Brit, and For. Med. Chir. Rev., Januai'y, 1849. ETIOLOGY OF PHTHISIS. 195 consumptive parentage given by Dr. K. Thompson, of which there were born 385 children, of whom 194 became phthisical, and 37 died in child- hood, leaving only 154 exempt. 1. The effects of so-called hereditary influence in leading to phthisis, have been regarded as attributable to contagion from the parent sub- sequent to birth either directly or through the milk. If this were so it would obviously follow that maternal " inheritance" should be far more deadly and earlier manifested than paternal. For the child is from earliest infancy in more constant association with its mother, and infected milk supply of parental source can only come from the mother. Nothing of the kind is observed in practice, however; and statistics show (a) that the " influence of paternal inheritance is especially developed before 25 years of age, being loaded upon the period between 10 and 25, the acme of susceptibility being exhibited between 20 and 25;" but that (b) with re- gard to maternal inheritance " susceptibility is not marked before 15, but is especially loaded on the period from 15 to 25, the acme being reached between 20 and 25." 2. It is said that inheritance in part arises from transmission of the virus in the manner in which svphilis is transmitted, and manifests itself early in life in the form of scrofula or meningeal or peritoneal tubercle (See loc. cit., p. 60). Careful observation of the manifestations of scrofula in the form of caseous glands or diseased bones, undoubtedly favors the view that they are predisposed to by constitutional states, but is also con- vincing of the fact that they are called forth by local injury or distal irri- tation; a scratch, a cut, an eczema, a carious tooth, an otorrhcea, a catarrh of the bronchi or bowel, begets gland irritation and caseation follows. The manifestations of syphilis have, on the other hand, in their inde- pendence of such exciting causes and in their symmetry and early devel- opmental features, the special characters of a blood disease; of course in the many cases in which inheritance is not immediately from one or other parent, any comparison with syphilis is impossible. 3. A third hypothesis, which is at once in accord with previously held views, and those most recently advanced as to the nature of the disease, is that suggested rather than expressed by Dr. H. AVeber in his recent lectures at the College of Physicians, viz., that phthisis is inherited as a predisposition, an inherent quality of soil favorable to the development of phthisis, but which yet can only be fertilized by the specific spores of that disease. This may of course be so; there are abundance of spores about, and it comes to be almost a mere matter of account whether the phthisis be attributed to the spores or .to the morbid state of tissues pre- pared for their delectation. In its transmissibility from either parent, its occurrence consequent upon, or in anticipation of, declared disease in the parent, in its declared presence being not protective from, but pre- disposing to, future attacks, and in the fact of atavism being a frequent 196 DISEASES OF THE LUNGS AND PLEURAE. and important characteristic, phthisis is, with regard to heredity, strik- ingly different from syphilis and zymotic diseases and strikingly in accord with insanity and trophic diseases. (Thompson.) A careful and impartial examination of the cases which come before us cannot fail to convince that neglected catarrh is the most common ex- citing cause of phthisis, although there must for the present be some difference of opinion as to the connecting link between the consequences of simple catarrh and the onset of phthisis. CHAPTER XVIII. ON THE VARIETIES OF PHTHISIS. It was held by Laennec, and it has in recent times been vociferously maintained, that phthisis is one disease. It cannot, however, be ques- tioned that the range of pathological varieties within the sphere-of this single malady, is so great as to justify its sub-divisions for clinical purposes of prognosis and treatment into sub-groups and varieties. Without further apology, then, I shall endeavor to sketch the main features of the follow- ing types of the disease. Pneumonic Phthisis. Alveolar catarrh. Catarrhal phthisis. Acute pneumonic phthisis, (a) Confluent form, (b) Disseminated form. Chronic pneumonic phthisis. Fibroid phthisis. TUBERCULAE PHTHISIS. Acute. Chronic. Acute tuberculosis—rather an infective complication of phthisis and of some allied conditions than truly a variety of that disease. Other varieties separable for clinical convenience:— Bronchi-ectatic phthisis. Diabetic phthisis. Dust (colliers', millers', etc.,) phthisis. Abdominal phthisis. Laryngeal phthisis. Syphilitic disease of the lung a^-I syphilitic phthisis. There are further to be considered separately, on the grounds of mere convenience two of the prominent consequences of phthisis, about which are grouped some of the most characteristic features of the disease, viz.:— Lung excavation. Haemoptysis. A third consequence, of rarer occurrence, viz., pneumo-thorax, has been already fully dealt with in a preceding chapter. (Chap, vii., p. 88). 198 DISEASES OF THE LUNGS AND PLEURAE. Pneumonic Phthisis. Alveolar Catarrh.—Alveolar catarrh in the first and slightest degree, forms the connecting link between the prodromal catarrh of Niemeyer and catarrhal pneumonia. This condition is extremely com- mon, and very readily overlooked, for the signs by which it is recognized are only faintly marked. It must be considered as really the first stage of phthisis—through which all cases of pneumonic phthisis, and there- fore the majority of cases of pulmonary consumption pass. Whether this catarrh be specific from the first, in the sense of having been determined by the reception and germination of the tubercle bacillus, is a question sufficiently discussed in the section on etiology, and which need not further embarrass us at present. The pathology of this disease consists, as has been before intimated, in the proliferation of the epithelium of the air-cells by a catarrhal process of the most superficial kind. Tubercle, in the sense of miliary granulation, has nothing whatever to do with this process, which may, indeed, pass on to catarrhal pneumonia and the destruction of the lung without such tubercle taking any conspicuous part in it. The subject of alveolar catarrh has always been previously depressed ' in health, through tardy convalescence from some other disease, bad liv- ing, mental anxiety, or overwork; he has had a persistent, though it may be a slight, cough, for a longer or shorter time, and has during that time been getting thinner. Professor Niemeyer, who has more than any other author urged the importance of the early detection and treatment of this condition, regarded the presence of pyrexia as the one symptom above all others significant of alveolar catarrh, and he also justly attached great importance to the occurrence of streaky haemoptysis. The pyrexia may not amount to more than a slight evening rise of temperature, but it is attended with malaise and increased cough at night. At this stage the physical signs are very slight, but in conjunction with the symptoms are sufficient for diagnosis; the respiration is weaker at one apex, the inspiration being wavy, or even jerking. There are usually a few ronchi present, which, if limited to that apex, are very significant, and, in addition, there is heard at the extreme summit of the lung (supra-clavicular or supra-spinous region) a peculiar crumpling sound at the moment of cough, which differs both in time and degree from the crepitant sound audible at a somewhat later stage with the first inspiration following a cough. These physical signs, which are but very slight—and their recognition is of the more importance on this account—are those of a bronchial catarrh limited to one apex, associated with a decided imperfection of the res- piratory murmur at that apex, which, when taken in conjunction with the symptoms—more particularly emaciation, quick pulse and evening VARIETIES OF PHTHISIS, 199 pyrexia—afford unmistakable evidence of incipient phthisical disease, upon which we must advise most decidedy if we do not wish to see the patient pass beyond our control so far as positive cure is concerned. There is no clinical line of demarcation to be drawn between this condition and the prodromal catarrh which precedes it, or the catarrhal pneumonia into which it is apt to pass; they shade imperceptibly into one another. I only specially refer to this as the earliest recognizable stage of phthisis. Catarrhal Phthisis.—The following case is illustrative of catarrhal pneumonia in an early stage and bears out some of the above remarks respecting the most common etiology of this form of consumption. S.S., aged 29, a married woman engaged in domestic duties and suck- ling a child aged seven weeks, came under my notice as an out-patient in April, 1871. Her mother had died of consumption within two years of the patient's birth, and an elder sister had been affected with the disease in an early stage. She had enjoyed fair health until her first confine- ment, when she was with difficulty delivered of twins, only one of whom survived the birth. This child she suckled for eleven months, when she again became pregnant. Ever since her last confinement she had suffered from increasing debility, emaciation, and cough, and shortly before that time she had had slight haemoptysis. She was a tall, thin, anaemic woman, with the worn look so character- istic of over-lactation or rapid child-bearing; her large, heavy, pendulous breasts, marbled with large veins, increased by contrast the general flat- ness and narrowed antero-posterior diameter of the chest. There was no local flattening, however, at either apex, and the respiratory movements though generally deficient were not more so at one apex than at the other. On percussion over the summit of the left lung the resonance was somewhat less than on the opposite side; the respiratory sounds there were harsh, and accompanied by some moist crepitation which extended to the second rib. The respiratory murmur elsewhere was of fairly good quality, but somewhat feeble. The main symptoms complained of were troublesome cough and yellow expectoration, shortness of breath, general weakness, and giddiness in the head. The pulse was quick and weak5 the appetite indifferent, but digestion fairly good. The case was regarded as one of catarrhal-pneumonic phthisis in an early stage, the disease being limited to the left apex, and supervening upon the exhausting effects of more than thirty months' continuance, alter- nately, of gestation and lactation. She was directed immediately and completely to wean the child, to take abundance of appropriate food, with a moderate amount of beer. Some counter-irritation was applied at the left apex, and cod-liver oil and steel wine administered, with some seda- tive lozenges for the night cough. On again examining the chest a month later, the moist sounds were 200 DISEASES OF THE LUNGS AND PLEUR.E. no longer audible with ordinary respiration, but a few crackles were heard after cough. There was slight flattening at the left apex, which became more obvious on deep inspiration; the respiratory sounds were feeble there, while on the opposite side they were more developed, and on per- cussion the line of resonance of the right lung extended a little to the left of the mid-sternal line. There was no evidence of a cavity at the left apex, and no extension of the disease below. The health of the woman was, though improved, by no means restored; she was still anaemic and thin. Her cough was troublesome, especially in the morning, and expec- toration difficult—the efforts of coughing often causing vomiting at that time. She had neglected to completely wean her child. The pulse was quiet but weak; the appetite improved. Three weeks later she had very greatly improved in health and strength; some color had returned to the cheeks, and she was gaining flesh rapidly. This case would be included under the heading of pneumonic phthisis, by Addison; catarrhal-pneumonia, by Niemeyer, Herard and Cornil; an epithelial pneumonia by Andrew Clark. By Laennec it would be termed local pulmonary tuberculosis, and by some modern writers it would be spoken of as early bacillary phthisis. Bacilli were not recognized at the time this case occurred, but we know from abundant experience that they are to be found on sufficiently diligent search in all cases in which the signs of softening are present. It is fair to assume that, had this patient been in happier circum- stances, had her health not been depressed by the development, at her expense, of three infants and the maintenance of two of them, while she herself was doubtless not in the enjoyment of nutritious food in any great abundance, had she sought advice earlier (and taken it), she would never have become phthisical—her hereditary proneness to consumption might have remained a mere latent tendency. Had there been any family ten- dency to insanity, it is quite possible that the same evil conditions might have caused her to be afflicted with some form of puerperal mania. " It is true that privation, excess, errors in habits of life, the sedentary occu- pations, the pernicious influence of certain trades, grief, anxiety, and tbe other wasters of vital powers, will not suffice to induce consumption in all, or even in the greater proportion of individuals; for these agents so universally prevalent are part of the daily lot, or of the daily errors, of many more than fall victims to consumption. But it is also true that, if to any or all of these conditions that of inherited tendency to phthisis be superadded, very few indeed escape the disease." * This remark is well borne out by the above, amid numberless other cases which must be familiar to physicians. The points about the case which rendered the prognosis a favorable 1 Dr. Pollock, Elements of Prognosis in Consumption, p. 340. VARIETIES OF PHTHISIS. 201 one, with certain reservations, were:—1. The obvious and very sufficient determining cause. 2. The limitation of the disease to one apex. 3. The presence of considerable crepitation and some dullness, without any local flattening or marked difference in expansion. 4. The absence of fever at the time of coming under observation. 1. If the circumstances of the patient admitted of complete rest from the cares and anxieties of her position of life, and change to a purer air, there would scarcely have been a doubt as to the prognosis. Without these advantages the disease ceased to extend, the secretion sounds dried up, and flattening appeared with some corresponding development of the opposite lung. 2. In addition to the evidence of the integrity of the opposite lung, the encroachment of its margin towards the diseased side should always be anxiously looked for; it can be readily made out by percussion, and when the disease is one-sided, it precedes, often by a long interval, any decided apex flattening, and is always a sign of good augury in prognosis. 3. The late appearance of flattening—coincidently, that is to say, with the lessening and disappearance of moist sounds, which have been con- siderable—is an important sign of arrest of the disease, in contradistinc- tion, to flattening which comes on coincidently with an advance in the other physical signs, and which may be due, therefore, to sheer loss of lung substance, or to the presence of the indurative form of disease, •chronic pulmonary tuberculization, which, though of chronic course, is yet one of the most intractable of lung affections. Flattening must then only be considered in conjunction with other signs, and with especial regard to the period of its appearance. In the case before us it signified, together with the other signs, pulmonary collapse, with perhaps a few shrunken nodules, adhesion and some thickening of the pleura. I believe that most cases of "cured" early-stage phthisis are of the kind above related. The cure may remain permanent, but one must always bear in mind that catarrhal pneumonia is one of those diseases that are peculiarly prone to recur, resembling acute rheumatism, tonsilitis and some other diseases in this respect. The delicacy of the lungs, in- herited or acquired, which has led to the first attack remains, nay, is increased by that attack. Hence the previous health history 'of the patient helps us much in the prognosis in each individual case. Those cases in which the pulmonary delicacy is distinctly inherited are the least hopeful, those again in which the attack has been most dis- tinctly led up to by adverse conditions of a definite and remedial kind are the most favorable. Of course in each case the extent of lung involved' and the intensity of the disease, to be ascertained only by physical ex- amination, must, as already pointed out, most importantly enter into the question as to prognosis. The patient, whose case is above related, after some months had a 202 DISEASES OF THE LUNGS AND PLEURAE. second attack, resulting in extension of disease on the same side, involve- ment of the opposite lung, and a fatal termination. In January, 1877, in the course of some clinical lectures delivered at the Brompton Hospital,1 I related the following case in illustration of the rapid formation and cicatrization of a cavity at the right apex and the complete clearing up of all signs and symptoms. A. W., a pale, scrofulous-looking girl, who was in attendance at the time of lecture, had been under my observation at the hospital since March, 1872, when, at the age of fifteen, she first came to me as an out- patient. She had then a somewhat loud cough, which had troubled her all the winter, but there were no other definite symptoms and no dis- coverable pulmonary signs. Her family history was good, but she had been delicate since an attack of measles in childhood. She got well on ordinary treatment, but returned in October, 1874, and again improved, but was ailing during the winter. In the spring of 1875, her principal complaint was of a painful affection of the left breast; she still had no defi- nite pulmonary signs or symptoms beyond general delicacy and slight cough. In June, she had whooping-cough rather severely; and six weeks after she still whooped with the cough, which was attended also with thick difficult expectoration. On again examining her chest I was somewhat surprised to find dullness with very marked cavernous breathing and some gurgling below the right clavicle; moist crepitant rales were also rather sparsely scattered over the posterior base. Fever and hectic symptoms were now marked. The prognosis appeared grave, and I recommended her to obtain an in-patient's letter. She did not come into the hospital, however, until January; meanwhile she improved as an out-patient. In October the sounds were noted as being quite dry, and 'on her admission into my ward in January, I examined her chest with great care, and did s© repeatedly afterwards, but I could never discover more than some harshness and feebleness of breathing at the right apex. I take it that this was a case of solitary caseous abscess at the right apex, which cleared out and cicatrized. Such cases are, however, un- fortunately exceptional; this is the only one of the kind of which I have a definite and certain note. Other similar cases have, however, been re- ported, and post-mortem observation of cicatrices in the lungs leave little doubt that they occur more frequently than positive clinical experience would indicate; but they are rarely single and uncomplicated, as in this case. The patient A. W. remained well after leaving the Hospital in 1877, and early in 1883 was married. In the course of that year she had a miscarriage and suffered much from menorrhagia afterwards. In May, 1885, she again came under my observation with cough especially during the night and in the morning, and some loss of flesh. She was nursing 1 Lecture ii., Lancet, Jau. 27th, 1877. VARIETIES OF PHTHISIS. 203 entirely a child eight months old. At the right apex, the seat of former mischief, there was slight dullness and some deep crackling and catarrhal rales but no evidence of a cavity. A few bronchitic rales were scattered over the chest on both sides. The breath-sounds below the left apex were not quite satisfactory. It is very common to meet with cases in which the second attack does not affect the same part of the lung as the first, but the opposite apex or some other portion of the same lung. Acute Pneumonic Phthisis.—(1) Confluent form.—In other cases of phthisis of more acute character, still as a rule one-sided in the initial attack, the consolidation is more extensive and more dense, the disease being more " massed" in the affected lobe, occupying perhaps its entire extent. This form of the disease is very apt to be confounded with croupous pneumonia of the apex—it very rarely occurs at the base of the lung— the signs of consolidation being uniform over an extended area; bronchial breath-sound and crepitant rales, at first fine, then coarser, are heard, and the voice sound is bronchophonic. The onset of the disease is abrupt and stormy, with pain in the chest, short cough, scanty expectoration, sometimes haemoptysis, with raised temperature, rapid pulse, and frequent respirations. The croupous element does indeed enter into the formation of many of these massed consolidations of the lung and it may be only after its resolution that the true nature of the case is unmasked with the slower decay and softening of those centres which have undergone caseation. In the distinction of these cases, from the not uncommon instances of true croupous pneumonia of the apex the following considerations are important. 1. The temperature although maintained above the normal has even from the first a more fluctuating range than that of pneumonia. The tongue is as a rule moister and less typically coated than in pneumonia, and hectic sweatings very soon become marked. 2. No critical fall of temperature corresponds with, or follows upon, the appearance of moist sounds. 3. The haemoptysis if present is decided, not a mere rust color of the sputum. The sputum is more abundant and from the first, more or less purulent, containing bacilli (Plate II., Fig. 1) and alveolar elastic tissue (Fig. 18). 4. As the case proceeds amid the moist crepitant rales, which cannot be distinguished from those of resolving pneumonia, larger clicks are heard in several centres, which become more liquid and characteristic of pulmonary softening. 5. The breath-sound, which had become more or less completely masked by the numerous rales, again appears in patches corresponding 204 DISEASES OF THE LUNGS AND PLEURAE. with the large clicking rales and assumes a hollow tubular quality. The voice-sound over these areas becomes of a nasal, snuffling quality and finally there is distinct pectoriloquy. 6. The rapid emaciation and markedly hectic temperature of the patient, his profuse sweatings, and the increasingly copious and purulent expectoration, within a few weeks put aside all possible error of diagnosis. Cases of caseous phthisis by no means all exhibit at the first onset the stormy symptoms above sketched. But in all cases the physical signs rapidly extend, until a more or less considerable portion of one lung is involved, before the signs of breaking down into cavities are manifested. In persons of lymphatic temperament, who are the more common subjects of this form of phthisis, the fever may not be sufficiently violent, nor the other symptoms urgent enough to prostrate them in bed; but remittent fever, cough, expectoration, and hectic sweatings are invariably present and sufficiently manifest to excite alarm in parents and friends. ^s^ It is remarkable, however, to observe the rounded contour of features and the relative plumpness of figure maintained 'by patients even far on m this form of the malady, which is certainly most common in young girls and women. The features are usually pale with anaemic mucous membranes, but in the younger subjects the cheeks may be well-colored. Ihe chest formation is usually fairly good, and in common with the rest of the frame well-covered with a layer of adipose tissue. The muscular system is, however, poorly developed and languidly innervated, the pulse feeble, and the nervous system wanting in tone. I have pointed out that in the form of phthisis now under considera- tion there is a tendency to arrest. This is brought about:— (1) By elimination of the caseous products. VARIETIES OF PHTHISIS. 205 (2) By cicatricial contraction of the cavities thus formed. (3) By comoensatory development of the opposite lung. It is a mistake commonly and naturally enough made by the inexperi- enced observer, on having revealed to him through his stethoscope the signs of breaking down of pulmonary consolidation in one or more centres, to infer that a further step has been advanced towards a hopeless prog- nosis in the case before him. In a sense, however, and fully admitting the gravity of the case at the first moment of diagnosis, these phenomena of softening are equally essential and important steps towards amend- ment. Without them it is impossible for healing changes to ensue. At the same time this process of elimination is attended with dangers of its own which have to be reckoned with. Fig. 19.—Annie T.—Fluctuating hectic temperature—Acute pneumonic phthisis—Cavities rapid- Jy forming. (a) Suppurative fever necessarily attends the process. A fluctuating hectic temperature, night sweats, cough, and more or less profuse expec- toration, containing elastic tissue and bacilli; haemoptysis is rarely present to any great extent. The character of temperature chart marking this period of phthisis is precisely the same as that of an empyema, or an im- perfectly drained abscess in any other part of the body, or the more brief hectic period of typhoid fever. Figs. 19 and 20. (b) There is throughout this period a danger of the opposite lung becoming involved in separate centres, from inhalation of specific morbid products in course of expectoration. Whilst the possibility of secondary tuberculosis at this stage is not to be forgotten, it is, so far as I have ob- served, a complication of much more rare occurrence than in other stages. 206 DISEASES OF THE LUNGS AND PLEURAE. (c) The patient tends to become more and more exhausted, and to lose weight throughout this period, and in severe cases constitutional re- sources are seriously taxed by a downward course of from six weeks to three or four months. During the process of elimination, cavities gradually become mani- fested to auscultation, and perhaps increase by coalescence to form one or two amphoric areas. Some shrinking of lung from loss of substance may be observed, the heart's surface being uncovered more or less to right or left according to the side affected. Coincidently, however, with these alarming signs of lung destruction, it may in a goodly number of cases be observed, (a) that the opposite lung has not become affected to any material extent, and that the limits of the disease on the affected side have not extended but have perhaps even re- trenched. It is necessary here to warn the auscultator against mistaking morbid sounds heard on the healthy side but really consonated from the diseased side, for signs of new disease.1 (b) Before the subsidence of hectic phenomena, careful percussion and auscultation will reveal that the margin of healthy lung is encroach- ing upon the sternum until the whole sternal region is thus occupied. (c) The flattening of the affected side becomes more marked, and the area of cardiac pulsation more extended towards the diseased side, whilst the cardiac surface is being covered by the lung advancing from the healthy side. The percussion note becomes duller and more wooden, and the hollow breath-sounds are less and less abundantly accompanied by rales. It is to be further noted, especially in left-sided cases, that the morbid pulmonary signs shift towards the upper axillary and infra-spinous regions. (d) The range of temperature gradually contracts, and this restriction may often be observed not only with regard to the high, but also the low register, for it is very usual for the hectic period of this disease to be marked by sub-normal points in alternation with pyrexial peaks (see fig. 20). The other phenomena of hectic abate, the patient regains appetite and flesh, and in favorable cases and under favorable circumstances the cough and expectoration may cease, the cavities contract and convales- cence be fairly established. (e) In left-sided cases when the lung has considerably contracted and all pulmonary signs have become quiet, the patient frequently complains much of palpitation and occasional faintness and ready disturbance of the heart's action. These symptoms are due to the organ being somewhat displaced, its anterior surface being unprotected by lung in contact with 1 This fallacy has recently been pointed out by Dr. Skerritt in a paper On the Conduction of Physical Signs in Diseases of the Lungs, Brit. Med. Jour. 1884, vol. ii., page 1005. See also Chap. X., pp. 130, 131. VARIETIES OF PHTHISIS. 207 the depressed parietes, it being further bounded on the left by a thick- ened lung instead of its normal elastic cushion of support. (2) Disseminated form.—In other cases, of happily rare occurrence, acute phthisis attacks both lungs, commencing simultaneously in many centres. This form of the disease bears the same relationship to the pre- ceding that disseminated bears to confluent, broncho-pneumonia. It corresponds with the florid phthisis of some authors, the phthisie galo- pante of the French. Acute disseminated pneumonic phthisis is the most descriptive term for the disease. For, whatever views different writers may hold as to its origin or otherwise in tubercle, the rapid destruction of lung texture is unquestionably the result of inflammatory action. The Fro. 20.—Marked hectic type of temperature attending the rapid softening and elimination of extensive caseous consoiidation. Lucy B., late period of acute phthisis. symptoms are not essentially different from those of the more ordinary form of acute phthisis, but the dyspnoea is more urgent and the progress to a fatal issue rapid, and, as a rule, unbroken. The flushed face, bright eyes and alert mind contrast with the apathy, pallor and prostration of acute tuberculosis, and the physical signs at first of acute bronchial catarrh with the rapid development of numerous centres of crepitation, softening and excavation, are equally characteristic. The rapid breaking down of the broncho-pneumonic centres occurring first at the apices, is again a characteristic feature, distinguishing this from mor simple forms of broncho-pneumonia. Post mortem the lungs are found to present numerous areas of greyish- 208 DISEASES OF THE LUNGS AND PLEURAE. pink granular consolidation, with yellow caseous centres broken down into small cavities communicating widely with enlarged, more or less eroded and acutely inflamed bronchial tubes; no miliary granulations of tubercle are to be seen, although the smaller, yellow centres may at first sight resemble them. Except on grounds of clinical accuracy, the distinction between acute disseminated phthisis and acute tuberculosis is of little importance, for the prognosis in both is about equally fatal within a short period of from four weeks to two or three months. The high and fluctuating temperature, hectic sweatings, purulent, sometimes blood-stained, and soon nummulated sputa containing elastic tissue and bacilli, in association with the physical signs, will render it im- possible, except in the earliest stage, to confound this disease with acute bronchitis. An inquiry into the family history of a case of acute disseminated phthisis will always elicit evidence of a decided phthisical taint. CHAPTER XIX. CHRONIC PNEUMONIC PHTHISIS—FIBROID PHTHISIS. The following case exemplifies fairly well the transition stages be- tween chronic pneumonic and fibroid phthisis, a transition pathologically very easy, and clinically often to be observed. John B., aged 29, a butcher's assistant, came under my notice in March, 1871. He was a broad-chested, powerfully made man, of medium height and florid complexion. He had led a rough but sober life, having followed his present business, which included the slaughtering of animals for some years in Australia, and had enjoyed excellent health until shortly before Christmas, when, after getting wet, he caught a severe cold, which was followed by a cough, which had since increased, uninfluenced by treatment. Up to and at the time of his attendance, he was still follow- ing his employment, but he now did so with difficulty, complaining of his cough and of increasing weakness with decided emaciation. His father had died of consumption, brought on subsequent to the patient's birth by intemperance; there was no other hereditary tendency to the disease. The chest, as before said, was broad and well-formed, without flatten- ing or obvious impairment of expansion. The heart's apex beat in the natural situation. At the left clavicular and sub-clavicular region the percussion note was dull, the dullness extending to the fourth rib; pos- teriorly, the resonance was defective at the left supra-spinous fossa. Scattered over the dull regions there was coarse crepitation, mingled with a still larger humid crackle. These moist sounds were abundant, and masked to a great extent the respiratory murmur, which was decidedly harsh, but not distinctly bronchial. Its vesicular quality became gradu- ally restored as the stethoscope was passed downwards. At the posterior base there were some scattered sibilant rales. On the right side the per- cussion note was good, and the breath-sounds were natural. The sequence of events in this case appear to have been a more or less general bronchial catarrh, subsequently localized at the left apex, extend- ing thence into the alveoli, and there producing catarrhal pneumonia; yet the man continued his daily work, though constantly losing strength, for three or four months, during which time the catarrhal process ran on insidiously to a more deeply inflammatory degeneration of the alveolar walls. The disease had been acquired by exposure, the family tendency being slight, and the build of the chest not that of inherited tendency to phthisis. The physical signs at the present stage showed consolidated 14 210 DISEASES OF THE LUNGS AND PLEURAE. lobules of blocked alveoli, which were softening with varying degrees of rapidity; the coarse crepitation answering to the redux crepitation of pneumonia, the larger clicK being due to more profound destruction of tissue (softening). On the occasion of his first visit the pulse was quick and the tongue red, and although there was no elevation of temperature at the moment, it is probable that it rose slightly towards evening. The patient was treated with an alkaline mixture containing small doses of iodide of potassium, and with cod-liver oil. The next note of importance was taken on April 27, when the expansion of the left side of the chest was found to be decidedly impaired, the dullness had increased in hardness but not in extent, and was very marked, especially between the left margin of the sternum and the mid-clavicular line. In the space marked out by these two vertical lines (left sternal and mid-clavicular), the respiration was extremely feeble, and not attended with any rales; the heart's impulse was diffused to the second interspace, though the apex was only half an inch higher than natural. To the left, again, of the mid-clavicular line, the respiration was still feeble, and the rales much diminished, the dullness being somewhat greater than before. At the apex posteriorly there was bronchial respiration and imperfect pectoriloquy the bronchial rales at the base had cleared up. The reso- nance of the right lung extended to the left margin of the sternum. These signs showed:—1. That the disease had n 44 INDEX. Hemorrhage from lung (see ha tysis) Haemothorax, 97 Hamilton, 15, 181, 182 Hare, Dr., 17 Hastings, Dr., 162 Hay asthma, 171 Health resorts, 173, 287 Hensley, 3 Hereditary predisposition, 194 Hjaltelin, 125 Hudson, 60 Hutchinson, 6, 125 Hydatids of lungs, 197 symptoms, 197 treatment, 336. Hyeres, health resort, 173 Inflammation of lung, 125 alveoli, 179 larynx, 250 Inhalations in laryngeal phthisis, in phthisis, 308 Inspection of chest, 22 Intercostal fluctuation, 58 neuralgia, 47 Irvine, Pearson, 149 Jaccoud, 286, 290 Jackson, 115 Jagielski, 284 Jauja, 290 Jenner, Sir W., 114 Johnson, Dr. Geo., 246 Karrick, 284 Klebs and Mosler, 257 Klein, 14, 15, 128, 181, 188 Koch, 182, 186, 188 Koumiss, 284 Laennec, 30, 39, 182, 183 Lardaceous disease, 274 Laryngeal phthisis, 250 Larynx, ulceration of, 250 morbid anatomy, 251 diagnosis, 254 treatment, 320 Laryngoscope, use of, 253 Lausanne, health resort, 291 Les Avants, health resort, 291 Les Moulins, health resort, 297 Liebermann, 3 Lungs, alveoli of, 2 anatomy of, 1 circulation in, 2 contractile powers of, 4 elastic resilience of, 7 lymphatics of, 14 movements of, in phthisis, 183 muscular fibres in, 5 nerves of, 15 Lungs, residual tension of, 5 Lymphatics of lung, 14 Mackenzie, S., 262 Maclean, 68 McVail, 114 Madeira, health resort, 298 Mahomed, 30 Manitou, health resort, 290 Manometer, 5 figure of, 7 Maunsell, 128 Meningitis, tubercular, 268 case of, 268 diagnosis, 272 symptoms, 272 treatment, 326 Mentone, health resort, 297, 299 Meran, health resort, 291, 299 Micro-organisms in sputum, 45 in phthisis, 187 in pneumonia, 128 Middleton, 191 Monte Carlo, health resort, 297 Montreux, health resort, 292 Mosler and Klebs, 257 Murchison, 127 Murmurs, respiratory, 32 vesicular, 32 of glottic origin, 34 in displacement of heart, 61 Miiller, 5 Myalgia, 47 Nerves of lung, 15 Neuralgia, intercostal, 47 Niemeyer, 198, 200 Night sweats in phthisis, 309 agaricin in, 310 picrotoxin, 310 OSdema of lung, 123 INDEX. 345 CEdema of lung, symptoms, 123 treatment, 124 in pneumonia, 137 Paracentesis thoracis, 73 Palpation, 23 Parkes, 134 Pau, health resort, 298 Pavy, 262 Peacock, 239 Pectoriloquie aphonique, 44 Percussion, 24 Perichondritis, 49 Perls, 5 Peruvian Andes, 290 Phthisis, acute pneumonic, 203 confluent form, 203 diagnosis, 203 elastic tissue, 204 symptoms, 203 temperature in, 205 treatment, 304 disseminated form, 207 acute tubercular, 219 etiology of, 186 albuminoid disease in, 275 bronchi-ectatic, 260 catarrhal, 199 case of, 202 cavity stag-e, 225 chronic pneumonic (see fibroid) classification of, 197 climatic causes, 190 constitutional liability, 193 contagion in, 190 definition, 178 diabetic, 262 dust, 261 fibroid, 209, 211 etiology, 212 cachexia in, 216 case of, 213 diagnosis, 211, 216 pathology, 211, 217 prognosis, 216, 217 symptoms, 211 treatment, 315 hemorrhagic, 339 health resorts in, 287 micro-organisms in, 185, 187 (see also bacillus) pathology of, 178 Phthisis, prophylaxis in, 277 pulmonary fibrosis in, 180 pyrexia in, 305 respiratory movements in, 183 social conditions in, 193 treatment, 277 tubercular, 219 case of, 220 chronic, 222 ATarieties of: bronchiectatic, 260 catarrhal, 199 diabetic, 262 dust, 261 fibroid, 209, 211 galloping, 207 laryngeal, 250 pneumonic, 198 syphilitic, 266 tubercular, 219 Physical examination of chest, 16 Pleura, adhesions of, 51 anatomy of, 51 diseases of, 51 Pleurisy, adhesions in, 51 etiology, 51 classification of, 51 diagnosis, 61 displacement of heart in, 56 dull triangle in, 55 effusion in, 62 locals from extension, 64 pathology, -52 secondary or septic, 65 simple, 51 symptoms, 52 Skodiac resonance in, 54 suppurative, 65 symptoms of, 66 treatment; 62 varieties, 51 Pneumatometry, 18 Pneumonia, 125 abscess in, 136, 143 etiology of, 125 climatic influence, 125 exciting causes, 126 Pneumonia, epidemics of, 125 gangrene in, 136 infectious, 127 oedema of the lung in, 137 pathology of, 129 34G Pneumonia, pneumonococci, 127 prognosis in, 137 purulent infiltration in, 130, 143 pythogenic, 134 case of, 134 temperature in, 135 septic causes, 127 sphacelus of lung in, 143 stages of, 129 symptoms, 131 terminations, 136 treatment of, 139 Pneumo-thorax, 88 bruit d'airain in, 91 diagnosis, 94 displacement of heart, 93 physical signs in, 91 prognosis, 95 symptoms, 90 treatment, 96 Potain's cork adjustment, 76 Pressure signs in pleurisy, 59 Promontogno, health resort, 290 Pulmonary circulation, 2 Pyrexia, 305 antipyrin, 307 arsenic in, 305 quinine in, 305 salkwlic acid, 306 Quito, health resort, 290 Ragatz, health resort, 290 Rales, 39 caA'ernous, 40, 42 crackling, 41 crepitant, 40 sub-crepitant, 41 Recruits, chest of, 18 Reybard, 75 Remak, 15 Residual tension, 5 Resonance, amphoric, 44 Skodaic, 54 Respiratory function, mechanism, 3 in new-born child, 3 movement, 9 schema for representing, 9, 13 statics of, 12 Rheumatism, aponeurotic, 47 Rhonchal fremitus, 40 Rickety thorax, 50 INDEX. Riegel, 99 Rindfleisch, 111, 114, 227, 228 Ringer, Dr., 80 Riviera, health resort, 295 Roberts, 63 Rocky mountains, 290 Roe, 63 Roger and Barth, 33, 34, 38 Rokitansky, 234 Rosenthal, 99 St. Moritz, health resort, 173, 278, 287 Salter, 5, 6, 7, 164 Samaden, health resort, 287 Sanderson, Burdon, 9, 14, 15, 181 Santa Fe de Bogota, health resort, 290 Sarcomata in mediastinum, 328 Schema of respiration, 9, 13 Schnitzler, 122 Seewis, health resort, 290 Shape of chest, 17 Sieveking, 18 Simon, 186 Skerrit, 206 Skoda, 30, 33 Skodaic resonance, 54 Sounds, voice, 43 varieties of, 44 Spirometry, 19 Spittal, 30, 33 Sputum, elastic tissue in, 45 examination of, 44 in phthisis, 204, 228 in pneumonia, 128 micro-organisms in, 45 Sputum, mould in, 46 Stirling, 15 Strieker, 5 Stridor, 40 Sturges, 99, 127, 137 Surgical treatment of bronchi-ectatic cavities, 158 of empyemata, 78 of hydatids of the lung, 336 of pleuritic effusions, 70 of pulmonary cavities, 158 Table of terms, 26, 338 of thoracic resilience, 8 of vital capacity, 19 Taylor, F., 262 INDEX. 347 Temperature in erysipelas, 132 in pneumonia, 132 in pythogenic pneumonia, 135 in tubercular meningitis, 273 Thompson, Reginald, 37, 60, 194, 195, 239 Thoracentesis, 78 Thorax, deformities of, 50 alar, 50 resilience of, 8 table of, 8 rickety, 50 organs in, 21, 22 Tissue, elastic, in sputum, 45, 204, 228 Topography of chest, 20 Tracings in emphysema, 118 Traube, 6, 12, 68 Triangle, the dull, 54 Trousseau, 63, 71, 72 Tubercle, nature of, 186 views of, 186 Tubercle-bacilli (see bacilli) Tubercular meningitis, 268 Tuberculosis, 197, 222. Tumours, mediastinal, 328 diagnosis, 331 symptoms, 329 varieties, 328 Turbie-sur-mer, health resort, 297 Ulceration of the bowel, 255 Ulceration of the bowel, acute, 255, 318 chronic, 319 treatment of, 318 of the bronchus, 148 effects of, 148 of the larynx, 250 Vesicular murmurs, 32 Villemin, 186 Voice sounds, 43 Vomiting with cough, 324 Voyages, sea, in phthisis, 292 cases suitable for, 293 Waldenburg, 18, 122, 239 Walshe, 18, 36, 40, 68 Waters, 115 Weber, Hermann, 189, 195, 239, 288, 290, 293 Weigert-Koch method, 45 Wells, Sir Spencer, 162 Welch, 126 Wiesen, health resort, 173, 287 Wilks, 262 Williams, C. J. B., 31, 40, 164, 286 Williams, Dawson, 262 Yeo, Burney, 286 Zeigler, 181 •v~-,-*/vii&< NLH 051107m: 7 NATIONAL LIBRARY OF MEDICINE .V,VVV. 5S55MSMM^A«AVVv\Warav