Cabot—Physical Diagnosis 
Radiograph op a Child’s Thorax and Abdomen. The 
Heart, Liver and a Renal Neoplasm Are Made Visible 
by the Air around Them in the Lungs and Intestines. 
(Frontispiece) PHYSICAL DIAGNOSIS 
BY / 
RICHARD C. CABOT, M. D. 
w* ’ 
PROFESSOR OF MEDICINE IN HARVARD UNIVERSITY 
FORMERLY CHIEF OF THE WEST MEDICAL SERVICE 
MASSACHUSETTS GENERAL HOSPITAL 
lEigbtb lEDiticm 
REVISED AND ENLARGED, WITH SIX PLATES 
AND 279 FIGURES IN THE TEXT 
NEW YORK 
WILLIAM WOOD AND COMPANY 
MDCCCCXXIII Copyright, 1923 
BY WILLIAM WOOD AND COMPANY 
Printed in the United States of America 
THE MAFUE PRESS - YORK PA TO 
FREDERICK C. SHATTUCK, M. D. 
FORMERLY JACKSON PROFESSOR OF CLINICAL MEDICINE 
IN HARVARD UNIVERSITY 
IN EVIDENCE OF MT APPRECIATION OF 
THE EXAMPLE OF SINCERITY, COMMON SENSE, AND ENTHUSIASM 
ESTABLISHED BY HIM IN THE TEACHING AND 
THE PRACTICE OF MEDICINE PREFACE TO THE EIGHTH EDITION 
The number of changes since the last edition has been so great as 
to require a complete resetting of the book. The section on emphy- 
sema has been radically changed. The chapter on electro-cardio- 
graph has, with Dr. Paul D. White’s help, been brought up to date. 
I wish to thank him here for expert and generous aid. 
The increasing value of x-ray in the diagnosis especially of pul- 
monary and genito urinary diseases has led me to add many 
additional instructions and many new sentences. A number of new 
X-ray pictures have been inserted. For them I am indebted to Dr. 
George W. Holmes and his associates in the X-ray department of 
the Mass. General Hospital. 
R. C. C. 
August, 1923 PREFACE 
This book endeavors to present an account of the diagnostic 
methods and processes needed by competent practitioners of the 
present date. It differs from other books on the subject in that it 
makes no attempt to describe technical processes with which the 
writer has no personal familiarity and gives no space to the descrip- 
tion of tests which he believes to be useless. 
To gain genuine familiarity with all the technical processes de- 
scribed in most books on physical diagnosis—such familiarity as 
makes one competent to use them with due regard for the sources 
and limits of error inherent in them—needs more than the life-time 
of one man. But unless one has one’s self used a technical process 
long enough to gain this sort of mastery over it, one cannot prop- 
erly describe it, far less recommend it to others. Because of my lack 
of personal acquaintance with such methods as cystoscopy, ophthal- 
moscopy, and laryngoscopy I have attempted no description of them, 
although I believe they should sooner or later be mastered by every 
internist. All that I have described I know by prolonged use. 
A book constructed on this basis should make obvious what its 
writer considers important and what unimportant, and reveal therein 
not only his opinions but his personal limitations. But I believe 
there is no longer a demand for books that attempt impartially to 
present all that has been or is now thought of value by some one. 
The personal equation cannot and should not be ignored. In diag- 
nosis as in therapeutics “ What do you find valuable?” is the question 
that our contemporaries ask of any one of us, not “What has been 
recommended ?” 
In the endeavor further to break down the false distinction be- 
tween clinical diagnosis and laboratory diagnosis I have described 
all the methods of getting at an organ—e.g., the kidney—in a sin- 
gle section. Palpation, thermometry, urinalysis are different proc- 
esses by which we may gather information about the kidney. The 
student should be accustomed to think of them and practice them 
in close sequence. 
VII VIII 
PREFACE 
For the same reason the most important methods of investigat- 
ing the stomach have been grouped together without any distinction 
of “clinical” and “laboratory” procedure. 
For the illustrations I owe many thanks to many persons, espe- 
cially to Drs. Frank Billings, A. E. Boycott, E. H. Bradford, E. R. 
Carson, J. Everett Dutton, R. T. Edes, Joel E. Goldthwait, J. S. 
Haldane, Frederick T. Lord, R. W. Lovett, H. C. Masland, S. J. 
Meltzer, Percy Musgrave, R. F. O’Neil, J. E. Schadle, William H. 
Smith, W. S. Thayer, and G. L. Walton; also to the editors of The 
Boston Medical and Surgical Journal, The St. Paul Medical Journal, 
American Medicine, The Journal of Experimental Medicine, and 
The Lancet. 
My assistant, Dr. Mary W. Rowley, has helped me very much 
with the index as well as with other parts of the book. 
190 Marlboro St., Boston. 
June, 1905. TABLE OF CONTENTS 
CHAPTER I 
DATA RELATING TO THE BODY AS A WHOLE 
Page 
I. Weight i 
1. Causes of Gain in Weight i 
2. Causes of Loss in Weight 2 
II. Temperature—Technique and Sources of Error 2 
1. Causes of Fever 3 
2. Subnormal Temperature 4 
3. Chills and Their Causes 3, 4 
4. Night and Day Sweats 4 
CHAPTER II 
THE HEAD, FACE, AND NECK 
I. The Cranial Vault 5 
1. Size, Shape 5 
2. Fontanels 6 
3. Hair 6 
II. The Forehead 7 
III. The Face as a Whole 8 
IV. Movements of the Head and Face 13 
V. The Eyes 14 
(а) Ocular Motions , 17 
(б) The Retina 17 
VI. The Nose 18 
VII. The Lips 20 
VIII. The Teeth 22 
IX. The Breath 23 
X. The Tongue 23 
XI. The Gums 25 
XII. The Buccal Cavity. 26 
XIII. The Tonsils and Pharynx 28 
XIV. The Neck 30 
1. Glands 31 
2. Abscess or Scars 33 
3. Thyroid Tumors 34 
4. Torticollis 34 
5. Vertebral Tuberculosis 35 
6. Bronchial Cysts and Fistulas 35 
7. Actinomycosis 36 
8. Cervical Rib 36 
9. Inflammatory or Dropsical Swelling of Neck 37 
IX X 
TABLE OF CONTENTS 
CHAPTER III 
THE ARMS AND HANDS; THE BACK 
PAGE 
The Arms. 
I. Paralysis 3 8 
II. Wasting of One Arm 40 
III. Contractures 4° 
IV. (Edema 41 
V. Tumors 41 
VI. Miscellaneous Lesions of the Forearm 43 
The Hands. 
I. Evidence of Occupation 45 
II. Temperature and Moisture 45 
III. Movements 45 
IV. Deformities 52 
The Nails 57 
The Back. 
I. Stiff Back 58 
II. Sacro-iliac Disease 59 
III. Spinal Curvatures 60 
IV. Tumors of the Back 60 
V. Prominent Scapula 61 
VI. Scaphoid Scapula. 61 
VII. Spina Bifida 61 
CHAPTER IV 
THE CHEST 
TECHNIQUE AND GENERAL DIAGNOSIS 
Introduction. 
I. Methods of Examining the Thoracic Organs 63 
II. Regional Anatomy of the Chest 63 
Inspection. 
I. Size 66 
II. Shape 66 
1. The Rachitic Chest 67 
2. The Paralytic Chest 67 
3. The Barrel Chest 68 
III. Deformities 69 
1. Curvature of the Spine 69 
2. Flattening of One Side of the Chest 70 
3. Prominence of One Side of the Chest 71 
4. Local Prominences 71 TABLE OF CONTENTS 
XI 
PAGE 
IV. Respiratory Movements. 72 
1. Normal Respiration 72 
2. Anomalies of Expansion 72 
(a) Diminished Expansion 73 
(b) Increased Expansion 73 
3. Dyspnoea 73 
V. Relation of Dyspnoea to Cyanosis 75 
VI. The Respiratory Rhythm 76 
x. Asthmatic Breathing 76 
2. Cheyne-Stokes Breathing 76 
3. Restrained Breathing 77 
4. Stridulous Breathing 78 
VII. Diaphragmatic Movements (Litten’s Phenomenon) 78 
VIII. The Cardiac Movements 80 
1. Normal Cardiac Impulse 80 
2. Displacement of the Cardiac Impulse 84 
3. Apex Retraction 85 
4. Epigastric Pulsation 86 
5. Uncovering of the Heart . 86 
IX. Aneurism and Other Causes of Abnormal Thoracic Pulsation .... 87 
X. The Peripheral Vessels 88 
1. Inspection of the Veins 88 
2. Arterial Phenomena .. 90 
3. Capillary Pulsation 91 
XI. The Skin and Mucous Membranes 92 
1. Cyanosis 92 
2. (Edema 93 
3. Pallor 93 
4. Jaundice 94 
5. Scars and Eruptions 94 
XII. Enlarged Glands. 94 
CHAPTER V 
PALPATION AND STUDY OF THE PULSE 
•c 
I. Palpation 96 
1. The Apex Beat 96 
2. Thrills 97 
3. Tactile Fremitus 98 
4. Friction, Pleural or Pericardial 100 
5. Palpable RMes 101 
6. Joint Frictions and Tendon Frictions 101 
7. Local Muscular Spasm 101 
8. Tender Points - . . . . 101 
The Pulse 102 
1. The Rate 104 
2. Rhythm 104 
3. Compressibility 104 XII 
TABLE OF CONTENTS 
PAGE 
4. Size and Shape of Pulse Wave 105 
5. Tension 106 
6. Size and Position of Artery 107 
7. Condition of Artery Walls 108 
III. Arterial Pressure and the Instruments for Measuring it 109 
1. Systolic or Maximum Pressure 111 
2. Diastolic Pressure 112,114 
3. Normal Readings 112,114 
4. Use of Data 112,114 
CHAPTER VI 
ARTERIOGRAMS, PHLEBOGRAMS AND 
ELECTROCARDIOGRAMS 
I. Heart Block 116 
II. Auricular Fibrillation 119 
III. Paroxysmal Tachycardia 120 
IV. Premature Beats (Extrasystoles) 121 
V. Coupling of Heart Beats and Alternation 123 
VI. Sinus Arrhythmia 124 
VII. Ventricular Preponderance 124 
CHAPTER VII 
PERCUSSION 
I. Technique 125 
/ Mediate Percussion ] 
\ Immediate Percussion j" 125 
2. Auscultatory Percussion 131 
3. Palpatory Percussion 132 
II. Percussion-Resonance of the Normal Chest 133 
1. Vesicular Resonance 133 
2. Dulness and Flatness 134 
3. Tympanitic Resonance 136 
4. Kronig’s Isthmus 136 
5. Cracked-pot Resonance 139 
6. Amphoric Resonance 139 
III. Sense of Resistance. 139 
CHAPTER VIII 
AUSCULTATION 
I. Mediate and Immediate Auscultation 142 
II. Selection of a Stethoscope 143 
III. The Use of the Stethoscope 147 
1. Selective Attention and What to Disregard 147 
2. Muscle Sounds 150 
3. Other Sources of Error 151 TABLE OF CONTENTS 
XIII 
PAGE 
IV. Auscultation of the Lungs 152 
1. Respiratory Types 154 
(a) Vesicular Breathing 156 
(b) Tubular Breathing 157 
(c) Broncho-vesicular Breathing 157 
(e) Asthmatic Breathing 157 
(/) Cog-wheel Breathing 157 
(g) Amphoric Breathing 158 
(h) Metamorphosing Breathing 158 
V. Differences between the Right and the Left Chest 158 
VI. Pathological Modifications of Vesicular Breathing 159 
1. Exaggerated Vesicular Breathing. . . 159 
2. Diminished Vesicular Breathing 160 
'VII. Bronchial Breathing in Disease 161 
VIII. Broncho-vesicular Breathing in Disease 162 
IX. Amphoric Breathing 162 
X. Rales 163 
1. Coarse Crackles 163 
2. Fine Crackles 164 
3. Musical 165 
XI. Cough. Effects on Respiratory Sounds 166 
XII. Pleural Friction 166 
XIII. Auscultation of the Voice Sound 167 
1. The Whispered Voice 167 
2. The Spoken Voice 168 
3. Egophony 169 
XIV. Phenomena Peculiar to Pneumo-hydrothorax 169 
1. Succussion 169 
2. Metallic Tinkle 170 
3. The Lung Fistula Sound 170 
CHAPTER IX 
AUSCULTATION OF THE HEART 
I. The Valve Areas 171 
II. Normal Heart Sounds 172 
III. Modifications in the Intensity of the Heart Sounds 174 
1. Mitral First Sound 174 
(a) Lengthening 174 
(b) Shortening. . . 175 
(c) Doubling 175 
2. The Second Sounds at the Base of the Heart 175 
(a) Physiological Variations 177 
Cb) Pathological Variations 177 
Accentuation of Pulmonic Second Sound 177 
Weakening of Pulmonic Second Sound 178 
Accentuation of the Aortic Second Sound 178 
Weakening of the Aortic Second Sound 178 XIV 
TABLE OF CONTENTS 
PAGE 
3. Modifications in Rhythm of Cardiac Sounds and Doubling of 
Second Sounds 179 
4. Metallic Quality of the Heart Sounds 180 
5. “Muffled” Heart Sounds 180 
IV. Sounds Audible Over the Peripheral Vessels 181 
CHAPTER X 
AUSCULTATION OF THE HEART, CONTINUED 
Cardiac Murmurs 182 
I. Terminology 182 
II. Mode of Production 183 
1. Place of Murmurs in the Cardiac Cycle 184 
2. Area of Transmission 185 
3. Intensity, Quality, and Length 188 
4. Relation to Heart Sounds 188 
5. Effects of Respiration, Exertion, and Position 189 
6. Metamorphosis of Murmurs 190 
III. Functional Murmurs . 190 
IV. Cardio-Respiratory Murmurs 192 
V. Arterial Murmurs 193 
CHAPTER XI 
ESTABLISHMENT AND FAILURE OF COMPENSATION IN 
VALVULAR DISEASE OF THE HEART 
I. Compensation Not Yet Established 194 
II. The Period of Compensation 194 
III. Failure of Compensation 195 
IV. Hypertrophy and Dilatation 196 
1. Causes 197 
2. Results 197 
3. Dilatation of the Heart 199 
(a) Predominant Dilatation of the Left Ventricle 201 
(b) Predominant Dilatation of the Right Ventricle 202 
CHAPTER XII 
RHEUMATIC HEART DISEASE 
Five Groups of Diseases Due to Circulatory Weakness 204 
I. Rheumatic Heart Disease 205 
1. Acute Endocarditis 206 
2. Rheumatic Pancarditis of Children 206 
3. Mitral Endocarditis (Rheumatic Type) 207 
(a) Early Stages 207 
(b) Late Mitral Disease—Stenosis 214 TABLE OF CONTENTS 
XV 
PAGE 
4. Aortic Disease (Rheumatic Type) 222 
1. Aortic Regurgitation ...222 
2. Aortic Stenosis 225 
5. Diseases of the Tricuspid and Pulmonary Valves 231 
1. Tricuspid Regurgitation . . 231 
2. Tricuspid Stenosis 234 
3. Pulmonary Regurgitation 234 
6. Combined Valvular Lesions 235 
1. Double Mitral Disease 236 
2. Aortic Regurgitation with Mitral Disease 237 
3. Aortic Regurgitation with Aortic Stenosis 237 
7. Pericarditis 238 
1. Dry or Fibrinous 238 
2. Pericardial Effusion 240 
3. Adherent Pericardium 245 
CHAPTER XIII 
SYPHILITIC HEART DISEASE 
I. Syphilitic Aortitis with or without Aneurism 248 
1. Aortic Regurgitation (Syphilitic Type) 248 
2. Physical Signs 249 
3. Capillary Pulsation 250 
4. Palpation 251 
5. Percussion and Auscultation 252 
II. Complications 254 
CHAPTER XIV 
SYPHILITIC AORTITIS WITH ANEURISM 
I. Inspection and Palpation 256 
1. Abnormal Pulsation 256 
2. Tumor 257 
3. Thrill. . 257 
4. Diastolic Shock 257 
5. Tracheal Tug 259 
II. Percussion 260 
III. Auscultation 260 
IV. Radioscopy 261 
V. Diagnosis 262 
CHAPTER XV 
HYPERTENSIVE CARDIO-VASCULAR DISEASE 
I. Physical Signs 268 
II. Fatty Degeneration 271 
III. Senile or Decrescent Arteriosclerosis 271 XVI 
TABLE OF CONTENTS 
CHAPTER XVI 
NEPHROGENOUS HEART DISEASE, GOITRE HEART, 
CONGENITAL MALFORMATIONS, MISCEL- 
LANEOUS CARDIAC LESIONS 
PAGE 
I. Nephritic (or Nephrogenous) Heart Disease 272 
II. Goitre Heart . 272 
III. Congenital Heart Disease 273 
1. Pulmonary Stenosis 274 
2. Aortic Coarctation. 274 
3. Patent Ductus Arteriosus 274 
4. Defective Interventricular Septum 275 
5. Defective Interauricular Septum 275 
6. Transposition of the Arterial Trunks 275 
7. Hypoplasia of the Aorta 275 
IV. Other Diseases which Weaken the Heart 275 
1. Acute Myocarditis • 275 
V. Miscellaneous Affections of the Heart 276 
1. Tachycardia 276 
2. Cardiac Symptoms of Nervousness 277 
Post Infectious Tachycardia, Tobacco, (Supposed Effect) 
Athlete’s Heart 278 
3. Bradycardia 279 
4. Heart Block ■. . 279 
5. Palpitation 279 
CHAPTER XVII 
DISEASES OF THE LUNGS 
BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
I. Tracheitis 281 
II. Bronchitis 281 
1. Acute 281 
2. Chronic 284 
III. Croupous Pneumonia 284 
(a) Inspection 285 
(b) Palpation 286 
(c) Percussion 286 
(d) Auscultation 287 
(e) Differential Diagnosis 290 
IV. Inhalation Pneumonia 291 
V. Broncho-Pneumonia 292 
VI. Pulmonary Tuberculosis 295 
1. Incipient Tuberculosis 295 
2. Moderately Advanced Cases 297 
3. Advanced Phthisis 300 
4. Hilus Tuberculosis 304 
5. Fibroid Phthisis 305 
6. Phthisis with Predominant Pleural Thickening 306 TABLE OF CONTENTS 
XVII 
PAGE 
7. Emphysematous Form of Phthisis 307 
8. Phthisis with Anomalous Distribution of the Lesions 308 
9. Acute Pulmonary Tuberculosis 308 
CHAPTER XVIII 
(DISEASES OF THE LUNGS, CONTINUED) 
I. “The Barrel Chest and Its Relations to Emphysema” 304 
2. Barrel Chest with Arteriosclerosis and Asthma 312 
3. Interstitial Emphysema 312 
4. Complementary Emphysema 313 
5. Acute Pulmonary Tympanites 313 
II. Bronchial Asthma 313 
III. Syphilis of the Lung 314 
IV. Bronchiectasis 315 
V. Examination of Sputa 317 
1. Origin 317 
2. Quantity ' 317 
3. Odor 317 
4. Gross Appearance 317 
5. Microscopic Examination 319 
CHAPTER XIX 
DISEASES AFFECTING THE PLEURAL CAVITY 
I. Hydrothorax 322 
II. Pneumothorax 322 
III. Pneumohydrothorax or Pneumopyothorax 324 
1. Differential Diagnosis 326 
IV. Pleurisy 328 
1. Dry Pleurisy 328 
2. Pleuritic Effusion 330 
(a) Percussion 330 
(b) Auscultation 335 
(c) Inspection and Palpation 336 
(d) Interlobar Empyema 338 
3. Pleural Thickening 339 
4. Encapsulated Pleural Effusions 341 
5. Pulsating Pleurisy and Empyema Necessitatis 342 
6. Differential Diagnosis of Pleural Effusions 342 
7. Carcinoma of the Pleura 344 
8. Cancer of the Bronchi and Lung 345 
9. Echinococcus of the Pleura 345 
10. Actinomycosis of the Pleura 345 
V. Cyto-Diagnosis of Pleural and Other Fluids 345 
1. Technique . 246 
2. Interpretation of Results 347 XVIII 
TABLE OF CONTENTS 
CHAPTER XX 
ABSCESS, GANGRENE, AND CANCER OF THE LUNG, PUL- 
MONARY ATELECTASIS, (EDEMA, AND HYPOSTATIC 
CONGESTION 
PAGE 
I. Abscess and Gangrene of the Lung 349 
II. Neoplasms of the Lung and Mediastinum 350 
III. Atelectasis 351 
IV. (Edema of the Lungs 352 
V. Hypostatic Pneumonia 353 
CHAPTER XXI 
THE ABDOMEN IN GENERAL, THE BELLY WALLS, PERI- 
TONEUM, OMENTUM, AND MESENTERY 
I. Examination of the Abdomen in General 354 
1. Technique . . . . v 354 
(a) Inspection 354 
(b) Palpation 356 
2. What can be felt Beneath the Normal Abdominal Walls . . „ . 357 
3. Palpable Lesions of the Belly Walls 358 
4. Abdominal Tumors 359 
(a) Percussion 361 
II. Diseases of the Peritoneum 362 
1. Peritonitis, Local or General 362 
2. Ascites 363 
3. Cancer and Tuberculosis 364 
III. The Mesentery 365 
1. Glands 365 
2. Thrombosis 365 
CHAPTER XXII 
THE STOMACH, LIVER, AND PANCREAS 
I. The Stomach 366 
1. Inspection and Palpation 366 
2. Use of the Stomach Tube 367 
3. Examination of Contents 369 
(a) Qualitative Tests 372 
(b) Quantitative Estimation of Free HC1 and of Total Acidity 372 
» 4. Bismuth X-ray Examination of the Stomach 373 
5. Incidence and Diagnosis of Gastric Diseases 375 
II. The Liver 377 
1. Pain 378 
2. Enlargement 378 
3. Atrophy 381 
4. Portal Obstruction 381 
5. Jaundice 382 
6. Loss of Flesh and Strength 384 TABLE OF CONTENTS 
XIX 
PAGE 
7. The Infection Group of Symptoms 384 
8. Cerebral Symptoms of Liver Disease 384 
III. The Gall Bladder and Bile Ducts 384 
1. Differential Diagnosis of Biliary Colic 385 
2. Enlarged Gall Bladder 385 
3. Cholecystitis 386 
IV. The Pancreas 386 
1. Cancer 387 
2. Acute Pancreatic Disease 387 
3- Cyst 387 
4. Bronzed Diabetes 387 
CHAPTER XXIII 
THE INTESTINES, SPLEEN, AND KIDNEY 
I. The Intestines 389 
1. Data for Diagnosis 389 
2. Appendicitis 391 
3. Chronic Appendicitis 393 
4. Intestinal Obstruction 393 
5. Cancer 394 
6. Examination of Contents 394 
7. Parasites 396 
II. The Spleen 401 
1. Palpation 401 
2. Percussion . 402 
3. Causes of Enlargement 403 
4. Differential Diagnosis of the Various Causes of Enlargement . . 404 
III. The Kidney 405 
1. Incidence and Data 405 
2. Characteristics Common to Most Tumors of the Kidney .... 407 
(a) Malignant Disease 409 
(b) Hydronephrosis and Cystic Kidney , 409 
(c) Perinephritic Abscess .....410 
(1d) Abscess of the Kidney 410 
(e) Floating Kidney 411 
3. Renal Colic and Other Renal Pain 411 
4. Examination of the Urine 413 
(a) Amount and Weight 413 
(b) Optical Properties 414 
(c) Significance of Sediments (Gross) 415 
5. Pyuria 416 
6. Hsematuria 417 
7. The “Red Test” 418 
8. Chemical Examination of the Urine 418 
(a) Reaction of Normal Urine 418 
(b) Tests for Albuminuria 419 
(c) Significance of Albuminuria 420 XX 
TABLE OF CONTENTS 
PAGE 
(d) Significance of Albumosuria 421 
(e) Glycosuria and Its Significance 421 
(/) The Acetone Bodies 422 
(g) Other Constituents 423 
9. Microscopic Examination of Urinary Sediments . , 423 
10. Summary of the Urinary Pictures Most Useful in Diagnosis. . . 428 
CHAPTER XXIV 
THE BLADDER, RECTUM, AND GENITAL ORGANS 
I. The Bladder 431 
1. Incidence and Data 431 
2. Distention 431 
3. The Urine as Evidence of Bladder Disease 433 
II. The Rectum ' 435 
1. Symptoms which should Suggest an Examination 435 
2. Methods . '. 436 
III. The Male Genitals 437 
1. The Penis 43& 
2. The Testes and Scrotum 438 
IV. The Female Genitals 44° 
1. Methods . 44° 
2. Lesions 440 
(a) In the External Genitals 440 
(b) In the Uterus 441 
(c) In the Fallopian Tubes 443 
(d) In the Ovaries 443 
CHAPTER XXV 
THE LEGS AND FEET 
I. The Legs 446 
1. Hip 446 
2. Groin 446 
3. Thigh 447 
4. Knee 451 
5. Lower Leg 452 
II. The Feet 456 
1. The Toes 460 
CHAPTER XXVI 
THE BLOOD 
I. Examination of the Blood 462 
1. Haemoglobin 462 
2. Study of the Stained Blood Film 464 
3. Counting the White Corpuscles 470 
4. Counting,the Red Corpuscles 471 XXI 
TABLE OF CONTENTS 
PAGE 
II. Interpretation of These Data 472 
1. Secondary Anaemia 472 
2. Chlorosis 473 
3. Pernicious Anaemia 473 
4. Leucocytosis 473 
5. Lymphocytosis 473 
6. Eosinophilia 473 
7. Leukaemia 476 
III. The Widal Reaction 477 
IV. The Wassermann Reaction 478 
V. Blood Parasites 478 
1. Malaria 478 
2. Trypanosomiasis 479 
3. Filariasis 479 
CHAPTER XXVII 
THE JOINTS 
I. Examination of the Joints 480 
1. Methods and Data 480 
2. Technique 481 
II. Joint Diseases 484 
1. Infectious Arthritis 485 
2. Atrophic Arthritis 488 
3. Hypertrophic Arthritis 490 
4. Gouty Arthritis 496 
5. Haemophilic Arthritis 496 
6. Relative Frequency of the Various Joint Lesions 496 
CHAPTER XXVIII 
THE NERVOUS SYSTEM 
I. Examination of the Nervous System 497 
1. Disorders of Motion 497 
2. Disorders of Sensation 500 
3. Reflexes 501 
4. Electrical Reactions 506 
5. Speech and Handwriting 506 
6. Trophic Vasomotor Disorders 507 
7. The Examination of Psychic Functions; Coma 507 
8. Examination of the Cerebro-Spinal Fluid 510 
Index. 513 PHYSICAL DIAGNOSIS 
CHAPTER I 
DATA RELATING TO THE BODY AS A WHOLE 
I. Weight 
To weigh the patient should be part of every physical examina- 
tion, and every physician’s office should contain a good set of scales. 
1. Gain in weight, aside from seasonal changes, the increase in 
normal growth, and convalescence from wasting diseases, means 
usually: 
(a) Obesity. 
(b) The accumulation of serous fluid in the body—dropsy, evi- 
dent or latent. 
The first of these needs no comment. Latent accumulation of 
fluid, not evident in the subcutaneous tissues or serous spaces, oc- 
curs in some forms of uncompensated cardiac or renal disease and in 
diabetes, and gives rise to an increase in weight which may delude the 
physician with the false hope of an improvement in the patient’s 
condition, but in reality calls for derivative treatment (diuresis, 
sweating). 
Obvious dropsy has, of course, the same effect on the weight and 
the same significance. 
(e) Myxoedema is a cause of increased weight, i.e., especially when 
the myxoedematous infiltration is widespread (see below, page u). 
2. Loss of Weight.—The aging process is so often associated with 
loss of weight that some writers speak of the 11 cachexia of old age." 
In some, a rapid loss of superfluous fat may occur at moderate age, 
e.g., at fifty-five, and may give rise to grave apprehension though the 
general health remains good and no known disease develops. 
Aside from this physiological change of later life, most cases of 
loss of weight are due to: 
(a) Malnutrition. 
(b) Loss of sleep (whether from pain or other cause). 
(c) Infectious fevers and other toxasmic states. 
1 2 
PHYSICAL DIAGNOSIS 
Under the head of malnutrition come the cases of oesophageal 
stricture, chronic dyspepsia (usually with peptic ulcer) and gastric 
cancer, chronic diarrhoea, the atrophies of infancy, diabetes mellitus, 
and the rare cases of anorexia nervosa. 
Loss of sleep is, I believe, the chief factor in the emaciation oc- 
curring in many painful illnesses as well as in various other types 
of disease. It is only in this way that I can account for the marked 
emaciation in many cases of thoracic aneurism and of gall-stones. 
Toxaemia is, I suppose, accountable for part at least of the ema- 
ciation in neoplasms, typhoid, cirrhotic liver, and tuberculosis. It is 
especially important to suspect tuberculosis and look for it in any 
patient who has lost weight without any obvious cause, for such a loss 
is often an early symptom of the disease. 
Accelerated or increased metabolism is present in Graves’ disease 
and may be one of the earliest symptoms. Even if the patient takes 
more than his normal share of food he may lose weight steadily. 
II. Temperature 
The method of taking temperature is too familiar to need expla- 
nation, but the student should be aware of the fact that hysterics 
and malingerers can and often do raise the mercury in the bulb by 
various manoeuvres, unless they are vigilantly watched. Dipping 
the bulb into hot water, shaking the mercury upward toward the 
higher degrees of the scale, and possibly friction with the tongue (?) 
are to be suspected. 
In comatose or dyspnoeic patients and in infancy the temperature 
is best taken by rectum. In others we must be sure that the lips do 
not remain open during the test, so as to reduce the temperature of 
the mouth. 
i. Fever, i.e., a temperature above 990 F., has much more diag- 
nostic value in adults than in infancy and childhood. In the latter 
it is often impossible to make out any pathological condition to 
account for a fever. After childhood the vast majority of fevers 
are found to be due to: 
(a) Infectious disease or inflammation of any type. 
(b) Toxaemia without infection—a much less common and less 
satisfactory explanation. Cancer of the liver and Graves’ disease are 
examples. TEMPERATURE 
3 
(c) Disturbance of heat regulation—as in sunstroke, after the use 
of atropine, and in nervous excitement, e.g., just after entering a 
hospital.1 
(d) After haemorrhage there may be marked fever for which no 
cause is clear. 
For such causes we search when the thermometer indicates fever. 
Types of fever often referred to are: 
(а) 11 Continued fever,” one which does not return to normal at 
any period in the twenty-four hours, as in many cases of typhoid, 
pneumonia, and tuberculosis. 
(б) “Intermittent,” “hectic,” or “septic” fever, one which disap- 
pears once or more in twenty-four hours, as in double tertian mala- 
ria and septic fevers of various types (including mixed infections in 
tuberculosis). 
A fever which disappears suddenly and permanently is said to 
end by “crisis,” while one which gradually passes off in the course of 
several days ends by “lysis.” 
Long-continued fevers—i.e., those lasting two weeks or more 
without obvious cause—are usually due (in the temperate zone) to 
one of three causes:—Typhoid, tuberculosis, sepsis. 
In 1,000 “long fevers” (as above defined) the following causes were 
found in the medical records of the Massachusetts General Hospital: 
Typhoid Fever 586 
Tuberculosis 192 
Pyogenic Infections 148 
Epidemic Meningitis 27 
“Influenza” 10 
Infectious Arthritis (‘ ‘ rheumatism 9 
Leucaemia 5 
Cancer 4 
Syphilis 2 
Miscellaneous 17 
926, or 92.6 per cent. 
74, or 7.4 per cent. 
Since the last 7.4 per cent, here listed represent fevers whose cause 
is usually obvious, it is substantially true to say that any long obscure 
fever arising in the temperature zones is due to typhoid, tuberculosis or 
sepsis. Under sepsis I include vegetative endocarditis (“benign” 
or “malignant”), urinary and biliary infections, all local inflammatory 
1 The latter event may also reduce (temporarily) a high fever to normal or 
below it. In coma from any cause (uraemia, cerebral hemorrhage, diabetic coma) 
fever often occurs. 4 
PHYSICAL DIAGNOSIS 
processes and generalized bacterial infections with or without a known 
portal of entry. 
2. Subnormal temperature is often seen in wasting disease (can- 
cer), nephritis, uncompensated heart disease, and myxoedema. It 
is rarely of diagnostic value, but is a rough measure of the degree of 
prostration. It may be present in health. 
3. Chills (due usually to a sudden rise in temperature) are seen 
chiefly in: (a) Sepsis of any type, especially urinary or biliary sepsis;1 
(b) Malaria; (c) Onset of acute infections; (d) “Nervous” states. 
After the passage of a catheter, after or during labor, after 
infusion of saline solution or any serum or antitoxin a chill is often 
seen, but not easily explained. 
True chill, with shivering and chattering teeth, is distinguished 
from chilliness without any shivering. Chilliness is far less signifi- 
cant and often goes without fever; true chill rarely does. 
The cause of true chills can usually be determined by blood exami- 
nation (leucocytosis, malarial parasites) and by the general physical 
examination. Chills without any abnormal physical signs and with 
normal blood are most often due to sepsis in the kidney, liver or bile 
ducts. Fever without explanation is sometimes from dental sepsis or 
sinus infection. 
4. Night Sweats and Day Sweats. 
Sweating in disease seems to be conditioned by: (a) Fever (infec- 
tion); (6) Weakness; (c) Sleep. 
A phthisical patient who falls asleep in the daytime will sweat 
then and there, and the sweating will stop when he wakes. In typhoid 
fever and pneumonia sweating often begins in convalescence when 
the temperature is nearly or quite normal. In alcoholism, hyper- 
thyroidism, and neurasthenic states we sometimes see sweating 
without fever. In France pretty much all dispensary patients com- 
plain of night sweats, perhaps because of their sleeping habits. 
Sepsis, acute rheumatism, and tuberculosis are the infections 
most often accompanied by sweating. In rickets the head sweats 
especially. 
1 Staphylococcus or B. coli infections of the kidney and its pelvis, cholangitis 
with stone in the common bile duct. CHAPTER II 
THE HEAD AND FACE; THE NECK 
THE HEAD AND FACE 
Almost all that we can learn about the manifestations of disease 
on the head and face is to be learned by the use of our eyes, by inspec- 
tion, as the term is, and by x-ray. Other methods—percussion, 
palpation—yield but little. I shall begin at the top. 
I. The Cranial Vault 
1. The Shape and Size of the Cranium 
The shape and size of the cranium concern us, especially in children. 
(a) Abnormally small crania (microcephalia) are apt to mean idiocy 
of syphilitic origin, especially if the 
sutures are closed. 
(b) An abnormally large head is seen 
in hydrocephalus (see Fig. i), associated 
with enormous “open” areas uncovered 
by bone and a peculiar downward in- 
clination of the eyes, which are partly 
covered by the eyelids and show a white 
margin above the iris. This condition is 
to be distinguished from the: 
(c) Rachitic head, which is flatter at 
the vertex and more protuberant at the 
frontal eminences, giving it a squarish 
outline, contrasted with the globular 
shape and rounded vertex of the 
hydrocephalic. In rickets there are no 
changes in the eyes. 
(d) In congenital syphilis we see a 
square head, prominent in the forehead, sloping down to a narrow chin. 
(e) In adult life an enlargement of the skull, due to bony thickening, 
forms part of the rare disease, osteitis deformans (Paget’s disease), 
associated with thickening and bowing of the long bones (see Fig. 2). 
Fig. 1.—Hydrocephalus. 
5 6 
PHYSICAL DIAGNOSIS 
(/) Myelomata of the skull may or may not be accompanied by a 
leuksemic blood and a greenish staining of the tumor tissues. They 
are recognized by the concurrent presence of the Bence-Jones protein 
in the urine, by the x-ray, the negative Wassermann reaction and finally 
the histological examination of an excised node (see Figs. 3 and 4). 
Hypernephromata may exhibit a cranial metastasis. With such 
a tumor the presence of hematuria and enlarged kidney is suggestive. 
2. The Fontanels 
The anterior and larger fontanel remains about the same size for 
the first year of life, then diminishes, and closes about the twentieth 
month. The posterior closes in about six weeks. In rickets, hydro- 
cephalus, hereditary syphilis, and cretinism, the fontanels and sutures 
remain open after the normal time limit. 
Fig. 2.—Paget’s Disease. (Edes.) a, Before onset of hyperostosis cranii. b. After 
onset of hyperostosis cranii. c, Later still. 
(a) Bulging fontanels mean increased intracranial tension (hydro- 
cephalus, hemorrhage, meningitis, or any acute febrile disease without 
dyspnoea). (b) Depressed fontanels are seen in severe diarrhoea, wasting 
diseases, collapsed states, and acute dyspnoeic conditions. 
3. The Hair 
(a) A rachitic child often rubs the hair off the back of its head 
by constant rolling on the pillow. (This is associated with profuse 
sweating of the head.) Patchy baldness occurs in the skin disease 7 
THE HEAD AND FACE 
alopecia, areata, and occasionally over the painful area in trigeminal 
neuralgia. 
(6) General loss of hair occurs normally after many acute fevers 
and with advancing age. Early baldness (under thirty-five) is often 
hereditary. Syphilis may produce a rapid loss of hair, local or general, 
and the same is true of myxcedema; but in both these diseases the hair 
usually grows again in convalescence. 
(c) Parasites (pediculi) are worth looking for in the dirtier classes 
and those associated with them (teachers). Their eggs adhere to 
the hairs and are familiarly known as “nits.” An eczema or itching 
dermatitis and an adenitis often results. 
Fig. 3.—Multiple Myelomata. 
Fig. 4.—Multiple Myelomata. 
II. The Forehead 
Scars, eruptions, and bony nodes are important. 
(а) Scars may be due to trauma or to old syphilitic periostitis. 
The epileptic often cuts his forehead in falling. 
(б) Eruptions often seen on the forehead are those of acne, syphilis, 
and smallpox. These may resemble each other closely, and are to be 
distinguished by the history, the presence of lesions on other parts of 
the body, and the concomitant signs (fever, prostration, etc.). 8 
PHYSICAL DIAGNOSIS 
(c) Nodes may be the result of many bumps in childhood or may 
be caused by a syphilitic periostitis or neoplasms (see Figs. 3, 4, 5 
and 7). The history must decide. 
(d) Evidence of frontal sinusitis may be found (see Fig. 9). 
The characteristic history of pain due to frontal sinusitis is that one 
wakes in the morning free from it, that within an hour or two, and 
usually at about, the same hour, a milder or severer ache over one 
Fig. 5.— Syphilis of the Frontal Bone. (Curschmann.) 
eyebrow begins, continues for a few hours, but ordinarily wears off by 
noon. The regular recurrence and localization are characteristic of 
sinusitis. 
III. The Face as a Whole 
Very characteristic even at a glance is the face of (a) acrome- 
galia. A strong family likeness seems to pervade all well-marked 
cases (see Figs. 7 and 8). The huge, bony “whopper jaw” is the 
most striking item, then the prominent cheek bones, and the ridge 
above the eyes. The nose and chin are very large. THE HEAD AND FACE 
9 
Fig. 6.—Gumma Involving Frontal Bone. 
Fig. 7.—Acromegalia. 10 
PHYSICAL DIAGNOSIS 
Fig. 8.—Typical Face in Acromegaly. 
Fig. 9.—Frontal Sinusitis. 
Fig. io.—Myxoedema. THE HEAD AND FACE 
11 
(b) Myxcedema (see Fig. io) is not so characteristic and might 
easily be mistaken for nephritis or normal stupidity with obesity. 
The presence of dry skin, falling hair, mental dulness, and subnormal 
temperature, all supervening simultaneously within a few weeks or 
months, makes us suspect the 
disease and test for low metabo- 
lism especially at or near the 
meno-pause. Palpation shows 
that the puffiness of the face is 
not true oedema, as it does not 
pit on pressure. 
(c) Cretinism—the infantile 
form of myxcedem a—can 
generally be recognized by sight 
Figs, ii and 12.—Cretinism 
alone (see Figs, n and 12). Here the tongue is often protruded, 
and there are often pot-belly and deformed legs. 
(d) In adenoids of the nasopharynx the child’s mouth is often 
open, the nose looks pinched, the expression is stupid (see Fig. 13). 
There is a history of mouth-breathing and snoring, with frequent 
“colds,” ear troubles and a high-arched palate. 12 
PHYSICAL DIAGNOSIS 
(e) In paralysis agitans and encephalitis lethargica the ‘ ‘ mask-like 
face shows almost no change of expression, whatever the patient says 
or does. The neck is usually inclined forward, and so rigid that when 
the patient wishes to look to right or left his whole body rotates like 
a statue on a pivot. In some cases tremor is absent and the character- 
istics just mentioned are then of great importance in diagnosis. 
Fig. 13.—Adenoid Face. (Schadle.) 
(/) In Graves' disease (thyrotoxicosis) the startled or frightened 
look is characteristic, though the expression is almost wholly due to the 
bulging of the eyes and their quick motions (Fig. 14). 
(g) In leprosy the general expression is of a superabundance of skin 
on the patient’s face, reminding us of some animal (“leonine face”) 
(Fig- is)- 
(h) In early phthisis one often notices the clear, delicate skin, 
fine hair, long eyelashes, wide pupils—“appealing eyes.” Pallor 
and a febrile flush (hectic) come later in some cases. 
(i) After vomiting the face has often a drawn, pinched, anxious 
look, which has often been supposed to be characteristic of general 
peritonitis, intestinal obstruction, or other diseases accompanied by 
vomiting; but I can not recognize any single expression as charac- 
teristic of peritoneal lesions. THE HEAD AND FACE 
13 
O') Chronic alcoholism may be shown not only in a red nose, but 
oftener in a peculiar, smoothed-out look, due, I suppose, to an extra 
but evenly distributed accumulation of subcutaneous fat. 
{k) An cedematous or swollen face is much more easily noticed by 
the patient or his friends than by one who is not familiar with his 
normal look. It usually points 
to nephritis, but may occur in 
heart disease, diabetes and 
sometimes (especially in the 
Fig. 14.—Exophthalmic Goitre. (Meltzer.) 
Fig. 15.—Face in Leprosy. 
morning) without any known cause. When combined with anaemia, the 
puffy face gives a peculiar “pasty” look (chronic glomerulo-nephritis). 
IV. Movements of the Head and Face 
i. The Shaking Head 
This occurs often in old age, occasionally in paralysis agitans 
(which oftener affects the hands), and in toxic conditions (alcohol 
tobacco, opium). In some cases no cause can be found. 
2. Spasms of the Face 
Spasms of the face, i.e., sudden, quick contractions of certain 
facial muscles, such as winking-spasm, jerking of a corner of the 
mouth, or sniffing, occur chiefly 14 
PHYSICAL DIAGNOSIS 
(a) As a matter of habit without other disease. This is chronic. 
(,b) As a part of the acute infectious disease chorea, with similar 
“restless” motions of the hands and feet. We often see these spasms 
in school-children; occasionally in pregnant women. The disease is 
probably due to the same streptococcus which produces (simultane- 
ously or at other times) the youthful types of polyarthritis (rheu- 
matic fever) and of endopericarditis. 
(c) By imitation, in schools and institutions, these spasms may 
spread like an epidemic. 
From habit spasms, which persist for months or years in one or 
two groups of muscles, true chorea is distinguished by its involvement 
of the hands, feet, and other parts, by its frequent association with 
tonsillitis, joint pain and endocarditis (see page 485), and by its short 
course (eight to ten weeks on the average). 
In hysterical conditions and hereditary brain defects, various 
other spasms occur (see below, page 499). 
V. The Eyes 
I shall not attempt to deal with lesions essentially local (such as 
a “sty”), but shall confine myself to data that have diagnostic value 
in relation to the rest of the body. 
i. CEdema of the Lids 
(Edema of lids, especially the lower, often accumulates in the 
night and is seen in the early morning, without known cause or after 
a debauch. In other cases it usually points to the existence of: 
(a) Nephritis (prove by urinary examination). 
(b) Anosmia (prove by blood examination). 
(c) Measles and whooping-cough (eruption, paroxysms of cough). 
Rarer causes are diabetes, trichiniasis, angioneurotic oedema, and 
erysipelas. 
Trichiniasis is recognized by the presence of fever, muscular ten- 
derness, and an excess of eosinophiles in the blood. 
In angioneurotic oedema and urticaria there is usually a previous 
history of similar transitory swellings in other parts of the body. 
The acute onset, red blush, high fever, and general prostration 
distinguish the oedema of erysipelas. THE HEAD AND FACE 
15 
2. Dark Circles under the Eyes 
may appear in any debilitated state, e.g., from loss of sleep, hunger, 
menstruation, masturbation, etc. 
3. Conjunctivitis 
This affection forms part of hay fever, measles, streptococcus in- 
fections, typhus, trichiniasis and yellow fever. It also occurs as an 
independent infection. It follows overdoses of iodide of potash or 
arsenic. The whole conjunctiva is reddened, in contradistinction from 
the reddening about the iris seen in iritis. 
Phlyctenular conjunctivitis and keratitis occurs especially in ill- 
nourished children of poor and ignorant parents living in congested 
districts, i.e., under the conditions producing tuberculosis. Its 
cause is unknown. It produces a yellowish-red ulcerated streak 
growing in from the conjunctiva across the margin of the cornea. 
4. Jaundice 
Jaundice, the yellow coloration of the white of the eye by bile 
pigment, is easily recognized when well marked, and can be con- 
founded only with subconjunctival fat, which differs from jaundice 
in that it appears in spots and patches, not covering the whole sclera, 
as jaundice does. In mild cases only the posterior portions of the 
sclera are tinted yellow, while the anterior part around the iris may 
show a bluish-white tinge in contrast. This state of things is hard to 
distinguish from the appearances seen in the eyes of many apparently 
healthy people. The presence of bile in the urine often clears up 
the question. 
The skin, mucous membranes, urine, and sweat are also bile- 
stained in most cases, and the circulation of the bile in the blood 
often produces slow pulse, itching,1 and mental depression. Lack of 
bile in the gut leads to flatulence and clay-colored fatty stools. 
The commonest causes are: (a) Biliary obstruction (catarrh, stone 
or tumors obstructing the larger bile ducts, hepatic cirrhosis, or 
syphilis constricting them). 
(b) Hemolysis (malaria, sepsis, icterus of the new-born, pernicious 
anasmia) producing obstruction of fine bile ducts. 
1 In gall-stone cases one often finds itching without jaundice. 16 
PHYSICAL DIAGNOSIS 
5. Argyria 
Since the prevalent use of silver salts in the treatment of ocular 
disease, a brownish staining of the conjunctiva and sclera not infre- 
quently results, even after moderate doses. Individual hypersensi- 
tiveness doubtless plays a part. 
6. The Pupils 
The normal reflexes to light are best tested with an electric flash 
light which produces a brisk and obvious contraction of the healthy 
pupil. To test the reaction to distance turn the patient away from 
the light and let him look at the farthest corner of the room. The pupil 
expands. Make him look at your finger a few inches distant from 
his eyes. The pupil contracts. Each pupil should be examined 
separately. 
The value of the pupils in diagnosis has been greatly overestimated. 
There are few conditions except tabes and paresis in which they yield 
us important diagnostic evidence, for, although they are very often 
abnormal, the abnormalities are seldom characteristic of any single 
pathological condition and throw little light on the diagnosis. Espe- 
cially in coma the condition of the pupils, on which much stress has 
been laid in textbooks, is, in my own experience, misleading or useless 
as a diagnostic guide. 
(a) The Argyll-Roberts on pupil reacts to distance, but not to light. 
It is of great value as a factor in the diagnosis of tabes dorsalis and 
dementia paralytica. 
(b) Dilated pupils.—(a) Many phthisical patients show a more or 
less transient dilatation of one or both pupils. (b) Blindness or defi- 
cient sight (from any cause) may cause dilatation of the pupil. (c) 
Other common causes are distress or strong emotion from any cause, 
many fevers and comatose states, and the use of mydriatic drugs. 
(c) Contracted pupils are common in old age and in photophobia 
from any cause. Disease high up in the spinal cord (tabes, general 
paralysis, etc.) may produce contraction (spinal niyosis) by paralyzing 
the sympathetic dilators. Aortic aneurism may produce in the same 
way contraction of one pupil (see below, page 259). 
(d) Contraction with irregular outline and sluggish reactions is 
often seen in iritis as a result of adhesions to the lens (posterior syne- 
chias), also in syphilis and without known cause. THE HEAD AND FACE 
17 
7. The Cornea 
(a) Arcus senilis, a grayish ring at the circumference of the cornea 
is one of the classical signs of old age and arteriosclerosis, but is occa- 
sionally seen in normal young adults. 
(b) Syphilitic keratitis, usually seen in the hereditary form of 
the disease, produces an irregularly distributed haziness of the cornea, 
usually in both eyes and before the sixteenth year. Diagnosis depends 
on other evidences of syphilis. 
(c) Gonorrheal ophthalmia is a common cause of opacities in the 
cornea and so of the types of blindness produced in infancy. 
(d) Trauma of the eyes by cuts and blows is a not infrequent cause 
of scars which impair vision. 
(a) Ocular Motions 
(a) Ptosis, or dropping of the eyelid, is usually unilateral and 
dependent on paralysis of the third nerve. Its most frequent cause 
is basal syphilitic meningitis. The eye is usually drawn out by the 
action of the unparalyzed external rectus. Moderate, bilateral ptosis 
is common in hysterical and neurasthenic conditions, in botulism and 
in sleeping sickness. 
(■b) Squint (strabismus) is called external if the eye turns out, 
internal if it turns in. Of its many types and causes I mention only 
the acute cases due to intracranial lesions, such as tuberculous and 
epidemic meningitis, syphilis, tumors. 
(c) Nystagmus is a rapid, usually horizontal oscillation of both 
eyeballs. It may be the result of albinism or of various local eye 
troubles, but is an important member of the symptom group char- 
acteristic of multiple sclerosis. It may, however, occur in other brain 
lesions and in health. Rarely the oscillation is vertical. 
(b) The Retina 
The lesions of greatest interest in general medicine are: Retinal 
hemorrhage, arterio-sclerosis, optic neuritis, and optic atrophy. 
(a) Retinal hemorrhages, with or without other retinal changes, are 
important signs of nephritis, grave anaemias, and diabetes. 
(b) Arterior-sclerosis may appear earlier or more clearly in the 
retina than elsewhere. 
(c) Papillary edema (choked disc) is of value in the diagnosis of 
intracranial pressure, for example in brain tumors, tuberculous men- 
ingitis, brain abscess, and in some cases hemorrhage. 18 
PHYSICAL DIAGNOSIS 
(<d) Optic atrophy may be the end result of any of the types of 
optic neuritis just mentioned, or in a primary form is important evi- 
dence of tabes dorsalis. Many cases occur without any known cause 
VI. The Nose 
i. Size and Shape.—The enlargement of all the tissues of the nose 
occurring in acromegaly has already been mentioned. In myxcedema 
Fig. i6.-—Syphilitic Depression of the Nasal Bones. 
the nostrils are sometimes thickened and the whole nose loses its 
delicacy of shape. A red nose is popularly and correctly associated 
with alcoholism, but in many cases identical appearances are produced 
by acne rosacea or by lupus erythematosus, as well as by circulatory 
anomalies without any other disease. 
Falling in of the bridge of the nose may be due to syphilis of the 
nasal bones, especially when there are scars over the sunken portion, 
but is sometimes present without any disease. See Fig. 16. 
Perforation of the septum (syphilitic) is often unknown to the 
patient and may be important in diagnosis. Occasionally it is due to 
mild non-syphilitic inflammations of the septum. The habit of put- THE HEAD AND FACE 
19 
ting a hand electric flash light against the side of the nose in the 
routine of physical examination is valuable. 
The small, narrow nose associated with adenoid growths has already 
been mentioned. 
2. The nostrils move visibly in many conditions involving dyspnoea 
(diseases of the heart and lungs, acute infections, etc.), and this is 
Fig. 17.—Epithelioma. 
sometimes useful in suggesting to the physician the possibility of 
pneumonia, hitherto unsuspected. Dried blood in the nostrils may be 
of value as evidence of recent nosebleed. 
3. Nosebleed suggests especially trauma, vascular hypertension, 
infectious fevers (particularly typhoid and. juvenile endocarditis); 
also hemorrhagic diseases (purpura, haemophilia, acute leukaemia). 
4. A nasal discharge in a young infant (“snuffles”) suggests hered- 
itary syphilis. In adults the familiar “cold in the head” may need a 
bacteriological examination to exclude the possibility of nasal diph- 
theria or to confirm a diagnosis of influenza. 
5. A small, indolent, long-standing sore on the nose or near the 
corner of the eye should always suggest epithelioma (see Fig. 17) and 
tuberculosis. Microscopic examination may be necessary to determine 
the diagnosis. 20 
PHYSICAL DIAGNOSIS 
6. The consideration of local disease within the nose does not fall 
within the scope of this book, but is suggested by local pain, difficulty 
in breathing through the nose, frequent “colds,” and asthma. 
(For the examination of the ears, see below, p. 482.) 
VII. The Lips 
1. Pallor of the mucous membrane of the lips suggests, though it 
never proves, anasmia. No diagnosis of anaemia should be made 
without at least testing the haemoglobin (Tallqvist’s scale). One 
minute suffices. 
2. Cyanosis, a purplish or slatey-blue color of the lips, occurs in 
some healthy persons from simple “weathering.” When well marked, 
however, it should always suggest:—(a) Heart disease (especially 
mitral or congenital lesions).—(b) Lung diseases (especially emphy- 
sema and pneumonia). (c) Polycythaemia.—(d) Poisoning by ace- 
tanilid or other coal-tar antipyretics, producing methasmoglobinaemia.1 
The last is easily tested by noting the brownish (not red) tint of the 
blood when soaked into filter paper, as in performing Tallqvist’s 
haemoglobin test; the test should be confirmed by the history. Disease 
of the heart or lung is identified by physical examination of the chest. 
3. Parted lips, an open mouth, may be a mere habit or may be due 
to nasal obstruction (adenoids). Idiots and cretins are very apt to 
keep their mouths open, whether there is enlargement of the tongue 
or not. Dyspnoea may compel a patient to keep his mouth open so 
as to get more air. 
In cold weather a crack or fissure may appear, usually in the centre 
of the lower lip, and in poorly nourished individuals may persist for 
weeks. At the corners of the mouth fissures or cracks may be due to 
chapping or “cold-sores” (herpes), but if they persist for weeks in 
young children they are very suggestive of syphilis. White linear 
scars radiating from the corners of the mouth are presumptive evidence 
of healed syphilitic lesions, oftenest congenital. 
4. The mucous patches of syphilis—white, sharply bounded areas 
about the size of the little-finger nail—are often seen at the junction 
of the skin with the labial mucous membrane, especially at the corners 
of the mouth. 
1 Cyanosis of intestinal origin occurs in connection with certain diseases involv- 
ing excessive intestinal decomposition. (See Gibson, Quarterly Journal of Medi- 
cine, Oct., 1907, p. 29.) THE HEAD AND FACE 
21 
5. Herpes (“cold sores”) is due to a lesion of the Gasserian ganglion 
with resulting “trophic” disturbances of the regions supplied by the 
trigeminal nerve. Appearing first as a cluster of vesicles (“water 
Fig. 18.—Epithelioma of the Lip. 
Fig. 19.—Chancre of the Lip. 
blisters”) which break and leave a small sore near the mouth, herpes 
is to be distinguished by: (a) its distribution near the terminations of 
some branch or branches of the trigeminal nerve (“herpes frontalis, 
nasalis. labialis”); (b) by its lasting but a few days; and (c) by the 
absence of similar lesions else- 
where. It may be connected with 
a “cold” (which is often a disease 
of the trigeminus), with pneu- 
monia, malaria or meningitis, but 
it frequently occurs without any 
discoverable cause. Herpetic 
stomatitis (“canker sores”) may 
accompany it. 
6. Epithelioma1 of the lip and 
chancre should be suspected when- 
ever a long-standing sore is dis- 
covered there. Epithelioma occurs 
almost always on the lower lip in 
a man past middle life (see Fig. 
18). It lasts longer than chancre, 
is slower in producing glandular 
enlargement at the angle of the 
jaw, and is not associated with other syphilitic lesions. 
Fig. 20.—-Angioneurotic CEdema of 
Lower Lip. 
1 It does harm to call this lesion “ cancer ” because this term is so firmly associ- 
ated in the lay mind with metastasis, recurrence, and death that unnecessary 
suffering may result when the patient or his family learns that he has “cancer.” 22 
PHYSICAL DIAGNOSIS 
7. Chancre of the lip is commoner in women and may occur at any 
age, especially under forty. The sore usually lasts but a few weeks, 
excites early enlargement of the glands, and is usually associated with 
other manifestations of syphilis (see Fig. 19). 
8. Angioneurotic oedema appears as a sudden, painless, apparently 
causeless swelling of the whole lip (see Fig. 20), which may attain 
double its normal size. The diagnosis depends on the exclusion of all 
known causes (trauma, infection, insect bites) and on the history of 
similar swellings (on the lip or elsewhere) in the past. 
9. The enlargement of the lips in myxoedema and cretinism has been 
mentioned above (page 19). 
10. Hare-lip is a vertical slit (congenital deficiency) in the upper 
lip opposite to the nostril; it is often connected with an antero-posterior 
cleft through the hard palate (“cleft palate”). The lesion may be 
double, leaving a small island of tissue continuous with the nasal 
septum (intermaxillary bone). Diagnosis is made at a glance. 
VIII. The Teeth 
The first set of teeth is fairly constant in its order and date of 
appearance. In Fig. 21 the number of the month when each tooth 
is most apt to appear is marked on the tooth. The second set (per- 
Fig. 2i.—-Diagram Showing the 
Month at which Each Tooth (of 
the First Set) Should Appear. 
Fig. 22.—Notched Incisors in Congenital 
Syphilis. 
manent teeth) arrives (less regularly) between the sixth and the 
fifteenth year, except the “wisdom teeth,’’ which appear about the 
twenty-first year. 
i. Rickets or cretinism often delays dentition considerably. THE HEAD AND FACE 
23 
2. Congenital syphilis may be associated with various deformities 
of the central incisors (permanent). The most constant deformity 
is that shown in Figs. 22 and 22a. 
3. Teeth-grinding.—Nervous, delicate, 
oversensitive children often grind their 
teeth in their sleep. There is no founda- 
tion for the popular superstition that 
this act indicates “worms.” 
Fig. 22a.—Hutchinsonian Teeth. 
IX. The Breath 
Foul breath is oftenest due to local causes such as: 
(a) Foul teeth and gums (neglect, Riggs’ Disease). 
(b) Stomatitis of any variety. 
(c) Follicular Tonsillitis with cheesy deposits in the crypts. 
(d) Nasal Disease. 
Rarer causes are abscess or gangrene of the lung, in which the breath 
may be intensely foul; the source of the odor is made evident by the 
sputa. 
Acetone breath has a faintly sweetish odor, which has been com- 
pared to that of chloroform, new-mown hay, and rotting apples. It 
occurs not only in diabetes, but in various conditions involving 
starvation (vomiting, fevers), and especially, but not only, a lack of 
carbohydrates.1 
In urcemia a foul odor is often noticed, and an ammoniacal(“ urin- 
ous”) smell has been mentioned by many writers. In typhoid and in 
syphilis some persons seem to detect a characteristic odor, but the 
evidence is insufficient. Alcoholic breath is often of value in correcting 
the false statements of its possessor. In comatose persons we must 
remember that a drink may have been taken just before an attack of 
apoplexy or any other cause for coma, so that an alcoholic breath in 
comatose patients does not prove that the coma is due to alcohol. 
In poisoning by illuminating gas the gaseous odor of the breath 
may be noticed. 
X. The Tongue 
The act of protruding the tongue may give us valuable information 
on the condition of the nervous system. 
1 See Taylor: “Studies on an Ash-free Diet.” University of California 
Publication, July 30th, 1904. 24 
PHYSICAL DIAGNOSIS 
(а) The hesitating, tremulous tongue of typhoidal states is very 
characteristic. Simple tremor is seen in alcoholism, dementia par- 
alytica, and weakness. A tongue protruded very far means usually a 
neurasthenic individual who is in the habit of examining it in a looking 
glass. 
(б) If the tongue is protruded to one side, it usually means facial 
paralysis as part of a hemiplegia; rarely it is due to lesions of the 
hypoglossal nerve or its nucleus 
(in bulbar paralysis or tabes). 
(c) A coated tongue (due 
mostly to lack of saliva) is 
not often of much value in 
diagnosis, and there is no need 
to distinguish the varieties and 
colors of coats; but a few 
suggestions may be obtained 
from it. Many persons who 
seem otherwise perfectly 
healthy have coated tongues 
in the early morning. This 
is especially true in mouth-breathers, in smokers, and in those who 
keep late hours. 
In those whose tongues are usually clean the appearance of a coat 
is associated often with arrested digestion, constipation, or fevers. 
A clean tongue in a dyspeptic suggests peptic ulcer. This point 
I have found of more value than any inference from a coated tongue. 
A dry, brown-coated, perhaps cracked tongue goes with uraemia, 
exhausted states and wasting diseases with or without fever. 
(d) Cyanosis and jaundice may be seen in the tongue but better 
elsewhere. 
(e) Indentation of the edges of the tongue by the teeth occurs 
especially in foul, neglected mouths, but has no diagnostic value. 
(/) Herpes (“canker”) often occurs on the tongue; it begins as a 
group of vesicles, but these rupture so soon that we usually see first a 
very small, grayish ulcer with a red areola. It heals in a day or two, 
i.e., more quickly than the syphilitic mucous patch or any other lesion 
with which it is likely to be confounded. 
(g) Cancer, tuberculosis, and syphilis may attack the tongue and 
form deep, long-standing ulcerations. Syphilis can usually be diag- 
nosed by the history, the presence of other syphilitic lesions, the 
Wassermann reaction, and the therapeutic test (see Fig. 23). Cancer 
Fig. 23.—Syphilis of the Tongue. THE HEAD AND FACE 
25 
and tuberculosis should be diagnosed by microscopic examination, 
though cancer is more commonly found in men (especially smokers) 
past middle life and on the side of the tongue. A local reaction after 
the injection of tuberculin may be of decisive importance. 
(h) “ Simple ulcers ” are due to irritation from a tooth or to trauma, 
and heal readily if their cause is removed. 
(i) Deep fissures of the tongue are sometimes due to syphilis, which 
is recognized in other lesions, by history, or by the Wassermann test. 
(j) Leukoplakia buccalis (lingual corns) refers to whitish, smooth, 
hard patches of thickened epithelium, usually on the dorsum of the 
tongue is smokers, running a chronic course without pain or ulceration, 
but important because epithelioma has been known (and not rarely) 
to develop in them. 
(k) Geographic tongue is a desquamation of the lingual epithelium 
in sinuous or circinate areas, which spread and fuse at their edges, 
while the central portions heal, giving a look something like the moun- 
tain ranges in a geographical map. It usually gives no trouble unless 
the patient’s attention becomes concentrated on it. 
il) Hypertrophy of the tongue has already been mentioned in 
connection with myxoedema and cretinism. It may occur indepen- 
dently as a congenital affection. 
XI. The Gums 
(a) A lead line should be looked for in every patient as a matter 
of routine, as it may not be suggested by anything in the patient’s 
symptoms or history, yet may be the key to the whole case. 
The deposit of lead sulphide in (not on) the gums is not blue, but 
gray or black; and is not a line, but a series of dots and lines arranged 
near the free margin of the gums. Where there are no teeth there is no 
lead line. In faint or doubtful cases a hand lens is of great assistance 
and shows up the dotted arrangement of the deposit very clearly (see 
Fig. 24). It is unfortunate that the term “blue line’’ has become 
attached to these gray-black dots. 
(b) A bismuth line—as in poisoning from the injection of bismuth 
paste—may present all the appearances of a lead line, though in some 
cases the staining is more diffuse and occurs at some distance from a 
tooth as well as at the free margin of the gum. The analyses of the 
feces and the history of the case serve to distinguish it from a lead line. 
(c) Sordes, a collection of epithelium, bacteria, and food particles, 
accumulates about the roots of the teeth with great rapidity in febrile 
cases, but has no considerable diagnostic importance. 26 
PHYSICAL DIAGNOSIS 
(d) Spongy and bleeding gums occur as part of the disease '‘scurvy, ” 
after overdoses of mercury or potassic iodide, in various debilitated 
states, and sometimes without known cause. The teeth are loosened 
and the flow of saliva is usually profuse. The stench from such cases 
is often intolerable. 
(e) Suppuration about the roots of the teeth (pyorrhoea alveolaris) 
is common in elderly people and in neglected mouths, and seems in 
Fig. 24.—Lead-dots in the Gums. (Use hand lens in looking at this picture and 
examine the gums not the teeth.) 
some cases to have some constitutional effects; but in most cases its 
effects appear to be wholly local. 
(/) Gumboil (alveolar abscess), is easily recognized by the familiar 
signs of abscess associated with a diseased tooth. Dental abscesses 
are an important cause of obscure fevers and joint pains. 
(g) “Epulis” is a word applied to various soft tumors springing 
from the jaw bone or occasionally from the gums themselves. Many 
of them are sarcomatous, but microscopic examination is necessary to 
distinguish these from fibroma, granuloma, and angioma. 
XII. The Buccal Cavity 
i. Eruptions 
(а) Koplik's spots in measles are of much importance. They 
appear chiefly in the inside of the cheeks, opposite the line of closure of 
the molars, and consist of minute, bluish-white spots, each surrounded 
by a red areola and sometimes fusing into larger red areas. 
(б) The syphilitic mucous patch (see above) should be looked for 
in suspicious cases, not only in easily accessible parts of the mouth, THE HEAD AND FACE 
27 
but round the roots of the gums, where the cheeks or lips have to be 
pushed away to afford a good view. 
2. Pigmentations 
In Addison’s disease brown spots or patches often occur on any 
part of the mucous membrane of the mouth. They may also occur in 
negroes without any disease and after ulcerations (e.g., from a tooth), 
so that they are not distinctive of Addison’s disease. 
3. Gangrene 
Gangrene (stomatitis gangrenosa, “noma”), a rare disease of 
weakly children, starts as a hard red spot inside the cheek and usually 
not far from the corner of the mouth (see Fig. 25). There is a swelling 
Fig. 25.—Gangrenous Stomatitis (“noma”). 
of the whole cheek, especially under the eye. The odor of gangrene is 
usually the first thing to make clear the diagnosis. Then the gangrene 
appears externally as a black patch on the cheek, surrounded by a red 
halo. 28 
PHYSICAL DIAGNOSIS 
XIII. The Tonsils and Pharynx 
Method of Examination.—Place the patient facing a good light, 
natural or artificial. An electric flash light is especially convenient. 
Ask him to open his mouth without protruding the tongue. Ask him 
to say “Ah.” Then gently press down and forward on the dorsum 
of the tongue (not too far back) with a spoon or tongue depressor,1 
until a good view of the throat is obtained. 
Look especially for: 
1. Inflammations (redness, eruptions, spots, or membranes). 
2. Ulcerations. 
3. Swellings. 
4. Reflexes. 
i. Inflammations 
(a) General redness means a mild or early pharyngitis, but may 
precede severe diseases like diphtheria and scarlet fever. 
(b) Yellowish-white spots on the tonsils, more or less confluent, 
mean follicular tonsillitis in the vast majority of cases, but only by 
culture can we exclude diphtheria with certainty. Fever and head- 
ache are usually present. 
(c) A membrane, continuous and grayish-white over one or both 
tonsils, especially if it extends to soft palate and uvula, means diph- 
theria in almost every case.2 Rarely a similar membrane is seen in 
streptococcus throats with or without scarlet fever. Cultures alone 
can decide. 
(d) The eruptions of smallpox and chickenpox may be distributed 
in the pharynx as well as over the rest of the respiratory tract. They 
are recognized by association with more characteristic skin lesions and 
constitutional signs. 
2. Ulcerations 
(a) Deep chronic, painless or but slightly painful ulcerations of 
the tonsils or soft palate are oftenest due to syphilis. Improvement 
1 If the patient is especially nervous, it is sometimes well to let him press down 
his tongue with his own forefinger. 
2 Thrush, a rather rare disease of ill-nourished infants, due to a fungus of the 
yeast order, may produce on the pharynx, tongue, or in any part of the mouth, 
patches of white membrane. As the disease is almost wholly local and without 
constitutional manifestations, it is passed over briefly here. 
Streaks of mucus or bits of milk coagulum are sometimes mistaken for a mem- 
brane. THE HEAD AND FACE 
29 
under treatment and the manifestations of syphilis elsewhere make the 
diagnosis possible. 
(b) Tuberculosis may produce similar deep ulcerations, easily 
recognized by their association with tuberculosis of the lung or larynx. 
Occasionally smaller “miliary” tubercles, not unlike “canker sores,” 
are seen in the tonsillar region. Tuberculous lesions are usually very 
painful and tender, syphilitic lesions almost free from tenderness. The 
chronic course of pharyngeal tuberculosis and the presence of other 
tuberculous lesions identify it. 
(c) Malignant disease (oftenest sarcoma) may attack the tonsil, 
and forms a painful, tender and finally ulcerating tumor. No other 
lesion of the tonsil grows so fast and invades surrounding parts so 
extensively except abscess; in abscess the pain, fever, and constitu- 
tional manifestations are far greater. 
3. Swellings 
(a) Chronic swollen or protruding tonsil (unilateral or bilateral) 
without fever or constitutional symptoms may represent hypertrophy 
following acute tonsillitis or may be part of the general adenoid hyper- 
trophy common in children’s throats. Tonsils may be small or buried 
and yet full of pus. Their size is of no particular importance in 
judging of the harm done by them. 
(h) Acute swollen tonsil is usually part of follicular tonsillitis (see 
above), but may occur without spots, and often accompanies scarlet 
fever. Swelling, pain in swallowing, and fever are the essentials of 
diagnosis. Our chief care should be to exclude: 
(c) Peritonsillar abscess (quinsy sore throat). Here the swelling is 
usually unilateral and greater than in follicular tonsillitis. The pain, 
which is often severe, is continuous and not merely on swallowing. 
Fever, constitutional symptoms, and swelling of the glands at the 
angle of the jaw are all more marked than in follicular tonsillitis. The 
pain, which is often severe, is continuous and not merely on swallow- 
ing. Fever, constitutional symptoms, and swelling of the glands at 
the angle of the jaw are all more marked than in follicular tonsillitis. 
The voice is nasal or suppressed, and there is often salivation. The 
pillars of the fauces and the soft palate take part in the swelling and 
the throat may be almost blocked by it. The suffering increases until 
the abscess breaks or is opened. Fluctuation is often late and 
indefinite, but should always be sought for. 
(d) Retropharyngeal Abscess.—A swelling in the back of the 
pharynx near the vertebra occurs not infrequently during the first 30 
PHYvSICAL DIAGNOSIS 
year of life. A peculiar cry or cough, like the bark of a puppy or the 
call of a heron, is very often associated (the French “cri de canard”). 
The parents are often unaware that the throat is the seat of the trouble, 
and only digital examination proves the presence of bulging and 
fluctuation, usually on one side of the posterior pharyngeal wall. 
A similar abscess of chronic course may complicate tuberculous 
cervical caries (see below, page 31). 
(e) Swollen uvula, with transparent oedema of its tip, often com- 
plicates a pharyngitis or any lesion with violent cough. Elongation 
of the uvula may bring it into contact with the tongue and by tickling 
excite cough. 
(f) Perforation of the soft palate or its adhesion to the back of the 
pharynx means syphilis almost invariably, and, as it may be the only 
sign of an old infection, it is a valuable piece of evidence. 
4. Reflexes 
(а) Lively or exaggerated pharyngeal reflexes, such that the patient 
gags and coughs as soon as one touches the dorsum of the tongue, 
are seen in many normal persons and in many alcoholics. It is this 
condition, combined with a smoker’s pharyngitis, that leads to many 
cases of morning vomiting in alcoholics. 
(б) Diminished or absent reflexes (with paralysis of the palate) occur 
in postdiphtheritic neuritis and bulbar paralysis. Fluids are regurgi- 
tated through the nose and the voice has a peculiar intonation. 
To test for paralysis, ask the patient to say “Ah.” In unilateral 
paralysis one side of the palate remains motionless; in bilateral paraly- 
sis the whole palate is still. 
(c) Diminished or absent gag-reflex is often seen (without palatal 
paralysis) in “nervous” people and neurasthenic states, associated 
with corneal anaesthesia and lively knee jerks. 
XIV. The Neck 
Long, thin necks are often seen in phthisical individuals, and short 
necks in the barrel-chested, but nothing more than a bare hint can be 
derived from such facts. The lesions oftenest searched for in the 
neck are: i. Enlarged'glands (cervical adenitis). 2. Abscesses and 
scars. 3. Thyroid tumors. 4. Pulsations (see below page 89). 
5. Torticollis and other lesions simulating it. 6. Tuberculosis of the 
cervical vertebras. 7. Evidence of meningitis. THE NECK 
31 
Rarer lesions will be mentioned below. 
i. Chains of Enlarged Glands 
radiate in all directions from the angle of the jaw—upward, in front 
of the ear and behind it, forward along the ramus of the jaw, and 
downward to the clavicle. The areas drained by the different groups 
overlap so much that it is not necessary to distinguish them. 
The commonest causes of enlargement are: 
(a) Tonsillitis and other inflammations within or around the mouth 
(diphtheria, the exanthemata, “cankers,” carious teeth, etc.). Glandu- 
Fig. 26.—Tuberculous Glands. 
lar swellings due to these causes are usually acute and more or less 
tender; most of them disappear in a fortnight or less, but some persist 
(without pain) indefinitely. 
(.b) Tuberculosis; long-standing cervical adenitis in children and 
young adults, with a tendency to involve the skin and to suppurate, 
is usually tuberculous. Certain diagnosis needs microscopic exami- 
nation, animal inoculation, the tuberculin test and the Wassermann. 32 
PHYSICAL DIAGNOSIS 
{c) Syphilis; small, non-suppurating glands, occurring in the neck 
and about the occiput in adults, often accompany syphilis, but the 
diagnosis depends on the presence of unmistakable syphilitic lesions 
elsewhere. Occasionally syphilitic glands are large and soft. 
(d) Hodgkin's disease; chronic, large, rarely suppurating glands in 
the neck, axillas, and groins, with slight splenic enlargement and nor- 
mal blood, suggest Hodgkin’s disease, but microscopic examination is 
Fig. 27.—Hodgkin’s Disease, Six Months Duration. 
necessary to exclude tuberculosis. A superficial gland can be excised 
under cocaine, with very little pain. 
(e) Lymphoid Leukaemia. No distinguishing characteristics can 
be found in the glands, but any nodular enlargement in the neck 
should lead us to examine a film specimen of blood; the leuksemic 
blood changes can be easily and quickly recognized. 
(/) Malignant disease (near by or at a distance) may enlarge the 
cervical glands. Cancer of the lip or tongue, sarcoma of the tonsil, 
and, among distant lesions, cancer of the stomach or pleura have 
caused enlargement of these glands in cases under my observation. THE NECK 
33 
(g) If the parotid gland alone is swollen and there are fever and 
pain on chewing, the case is probably one of mumps, especially if 
there are other cases in the vicinity. Malignant disease and ordinary 
sepsis may also attack the parotid. 
(h) German measles may be 
accompanied by swelling of the 
posterior cervical or occipital 
glands without the involvement 
of any other. 
Figs. 28 and 29.—Cervical Abscess in Pott’s Disease. (Bradford and Lovett.) 
2. Abscess or Scars 
Abscess or scars in the sides and front of the neck generally result 
from glandular tuberculosis; hence the presence of scars may be of 
value in the diagnosis of doubtful cases with a suspicion of tubercu- 
losis in later life. Aside from glandular abscesses (tuberculous or 
septic) it is rare to find any suppuration in the neck, except in the nape, 
where deep, septic abscess (carbuncle) and superficial boils are 
common. High Pott’s disease complicated by abscess (see 
Figs. 28 and 29) 34 
PHYSICAL DIAGNOSIS 
occur chiefly in two diseases; 
(a) Simple goitre (unilateral or bilateral). 
(b) Goitre with exophthalmos, tachycardia, and tremor, sweating 
and loss of weight (Thyrotoxicosis or Graves’ disease). 
The tumor may look the same in these two diseases (see Fig. 30); 
it varies in outline and consistency according to the amount of gland 
tissue and fibrous or cystic 
degeneration that is present. 
Owing to its connection with the 
larynx it moves up and down 
somewhat when the patient 
swallows, but is not attached to 
any other structures in the 
neck. The enlargement is often 
unilateral or largely so. If very 
vascular, the tumor may vary 
greatly in size from moment to 
moment or at certain times 
(i.e., menstruation, pregnancy). 
Since the normal thyroid 
can rarely be felt, atrophy of the 
gland (as in myxoedema) is 
unrecognizable. 
Cancer or sarcoma also occur in the thyroid and may be difficult 
to distinguish from goitre. Malignant tumors are usually painful, 
grow fast, are accompanied by emaciation and anasmia, are often 
harder and more nodulated than benign goitres, and invade the neigh- 
boring tissues and lymphatics. Histological examination should 
decide in doubtful cases. 
4. Torticollis (Wry-neck) and Other Lesions Resembling It 
(а) Spasm (tonic, rarely clonic) of the sterno-mastoid and trapezius 
may be due to irritation of the spinal accessory nerve by swollen glands, 
abscess, scar, or tumor, but more often occurs without known cause 
(“rheumatic” and nervous” cases). The muscle is rigid and tender. 
(б) Congenital torticollis (a counterpart of club-foot) is due to 
shortness of the muscle without spasm. It is almost always right-sided 
and associated with facial asymmetry. 
(c) Dislocation of the upper cervical vertebroe causes a distortion of 
the neck much like that of torticollis (see Fig. 31). The diagnosis 
3. Thyroid Tumors 
Fig. 30.—Simple Goitre. 35 
THE NECK 
depends on the history of injury, the absence of true muscular spasm 
and the x-ray picture. 
(,d) Compensatory cervical deviations: (i) When there is marked 
lateral curvature of the spine, with or without Pott 's disease, the head 
may be inclined so far to the opposite side that torticollis is simulated, 
(see below, page 72). (2) When the power of the two eyes is mark- 
edly different, as in some 
varieties of astigmatism, the 
head may be habitually 
canted to one side to assist 
vision. (3) In some cases due 
to none of the above causes, 
habit or occupation (heavy 
loads on one shoulder) seem 
to produce the condition. 
(e) Forced attitude from 
cerebellar disease may re- 
semble torticollis. The diag- 
nosis depends on the other 
evidences of intracranial dis- 
ease. 
5. Cervical Pott's Disease 
(Vertebral Tuberculosis) 
has the characteristics alluded to below in the section on joint tuber- 
culosis, viz., stiffness due to muscular spasm, malposition of the bones 
and of the head, and abscess formation (see page 33). 
Diagnosis depends on wry-neck with stiffness of the muscles of the 
back and neck and pain in the occiput—a very characteristic symptom- 
group. The chin is often supported by the hand. “Rheumatic” 
or traumatic torticollis, however, may present all these symptoms, 
and diagnosis may be impossible without the aid of time and ther- 
apeutic tests. 
Fig. 31.—Dislocation of the Cervical Vertebrae. 
(Walton.) 
6. Branchial Cysts and Fistulas 
These, due to persistence of parts of the foetal branchial clefts,- are 
not very uncommon (see-Fig. 32). 
A branchial cyst is a globular or ovoid fluctuating sac, hanging or 
projecting from the side of the neck or the region of the hyoid bone, 36 
PHYSICAL DIAGNOSIS 
painless and slow of growth. It may transmit the motions of the 
carotids and be mistaken for aneurism, but has no expansile pulsation 
and occurs in youth, when 
aneurism is practically un- 
known. Some such cysts 
may be emptied by external 
pressure.1 
Branchial cysts may con- 
tain serous, mucous, or sero- 
sanguineous fluid, or hair and 
sebaceous material, according 
as their lining wall is derived 
from ectoderm or entoderm. 
Diagnosis depends on the 
position and consistency of 
the growth and on the results of aspiration. 
Branchial fistula (congenital) may open externally in the neck, and 
occasionally are complete from neck to pharynx. They may become 
occluded and suppuration result. 
Fig. 32.—Branchial Cyst. 
7. Actinomycosis 
Actinomycosis, though it 
usually arises in the lower jaw 
bone, may appear externally in 
the neck. A denser infiltration 
with bluish-colored, semifluctuat- 
ing areas in it, but without any 
distinct lumps or sharp outlines, 
is strongly suggestive of acti- 
nomycosis, and should always 
lead to a microscopic examina- 
tion of excised portions or of the 
discharge. 
Fistulas may form, but are less 
common than in tuberculosis. 
springing from the seventh cer- 
vical vertebra and ending free or 
8. A Cervical Rib 
Fig. 33.—Mediastinal Neoplasm with Cervica 
Metastases and Obstructed Vena Cava. 
1 A patient of mine can produce a gush of foul fluid in the mouth by pressure 
over a small cyst in the neck. THE NECK 
37 
attached to the first thoracic rib, appears in the neck as an angular 
fulness which pulsates, owing to the presence of the subclavian artery 
on top of it. It rarely produces any symptoms and is generally 
Fig. 33a.—Anthrax Infection of the Neck. 
encountered when percussing the apex of the lung. The bone can,- be 
felt behind the artery by careful palpation and demonstrated by 
radiography. Pain or wasting in the arm, and occasionally throm- 
bosis or gangrene may occur and may be cured by removing the rib. 
9. Inflammatory or Dropsical Swelling of Neck 
Venous thrombosis, aneurism, mediastinal tumors and inflammatory 
exudates (see Fig. 33a) may produce oedema in the neck. CHAPTER III 
THE ARMS AND HANDS; THE RACK 
THE ARMS 
Most of the lesions of these parts are joint lesions and are dealt 
with in the section on joints. Others fall under the province of the 
neurologist or the dermatologist, but must be briefly mentioned here. 
I. Paralysis of One Arm 
Paralysis of most or all the muscles of one arm occurs oftenest in: 
(a) Hemiplegia—with paralysis of the leg and often of the face on 
the same side. (6) Pressure neuritis—traumatic or from new growths. 
(c) Obstetrical paralysis—neuritis from injury during parturition. 
(d) Lead or alcoholic neuritis—extensors of wrist especially, and often 
in both arms, (e) Anterior poliomyelitis—infantile paralysis. (/) 
Hysteria and traumatic neuroses.1 (g) Subdeltoid bursitis is a common 
result of falls in which one strikes upon the shoulder, and of other 
injuries to the upper arm, though it may come on without any known 
cause. A soreness and stiffness of the shoulder is soon followed by 
inability to use the deltoid or to lift the arm from the side. Atrophy 
supervenes with astonishing rapidity and recovery may be a matter of 
many weeks. Disuse is undoubtedly a factor in this. 
Pressure Neuritis.—The history of the case is of the greatest im- 
portance. During surgical anaesthesia the brachial plexus or the mus- 
culo-spiral nerve may be compressed, and paralysis is noted as soon 
as the patient comes out of anaesthesia. In a similar way in deep sleep, 
especially drunken sleep with the arm banging over a bench or doubled 
under the body, the nerves may be injured. Pressure from a crutch 
or from the head of the humerus in fractures or dislocations, or even 
a violent fall on the shoulder without injury of bones, may result in 
a paralyzed arm (with or without subdeltoid bursitis). 
Diagnosis rests on the history, and on the fact that not only the 
muscles of the shoulder group and the extensors of the wrist are 
1 Less common are paralyses due to lesions of the arm centre in the cerebral 
cortex (tumor, softening, cyst abscess, hemorrhage, thromboses, or embolism). 
38 THE ARMS 
39 
affected, but also the supinator longus, while in the toxic paralyses, 
especially lead, the supinator longus is spared. 
Obstetrical Neuritis.—In instrumental deliveries or when forcible 
traction on the child’s arm has been necessary, a paralysis of the 
arm often results, with or without fractures, and, what is important, 
is often not noticed till some years later, and then thought to have 
Fig. 34.-—Wrist Drop, following Lead Neuritis. 
just arisen; thus it may be mistaken for anterior poliomyelitis or other 
lesions. 
Toxic Neuritis.—Lead or alcohol produces usually a weakness of 
both forearms, especially the extensors of the wrist (“wrist-drop”), 
but one side may be predominantly affected and other muscles are 
involved in most severe cases. The history, the other signs of lead 
poisoning, and the soundness of the supinator longus distinguish it 
from other paralyses. (See Fig. 34.) 
All these forms of neuritis are apt to be accompanied either by 
pain, by anaesthesia, or by paraesthesia, which helps to distinguish them 
from the cerebral and spinal paralyses next described. 
Acute Anterior Poliomyelitis.—Paralysis attacks a child suddenly 
and without apparent cause, usually after “a feverish turn.” Either 
the upper arm group (deltoid, biceps, brachialis anticus, and supinator 40 
PHYSICAL DIAGNOSIS 
longus) or the lower arm group (flexors and extensors of wrist and 
fingers) may be affected. The arm is flabby and painless, the muscles 
waste rapidly, and the electrical reactions show degeneration, often 
within a week. 
Hysterical and Traumatic Neuroses.—The history and mode of 
onset, the frequent association of sensory symptoms which do not 
fit the distribution of any peripheral nerve, spinal segment, or cortical 
area, the normal reflexes and electrical reactions distinguish most 
cases of this type, but diagnosis is sometimes impossible. 
Paralysis of both arms is much less common than paralysis of one 
arm, and occurs chiefly in poisoning by lead and in multiple neuritis. 
Rarely it is seen in the late stages of chronic diseases of the spinal cord. 
II. Wasting of One Arm 
(а) Rapid atrophy occurs in all the types of neuritis mentioned, 
also in subdeltoid bursitis, poliomyelitis and progressive muscular 
atrophy. In the latter it occurs without complete paralysis, though the 
wasted muscles are weak. Progressive muscular atrophy usually 
begins in the muscles at the base of the thumb and between it and the 
index finger. Less often the disease begins in the deltoid. In either 
case the rest of the arm muscles are later involved. 
In the atrophies just mentioned a lack of trophic or nourishing 
functions which should flow down the nerve is usually assumed to 
explain the wasting (“ trophic atrophy ’ ’). From this we distinguish the 
atrophy due simply to disuse of the muscles without nerve lesions. 
(б) Slow atrophy of disuse occurs in the arm in hemiplegia, infantile 
or adult, and in other cerebral lesions involving the arm centre or the 
fibres leading down from it. 
(c) Cervical rib occasionally leads to wasting as well as pain in the 
corresponding arm. 
(d) The atrophy often seen in hysterical cases is probably due to 
disuse and is similar to that occurring in an arm that has been splinted 
after fracture or dislocation. 
III. Contractures of the Arm 
After cerebral lesions involving the arm centre, and in almost any 
spinal or peripheral nerve lesion which involves one set of muscles and 
spares another, the sound muscles contract (or overact) and permanent 
deformities result. In hysteria similar contractures occur. Contrac- THE ARMS• 
41 
tures have in themselves little or no diagnostic value, but indicate a 
late and stubborn stage of whatever lesion is present. 
IV. CEdema of the Arm1 
Causes.—1. Clot of axillary or brachial vein, usually from heart 
disease or from: 2. Pressure of scar tissue or of tumors—aneurism, 
cancer of axillary glands, lung or mediastinum, Hodgkin’s disease. 
3. Nephritis, when the patient has lain long on one side. 4. Inflam- 
mation, usually with evidence of lymphangitis spreading up the arm 
from a septic wound on the hand. 5. Deep axillary abscess—an 
insidious painful septic focus, not depending on tuberculosis or on any 
form of adenitis, may burrow so deeply in the axilla that oedema of 
the arm (as well as pain) is produced. Leucocytosis and slight fever 
accompany it. The diagnosis is easily made from the above data 
provided we are aware of the existence of this uncommon but distinct 
clinical entity. 
The diagnosis of the cause of oedema is usually easy in the light of 
the facts brought out by the general physical examination (heart, 
urine, local lesions, etc.). 
The arteries of the arm (brachial and radial) are to be investigated 
for changes in the vessels (see page 90) and for the evidence given by 
their pulsations as to the work of the heart (see page 102). 
V. Tumors of the Upper Arm 
In the upper arm we have: i. Fatty tumors. 2. Sarcoma of the 
humerus. 3. Ruptured biceps. 4. Syphilitic nodes on the humerus. 
5. Tuberculosis of the humerus. 6. Gouty deposits in the triceps 
tendon. 
Fatty tumors are recognized by the history of long duration and 
very slow growth, by their superficial position, usually external to the 
muscles, and soft, lobulated feel. 
Sarcoma forms the only large tumors springing from the humerus. 
It is usually hard and obviously deep seated (see Fig. 35). 
Ruptured biceps. The lower half of the biceps projects sharply 
when the muscle is contracted, looking as if the biceps had slid down 
from its normal site. This appearance suddenly following a wrench 
or strain of the biceps is diagnostic. 
1 Distinguished, like all oedema, by the fact that a dent made by pressing with 
the finger does not at once disappear when the pressure is removed. 42 
PHYSICAL DIAGNOSIS 
Syphilitic nodes are flattened elevations on the bone, usually about 
the size of a half-dollar, and feel like the callus after a fracture, but 
project only from one side of the bone. There is pain, especially 
at night, and moderate tenderness. A history or other and more 
characteristic lesion of syphilis, a radiogram or a Wassermann reaction 
may be necessary for diagnosis. 
Tuberculous lesions1 are much more common on the forearm bones, 
but are occasionally seen on the humerus near the epiphyseal ends. 
Fig. 35.—Sarcoma of Humerus. 
They usually involve and perforate the skin, leaving an indolent, sup- 
purating sinus leading to necrosed bone. The evidence of tuberculosis 
in other organs and the slow, “cold” progress of the lesion assist the 
diagnosis. In doubtful cases the local reaction after the subcutaneous 
injection of tuberculin may be of distinct value. Pain, tenderness, 
1 Coccidioidal Granuloma, a rare disease clinically identical with tuberculosis, but 
due to a wholly different organism, an animal parasite resembling a coccidium, has 
been described by Rixford, Gilchrist, Montgomery, and others. THE ARMS 
43 
oedema, redness and heat may then appear or may be increased if 
already present. 
Gouty tophi are sometimes seen along the fasciae covering the triceps 
tendon. They are hard and painless. The diagnosis depends upon 
the peculiar situation of the lesions and their association with other 
evidences of gout.1 
VI. Miscellaneous Lesions of the Forearm 
Bowing of the forearm bones occurs in rickets and in Paget’s disease 
(see Fig. 242, p. 45c). The lesions in the other parts of the body 
make the diagnosis clear. 
Fig. 36.—Rachitic Epiphysitis. 
Fig. 37.—Sarcoma of Ulna. 
Local lesions of the bones of the forearm are chiefly tuberculous 
and syphilitic, both of which have been sufficiently described in the 
last section. 
In the wrist bones we find: 
i. Rachitic enlargement of the epiphyses. In rickets the terminal 
epiphyses at the wrists take part in the general epiphyseal enlargement 
1 Bursitis over the olecranon (“miner’s elbow”) produces a tender fluctuating 
swelling over the tip of the elbow. 44 
PHYSICAL DIAGNOSIS 
so common in the disease. The diagnosis is easy, for there is no other 
disease of infancy producing general enlargement of the epiphyses 
(see Fig. 36). 
2. Hypertrophic pulmonary osteoarthropathy (Figs. 38, 39, and 40). 
An enlargement of the lower ends of the radius and ulna, with clubbing 
of the fingers (see below, page 54), is recognized by the x-ray picture 
and by its association with pulmonary or pleural diseases of many 
years’ duration (bronchiectasis, phthisis, empyema). 
Fig. 38.—Hypertrophic Pulmonary Osteo-arthropathy. (Thayer.) 
3. Acromegalia (see page 8) affects chiefly the bones and soft tissues 
of the hand. The x-ray picture is characteristic. 
4. Hypertrophic, atrophic, or tuberculous disease of the wrist-joint 
will be described below (see Examinations of the joints, page 481). 
5. “Weeping sinew” or “ganglion” (tenosynovitis) forms a fluc- 
tuating, spindle-shaped swelling along one of the tendons of the 
wrist, slow and almost painless in its course. It may be tuberculous, 
in which case the sac is generally divided into several parts (“com- 
pound ganglion”); tubercle bacilli may occasionally be demonstrated 
in the exudate. 
6. Neoplasms (see Fig. 37). THE HANDS 
45 
THE HANDS 
I. Evidence of Occupation 
The horny, stiffened hands of the “son of toil,” the stains of paint 
in house painters, the flattened, calloused finger-tips of the violinist 
the worn fingers of the sewing 
woman, afford us items of infor- 
mation which are sometimes useful 
and worth a rapid glance in routine 
examination. 
II. Temperature and Moisture 
(a) The cold, moist hand is 
most commonly felt in ‘ ‘ nervous ’ ’ 
people under forty. It is almost 
never seen in heart disease, which 
its possessor often fears, and does 
not mean “poor circulation,” but 
vasomotor disturbances of neurotic 
origin. 
(h) Cold, dry extremities—hands, 
feet, nose, ears—may mean simply 
fatigue, exposure to low tempera- 
ture, or insufficient exercise; but in 
the course of chronic disease they 
usually mean weakness of the 
heart, and hence are serious. 
(c) Warm, moist hands are felt 
in thyrotoxicosis, and if the warmth 
and moisture are present most of 
the time this disease is strongly 
suggested, and a search for tremor, 
rapid heart, goitre, and bulging 
eyes should be made. 
(d) The hot, dry hand ordinarily means fever, as temperature 
record will demonstrate. 
Fig. 39.—Radiographs of the Hand 
and Arm of a Case of Hypertrophic 
Pulmonary Osteoarthropathy (the left 
figure) compared with the hand and arm 
of a normal individual of the same height 
(the right figure). Note especially the 
thickening of the radius and ulna. 
(Thayer.) 
ill. Movements of the Hands 
(a) The manner of shaking hands gives us vague but useful impres- 
sions of the patient’s temperament. The nervous, cramped, half- 46 
PHYSICAL DIAGNOSIS 
opened hand, which never really grasps and gets away as soon as possi- 
ble; the firm, hearty grasp; the limp, “wilted” hand—furnish hints of 
character that every physician must take account of. 
In fevers or toxsemic states (typhoid, alcoholism) there are two 
sets of movements which recur so often that names have been given 
them, viz.: 1. Carphologia—picking and fumbling at the bed clothes. 
2. Subsultus tendinum—involuntary twitching and jerking of the ten- 
Fig. 40.—Radiograph of the Wrists in Hypertrophic Pulmonary Osteo-arthropathy 
• (v. Ziemssen’s Atlas.) 
dons in the wrist and on the back of the hand, usually associated with 
tremor and carphologia. 
{b) Tremor of the Hands— To test for ordinary tremor, we ask the 
patient to extend and separate his fingers widely. The motions are 
then apparent. 
Causes: i. Nervousness, cold, or old age. 2. Fever and toxaemia. 
3. Alcohol (less often lead, tobacco, morphine, or other drugs). 
4. Graves’ disease. 5. Paralysis agitans. 6. Multiple sclerosis. 7. 
Hysteria. 
Most of these tremors need no comment. The intention tremor 
of multiple sclerosis (sometimes seen also in hysteria) is often exag THE HANDS 
47 
gerated into coarse shaking movements when the patient tries to pick 
up a pin, drink a glass of water, or do any other act calling for the 
volitional coordination of the small hand muscles. In the presence of 
such a tremor we should look for nystagmus (see above, page 17), a 
spastic gait (see page 497), and a slow, staccato speech. This group 
of symptoms suggests multiple (or insular) sclerosis. 
| Fig. 41.—Athetosis. Successive positions of the hands. (Curschtnann.) 
In direct contrast with this is the pill-rolling tremor of paralysis 
agitans, which usually ceases during voluntary movements. The thumb 
and forefinger are near or touch one another, and move as if they were 
rolling a bread-pill. This tremor is usually associated with an immov- 
able, expressionless face, a stiffened neck and back, and a peculiar 
attitude and gait (see below, page 498). 48 
PHYSICAL DIAGNOSIS 
The other varieties of tremor can usually be recognized by the 
history and associated symptoms. 
(c) Spasms or coarse twitchings of the hand due to: 
i. Jacksonian epilepsy—convulsive attacks which begin in and 
may remain confined to one set of muscles, often preceded by prick- 
ling or other paraesthesia of the part affected, but without loss of con- 
sciousness. These muscle spasms 
are due usually to an irritation of 
the corresponding motor 'area in 
the cortex cerebri (tumor, soften- 
ing, chronic meningitis, etc.), but 
may also occur in ■*'uraemia and 
diementia paralytica. Coma and 
general spasms may follow. 
2. Professional Spasm.— 
Writers, violin-players, and others 
who use one set of muscles con- 
Fig. 42.—Tetany. (Masland.) 
Fig. 43.—Tetany. 
tinually are often attacked with painful cramps in the muscles used 
(“writer’s cramp”). Weakness and usually far more pro- 
minent than spasm. 
3. Chorea and Choreiform Movements.—True, acute, infectious 
chorea (Sydenham’s) occurs chiefly in children between five and 
fifteen, generally in those who have joint troubles or heart disease, and 
ends in eight or ten weeks. The hands are usually affected first, and 
their movements are like those of restlessness and are quasi-purposive, 
i.e., movements that might have been made intentionally, though they THE HANDS 
49 
Fig. 44.—Tetany. 
Fig. 45.—Tetany. 50 
PHYSICAL DIAGNOSIS 
are not. At first sight one would surely think the child was simply 
fidgety. 
Similar movements occur in pregnant women or sometimes after 
parturition, but the type is much severer and is apt to be associated 
with maniacal symptoms. 
Fig. 46.—Tetany. 
Fig. 47.—Atrophic Arthritis with “Flipper Hand.” 
Habit spasms or tics are much commoner in the face, throat and 
shoulders but also reach the hands occasionally. They constitute an 
independent chronic neurosis and may or may not be associated with THE HANDS 
51 
mental or emotional disturbances. Winking and nodding movements 
are commonest. They have no relation to infectious chorea, to the 
joints or the heart. 
Post-hemiplegic chorea refers to similar movements in the paralyzed 
hands of hemiplegic cases (children or adults). True infectious chorea 
may also affect only one-half the body (hemichorea). 
Fig. 48.—Spade Hand in Myxcedema. 
In hysteria or by a short of psychic contagion similar movements are 
sometimes taken up in schools and institutions, and last till their cause 
is understood and removed. 
Chronic choreiform movements occur also in the rarer congenital 
forms of paralysis with or without idiocy. 52 
PHYSICAL DIAGNOSIS 
4. Athetosis (see Fig. 41) means slow twisting and bending move- 
ments of the fingers, quite involuntary and always secondary to 
organic cerebral lesions (hemiplegia, infantile cerebral paralysis). 
5. Tetany (see Figs. 42, 43, 44, 45 and 46)—a peculiar spasm of 
the hands (often of the feet as well), occurring in the course of diseases 
involving obstruction of the pylorus, in children, in nursing women, 
after gastric lavage, and after thyroidectomy,1 usually lasting minutes 
1 When the parathyroid glands are accidentally removed, 
or hours—rarely days. The gastric or obstructive type of tetany 
(with or without uremia) seems to depend on the modifications of the 
gastric acidity and so of the haemic alkalinity. 
IV. Deformities of the Hands 
1. “ Claw hand ’ ’ results from paralysis of the interossei and lumbri- 
cales with contractures, and occurs when the median or ulnar nerves 
are paralyzed, and in progressive muscular atrophy, syringomyelia, and 
chronic poliomyelitis. 
2. “Flipper hand" (see Fig. 47), a common result of the contrac- 
tures in late cases of atrophic arthritis. Other deformities of the 
fingers are common in this disease and in gout. 
3. “ Hemiplegic hand, ’ ’ a result of the contractures following hemi- 
plegia from any cause. 
4. Myxcedema results in thickening and coarsening of the tissues 
of the hand (“spade hand”) without bony enlargement; but the spade 
hand is a fairly common type without myxoedema, and one needs to see 
it rapidly develop in connection with other myxoedematous lesions 
before it can have diagnostic significance. (The same is true of the 
myxoedematous face.) (See Fig. 48.) 
5. Acromegalia produces general enlargement of the bones and 
other tissues of the hands and feet. 
6. Pulmonary Osteo-athropathy.—Any long-standing disease of 
the heart, lungs, or pleura, and any abdominal tumor (liver, spleen) 
which elevates the diaphragm and reduces lung capacity, may be 
followed by this peculiar hypertrophic change in all the tissues of the 
extremities. Mild forms produce “ clubbed fingers," a bulbous enlarge- 
ment of the finger-tips with double curvation of the nails, lateral and 
antero-posterior1 (see Fig. 51). In severer forms the bones of the 
hand and wrist are also considerably enlarged (see Figs. 38 and 40). 
1 Clubbed fingers are occasionally seen in a variety of other diseases: e.g., 
hepatic abscess, nephritis, congenital syphilis; and even in apparently healthy 
persons. THE HANDS 
53 
Fig. 49.—a, Acromegalic Hand, b, Normal Hand. 
Fig. 50.—Atrophic Arthritis. 54 
PHYSICAL DIAGNOSIS 
Fig. 51.—Clubbed Fingers. 
Fig. 52.—Clubbed Fingers. THE HANDS 
55 
7. Heberden ’s nodes, later described under the head of hypertrophic 
arthritis, are here pictured (Fig. 54). The distinction from gout will 
later be referred to (page 482). 
8. Atrophic arthritis (Fig. 47) (further described on page 488) 
presents its most typical lesions in the hands and wrists. The con- 
Fig. 53.—Raynaud’s Disease. 
Fig. 54.—Heberden’s Nodes. 
striction line opposite the articulation is observed in late cases, but 
ordinarily multiple spindle-joints symmetrically arranged are all that 
we see. The boggy feel, the trophic disturbances, and the chronic 
course are usually diagnostic; but .v-ray examination is necessary to 
establish the diagnosis which is important because of the unfavorable 
prognosis which it involves. 56 
PHYSICAL DIAGNOSIS 
9. Syphilitic and tuberculous dactylitis (see Fig. 55), seen as a rule 
in young children, are not distinguished from each other by the physi- 
cal signs. Diagnosis rests upon the history, the course, the x-ray, the 
Wassermann reaction, the results of giving tuberculin or Salvarsan, 
and the evidence of syphilitic or tuberculous lesions elsewhere. In 
either disease we have a chronic, almost painless, boggy, red enlarge- 
ment of one phalanx, or more, due to an indolent inflammation which 
starts from the bone or periosteum and usually burrows to the surface, 
to produce a chronic discharging sinus or ulcer. 
Fig. 55.—Tuberculous Dactylitis. 
10. Raynaud's disease attacks the fingers more often than any 
other part. Osier distinguishes three grades of intensity: A Local 
syncope (“dead fingers”) following exposures to slight cold or emo- 
tional strain. The fingers become white and cold. The condition 
usually passes off in an hour or two. From similar causes we may 
have: B. Local asphyxia (“chilblains”), producing congestion and 
swelling with or without pain and stiffness and with heat or coldness 
of the part. C. Local or symmetrical gangrene. If local asphyxia 
persists, gangrene results. (See also under Erythromelalgia, p. 459.) 
11. Morvan's Disease.—As a part of syringomyelia multiple 
arthropathies (atrophic arthritis) and painless felons may develop in 
the hands (see Fig. 56). The appearances may strongly suggest: THE NAILS AND FINGER TIPS 
57 
12. Leprosy, in which there is likewise anesthetic necrosis of 
phalanges; but the two diseases can usually be distinguished by a 
study of the lesions and symptoms in other parts of the body. 
13. Dupuytren’s contraction of the palmar fascia is commonest in 
adult men, and gradually produces a permanent, painless flexion of 
Fig. 56.—Morvan’s Disease. 
the little finger in one or both hands. A tense band is felt in the palm. 
The ring finger may also be affected; less often the others. If burn and 
felon are excluded, the diagnosis is obvious. 
THE NAILS AND FINGER TIPS 
i. The nutrition of the nails suffers in chronic skin diseases, in 
myxoedema, in many nerve lesions (neuritis, hemiplegia, syringomyelia, 
etc.), dementia paralytica; also in atrophic arthritis. 58 
PHYSICAL DIAGNOSIS 
2. A transverse ridge and groove on the nails often form when their 
growth is resumed after an acute illness. The movement of this ridge 
from the matrix to the free edge is said to take about six months 
(see Fig. 57). 
3. Hang-nails possess a certain 
medical interest, because in some 
individuals they become sore when 
the general condition is below par, 
and constitute a rough index of the 
degree of resistance to infection. 
Thejr may become infected and 
lead on to suppuration (paronychia). 
4. Indolent sores around the 
nail should rouse the suspicion of 
tuberculosis or syphilis, especially 
in a child. 
5. (a) Cyanosis, the slatey or 
purplish-blue color of venous con- 
gestion, can be well seen in the 
nails, (h) Anaemia, if well marked, 
blanches the tint of the tissues seen through the nail, but the diagnosis 
should invariably be confirmed by a haemoglobin estimate. 
6. Incurvation of the nails has already been referred to as a part of 
the condition known as “clubbed fingers’’ (page 54). 
7. Capillary pulse (see below, page 91). 
8. Tender finger ends not infrequently occur in septic endocarditis 
and may help in the diagnosis of that disease. Minute ecchymoses are 
occasionally present as well. Both phenomena are, I suppose, 
embolic. 
Fig. 57.—Grooved Nails after Acute 
Illness. 
THE BACK 
The evidences of spinal tuberculosis, spinal curvature, and of the 
spinal form of infectious and of hypertrophic arthritis will be described 
later (page 480 et eeq.). 
I. Stiff Back 
“Stiff back’’ may be due not only to the joint troubles just men- 
tioned, but also and more commonly to lumbago, a painful affection 
of the lumbar muscles without known pathologic basis. Clinically it 
is characterized by pain when the muscles are used, as in bending THE BACK 
59 
forward to tie one’s shoes and in recovering the upright position. 
There is no bony soreness, no involvement of the sacro-iliac joints, and 
sideways bending is usually freer than in hypertrophic arthritis. The 
pain of lumbago does not radiate around the chest or down the legs, 
and is not especially aggravated by coughing or sneezing, but it some- 
times extends down low into the fascia of the lumbar muscles over the 
sacrum. The age of the patient (usually over thirty) distinguishes 
most cases of lumbago from spinal tuberculosis. “Stiff neck” often 
accompanies or precedes it and some relation to meteoric conditions 
can often be traced. The disease is self limited and should end in a 
few days or at most a few weeks. Cases of longer duration are prob- 
ably due to infectious or hypertrophic spinal arthritis or to tuberculosis. 
Metastatic cancer of the vertebrae often follows cancer of the breast, 
producing a stiff, painful spine. The x-r&y picture is usually 
characteristic. 
II. Sacro-iliac Disease 
Tuberculosis of this joint has long been known and calls attention 
to its presence by pain, psoas spasm, and a limp. If the wings of the 
ilium are forcibly pressed together, the pain in the joint is much 
increased. Abscess formation is often the first distinctive sign. The 
motions at the hip-joint are not restricted and the local signs of verte- 
bral caries are absent. The duration of the disease, the local reaction 
after tuberculin injection and the formation of abscess distinguish it 
from other lesions of the sacro-iliac joint. 
Goldthwait1 has shown that the sacro-iliac joint is subject 
to most of the diseases of other joints, and that some (e.g., hyper- 
trophic arthritis) are not at all uncommon there. Many of the pains in 
the back complained of by women during menstruation or in pelvic 
disorders are referred precisely to the sacro-iliac articulation and are 
probably due to lesions of that joint. Many cases diagnosed as 
“lumbago” are probably due to one or another sacro-iliac lesion, 
strain, sprain or subluxation. The diagnostic points are—on the 
positive side: (a) Pain or tenderness directly over the joint. Such 
pain may be elicited by raising the leg while the knee is kept stiff. It is 
also referred in many cases to the course of the sciatic nerve so that 
many, perhaps most, cases of so-called sciatica are due in fact to sacro- 
iliac disease. It is often worse at night. (b) Abnormal mobility of 
the sacro-iliac joint, (c) A tendency to lean the trunk away from 
1 Goldthwait: Boston Medical and Surgical Journal, March 9th, 1905. 60 
PHYSICAL DIAGNOSIS 
the affected side when standing. (d) Limitation of lateral bending 
of the spine to one side or the other when the patient stands with 
the knees .stiff. 
On the negative side the absence of limitation in the motions 
at the hip-joint, the negative x-ray, the free forward bending (when 
the patient sits during the test), the absence of fever, leucocytosis and 
abscess formation are important. 
A strong nervous element is present in many cases. 
III. Spinal Curvatures 
Diagnosis is not difficult, provided we are led to examine the back 
at all. 
(a) Kyphosis or backward convexity of the spine, if sharply angular 
usually means Pott’s disease (tuberculosis). If the curve is gentle and 
gradual it may be due to “ round shoulders,” to hypertrophic arthritis, 
to barrel chest, Paget’s disease, or rickets. The rachitic curve is 
flaccid, is due simply to muscular weakness, and is associated with 
other evidences of rickets. In barrel chest and Paget’s disease the 
kyphosis goes with the other signs of those diseases. In hypertrophic 
arthritis the curve is rigid, irreducible, and usually painless. “Round 
shoulders” can be straightened by muscular exertion, and represent 
a habit of posture. 
(b) Lordosis, an exaggeration of the normal forward convexity of 
the lumbar spine, is seen in tuberculosis of the hip or spine, in paralysis 
of the dorsal or abdominal muscles (especially muscular dystrophy), 
and in abdominal tumors (pregnancy), which need to be counter- 
balanced by backward bending. 
(c) Scoliosis is a combination of lateral curvature with twisting of 
the spine. In slight or doubtful cases the tips of the spinous processes 
should be marked with a colored pencil, which makes the deviation 
easily visible. Severe cases cannot be mistaken. 
IV. Tumors of the Back 
(a) Aneurism of the descending aorta may point in the back near 
the angle of the left scapula (see below, page 263). It is the only 
pulsating tumor of this region. 
(b) Perinephritic abscess usually points between the crest of the 
ilium and the twelfth rib, a few inches from the spine (see page 410). THE BACK 
61 
(c) Tuberculous abscess (“cold abscess”), originating in vertebral 
tuberculosis, may point in the same region, though more often it fol- 
lows down the sheath of the psoas and points near Poupart’s ligament. 
“ Cold abscess,” starting from a necrosed rib, is often seen in the back. 
The probe leads to dead bone at the end of the sinus. Microscopic 
examination of excised pieces is the only way of excluding actinomycosis, 
though this disease is less apt to form sinuses. 
(d) Sarcoma of the scapula, the only tumor of the scapula that is 
often seen, occurs in children and rarely after the second decade. 
With a solid, nearly painless tumor of this bone in a child, sarcoma 
should always be suspected. Benign exostoses are possible, but usually 
occur later in life. Histological examination will decide. 
(e) Epithelioma, arising from the skin of the back, presents the 
ordinary evidences of this form of cancer. 
(/) The multiple subcutaneous abscesses due to glanders (“farcy 
buds”) are more common on the extremities, but may be found on the 
trunk as well. Flattened, oval fluctuating nodes with slight tender- 
ness are suggestive. Bacteriological examination of the purulent 
contents settles the diagnosis. 
V. Prominent Scapula 
This is due usually to: 
(a) Lateral curvature of the spine (see above). 
(b) Serratus paralysis, recognized by the startling prominence of 
the scapula if the patient pushes forward with both hands against 
resistance (“angel-wing” scapula). 
VI. Scaphoid Scapula 
In congenital syphilis and some non-syphilitic conditions the median 
or vertebral border of the scapula is sometimes markedly concave. 
VII. Spina Bifida 
A congenital, saccular tumor, connecting through a bony defect 
with the interior of the spinal canal at any point between the occiput 
and the sacrum; nine-tenths of all cases occur in the lowest third of the 62 
PHYSICAL DIAGNOSIS 
spinal column. There is no other congenital tumor in this position 
communicating with the spinal canal. 
Fig. 58.—Spina Bifida with Meningocele. 
In the sacral region there are other congenital sinuses, tumors, 
dermoid cysts, lipomata, and others. Their nature can be learned 
only by incision. It is important to settle their relation to spina bifida 
by the presence or lack of communication with the spinal canal. CHAPTER IV 
THE CHEST 
TECHNIQUE AND GENERAL DIAGNOSIS 
INTRODUCTION 
I. Methods of Examining the Thoracic Organs 
To carry out a thorough examination of the chest we do five 
things: i. We look at it; technically called “inspection.” 2. We 
feel of it; technically called “palpation.” 3. We listen to the sounds 
produced by striking it; technically called “percussion.” 4. We 
listen to the sounds produced within it by physiological or pathological 
processes; technically called “auscultation.” 5. 
We study pictures thrown on the fluoroscopic 
screen or on a photographic plate by the 
Roentgen rays as they traverse the chest; 
technically called “radioscopy.” 
Measuring the dimensions or movements ol 
the chest (“mensuration”) and the spirometric 
measurement of “vital capacity” are often men- 
tioned as co-ordinate with the above methods, but 
yield very little information of practical value. 
Without some knowledge of the regional 
anatomy of the chest no intelligent investigation 
of the condition of the thoracic organs can be 
carried on. Accordingly, I shall begin by re- 
calling very briefly some of the most essential 
anatomical relations. 
II. Regional Anatomy of the Chest 
It seems to me a mistake to divide the chest 
into arbitrary portions and to describe physical 
signs with reference to such division. The 
seat of any lesion can best be described by giving its relation to 
the clavicle, sternum, or ribs on the front and sides of the chest, and to 
Fig. 59.—The Mid- 
axillary Line. 
63 64 
PHYSICAL DIAGNOSIS 
the scapulas and ribs behind. Thus we may speak of rales as heard 
“above the left clavicle in front,” “below the right scapula behind,” 
“between the seventh and ninth ribs in the axilla,” and so on. When 
we want to state more exactly what part of the axilla anteroposteriorly 
is affected we may refer to the ‘ ‘ mid-axillary line ’ ’ (see Fig. 5 9); or better, 
we may place the lesion by measuring the number of centimetres or 
inches from the median line of the sternum. In a similar way the place 
of the apex impulse of the heart (whether in the normal situation or 
farther toward the axilla) can be determined by measuring from the 
Upper lobe of left 
lung. 
Right lung. 
Right auricle. 
Left ventrical, 
Lower lobe of left 
lung. 
Liver. 
Stomach 
Fig. 6o.-—Position of the Heart, Lungs, Liver and Stomach. The dotted lines corre- 
spond to the outlines of the lung; the heavy continuous line represents the heart; while 
the position of the liver and of the lower border of the stomach is indicated by light 
continuous lines. The ribs are numbered. 
median line of the sternum. Measurements referring to the nipple 
are useless in women with relaxed or hypertrophied breasts. But as 
a general rule they convey more useful and reliable information than 
measurements from mid-sternum. 
If, then, we confine ourselves chiefly to the bones of the chest as 
landmarks, and fix, with reference to them, the position of any portion 
of the internal organs which we desire to study, it becomes unnecessary 
to memorize any technical terms or to learn the position of any arbi- 
trary lines and divisions such as are frequently forced upon the student. 
The only points which it is necessary to memorize once for all are: 
1. The position of the heart, lungs, liver, and spleen with reference 
to the bones of the chest. 
2. The position of certain points which experience has taught us 
have a certain value in physical diagnosis. I mean (a) the so-called INTRODUCTION 
65 
“valve areas” of the heart, which do not correspond to the actual 
position of the valves, for reasons to be explained later on, and (b) 
the percussion outlines of the heart, liver, and spleen. These outlines 
do not correspond in size with the actual dimensions of the organs 
within, yet there is a definite relation between the two which remains 
relatively constant, so that we can infer the size of the organ itself from 
the outlines which we determine by percussion. The position of the 
Upper lobe. 
Upper 
lobe. 
Middle 
lobe. 
Lower lobe. 
Spleen. 
Lower lobe, 
Liver- 
Fig. 61.—Position of the Left Lung from 
the Side, and of the Spleen. 
Fig. 62.—Position of the Right Lung from 
the Side, and .of the Liver. 
organs themselves is shown in Figs. 60, 61, and 62. It will be noticed 
in Fig. 58 that the lungs extend up above the clavicles and overlap the 
liver and the heart—facts of considerable importance in the physical 
examination of these organs, as will be later seen. It is also to be 
noticed how small a portion of the stomach is directly accessible to 
physical examination, the larger part of it lying behind the ribs and 
covered by the liver. The normal pancreas and kidneys are practically 
inaccessible to physical examination. 66 
PHYSICAL DIAGNOSIS 
The percussion outlines—corresponding to those portions of the 
heart, liver, and spleen which lie immediately beneath the chest walls— 
will be illustrated in the section on Percussion (see page 125). 
INSPECTION 
Much may be learned by a careful inspection of all parts of the 
chest, but only in case the clothes are wholly removed. A good light 
is essential, bat this does not always mean a direct light; for example, 
when examining the front of the chest it is often better to have the 
patient stand with his side to the window so that the light strikes 
obliquely across the chest, accenting every depression and making 
every pulsation a moving shadow. In searching for abnormal pulsa- 
tions, this oblique light is especially important. 
In examining the thorax we look for the following points: 
1. The size. 
2. The general shape and nutrition. 
3. Local deformities or tumors. 
4. The respiratory movements of the chest walls. 
5. The respiratory movements of the diaphragm. 
6. The normal cardiac movements. 
7. Abnormal pulsations (arterial, venous or capillary). 
8. The peripheral vessels. 
9. The color and conditions of the skin and mucous membranes. 
10. The presence or absence of glandular enlargement. 
I. Size 
Small chests are seen in patients who have been long in bed from 
whatever cause; also in those who have suffered in infancy from 
rickets, adenoid growths in the naso-pharynx, or a combination of the 
two diseases. Abnormally large chests (“barrel chest”) are seen chiefly 
in elderly people with stiff cartilages. Of course the chests of healthy 
individuals vary a great deal in size at any given age, and I refer 
only to variations greater than those normally found. 
II. Shape 
There are marked differences in shape between the child’s and the 
adult’s chest in health. A child’s trunk, as compared with that of 
an adult, is far more nearly cylindrical; that is, the anteroposterior INSPECTION 
67 
diameter is nearly as great as the lateral. The adult’s chest is at first 
flattened from before backward. Later it returns more nearly to the 
childish shape as cartilages stiffen (“barrel chest’’). 
In childhood the commonest pathological modifications are due 
to adenoids or to rickets; in middle and later life to calcified cartilages, 
to phthisis, or old pleuritic disease. 
1. The Rachitic Chest 
The sternum generally projects (“pigeon breast"), but in some 
cases, especially when rickets is combined with adenoid hypertrophy, 
there may be a depression at the 
root of the sternum resulting in the 
condition known as ‘ ‘ funnel breast ’ ’1 
(Fig. 63). The sides of the chest 
are compressed laterally and slope 
in to meet the sternum as the sides 
of a ship slope down to meet the 
keel (pectus carinatum) (Figs. 65 
and 66). From the origin of the 
ensiform cartilage a depression or 
groove is to be seen running down- 
ward and outward to the axilla and 
corresponding nearly to the attach- 
ment of the diaphragm. This is 
sometimes spoken of as11 Harrison ’s 
groove.’’ The lower margin of the 
ribs in front often flares out, owing 
to the enlargement of the liver 
and spleen below and the pull of 
the diaphragm above. Along the 
line of the chondro-costal articula- 
tion there is to be felt, and some- 
times seen, a line of eminences or 
swellings, to which the name of “rachitic rosary’’ has been given. 
Fig. 63.—Funnel Breast. 
2. The “Paralytic Thorax” 
Fig. 67 conveys a better idea of this form of chest than any descrip- 
tion. The normal anteroposterior flattening is exaggerated so that 
such persons are spoken of as “flat-chested." The clavicles are very 
1 In some cases this condition appears to be congenital. 68 
PHYSICAL DIAGNOSIS 
prominent, owing to falling in of the tissues above and below them; 
the shoulders are stooping, the scapulae prominent, and the neck is 
generally long. The angle where the ribs meet at the ensiform carti- 
lage, the so-called “costal angle,” is in such cases very sharp. This 
type of chest has often been supposed to be characteristic of phthisis, 
but may be found in persons with perfectly healthy lungs. On the 
T Fig. 64.—Acquired Depression at the Root of the Ensiform Cartilage. The patient 
is a shoemaker of seventy, who has all his life pressed against his breast bone the shoe on 
which he worked. 
other hand, phthisis frequently exists in persons with normally shaped 
chests or with abnormally deep chests (Woods Hutchinson). (See 
Fig. 178, page 299.) 
3. The “ Barrel Chest " 
Nothing is less like a barrel than the “barrel chest." It represents 
an extreme degree of the physiological enlargement of the thorax seen 
so often after middle life, especially in males. Its most striking 
characteristic is its greatly increased anteroposterior diameter, 
so that it approaches the form of the infant’s chest. The costal angle 
is very obtuse, the shoulders are high, and the neck is short. The INSPECTION 
69 
respiratory movements of the barrel chest will be spoken of later (see 
Figs. 68 and 69). 
(a) Nutrition of the Chest Walls 
Emaciation is readily appreciated by inspection. The ribs are 
unusually prominent, the scapulae stand out, and the clavicles project. 
Fig. 65.—Pigeon Breast. 
All this may be seen independently of any change in the shape of the 
chest such as was described above under the title of Paralytic Thorax. 
Tuberculosis of the apices of the lungs may produce a marked falling 
in of the tissues above and below the clavicle independent of any 
emaciation of the chest itself. 
III. Deformities 
The abnormalities just enumerated are symmetrical and affect the 
whole thorax. Under the head of Deformities, I shall consider chiefly 
such abnormalities as affect particular portions of the chest and not 
the thorax as a whole. 
1. Spinal Curvatures and Twists1 
Slight degrees of deformity are best seen by marking with a skin- 
pencil the position of the spinous processes (see Fig. 71). The more 
marked cases of lateral curvature, which are usually accompanied by a 
certain amount of twisting, give rise to considerable displacement of 
1 See also page 60. The lesions are referred to here only in relation to their 
effects on heart and lungs. 70 
PHYSICAL DIAGNOSIS 
the thoracic organs and render unreliable the usual bony landmarks, 
with reference to which we judge of the position of the intrathoracic 
organs. By such deformities the apex of the heart may be pushed 
up into the fourth space or out into the axilla, or portions of the lungs 
may be compressed and made atelectatic. The bulging on the convex 
Fig. 66.—Pigeon Breast. 
side of the curve may simulate an aneurismal tumor. Pott’s disease 
of the spine should be looked for as a part of the routine inspection of 
the chest. It is sometimes better felt than seen. 
2. Flattening of One Side of the Chest 
In chronic phthisis, cirrhosis of the lung, or long-standing pleurisy 
(serous, fibrous or purulent), marked falling in of one side of the chest 
is often to be seen (see Figs. 67 and 73). The shrinkage of the affected 
side is made more obvious by contrast with the compensatory hyper- 
trophy of the sound lung, which makes the sound side unusually 
full and prominent. INSPECTION 
71 
3. Prominence of One Side of the Chest 
In pneumothorax or pleural effusions, and sometimes m malignant 
disease of the lung or pleura, there is 
a marked increase in the size of the 
affected side of the chest. In pneu- 
mothorax or pleuritic effusion we 
usually see, in addition to the above 
enlargement of the affected side, a 
smoothing out of the intercostal de- 
pressions so that the surface of that 
side is much more uniform than the 
Fig. 67.—The Paralytic Thorax. 
Fig. 68.—Barrel Chest in a Case of 
Bronchial Asthma (set. 13). 
other side. Bulging of the interspaces from great pressure within 
the chest rarely occurs. I have never seen it. 
4. Local Prominences 
In nearly one-quarter of all healthy chests that part of the thoracic 
wall which overlies the heart (the so-called “precordial region’’) is 
abnormally prominent. The cause of this condition is much disputed. 
A similar prominence may be brought about in children (whose thoracic 
bones are very flexible) and occasionally in older patients, by the out- 72 
PHYSICAL DIAGNOSIS 
ward pressure of an enlarged heart or of an effusion in the pericardial 
sac. The prominences due to spinal curvature have been already 
mentioned. Less common causes of local prominence are: 
1. Aneurism of the arch of the aorta. 
2. Tumor of the chest wall (lipoma, sarcoma, gumma), of the 
lung, mediastinum, or of the thoracic glands pressing their way 
outward. 
3. “Cold abscess’’ (tuberculosis, actinomycosis) of a rib or of the 
sternum. 
4. Empyema perforating the chest wall, the so-called “empyema 
necessitatis. ” 
IV. The Respiratory Movements 
1. Normal Respiration 
During normal respiration, one sees the ribs move outward and 
upward with inspiration, and downward and inward with expiration. 
Possibly one catches some hint of 
the movements of the diaphragm at 
the epigastrium. In men, diaphrag- 
matic breathing is more marked, while 
in women breathing is mostly of the 
“costal type;” that is, is done by the 
intercostal muscles. In certain dis- 
eases an exaggeration of the costal or 
of the diaphragmatic type of breath- 
ing may be seen. When costal 
cartilages become ossified, the ribs 
move little, and most of the work of 
respiration is performed by the dia- 
phragm, whose pull upon the lower 
ribs can sometimes be distinctly seen 
during inspiration. On the other 
hand, when the diaphragm is pushed 
high and held there by the presence of fluid or a solid tumor, as in 
cirrhosis of the liver or leukaemia, the breathing has largely to be per- 
formed by the ribs, and becomes, as we say, costal in type (see below, 
p. 80). 
Fig. 69.—Barrel Chest. 
2. Anomalies of Expansion 
If we watch the patient while he takes a full breath, we may notice 
certain variations from the normal type of respiratory movements. INSPECTION 
73 
We may see: (i) Diminished expansion of one side (as a whole, or at 
the apex). (2) Increased expansion of the other side. 
(1) If diminished expansion of one side is due to pleuritic effusion, 
pneumothorax, or solid tumor of the lung or pleura, the affected side 
is usually distended as well as 
immobile. When, on the other 
hand, the lung is retracted or 
bound down by adhesions, as 
in phthisis, old pleurisy, oc- 
clusion of the bronchus, or 
from the pressure of an aneu- 
rism, we have immobility 
combined with a retraction of 
the affected side. In tubercu- 
lous disease at the apex of the 
lungs we may see one side or 
both sides fail to expand at 
the top. Restriction of the 
motion of one side of the chest 
may also be due to pain or to 
pressure from below the dia- 
phragm. An enlarged liver or 
spleen and tumors of the 
hepatic or splenic region may 
in this way prevent the normal 
expansion of one or the other 
side of the thorax. Occasion- 
ally a hemiplegia or a unilat- 
eral paralysis of the diaphragm results in diminished movement of one 
side of the chest. 
(2) Increased expansion of one side of the chest is observed prin- 
cipally as a compensatory or vicarious overfunctioning of that side when 
the other side of the chest is thrown out of use by a large pleuritic 
effusion, by pneumothorax, long-standijig pleurisy with contraction, 
or other causes. 
Fig. 70.—Lateral Curvature. Scoliosis. 
3. Dyspnoea 
This term is often used rather loosely to include: (i) Difficult 
breathing, whether rapid or slow. (2) Unusually deep breathing 
whether difficult or not. (3) Rapid breathing. 74 
PHYSICAL DIAGNOSIS 
True dyspnoea or difficult breathing is almost always rapid as well, 
and does not differ at all from the well-known phenomenon of being 
“out of breath” after a hard run or any violent exertion. Conceive 
these conditions as persisting over hours or days, and we have the 
phenomenon known as dyspnoea. The breathing is not only quick 
but labored; that is, performed with difficulty, and unusual muscles, 
not ordinarily called upon for respiration, come into play and are 
seen working above the clavicle and elsewhere. More or less distress 
is generally expressed in the face, and there is often a blueness of the 
lips or a dusky color throughout the face. The commonest causes 
of dyspnoea are the various forms of heart disease, pneumonia, large 
pleuritic effusion, asthma, and phthisis. The researches of Barcoft 
and Thomas Lewis1 make it probable that there are two types of 
dyspnoea—Mechanical and Chemical. 
(a) Mechanical dyspnoea is associated with a decrease of O2 and 
an increase of C02 in the blood, hence with a proportionate cyanosis. 
It is seldom marked in bed-ridden patients and does not increase at 
night unless the patient slips down from his sitting position. It is 
increased by pressing on the abdomen so as to drive blood to the 
heart. It is seldom if ever periodic. 
(b) In chemical dyspnoea there is no excess of CO2 in the blood and 
no considerable cyanosis. It is commonly seen in bed-ridden patients, 
is worse at night even when there is no orthopnoea and so no slipping 
down. It is not increased by abdominal pressure. Finally it is associ- 
ated with the presence or increase of an unknown nonvolatile acid in 
the blood, in other words with acidosis. Thereby it is made compar- 
able with the dyspnceic acidosis after long hard exercise (lactic acid 
from the contracting muscles) and with the acidosis of diabetic air 
hunger (ffioxybutyric acid). An acidosis has also been demonstrated 
in the hyperpnoea of normal persons at high altitudes, in diabetes, 
uraemia, lobar pneumonia, thyrotoxicosis, tuberculous pneumothorax 
and eclampsia. 
This type of dyspnoea is often called “uraemic” but the term is 
too vague to be of value at present. 
(c) The mechanical and chemical causes of dyspnoea often act 
simultaneously. 
Dyspnoea may affect especially inspiration, as, for example, when 
a foreign body lodges in the larynx, or in ordinary “croup. ” In such 
cases we speak of “ inspiratory dyspnoea, ” distinguishing it from l‘expira- 
1 Thos. Lewis: Lectures on the Heart (P. B. Hoeber, New York, 1915). INSPECTION 
75 
tory dyspnoea ” such as occurs in asthma and in barrel-chested persons. 
In the latter condition the breath seems to enter the chest readily, but 
the difficulty is to get it out again. Expiration is greatly prolonged 
and often wheezey. 
Combined types in which both respiratory acts are difficult are 
more common. 
Sucking-in of the interspaces in the lower axillary regions or below 
the clavicles may be seen in connection with dyspnoea whenever the 
lungs are prevented by some cause from properly expanding during 
inspiration. This may occur in obstruction at the glottis.1 
Simple rapidity of breathing should be distinguished from dys- 
pnoea. In adults the normal rate of respiration is about 18 per 
minute. In children, it is considerably quicker and more irregular. 
It is not desirable to attempt here to enumerate all the causes which 
may lead to a quickening of the respiration. Among the commoner 
are muscular exertion, emotion, hysteria, diseases of the heart and 
lungs, and fluid or solid accumulations below the diaphragm, which 
push up that muscle and cause it to encroach abnormally upon the 
thoracic cavity. Most of the infectious fevers are also apt to be 
accompanied by quickened breathing, especially but not exclusively 
when the fever is associated with a disease of the heart, lungs, pleura, 
or pericardium. Further chemical study of the blood will help us 
doubtless more accurately to divide and classify the varieties of 
breathlessness. The purely mechanical types are probably seen but 
rarely in bed-patients. In this, as in many other fields of medicine, 
the mechanical wanes and the chemical steadily waxes in etiological 
significance. 
V. Relation of Dyspncea to Cyanosis 
These two phenomena go parallel in degree and coincide in ap- 
pearance and disappearance so long as we are dealing with the me- 
chanical type of obstruction to respiration (as in the rheumatic 
type of heart disease or in obstruction of the upper air passages). 
In the chemical or acid type of dyspnoea cyanosis is absent or dis- 
proportionately slight. On the other hand, in polycythasmia, in 
some extremely barrel-chested persons and in congenital heart disease, 
there may be striking cyanosis with little or no dyspnoea. Here it 
is the crowding of the peripheral capillaries with red blood cells that 
1 Slight retraction of the lower interspaces in the axilla during inspiration is 
often seen in health. In disease this phenomenon is greatly exaggerated. 76 
PHYSICAL DIAGNOSIS 
is chiefly responsible for the patient’s color. An actual hyper- 
activity of the marrow exists in many of these cases and the red cells 
are increased not only at the periphery but in the larger blood vessels 
and internal organs (“primary or secondary polycythasmia”). 
VI. Changes in the Respiratory Rhythm 
1. Asthmatic Breathing 
In asthma the normal rhythm is reversed; audible expiration be- 
comes longer than inspiration. Inspiration may be represented by 
a short gasp, while expiration becomes a prolonged wheeze. Dysp- 
noea is usually very marked. In barrel-chested persons we get 
the same type of breathing so far as rhythm is concerned but the dysp- 
noea is not usually so extreme and the auxiliary muscles of respiration 
are not so apt to be called into use. In many barrel-chested persons 
one sees the thorax move all as one piece, “cm cuirasse,” owing to a 
senile fixation of the bones of the thorax from ossification of the car- 
tilaginous portions. In hereditary syphilis or phthisis this fixation 
may occur in youth or early middle age. Weak heart and pulmonary 
oedema are usually the main factors in the so-called “emphysematous 
dyspnoea.” 
2. Cheyne-Stokes Breathing 
An anomaly of respiratory rhythm in which short, recurrent parox- 
ysms of dyspnoea are preceded and followed by periods in which no 
respiration occurs (apncea). If we represent the normal respiratory 
movement by an up-and-down line, the Cheyne-Stokes type of 
breathing would appear as in Fig. 71. The period of apnoea may 
Fig. 71.—Cheyne-Stokes Respiration. 
last from one to ten seconds; then short, shallow respirations begin 
and increase rapidly, both in volume and in rate, until a maximum 
of marked dyspnoea is reached, when a diminution in the rate and 
depth of the act begins, and the patient gradually returns to the 
apnoeic state. The length of the whole paroxysm may be from 30 
to 70 seconds. During the apnoeic period the patient is apt to drop 
asleep for a few seconds and the pupils may become contracted. When INSPECTION 
77 
the paroxysm of dyspnoea is at its height, he is apt to cough and shift 
his position restlessly, or in case the whole phenomenon occurs during 
sleep he moves uneasily in his sleep at this period. Modified types of 
this also occur, in which there is rhythmic increase and decrease in the 
depth and rapidity of respiration but without any intervening period 
of apnoea (“Biot’s breathing”). This type of breathing is most often 
seen in various types of cardiac, renal, or cerebral disease. Conner has 
recorded many varieties in tuberculous meningitis. Respiratory 
arrhythmias are generally more marked at night but may occur only 
at that time. Often in healthy children and occasionally in sound 
adults, Cheyne-Stokes breathing occurs during sleep and rarely even 
in waking hours. It is especially apt to occur when the person lies 
on the back and may be checked either in health or disease by turning 
on the side (Edsall). As a rule continuous Cheyne-Stokes breathing 
is a sign of grave prognostic significance, but patients have been 
known to recover completely after weeks or even months of it. It 
is due probably to a relative numbness of the respiratory center 
which allows its usual chemical excitants to accumulate (in the 
apnoeic pause) until they can break through its insensibility and make 
it start the breathing again. 
3. Restrained or “Catchy ” Breathing 
When the patient has a “stitch in the side,” due to dry pleurisy, 
or to other causes, the inspiration may be suddenly interrupted in 
the middle, owing to a seizure of pain which makes the patient stop 
breathing as quickly as he can. The same conditions may produce 
very shallow breathing as the patient tries to avoid the pain which 
a full inspiration will cause. This type of restrained breathing is 
often seen in pleurisy and pneumonia, and in the latter disease ex- 
piration is often accompanied by a little moan or grunt of discomfort. 
Shallow and irregular breathing is often seen in states of pro- 
found unconsciousness from any cause, sucn as apoplexy or poison- 
ing. A few deep respirations may be followed by a number of shallow 
and irregular ones. 
Sterno-mastoid breathing. When death is imminent in any disease, 
the respiration may become very irregular and gasping, and it is apt 
to be accompanied by a peculiar nodding movement of the head, 
the chin being thrown quickly upward during inspiration and falling 
slowly during expiration. I have known but one patient to recover 
after this type of breathing had set in. 78 
PHYSICAL DIAGNOSIS 
After severe hemorrhage the breathing may be of a sighing type 
as well as very shallow. 
4. Stridulous Breathing 
A high-pitched, crowing or barking sound is heard during inspira- 
tion when there is obstruction of the entrance of air at or near the 
glottis. This type of breathing occurs in spasm or oedema of the 
glottis, “croup,” laryngismus stridulus and post-pharyngeal abscess; 
it forms the “whoop” in the paroxysms of whooping-cough. Laryn- 
geal or tracheal obstructions due to foreign bodies, to tumors within 
or pressure from without the air-tubes, may cause a similar type of 
respiration. It is in these cases more especially that we see the suck- 
ing-in of the interspaces mentioned above (see p. 75). 
VII. Diaphragmatic Movements 
1. The Phrenic Wave 
The normal movements of the diaphragm may be rendered visible 
by the following procedure, suggested by Litten in 1892: The patient 
Fig. 72.—Litten’s Diaphragm Shadow. Proper position of patient and of observer. 
The shadow is best seen near L. 
lies upon his back with the chest bared and the feet pointed directly 
toward a window. Cross lights must be altogether excluded by dark- 
ening any other windows which the room may contain1 (see Fig. 72). 
The observer stands at the patient’s side. As the ribs rise with the 
1 If it is convenient to move the patient’s bed into the proper position with 
relation to the window, or if the foot-board interferes, or if the observation has to be 
made after dark, a dark lantern or electric hand lantern held in the hand answers 
very well. INSPECTION 
79 
movement of inspiration, a short, narrow shadow moves down the 
axilla from about the seventh to about the ninth or tenth rib. During 
expiration the shadow rises again to the point from which it started, 
but is less easily seen. This phenomenon is to be seen on both sides 
of the chest, less well in the back, and sometimes in the epigastrium. 
It is best seen in spare, muscular young men, but is never absent in 
health except in those who are very fat, or who cannot or will not 
breathe deeply. The latter condition occurs in hysteria and in some 
very stupid persons. In the observation of several thousand cases,* I 
have never known it absent 
in health except under these 
conditions. 
In normal chests, the ex- 
cursion of the shadow is about 
two and a half inches; with 
very forced breathing three 
and a half inches. The me- 
chanism of this phenomenon 
is best understood by imagin- 
ing a coronal section of the 
thorax as seen from the front 
or back (see Fig. 73). At the end of expiration, the diaphragm lies 
flat against the thorax from its attachment up to about the sixth rib. 
During inspiration it11 peels of” as it descends and allows the edge of 
the lung to come down into the chink between the diaphragm and 
thorax. This “peeling off” of the diaphragm and the descent of the 
lung during inspiration give rise to the moving shadow above 
described. 
By thus observing the excursion of the diaphragm we can obtain 
a good deal of information of clinical value. 
In pneumonia of the lower lobe, pleuritic effusion, extensive pleu- 
ritic adhesions, or in well marked barrel chest, the shadow is absent. 
This is explained by the fact that in these conditions the diaphragm is 
held off from the chest wall so that its movements communicate no 
shadow. In pleuritic adhesions the movements of the diaphragm are 
prevented. In early phthisis I have generally found the excursion of 
the diaphragm diminished upon the affected side, owing to a loss of 
elasticity in the effected lung and in part probably to pleuritic adhesions. 
On the other hand, fluid or solid tumors below the diaphragm, unless 
very large, do not prevent the descent of that muscle, and so do not 
abolish the diaphragm shadow. In cases in which the diagnosis is 
Pig. 73.—Excursion of the Diaphragm 
during Forced Respiration. R, Ribs; E, posi- 
tion of the diaphragm at end of expiration; 7, 
position of diaphragm at end of inspiration. 80 
PHYSICAL DIAGNOSIS 
in doubt between fluid in the right pleural cavity and an enlarge- 
ment of the liver upward or a subdiaphragmatic abscess, the preser- 
vation of the Litten’s phenomenon in the latter two affections may 
be of some value in diagnosis. Very large accumulations of ascitic 
fluid may so far restrain the diaphragmatic movements that no shadow 
can be seen. 
This method frees us to a considerable extent from the need of 
using the spirometer to determine the capacity of the lungs. By 
measuring the excussion of the phrenic shadow and taking account 
of the thoracic movement, we obtain a fair idea of the respiratory 
capacity (so called “vital capacity”) of the individual. 
2. The III Effects of a High Diaphragm 
(а) The permanently raised position into which the midriff is 
forced by abdominal stasis with ascites and engorged liver, by extreme 
obesity, by abdominal tumors or dropsies and by gaseous distention, 
is an important factor in the dyspnoea and in the pulmonary lesions 
which these conditions produce. Pulmonary engorgement, infarct 
and broncho pneumonia are favored by high diaphragm. 
(б) Moreover since the pumping action exerted by the midriff on 
the blood of the splanchnic area is an important factor in maintaining 
the circulation, the feeble, restricted motions of a high diaphragm 
handicap the heart and throw extra work upon it. 
(c) Lewis has shown that free diaphragmatic breathing raises 
blood pressure and that a purely or largely costal breathing lowers it. 
Lowered blood pressure appears therefore to be a further disadvantage 
resulting from a high fixed position of the diaphragm. 
Permanently low diaphragm (splanchnoptosis) is believed to pro- 
duce circulatory disturbance since in its steady depression (as in its 
permanent exaltation) it cannot pump along the splanchnic blood 
effectively. 
Unilateral displacement of the diaphragm will be further referred 
to in the section on subphrenic abscess. 
VIII. Observation of the Cardiac Movements 
i. The Normal Cardiac Impulse 
With each systole of the heart there may be seen in the great 
majority of normal chests an outward movement of a small portion of 
the chest wall just inside and below the left nipple. This phenomenon INSPECTION 
81 
is known as the cardiac impulse.1 It is now generally admitted that 
the “apex impulse” is caused by the impact of a portion of the right 
ventricle against the chest wall and not by the apex of the heart itself. 
(The bearings of this fact, which have not, I think, been generally 
appreciated, will be discussed presently.) The position of the maxi- 
mum impulse in adults is usually in the fifth intercostal space just 
inside the nipple line. In children under the age of six it is often in 
Fig. 74.—Showing Amount of Shifting of the Apex Impulse with Change of Position 
The inner dot represents the position of the impulse when the patient lies on his back; 
the outer dot corresponds to the position of the apex with patient on left side. 
the fourth interspace and outside the nipple; while in persons with 
low diaphragm it may descend as low as the sixth interspace. In 
adults it is occasionally absent even in perfect health and under 
certain pathological conditions to be later mentioned. 
(a) The position of the impulse varies to a certain extent according 
to the position of the body. If the patient lies upon the left side, the 
heart’s apex swings out toward the axilla, so that the visible impulse 
shifts from one to two and one-half inches to the left (see Fig. 74). 
1 For a more detailed description of the normal position of the cardiac impulse, 
see next page. 82 
PHYSICAL DIAGNOSIS 
A slight shift to the right can also be brought about by lying upon the 
right side, and, as a rule, the impulse is less visible in the recumbent 
than in the upright position. Since the heart is lifted with each 
expiration by the rise of the diaphragm and falls during inspiration, 
a corresponding change can be observed in the apex beat, which, in 
forced breathing, may shift as much as one interspace. Of the changes 
in the position of thejmpulse brought about by disease, I shall speak 
in a later paragraph. 
(b) Relation of the maximum cardiac impulse to the apex of the 
heart.—I mentioned above that the maximum cardiac impulse is not 
Fig. 75.—The is the Maximum Cardiac Impulse. That to the right is the 
true apex of the heart, as obtained by percussion. The ribs are numbered. 
due to the striking of the apex of the heart against the chest wall, but 
to the impact of a portion of the right ventricle. The practical impor- 
tance of this fact is this: When we are trying to localize the apex of 
the heart in order to determine how far the organ extends to the left 
and downward, it will not do to be guided by the position of the 
maximum impulse, for the apex of the heart is almost always to be 
found three-fourths of an inch or more farther to the left (see Fig. 75). 
This may be proved by percussion (vide infra, p. 125), and by fluoro- 
scopy. The true position of the cardiac apex thus determined corre- INSPECTION 
83 
sponds usually not with the maximum impulse, but with the point 
farthest out and farthest down at which any localized rise and fall 
synchronous with the heart beat can be felt. 
(c) Besides the definite and localized impulse which has just been 
described, it is often possible to see that a considerable section of the 
chest wall in the precordial region is lifted “ en masse. ” The phenome- 
non is the “ Her zenstoss” of the Germans, with which the “ Spitzentoss" 
or apex impluse is contrasted. A variable amount of “Herzentoss” 
can be seen and felt over any normal heart when it is acting rapidly and 
forcibly, and in thin, nervous subjects or in children even when the 
heart is beating quietly. It is more marked in cardiac neuroses, in 
Graves’ disease, when the heart is hypertrophied, and when there is 
more or less stiffening of the ribs with loss of their natural elasticity. 
At times it may be impossible to localize any one point to which we 
can give the name of apex impulse, and what we see is the rhythmical 
rise and fall of a section of the chest as large as the palm of the hand 
or larger. In many fat people and in those with thick, stiff chest 
walls it is often impossible to make out any cardiac impulse. Some- 
times we can feel it when the patient lies on his left side, and allowing 
for its normal lateral swing, we may in this way calculate its ordinary 
position. In old people palpation is often useless and we fall back on 
percussion, blood pressure and the x-ray. 
(d) X-ray measurements of the normal heart:—The normal adult 
heart x-rayed in the upright position at a distance of 7 feet extends 
from 7 to 11 cm. to the left of the median line and from 3 to 5 cm. to 
the right of the median line. The heavier the person the larger the 
heart. Women’s hearts average about 1 cm. smaller in each direction. 
The transverse diameter of the great vessels is usually between 4 
and 6.5 mm. 
Percussion agrees fairly well with the measurements to the left of 
the median line (where also palpation usually serves us excellently) 
but is unreliable on measurements to the right of the median line. 
(e) Character of the cardiac impulse.—Palpation is considerably 
more effective than inspection in giving us information as to the 
nature of the cardiac movements which give rise to the “ apex beat, ” but 
even inspection sometimes suffices to show that the impulse has the 
slow forcible thrust characteristic of hypertrophy or is of the nature 
of a short tap, a peristaltic wave, or a diffuse slap against the chest 
wall. In some cases a distinct undulation can be seen passing from 
the apex region upward toward the base of the heart, or in the opposite 
direction. 84 
PHYSICAL DIAGNOSIS 
2. Displacement of the Cardiac Impulse 
To one familiar with the position, extent, and character of the 
normal cardiac impulse, any displacement of this impulse from its 
normal site or any superadded pulsation in another part of the chest is 
apparent at a glance. I will consider first the commonest forms of 
dislocation of the apex impulse. 
(а) Displacement of the cardiac impulse due to hypertrophy and 
dilatation of the heart.—By far the most common directions of dis- 
placement are toward the left axilla and downward. As a rule, it is 
displaced in both these directions at once. I shall return to this sub- 
ject more in detail under the heading Cardiac Hypertrophy, but here I 
may say that enlargements of the left ventricle tend especially to 
displace the apex impulse downward, while enlargements of the right 
ventricle are more commonly associated with displacement of the 
impulse toward the axilla. 
(б) Next to hypertrophy and dilatation of the heart perhaps the 
commonest cause of dislocation of the cardiac impulse is pressure from 
below the diaphragm. When the diaphragm is raised by a large 
accumulation of gas or fluid, by pregnancy or by solid tumors of large 
size, we may see the apex beat of the normal heart in the fourth inter- 
space and often an inch or more inside the nipple line. 
(c) Of nearly equal frequency is displacement of the heart due to 
left-sided pleuritic effusion or to pneumothorax (see below, p. 322). 
When a considerable amount of air or fluid accumulates in the left 
pleural cavity, the heart is displaced bodily to the right so that it may 
be concealed behind the sternum or be visible beyond it to the right; 
in extreme cases it may be dislocated beyond the right nipple. Right 
pleuritic effusions have far less effect upon the position of the cardiac 
impulse, but when a very large amount of fluid accumulates we may 
see the impulse displaced considerably toward the left axilla. 
(d) I have mentioned causes tending to push the heart to the right, 
to the left, or upward. Occasionally the heart is pushed downward by 
an aneurismal tumor or a neoplasm of the mediastinum. In these 
cases there is usually more or less displacement to the left as well. 
As a result of arteriosclerosis or cardiac hypertrophy the aorta may 
sag or stretch a little, the diaphragm may stand lower, so that the 
apex beat descends to the sixth interspace, or (more often) is lost to 
sight and touch behind the bunch of convergent costal cartilages just to 
the left of the ensiform. Very frequently in barrel-chested men past 
forty-five the whole heart sinks considerably, so that a marked systolic INSPECTION 
85 
retraction (less often pulsation) is seen below the ensiform in 
the epigastrium. 
(e) Displacement of the cardiac impulse resulting from adhesions 
of the pericardium to the pleura, with subsequent contraction, occurs 
in fibroid phthisis and in some cases of long-standing disease of the 
pleura. Through the effect of negative pressure the heart may be 
sucked into the space formerly occupied by a portion of the lung, when 
the latter has become contracted by disease. It seems probable, 
however, that in the majority of cases adhesions between the pleura 
and pericardium play a part in such displacement. By these means 
the heart may be displaced to the right of the sternum, as it is by 
left-sided pleuritic effusion. It is often drawn upward as well as to the 
right in such cases because the contraction takes place in the upper 
part of the lung. More rarely we see the heart drawn toward the left 
clavicle in fibroid phthisis of the left apex. 
(/) Distortion of the thorax due to spinal curvature or other causes 
may bring about a considerable displacement of the heart from its 
normal position. 
(g) Dextrocardia and Situs Inversus.—In rare cases a displacement 
of the apex impulse to the right of the sternum may be due either to a 
transposition of all viscera (the liver being found upon the left, the 
spleen upon the right, etc.), or to dextrocardia, in which the heart 
alone is transposed while the other viscera retain their normal places. 
(a) Summary 
The apex impulse is displaced by: 
(а) Hypertrophy and dilatation of the heart. 
(б) Pressure from below the diaphragm. 
(c) Air or fluid in one pleural cavity especially the left. 
(d) Aneurism, mediastinal growths, and sagging of the aorta. 
(e) Fibroid phthisis and chronic pleurisy. 
(/) Spinal curvature. 
(g) Transposition of the heart or of all the viscera. 
3. Apex Retraction 
Before leaving the subject of the cardiac impulse it seems best to 
speak of those cases in which during systole we see a retraction of one 
or more interspaces at or near the point where the cardiac impulse 
normally appears. 86 
PHYSICAL DIAGNOSIS 
(a) In by far the greater number of instances such retraction is 
due to negative pressure produced within the chest by the vigorous 
contraction of a more or less hypertrophied and dilated heart. In 
these cases the retraction is usually balanced by an impulse in the 
next interspace so that a “walking beam” appearance or tilting of a 
piece of the chest wall results. 
(.b) In rarer cases several interspaces, both in the precordial 
region and in the left lower axilla and back, may be drawn in as a 
result of adhesions between the pericardium and the chest wall, such 
as form in cases of adherent pericardium and fibrous mediastinitis1 
(see below, pages 245 and 246). 
4. Epigastric Pulsation 
In a considerable portion of healthy adults a pulsation or retrac- 
tion at the epigastrium synchronous with the systole of the heart is to 
be seen from time to time. Such pulsation has often been considered 
evidence of hypertrophy of the right ventricle, but atopsy findings 
do not substantiate this belief. In some cases epigastric pulsation is 
to be explained as the transmission of the heart’s impulse through the 
liver, or as a lifting of that organ by the movements of the abdominal 
aorta. In other cases it is due to bathycardia (“low heart”—a con- 
dition very common in arteriosclerosis). 
5. Visible Pulsations due to Uncovering of Portions of the Heart 
Normally Covered by the Lungs 
One of the commonest causes of visible pulsations in parts of the 
chest where normally none is to be seen is retraction of the lung. 
(а) In chlorosis we saw such pulsations frequently before that 
disease became so rare. In that disease, as in other debilitated states, 
the lungs are often not adequately expanded owing to the superficiality 
of the respiration, and accordingly their margins do not cover as much 
of the surface of the heart as they do in healthy adults. This results in 
rendering visible, in the second, third, or fourth left interspace near 
the sternum, pulsations transmitted from the conus arteriosus or from 
the right ventricle. Less commonly, similar pulsations due to the 
uncovered aorta may be seen on the right side of the sternum. 
(б) A rarer cause of retraction of the lungs is phthisis or chronic 
interstitial pneumonia. In these diseases a very large area of pulsation 
1 Or more often as a result of simple cardiac hypertrophy. Most cases of aortic 
regurgitation in thin young patients show this systolic retraction in the left lower 
back. INSPECTION 
87 
may be seen in the precordial region owing to the entire uncovering 
of the heart by the retracted lung, even when the heart is not drawn 
out of its normal position. 
IX. Aneurism and Other Causes of Abnormal Thoracic 
Pulsation 
So far I have spoken altogether of pulsations transmitted directly 
to the thorax by the heart itself, but we have also to bear in mind that 
an aneurism may transmit to the chest wall pulsations which it is 
exceedingly important for us to recognize and properly to interpret. 
Fig. 76.—Position When Looking for Slight Aneurismal Pulsation. 
No disease is easier to recognize than aneurism when the growth has 
perforated the chest wall and appears as a tumor externally, but it 
is much more important as well as much more difficult to recognize 
the disease while it is confined within the thorax. In such cases, 
the movements transmitted from the aorta to the chest wall may be 
so slight that only the keenest and most thorough inspection controlled 
by palpation will detect them. When slight pulsations are searched 
for, the patient should be put in the position shown in Fig. 76, and the 
observer should place himself so that his eye is as nearly as possible on 
a level with the chest and looks across it so that he sees it in profile. 
In this position, or in a sitting position with tangential light, he can 
make out pulsations which are totally invisible if the patient sits 
facing the light. 88 
PHYSICAL DIAGNOSIS 
Pulsations due to aneurism are most apt to be seen in the first 
or second right interspace near the sternum, and not infrequently the 
clavicle and the adjacent parts may be seen to rise slightly with every 
beat of the heart, but in any part of the chest wall pulsations due to 
an aneurism are occasionally to be seen, and should be looked for 
scrupulously whenever the symptoms of the case suggest the possibility 
of this disease (see below, p. 256). 
i. Pulsating Pleurisy 
In cases of purulent pleurisy in which the fluid has worked its way 
out between the ribs so that it is covered only by the skin and sub- 
cutaneous tissues, a pulsation transmitted from the heart may become 
visible, and the resemblance to the pulsation seen in aneurism may be 
confusing. Such pulsation is apt to be seen in the upper and front 
portions of the chest. Very rarely a pleuritic effusion which has not 
burrowed into the chest wall may transmit to the latter a wavy move- 
ment corresponding to the motions set up in the fluid by the cardiac 
contractions. I have never seen a pulsating pleurisy. 
X-. Inspection of the Peripheral Vessels 
In the study of all diseases of the heart and lungs it is important 
to take account of all vascular phenomena apparent in the neck or in 
the extremities, since such phenomena have a very direct bearing upon 
the interpretation of the conditions obtaining within the chest. In- 
spection plays a very large part in the study of these vascular phe- 
nomena. We should look for: (a) Venous phenomenia; (b) Arterial 
phenomena; (c) Capillary phenomena. 
i. Inspection of the Veins 
i. The condition of the veins of the neck is of considerable impor- 
tance in the diagnosis of diseases of the heart and lungs. Where the 
tissues of the neck are more or less wasted, the veins may be quite 
prominent even when no disease exists within the chest, and in such 
cases they may be more or less distended during each expiration, 
especially if dyspnoea or cough is present. If the overdistended veins 
are completely emptied during deep inspiration and on both sides of 
the neck, we can usually infer that there is an overdistention of the 
right side of the heart. When a similar phenomenon occurs on one 
side only, it may mean pressure upon one innominate vein. So far I 
have spoken of venous changes synchronous with respiration, but we 
may have also INSPECTION 
89 
2. A presystolic pulsation or undulation seen either in the external 
jugular vein or in the bulbus jugularis between the two attachments 
of the sternomastoid muscle. Such pulsation or undulation, which 
is to be seen just before each systole of the heart, is not necessarily 
anything abnormal and must be carefully distinguished from 
3. Systolic venous pulsation, such as occurs in what I suppose is 
one of the most common valvular diseases of the heart, relative tri- 
cuspid regurgitation,1 as well as in a good many other conditions. 
Fig. 77.—Tortuous Veins on Chest and Abdomen. (Autopsy showed obliteration of the 
vena cava inferior.) 
Systolic venous pulsation is more often seen upon the right side than 
upon the left side of the neck. There may be a wave during the systole 
of the auricle and another during the systole of the ventricle, the latter 
closely following the former. In any case in which a doubt arises 
whether a pulsation in the veins of the neck is due to tricuspid regur- 
gitation, it is well to try the experiment of emptying the vein by strok- 
1 A pulsating carotid may transmit an up-and-down motion to the veins over- 
lying it. In such cases, if the veins be emptied by “milking” them upward,they 
will not refill from below. 90 
PHYSICAL DIAGNOSIS 
ing it from below upward. If it immediately fills from below, we may 
be practically certain that tricuspid regurgitation is present. In 
the vast majority of cases of venous pulsation due to other causes or 
'occurring in healthy persons a vein will not refill from below if emptied 
in the manner above described. The finer points relating to the varia- 
tions in the cervical venous pressure are recognized by phlebograms 
traced by MacKenzie’s instrument or in some similar way. 
Fig. 78.—Enlarged and Tortuous Brachial Arteries (Arteriosclerosis). 
The venous waves so recorded tell us much that is interesting and 
some things that are important about the behavior of the auricles. 
(See below, p. 117.) 
4. Rarely, superficial veins may be seen to pulsate in other parts 
of the body, especially in aortic regurgitation, and occasionally large 
and tortuous veins may be seen pulsating upon the thoracic or abdom- 
inal wall, representing an attempt at collateral circulation when one 
or the other vena cava is compressed (Fig. 77).1 
2. Arterial Phenomena 
i. In thin or nervous persons pulsations are not infrequently to be 
seen in the carotids independent of any abnormal condition of the 
heart. 
1 Enlarged veins about the navel, the so-called “caput Medusae,” are commonly- 
found in text-books, but rarely in cirrhosis of the liver. I have never seen them. INSPECTION 
91 
2. Very violent throbbing of the carotids, more noticeable than 
the normal, often occurs in severe anaemias and occasionally in simple 
overaction of the heart, e.g., in Graves’ disease. From the same 
causes, visible pulsation may occur in the subclavian, axillary, brachial, 
and radial arteries, as well as in the large arterial trunks of the lower 
extremity. 
3. In arterio-sclerosis occurring in spare, elderly men, one often 
notices a lateral excursion of the tortuous brachial arteries synchronous 
Fig. 79.—Enlarged and Tortuous Brachial Artery (Arterio-sclerosis). 
with every heart beat. An up-and-down pulsation may occur at the 
same time. Not infrequently the arteries which are stiffened by 
arterio-sclerosis (see below, page 108) stand out visibly as enlarged, 
tortuous cords along the inner side of the biceps muscle (see Figs. 78 
and 79), and occasionally the course of the radial artery may be traced 
over a considerable distance in the forearm. In rare cases inequalities 
produced in the arterial wall by deposition of lime salts may be visible 
as well as palpable. The temporal artery (unlike the brachial) is 
normally tortuous. Its course has therefore no relation to arterio- 
sclerosis. It is visible in many normal persons. 
If a microscopic slide is placed against the mucous membrane of 
the lower lip so as partially to blanch its surface, one may see, with 
each beat of the heart (in cases of aortic regurgitation and in some 
3. Capillary Pulsation 92 
PHYSICAL DIAGNOSIS 
other conditions presently to be mentioned), a delicate flushing of the 
blanched surface beneath the glass slide. The same pulsation is 
sometimes to be observed under the finger nails, or may be still better 
brought out by holding a pocket electric flash light against the finger 
pulp so as to transilluminate it. The paling and flushing with each 
heart beat is well seen. This phenomenon will be referred to again 
when we come to speak of aortic regurgitation. Here it suffices to 
say that it is not in any way peculiar to that disease, but occurs 
occasionally in health, in anaemia, in thyrotoxicosis, i.e. in conditions 
associated with large pulse pressures (see below, pp. 112-114), as well 
as in any area of inflammatory hyperaemia (jumping toothache, 
throbbing felon, etc.). 
XI. Inspection of the Skin and Mucous Membranes 
Light may be thrown upon the diagnosis of very many diseases 
by observing the color and condition of the cutaneous surfaces as well 
as of the mucous membranes. We should look for the following 
conditions: 
(1) Cyanosis. 
(2) (Edema. 
(3) Pallor. 
(4) Jaundice. 
(5) Scars and eruptions. 
i. Cyanosis 
By cyanosis we mean a purplish or grayish blue tint noticeable 
especially in the face, in the lips, and under the nails. There are 
many degrees of cyanosis, from the slight purplish tinge of the lips, 
which a little overexertion or slight exposure to cold may bring out, 
up to the gray-blue color seen in advanced cases of pulmonary or 
cardiac disease, or the dark reddish-blue seen in congenital malforma- 
tions of the heart. Cyanosis makes a very different impression upon 
us when it is combined with pallor on the one hand or with jaundice on 
the other. When combined with pallor, one gets various ashy-gray 
tints, while the admixture of cyanosis and jaundice results in a color 
very difficult to describe, sometimes approaching a greenish hue. The 
commonest causes of cyanosis are; 
(a) Valvular or parietal disease of the heart. 
(b) Extreme types of the barrel chest. INSPECTION 
93 
(c) Asthma. 
(d) Pneumonia. 
(e) Phthisis. 
(/) Obstruction of the superior vena cava by mediastinal tumors 
or other causes. 
(g) In some persons a certain degree of cyanosis of the lips exists 
despite perfect health. This is especially true of weather-beaten 
faces and those of the so-called “full-blooded” type. 
(h) Methsemoglobinaemia, such as occurs after the excessive use 
of coal-tar analgesics (antifebrine in headache powders, etc.). 
A rare but very striking type of cyanosis is that seen in cases of 
congenital heart disease, in which the lips may be indigo blue in 
color or almost black while yet no dyspnoea is present. 
Cyanosis of intestinal origin has been described by English writers. 
It is distinctly rare. 
In polycythasmia the face and lips may show the ordinary tint 
of cyanosis or may be of a deep red peculiar to this disease. 
2. (Edema 
(Edema, or the accumulation of serous fluid in the subcutaneous 
spaces, is usually appreciated by palpation rather than by inspec- 
tion, but sometimes makes the face look very puffy, especially under 
the eyes. This is not a common occurrence in diseases of the chest, 
in connection with which such oedema as takes place is usually to be 
found in the lower extremities and is appreciable rather by palpation 
than by inspection. If we are not familiar with a patient’s face, 
we often do not perceive in it the changes of outline due to oedema 
which a friend would notice at once. Clothing is apt to leave grooves 
and marks wherever it presses tightly upon the oedematous tissues, 
as around the waist or over the shoulders. In the legs, the presence 
of oedema may be suggested by an unnaturally smooth, glossy appear- 
ance of the skin. Such impressions, however, may be false unless 
controlled by palpation, for simple obesity may produce very similar 
appearances. 
3. Pallor 
Pallor suggests, though it does not in any way prove, anaemia. 
Pallor of the mucous membranes, as seen in the lips and conjunctivae, 
is much more apt to be a sign of real anaemia than is pallor of the 94 
PHYSICAL DIAGNOSIS 
skin. At best, pallor is only a sign which suggests to us to look 
further into the case in one or another direction, and of itself proves 
nothing of importance. Haemorrhage, cancer, nephritis, septicaemia 
and pernicious anaemia are the commonest causes of anaemia. Pallor 
without ancemia is often seen in tuberculosis, in arteriosclerosis and 
in the psychoneuroses. 
4. Jaundice 
The yellowish tint which appears in the skin, and especially in 
the conjunctivae, when the escape of bile from the liver is hindered 
(catarrhal jaundice, gall-stones, cancer, cirrhosis), or when rapid 
hemolysis has occurred (malaria, sepsis). 
5. Scars and Eruptions 
The scars of old tuberculous glands in the neck, the scars of 
varicose ulcers along the shin bones, the various scars and eruptions 
of syphilis, of the exanthemata, of traumata and of surgical opera- 
tions are of value in tracing the past history and interpreting the 
present illness. Without attempting to enter the field of dermatology 
it may be here mentioned that for the internist the skin lesions most 
important of recognition are those just mentioned and, in addition, 
drug eruptions, cutaneous neoplasms and the various causes of 
pigmentation. 
XII. Enlarged Glands 
Routine inspection may reveal the presence of enlarged glands in 
the neck or axillae or groins, and may thereby give us a clew to the 
nature of the underlying disease; for example, the presence of enlarged 
glands in the neck, especially if there are any scars, sinuses, or other 
evidence that suppuration is going on or has formerly taken place 
in them, suggests the possibility of glandular tuberculosis or of an 
enlargement of the bronchial and mediastinal glands. In children 
cervical adenitis is most often a sign of bad teeth, tonsillitis and 
head lice. Again, malignant disease of the chest or abdomen is some- 
times associated with the metastatic nodules over the clavicle (see 
Fig. 80), and a microscopic examination of them may thus reveal 
the nature of the intrathoracic disease to which they are secondary. 
Very large and matted masses of glands above the clavicle, which INSPECTION 
95 
have never suppurated and have been painless and slow in their 
growth, suggest the presence of similar deposits in the mediastinum 
as a part of the symptom complex known as “Hodgkin’s disease.” 
The presence of a goitre or enlargement of the thyroid gland may 
account for a well-marked dyspnoea. Axillary adenitis means most 
often peripheral sepsis, next tuberculosis, then metastatic cancer, 
Fig. 8o.—Sarcoma of Sternum and Cervical Glands. (Curschmann.) 
leucaemia and Hodgkin’s disease. Inguinal adenitis (suppurative)1'is 
most often a result of gonorrhoea. If non-suppurative, it is usually 
due to sepsis in the leg, syphilis, leucaemia, Hodgkin’s disease and 
metastatic cancer. 
Syphilis produces general glandular enlargement; the posterior 
cervical and the epitrochlear glands are often involved, but this is 
also the case in many diseases other than syphilis. CHAPTER V 
PALPATION AND THE STUDY OF THE PULSE 
I. Palpation 
The most important points to be determined by palpation—that 
is, by laying the hand upon the surface of the chest—are: 
(1) The position and character of the apex heat of the heart. 
(2) The presence of a “thrill” (see below). 
(3) The vibrations of the spoken voice (“tactile fremitus"). 
(4) The presence of pleuritic or pricardial friction. 
(5) Local muscular spasm. 
Other less important data furnished by palpation will be mentioned 
later. 
t. The Apex Beat 
(а) In feeling for the apex impulse of the heart, one should first 
lay the palm of the hand lightly upon the chest just below the left 
nipple. In this way, we can appreciate a good deal about the move- 
ments of the heart, and confirm or modify what we have learned 
by inspection. One learns, in the first place, whether the heart beat 
is regular or not, and in case it is irregular, something as to the nature 
and degree of the arrhythmia; further one gets a more accurate idea 
than can be obtained through inspection regarding the character 
of the cardiac movements. The powerful, slow, widespread impulse 
of a hypertrophied heart, the sudden rap characteristic of mitral 
stenosis may be thus appreciated. 
(б) After this, it is best to lay the tips of two or three fingers 
over the point where the maximum impulse is to be seen, and follow 
it outward and downward until one arrives at the point farthest 
to the left and farthest down at which it is still possible to feel any 
up-and-down movement. The point usually corresponds with 
the apex of the heart, as determined by percussion or fluoroscopy. 
It does not correspond with the maximum cardiac impulse, but is often 
to be found at least an inch farther to the left and downward (see 
above, Fig. So). 
96 PALPATION AND THE STUDY OF THE PULSE 
97 
Sometimes one can localize by palpation a cardiac impulse which 
is not visible; on the other hand, in some cases we can see pulsations 
that we cannot feel. Both methods must be used in every case. 
When x-ray measurements cannot be had, palpation and inspec- 
tion of the region give us the most reliable data that we have regard- 
ing the size of the heart. Percussion is often interfered with by the 
presence of gas in the stomach, of fluid or adhesions in the pleural 
cavity, or by the ineptness of the observer, but it is almost always 
possible with a little care to make out by a combination of palpation 
and inspection the position of the apex of the heart. When we can 
neither feel it nor see it, we may have to fall back upon auscultation, 
considering the apex of the heart to be at or near the point at which 
the heart sounds are heard loudest. When endeavoring to find the 
apex of the heart, we must not forget that the position of the patient 
influences considerably the relation of the heart to the chest walls. 
If the patient is leaning toward the left or lying on the left side, the 
apex will swing out several centimeters toward the left axilla. If 
the peripheral blood pressure is permanently high, it is well to conclude 
that the heart is enlarged, whatever the other physical signs. 
When feeling for the cardiac impulse with the palm of the hand, 
we are in a good position to notice the presence or absence of a very 
important physical sign to which we give the name of “thrill.” The 
feeling imparted to the fingers by the throat of a purring cat is very 
much like the palpable “thrill” over the precordia in certain disease 
of the heart to be mentioned later. It is a vibration of the chest 
wall, usually confined to a small area in the region of the apex impulse, 
but sometimes felt in the second right intercostal space or elsewhere 
in the precordial region. This vibration or thrill almost always 
occurs intermittently, i.e., only during a portion of the cardiac cycle. 
When felt in the apex region, it usually occurs just before the cardiac 
impulse; this fact we express by calling it a “presystolic thrill;” but 
occasionally we may feel a systolic thrill at the apex—one, that is, 
which accompanies the cardiac impulse. The word thrill should be 
used to denote only a purring, vibrating sensation communicated to 
the fingers by the chest wall. It is incorrect to speak of a thrill as 
if it were something audible. 
We must especially distinguish a thrill from the slight systolic 
shudder or jarring which is often palpable over the whole precordia in 
functional neuroses of the heart or in conditions of mental excitement. 
2. Thrills 98 
PHYSICAL DIAGNOSIS 
As a rule we can appreciate a thrill more easily if we lay the palm 
very lightly upon the chest, using a little pressure as possible. Firm 
pressure may prevent the occurrence of the vibrations which we 
desire to investigate. Of the thrills felt over the base of the heart, 
more will be said in Chapter X. At the apex nothing should be called 
a “thrill” unless it lasts longer than a normal heart sound. Many a 
forcible first sound in an excited, nervous subject is miscalled a thrill. 
3. Vibrations Communicated to the Chest Wall by the Voice 
“ Tactile fremitus” is the name given to the sense of vibration 
communicated to the hand if the latter is laid upon the chest while 
the patient repeats some short 
phrase of words. The classical 
method of testing tactile fre- 
mitus is to ask the patient to 
count “one, two, three,” or to 
repeat the words “ninety-nine” 
while the palm or the edge of 
the hand is laid upon the chest. 
The amount of fremitus to be 
obtained over a given part of the 
thorax varies, of course, accord- 
ing to the loudness of the words 
spoken, and is influenced also 
by the vowels contained in them. 
A certain uniformity is obtained 
by getting the patient to repeat always the same formula. Thus, he 
is likely to use the same amount of force each time he repeats them 
and to use approximately the same pitch of voice. 
Other things being equal, the fremitus is greater in men than in 
women, in adults than in children, and is more marked in those whose 
voices are low pitched than in those whose voices are relatively shrill. 
The amount of fremitus also varies widely in different parts of the 
healthy chest. A glance at Fig. 81 will help us to realize this. The 
parts shaded darkest communicate to the fingers the most marked 
fremitus, while in the parts not shaded at all, little or no fremitus is 
felt. Intermediate degrees of vibration are represented by inter- 
mediate tints of shading. From this diagram we see at once (a) that 
the maximum of fremitus is to be obtained over the apex of the right 
Fig. 8i. —Distribution of Tactile Fremitus. PALPATION AND THE STUDY OF THE PULSE 
99 
lung in front1, (6) that it is greater in the upper part of the chest than 
in the lower, and somewhat greater throughout the right chest than 
in corresponding part of the left. This natural ineuqality of the two 
sides of the chest cannot be too strongly emphasized. 
Comparatively little fremitus is to be felt over the scapulae be- 
hind, and still less in the precordial region in front. The outlines 
of the lungs can be quite accurately mapped out by means of the 
Fig. 82. —Showing Point at Which Pleural Friction is Most Often Heard 
tactile fremitus in adults of low-pitched voice. In children, as has 
been already mentioned, fremitus is usually very slight and may be 
entirely absent, and in many women it is too slight to be of any 
considerable diagnostic value. Again, some very fat persons and 
those with thick chest walls transmit but little vibration to their chest 
walls when they speak. On the other hand, in emaciated patients 
or in those with thin-walled, flexible chests, the amount of fremitus 
is relatively great. 
1 Owing to the more direct connections through the right bronchus with the 
larynx. 100 
PHYSICAL DIAGNOSIS 
Bearing in mind all these disparities—disparities both between 
persons of different age and different sex, and between the two sides 
of the chest in any one person—we are in a position to appreciate 
the modifications to which disease gives rise and which may be of 
great importance in diagnosis. These variations are: 
(a) Diminution or absence of fremitus. 
(b) Increase of fremitus. 
(а) If the lung is pushed away from the chest wall by the presence of 
air or fluid, or tumor (pneumothorax, pleurisy, hydrothorax, neoplasms) 
in the pleural cavity, we get a diminution or absence of tactile frem- 
itus—diminution where the layer of fluid or air is very thin, absence 
where it is of considerable thickness. 
(б) Solidification of the lung due to phthisis or pneumonia is the 
commonest cause of an increase in tactile fremitius. Further details 
as to the variations in amount of fremitus in different diseases may 
be found in later chapters in this book. 
4. Friction, Pleural or Pericardial 
In many cases of inflammatory roughening of the pleural sur- 
faces (“dry pleurisy”), a grating or rubbing of the two surfaces upon 
each other may be felt as 
well as heard during the 
movements of respiration, 
and especially at the end of 
inspiration. Such friction is 
most often felt at the bottom 
of the axilla, on one side or 
the other, where the dia- 
phragmatic pleura is in close 
apposition with the costal 
layer (see Fig. 82, p. 99). 
Similarly, in roughening 
of the pericardial surfaces 
(“dry” or “plastic” peri- 
carditis) it is occasionally 
possible to feel a grating or 
rubbing in the precordial region more or less synchronous with the 
hearts movements. Such friction is most often to be felt in the region 
of the fourth left costal cartilage (see Fig. 83). 
Fig. 83. —Showing Point (P) at Which Peri- 
cardial Friction is Most Often Heard. PALPATION AND THE STUDY OF THE PULSE 
101 
Palpable friction is of great value in diagnosis because it is a sign 
about which we can feel no doubt; as such it frequently confirms our 
judgment in cases in which the auscultatory signs are less clear. Fric- 
tion sounds heard with the stethoscope may be closely simulated 
by the rubbing of the stethoscope upon the skin, but palpable friction 
is simulated by nothing else, unless occasionally by 
5. Palpable Rales 
Occasionally low pitched, snoring rales communicate a sensation 
to the hand placed upon the chest in the region beneath which the 
rales are produced; to the practised hand this sensation is quite differ- 
ent from that produced by pleural friction, although the difference 
is hard to describe. 
6. Joint Frictions and Tendon Frictions 
F. T. Lord has called attention to grinding, grazing or snapping 
noises heard over the back and shoulders of patients especially when 
their arms are crossed on the chest so as to draw the scapulae forward. 
Some of these sounds are produced in the shoulder-joint, others in 
the fascia or muscle-bands about the scapulae. Since these frictions 
can be felt as well as heard they are mentioned here. Relaxing all 
the muscles, and listening over the shoulder-joint, usually prevents 
our mistaking such sounds for rales or pleural friction. 
7. Local Muscular Spasm 
Pottenger has called attention to the importance of increased 
tension or rigidity in muscular bundles overlying a focus of tubercu- 
losis in the lung. In some cases this is easily appreciated and may 
be of value in diagnosis. 
8. Tender Points upon the Thorax 
In mitral disease, dry pleurisy, necrosis of the rib, and some times 
in phthisis, one finds areas of marked tenderness in different parts of 
the chest. In mitral disease and “effort syndrome” it is the parts 
near the apex impulse that are sore. 
The tenderness in phthisis is most apt to be in the upper and 
front portions of the chest. In neurotic individuals we sometimes 
find a very superficial tenderness over parts of the thorax; in such 
cases pain is produced by very light pressure, but not by firm pressure 
at the same point. 102 
PHYSICAL DIAGNOSIS 
The presence of pulsations in parts-of the chest where normally 
there should be none is suggested by inspection and confirmed by 
palpation. It is not necessary to repeat what was said above *as to 
the commonest causes of such abnormal pulsations. When searching 
for slight, deep-seated pulsation (e.g., from an aortic aneurism), it is 
well to use bimanual palpation, keeping one hand on the front of the 
chest and the other over a corresponding area in the back. 
The temperature and quality of the skin are often brought to 
our attention during palpation. After a little practice one can 
usually judge the temperature within a degree or two simply from 
the feeling of the skin. Any roughness, dryness, or loss of elasticity 
of the skin (myxoedema, diabetes, long-standing pyrexia, or wasting 
disease) is easily appreciated as we pass the hand over the surface of 
the thorax or down the arms. The same manipulation often brings 
to our attention in cases of alcoholism an unusually smooth and satiny 
quality of the cutaneous surface. 
II. The Pulse; Preliminary Study 
Fifty years ago the study of the pulse furnished the physician 
with most of the available evidence regarding the condition of the 
heart. At present this is not the case. With the increase of our 
knowledge of the direct physical examination of the heart and of the; 
various methods of measuring the systolic or diastolic pressure on the 
peripheral arteries, the amount of information furnished exclusively 
by the pulse proportionately decreased, until within the past ten 
years when the researches of Wenckebach, the studies of MacKenzie 
upon the venous pulse, the electrocardiographic work of Einthoven 
have focussed attention anew upon vascular phenomena as a means 
of estimating heart function. 
Despite the more accurate and detailed information to be obtained 
by the newer methods, simple manual palpation of the radial pulse is 
still an important factor in diagnosis, prognosis, and treatment, 
and will remain so, because it gives us quickly, succinctly, and in 
almost every case a great deal of valuable information which it would 
take more time and trouble to obtain in any other way. As we feel 
the pulse, we get at once a fact of central importance in the case; 
by the pulse the steps of our subsequent examination are guided. In 
emergencies or accidents the pulse gives us our bearings and tell us 
whether or not the patient’s condition is one demanding immediate 
succor—e.g., hypodermic stimulation—and whether the outlook is PALPATION AND THE STUDY OF THE PULSE 
103 
bright or dark. To gather this same information in any other way 
would involve losing valuable time. 
Again, when one has to see a large number of patients in a short 
time, as in visiting a hospital ward or on the crowded days of private 
practice, the pulse is an invaluable short cut to some of the most impor- 
tant data. 
Moreover, there are some important inferences which the pulse 
and only the pulse enables us to make. They are not numerous, but 
their value may be great. Delay in one radical pulse when taken in 
connection with other signs may furnish decisive evidence of aneu- 
rism of the aortic arch; arterial degeneration may betray its presence 
chiefly in the peripheral arteries. 
Since, then, direct palpation of the radial pulse furnishes informa- 
tion of crucial importance in a few diseases, and is a quick, reliable, 
and convenient indication of the general condition of the circulation in 
all cases, it is essential that we should study it carefully both in health 
and in disease. 
How to Feel the Pulse 
(a) We usually feel for the pulse in the radial artery because 
this is the most superficial vessel which is readily available. Oc- 
casionally, as when the wrists are swathed in surgical dressings or 
tied up in a straight-jacket, we make use of the temporal, facial, 
or carotid arteries. Hoover believes that the femoral artery is better 
than the radial when one wishes to judge blood pressure, but this 
datum seems to me one that should always be secured by instrumental 
means. In searching for evidence of arterial degeneration the brachial 
arteries should always be palpated. 
(b) Both radials should usually be felt at the same time. By 
making this a routine practice many mistakes are avoided and any 
difference in the two pulses is appreciated. 
(c) The tips of three fingers (never the thumb) should be laid 
upon the artery, and the following points noted: 
1. The rate of the pulse. 
2. The rhythm of the pulse. 
3. The amount of force necessary to obliterate it (compressibility). 
4. The size and shape of the pulse wave. 
5. The size and position of the artery. 
6. The condition of the artery walls. 
Each of these points will now be considered in detail. 104 
PHYSICAL DIAGNOSIS 
1. The Rate of the Pulse 
In the adult male the pulse averages 72 to the minute, in the female 
80. In children it is considerably more frequent. At birth it averages 
about 130, and until the third year it is usually above 100. In some 
families a slow pulse, 60 or less, is hereditary; on the other hand, it 
is not very rare to observe a permanent pulse rate of 90 or more in a 
normal adult (see below, p. 276). Exercise or emotion quickens the 
pulse very markedly, and after food it is somewhat accelerated. 
Some account of the causes of pathological quickening or slowing of 
the pulse will be found on pages 278 and 279. 
2. Rhythm 
The pulse may be irregular in force, in rhythm, or (as most com- 
monly happens) in both respects. As a rule, irregularities in force are 
the more serious, whether occurring as alternation (see page 123) or 
in the absolute type of arrhythmia which is associated with auricular 
fibrillation (see below, p. 119). Intermittence or irregularity in 
rhythm alone (respiratory arrhythmia and premature beats) is much 
less ominous. 
Special types of irregularity will be discussed later in connection 
with the instrumental study of phlebograms and arteriograms. 
In general it may be said (a) that irregularity in the force of the 
pulse beats is a serious sign, if overexertion and temporary toxic 
influences (tobacco, tea, etc.) can be ruled out; (b) that it is far more 
serious when occurring in connection with diseases of the aortic valve 
than in mitral disease; and (c) that it often occurs in connection with 
sclerosis of the coronary arteries and myocardial weakening. 
3. Compressibility, or Systolic Arterial Pressure 
There is no single datum concerning the pulse more important 
than the amount of force needed to obliterate its beat. Until recently 
we have had no more accurate method of measuring the systolic 
blood pressure than that depending on direct digital compression. 
This method seems to me so unreliable that it should be abandoned 
in favor of the instrumental method presently to be described. 
4. The Size and Shape of the Pulse Wave 
Of the use of the sphygmograph for representing pulse waves I 
shall speak later. The points discussed in this section are appre- 
ciable to the fingers. PALPATION AND THE STUDY OF THE PULSE 
105 
I. The size of the pulse wave—the height to which it lifts the finger 
—depends on two factors: 
(a) The force of the cardiac contractions (systolic arterial pressure). 
(b) The tightness or looseness of the artery (tension, or diastolic 
pressure). 
If the arteries are contracted and small, the pulse wave corre- 
sponds, while if they are large and relaxed, it needs only a moderate 
degree of power in the heart to produce a high pulse wave. If the 
tension remains constant the size of the pulse wave depends on the 
force of the heart’s contraction. If the heart power remains con- 
stant, the size of the pulse wave depends on the degree of vascular 
tension. Vascular tension is estimated in ways to be described 
presently, and after allowing for it, we are enabled to estimate 
the power of the heart’s contraction from the height of the pulse 
wave. 
II. The shape of the pulse wave is also of importance. 
(a) It may have a very sharp summit, rising and falling back 
again suddenly; this is known as an ill-sustained pulse or a “Corrigan” 
pulse, and may be due to a lack of sustained propulsive power in the 
contracting heart muscle, to low vascular tension, diminished vascular 
elasticity, or to a combination of the three causes. A weak heart 
with low arterial tension often produces such a pulse wave—decep- 
tively high and giving at first an impression of power in the heart 
wall, but ill sustained and easily compressible. This is the “bounding 
pulse” of early infectious processes. An exaggeration of this type of 
pulse is to be felt in aortic regurgitation (see page 222) and in many 
cases of arteriosclerosis. Thyrotoxicosis also produces it. 
(b) In sharp contrast with the above is the pulse wave which 
lifts the finger gradually and slowly, sustains it for a relatively long 
period, and then sinks gradually down again. Such a pulse with a 
“long plateau” instead of a sharp peak is to be felt most distinctly 
in aortic stenosis, less often in mitral stenosis and other conditions 
(see page 228). 
(c) The dicrotic pulse wave is one in which the secondary wave, 
which the sphygmograph shows to be present in the normal pulse, 
is much exaggerated, so that a distinct “echo” of the primary wave 
is felt after each beat. If the heart is acting rapidly, this dicrotic 
wave does not have time to fall before it is interrupted by the primary 
wave of the next beat, and so appears in the sphygmographic tracing 
as a part of the up-stroke of the primary wave. This is known as the 
11 anacrotic pulse.” 106 
PHYSICAL DIAGNOSIS 
(d) The shape of the high-tension pulse wave will be described 
in the next section. 
5. Tension, or Diastolic Arterial Pressure 
The degree of contraction of the vascular muscles determines 
the size of the artery and (to a great extent) the tension of the blood 
within it. But if the heart is acting feebly, there may be so little 
blood in the arteries that even when tightly contracted they do not 
subject the blood within them to any considerable degree of tension. 
Fig. 84.—Sphygmographic Tracing of Low Tension Pulse. 
To produce high tension, then, we need two factors: a certain degree 
of power in the heart muscle, and contracted arteries. To produce low 
tension we need only relaxation of the arteries, and the heart may be 
either strong or weak. 
Fig. 85.—Sphygmographic Tracing of High Tension Pulse. 
The pulse of low tension collapses between beats, so that the ar- 
tery is less palpable than usual or cannot be felt at all. Normally, 
the artery can just be made out between beats, but any consider- 
able lowering of arterial tension makes it altogether impalpable 
except during the period of the primary wave and of the dicrotic 
wave, which is often very well marked in pulses of low tension. The 
shape of the wave under these conditions has already been described 
(see Fig. 84). 
The pulse of high tension is perceptible between beats as a distinct 
cord which can be rolled between the fingers, like one of the tendons PALPATION AND THE STUDY OF THE PULSE 
107 
of the wrist. It is also difficult to compress in most cases, but this 
may depend rather on the heart’s power than on the degree of vas- 
cular tension. A high-tension pulse is often indistinguishable from 
one stiffened by arteriosclerosis {vide infra). The pulse wave is 
usually of moderate height or low, and falls away slowly with little 
or no dicrotic wave (see Fig. 85). 
6. The Size and Position of the Artery 
I have often known errors to occur because a small artery is mis- 
taken for a small pulse wave. The size of the branches of the arterial 
tree varies a great deal in different individuals of the same weight 
and height, and if the radial is unusually small and a hurried ob- 
servation gives us the impression (true, so far as it goes) that there is 
very little in the way of a pulse to be felt, we are apt to conclude 
(wrongly, perhaps) that the heart’s work is not being properly per- 
formed. The effort to obliterate such a pulse, however, may set us 
right by showing that despite the small size of the vessel (and con- 
sequently of the pulse wave) it takes as much force as it normally 
does to obliterate it. But in many cases we can determine the 
question satisfactorily often by using some instrument for measuring 
arterial pressure. Thus, a small pulse wave (in a congenitally small 
artery) may be distinguished from a weak pulse. From the con- 
tracted artery of high vascular tension we distinguish the congenitally 
small artery because the latter is not to be rolled beneath the fingers, 
and is not more than normally palpable between the pulse beats. 
Blood pressure measurements, however, are the only reliable guide in 
such cases. 
’Not infrequently the nurse reports in alarm that the patient has 
no pulse, when in reality the pulse is excellent but the artery mis- 
placed so as to be impalpable in the ordinary situation. It may be 
simply more deeply set than normal, so that the fingers cannot get 
at it, or it may run superficially over the end of the radius toward 
the “anatomical snuff box.’’ Other anomalies are less common. 
As a rule, the other radial artery is normally placed and can be used 
as a standard, but occasionally both radials are anomalous and we 
may be compelled to use the temporal or facial instead. 
1 ‘ ‘ Arterio-sclerosisl’ is here used to mean any anatomical change in the arterial 
walls that permanently diminishes their elasticity. No single histological entity 
is referred to. 108 
PHYSICAL DIAGNOSIS 
7. The Condition of the Artery Walls 
Arteriosclerosis is manifested in the peripheral arteries, especially 
in the brachial, in the following forms: 
(a) Simple stiffening of the arteries without calcification. 
(b) Tortuosity of the arteries.1 
(c) Calcification. 
Simple stiffening without calcification is due to fibrous thickening 
of the vessel and produces a condition of the arteries not manually 
to be distinguished from high tension. The artery can be rolled under 
the fingers, stands out visibly between the heart’s beats, but is not 
incompressible, has a smooth surface, and is not always tortuous. 
If it is tortuous as well as stiff, we may conclude that there is an 
histological degeneration at any rate, whether or not there is increased 
tension as well. In the majority of cases the two conditions are 
associated and do not need to be distinguished. 
The normal radial artery is straight;1 hence any deviation is 
evidence of changes in its walls and is easily recognized as we run 
our fingers up and down the vessel. 
Calcification of an artery produces usually a beading of its sur- 
face. As we move the fingers along the artery, quickly and with 
very slight pressure, a series of transverse ridges or beads can be 
felt. The qualities of the pulse wave within can usually be appre- 
ciated fairly well, in this type of artery, but in very advanced cases 
the calcification is diffuse and converts the radial into a rigid “pipe 
stem’’—absolutely incompressible—unless we break the calcified 
coat—and easily mistaken for a tendon. In such an artery little or 
no pulse can be felt. 
Such are the points to be noted in a cursory, manual study of the 
pulse. To enumerate the characteristics of the pulse in the many dis- 
eases in which it affords us valuable information is beyond the scope of 
this book. The qualities to be expected in the pulse in connection 
.with the different diseases of the heart are described in the sections on 
those diseases. Here it will suffice to enumerate some of the con- 
ditions in which vascular tension is usually increased or diminished. 
Low tension is produced by moderate exercise, by warmth (e.g., 
a warm bath), by food. Among pathological conditions we may 
mention diarrhoea, Addison’s disease, pernicious anasmia, many in- 
fectious fevers and debilitated states. 
1 Tortuosity in the temporal artery, however, is normal. PALPATION AND THE STUDY OF THE PULSE 
109 
Temporary high tension is produced by exercise and emotion; also 
by cold (e.g., cold bathing, malarial chills). Vascular tension is almost 
always high in toxaemias of pregnancy during and before eclamptic 
spasms and parturition. 
Increase of intracranial pressure (as by cerebral hemorrhage or 
trauma) has a similar but more lasting effect. 
Permanent high tension is due to subacute or chronic nephritis, to 
arterio-sclerosis or to unknown causes (Allbutt’s “ Hyperpiesia). 
In valvular heart disease without nephritis or arterio-sclerosis 
the tension is usually normal or slightly lowered. 
III. Arterial Pressure and the Instruments for Measuring It 
Within the past decade a number of instruments have come into 
use, the object of which is to tell us with some approach to accuracy 
Fig. 86.—Mercer’s Type oi Riva-Rocci Sphygmomanometer, 
the lateral pressure in the peripheral arteries. We have long attempted 
to estimate this pressure, by simple digital compression and palpation, 
but today it is recognized universally that digital methods are wholly 110 
PHYSICAL DIAGNOSIS 
unreliable and that only by instrumental methods can we measure 
arterial tension and so estimate the heart’s power. 
Here as elsewhere in this book I shall describe only such instruments 
and methods as seem to me the best. I shall not attempt to cover the 
whole field or to conceal such personal preferences as are based on 
experience. 
For clinical work instruments of the Riva-Rocci type have now 
displaced all others in this country) e.g., Nicholson’s or the Bauman- 
Fig. 87.—Nicholson’s Type of Riva-Rocci Sphygmomanometer. 
ometer). There are many variations and types all essentially the 
same and all good so long as a mercury column is their basis. Despite 
the inconveniences of transporting a mercury column, it remains the 
most reliable method. Instrument of any other type (e.g., those 
using springs to measure pressure) are always getting out of order 
and have to be constantly standardized by comparison with the 
mercury column. 
All instruments of the Riva-Rocci type consist essentially of an 
inflatable rubber armlet, so arranged that it can be fitted closely 
around the upper arm, a mercury manometer of the ordinary type, PALPATION AND THE STUDY OF THE PULSE 
111 
and an air-pump (see Figs. 86 and 87). The air forced from the pump 
is distributed into the rubber armlet and into the manometer at the 
same time, and experiments have shown that the actual pressure in the 
armlet is practically identical at any given time with that in the 
manometer. 
1. Measurement of Systolic Pressure 
(a) Palpatory Method 
Pump in air until the radial pulse stops, and at that instant note 
the height of the mercury column. The reading thus obtained is 
taken to represent the systolic or maximum pressure in the brachial 
artery. To raise the mercury column slightly above the point at 
which the pulse stops, then let the column slowly fall and note the 
point on the scale at which we feel the return of the pulse, is easier 
and no less accurate than to fix the point at which the pulse first 
disappears. This method is inferior to the auscultatory method 
described below. 
It is true that the air within the rubber armlet has to overcome not 
only the pressure within the radial artery, but the resistance of the 
artery wall and the elasticity of the soft parts around it. The former 
factor has been shown to represent a pressure of not more than 2 or 
3 mm. Hg, provided the artery walls are normal. If arteriosclerosis 
is present, it has been estimated by Herringham that the artery may 
oppose a resistance of 15 to 20 mm. Hg. The more carefully conducted 
experiments of Janeway, however, convince me that Herringham is 
wrong and that sclerosed arteries offer a direct resistance of less than 5 
mm. Hg. The amount of error thus introduced is not of importance. 
The resistance of the soft parts around the artery is a factor of no 
A huge arm gives no higher reading than a shrivelled one, as has been 
shown by Janewav in a patient one of whose arms was congenitally 
atrophied while the other was enormous. 
(b) Auscultatory Method 
A better way to measure systolic pressure is by listening with the 
stethoscope over the brachial artery just peripheral to the cuff, and 
noting when the tapping systolic sound disappears, or better when it 
first reappears as the mercury falls. 112 
PHYSICAL DIAGNOSIS 
2. Measurement of Diastolic Pressure 
The auscultatory method (Korotkoff) just described is especially 
useful in the measurement of diastolic or minimum blood-pressure. 
The air is allowed gradually to leak out of the cuff and, as the mercury 
column descends, one listens with the stethoscope just below the cuff. 
The sharp systolic sound reappears, (record systolic pressure) becomes 
loud, and remains so until we reach a point 30-90 mm. below the sys- 
tolic reading. Then the sound suddenly changes from a sharp tap to a 
dull, feeble thud. The height of the mercury column at the instant 
when this change appears is best taken as the diastolic pressure. At a 
point 5 to 10 mm. of mercury below this, the arterial sound disappears 
altogether and some use this disappearance point to represent the 
diastolic pressure. The sudden-weakening point is, however, more 
accurate. 
3. Normal Readings 
With any of the various types of Riva-Rocci instrument, the aver- 
age readings in healthy adults are approximately as follows: Systolic, 
110-13 5 mm. Hg. Diastolic, 60-90 mm. Hg. 
The “pulse pressure,’’ i.e., the difference between any individual’s 
systolic and diastolic pressure, averages 30-60 mm. Hg. 
In women systolic pressure runs about 10 mm. lower than in men. 
Children under 2 years 75-90 mm. In older children, 90-110 mm. 
Excitement or exercise raises the pressure temporarily but considerably. It 
is 5-10 mm. lower in recumbency than in the sitting position. 
4. The Use of the Data Obtained by these Instruments 
Whenever it is important for us to know the tension of the per- 
ipheral arteries, a sphygmomanometer is indispensable. The Riva- 
Rocci instrument as modified by Nicholson and others has now 
secured a firm position in the routine work of good clinicians all over 
this country. 
(a) High Systolic Blood-pressure 
Slight increase of systolic blood-pressure is (fortunately for our 
diagnosis) rarely encountered. As a rule if we find blood pressure 
high it is very high, obviously high, 160-250 mm. Hg., and not in 
the more dubious immediate regions (140-160). In at least 95 per 
cent, of the cases a permanent or long standing hypertension is associ- ARTERIAL PRESSURE 
113 
ated with obvious hypertrophy of the heart and due to all the well 
known causes of cardiac hypertrophy except rheumatic endocarditis with 
valve lesions. Accordingly the types of high systolic blood pressure 
are those due to: 
1. Unknown cause (Allbutt's “Hyper piesia"). 
2. Chronic nephritis.l 
3. Arteriosclerosis.2 
4. Syphilitic aortitis with aortic regurgitation. 
5. Thyrotoxicosis (Graves’ disease). 
Less important are the transitory effects of puerperal autointoxi- 
cation, of acute brain-pressure as in apoplexy, skull fractures, and 
meningitis; also of acute pain (as in gout, tabetic crises, lead colic, 
biliary colic and during child birth). 
Clinically it is easy to exclude in most cases all the causes of 
hypertension just listed except three: “primary ” or toxic hypertension 
(Allbutt), chronic nephritis, and arteriosclerosis. Hence vascular hyper- 
tension and high blood-pressure should always make us suspect these dis- 
eases even though the urine and the peripheral arteries give no convincing 
sign of them. 
We may thus detect in life insurance examinations and elsewhere 
many cases that would otherwise pass altogether unnoticed. On the 
other hand the negative value of a normal blood-pressure is very great. 
It helps us to exclude chronic nephritis in the vast majority of cases, 
and except in the aged raises a presumption against the existence of 
arterio-sclerosis. 
(b) Low Systolic Blood-pressure 
Much less valuable in diagnosis are the abnormally low blood- 
pressure readings. We seldom get much help from them. The 
lowest readings occur in Addison’s disease (even to 50 mm.), after 
haemorrhage, infectious fevers (tuberculosis, pneumonia, typhoid) 
and surgical “shock.” Occasionally attacks of faintness, vertigo, 
headache and muscular debility are associated (especially in young 
adults) with a hypotension of unknown origin. 
1 i.e., any nephritis of more than a few weeks duration. 
2 Especially if the thoracic, aortic and splanchnic arteries are extensively 
diseased. 114 
PHYSICAL DIAGNOSIS 
(c) Diastolic Pressure 
The conclusions about the strength of the heart muscle recently 
drawn by several writers from formulas based on pulse pressure and 
its relations to systolic and diastolic pressure seem to me to rest on 
quite uncertain theoretic foundations. They are not verified by 
clinical observation or by autopsy results. 
Diastolic pressure should be measured in every case showing high 
systolic pressure, and when we have learned the technique it is about 
as easy to measure both systolic and diastolic pressure by the auscul- 
tatory method and in every case. The high systolic pressures of 
aortic regurgitation is rendered relatively unimportant by the corre- 
spondingly depressed diastolic pressure. The same is true in many 
cases of arterio-sclerosis and hyperthyroidism. 
High systolic pressures as measured in office patients or in any 
anxious or excited person are often temporary and significant of 
nothing except the patient’s state of mind. But the particular value of 
measuring diastolic pressure is that it is influenced little or not at all 
by emotional states and remains low even when the systolic pressure 
is raised by emotion to 140 or even higher. 
Moreover in some cases of pathological and serious hypertension 
it is chiefly the diastolic pressure that is elevated, e.g., systolic only 160 
■—diastolic 120. 
On the whole, then, diastolic pressure is decidedly more important 
than systolic pressure in diagnosis. A permanently high diastolic 
pressure (over 100 mm. Hg.) is almost always due to nephritis, 
arteriosclerosis or hyperpiesia, while a permanently or temporarily high 
systolic pressure (140-160) may mean very little. 
Systolic pressures above 160 are usually associated by high diasto- 
lic pressures. Aortic regurgitation is the only exception of importance, 
though in thyrotoxicosis and arteriosclerosis we may find the 
same thing. CHAPTER VI 
CARDIAC PHYSIOLOGY AND PATHOLOGY AS RE- 
VEALED BY ARTERIOGRAMS, PIILEBOGRAMS, 
AND ELECTROCARDIOGRAMS 
In the early editions of this book I referred to the sphygmograph 
as a fascinating but useless little toy. As an instrument for recording 
the shape of pulse waves it went out of use, because it was hopelessly 
unreliable. To record the time relations of the pulse waves it has 
come back into use, so that Lewis, one of the most distinguished 
investigators in the field of phlebographic and electrocardiographic 
work, is able to state, in his recent monograph1 that “the mechanism 
of the heart may be identified in the majority of cases in which it is 
irregular by a careful examination of the radial pulse tracing alone.” 
We may come back to the sphygmograph and to the results 
obtained through it, and, interpreting our old data in the light of newer 
researches, we may be able to read far deeper and more intelligible 
meanings into them. But whether this is true or not I feel convinced 
by my own experience with tracings of the venous pulse and by my 
study of other’s work with electrocardiograms that neither method 
is likely ever to be used by the practitioner for whom this book is 
intended. I desire therefore, in this chapter, to state the results 
accomplished by the newer methods without attempting to describe or 
recommend the technique. 
The advances achieved through phlebographic and electrocardio- 
graphic work may be summed in a classification of the arrhythmias 
or better as a new grouping of the disturbances in the heart beat. 
1. Heart block, partial or total. 
2. Auricular fibrillation and absolute irregularity of the pulse. 
3. Paroxysmal tachycardia and auricular flutter. 
4. Premature contraction of auricle or ventricle. 
5. Alternation. 
Paul D. White’s article in the Amer. Journ. Med. Sc., June, 1915, 
gives us an interesting statistical picture of these disturbances and 
serves as a table of contents, a classification and rough estimate of 
1 Thomas Lewis: “The Mechanism of the Heart Beat,” Shaw & Sons, London, 
1911, a work to which I am profoundly indebted. 
115 116 
PHYSICAL DIAGNOSIS 
the size of each class. At the end of eight months work at the Mass. 
General Hospital, White’s results could be compressed into the 
following table. 
Disturbances of the Heart Beat Found in 300 Cases of Cardio-vascular 
Disease (Paul D. White) 
1. (a) Ventricular premature beats in 119 cases. 
(b) Auricular premature beats in 22 cases. 
2. Auricular fibrillation in 71 cases. 
3. Alternation in 71 cases. 
4. Delayed conduction and heart block in 22 cases. 
5. Paroxysmal tachycardia 9 cases. 
Auricular flutter 6 cases. 
6. Sinus arrhythmia (Disturbances of im- 
pulse production). No records kept. 
Blashford & Willis (Arch, of Int. Med., Jan., 1918), found: In 3500 electro- 
cardiograms 
1. Auricular fibrillation 363 cases. 
2. Ventricular premature beats 316 cases. 
3. Auricular premature beats 160 cases. 
4. Paroxysmal tachycardia 5 cases. 
5. Auricular flutter 9 cases. 
The meaning of these terms will next be explained, though the order of numer- 
ical frequency will no longer be followed. 
I. Heart Block 
In the normal heart the impulse of contraction starts at the sino- 
auricular node, a mass of specialized muscular tissue at the superior 
cavo-auricular junction, spreads through the bundle of His in the mem- 
branous interventricular septum, and is distributed thence through 
the Purkinje fibres to the ventricles and their papillary muscles. Since 
the sino-auricular node just mentioned is apparently responsible 
for the organization of beat after beat, and determines the rate of 
the heart, it is now often spoken of as “the pace-maker.” 
If the transmission of impulses is blocked by disease in the bundle 
of His (usually gumma or fibro-calcareous degeneration), we get the 
following series of disasters, each worse than the last: 
(a) A prolongation of the interval between auricular systole and 
ventricular systole (“the A-s—V-s interval,” normaly from .1 to .2 
of a second) to twice or thrice its normal length. 
(b) “Dropped beats,” i.e., an occasional “silence" of the ventricle 
in answer to the regular auricular contraction preceding it. ARTERIOGRAMS, PHLEBOGRAMS, AND ELECTROCARDIOGRAMS 
117 
(c) Regularly recurring “dropped beats’’ every tenth beat or 
oftener. 
(d) The establishment of a 3 :i or 2 :i rhythm i.e., three or two beats 
of the auricle for every beat of the ventricle. 
(e) Complete dissociation of auricle and ventricle. No impulses 
pass down. The ventricle may stand still for good and all or may 
gradually initiate a slow rhythm of its own (approximately 32 per 
minute). 
If the ventricular silence lasts three to five seconds the patient 
usually loses consciousness for a moment. Silence of ten to twenty 
seconds usually results in epileptiform convulsions. When these 
cerebral phenomena are associated with more or less heart block we 
have the Stokes-Adams syndrome. Silence over ninety seconds means 
death. (Lewis, loc. cit., p. 266.) 
Heart block in slight grades (see (a) above) is often a result of 
“rheumatic” infection of the heart, especially (as Mackenzie and 
Lewis have shown) in cases of mitral stenosis. Lewis found an A-s—- 
V-s interval of over .2 seconds in nearly 17 per cent, of 84 cases of 
comparatively well-compensated out-patient cases of mitral stenosis. 
In ward patients it is one of the rarest types of arrhythmia. In 
White’s series it was found but 22 times among 300 cases of cardio- 
vascular disease. 
When the A-s—V-s interval is already increased, the act of swallow- 
ing, pressure on the vagus in the neck or the administration of digitalis 
may increase the grade of heartblock, and may lead to a 2:1 to 3:1 
rhythm, or to complete dissociation of auricle and ventricle, always a 
very serious condition. 
To diagnose heart block we need electrocardiograms or venous 
pulse tracings made synchronously with arterial pulse tracings, so that 
the time relation of auricular contraction (shown in the neck veins) to 
ventricular contraction (shown in the carotid or radial artery) can be 
demonstrated. Mackenzie’s polygraph records upon the same strip 
of paper the movements of the auricle (neck vein), of the ventricle 
(radial pulse or carotid), and of a time marker from which we can 
calculate very exactly any delay in the passage of the contraction wave 
from auricle to ventricle. Sometimes we can see in the neck or hear 
with the stethoscope1 something corresponding to the auricle move- 
1 Stokes noted that the dropped beats (auricular movements) in heart block 
produced “small sounds which may give the illusion of reduplication of either 
sound.” Hirschfelder describes them as “very soft distant sounds like the ticking 
of a watch” and “best heard along the left sternal margin.” 118 
PHYSICAL DIAGNOSIS 
ments, and, comparing these facts with the palpable radial impulse, 
may recognize the severer grades of heart block, but no certainty 
can be obtained without the use of venous pulse tracings or electro- 
cardiograms. In the latter we have a record of the electrical changes 
corresponding to the earliest contraction wave in the auricles and in 
the ventricles respectively—the two waves recorded in the same 
tracing so that no time comparisons or measurements of different 
curves are necessary. 
Luckily for those who cannot get the time and money necessary 
for the use of these methods, there are relatively few cases in which it 
is imperatively necessary for any purpose of diagnosis, prognosis, or 
treatment that we should recognize heart block. Were it a commoner 
or a more curable condition the general practitioner would sometimes 
be at a great disadvantage. As it is, we can often recognize and treat 
the disease underlying heart block with about the same measure of success 
whether the heart block itself escapes us or not; but in heart block 
itself there is sometimes effective treatment by thyroid extract, which 
tends to decrease the grade of block and increases the idio-ventricular 
rate. 
In 3219 cases electrocardiographed at the Massachusetts General 
Hospital between October 21, 1914 and March 15, 1922, the following 
figures were obtained by Paul D. White: 
Cases 
Per 
Cent. 
Auriculoventricular block, 
Complete 
Partial 
2? 
129 
156 
0.8 
4.0 
4.8 
Intraventricular block, 
Bundle branch 
Lesser degree (“aberration”) 
41 
89 
130 
I .2 
2.8 
4.0 
All cases showing auriculoventricular or intra- 
ventricular block 
‘ ‘ Sinoauricular block ” 
252 
11 
7.8 
0-3 
Dr. White adds the following definitions: 
Complete auriculoventricular block consists of complete dissociation 
between the auricular and ventricular contractions, with an idio- 
ventricular rate of sixty or less. 
Partial auriculoventricular block consists of partial dissociation 
between the auricular and ventricular activity, in which the P-R 
interval is abnormally long (.2 second or over in this series), or in which ARTERIOGRAMS, PHLEBOGRAMS, AND ELECTROCARDIOGRAMS 
119 
there are dropped beats, and where ventricular escape is not primarily 
the cause of the dissociation. 
Intraventricular block is the expression used for delay or blocking in 
the arborizations of the auriculoventricular conduction system below 
the bifurcation of the bundle of His. 
“ Sinoauricular block ” is that condition of the cardiac mechanism 
in which the sinoauricular node fails to function either at intervals or 
continuously. 
In White’s opinion intraventricular block is of greater significance 
than auriculoventricular block. To detect the former one needs 
the electrocardiograph.1 
II. Auricular Fibrillation 
The researches of Mackenzie in 1904-5 brought out the fact that 
when a heart is absolutely and perpetually irregular, i.e., when no 
two successive beats have the same duration (as shown by a radial 
pulse tracing), the venous pulse tracing shows no sign of the normal 
auricular wave, but corresponds with the ventricular systole. This 
was thought at first to be due to auricular paralysis, but further 
electrocardiographic research has brought convincing evidence that 
the auricle is in fact fibrillating, i.e., the seat of innumerable, incoor- 
dinate contractions, each limited to a small bundle of muscle fibres. 
The fibrillating auricle is quite ineffectual and remains in the diastolic 
position. This condition has long been familiar in animal experimen- 
tation, but has not until the last few years been capable of recognition 
in man. 
Though venous pulse tracings and electrocardiographic records 
are necessary for the absolute demonstration of auricular fibrillation 
in any case, the presence of an absolutely irregular pulse (delirium 
cordis) is practically equivalent to proof of auricular fibrillation. 
The exceptions to this rule are negligible. Since the auricles are of 
use chiefly as temporary reservoirs, the circulation can and does go 
on for months and years despite the absence of any effectual con- 
traction of the auricle. The ventricle and the peripheral arteries do 
the work, while the quivering, distended auricle showers impulses at 
the upper end of His’ bundle. “From this turmoil of the auricle a 
rapid and haphazard succession of waves escapes”2 along the bundle 
and produces the absolutely irregular pulse. 
1 Paul D. White: Observations on Heart Block, in Transactions of the Associa- 
tion of American Physicians, 1922. 
2 Lewis, loc. cit., p. 247. 120 
PHYSICAL DIAGNOSIS 
Auricular fibrillation thus defined produces the great majority of 
all the arrhythmias clinically observed in the failing heart. The 
irregular pulse of most cases of rheumatic endocarditis and of myo- 
cardial insufficiency (the familiar arteriosclerotic or cardiorenal 
types) is of this kind. 
Auricular fibrillation usually lasts as long as the period of failing 
compensation which it accompanies. But the auricles may go on 
fibrillating even after compensation is restored. 
Occasionally short flights of fibrillation occur with normal rhythm 
before and after them (“paroxysmal fibrillation”). 
III. Paroxysmal Tachycardia 
Excluding the periods of accelerated heart action due to emotional 
strain, muscular exertion and infectious disease, we have but one 
condition in which the heart suddenly becomes rapid, without irregu- 
larity and without previous evidence of cardiac disease. This con- 
dition, long known as paroxysmal tachycardia, has been illuminated 
by recent researches. It is a relatively rare condition, occurring nine 
times among 300 cases investigated by White (see table, p. 116). 
We now know, through electrocardiographic investigations, that while 
in the vast majority of these tachycardias the cardiac impulse comes 
down from the auricle in the ordinary way, it does not arise at the 
ordinary place, i.e., at the pace-maker, but starts up like an insurrec- 
tion at some other point in the auricular muscle (“heterogeneous 
impulses ”). Rarely does such a tachycardia originate in the ventricle 
or in the bundle of His. The present condition of our knowledge 
is fairly represented by the diagram from Lewis {loc. cit., p. 191) 
reproduced on page 122. 
This diagram suggests the “close relation” of paroxysmal tachy- 
cardia to the more serious auricular fibrillation just described and 
to the commoner and less serious forms of arrhythmia due to premature 
beats. 
Histologically nothing definite is known about the cause of par- 
oxysmal tachycardia. 
1. Auricular Flutter 
When the auricular rate rises above 200 but remains regular, 
while the ventricle beats at a slower rate (usually }/£) owing to heart 
block, the term flutter is arbitrarily applied. It occurs in cases of 
toxic goitre and of mitral stenosis or other “rheumatic” forms of ARTERIOGRAMS, PHLEBOGRAMS, AND ELECTROCARDIOGRAMS 
121 
heart disease. It may occur despite good compensation and is not 
in itself of much importance. Its import depends on what else is 
wrong with the heart. Chronic cases may be cured by large doses 
of digitalis. 
IV. Premature Beats (Extrasystoles) 
i. Ventricular—Of all disturbances of rhythm (excluding the 
semi-physiological sinus arrhythmia) ventricular premature beats 
are the commonest. Paul White1 found them in 119 out of 300 cases 
of cardiac disease examined within eight months at the Mass. General 
Hospital. In the decompensated cases it is relatively rare (10 per 
cent.) compared to fibrillation and alternation. Like many of the 
newly discovered cardiac anomalies, ventricular escape is comparable 
to insubordination or civil war in the heart. It is recognized: 
(a) In part by the fact that the pause following it in the arterio- 
gram is “compensatory, ” i.e., just makes up for the shortening of the 
pause before the premature beat. 
(b) Because such premature beats are usually weak and barely 
palpable at the wrist, while the succeeding beat is unusually strong— 
another form of compensation. 
(c) By auscultation; the second sound is often found to be absent, 
only the first sound is heard. 
The ventricular origin of the contraction is shown by the fact that 
the venous curve from the jugular exhibits a regular uninterrupted 
rhythm of auricular waves in the tracing. 
2. Auricular.—Premature contractions arising in the auricle and 
leading to a similarly premature ventricular beat are less commonly 
seen than “ventricular extrasystoles.” In White’s series there were 
but 22 cases as compared with 119 of the ventricular type. The 
pause following such a beat may be compensatory in the sense ex- 
plained above, but usually it is not so. 
The electrocardiogram shows that these abnormal beats do not 
arise at the pace-maker, but from some other part of the auricle— 
another example of cardiac civil war or uncoordinated independent 
action by a portion of the heart muscle. In the same way the ven- 
tricular extrasystoles are shown to arise from some abnormally active 
bit of ventricular muscle. 
3. The clinical significance of premature beats is not yet clear. 
Mackenzie believes that they have little or no importance either in 
1 Paul D. White: Alternation: Am. Journ. of Med. Sciences, June, 1915. 122 
PHYSICAL DIAGNOSIS 
SINUS 
AURICLE 
A-V JUNCTION 
VENTRICLE 
SINUS 
AURICLE 
A-V JUNCTION 
VENTRICLE 
SINUS 
AURICLE 
A-V JUNCTION 
VENTRICLE 
I. Occasional premature beats (“auricular extrasystoles’’). Indicated in red. 
II. A short period of paroxysmal tachycardia. Indicated in red. 
III. Absolute arrhythmia (auricular fibrillation). 
Lewis’ experiments indicate that these three disturbances represent three increasing 
degrees of typical impulse-formation, “all stages of one or the same process’’ of disorder 
or civil war in the heart muscle. 
Fig. 88.— (After Lewis.) ARTERIOGRAMS, PHLEBOGRAMS, AND ELECTROCARDIOGRAMS 
123 
diagnosis or prognosis. In many cases they certainly represent one 
of the mildest and most harmless types of arrhythmia, but whether 
this is always true is not yet clear. Their significance probably de- 
pends on the associated anomalies discoverable in the circulation. If 
the heart is sound in every other respect, premature beats have no 
considerable importance. If, however, hypertension or valvular 
lesions are also present the “extrasvstole” may be an early sign of 
failing compensation. 
V. Coupling of the Heart Beats 
In uncompensated heart disease of any type, when the auricle is 
fibrillating, coupling of the ventricular beats often follows the ad- 
ministration of digitalis. Indeed, in the vast majority of cases we 
can assume that the patient has recently been taking digitalis if we 
find the beats coming in close-knit pairs with pauses of varying 
lengths between the pairs. Other types of coupling also occur, but 
will not be mentioned here. 
1. Alternation 
In the healthy but overtaxed and rapidly beating heart, in many 
cases of paroxysmal tachycardia, and in the myocardial insufficiency 
Fig. 89.—Radial Tracing in a Case of Alternation. (Paul D. White.) 
of the senile heart, one may find a regular alternation of strong and 
weak beats with or without a disturbance of rhythm. An auricular 
beat precedes each ventricular beat in normal fashion. 
The weak beat appears in the arteriogram (see Fig. 89). It may 
also be noticed while taking the blood-pressure by the auscultatory 
method: as one slowly lets the mercury column fall one may suddenly 
begin to hear a doubled rate in the tapping sounds, as the smaller 
waves begin to come through. Thereafter for a few beats one may 
hear that every other beat is accented. 124 
PHYSICAL DIAGNOSIS 
When permanent, alternation is always a serious symptom and 
means that “the heart muscle is in a precarious condition, be it 
structural or functional.” (Lewis, loc. cit., p. 278.) 
Immediately following a premature beat, a few alternating beats 
may often be recognized, as has recently been shown by Paul White. 
In these cases alternation is not always of serious import. White’s 
studies revealed 71 cases of alternation among 300 patients with 
cardiovascular disease. But in 79 per cent, the alternation was 
inconstant and occurred only for a few beats following premature 
contractions. Only in 15 out of 71 cases (21 per cent.) was the alter- 
nation constant, and so ominous. 
VI. Sinus Arrhythmia 
I include here, for convenience, a cardiac irregularity which is not 
pathological. It is supposedly due to change in vagal tone and is 
present in some degree in most sound young adults and many older 
people. The cardiac contractions take place in the normal way, 
but their rate waxes and wanes—usually quickening with inspiration 
and slowing with expiration, occasionally without any such connection. 
VII. Ventricular Preponderance 
Besides the arrhythmias and defects of contraction, an excessive 
contractile force either of the left ventricle or of the right appears in 
some of the electrocardiograms. This tells us which ventricle is the 
larger and so helps in some doubtful diagnoses. For instance, between 
mitral stenosis and goitre heart, right sided predominance in the elec- 
trocardiogram favors stenosis. CHAPTER VII 
PERCUSSION 
i. Technique 
There is no other method of physical examination which needs 
so much practice as percussion, and none that is so seldom thor- 
oughly learned. Many physicians never succeed in acquiring a 
facility in the use of it sufficient to make them rely upon their results. 
Undoubtedly one of the greatest difficulties arises from the necessity 
of being at once active and passive—-at once the percussor and the 
one who listens to the percussion. Students half unconsciously get 
to treat the percussion as an end in itself, and hammer away indus- 
triously without realizing that two-thirds of the attention must be 
given to listening, while the percussion itself should become semi- 
automatic. 
It is undoubtedly an advantage to possess a musical ear, but this 
is by no means a necessity. Some of the most accurate percussors 
that I know possess absolutely no musical ear—no ear, that is, for 
pitch—-and form their judgments in percussing upon the quality or 
intensity of the note, and upon the sense of resistance. 
In this country practically all percussion is done with the fingers; 
in Europe instruments are still used to a considerable extent. 
i. Mediate and Immediate Percussion 
Percussion may be either “mediate” or “immediate,” the lat- 
ter term referring to blows struck directly upon the chest with the 
flat of the hand, or upon the clavicles with the tip of the second 
finger. 
(a) Methods 
Mediate percussion (which is used ninety-nine hundredths of the 
time) is performed as follows: 
The patient should either lie down or sit with his back against 
some support. The reason of this is that for good percussion one 
125 126 
PHYSICAL DIAGNOSIS 
needs to press very firmly with the middle finger of the left hand 
upon the surface of the chest, so firmly that if the patient is sitting 
upon a stool without support for his back, it will need considerable 
exertion upon his part to avoid losing his balance. 
In percussing the front of the chest it is important to have the 
patient sitting or lying in a symmetrical position—that is, without any 
twist or tilting to one side. His head should point straight forward 
Fig. 90.—Position of the Hands When Percussing the Right Apex. 
and his muscles must be thoroughly relaxed. Many patients, when 
stripped for examination, swell out their chests and sit up with a 
military erectness. The muscular tension thus produced modifies 
the percussion note and causes an embarrassing multitude of muscle 
sounds which greatly disturb auscultation. Some muscular tensions 
which produce dulness are probably due to reflex stimulation from 
disease within the chest and cannot be voluntarily relaxed. PERCUSSION 
127 
Fig. 91.—Position of the Hands When Percussing the Left Apex. 
Fig. 92.—The Right Way to Percuss—i.e., From the Wrist. 128 
PHYSICAL DIAGNOSIS 
Having placed the patient in an easy and symmetrical position, 
our percussion should proceed according to the following rules: 
(1) Always, press as firmly as possible upon the surface of the 
chest with the second finger of the left hand1 on the dorsum of which 
Fig. 93.—The Wrong Way to Percuss—i.e.. From the Elbow. 
the blow is to be struck. Raise the other fingers of the left hand from 
the chest so as not to interfere with its vibrations. 
(2) Strike a quick, perpendicular, rebounding blow with the tip 
of the second finger2 of the right hand upon the second finger of the 
left just behind the nail, imitating as far as possible with the right 
hand the action of a piano-hammer. The quicker the percussing 
finger gets away again after striking, the clearer will be the note 
obtained. 
1 Left-handed percussors will, of course, keep the right hand upon the chest and 
strike with the left. 
2 When percussing the right apex I prefer to strike upon the thumb (see Figs. 96 
and 97) as it is almost impossible when standing directly in front of the patient to 
fit any of the fingers comfortably into the right supraclavicular fossa. PERCUSSION 
129 
(3) Let all the blows struck in any one part of the chest be uniform 
in force. 
(4) Strike from the wrist and not from the elbow (see Figs. 92 
and 93). The wrist must be held perfectly loose. 
(5) Keep the percussing finger bent at a right angle as in Fig. 94. 
The force to be used in percussion depends upon the purpose 
for which the percussion is used—that is, upon what organ we are 
percussing—and also upon the thickness of the muscles covering 
Fig. 94.—Proper Position of the Right Hand During Percussion, 
that part of the chest. For example, it is necessary to percuss very 
strongly when examining the back of a muscular man, where an 
inch or two of muscle intervenes between the finger on which we 
strike and the lung from which we desire to elicit a sound. Over 
the front of the chest and in the axillae the muscular covering is, much 
thinner, and hence a lighter blow sufficies. In children or emaciated 
patients, or in any case in which the muscular development is slight, 
percussion should be as light as is sufficient to elicit a clear sound. 
Heavy percussion is sometimes necessary but always unsatisfactory, 
in that the sound which it elicits comes from a relatively large area 130 
PHYSICAL DIAGNOSIS 
of the chest and does not therefore give us information about the condi- 
tion of any sharply localized area. If a carpenter, in tapping the wall 
to find the position of the studs, strikes too hard, he will fail to find the 
beam, because the blow delivered over the spot behind which the beam 
is situated is so forcible as to bring out the resonance of .the hollow 
parts around. It is the same with medical percussion. Heavy percus- 
sion is always inaccurate. It may be necessary where the muscles 
Fig. 95.—Proper Position of the Patient During Percussion of the Back. 
are very thick, but its value is then proportionately diminished. On 
the other hand, it is possible to strike so lightly that no recognizable 
sound is elicited at all. The best percussion, therefore, is that which is 
just forcible enough to elicit a clear sound without setting a large area 
of chest wall in vibration. 
When we desire to percuss the back, it is important to get the 
scapulas out of the way as far as possible. To accomplish this, we 
put the patient in the position shown in Fig. 95, the arms crossed 
upon the chest. This position sometimes produces crackling or 
grazing sounds transmitted from the shoulder-joint or from the taut 
muscle-bands. In case of doubt the hands should be dropped loosely 
at the sides (F. T. Lord). The patient should be made to bend for- PERCUSSION 
131 
ward; otherwise the left hand of the percussor will be uncomfortably 
bent backward and his attention thereby distracted (see Fig. 96). 
When the axillag are to be percussed, the patient should put the 
hands upon the top of the head. 
2. Auscultatory Percussion 
If while percussing one auscults at the same time, letting the 
chest piece of the stethoscope rest upon the chest, or getting the 
patient or an assistant to hold it there, the sounds produced by 
Fig. 96.—Wrong Position for Percussing the Back. The patient should be bent 
forward.' 
percussion are greatly intensified, and changes in their volume, pitch, 
or quality are very readily appreciated. The blows must be very 
lightly struck, either upon the chest itself or upon the finger used as a 
pleximeter in the ordinary way. Some observers use a short stroking 
or scratching touch upon the chest itself without employing any 
pleximeter. • • '• nm-Vdo 132 
PHYSICAL DIAGNOSIS 
This method is used especially in attempting to map out the 
borders of the heart and in marking the outlines of the stomach. 
In the hands of skilled observers it often yields valuable results, 
but one source of error must be especially guarded against. The 
line along which we percuss, when approaching an organ whose bor- 
ders we desire to mark out, must neither approach the chest piece of 
the stethoscope nor recede from it. In other words, the line along 
which we percuss must always describe a segment of a circle whose 
Percussion arc 
Chest piece of 
Stethoscope. 
Fig. 97.—Auscultatory Percussion, Showing the Arc along which such Percussion should 
be made. 
centre is the chest piece of the stethoscope (see Fig. 97). If we 
percuss, as we ordinarily do, in straight lines toward or away from the 
border of an organ, our results are wholly unreliable since every 
straight line must bring the point percussed either closer to the stetho- 
scope or farther from it, and the intensity and quality of the sounds 
conducted through the instrument to our ears vary directly with its 
distance from the point percussed. 
It will be readily seen that the usefulness of auscultatory per- 
cussion is limited by this source of error, and that considerable practice 
is necessary before one can get the best results from this method. 
Nevertheless it has, I believe, a place, though not an important 
one, among serviceable methods of physical examination. 
3. Palpatory Percussion 
Some German observers use a method of percussion in which 
attention is fixed directly or primarily on the amount of resistance 
offered by the tissues over which percussion is made. Even in or- PERCUSSION 
133 
dinary percussion the amount of resistance is always noted by expe- 
rienced percussors, but the element in sound is usually the main 
object of attention. Palpatory percussion is rather a series of short 
pushes against various points on the chest wall, but some sound is 
elicited and probably enters into the rather complex judgment which 
follows. 
Normal dulness of 
the right apex. 
Deep cardiac 
dulness. 
Superficial cardiac 
dulness. 
Liver dulness 
Liver flatness 
Traube’s semilunar 
•tympanitic space. 
Fig. 98.—Percussion Outlines in the Normal Chest 
In this country palpatory percussion is but little employed. 
Some physicians use a bit of flexible rubber for direct percussion, 
but I have seen no advantage gained by it. 
II. Percussion Resonance of the Normal Chest 
The note obtained by percussing the normal chest varies a great 
deal in different areas. In Fig. 98, the parts shaded darkest are 
those that normally give least sound when percussed in the manner 
described above, while from the lightest areas the loudest and clear- 
est sound may be elicited. 
i. Vesicular Resonance 
The sound elicited in the latter areas is known as normal or 
“ vesicular ” resonance, and is due to the presence of a normal amount 
of air in the vesicles of the lung underneath. If this air-containing 
lung is replaced by a fluid or solid medium, as in pleuritic effusion 
or pneumonia, it is much more difficult to elicit a sound, and such 
sound as is produced is short, high pitched, and has a feeble carrying 
power when compared with the sound elicited from the normal lung. 134 
PHYSICAL DIAGNOSIS 
This-short, feeble, high-pitched sound is known technically as a “dull" 
or “flat" sound, flatness designating the extreme of the qualities that 
characterize dulness. Over the parts shaded dark in Fig. 98, we 
normally get a dull or flat tone, the darkest portions being flat and 
the others dull. The heavy shadow on 
the right corresponds to the position oc- 
cupied by the liver, or rather by that part 
of it which is in immediate contact with 
the chest wall. The upper portion of the 
liyer is overlapped by the right lung (see 
Fig. 98), and hence at this point we get a 
certain amount of resonance on percussion, 
although the tone is not so clear as that to 
be obtained higher up. Below the sixth 
rib we find true flatness near the sternum 
and for a few inches to the right of this 
ppint. As we go toward the axilla, the 
line of lung resonance slopes down, as is 
seen in Fig. 98. In the back resonance 
extends to the ninth or tenth ribs. 
Upper 
lobe. 
Lower 
lobe. 
Splenic 
arear ' 
2. Normal Dull Areas 
On the left side, the main dull area cor- 
responds to the heart, which at this point 
approaches the chest wall, and over the 
portion shaded darkest is uncovered by 
the lung. The part - here lightly shaded corresponds to that por- 
tion of the heart which is overlapped by the margin of the right and 
left lungs. 
Over the portion of the heart not overlapped by the lung (see 
Fig. 98, p. 133) the percussion note is nearly flat to light percussion, and 
very dull even when strongly percussed. This little quadrangular area 
is known as the “ superficial cardiac space, ” and the dulness correspond- 
ing to it is referred to as the “superficial”. cardiac dulness, while the 
dulness corresponding to the outlines of the heart itself beneath the 
overlapping lung margins is-called the “deep” cardiac dulness. 
When the heart becomes enlarged, both of these areas, the deep and 
the superficial, are enlarged, the former corresponding to the increased 
size of the heart itself, while the superficial cardiac space is extended 
because the margins of the lungs are pushed aside and a larger piece 
Fig. 99.—Position of the Left 
Lung in the Axilla. PERCUSSION 
135 
of the heart wall comes in contact with the chest wall. Accordingly, 
either the superficial or the deep dulness may be mapped out as a 
means of estimating the size of the heart. ; 
The deep cardiac dulness is much more satisfactory as a means 
of estimating the size of the heart, but much more difficult to 
map out. The longer that I have tried to percuss the heart area, and 
the more I have watched others attempt to do so, correlating the results 
with post-mortem facts and x-ray findings, the less I believe in the 
value of cardiac percussion. I rarely attempt it. 
It is a disputed point whether light or forcible percussion should be 
used when we attempt to map out the deep cardiac dulness. I find 
that as years go on I very seldom percuss out any cardiac border 
except the left and that only in the few cases in which the cardiac apex 
cannot be palpated. Much too great stress has been laid on percussion 
of the heart. Palpation and blood-pressure measurements usually 
give all essential information. When they do not, x-ray is usually the 
qnly reliable way to find out the heart’s size. 
Good observers are to be found on each side of this question, and 
I have no doubt that cardiac percussion works well in skilled hands. 
Personally I have found it nearly useless. 
Whatever method we use we must percuss successive points along 
a line running at right angles to the border of the organ which we 
wish to outline until a change of note is perceived. 
If now we look at the upper part of the chest in Fig. 98, we notice 
at once that the two sides are not shaded alike: the left apex is dis- 
tinctly lighter colored than the right. This is a very important point 
qnd one not sufficiently appreciated by students. The apex of the 
normal right lung is distinctly less resonant than the apex of the left 
in a corresponding poition. 
In percussing at the bottom of the left axilla, we sometimes find a 
small oval area of dulness corresponding to that outlined in Fig. 99. 
This is the area of splenic dulness, so called, and corresponds to that 
portion of the spleen which is in contact with the chest wall. This 
dull area is to be made out only in case the stomach and colon are not 
overdistended with air. When these organs are full of gas as is not 
infrequently the case, there is no area of splenic dulness and the whole 
region gives forth, when percussed, a note of a quality next to be 
described, namely, “ tympanitic. ” In my experience, percussion of the 
spleen is of very little use when we want it most, i.e., in infectious 
diseases like typhoid, malaria or sepsis. If the edge of the organ can 
be felt it is almost always enlarged; if the edge cannot be felt the 136 
PHYSICAL DIAGNOSIS 
results of percussion are most unreliable. In leucaemia and other 
diseases which greatly enlarge the spleen we can accurately percuss 
out its upper border, but this has little practical value. 
3. Tympanitic Resonance 
Tympanitic resonance is that obtained over a hollow body, like 
the stomach when moderately distended with air.1 It is usually 
of a higher pitch than the resonance to be obtained over the normal 
lung, and may be elicited by percussion lighter than that needed 
to bring out the lung resonance. It differs also from the vesicular or 
pulmonary resonance in quality, in a way easy to appreciate but 
difficult to describe. Tympanitic resonance is usually to be heard 
-when one percusses over the front of the left chest near the ensiform 
cartilage and for a few inches to the left of this point over the area 
corresponding with that of the stomach bubble as seen by #-ray. 
This tympanitic area, known as “Traube’s semilunar space,” varies a 
great deal in size according to the contents of the stomach. It is 
bounded on the right by the liver flatness, above by the pulmonary 
resonance, on the left by the splenic dulness, and below by the reso- 
nance of the intestine, which is also tympanitic, although its pitch is 
different owing to the different size and shape of the intestine. 
(The right axilla shows normal lung resonance down to the point 
at which the liver flatness begins, as shown in Fig. 98.) 
In the back, when the scapulas are drawn forward, as shown in Fig. 
95, page 130, percussion elicits a clear vesicular resonance from top to 
bottom on each side, although the top of the right lung is always 
slightly less resonant than the top of the left, and sometimes the bot- 
tom of the right lung is slightly less resonant than the correspond- 
ing portion of the left. 
4. Kronig's Isthmus 
In percussing the apices behind one can map out on each trapezius 
muscle a band of resonance bounded by the dulness of the neck struc- 
ture on the median side and of the dulness of the shoulder structures 
outwardly. This strip, known as Kronig’s isthmus, is narrowed in 
chronic (usually tuberculous) disease of the lung apex, as lung retrac- 
tion replaces resonance by dulness. 
1 Extreme distention here, as in a snare drum, is associated with a dull percussion 
note (see below p 30). PERCUSSION 
137 
The normally resonant strip 4 to 6 cm. wide may in disease be 
reduced to 2 or 3 cm. 
It should be remembered, however, that in the majority of cases 
the resonance throughout the back is distinctly less than that obtained 
over the front, on account of the greater thickness of the back muscles. 
Yet in children or emaciated persons, or where the muscular develop- 
ment is slight, there may be as much resonance behind as in front. 
Importance o f Percussing Symmetrical Points.—Since we depend for 
our standard of resonance upon comparison with a similar spot on the 
Fig. ioo.—The arrows point to Kronig’s Isthmus. 
outside of the chest, it is all-important that in making such comparisons 
we should percuss symmetrical points, and not, for example, com- 
pare the resonance over the third rib in the right front with that over 
the third interspace on the left, since more resonance can always 
be elicited over an interspace than over a rib. This comparison of 
symmetrical points, however, is interfered with by the presence of the 
heart on one side and the liver on the other, as well as by the fact 
that the apex of the right lung is normally less resonant than that of 
the left. A resonance which would be pathologically feeble if obtained 
over the left top may be normal over the right. Where both sides 
are abnormal, as in bilateral disease of the lung, or where fluid accu- 
mulates in both pleural cavities, we have to make the best comparison 
we can between the sound in the given case and an ideal standard 
carried in the mind. 
It must always be remembered that the amount of resonance 
obtained at any point by percussion depends upon how hard one 138 
PHYSICAL DIAGNOSIS 
strikes, as well as upon the conditions obtaining within the chest. 
A powerful blow over a diseased lung may bring out more resonance 
than a lighter blow over a normal lung. To strike with perfect 
fairness and with equal force upon each side can be learned only by 
considerable practice. Furthermore, the distance from the ear to 
each of the tw;o points, the resonance of which we are comparing, must 
be the same—that is, we must stand squarely in front or squarely 
behind the patient, otherwise the note coming from the part farther 
from the ear will sound duller than that coming from the nearer side. 
The normal resonance of the different parts of the chest can be 
considerably modified by the position of the patient, by deep breathing, 
by muscular exertion, and by other less important conditions. If, 
for example, the patient lies upon the left side, the heart swings out 
toward the left axilla and its dulness is extended in the same direction. 
Deep inspiration distends the margins of the lungs so that they 
encroach upon and reduce the area of the heart dulness and liver 
dulness. After muscular exertion the lungs become more than 
ordinarily voluminous, owing to the temporary distention brought 
about by the unusual amount of work thrown upon them. 
The area of cardiac dulness is increased in any condition involving 
insufficient lung expansion. Thus, in children, in debility, chlorosis, 
or fevers, the space occupied by the lungs is relatively small and the 
dull areas corresponding to the heart- &nd liver are proportionately 
enlarged. In old age, on the other hand, when the lungs have lost 
part of their elasticity and sag down over the heart and liver, the 
percussion dulness of these organs is reduced. 
Conditions Modifying the Percussion Note in Health.—The develop- 
ment of muscle or fat as well as the thickness of the chest wall will 
influence greatly the amount of resonance to be obtained by percussion. 
Indeed, we see now and then an individual in no part of whose chest 
can any clear percussion tone be elicited. In women, the amount of 
development of the breasts has also great influence upon the percussion 
note. In children, the note is generally clearer, and only the lightest 
percussion is to be used on account of the thinness of the chest wall. 
In old people whose chests are almost always more or less barrel- 
shaped, a shade of tympanitic quality is added to the normal vesicular 
resonance. Distention of the colon with gas often obliterates the liver 
dulness by rotating that organ so that only its edge is in contact with 
the chest wall, and if there is wind in the stomach, a variable amount 
of tympany is heard on percussing the lower left front and axilla 
or even in the left back. PERCUSSION 
139 
If a patient is examined while lying on the side, the amount of 
resonance over the lung corresponding to the side on which he lies 
is usually less than that of the side which is uppermost, because there 
is more air in the latter.1 Whatever the patient’s position, the 
amount of resonance is also greater at the end of inspiration than at 
the end of expiration, for the reason just given. As the lungs expand 
with full inspiration, their borders must move so as to cover a larger 
portion of the organs which they normally overlap. Portions of 
the chest which at the end of expiration are dull or flat, owing to the 
close juxtaposition of the heart, liver, or spleen, become resonant 
at the end of inspiration. For example, the lower margin of the right 
lung moves down during inspiration so as to cover a considerably 
larger portion of the liver. 
Percussion as a Means of Ascertaining the Movability of the Lung 
Borders.—It is sometimes of importance to determine not merely 
the position of the resting lung but its power to expand freely. This 
can be ascertained by percussion in the following way: The lower 
border of the lung resonance, say in the axilla, is carefully marked 
out. Then percussion is made over a point just below the level of 
the resting lung and at the same time the patient is directed to inspire 
deeply. If the lung expands and its border moves down, the percussion 
note will change suddenly from dull to resonant during the inspiration. 
An excursion of two or three inches can often be demonstrated by this 
method, which is especially important for the anterior and posterior 
margins of the lungs. In the axilla kitten’s phrenic shadow will give 
us the same information. 
The mobility of the borders of the lung, as determined by this 
method, is of considerable clinical importance, for an absence of 
such mobility may indicate pleuritic adhesions. Its amount depends 
upon various conditions and varies much in different individuals, but 
complete absence of mobility is always pathological. 
5. Cracked-pot Resonance 
When percussing the chest of a crying child, we sometimes notice 
that the sound elicited has a peculiar “chinking" quality, like that 
produced by striking one coin with another, but more muffled. The 
sound may be more closely imitated, and the mode of its production 
illustrated, by clasping the hands palm to palm so as to enclose an 
1 There is also a shade of tympany associated with the dulness of the feebly 
expanded lung of the lower side. 140 
PHYSICAL DIAGNOSIS 
air space which communicates with the outer air through a chink left 
open, and then striking the back of the under hand against the knee. 
By the blow, air is forced out through the chink with a sound like that 
of metallic coins struck together. 
In disease, the cracked-pot sound is usually produced over a 
superficial and empty pulmonary cavity (as in advanced phthisis) 
from which the air is suddenly expelled by the percussion stroke. 
It is much easier to hear this peculiar sound if, while percussing, 
one listens with a stethoscope at the patient’s open mouth. The 
patient himself holds the chest piece of the instrument just in front 
of his open mouth, leaving the auscultator’s hands free for percussing. 
6. Amphoric Resonance 
A low-pitched hollow sound approximating in quality to tym- 
panitic resonance, and occasionally obtained over pulmonary cavities 
or over pneumothorax, has received the name of amphoric resonance. 
It may be imitated by percussing the trachea or the cheek when 
moderately distended with air. 
(a) Summary 
The varieties of resonance to be obtained by percussing the norma 
thorax are: 
(1) Vesicular resonance, to be obtained over normal lung tissue. 
(2) Tympanitic resonance, to be obtained in Traube’s semilunar 
space. 
(3) Diminished resonance or dulness, such as is present over the 
scapulas, and 
(4) Absence of resonance or flatness, such as is discovered when 
we percuss over the lowest ribs in the right front. 
(5) Cracked-pot resonance, sometimes obtainable over the chest of 
a crying child. 
(6) Amphoric resonance, obtainable over the trachea. 
Any of these sounds may denote disease if obtained in portions 
of the chest where they are not normally found. Each has its place, 
and becomes pathological if found elsewhere. 
III. Sense of Resistance 
While percussing the chest we must be on the lookout not only 
for changes in resonance, but for variations in the amount of resis- 
tance felt underneath the finger. Normally the elasticity of the PERCUSSION 
141 
chest walls over the upper fronts is considerably greater and the 
sense of resistance considerably less than that felt over the liver. 
In the axillae and over those portions of the back not covered by 
the scapulae, we feel in normal chests an elastic resistance when 
percussing which is in contrast with the dead, woodeny feeling which 
is communicated to the finger when the air-containing lung is replaced 
by fluid or solid contents (pleuritic effusion, pneumonia, phthisis, etc.). 
Muscle spasm over pleurisy or diseased lung may also increase the sense 
of resistance (Pottenger). In some physicians this sense of resistance 
is very highly developed and as much information is obtained thereby 
as through the sounds elicited. CHAPTER VIII 
AUSCULTATION 
I. Mediate and Immediate Auscultation 
Auscultation may be practiced by placing one’s ear directly 
against the patient’s chest (immediate auscultation) or with the 
help of a stethoscope (mediate auscultation). 
Each method has its place. Immediate auscultation is said to 
have advantages similar to those of the low power of the micro- 
scope, in that it gives us a general idea of the condition of a rela- 
tively large area of tissue, while the stethoscope may be used, like 
the oil immersion lens, to bring out details at one or another point. 
On the other hand, I am firmly convinced that the unaided ear 
can perceive sounds, conducted from the interior of the lungs—sounds 
quite inaudible with any stethoscope—and that in this way the faint 
tubular breathing produced by deep-seated areas of solidified lung 
may be recognized. 
Immediate auscultation may be objected to: 
(а) On grounds of delicacy (when examining persons of the opposite 
sex). 
(б) On grounds of cleanliness (although the chest may be cov- 
ered with a towel so as to protect the auscultator to a certain extent). 
(c) Because we cannot conveniently reach the supraclavicular or 
the upper axillary regions in this way. 
(d) Because it is difficult to localize the different valvular areas 
and the sites of cardiac murmurs if immediate auscultation is employed. 
On account of the latter objection the great majority of observers 
now use the stethoscope to examine the heart. For the lungs, both 
methods are employed by many experienced auscultators. I have 
already mentioned the importance of immediate auscultation in the 
search for deep-seated areas of pneumonia. Attention has also been 
called by Conner (Assoc, of American Physicians, 1907, p. 113) to the 
fact that the diastolic murmur of aortic insufficiency is sometimes 
audible to the unaided ear when it cannot be heard with any form 
of stethoscope. Faint, high-pitched blowing sounds are those which 
the free ear is especially adapted to detect. 
142 AUSCULTATION 
143 
This is doubtless due, as Conner explains, to the fact that the tubes 
of the stethoscope do not conduct high-pitched sounds well. With 
the free ear we have also the opportunity to detect the bone-con- 
ducted sounds which are missed in mediate stethoscopic auscultation. 
II. Selection of a Stethoscope 
(1) It is as rash for any one to 
select a stethoscope without first 
trying the fit of the ear pieces in 
his ears as it would be to buy a new 
hat without trying it on. What 
.suits A. very well is quite impossible 
for B. It is true that one can get 
used to almost any stethoscope as 
one can to almost any hat, but it is 
not necessary to do so. The ear 
pieces of the ordinary stethoscope 
are often too small and rarely too 
large. In case of doubt, therefore, 
it is better to err upon the side of 
getting a stethoscope with too large 
rather than too small ends. 
(2) The binaural stethoscope, 
which is now used almost exclu- 
sively in this country, maintains its 
position in the ears of the auscul- 
tator either through the pressure of a rubber strap 
stretched around the metal tubes leading to the ears, 
or by means of a steel spring connecting the tubes. 
Either variety is usually satisfactory, but I prefer a 
stethoscope made with a steel spring (see Fig. 101) 
because such a spring is far less likely to break or lose 
its elasticity than a rubber strap. A rubber strap can 
always be added if this is desirable. It is important 
to pick out an instrument possessing a spring not strong enough to 
cause pain in the external meatus of the ear and yet strong enough to 
hold the ear pieces firmly in place. Persons with narrow heads need 
a much more powerful spring or strap than would be convenient for 
persons with wide heads. 
(3) The rubber tubing used to join the metallic tubes to the 
chest piece of the instrument' should be as flexible as possible (see 
Fig. 102.—'Cam- 
man Stethoscope 
with Stiff Tubing 
and Rubber Strap. 
Fig. ioi.—Stetho- 
scope Fitted with 
Long Flexible 
Tubes, Especially 
Useful When Ex- 
amining Children. 144 
PHYSICAL DIAGNOSIS 
Fig. 107). Stiff tubing (see Fig. 102) makes it necessary for the aus- 
cultator to move his head and body from place to place as the examina- 
tion of the chest progresses, while if flexible tubing is used the head 
need seldom be moved and a great deal of time and fatigue is thus 
saved. Stiff stethoscopes are 
especially inconvenient when 
examining the axilla. 
(4) Jointed stethoscopes 
which fold up or take apart 
should be scrupulously avoi- 
ded. They are a delusion 
and a snare, apt to come apart 
at critical moments, and to 
snap and creak at the joints 
when in use, sometimes pro- 
ducing in this way sounds 
which may be easily mistaken 
for rales. Such an instrument 
is no more portable nor com- 
pact than the ordinary form 
with flexible tubes. It has, 
therefore, no advantages over 
stethoscopes made in one 
piece and possesses disadvan- 
tages which are peculiarly 
annoying. 
(5) The Chest Piece.—The 
majority of the stethoscopes 
now in use have a chest piece of hard-rubber, 
wood or metal with a diameter of about seven- 
eighths of an inch. Chest pieces of larger diam- 
eter than this are to be avoided as they are very difficult to main- 
tain in close apposition with thin chests. To avoid this difficulty 
the chest piece is sometimes made of soft-rubber or its diameter still 
further reduced. 
(6) The Bowles Stethoscope.—(See Figs. 103 and 104.) Within 
recent years there has been introduced an instrument which, for 
many purposes, seems to me far superior to any other form of stetho- 
scope with which I am acquainted. Its peculiarity is the chest piece, 
which consists of a very shallow steel cup (see Fig. 105) over the 
mouth of which a thin metal plate or a bit of pigskin is fastened. 
Fig. 103.—Bowles’ 
Stethoscope. Front 
view. * 
Fig. 104.—Combination 
Bowles’ Stethoscope. AUSCULTATION 
145 
The metal or pigskin diaphragm serves simply to prevent the tissues 
of the chest from projecting into the shallow cup of the chest piece 
when the latter is pressed against the chest, and does not in any 
other way contribute to the sounds which we hear with the instru- 
ment. This is proved by the fact that we can hear as well even 
when the diaphragm is cracked across in several directions. 
With this instrument almost all sounds produced within the chest 
can be heard much more distinctly than in any other variety of 
stethoscope. Cardiac murmurs which are inaudible with any other 
Fig. 105.—Chest Piece of Bowles’ Stethoscope. On the right the shallow cup com- 
municating with the ear tubes. On the left the diaphragm which covers the cup, and 
the ring which holds it in place. 
stethoscope may be distinctly heard with this. Especially is this 
true of all high-pitched sounds and of the murmurs of aortic regurgi- 
tation. Yet it is useful for examination not merely of the heart, but 
of the lungs as well. For any one who has difficulty in hearing the 
ordinary cardiac or respiratory sounds, or for one who is partially 
deaf, the instrument is invaluable. As the metal rim of the chest is 
apt to get unpleasantly cold, it is best to cover it with a bit of rubber 
or kid. This saves the patient some discomfort and also tends to pre- 
vent the instrument from slipping on the skin. The flat chest piece 
makes the instrument very useful in listening to the posterior por- 
tions of the lungs in cases of pneumonia in which the patient is too 
sick to be turned over or to sit up. Without moving the patient at 
all we can work the chest piece in under the back of the patient by 
pressing down the bed-clothes, and in this way can listen to any part 
of the chest without moving the patient. A further advantage of the 
instrument is that it enables us to gain an approximately accurate 
idea of the heart sounds without undressing the patient. Respira- 146 
PHYSICAL DIAGNOSIS 
tory sounds cannot well be listened to through the clothes, as the 
rubbing of the latter may simulate rales. 
There are two purposes for which I have sometimes found the 
Bowles stethoscope inferior to the ordinary stethoscope: 
(1) For listening over the apex of the lung for fine rales, e.g., in 
incipient phthisis. 
(2) For listening for low-pitched or superficial sounds, such as a fric- 
tion rub or a presystolic murmur.1 When I desire to listen for fine 
rales at an apex, for a friction rub, 
or for a presystolic murmur, I sepa- 
rate the chest piece of the Bowles 
stethoscope from the hard-rubber 
bell into which it is inserted, 
thereby converting the instrument 
into one of the ordinary form. 
With an extra-hard-rubber bell 
attached, the instrument is no 
more bulky than an ordinary 
stethoscope, and far more efficient. 
When used for listening to the 
respiration, the Bowles instrument 
gives us information similar in 
some respect to that obtained by 
the use of the free ear—that is we 
are through it enabled to ascertain 
by listening at one spot the con- 
dition of a much larger area of the 
chest than can in any other way 
be investigated. 
Owing to the fact that both 
cardiac and respiratory sounds are 
magnified by the Bowles stethoscope, this instrument is especially 
well adapted for use with some sort of an attachment whereby several 
sets of ear pieces are so jointed by tubing to one chest piece that 
several persons may listen at once. Bowles’ multiple stethoscope, 
fitted for six and for twelve observers, is seen in Figs. 106 and 107, and 
Fig. 106.—Bowles’ Multiple Stethoscope 
for Six Students. 
1 It has frequently been observed, when listening with the ordinary stethoscope, 
that a presystolic murmur can be better heard if only the very lightest pressure is 
made with the stethoscope. The fact that a thrill is communicated to the chest 
wall, and that that thrill is connected with the audible murmur explains my calling 
this murmur a superficial one. AUSCULTATION 
147 
the method of its use in Fig. 108. In the teaching of auscultation this 
instrument is of some value, saving as it does the time of the instruc- 
tor and of the students and the strength of the patient. The sounds 
conducted through any one of the twelve tubes used in this instrument 
are as loud as those to be heard with a single instrument of the ordi- 
nary form, although far 
fainter than those to be 
heard with a single 
Bowles stethoscope. 
III. The Use of the 
Stethoscope 
Having secured an 
instrument which fits 
the ears satisfactorily, 
the beginner may get a 
good deal of practice by 
using it upon himself, 
especially upon his own 
heart. The chief point 
to be learned is to dis- 
regard various irrelevant 
sounds and to concen- 
trate attention upon 
those which are relevant. 
Almost any one hears enough with a stethoscope, and most beginners 
hear too much. No great keenness of hearing is required, for the 
sounds which we listen for are not, as a rule, difficult to hear if atten- 
tion is concentrated upon them. 
Fig. 107.—Bowles’ Multiple Stethoscope for 
Twelve Students. 
i. Selective Attention and What to Disregard 
Accordingly, the art of using a stethoscope successfully depends 
upon the acquisition of two powers— 
(a) A knowledge of what to disregard. (b) A selective atten- 
tion or concentration upon those sounds which we know to be of 
importance. 
Among the sounds which we must learn to disregard are the 
following: 148 
PHYSICAL DIAGNOSIS 
(1) Noises produced in the room or its immediate neighborhood, 
but not connected with the patient himself. It is, of course, easier 
to listen in a perfectly quiet room where there are no external noises 
which need to be excluded from attention, but as the greater part 
of the student’s work must be done in more or less noisy places, 
Fig. 108.—Bowles’ Multiple Stethoscope in Use. Twelve students listening at once. 
it is for the beginner a practical necessity to learn to withdraw his atten- 
tion from the various sounds which reach his ear from the street, 
from other parts of the building, or from the room in which he is 
working. This is at first no easy matter, but can be accomplished 
with practice. 
(2) When the power to disregard external noises has been ac- 
quired, a still further selection must be made among the sounds 
which come to the ear through the tubes of the stethoscope. Noises 
produced by friction of the chest piece of the stethoscope upon the 
skin are especially deceptive and may closely simulate a pleural or 
pericardial friction sound. It is well for the student to experiment 
upon the nature and extent of such “skin rubs” by deliberately AUSCULTATION 
149 
moving the chest piece of the stethoscope upon the skin and listen- 
ing to the sounds so produced. Mistakes can be avoided in the 
majority of cases by holding the chest piece of the stethoscope very 
firmly against the chest. This can be easily done when the patient 
is in the recumbent position, but when the patient is sitting up it 
may be necessary to press so hard with the chest piece of the stetho- 
scope as to throw the patient off his balance unless he is in some 
way supported; accordingly, it is my practice in many cases to put 
the left arm around and behind the patient so as to form a support, 
against which he can lean when the chest piece of the stethoscope 
is pressed strongly against his chest. When listening to the back 
of the chest, the manoeuvre is reversed. If the skin is very dry, the 
ribs are very prominent, or the chest is thickly covered with hair, 
it may be impossible to prevent the occurrence of adventitious sounds 
due to friction of the chest piece upon the chest, no matter how firmly 
the instrument is held. In case of doubt, and in any case in 
which a diagnosis of fine rales or of pleural or pericardial friction is 
in question, the chest piece of the stethoscope, the fingers of the 
hand which holds it and the surface of the chest, at the point where 
we desire to listen, should be moistened and any hair that may be pres- 
ent thoroughly wetted with a sponge, so that it will lie flat upon 
the chest. Otherwise the friction of the hair under the chest piece 
of the stethoscope may simulate crepitant rales as closely as “skin 
rubs” simulate pleural friction. 
(3) The friction of the fingers of the auscultator upon the chest 
piece or on some other part of the stethoscope frequently gives rise 
to sounds closely resembling rales of one or another description. 
The nature of these sounds can be easily learned by intentionally 
moving the fingers upon the stethoscope. They are to be avoided 
by wetting the fingers, grasping the bell firmly, and by touching it 
with as few fingers as will suffice to hold it close against the 
chest. 
(4) Noises produced by a shifting of the parts of the stetho- 
scope upon each other are especially frequent in stethoscopes made 
in several pieces and jointed together. A variety of snapping and 
cracking sounds, not at all unlike certain varieties of rales, may 
thus be produced, and if we are not upon our guard, may lead to 
errors in diagnosis. Stethoscopes which have no hinges and which 
do not come apart are far less likely to trouble us in this way. 
(5) When a rubber band is used to press the ear pieces more 
firmly into the ears, a very peculiar sound may be produced by the 150 
PHYSICAL DIAGNOSIS 
breathing of the auscultator as it strikes upon the rubber strap. It 
is a loud musical note, and may be confused with coarse, dry rales. 
When one has learned to recognize and to disregard the noises 
produced in the ways above indicated, there is still one set of sounds 
which are very frequently heard, yet which have no significance for 
physical diagnosis, and must therefore be disregarded; I refer to 
2. Muscle Sounds 
Patients who hold themselves very erect, patients who are chilly 
or nervous, or who for any reason contract the muscles over which 
we are listening, produce in these muscles a characteristic set of 
sounds. The contraction of any muscle in the body produces sounds 
similar in quality to those heard over the chest, but of less intensity. 
Those who have the faculty of contracting the tensor tympani 
muscle at will can at any time listen to a typical muscle sound. Or 
close both ears with the fingers and strongly contract the masseter 
muscle, with the teeth clenched. A low-pitched muscle sound will 
be heard. 
It is well also to have a patient contract one of the pectorals and 
then listen to the sound thus produced. In some cases a continuous, 
low-pitched roar or drumming is all that we hear; in other cases we hear 
nothing but the breath sounds during expiration, while during inspira- 
tion the breath sound is obscured by a series of short, dull, rumbling 
sounds, following each other at the rate of from five to ten in a second. 
Occasionally the sound is like the puffing of the engine attached to 
a pile-driver, or like a stream of water falling upon a sheet of metal 
just slowly enough to be separated into drops and heard at a con- 
siderable distance. As already mentioned, we are especially apt to 
hear these sounds at the end of forced inspiration, owing to the con- 
traction of voluntary muscles during that portion of the respiratory 
act. They are most often heard over the upper portion of the chest 
(over the pectorals in front and over the trapezius behind), but in 
some persons no part of the chest is free from them. It is a curious 
fact that we are not always able to detect by sight or touch the muscu- 
lar contractions which give rise to these sounds, and the patient himself 
may be wholly unaware of them. Under such circumstances they are 
not infrequently mistaken for rales, and I am inclined to think that 
many of the sounds recorded as “crumpling,” “obscure,” “muffled,” 
“distant,” or “indeterminate” rales are in reality due to muscular 
contraptions. The adjectives “muffled” and “distant” give us an AUSCULTATION 
151 
inkling as to the qualities which distinguish muscular sounds from 
rales. Rales can often be counted, are more clean cut, have a more 
distinct beginning and end, seem nearer to the ear, and possess more of 
a crackling or bubbling quality than muscle sounds. 
The joint sounds and fascial rubbings described by F. T. Lord 
have already been referred to. General relaxation of all muscles 
usually quiets them. 
3. Other Sources of Error 
Another source of confusion, which for beginners is very trouble 
some, especially if they are using the ordinary form of stethoscope 
with a bell-shaped chest piece, arises in case the chest piece is not 
held perfectly in apposition with the skin. If, for example, the 
stethoscope is slightly tilted to one side so that the bell is lifted from 
the skin at some point, or if one endeavors to listen over a very uneven 
part of the chest on which the bell of the stethoscope cannot be 
made to rest closely, a roar of external noises reaches the ear through 
the chink left between the chest piece and the chest. After a little 
practice one learns instantly to detect this condition of things and 
so to shift the position of the chest piece that external noises are 
totally excluded; but by the beginner, the peculiar babel of external 
noises, which is heard whenever the stethoscope fails to fit closely 
against the chest, is not easily recognized, and hence he tends to attrib- 
ute some of these external sounds to diseased conditions within the 
chest. 
Again, it is not until we have had considerable practice that our 
sense of hearing comes instantly to tell us when something is wrong 
about the stethoscope itself; when, for example, one of the tubes is 
blocked, kinked, or disconnected, or when we are holding the stetho- 
scope upside down, so that the ear pieces point downward instead of 
upward (see Figs. 109 and no). It is only when we have learned 
through long practice about how much we ought to hear at a given 
point in the normal chest that we recognize at once the fact that we 
are not hearing as much as we should, in case some one of the above 
accidents has happened. Many beginners do not listen long enough 
in any one place, but move the chest piece of the stethoscope about 
rapidly from point to point, as they have seen experienced auscultators 
do; but it is remarkable how much more one can hear at a given point 
by simply persevering and listening to beat after beat, or breath after 
breath. It is sometimes difficult to -avoid the impression that the 152 
PHYSICAL DIAGNOSIS 
sounds themselves have grown louder as we continue to listen, espe- 
cially if we are in any doubt as to what we hear. Therefore, if we hear 
indistinctly, it is important to keep on listening, and to fix the atten- 
tion successively upon each of the different elements in the sounds 
under consideration. In difficult cases we should use every possible 
aid toward concentration of the attention, and where it is possible, 
all sources of distraction should be eliminated. Thus, in any case of 
doubt, I think it is important for the auscultator to get himself into 
Fig. 109.—Stethoscope Held 
Right Side Up. 
Fig. iio.—Stethoscope Held 
Wrong Side Up. 
as comfortable a position as he can, so' that his attention is not 
distracted by his own physical discomforts. Many auscultators shut 
their eyes when listening in a difficult case so as to avoid the distraction 
of impressions coming through the sense of sight. It goes without 
saying that if quiet can be secured in the room where we are working, 
and outside it as well, we shall be enabled to listen much more profit- 
ably. Hawes1 has studied the sources of error in auscultation with 
special reference to the diagnosis of tuberculosis. He gives the 
following figures: In 250 cases muscle sounds were marked in 57, 
slight in 25, absent in 168. Joint sounds were present in 126 of 250, 
tendon or bursal sounds in 10 cases, atelectatic crackles in 5 cases. 
In 55 instances, or 22 per cent., the joint sounds resembled rffies. 
IV. Auscultation of the Lungs 
In the majority of cases ordinary quiet breathing is not forcible 
enough to bring out the sounds on which we depend for the diagnosis 
of the condition of the lungs. Deep or forced breathing is what we 
need. 
1 Hawes: Boston Med. and Surg. Journ., June 18, 1914. AUSCULTATION 
153 
As a rule, the patient must be taught how to breathe deeply, which 
is best accomplished by personally demonstrating the act of deep 
breathing and then asking him to do the same. Two difficulties are 
encountered: 
(a) The patient may blow out his breath forcibly and with a noise, 
since that is what he is used to doing whenever he takes a long breath 
under ordinary circumstances; or 
(b) It may be that he cannot be made to take a deep breath at all. 
The first of these mistakes alters the sounds to be heard with the 
stethoscope in any part of the chest by disturbing both the rhythm 
and the pitch of the respiratory sounds. In this way the breathing 
may be made to sound tubular or asthmatic throughout a sound chest. 
This difficulty can sometimes be overcome by demonstrating to the 
patient that what you desire is to have him open his mouth, take a 
full breath and then simple let it go, but not blow it forcibly out. In 
some cases the patient cannot be taught this, and we have to get on 
the best we can despite his mistakes. When he cannot be made to 
take a full breath at all, we can often accomplish the desired result by 
getting him to cough. The breath just before and after a cough is 
often of the type we desire. The use of voluntary cough in order to 
bring out rales will be discussed later on. Another useful manoeuvre 
is to make the patient count aloud as long as he can with a single 
breath. The deep inspiration which he is forced to take after this 
task is of the type which we desire. 
1. Respiratory Types 
In the normal chest two types of breathing are to be heard: 
(1) Tracheal, bronchial, or tubular breathing. 
(2) Vesicular breathing. 
Tracheal, bronchial, or tubular breathing is to be he’ard in normal 
cases if the stethoscope is pressed against the trachea, and as a rule it 
can also be heard over the primary bronchi, in front or behind (see 
Figs, hi and 112). 
Vesicular breathing is to be heard over most of the remaining por- 
tions of the lung—that is, in the front of the thorax except where the 
heart and the liver come against the chest wall, in the back except 
over the scapulae, and in the axillae. Two exceptions to this state- 
ment will be mentioned later. 154 
PHYSICAL DIAGNOSIS 
(a) Characteristics of Vesicular Breathing 
Vesicular breathing—that heard over the air vesicles or paren- 
chyma of the lung—has certain characteristics which I shall try to 
describe in terms of intensity, duration, and pitch. 
Of the quality of the sounds heard over this portion of the lung 
there is little can be said; it sounds something like the swish of the wind 
Fig. iii.—Position of Trachea and 
Bronchi from the Front. 
Fig. 112.—Position of Trachea and 
Bronchi from the Back. 
in a grove of trees some distance off, and hence is sometimes spoken 
of as “breezy.” 
The intensity, duration, and pitch of the inspiration as compared 
with that of the expiration may be represented as in Fig. 113. In 
this figure, as in all those to be used in description of respiratory 
sounds— 
(1) I represent the inspiration by an up-stroke and the expira- 
tion by a down-stroke (see the direction of the arrows in Fig. 113). 
(2) The length of the up-stroke as compared with that of the 
down-stroke corresponds to the length of inspiration compared with 
expiration. 
(3) The thickness of the up-stroke as compared with the down- 
stroke represents the intensity of the inspiration as compared with 
the expiration. 
(4) The pitch of inspiration as compared with that of expiration 
is represented by the sharpness of the angle which the up-stroke makes 
with the perpendicular as compared with that which the down-stroke AUSCULTATION 
155 
makes with the perpendicular. The pitch of a roof may be thought 
of in this connection to remind us of the meaning of these symbols. 
If now we look again at Fig. 113 we see that when compared with 
expiration (the down-stroke), the inspiration is— 
(a) More intense. 
(b) Longer. 
(c) Higher pitched. 
Our comparison is invariably made between inspiration and expira- 
tion, and not with any other sound as a standard. 
Now, this type of breathing (which, as I have said, is to be heard 
over every portion of the lung except those portions immediately 
Fig. i 13.—Vesicular 
Breathing. 
Fig. 114.—Distant 
Vesicular Breathing. 
Fig. 115.—Exaggerated 
Vesicular Breathing. 
adjacent to the primary bronchi), is not heard everywhere with equal 
intensity. It is best heard below the clavicles in front, in the axillae, 
and below the scapulae behind; over the thin, lower edges of the lung, 
whether behind or at the sides, it is feebler, though still retaining its 
characteristic type as revealed in the inspiration and expiration in 
respect to intensity, duration, and pitch. To represent distant 
vesicular breathing graphically we have only to draw its symbol on a 
smaller scale (see Fig. 114). On the other hand, when one listens to 
the lungs of a person who has been exerting himself strongly, one hears 
the same type of respiration, but on a larger scale, which may then be 
represented as in Fig. 115. This last symbol may also be used to 
represent the respiration which we hear over normal but thin-walled 
chests; for example, in children or in emaciated persons. It is some- 
times known as “exaggerated” or “puerile” respiration. When one 
lung is thrown out of use by disease so that increased work is brought 
upon the other, the breath sounds heard over the latter are increased 
and seem to be produced on a larger scale. Such breathing is some- 
times spoken of as “rough” breathing. 
It is very important to distinguish at the outset between the 
different types of breathing, one of which I have just described, and 
the different degrees of loudness with which any one type of breathing 
may be heard. 156 
PHYSICAL DIAGNOSIS 
(b) Bronchial or Tracheal Breathing in Health 
Bronchial breathing may be symbolically represented as in Fig. 116, 
in which the increased length of the down-stroke corresponds to the 
increased duration of expiration, and the greater thickness of both 
lines corresponds to the greater intensity of both sounds, expiratory 
and inspiratory, while the sharp pitch of the “gable” on both sides of 
the perpendicular corresponds to the high pitch of both sounds. Ex- 
piration, in most cases, slightly exceeds inspiration both in intensity 
Fig. ii6.—Bronchial Breath- 
ing of Moderate Intensity. 
Fig. ii7.—Distant Bronchial 
Breathing. 
Fig. 118.—Very Loud 
Bronchial Breathing. 
and pitch, and considerably exceeds it in duration, while as com- 
pared with vesicular breathing almost all the relations are reversed. 
Bronchial breathing has also a peculiar quality which can be better 
appreciated than described. 
In the healthy chest this type of breathing is to be heard if one 
listens over the trachea or primary bronchi (see above, Fig. in), but 
practically, one hardly ever listens over the trachea and bronchi except 
by mistake, and the importance of familiarizing one’s self with the 
type of respiration heard over these portions of the chest is due to the 
fact that in certain diseases, especially in pneumonia and phthisis, 
we may hear bronchial breathing over the parenchyma of the lung 
where normally vesicular breathing should be heard. 
The student should familiarize himself with each of these types 
of breathing, the vesicular and the bronchial, concentrating his at- 
tention as he listens first upon the inspiration and then upon the 
expiration, and comparing them with each other, first in duration, 
next in intensity, and lastly in pitch. To those who have not a musical 
ear, high-pitched sounds convey the general impression of being 
shrill, while low-pitched sounds sound hollow and empty, but the 
distinction between intensity and pitch is one comparatively difficult 
to master. Distant bronchial breathing may be represented in Fig. 
116, and is to be heard over the back of the neck opposite the position 
of the trachea and bronchi. Fig. 118 represents very loud bronchial 
breathing such as is sometimes heard in pneumonia. AUSCULTATION 
157 
(c) Broncho-Vesicular Breathing in Health 
As indicated by its name, this type of breathing is intermediate 
between the two just described, hence the terms “mixed breathing,” 
or “atypical breathing” (“unbestimmt”). Its characteristics may 
be symbolized as in Fig. 119. In the normal chest one can become 
familiar with broncho-vesicular breathing, by examining the apex of 
the right lung, or by listening over the trachea or one of the primary 
bronchi, and then moving the stethoscope half an inch at a time toward 
Fig. i 19.—Two Common Types of 
Broncho-Vesicular Breathing. 
Fig. 120.—Distant Broncho-Vesicular 
Breathing. 
one of the nipples. In the course of this journey one passes over points 
at which the breathing has, in varying degrees, the characteristics 
intermediate between the bronchial type from which we started and 
the vesicular type toward which we are moving. Expiration is a 
little longer, intenser, or higher pitched than in vesicular breathing, 
and inspiration a little shorter, feebler, or lower pitched; but since 
these characteristics are variously combined, there are many 
subvarieties of broncho-vesicular breathing which, for purposes of con- 
venience (see below, page 300), I have called the first type of broncho- 
vesicular breathing (see Figs. 119, a, and 120, a) and the second type of 
broncho-vesicular breathing (Figs. 119, b, and 120, b) or B-V—I, and 
B-V—II. The first type is identical with that often called “sharp”— 
because inspiration is sharp or high pitched. In this type the inspira- 
tion is often segmented (“cog-wheel breathing”). 
(e) The Breathing in Asthma 
In this type of breathing, both sounds are usually obscured to a 
great extent by the presence of piping and squeaking rales (see below). 
(/) Interrupted or “Cogwheel ” Breathing 
As a rule, only the inspiration is interrupted, being transformed 
into a series of short, irregular, jerky puffs as shown in Fig. 123. 158 
PHYSICAL DIAGNOSIS 
Very rarely the expiration is also divided into segments. Inspiration 
is also abnormally high pitched in most cases. When heard over the 
entire chest, cogwheel breathing is usually the result of nervousness, 
fatigue, or chilliness on the patient’s part. With the removal of these 
causes, this type of respiration is confined to a relatively small portion 
of the chest, and remains present despite the ex- 
clusion of fatigue, nervousness, or cold. It points 
to a local catarrh in the finer bronchi such as to 
render difficult the entrance of air into the alveoli. 
As such, it has a certain significance in the diag- 
nosis of early phthisis, a significance similar to 
that of rales or other signs of localized bronchitis 
(see below). Cogwheel breathing must be dis- 
tinguished from cardio-respiratory murmurs which 
have the qualities of breath sounds, but occur 
simultaneously with each cardiac systole. Such murmurs are very often 
heard at the left base behind, but have, so far as I know, no clinical 
importance. 
Fig. 121.—Asth- 
matic Breathing. 5, 
s, s, squeaking (musi- 
cal) r&les. 
Fig. 122.—Cogwheel Breathing. 
Fig. 123.—Metamorphosing Breathing. 
(g) Amphoric or Cavernous Breathing (see below, p. 162). 
(h) Metamorphosing Breathing 
Occasionally, while we are listening to an inspiration of normal 
pitch, intensity, and quality, a sudden metamorphosis occurs and the 
type of breathing changes from vesicular to bronchial or amphoric 
(see Fig. 123), or the intensity of the breath sounds may suddenly be 
increased without other change. These metamorphoses are usually 
owing to the fact that a plugged bronchus is suddenly opened by the 
force of the inspired air, so that the sounds conducted through it 
become audible. 
V. Differences between the Two Sides of the Chest 
(a) Over the apex of the right lung—that is, above the right clav- 
icle in front, and above the spine of the scapula behind—one hears in AUSCULTATION 
159 
the great majority of normal chests a distinctly broncho-vesicular type 
of breathing. In a smaller number of cases this same type of breathing 
may be heard just below the right clavicle. These facts cannot be too 
strongly insisted upon, since it is only by bearing them in mind that we 
can avoid the mistake of diagnosing a beginning consolidation of the 
right apex where none exists. Breath sounds which are perfectly normal 
over the right apex would mean serious disease if heard over similar por- 
tions of the left lung. It will be remembered that the apex of the right 
lung is also duller on percussion than the corresponding portion of the 
left, and that the voice sounds and tactile fremitus are normally more 
intense on the right (see Fig. 86). The best explanation of these dif- 
ferences seems to me that given by Petterolf (Archives of Int. Med., 
Feb., 1909), who has shown that the apex of the right lung is in close 
contact with the trachea, while the left lung-apex is separated from 
the trachea by the large blood vessels, the gullet and other structures. 
The tracheal or bronchial sounds are therefore better transmitted to 
the right lung. 
(b) At the base of the left lung, posteriorly, one often hears a 
slightly rougher or more noisy type of breathing than at the right base. 
The vicinity of the stomach bubble may explain this.1 
VI. Pathological Modifications of Vesicular Breathing 
Having now distinguished the different types of breathing and 
described their distribution in the normal chest, we must return to 
the normal or vesicular breathing in order to enumerate certain of its 
modifications which are important in diagnosis. 
i. Exaggerated Vesicular Breathing (“Compensatory ” Breathing) 
(a) It has already been mentioned that in children or in adults 
with very thin and flexible chests the normal breath sounds are heard 
with relatively great distinctness; also that after any exertion which 
leads to abnormally deep and forcible breathing a similar increase in 
the intensity of the respiratory sounds naturally occurs. 
(b) The term 11 compensatory breathing, ” or “vicarious” breathing, 
refers to vesicular breathing of an exaggerated type, such as is heard, 
for example, over the whole of one lung when the other lung is thrown 
out of use by the pressure of an accumulation of air or fluid in the 
1 If the patient lies on the side, that side shows a slightly more tubular respira- 
tion with increased voice, whisper, and fremitus. This must be allowed for in all 
comparisons made in this position. 160 
PHYSICAL DIAGNOSIS 
pleural cavity. A similar exaggeration of the breathing upon the 
sound side takes place when the other lung is solidified, as by tuber- 
culosis, pneumonia, or malignant disease, or when it is compressed by 
the adhesions following pleuritic effusion, or by a contraction of the 
bones of that side of the chest such as occurs in spinal curvature. 
2. Diminished Vesicular Breathing 
The causes of a diminution in the intensity of the breath sounds, 
without any change in their type, are very numerous. I shall mention 
them in an order corresponding as nearly as possible to the relative 
frequency of their occurrence. 
(a) Fluid, Air or Solid in the Pleural Cavity.—Probably the 
commonest cause for a diminution or total abolition, of normal breath 
sounds is an accumulation of fluid in the pleural cavity such as occurs 
in inflammation of the pleura or by transudation (hydrothorax). In 
such cases the layer of fluid intervening between the lung and the 
stethoscope of the auscultator causes retraction of the lung so that 
little or no vesicular murmur is produced in it, and hence none is 
transmitted to the ear of the auscultator. An accumulation of air in 
the pleural cavity (pneumothorax) may diminish or abolish the breath 
sounds precisely as a layer of fluid does; in a somewhat different way a 
thickening of the costal or pulmonary pleura or a malignant growth of 
the chest wall may render the breath sounds feeble or prevent their 
being heard, because the vibrations of the thoracic sounding-board are 
thus deadened. Whichever of these causes, fluid or air or solid, inter- 
venes between the lung and the ear of the auscultator, the breath 
sounds are deadened or diminished without, as a rule, any modification 
of their type. The amount of such diminution depends roughly on 
the thickness of the layer of extraneous substance, whether fluid, air, 
or solid. 
Total absence of breath sounds may therefore be due to any one of 
these causes, provided the layer intervening between the lung and 
chest wall is of sufficient thickness to produce complete atelectasis of 
the lung or to deaden the vibrations of the chest wall. 
(b) In the earliest stages of pneumonia the breathing may be 
feeble or nearly suppressed, not bronchial. In bronchitis the breath 
sounds are sometimes considerably diminished owing to the filling up 
of the bronchi with secretion. This diminution, however, usually 
attracts but little attention, owing to the fact that the bubbling and 
squeaking sounds, which result from the passage of air through the AUSCULTATION 
161 
bronchial secretions, distract our notice to such an extent that we find 
it difficult to concentrate attention upon the breath sounds, even if 
we do not forget altogether to listen to them. When, however, we 
succeed in listening through the rales to the breath sounds themselves, 
we usually notice that they are very feeble, especially over the lower 
two-thirds of the chest. CEdema of the lung may diminish the breath 
Sounds in a similar way. ’ -a • me fr.':' ■ 
(c) Pain in the ,thorax, such as is produced by dry pleurisy or 
intercostal neuralgia, diminishes the breath sounds because it leads 
the patient to restrain, so far as possible,, the movements of his chest, 
and; so of his lungs. If, for any other reason, the full expansion of the 
lung does not take place, whether on account of the feebleness of the 
fespiratory movements or because the lung is mechanically hindered 
by the presence of pleuritic adhesions, the breath sounds are propor- 
tionately feeble. , « f ' ■ : lift 
(d) Occlusion of the upper air passages, as by spasm of oedema of the 
glottis, renders the'breathing very feeble on both sides of the chest. 
If one of the primary bronchi is occluded, or narrowed as the result 
of a gumma or' a tumor, or by an enlarged gland from without, we 
may get a unilateral enfeeblement of the breathing.*; m 
(e) Atele'cctasis, -especially in' new-born infants, gives feeble or 
absent breathing the portion affected. Occasionally a paralysis 
of the muscles of respiration , on one or both sides is found to result in a 
unilateral or bilateral enfeeblement of the breathing. 
(f) Relaxation of the lung above a high diaphragm, itself raised by 
abdominal tumors, gaseous or fluid accumulations, often produces an 
area of dulness and feeble breathing with more or less broncho- 
vesicular quality. A'-rav helps us very much in recognizing this 
Condition. ■ vm/'A.' ,, • ' ' 
One Should remember, when estimating the intensity of the 
breathing, that the sounds heard over the right base’are, normally, 
feebler than those over the left base. 
VTl. Bronchial or Tubular Breathing in Disease 
v: (a) 1 have already described'the occurrence of bronchial breathing 
in parts of the normal chest, namely, over the trachea and primary 
bronchi. In disease, bronchial breathing may be heard elsewhere in 
the chest and usually points to solidification of that portion of lung 
from which it is conducted. It is heard, most cOmmonlv in phthisis 
(sec below, p, 285)- • robuooo ?\ « Ui f s lo qoJ edi aaoras pniwo.'d 162 
PHYSICAL DIAGNOSIS 
(b) Croupous pneumonia is probably the next most frequent cause 
of bronchial breathing, although by no means every case of croupous 
pneumonia shows this sign. For a more detailed account of the 
conditions under which it does or does not occur in croupous pneumo- 
nia, see below, p. 287. Lobular pneumonia is rarely manifested by 
tubular breathing. 
(c) In about one-third of the cases of pleuritic effusion, distant 
bronchial breathing is to be heard over the fluid. On account of the 
feebleness of the breath sounds in such cases they are often put down 
as absent, as we are so accustomed to associate intensity with the 
bronchial type of breathing. One should be always on the watch for 
any degree of intensity of bronchial breathing from the feeblest to the 
most distinct. In empyema—especially in children—the bronchial 
breathing heard over the fluid may be intense and often leads to a 
false diagnosis of unresolved pneumonia or phthisis. 
When the breath sounds are enfeebled at the base of the thorax by 
accumulation of fluid there is usually a layer of bronchial or broncho- 
vesicular breathing a little higher up near the root of the lung which 
is relaxed above the fluid. (See also changes associated with peri- 
cardial effusion, p. 239.) 
(d) Rarer causes of bronchial breathing are pleural thickening, 
hemorrhagic infarction of the lung, syphilis, or malignant disease, any 
one of which may cause a solidification of a portion of the lung. 
VIII. Broncho-vesicular Breathing in Disease 
Respiration of this type should be carefully distinguished from 
puerile or exaggerated breathing, in which we hear the normal vesicu- 
lar respiration upon a large scale. I have already mentioned that 
broncho-vesicular breathing is normally to be heard over the apex of 
the right lung. In disease, broncho-vesicular breathing is heardpn 
other portions of the lung, and usually denotes a moderate degree of 
solidification of the lung, such as occurs in early phthisis or in the 
earliest and latest stages of croupous pheumonia. In cases of pleuritic 
effusion, one can usually hear broncho-vesicular breathing over the 
upper portion of the affected side, owing to the retraction of the lung 
at that point. 
IX. Amphoric Breathing (Amphora = A Jar) 
Respiration having a hollow, empty sound like that made by 
blowing across the top of a bottle, is occasionaly heard in disease AUSCULTATION 
163 
over pulmonary cavities (e.g., in phthisis) or in pneumothorax, i.e., 
under conditions in which the air passes in and out of a large empty 
cavity within the chest. Amphoric breathing never occurs in health. 
The pitch of both sounds is low, but that of expiration lower than that of 
inspiration. The intensity and duration of the sounds vary, and the 
distinguishing mark is their quality which resembles that of a whispered 
“who." 
X. Rales 
The term “rales” is applied to sounds produced by the passage of 
air through bronchi which contain mucus or pus, or which are narrowed 
by swelling of their walls.1 Rales are best classified as follows: 
(1) Crackling r&les, coarse or fine. When these are loud or sharp 
we call them consonating. 
(2) Musical rales (squeaks or groans). 
Each of these varieties will now be described more in detail- 
1. Coarse Crackles (or Bubbles) 
The nature of these is sufficiently indicated by their name. The 
coarsest or largest bubbles are those produced in the trachea, and 
ordinarily known as the “ death rattle. ” Tracheal rales occur in any 
condition involving either profound unconsciousness or very great 
weakness, so that the secretions which accumulate in the trachea are 
not coughed out. Tracheal rales are by no means a sure precursor of 
death, although they are very common in the moribund state. They 
can usually be heard at some distance from the patient and without a 
stethoscope. In catarrh of the smaller bronchi, large bubbling rales 
are occasionally to be heard. In phthisical cavities one sometimes 
hears coarse, bubbling rales of a very metallic and gurgling quality 
(see below, p. 302). The finer grades of rales correspond to the finer 
bronchi. 
In the majority of cases these rales are most numerous during 
inspiration and especially during the latter part of this act. Their 
relation to respiration may be represented graphically as in Fig. 124, 
using large dots for coarse rales and small dots for fine rales. Musical 
rales can be symbolized by the letter 5 (squeaks). 
1 Rales are of all auscultatory phenomena the easiest to appreciate, provided we 
exclude various accidental sounds which may be transmitted to the ear as a result of 
friction of the stethoscope against the skin or against the fingers of the observer. 
(See above, page 144.) 164 
PHYSICAL DIAGNOSIS 
2. Fine Crackling Rales 
These differ from the. preceding variety merely by the absence of 
any distinct bubbling quality. They are usually to be heard in cases 
of bronchopneumonia (tuberculous or not) and in other diseases 
causing pulmonary condensation so that the tiny explosions of fluid 
in the bronchi resonate or corisonate in the surrounding solid patches. 
They are especially apt to come at the end of inspi- 
ration, a large number being evolved in a very short 
space of time, so that one often speaks of an “explosion 
of fine cfackling rales ” at the end of inspiration. There 
is some doubt whether or not fine crackles can be pro- 
duced in a pleural exudate, old of new, but personally 
I 'am convinced that they are not infrequently so 
produced. 
The finest sounds'of this type are very much like the 
noise* which is heard when one takes a lock of hair be- 
tween the thumb and first finger, and rubs the hairs 
upon each other while holding them close to the ear. A very large 
number of minute crackling sounds is heard following each other in 
rapid succession. To the inexperienced ear they may seem to blend 
into a continuous souqd, but with practice the component parts may 
be distinguished. This type of rales is especially apt to dccur during 
inspiration alqne, but not very infrequently they are heard during 
expiration as well. 
They are oftenest heard at the end of a case of pneumonia, less 
frequently at its beginning. In tuberculosis, infarction, pulmonary 
abscess or oedema they are occasionally heard. If the chest is covered 
with hair, sounds precisely like crepitant rales may be heard 
when the stethoscope is placed upon the hairy portions. To avoid 
mistaking these sounds for rales one must thoroughly wet the hair. 
Fig. 124 — 
Explosion o f 
Fine Reties at 
End of Inspi7 
ration. 
(a) Crackling Rales in Atelectasis 
Fine crackles are very often to be heard: along the thin margins 
of the lungs at the base of the axillae and in the back, especially when 
a, middle-aged or elderly .patient who is breathing superficially first 
takes deep breaths.. In such cases; they usually disappear after 
the first few respirations, and are then to be explained by the tearing 
apart of the slightly agglutinated surfaces of the finer bronchioles. 
If is by no means' invariably the ease, however, that such crep- 
itant rales are merely transitory in their occurrence. In a small AUSCULTATION 
165 
number of cases they persist despite deep breathing. The frequency 
of crepitant rales, persistent or transitory, heard over the inferior 
margin of the normal lung at the bottom of the axilla, is shown by 
the following figures: Out of 356 normal chests to which I have 
listened especially for these rales, I found 228, or 61 per cent., which 
showed them on one or both sides. They are very rarely to be heard 
in persons under twenty years of age. After forty-five, on the other 
hand, it is unusual not to find them. *In my experience they are 
considerably more frequent in the situation shown in Fig. 182 than in 
any other part of the lung, but they may be occasionally heard in the 
back or elsewhere.. In view of these facts, it seems to me that we 
must recognize that it is almost if not quite physiological to find the 
finer varieties of crackling rales at the base of the axillse in persons over 
forty years old. I have supposed these rales to be due to a partial 
atelectasis resulting from disuse of the thin lower margin of the lungs. 
Such portions of the lung are ordinarily not expanded unless the 
respirations are forced and deep.1 
In certain cases of dry > pleurisy there occur fine crackling sounds 
which can scarcely be differentiated from crepitant rales. I shall: 
return to the description of them, in speaking of pleural friction (see 
below, p. 328). j a;; : .0 .. a, ■ 
3. Musical Rales (Squeaks ahd Groans) 
The passage of air through moist bronchial tubes narrowed by1 
inflammatory swelling of their lining membrane (bronchitis), by drop- 
sical effusions or by spasmodic contraction (asthma), gives rise not 
infrequently to a multitude of musical sounds: j Such a stenosis occur- 
ring in relatively large bronchial tubes produces a deep-toned groaning 
spund, while narrowing of the finer tubes results in piping, squeaking, 
whistling noises of various qualities. Such sounds are often known 
as “dry rales” in contradistinction to those above described, but as 
many non-musical crackling rales have also a very dry sound, it seems- 
to me best to apply the more distinctive term “musical rales” to all 
adventitious sounds of distinctly musical quality, giving up the term 
“dry” altogether. Musical rdles are of all adventitious sounds the 
easiest to recognize but also the most fugitive and changeable. They 
appear now here, now there, shifting from minute to minute, and may 
totally disappear from the chest and reappear again within a very 
1 So as to expand the lung and produce the “ entfaltungsgerausch ” of the 
Germans. 166 
PHYSICAL DIAGNOSIS 
short time. This is to some extent true of all varieties of rales, but 
especially of the squeaking and groaning varieties. A cough may elicit 
them. 
Musical rales are heard, as a rule, more distinctly during expiration, 
especially when they occur in connection with asthma. In these dis- 
eases one may hear quite complicated chords from the combinations of 
rales which vary in pitch. 
XI. The Effects of Cough 
The influence of coughing upon rales may be either to intensify 
them and bring them out where they have not previously been heard, 
or to clear them away altogether. Lying on the side multiplies and 
intensifies rales on the lower side. Other effects of coughing upon 
physical signs will be mentioned later. 
XII. Pleural Friction 
The surfaces of the healthy pleural cavity are lubricated with 
sufficient serum to make them pass noiselessly over each other during 
the movements of respiration. But when the tissues become abnor- 
mally dry, as in Asiatic cholera, uraemia, or when the serous surfaces are 
roughened by the presence of a fibrinous exudation, as in ordinary 
pleurisy, the rubbing of the two pleural surfaces against one another 
produces peculiar and very characteristic sounds known as “pleural 
friction sounds.” The favorite seat of pleural friction sounds is at the 
bottom of the axilla, i.e., where the lung makes the widest excursion 
and where the costal and diaphragmatic pleura are in close apposition 
(see Fig. 82). In some cases pleural friction sounds are to be heard 
altogether below the level of the lung. In others they may extend up 
several inches above its lower margin, and occasionally it happens 
that friction may be appreciated over the whole lung from the top to 
the bottom. Sometimes friction sounds are heard only at the apex 
of the lung in early tuberculosis. 
The sound of pleural friction may be closely imitated by holding 
the thumb and forefinger close to the ear, and rubbing them past each 
other with strong pressure, or by pressing the palm of one hand over 
the ear and rubbing upon the back of this hand with the fingers of the 
other. Pleural friction is usually a catchy, jerky, interrupted, irregu- 
lar sound, and is apt to occur during inspiration only, and particu- 
larly at the end of this act. It may, however, be heard with both 
respiratory acts, but rarely, if ever, occurs during expiration alone. auscultation 
167 
The intensity and quality of the sounds vary a great deal, so that they 
may be compared to grazing, rubbing, rasping, and creaking sounds. 
They are sometimes spoken of as “leathery." As a rule, they seem 
very near to the ear, and are sometimes startlingly loud. In many 
cases they cannot be heard after the patient has taken a few full 
breaths, probably because the rough pleural surfaces are smoothed 
down temporarily by the friction which deep breathing produces. 
After a short rest, however, and a period of superficial breathing, 
pleural friction sounds often return and can be heard for a short time 
with all their former intensity. They are • increased by pressure 
exerted upon the outside of the chest wall. Such pressure had best be 
made with the hand or with the Bowles stethoscope, since the sharp 
edges of the chest-piece of the ordinary stethoscope may give rise to 
considerable pain; but if such pressure is made with the hand, one 
must be careful not to let the hand shift its position upon the skin, 
else rubbing sounds may thus be produced which perfectly simulate 
pleural friction. In well-marked cases friction can be felt if the 
hand is laid over the suspected area; occasionally the vibrations are 
so coarse that they can be heard and felt by the patient himself or 
by those around him. I have already mentioned F. T. Lord’s1 ac- 
count of a sound a good deal like pleural friction, often heard over 
the scapulae when examining patients whose arms are folded across 
the chest with each hand on the opposite shoulder. The sound ap- 
parently starts in the shoulder-joint on one side or both sides—usually 
both. It is less jerky and irregular than pleural friction, can often 
be abolished by shifting the position of the arms, and causes no pain. 
XIII. Auscultation of the Spoken or Whispered Voice Sounds 
The more important of these is: 
1. The Whispered Voice 
The patient is directed to whisper “one, two, three,” or “ninety- 
nine,” while the auscultator listens over different portions of the chest 
to see to what degree the whispered syllables are transmitted. In 
the great majority of normal chests the whispered voice is to be heard 
only over the trachea and primary bronchi in front and behind, while 
over the remaining portions of the lung little or no sound is to be 
heard. When, on the other hand, solidification of the lung is present, 
the whispered voice may be distinctly heard over portions of the lung 
1 P. T. Lord: Boston Med. & Surg. Journal, Oct. 21, 1909. 168 
PHYSICAL DIAGNOSIS 
relatively distant from the trachea and bronchi; for example, over the 
lower lobes of the lung, behind. The usefulness of the whispered voice 
in the search for /small areas, of solidification or for the boundaries of a 
solidified area is great, especially in pneumonia when we wish .to save 
the patient the pain and fatigue of taking deep breaths. Whispered 
voice sounds, are practically equivalent to a forced expiration and can 
be obtained with very little exertion on the patient’s part. The in- 
creased transmission of the whispered voice is, in my opinion, a more 
delicate test for solidification than tubular breathing. The latter 
sign is present only when a considerable area of lung tissue is solidified, 
while the increase of the whispered voice may be obtained over much 
smaller areas. Retraction of the lung above the level of a pleural 
effusion causes a moderate increase in the transmission of the whispered 
voice, and at times this increased or bronchial whisper is to be heard 
over the fluid itself, probably by transmission from the compressed 
lung above. • \ . 
Where the lung is completely solidified the whispered words may 
be clearly distinguished over the affected area. In lesser degrees of 
solidification the syllables are more or less blurred. 
2. The Spoken Voice 
The evidence given us by listening for the spoken voice in various 
parts of the chest is considerably less in value than that obtained 
through the whispered voice. As a rule, it corresponds with the 
tactile fremitus, being increased in intensity by the same causes which 
increase tactile fremitus, viz., solidification or condensation of the lung, 
and decreased by the same causes which decrease tactile fremitus— 
namely, by the presence of air or water in the pleural cavity, by the 
thickening of the pleura itself, or by an obstruction of the bronchus 
leading to the part over which we are listening. In some cases the 
presence of solidification of the lung gives rise not merely to an increase 
in transmission of the spoken voice, but to a change in its quality, so 
that it sounds abnormally concentrated, nasal, and near to the listen- 
er’s ear. The latter change may be heard over areas where tactile 
fremitus is not increased, and even where it is diminished. Where 
this change in the quality of the voice occurs, the actual words spoken 
can often be distinguished in a way not usually possible over either 
normal or solidified lung. “Bronchophony,” or the distinct trans- 
mission of audible words, and not merely of diffuse, unrecognizable 
voice sounds, is "considerably commoner in the solidifications due to AUSCULTATION 
169 
pneumonia than in those due to phthisis; it occurs in some cases of 
pneumothorax and pulmonary cavity. 
3. Egophony 
Among the least important of the classical physical signs is a 
nasal or squeaky quality of the sounds which reach the observer’s 
ear when the patient speaks in a natural voice. To this peculiar 
quality of voice the name of “egophony” has been given. It is most 
frequently heard in cases of moderate-sized pleuritic effusion just 
about the level of the lower angle of the scapula and in the vicinity of 
that point. Less often it is heard at the same level in front. It is 
very rarely heard in the upper portion of the chest and is by no means 
constant either in pleuritic effusion or in any other condition. A point 
at which it is heard corresponds not, as a rule, with the upper level of 
the accumulated fluid, as has been frequently supposed, but often with 
a point about an inch farther down. The presence of egophony is in 
no way distinctive of pleuritic effusions and may be heard occasionally 
over solidified lung. 
XIV. Phenomena Peculiar to Pneumohydrothorax and Pneumo- 
pyothorax 
Now and then a patient consults a physician, complaining that he 
hears noises inside him as if water were being shaken about. One 
such patient expressed himself to me to the effect that he felt “like a 
half-empty bottle.” In the chest of such a patient, if one presses the 
ear against any portion of the thorax and then shakes the whole patient 
strongly (succussion), one may hear loud splashing sounds due to air 
and fluid within. The sound itself is often miscalled “succussion.” 
Such sounds are absolutely diagnostic of the presence of both air and 
fluid. Very frequently they may be detected by the physician when 
the patient is not aware of their presence. Occasionally the splashing 
of the fluid within may be felt as well as heard. It is essential, of 
course, to distinguish splashing due to the presence of air and fluid in 
the pleural cavity from similar sounds produced in the stomach, but 
this is not at all difficult in the majority of cases. It is a bare possibility 
that succussion sounds may be due to the presence of air and fluid in 
the pericardial cavity, or in the stomach or gut escaped into the 
thorax through a relaxed or ruptured diaphragm. In accident cases 
this possibility must be remembered. 
i. Succussion Sounds 170 
PHYSICAL DIAGNOSIS 
It is important to remember that splashing is never to be heard 
in simple pleuritic effusion or hydrothorax. The presence of air, as 
well as liquid, in the pleural cavity is absolutely essential to the pro- 
duction of succession sounds.1 
2. Metallic Tinkle or Falling-Drop Sound 
When listening over a pleural cavity which contains both air and 
fluid, one occasionally hears a liquid, tinkling sound, due possibly 
to the impact of a drop of liquid falling from the relaxed lung above 
into the accumulated fluid at the bottom of the pleural cavity, but 
probably to r&les produced in the tissues around the cavity. It is 
stated that this physical sign may in rare cases be observed in large 
sized phthisical cavities as well as in pneumohydrothorax and 
pneumopyothorax. 
3. The Lung-Fistula Sound 
When a perforation of the lung occurs below the level of the fluid 
accumulated in the pleural cavity, bubbles of air may be forced out 
from the lung and up through the fluid with a sound reminding one of 
that made by children when blowing soap-bubbles. I have never 
heard this sound. 
1 It is well for the student to try for himself the following experiment, which I 
have found useful in impressing these facts upon the attention of classes in physical 
diagnosis: Fill an ordinary rubber hot-water bag to the brim with water. Invert 
it and squeeze out forcibly a certain amount (perhaps half) of the contents, by 
grasping the upper end of the bag and compressing it. While the water is thus 
being forced out, screw in the nozzle of the bag. Now shake the whole bag, and 
it will be found impossible to produce any splashing sounds owing to the fact that 
there is no air in the bag. Unscrew the nozzle, admit air, and then screw it in 
again. Now shake the bag again and loud splashing will be easily heard. CHAPTER IX 
AUSCULTATION OF THE HEART 
In the routine examination of the heart, most observers listen in 
four places: 
(1) At the apex of the heart in the fifth intercostal space near the 
nipple, the “mitral area." 
(2) In the second left intercostal space near the sternum, the 
“pulmonic area." 
(3) In the second right intercostal space near the sternum, the 
“aortic area." 
I. “Valve Areas” 
Pulmonic area 
Aortic area. 
Tricuspid area 
Mitral area. 
Fig. 125.—The Valve Areas, 
(4) At the bottom of the sternum near the ensiform cartilage, 
the “ tricuspid area." 
These points are represented in Fig. 125 and are known as “valve 
areas." They do not correspond to the anatomical position of any 
one of the four valves, but experience has shown that most of the 
sounds heard best at the apex can be proved (by post-mortem exami- 
nation) to be produced at the mitral orifice. They are probably 
transmitted through the papillary muscle whose base or insertion is 
near the apex region. Similarly, sounds heard best in the second left 
intercostal space are proved to be produced at the pulmonary orifice; 
171 172 
PHYSICAL DIAGNOSIS 
those which are loudest at the second right intercostal space to be pro- 
duced at the aortic orifice;1 more often, however, aortic murmurs are 
best heard over the third and fourth left costal cartilages (‘ ‘ secondary 
aortic area ”). I can recognize no tricuspid murmurs. 
II. The Normal Heart Sounds 
A glance at Fig. 126, which represents the anatomical positions of 
the four valves above referred to, illustrates what I said above; 
namely, that the traditional valve areas do not correspond at all with 
the anatomical position of the valves. If now we listen in the 11 mitral 
area,” that is, in the region of the apex impulse of the heart, keeping 
Pulmonic valve. 
Aortic valve. 
Tricuspid valve. 
Mitral valve. 
Fig. 126.—Anatomical Position of the Cardiac Valves 
at the same time one finger on some point at which the cardiac impulse 
is palpable, one hears with each outward thrust of the heart a low, 
dull sound, and in the period between the heart beats a second sound, 
shorter and sharper in quality.2 
That which occurs with the cardiac impulse is known as the first 
sound; that which occurs between each two beats of the heart is known 
as the second sound. The second sound is generally believed to be 
due to the closure of the semilunar valves. The cause of the first 
1 For the exceptions to this rule, see below, page 224. 
2 The first sound of the heart, as heard at the apex, may be imitated by holding 
a linen handkerchief by the corners and suddenly tautening one of the borders. 
To imitate the second sound, use one-half the length of the border instead of the 
whole. AUSCULTATION OF THE HEART 
173 
sound has been a most fruitful source of discussion, and no one expla- 
nation of it can be said toibe generally: received. Perhaps the most 
commonly accepted view attributes .the first or systolic sound of the 
heart to a combination of two elements— 
;(&) The contraction of the heart muscle itself. 
(b) The sudden tautening of the mitral curtains. 
Following the second sound there is a pause corresponding to the 
diastole of the heart. Normally this pause occupies a little more 
time than the first and second sounds of the heart taken together. In 
disease it may be much shortened. p. ; 
The first sound of the heart is not only longer and duller than the 
second (it is often spoken of as “booming” in contrast with the “snap- 
ping” quality of the second sound), but is also considerably more 
intense, so that it gives us the impression of being accented like the 
first syllable of a trochaic rhythm. After a little practice one grows 
so accustomed to this rhythm that one is apt to rely upon his apprecia- 
tion of the rhythm alone to identify the first or systolic sound. This 
is, however, an unsafe practice and leads to many errors. Our impression 
as to which of the sounds of each cardiac cycle corresponds to systole 
should always-be verified either by sight or touch. We must either 
see or feel the cardiac impulse) and assure ourselves that it is synchron- 
ous with the heart sound which we take to be systolic.1 This point is 
of especial importance in the recognition and Identification of cardiac 
murmurs, as will be seen presently. I v : 
So far, I have been describing the normal heart sounds heard in 
the “mitral area,” that is, at the apex of the heart. If now we listed 
over the pulmonary area (in the second left intercostal space), we often 
find that the rhythm of the sounds lias changed and that here the stress 
seems to fall upon the “second sound,” i.e<, that corresponding 
to the beginning of diastole; in other words,,: the first Sound of;the heart 
is here heard more feebly and the second, sound more distinctly. 
The sharp, snapping quality of the latter is here even more marked) 
than at the apex, and despite the feebleness of the first sound in 
this area we can usually recognize its relatively dull and prolonged 
quality.. ■ /yy ij; ;: ,i;j . 
Over the traditional aortic area (i.e., the second right space) the 
rhythm is the same as in the pulmonary area, although the second 
sound may be either stronger or weaker, than the corresponding sound 
on the other side of the sternum (see below, p. 176). . ) '■ ■ 
1 When the cardiac impulse can be neither seen nonfelt, the pulsation of the 
carotid will generally guide us. The radial pulse is not a safe guide. 174 
PHYSICAL DIAGNOSIS 
Over the tricuspid area one hears sounds practically indistinguish- 
able in quality and in rhythm from those heard at the apex.1 
When the chest walls are thick and the cardiac sounds feeble, it 
may be difficult to hear them at all. In such cases the heart sounds 
may be heard much more distinctly if the patient leans forward and 
toward his own left. Such a position of the body also renders it easier 
to map out the outlines of the cardiac dulness by percussion if we allow 
for the swing of the heart to the left. 
In cardiac neuroses, thyrotoxicoses and during excitement or emo- 
tional strain, the first sound at the apex is not only very loud but has 
often a curious metallic reverberation (“cliquetis metallique”) corre- 
sponding to the trembling, jarring cardiac impulse (often mistaken 
for a thrill) which palpation reveals. 
III. Modifications in the Intensity of the Heart Sounds 
It has already been mentioned that in young persons with thin, 
elastic chests, the heart sounds are heard with greater intensity than in 
older persons whose chest walls are thicker and stiffen In obese, 
indolent adults it is sometimes difficult to hear any heart sounds at 
all, while in young persons of excitable temperament the sounds may 
have a very intense and ringing quality. Under diseased conditions 
either of the heart sounds may be increased or diminished in intensity. 
I shall consider 
1. The First Sound at the Apex (sometimes Called the Mitral First 
Sound) 
(a) Increase in the intensity of the first sound at the apex of the 
heart occurs in any condition which causes the heart to act with 
unusual degree of force, such as thyrotoxicosis, exertion, or excite- 
ment. In the earlier stages of infectious fevers a similar increase in 
the intensity of this sound may sometimes be noted. Hypertrophy 
of the left ventricle sometimes has a similar effect upon the sound, 
1 A third heart sound (or reduplication of the second sound) is audible on careful 
auscul tation in a considerable proportion of healthy young individuals—especially if 
they lie on the left side. Bari6 described it in 1893 (Semaine med.t 1893, xiii, 474), 
and Thayer (Boston Med. & Surg. Journ., May 7, 1908) has recently recalled it to 
notice, believing it due to “the sudden tension of the mitral and perhaps at times 
tricuspid valves occurring at the end of the first and most rapid phase of diastole.” 
This is probably identical with the double second sound of mitral stenosis and with 
one of the types of gallop rhythm. No diagnostic significance is as yet clearly 
associated with it. AUSCULTATION OF THE HEART 
175 
but less often than one would suppose, while weakening of the left 
ventricle, contrary to what one would suppose, is not infrequently 
associated with a loud, forcible first sound at the apex. In mitral 
stenosis the first sound is usually very intense, and is often spoken of as 
a “thumping first sound” or as a “sharp slap.” 
(b) Shortening and weakening of the first sound at the apex. 
In the course of continued fevers and especially in typhoid fever 
the granular degeneration which takes place in the heart muscle is 
manifested by a shortening and weakening of the first sound at the 
apex, so that the two heart sounds come to seem much more alike 
than usual. In the later stages of typhoid, the first sound may become 
almost inaudible. The sharp “valvular” quality, which one notices 
in the first apex sound under these conditions, has been attributed to 
the fact that weakening of the myocardium has caused a suppression 
of one of the two elements which go to make up the first sound, namely, 
the muscular element, so that we hear only the short, sharp sound due 
to the tautening of the mitral curtains. Arterio-sclerosis, or any other 
change which tends to enfeeble the heart wall, produces a weakening 
and shortening of the first sound similar to that just described. Simple 
weakness in the mitral first sound without any change in its duration 
or pitch may be due to fatty overgrowth of the heart, to emphysema 
or pericardial effusion in case the heart is covered by the distended 
lung or by the accumulated fluid. All in all, however, these changes 
in the first sound are of very little diagnostic use. 
(c) Doubling of the first sound at the apex. 
It is not uncommon in healthy hearts to hear in the region of the 
apex impulse a doubling of the first sound so that it may be suggested 
by pronouncing the syllables “turrupp” or “trupp.” In health this 
is especially apt to occur at the end of expiration. In disease it is 
associated with many different conditions involving an increase in the 
work of one or the other side of the heart. It seems to be unusually 
frequent in the weakened heart of nephritis and arteriosclerosis, but 
is not of much importance. 
2. Modifications in the Second Sounds as Heard at the Base of the 
Heart 
(a) Physiological Variations 
The relative intensity of the pulmonic second sound, when com- 
pared with the second sound heard in the conventional aortic area, 
varies a great deal at different periods of life. Attention was first 176 
PHYSICAL DIAGNOSIS 
called to this by Vierordt,1 and it has of late years been recognized 
by the best authorities on diseases of the heart. 
The work of Dr. Sarah R. Creighton, done in my clinic during the 
summer of 1899, showed that in 90 per cent, of healthy children under 
ten years of age, the pulmonic second sound is louder than the aortic. 
In the next decade (from the tenth to the twentieth year) the pulmonic 
second sound is louder in two-thirds of the cases. About half of 207 
cases, between the ages of twenty and twenty-nine, showed an accen- 
DECADES. 
PERCENTAGES. 
Fig, i 26a,“Showing the Per Cent, of Accentuated Pulmonic Second Sound in Each 
Decade. Based on 1,000 cases. ; , ,, ; : ,: 
tuation of the pulmonic second, while after the thirtieth yehr the 
number of cases showing such accentuation became smaller with each 
decade, until after the sixtieth year we found an accentuation of the 
aortic second in sixty-six out of sixty-eight cases examined. These facts 
are exhibited in tabular form in Figs. 126a and 127, and appear to show 
that the relative intensity of the two sounds in the aortic and pulmonic 
arteries depends primarily upon the age of the individual, the pulmonic 
1 Vierordt: “Die Messung der Intensitat der Herztone” (Tubingen, -1885). 
See also Hochsinger, “ Die Auscultation des kindlichen Herzens;” Gibson, “ Diseases 
of the Heart” (1898); Rosenbach, “Diseases of the Heart” (i960); Allbutt, 
“ System of Medicine.” AUSCULTATION OF THE HEART 
177 
sound predominating in youth and the aortic in old age, while in the 
period of middle life there is relatively little discrepancy between the 
two. It is, therefore, far from true to suppose that we can obtain evi- 
dence of a pathological increase in the intensity of either of the second 
sounds at the base of the heart simply by comparing it with the other. 
Pathological accentuation of the pulmonic second sound must mean a 
greater loudness of this sound than should be expected at the age of the 
patient in question, and not simply a greater intensity than that of the 
DECADES. 
PERCENTAGES. 
Fig. 127.—Showing the Per Cent, of Accentuated Aortic Second Sound in Each Decade 
Based on 1,000 cases. 
aortic second sound. The same observation obviously applies to 
accentuation of the aortic second sound. 
Both the aortic and the pulmonic second sounds are sometimes 
very intense during emotional excitement, in Graves’ disease, after 
muscular exertion, and sometimes without any obvious cause. 
(b) Pathological Variations 
Accentuation of the Pulmonic Second Sound 
Pathological accentuation of the second sound occurs especially in 
conditions involving a backing up of blood in the lungs, such as occurs 178 
PHYSICAL DIAGNOSIS 
in stenosis and insufficiency of the mitral valve, or in obstructive 
disease of the lungs (bronchitis, phthisis, chronic interstitial pneu- 
monia). Indirectly, accentuation of the pulmonic second sound points 
to hypertrophy of the right ventricle, since without such hypertrophy 
the work of driving ihe blood through the obstructed lung could not 
long be performed. If the right ventricle becomes weakened the 
accentuation of the pulmonic second sound is no longer heard. 
Weakening or Absence of the Pulmonic Second Sound 
Weakening of the pulmonic second sound is a very serious symptom, 
sometimes to be observed in cases of pneumonia or cardiac disease 
near death. 
Pulmonary stenosis also weakens or abolishes the second sound, 
and in many other types of congenital heart disease the pulmonic, as 
well as the aortic, second sound in inaudible. I have found it absent 
in aortic stenosis. Indeed, I think it may be stated that with any 
very loud systolic murmur at the base of the heart, we may find the 
pulmonic second sound gone; why I do not know. 
Accentuation of the Aortic Second Sound 
I have already shown that the aortic second sound is louder than 
the corresponding sound in the pulmonary area in almost every 
individual over sixty years of age and in most of those over forty. A 
still greater intensity of the aortic second sound occurs— 
(a) In nephritis, arterio-sclerosis, or any condition which increases 
arterial tension and so throws an increased amount of work upon the 
left ventricle. Directly, therefore, a pathologically loud aortic sound 
points to increased resistance in the peripheral arteries and indirectly 
to hypertrophy of the left ventricle. 
(b) A similar increase in the aortic second sound occurs in aneu- 
rism or sclerosis of the arch even without high blood-pressure. 
Diminution in the Intensity of the Aortic Second Sound 
Whenever the amount of blood thrown into the aorta by the 
contraction of the left ventricle is diminished, as is the case especially 
in mitral stenosis and in most cases of aortic stenosis, the aortic 
second sound is weakened so that at the apex it may be inaudible. 
A similar effect is produced by any disease which weakens the walls of 
the left ventricle. Relaxation of the peripheral arteries has the AUSCULTATION OF THE HEART 
179 
same effect. In conditions of collapse the aortic second sound may- 
be almost or quite inaudible. 
In persons past middle life the second sounds are often louder in 
the third or fourth interspace than in the second, so that if we listen 
only in the second space we may gain the false impression that the 
second sounds are feeble. 
Accentuation of both the second sounds at the base of the heart 
may occur in health from nervous causes or when the lungs are re- 
tracted by disease so as to uncover the conus arteriosus and the aortic 
arch. Under these conditions the second sound may be seen and felt 
as well as heard. In a similar way, an apparent increase in the inten- 
sity of either one of the second sounds at the base of the heart may 
be produced by a retraction of one or the other lung. 
Summary.—(i) The mitral first sound is increased by whatever 
induces increased vigor of the heart, and among valvular diseases, 
especially by mitral stenosis. It is weakened or reduplicated when 
the heart is weakened. Any of these changes may occur tempo- 
rarily from physiological causes. 
(2) The pulmonic second sound is usually more intense than the 
aortic in children and up to early adult life. Later the aortic second 
sound predominates. Pathological accentuation of the second 
pulmonic sound usually points to obstruction in the pulmonary circu- 
lation (mitral disease, etc.). Weakening of the pulmonic second 
means failure of the right ventricle and is serious. 
(3) The aortic second sound is increased pathologically by any 
cause which increases the work of the left ventricle (arterio-sclerosis, 
chronic nephritis). It is diminished when the blood stream, thrown 
into the aorta by the left ventricle, is abnormally small (mitral disease, 
cardiac failure). 
(4) Changes in the tricuspid sounds are rarely recognizable, while 
changes in the first sound as heard in aortic and pulmonic areas have 
little practical significance. 
3. Modifications in the Rhythm of the Cardiac Sounds 
(i) Whenever the walls of the heart are greatly weakened by 
disease—for example, in the later weeks of a case of typhoid fever—the 
diastolic pause of the heart is shortened so that the cardiac sounds 
follow each other almost as regularly as the ticking of a clock; hence 
the term “tick-tack heart.” As this rhythm is not unlike that heard 
in the foetal, the name of “embryocardia” is sometimes applied to 180 
PHYSICAL DIAGNOSIS 
it. The “tick-tack” rhythm may be heard in paroxysmal tachy- 
cardia, in thyrotoxicosis, infectious diseases and in any condition 
leading to collapse. 
(2) The term gallop rhythm refers to conditions in which three 
sounds are audible at or near the apex. 
(a) The commoner type is the presystolic gallop rhythm in which an 
extra sound occurs just before the ordinary first sound of the heart 
(practically a double first sound with accent on the second half). 
Such a rhythm may occur temporarily in any heart which is excited 
or overworked from any cause, but when permanent it is usually a 
sign of grave cardiac weakness (nephritic cases, arterio-sclerosis, 
chronic valvular disease, goitre, etc.). 
(b) Protodiastolic Gallop Rhythm (doubling of the second sounds at 
the base of the heart). The extra sound is not easily distinguished 
from the so-called “third heart sound” referred to on page 217 and 
most constantly heard in the early stages of mitral stenosis, but the 
interval between the two parts is longer in the latter case. 
At the end of a long inspiration this change may be observed in 
almost any healthy persons if one listens at the base of the heart. It 
is still better brought out after muscular exertion or by holding the 
breath. 
In mitral stenosis the double diastolic sound is also to be heard at 
the apex, and in the diagnosis of this disease this “double shock sound ” 
during diastole may be an important piece of evidence, and may 
sometimes be felt and seen as well as heard. Just what its mechanism 
is, is disputed. Except in mitral stenosis, it has no especial clinical 
significance. 
4. Metallic Heart Sounds 
The presence of air in the immediate vicinity of the heart, as, for 
example, in pneumothorax or in gaseous distention of the stomach or 
intestine, may impart to the heart sounds a curious metallic quality 
such as is not heard under any other conditions. 
5Muffling,” “Prolongation, ” or 11 Unclearness” of the Heart Sounds 
These terms are not infrequently met with in literature, but their 
use should, I think, be discontinued. The facts to which they refer 
should be explained either as faintness of the heart sounds, due to the 
causes above assigned, or as faint, short murmurs. In their present 
usage such terms as “muffled” or “unclear” heart sounds represent AUSCULTATION OF THE HEART 
181 
chiefly an unclearness in the mind of the observer as to just what it is 
that he hears, and not any one recognized pathological condition in 
the heart. 
IV. Sounds Audible over the Peripheral Vessels 
(1) The normal heart sounds are in adults audible over the carotids 
and over the subclavian arteries. In childhood and youth only the 
second heart sound is thus audible. 
(2) In about 7 per cent, of normal persons a systolic sound can be 
heard over the femoral artery. This sound is obviously not trans- 
mitted from the heart, and is usually explained as a result of the 
sudden systolic tautening of the arterial wall. 
In aortic regurgitation this arterial sound is almost always audible 
not only in the femoral but in the brachial and even in the radial, and 
its intensity over the femoral becomes so great that the term ‘ ‘ pistol- 
shot” sound has been applied to it. In fevers, exophthalmic goitre, 
and other diseases involving a large pulse pressure, a similar arterial 
sound is to be heard much more frequently than in health. CHAPTER X 
AUSCULTATION OF THE HEART: CONTINUED 
CARDIAC MURMURS 
I. Terminology 
The word “ murmur ” is one of the most unfortunate of all the terms 
used in the description of physical signs. No one of the various 
blowing, whistling, rolling, rumbling, or piping noises to which the 
term refers, sounds anything like a “murmur” in the ordinary sense 
of the word. Nevertheless, it does not seem best to try to replace it 
by any other term. The French word “souffle” is much more 
accurate and has become to some extent Anglicized. Under the head 
of cardiac murmurs are included all abnormal sounds produced within 
the heart itself. Pericardial friction sounds and those produced in 
that portion of the lung or pleura which overlies the heart are not 
considered ‘ ‘ murmurs. 
II. Mode of Production 
With rare exceptions all cardiac murmurs are produced at or near 
one of the valve orifices, either by disease of the valves themselves 
resulting in shrivelling, thickening, stiffening, and narrowing of the 
valve curtains, by a stretching of the orifice into which the valves 
are inserted, or by disease of the aortic arch. 
Diseases of the valves themselves may lead to the production of 
murmurs: 
(a) When the valves are too stiff and short to close (incompe- 
tence, insufficiency, or regurgitation). 
(b) When the valves fail to open at the proper time (stenosis or 
obstruction). 
(c) When the surfaces of the valves or of the parts immediately 
adjacent are roughened so as to prevent the smooth flow of the blood 
over them. 
(d) When the orifice which the valves are meant to close is dilated 
as a result of dilatation of the heart chamber of which it forms the 
entrance or exit. The valves themselves cannot enlarge to keep pace 
182 AUSCULTATION OF THE HEART 
183 
with the enlargement of the orifice, and hence no longer suffice to 
reach across it. 
The presence of any one of these lesions gives rise to eddies in the 
blood current and thereby to the abnormal sounds to which we give 
Fig. 128.—Diagram to Illustrate the Production of a Cardiac Murmur Through 
Regurgitation from the Aorta or in an Aneurismal Sac. The arrow shows the direction 
of the blood current and the curled lines the audible blood eddies. 
the name murmurs.1 (See Figs. 129, 130 and 131.) When valves 
fail to close and so allow the blood to pass back through them, we 
speak of the lesion as regurgitation, insufficiency, or incompetence; if, 
for example, the aortic valves fail to close after the left ventricle has 
Fig. 129.—Diagram to Illustrate the Production of a Cardiac Murmur Through Stenosis 
of a Valve-Orifice. 
thrown a column of blood into the aorta, some of this blood regurgi- 
tates through these valves into the ventricle from which it has just 
been expelled, and we speak of the lesion as “aortic regurgitation," 
and of the murmur so produced as an aortic regurgitant murmur or a 
Fig. 130.—Diagram to Illustrate the Production of Cardiac Murmurs Through Rough- 
ening of a Valve. 
murmur of aortic regurgitation. If the mitral valve fails to open 
properly to admit the blood which should flow during diastole from 
the left auricle into the left ventricle, we speak of the condition as 
mitral stenosis or mitral obstruction. A similar narrowing of the aortic 
1 The method by which functional murmurs are produced will be discussed later. 
(See page 191.) 184 
PHYSICAL DIAGNOSIS 
valves such as to hinder the egress of blood during the systole of the 
left ventricle is known as aortic stenosis or obstruction. Valvular 
lesions of the right side of the heart (tricuspid and pulmonic valves) 
are comparatively rare, but are produced and named in a way similar 
to those just described. 
The facts most important to know about a murmur are: 
(1) Its place in the cardiac cycle. 
(2) Its point of maximum intensity. 
(3) The area over which it can be heard. 
(4) The effects of exertion, respiration, or position upon it. 
Less important than the above are: 
(5) Its intensity. 
(6) Its quality. 
(7) Its length. 
(8) Its relation to the normal sounds of the heart. 
Each of these points will now be taken up in detail: 
(1) Time of Murmurs.—The first and most important thing to 
ascertain regarding a murmur is its relation to the normal cardiac 
cycle; that is, whether it occurs during systole or during diastole, or in 
case it does not fill the whole of one of those periods, in what part of 
systole or diastole it occurs. It must be borne in mind that the period 
of systole is considered as lasting from the beginning of the first sound 
of the heart up to the occurrence of the second sound, while diastole 
lasts from the beginning of the second sound until the beginning of the 
first sound in the next cycle. Any murmur occurring with the first 
sound of the heart, or at the time whan the first sound should take 
place, or in any part of the period intervening between the first sound 
and the second, is held to be systolic. Murmurs which distinctly follow 
the first sound or do not begin until the first sound is ended are known 
as late systolic murmurs. 
On the other hand, it seems best, for reasons to be discussed more 
in detail later on, not to give the name of diastolic to all murmurs which 
occur within the diastolic period as above defined. Murmurs which 
occur during the last part of diastole and which run up to the first 
sound of the next cycle are usually known as “presystolic” murmurs. 
All other murmurs occurring during diastole are known as diastolic. 
The commonest of all the errors in the diagnosis of disease of the 
heart is to mistake systole for diastole, and thereby to misinterpret the 
significance of a murmur heard during those periods. This mistake 
would never happen if we were always careful to make sure, by means AUSCULTATION OF THE HEART 
185 
of sight or touch, just when the systole of the heart occurs. This may 
be done by keeping one finger upon the apex impulse of the heart or 
upon the carotid artery while listening for murmurs, or, in case the 
apex impulse or the pulsations of the carotid are better seen than felt, 
we can control by the eye the impressions gained by listening. It is 
never safe to trust our appreciation of the cardiac rhythm to tell us 
which is the first heart sound and which the second. The proof of this 
statement is given by the numberless mistakes made through disre- 
garding it. Equally untrustworthy as a guide to the time of systole 
and diastole is the radial pulse, which follows the cardiac systole at an 
interval just long enough to mar our calculations. 
(2) Localizations of Murmurs.—To localize a murmur is to find its 
point of maximum intensity, and this is of the greatest importance in 
diagnosis. Long experience has shown that murmurs heard loudest in 
the region of the apex beat (whether this is in the normal situation or 
displaced), are in the majority of cases produced at the mitral valve. 
In about five per cent, of the cases mitral murmurs may be best heard 
at a point midway between the position of the normal cardiac impulse 
and the ensiform cartilage, or, (rarely), an inch or two above this 
situation. 
Murmurs heard most loudly in the second left intercostal space are 
usually produced at the pulmonic orifice or just above it in the conus 
arteriosus. Many congenital heart defects produce murmurs here. 
Murmurs produced at the aortic orifice may be heard best in the 
aortic area, but in a large proportion of cases are loudest on the other 
side of the sternum at or about the situation of the fourth left costal 
cartilage. Sometimes they are best heard at the apex of the heart 
in the axilla or over the lower part of the sternum (see below, Fig. 149). 
(3) Transmission of Murmurs.—If a murmur is audible over 
several valve areas, the questions naturally arise: “How are we to know 
whether we are dealing with a single valve lesion or with several ? Is 
this one murmur or two or three murmurs ?” Obviously the question 
can be asked only in case the murmur which we find audible in various 
places occupies everywhere the same time in the cardiac cycle. It 
must, for example, be everywhere systolic or everywhere diastolic. A 
systolic murmur at the apex cannot be supposed to point to the same 
lesion as a diastolic murmur, no matter where the latter is heard. 
But, if we hear a systolic murmur in various parts of the chest, say 
over the aortic, mitral, and pulmonic regions, how are we to know 
whether the sound is simple or compound, whether produced at one 
valve orifice or at several ? 186 
PHYSICAL DIAGNOSIS 
This question is sometimes difficult to answer, and in a given case 
skilled observers may differ in their verdict, but, as a rule, the difficulty 
may be overcome as follows: 
(1) Experience and post-mortem examination have shown that 
the murmur produced by each of the valvular lesions has its own 
characteristic area of propagation, over which it is heard with an 
intensity which regularly diminishes as we recede from a maximum 
whose seat corresponds with some one of the valve areas just described. 
These areas of propagation are shown in Figs. 142, 147, and 150. Any 
murmur whose distribution does not extend beyond one of these areas, 
and which steadily and progressively diminishes in intensity as we 
move away from the valve area over which it is loudest, may be 
assumed to be due to a single valve lesion and no more. Provided 
but one valve is diseased, this course of procedure gives satisfactory 
results. 
(2) When several valves .are diseased and several murmurs may 
be expected, it is best to start at some one valve area, say in the mitral 
or apex region, and move the stethoscope one-half an inch at a time 
toward one of the other valve areas, noting the intensity of any mur- 
mur we may hear at each of the different points passed over. As we 
move toward the aortic area, we may get an impression best expressed 
by Fig. 133. As we go on in the same direction the murmur may first 
grow fainter then louder (and perhaps change in pitch and quality 
as well) until a maximum is reached at the aortic area, beyond which 
the murmur again fades out. 
These facts justify us in suspecting that we are dealing with two 
murmurs, one produced at the tricuspid and one at the mitral orifice. 
The suspicion is more likely to be correct if there has been a change in 
the pitch and quality of the murmur as we neared the second orifice, 
and may be confirmed by the discovery of other evidences of a double 
lesion. But no diagnosis is satisfactory which rests on the evidence of 
murmurs alone. Changes in the size of the heart’s chambers or in the 
pulmonary or peripheral circulations are the most important facts in 
the case. Nevertheless the effort to ascertain, and graphically to 
represent the intensity of cardiac murmurs as one listens along the line 
connecting the valve areas has its value. An “hour-glass” murmur, 
such as that represented in Fig. 133 generally means two-valve lesions. 
An “hour-glass” shape may be found to represent the auditory facts 
as we move from the mitral to the pulmonic or to the aortic areas 
(see Fig. 131) and, as in the previous case, arouses our suspicion 
that more than one valve is diseased. AUSCULTATION OF THE HEART 
187 
It must not be forgotten, however, that “a murmur may travel some 
distance underground and emerge with a change of quality ” (Allbutt). 
This is especially true of aortic systolic murmurs, which are often 
heard well at the apex and at the aortic area, and faintly in the inter- 
vening space, probably owing to the interposition of the right ventricle. 
In such cases we fall back upon the other relevant facts shown by 
A-ray, blood-pressure, inspection, palpation, and percussion, upon the 
Fig. 131.—Mitral Disease and Aortic Stenosis. The systolic murmur is loudest 
at the extremities of the shaded area; and faintest at its “waist.” 
condition of the lungs and arteries as shown in the other symptoms 
and signs of the case (dropsy, cough, etc.), and upon the etiology. 
(3) Intensity of Murmurs.—Sometimes murmurs are so loud 
that they are audible to the patient himself or even at some distance 
from the chest. In one case I was able to hear a murmur eight feet 
from the patient. Such cases are rare and usually not serious, for the 
gravity of the lesion is not at all proportional to the loudness of the 
murmur; indeed, other things being equal, loud murmurs are less 
serious than faint ones, provided we are sure we are dealing with 
organic lesions. (On the distinction between the organic and func- 
tional murmurs, see below, p. 190.) 
A loud murmur means a powerful heart driving the blood strongly 
over the diseased orifice. When the heart begins to fail, the intensity 
of the murmur proportionately decreases because the blood does not 
flow swiftly enough over the diseased valve to produce as loud a sound 
as formerly. The gradual disappearance of a murmur known to be 
due to a valvular lesion is, therefore a very grave sign, and its reap- 
pearance revives hope. Patients are not infrequently admitted to a 188 
PHYSICAL DIAGNOSIS 
hospital with valvular heart trouble which has gone on so long that 
the muscle of the heart is no longer strong enough to produce a mur- 
mur as it pumps the blood over the diseased valve. In such a case, 
under the influence of rest and cardiac tonics, one may observe the 
development of a murmur as the heart wall regains its power, and 
the louder the murmur becomes the better the condition of the patient. 
On the other hand, when the existence of a valvular lesion has been 
definitely determined, and yet the compensation remains perfectly 
good (for example, in the endocarditis occurring in children in con- 
nection with chorea), an increase in the loudness of the murmur may 
run parallel with the advance in the valvular lesion. 
In general the most important point about the intensity of a mur- 
mur is its increase or decrease while under observation, and not its 
loudness at any one time. 
(4) Quality of Heart Murmurs.—It has been already mentioned 
that the quality of a heart murmur is never anything like the sound 
which we ordinarily designate by the word “murmur.” The com- 
monest type of heart murmur has a blowing quality whence the old 
name of 11 bellows sound." The sound of the letter “f” prolonged is 
not unlike the quality of certain murmurs. Blowing murmurs may 
be low-pitched like the sound of air passing through a large tube, 
or high-pitched approaching the sound of a whistle. This last type 
merges into that known as the musical murmur, in which there is a 
definite musical sound whose pitch can be identified. Rasping 
or tearing sounds often characterize the louder varieties of murmurs. 
Finally, there is one type of sound which, though included under 
the general name murmur, differs entirely from any of the other 
sounds just described. This is the “presystolic roll," which has a 
rumbling or blubbering quality or may remind one of a short drum- 
roll. This murmur is always presystolic in time and usually associated 
with obstruction at the mitral or tricuspid valves. Not infrequently 
some part of a cardiac murmur will have a musical quality while the 
rest is simply blowing or rasping in character. Musical murmurs do 
not give us evidence either of an especially serious or especially 
mild type of disease. Their chief importance consists in the fact that 
they rarely exist without some valve lesion,1 and are, therefore, of 
use in excluding the type of murmur known as “functional," pres- 
ently to be discussed, and not due to valve disease. Very often rasp- 
ing murmurs are associated either with the calcareous deposit upon 
a valve or very marked narrowing of the valve orifice. 
1 Rosenbach holds that they may be produced by adhesive pericarditis. AUSCULTATION OF THE HEART 
189 
Murmurs may be accented at the beginning or the end; that is, 
they may be of the crescendo type, growing louder toward the end, 
or of the decrescendo type with their maximum intensity at the 
beginning. 
(5) Length of Murmurs.—Murmurs may occupy the whole of 
systole, the whole of diastole, or only a portion of one of these periods, 
but no conclusions can be drawn as to the severity of the valve lesion 
from the length of the murmur. A short murmur, especially if 
diastolic, may be of very serious prognostic import. 
(6) Relations to the Normal Sounds of the Heart.—Cardiac murmurs 
may or may not replace the normal heart sounds. They may occur 
simultaneously with one or both sounds or between the sounds. These 
facts have a certain amount of significance in prognosis. Murmurs 
which entirely replace cardiac sounds usually mean a severer disease 
of the affected valve than murmurs which accompany, but do not 
replace, the normal heart sounds. Late systolic murmurs, which 
occur between the first and the second sound, are usually associated 
with a relatively slight degree of valvular disease. Late diastolic 
murmurs, on the other hand, have no such favorable significance. 
(7) Effects of Position, Exercise, and Respiration upon Cardiac 
Murmurs.—Almost all cardiac murmurs are affected to a greater or 
less extent by the position which the patient assumes while he is 
examined. Systolic murmurs which are inaudible while the patient 
is in a sitting or standing position may be quite easily heard when the 
patient lies down. On the other hand, a presystolic roll which is easily 
heard when the patient is sitting up may nearly disappear when he 
lies down. Diastolic murmurs are relatively little affected by the 
position of the patient, but in the majority of cases are somewhat 
louder in the upright position. 
The effects of exercise may perhaps be fitly mentioned here. 
Feeble murmurs may altogether disappear when the patient is at rest, 
and under such circumstances may be made easily audible by getting 
the patient to walk briskly up and down the room a few times. Such 
lesions are usually comparatively slight.1 On the other hand, mur- 
murs which become more marked as a result of rest are generally of 
the severest type. 
Organic murmurs are usually better heard at the end of expiration 
and become fainter during inspiration as the expanding lung covers 
the heart. This is especially true of those produced at the mitral 
1 For exception to this see below, page 208. 190 
PHYSICAL DIAGNOSIS 
valve, and is in marked contrast with the variations of functional mur- 
murs which are heard chiefly or exclusively at the end of inspiration. 
(8) Sudden Metamorphosis of Murmurs.—In acute endocarditis, 
when vegetations are rapidly forming and changing their shape upon 
the valves, murmurs may appear and disappear very suddenly. This 
metamorphosing character of cardiac murmurs, when taken in connec- 
tion with other physical signs, may be a very important factor in the 
diagnosis of acute endocarditis. In a similar way relaxation or 
rupture of one of the tendinous cords, occurring in the course of 
acute endocarditis, may effect a very sudden change in the auscultatory 
phenomena. 
III. Functional Murmurs 
Not every murmur which is to be heard over the heart points to 
disease either in the valves or in the orifices of the heart. Perhaps the 
majority of all murmurs are thus unassociated with valvular disease, 
and to such the name of “accidental,” “functional,” or “haemic” 
murmurs has been given. The origin of these “functional” murmurs 
has given rise to an immense amount of controversy, and it cannot be 
said that any one explanation is now generally agreed upon. To me, 
the most plausible view is that which regards most of them as due 
either to a temporary or permanent dilatation of the conus arteriosus, 
or to pressure or suction exerted upon the overlapping lung margins 
by the cardiac contractions. This explains only the systolic functional 
murmurs, which make up ninety-nine per cent, of all functional 
murmurs. The diastolic functional murmurs, which undoubtedly 
occur, although with exceeding rarity, are probably due to stretching of 
the aortic ring or to sounds produced in the veins of the neck and 
transmitted to the vena cava. 
Characteristics of Functional Murmurs.—(i) Almost all functional 
murmurs are systolic, as has before been mentioned. 
(2) The majority of them are heard best over the pulmonic valve 
in the second left intercostal space. From this point they are trans- 
mitted in all directions, and are frequently to be heard, although with 
less intensity, in the aortic and mitral areas. Not infrequently they 
may have their maximum intensity in one of the latter positions. 
(3) As a rule, they are very soft, short, and blowing in quality, 
though exceptionally they may be loud and rough. They almost 
never extend through the whole of systole. AUSCULTATION OP THE HEART 
191 
(4) They are usually not associated with evidence of enlargement 
of the heart nor with accentuation of the pulmonic second sound.1 
(5) They are usually louder at the end of inspiration. 
(6) They are usually heard over a very limited area, but to this 
rule there are exceptions. 
(7) They are especially evanescent in character; for example, they 
may appear at the end of a hard run or boat race or during an attack 
of fever, and disappear within a few days or hours. Respiration, 
position, and exercise produce greater variations in them than in 
‘ ‘ organic ’ ’ murmurs. 
(8) They are especially apt to be associated with anccmia, although 
the connection between anaemia and functional heart murmurs is by 
no means as close as has often been supposed. The severest types of 
anaemia, for example pernicious anaemia, may not be accompanied by 
any murmur, while, on the other hand, typical functional murmurs are 
often heard in patients whose blood is normal, and even in full health. 
Yet in three cases of intense anaemia I have heard diastolic murmurs 
loudest at the fourth left costal cartilage and leading to a diagnosis of 
aortic regurgitation. At autopsy the aortic valves were in each case 
sound, and I am at a loss to account for the murmurs.2 
The distinctions between organic and functional heart murmurs 
may be summed up as follows: 
Organic murmurs may occupy any part of the cardiac cycle; if 
systolic, they are often transmitted either into the axilla and back, or 
into the great vessels of the neck; they are usually associated with 
evidences of cardiac enlargement and changes in the second sounds 
at the base of the heart, as well as with signs and symptoms of stasis 
in other organs. Organic murmurs not infrequently have a musical 
or rasping quality, although this is by no means always the case. 
They are rarely loudest in the pulmonic area and are relatively unin- 
fluenced by respiration, position, or exercise. 
Functional murmurs are almost always systolic in time and usually 
heard with maximum intensity in the pulmonic area. They are 
rarely transmitted beyond the precordial region and are usually loudest 
at the end of inspiration. They are not accompanied by evidences of 
cardiac enlargement or pathological accentuation of the second 
sounds at the base of the heart, nor by signs of venous stasis or dropsy. 
1 In chlorosis the second pulmonic sound is often very loud (owing to the 
retraction of the lungs and uncovering of the conus arteriosus) and associated with 
a systolic murmur. 
2 Cabot and Locke: Johns Hopkins Bulletin, May, 1903. 192 
PHYSICAL DIAGNOSIS 
They are very apt to be associated with anaemia or with some special 
attack upon the resources of the body (e.g., physical overstrain or 
fever), and to disappear when such forces are removed. They are 
usually short and soft in quality; rarely musical. The very rare 
diastolic functional murmur occurs oftenest, so far as I am aware, in 
conditions of profound anasmia; i.e., when the haemoglobin is twenty- 
five per cent, or less, and of hypertension. 
IV. Cardio-Respiratory Murmurs 
When a portion of the free margin of the lung is fixed by adhesions 
in a position overlapping the heart, the cardiac movements may 
rhythmically displace the air in such piece of lung so as to give rise to 
sounds which at times closely simulate cardiac murmurs. These 
conditions are most often to be found in the tongue-like projection of 
the left lung, which normally overlaps the heart, but it is probably 
the case that cardio-respiratory murmurs may be produced without 
any adhesion of the lung to the pericardium under conditions not at 
present understood. Such murmurs may be heard under the left 
clavicle or below the angle of the left scapula, as well as near the apex 
of the heart,—less often in other parts in the chest. 
Cardio-respiratory murmurs may be either systolic or diastolic, 
but in the vast majority cases are systolic. The area over which they 
are audible is usually a very limited one. They are greatly affected 
by position and by respiration, and are heard most distinctly, if not 
exclusively, during inspiration, especially at the end of that act. 
(This fact is an important aid in distinguishing them from true cardiac 
murmurs, which are almost always fainter at the end of inspiration.) 
They are also greatly affected by cough or forced respiration or by 
holding the breath, whereas cardiac murmurs are relatively little 
changed thereby. Pressure on the outside of the thorax and in their 
vicinity'may greatly modify their intensity or quality, while organic 
cardiac murmurs are less influenced by pressure. As a rule, they have 
the quality of normal respiratory murmurs, and sound like an inspiration 
interrupted by each systole of the heart.1 
In case the effect of the cardiac movements is exerted upon a piece 
of lung in which a catarrhal process is going on, we may have systolic 
or diastolic crackles or squeaks, or any type of respiratory murmur 
except the bronchial type, since this is produced in solid lung which 
could not be emptied or filled under the influence of the cardiac move- 
1 For the distinction from cog-wheel breathing, see above, page 153. AUSCULTATION OF THE HEART 
193 
ments. Cardio-respiratory murmurs have no special diagnostic 
significance, and are mentioned here only on account of the importance 
of not confusing them with true cardiac murmurs. They were 
formerly thought to indicate phthisis, but such is not the case. 
V. Arterial Murmurs 
(1) Roughening or slight dilatation of the arch of the aorta, due to 
chronic endaortitis, is a frequent cause in elderly people of a systolic 
murmur, heard best at the base of the heart and transmitted into the 
vessels of the neck. From cardiac murmurs it is distinguished by 
the lack of any other evidence of cardiac disease and by the evidence 
of marked arteriosclerosis in the peripheral vessels (see further dis- 
cussion under Aortic Stenosis, p. 225, and under Aneurism, p. 261). 
(2) A narrowing of the lumen of the subclavian artery, due to 
some abnormality in its course, may give rise to a systolic murmur 
heard close below the clavicle at its outer end. The murmur is greatly 
influenced by movements of the arm and especially by respiratory 
movements. During inspiration it is much louder, and at the end of 
a forced expiration it may disappear altogether. Occasionally such 
murmurs are transmitted through the clavicle so as to be audible 
above it. 
(3) Pressure exerted upon any of the superficial arteries, carotid, 
femoral, etc.) produces a systolic murmur. Diastolic arterial mur- 
murs are peculiar to aortic regurgitation. 
(4) Over the anterior fontanella in infants and over the gravid 
uterus systolic murmurs are to be heard which are probably arterial 
in origin. 
(5) Thayer has recently described an epigastric murmur in a case 
of cirrhotic liver. CHAPTER XI 
establishment and failure of compensa- 
tion IN VALVULAR DISEASE OF THE HEART 
We may discriminate three periods in the progress of a case of 
valvular heart disease: 
(1) The period before the establishment of compensation. 
(2) The period of compensation. 
(3) The period of failing or ruptured compensation. 
In most cases of acute “rheumatic” endocarditis, whether of the 
relatively benign or of the malignant type, there is a time when the 
lesion is perfectly recognizable despite the fact that compensatory 
hypertrophy has not yet occurred. In some cases this period may last 
for months; the heart is not enlarged, there is no accentuation of either 
second sound at the base, there is no venous stasis, and our diagnosis 
must rest solely upon the presence and characteristics of the murmur. 
For example, in early cases of mitral lesion associated with chorea or 
rheumatism, the disease may be recognized by the presence of a 
long or musical murmur heard in the back as well as at the apex and 
in the axilla. In the earlier stages of aortic regurgitation occurring 
in young people as a complication of rheumatic fever, there may be 
absolutely no evidence of the valve lesion except the characteristic 
diastolic murmur. 
I. Compensation not yet Established 
II. The Period of Compensation 
Valvular disease would, however, soon prove fatal were it not for 
the occurrence of compensatory hypertrophy of the heart walls. To 
a certain extent the heart contracts as a single muscle, and increases 
the size of all its walls in response to the demand for increased work; 
but as a rule the hypertrophy predominates in one ventricle—that 
ventricle, namely, upon which especially demand is made for increased 
power in order to overcome an increased resistance in the vascular cir- 
cuit which it supplies with blood. Whatever increases the resistance 
194 HYPERTROPHY AND DILATATION 
195 
in the lungs brings increased work upon the right ventricle; whatever 
increases the resistance in the aorta or peripheral arteries increases 
the amount of work which the left ventricle must do. 
Now, any disease of the mitral valve, whether obstruction or 
leakage, results in engorgement of the lungs with blood, and hence 
demands an increased amount of work on the part of the right ventricle 
in order to force the blood through the overcrowded pulmonary 
vessels, hence' it is in mitral disease that we find the greatest com- 
pensatory predominance of the right ventricle. 
On the other hand, it is obvious that obstruction at the aortic 
valves or in the peripheral arteries with or without arterio-sclerosis, 
or nephritis demands an increase in power in the left ventricle, in 
order that the requisite amount of blood may be forced through ar- 
teries of reduced calibre, while if the aortic valve is so diseased that a 
part of the blood thrown into the aorta by the left ventricle returns 
into the ventricle, its work is thereby greatly increased, since it has to 
contract upon a larger volume of blood. 
In response to these demands for increased work, the muscular 
wall of the left ventricle increases in thickness, and compensation is 
thus established at the cost of an increased amount of work on the 
part of the heart.1 
III. Failure of Compensation 
Sooner or later in the vast majority of cases, the heart, handi- 
capped as it is by a leakage or obstruction of one or more valves, 
becomes unable to meet the demands made upon it by the needs of 
the circulation. Failure of compensation is associated with decrease of 
muscular tone and thence with weakening of the heart’s contraction. 
Not infrequently recurrent attacks of “failing compensation” represent 
a flare-up of a smouldering endocarditis as the accompanying leucocy- 
tosis (with or without fever) suggests. This is especially common in 
children but occurs also in young adults. Sometimes, however, 
neither mechanical nor infectious changes can be found. Whatever 
the cause may be, the result of ruptured compensation is venous stasis; 
that is, oedema or dropsy of various organs appears. If the left 
ventricle is especially weakened, dropsy appears first in the legs, on 
account of the influence of gravity, soon after in the genitals, lungs, 
liver, and the serous cavities. Engorgement of the lungs is especially 
marked in cases of mitral disease with weakening of the right ventricle, 
1 Rosenbach brings forward evidence to show that the arteries, the lungs, and 
other organs actively assist in maintaining compensation. 196 
PHYSICAL DIAGNOSIS 
and is manifested by dyspnoea, cyanosis, cough, and haemoptysis. 
In many cases, however, dropsy is very irregularly and unaccount- 
ably distributed, and does not follow the rules just given. In pure 
aortic disease, uncomplicated by leakage of the mitral valve, dropsy 
is a relatively late symptom, and precordial pain (angina pectoris) is 
more prominent. 
Functional Tests of Compensation.—After a considerable trial of 
the methods by which it has been proposed to test cardiac power 
through watching the heart’s response to measured “doses” of work, 
I am convinced that the best tests are the ordinary duties and pleasures 
of life, which step by step the patient naturally tries in convalescence. 
IV. Hypertrophy and Dilatation 
Since cardiac hypertrophy or dilatation are not in themselves dis- 
eases, but may occur in any disease of the heart (valvular or parietal), 
it seems best to give some account of them and of the methods by 
which they may be recognized, before taking up separately the differ- 
ent lesions with which they are associated. 
1. Causes 
1. Vascular hypertension (unknown cause, nephritis, arterio- 
sclerosis) . 
2. Valvular disease (mostly “rheumatic”). 
3. Syphilitic aortitis (with aortic regurgitation or aneurism). 
4. Adherent pericardium. 
5. Moderate hypertrophy and dilatation are often found in Graves’ 
disease, in pernicious anaemia and in leucaemia. 
In 1082 cases of hypertrophy and dilatation found in 4000 con- 
secutive necropsies at the Mass. General Hospital, the following 
possibly causative factors were present: 
Arteriosclerosis 
279 
Valvular heart disease 
79 
'Nephritis 
77 
Syphilitic aortitis 
24 
Chronic pericarditis 
24 
Pernicious anaemia 
8 
Leucaemia 
6 
Hyperthyroidism 
3 
Unknown cause 
210 
Total 
734 HYPERTROPHY AND DILATATION 
197 
Also the following combinations: 
Arterio-sclerosis- and nephritis 
126 
Arterio-sclerosis and chronic valvular endocarditis. 
36 
Arterio-sclerosis and myocarditis 
26 
Arterio-sclerosis and syphilitic aortitis 
• 17 
Chronic endocarditis and pericarditis 
11 
Nephritis and chronic valvular endocarditis. ...... 
10 
Other combinations 
122 
Grand Total 
1082 
I have never seen any evidence that excessive muscular work is 
by itself capable of causing cardiac hypertrophy and dilatation. I 
have never seen “athlete’s heart” in the sense of chronic hyper- 
trophy, or of acute dilatation produced in the previously sound heart 
by violent exertion. It is in the previously diseased heart that 
athletic “stunts” often produce failure. After a “Marathon run” 
the heart is of normal size or even smaller than usual. 
In valvular disease the greatest degree of hypertrophy is to be 
seen usually in relatively young persons, and especially when the 
advance of the lesion is not very rapid. 
Hypertrophy of the heart in valvular disease is also influenced by 
the amount of muscular work done by the patient, by the degree 
of vascular tension, and by the treatment. In the great majority 
of cases of hypertrophy, from whatever causes, both sides of the heart 
are affected, but we may distinguish cases in which one or the other 
ventricle is predominantly affected. . 
2. Signs 
(a) Cardiac hypertrophy affecting especially the left ventricle 
(a) High systolic blood pressure is the most constant and reliable 
of all signs of cardiac hypertrophy and is therefore mentioned here. 
(b) The apex impulse is usually lower than normal, often in the 
sixth space, occasionally in the seventh or eighth.1 It is also farther 
to the left than normal, but far less so than in cases in which the hyper- 
trophy affects especially the right ventricle. The area of visible 
pulsation is usually increased, and a considerable portion of the chest 
wall may be seen to move with each systole of the heart, while fre- 
quently there is a systolic retraction of the interspaces in place of a 
systolic impulse. 
1 This is due partly to a stretching of the aorta, produced by the increased 
weight of the heart. 198 
PHYSICAL DIAGNOSIS 
(c) Palpation confirms the results of inspection and shows us also 
that the apex impulse is unusually deliberate and diffuse as well as 
powerful (“heaving impulse”). Percussion shows in many cases that 
the cardiac dulness is more intense and its area increased downward 
and to a lesser extent toward the left.1 
(<d) If we listen in the region of the maximum cardiac impulse, we 
generally hear an unusually long and low-pitched first sound, which 
may or may not be of a greater intensity than normal. Often we 
hear nothing abnormal except a soft systolic murmur. A very loud 
first sound is much more characteristic of a cardiac weakness of neu- 
rosis than of pure hypertrophy of the left ventricle. 
The second sound at the apex (the aortic second sound transmitted) 
is usually much louder and sharper than usual. Auscultation in the 
aortic area shows that the second sound at that point is loud and ringing 
in character. Not infrequently the peripheral arteries (the sub- 
clavians, brachials, carotids, radials, and femorals) may be seen to 
pulsate with each systole of the heart. This sign is most frequently 
observed in cases of hypertrophy of the left ventricle, which are due 
to aortic regurgitation, but is by no means peculiar to this disease and 
may be repeatedly observed when the cardiac hypertrophy is due to 
arterio-sclerosis, Graves’ disease, or anaemia. 
The radial pulse wave has no constant characteristics, but depends 
rather upon the cause which has produced the hypertrophy than upon 
the hypertrophy itself. 
The electrocardiogram usually shows characteristic changes. 
(b) Cardiac Hypertrophy Affecting Especially the Right Ventricle 
It is much more difficult to be certain of the existence of enlarge- 
ment of the right ventricle than of the left. Practically we have but 
three reliable physical signs: 
(a) Increase in the transverse diameter of the heart, as shown by 
the position of the apex impulse and by percussion of the left border 
of the heart; and 
(b) Accentuation of the pulmonic second sound, which is often 
palpable as well as audible. 
(c) A characteristic alteration of the electrocardiogram. 
The apex beat is displaced both to the left and downward, but 
especially to the left. In cases of long-standing mitral disease, the 
1 Post mortem enlarged left ventricle is often found despite the absence of the 
above signs in life because it extends backward out of our reach. HYPERTROPHY AND DILATATION 
199 
cardiac impulse may be felt in mid-axilla, several inches outside the 
nipple, and yet not lower down than the sixth intercostal space. In a 
small percentage of cases (i.e.; when the right auricle is engorged), an 
increased area of dulness to the right of the sternum may be demon- 
strated. Accentuation of the pulmonic second sound is very fre- 
quent in hypertrophy of the right ventricle, though it is not constant 
or peculiar to that condition. It may be heard, for example, in cases 
of pneumonia when no such hypertrophy is present, but in the majority 
of cases of cardiac disease we may infer the presence, and to some extent 
the amount of hypertrophy of the right ventricle from the presence of a 
greater or lesser accentuation of the pulmonic second sound. The 
radial pulse shows nothing characteristic of this type of hypertrophy. 
Epigastric pulsation gives us no evidence of the existence of 
hypertrophy of the right ventricle, despite contrary statements in 
many text-books. Such pulsation is frequently to be seen in persons 
with normal hearts, and is frequently absent when the right ventricle 
is obviously hypertrophied. It is perhaps most often due to an 
unusually low position of the whole heart. 
3. Dilatation of the Heart 
Dilatation almost never occurs without accompanying hyper- 
trophy. Moreover, it cannot be considered as an unmixed evil. In 
Fig. 132.—Dilated Heart. From v. Ziemssen’s Atlas. 
aortic regurgitation and most other types of cardiac disease it is insepa- 
rably linked with hypertrophy and is present long before com- 
pensation fails. Probably it is the pathological fatigue of a dilated 200 
PHYSICAL DIAGNOSIS 
and hypertrophied heart that causes stasis and the other abnormalities 
next described. 
(1) Acute Dilatation.—Immediately after severe muscular exertion, 
as, for example, at the finish of a boat race, or of a two-mile run 
(especially in persons not properly trained), an acute cardiac dilatation 
has been said to occur. I have never seen this in healthy persons, 
though Hornung (Berl. klin. Woch., xlv, 1769) believes that with the 
Fig. 133.—The Base of the Contracted Heart Showing Sphincteric Action of the 
Muscular Fibres Surrounding the Mitral and Tricuspid Valves. The outer dotted line 
is the outline of the relaxed heart. The inner dotted circles show the size of the mitral 
and tricuspid valves during diastole, a, Outline of the heart when relaxed; b, outline of 
the relaxed tricuspid valve; c, outline of the mitral orifice during diastole. (After 
Spalteholz.) 
fluoroscope he has identified cases of acute dilatation in healthy per- 
sons after fright, sexual excitement, high altitude, and other strains. 
In debilitated or poorly nourished subjects, or when the heart has 
been previously weakened by diseases, such an acute dilatation may 
be serious or even fatal in its results. 
(2) Chronic dilatation wTith hypertrophy comes as a result of valvular 
disease or other causes, and gives rise to the same physical signs as 
those of acute dilatation, from which it differs chiefly as regards the 
accompanying physical phenomena and the prognosis. HYPERTROPHY AND DILATATION 
201 
The mitral and tricuspid orifices are closed not simply by the 
shutting of their valves, but also in part by the sphincter-like action 
of the circular fibres of the heart wall (see Fig. 133) and the contraction 
of the papillary muscles (Fig. 134). 
In birds, the tricuspid orifice has no valve and is closed wholly by 
the muscular sphincter of the heart wall. 
In conditions of very acute cardiac failure, such as may occur 
after a hard run, the papillary muscles are in all probability relaxed. 
Mitral curtains. 
Circular or 
sphincteric 
fibres. 
Cordea 
tendineae 
Endocardium. 
Papillary 
muscle. 
Myocardium. 
Pericardium 
Fig. 134.—The Mitral Valve Closed, Showing the Action of the Papillary Muscles, 
(After Spalteholz.) 
Briefly stated, the signs of predominant dilatation of the heart, 
whether acute or chronic, are: 
(a) Feebleness and irregularity of the apex impulse and of the 
radial impulse; (6) enlargement of the heart, as indicated by inspection, 
palpation, and percussion, and (sometimes) (c) widely spread systolic 
murmurs; (d) often gallop rhythm (see above, p. 180); (e) evidence 
of stasis at the periphery. 
(a) Predominant Dilatation of the Left Ventricle 
Inspection shows little that is not better brought out by palpation. 
Palpation reveals a “flapping” cardiac impulse, or a vague shock dis- 
placed both downward and to the left and diffused over an abnormally 
large area of the chest wall. Percussion verifies the position of the 
cardiac impulse. 202 
PHYSICAL DIAGNOSIS 
On auscultation, the first sound is usually very short and sharp, but 
not feeble unless it is accompanied by a murmur. A systolic murmur 
is sometimes heard at the apex of the heart. The aortic second sound, 
as heard in the aortic area and at the apex, is feeble. Peripheral blood- 
pressure sometimes falls. 
(b) Predominant Dilatation of the Right Ventricle 
The failure of muscular tone is shown in extreme cases by an 
increase in the area of cardiac dulness to the right of the sternum (cor- 
responding to the position of the right auricle), by feebleness of the 
pulmonic second sound and especially by cyanosis and signs of conges- 
tion and engorgement of the lungs. When this latter event occurs, 
one may have also systolic pulsation in the jugular veins, and rarely 
in the liver. 
The diagnosis of dilatation of the heart seldom rests entirely upon 
physical signs referable to the heart itself. In acute cases our diagnosis 
is materially aided by a knowledge of the cause, which is often toler- 
ably obvious. In chronic cases the best evidence of dilatation is often 
that furnished by the venous stasis which results from it. 
In conditions of profound nervous debility, excitement, or exhaus- 
tion, weakening of the cardiac muscles is often associated with systolic 
murmurs, which cease with the removal of their cause. Stress has been 
laid upon these points by Da Costa, by Prince, and recently in the 
World War. 
Systolic murmurs at the base and at the apex are often heard in 
aortic regurgitation with the dilatation of the left ventricle which that 
lesion produces, also in chronic nephritis and arterio-sclerosis. 
The results of any form of mitral disease occur in this order. 
(1) Dilatation and hypertrophy of the left auricle, which has to receive 
blood from the lungs but cannot empty itself freely into the left 
ventricle. 
(2) The overfilled left auricle cannot receive the blood from the 
lungs as readily as it should; hence the blood “backs up” in the lungs 
and thereby increases the work which the right ventricle must do in 
order to force the blood through them. Thus result oedema of the 
lungs, and— 
(3) Hypertrophy and dilatation of the right ventricle, which in 
turn becomes sooner or later overcrowded so that tricuspid leakage 
occurs. 
(4) The muscular capacity possessed by the right auricle is soon 
exhausted, and we get then— HYPERTROPHY AND DILATATION 
203 
(5) General venous stasis, which shows itself first as systolic pulsa- 
tion in the jugulars and in the liver, and later in the tissues drained by 
the portal and peripheral veins. This venous stasis increases the 
work of the left ventricle, and so we get— 
(6) Hypertrophy and dilatation of the left ventricle. Hypertrophy 
of the left ventricle is also produced by the increased work necessary 
to maintain sphincter action at the mitral orifice. 
At last the circle is complete. Every chamber in the heart is 
enlarged and fatigued. Failure is imminent. CHAPTER XII 
THE CLASSIFICATION OF CARDIO-VASCULAR 
DISEASES 
I have found it convenient to make four groups out of those whose 
illness appears to be due chiefly to circulatory weakness. The classi- 
fication which appears below is based on the figures which accompany 
it, and on the last ten years’ experience with diseases of the circulation 
in the wards and post-mortem room of the Massachusetts General 
Hospital. 
The tentative nomenclature and relative frequency of the different 
types is as follows: 
Occurrence in 6oo 
clinical cases, 
per cent. 
Occurrence in 126 
cases post mortem, 
per cent. 
I 
“ Rheumatic” 
46 
42 
2 
Syphilitic 
12 
13 
3 
Hypertensive (arteriosclerotic 
and nephritic) 
34 
40 
4 
Congenital malformations 
0 
1 
Doubtful cases1 
8 
4 
These two sets of figures do not overlap. The clinical cases were 
all studied between 1910 and 1914. Those autopsied had died 
between 1896 and' 1905. The two series were worked out at different 
times and without any comparison of the figures. 
1. The terms need some definition: “Rheumatic” here includes the 
cases of weakened myocardium, acute pericarditis, adherent pericar- 
dium, and valvular disease associated with: 
1 One-fifth of these are goitre hearts. 
204 CARDIOVASCULAR DISEASES 
205 
(a) Acute polyarthritis (non-gonorrhceal). 
(b) Acute chorea (Sydenham’s type). 
(c) Acute septic tonsillitis. 
(d) Primary endocarditis. 
Only cases with negative Wassermann are included. Sixty per 
cent, of the cases begin before the twenty-second year, and 60 per cent, 
are in girls. It seems probable but not proved that some type of 
streptococcus is the cause in all cases of this type. The proved gonor- 
rhoeal cases are so few that I have left them out of account. The 
scarlatinal cases are probably streptococcic. 
Cases of malignant or ulcerative endocarditis and Libman’s 
“subacute and chronic bacterial endocarditis” are here included in 
the same group. 
Ultimately the word “rheumatic” may well be changed to 
streptococcic. 
2. Syphilitic heart disease is here used to include syphilitic aortitis, 
(with and without aneurism), and all the weakened hearts associated 
with proved syphilis and without other obvious cause. Seventy per 
cent, of the cases are in middle-aged men. 
3. Hypertensive Heart Disease, Arteriosclerotic Type.—(a) The 
average age in my series is 59 years. The arteries show extensive 
changes. No evidence of syphilis or of the valve lesions ordinarily 
associated with “rheumatism” was discovered. I leave unanswered 
the question whether arteriosclerosis is a result or a cause of hyper- 
tension, though I incline to believe that the two are independent. 
(6) Nephritic {or Nephrogenous) Type.—Average age 36. Obvious 
nephritis of the glomerular or vascular type. Negative Wassermann. 
No valve lesions. 
The congenital malformations need no further explanation here. 
Other less defined types will be mentioned later (see page 275). 
I. RHEUMATIC HEART DISEASE 
Under this heading I shall discuss: 
(a) Acute endocarditis. 
(b) Pancarditis (especially in children). 
(c) Mitral disease. 
(d) Aortic disease. 
(e) Disease of the tricuspid and pulmonary valves 206 
PHYSICAL DIAGNOSIS 
The “rheumatic” type of myocarditis cannot, I believe, be recog- 
nized clinically and will not, therefore, be separately discussed. It 
will be referred to in connection with the discussion of Compensation. 
1. Acute Endocarditis 
There are no positive or characteristic physical signs of this form 
of the disease. We suspect it by reasoning from one member to 
another within a familiar pathologic group. When fever and leuco- 
cytosis without any other known cause are associated with acute arthritis 
or chorea, or persist unexplained after an acute tonsillitis has sub- 
sided, one may conjecture that acute endocarditis is present, i.e., soft, 
friable vegetations on the heart valves. The conjecture approaches 
knowledge if we find one or more cardiac murmurs which change in 
time, position, quality or intensity from day to day, and is confirmed 
if evidence of embolism appears in the subcutaneous tissues, in the 
kidney, spleen, brain, eye, or peripheral arteries. 
The diagnosis is seldom made without the presence of chronic 
“rheumatic” lesions in the heart, on some of which the acute process 
is often grafted. 
It is often present as a terminal lesion superimposed on chronic 
valvular defect, less often in chronic wasting diseases. It is some- 
times associated with a septic focus such as peritonitis. 
2. Rheumatic Pancarditis of Children 
The rheumatic {i.e., streptococcic) infections of children and young 
adults often attack simultaneously the endocardium, myocardium, 
and pericardium. 
It may be impossible to determine in a given case whether the 
infection has attacked one, two, or all three of these parts. Single, 
double, or triple invasion may produce identical signs, i.e., rapid, 
perhaps irregular heart action, a systolic murmur usually loudest in the 
apex region, and as time goes on more or less extension of the heart's 
borders. The evidence of acute pericarditis (see below, p. 238) may 
not be recognizable. If the aortic valve is affected we can generally 
make that out, but if the mitral alone is involved there are no signs 
in the early acute stages of the disease by which we can distinguish 
the systolic murmur of mitral vegetations from the similar murmur 
produced by acute rheumatic infection with or without pericarditis. 
Years ago I used to call these cases “mitral regurgitation” and 
this is still their popular title, but I have ceased to use it since I have CARDIOVASCULAR DISEASES 
207 
watched the disease get well and heard the murmur more and more 
faintly till it disappeared altogether. In such a case there may have 
been a true mitral regurgitation due to relaxation of the mitral sphinc- 
ter from weakening of the circular muscle fibres about the valve orifice. 
But without post-mortem this is conjecture only and though the 
necropsy often does not verify it we cannot deny that during life there 
may have been atony not demonstrable in the dead tissue. 
It will now describe separately the physical signs which tend to 
convince us that one or another element within the circulatory appa- 
ratus is especially affected by the “rheumatic” infection. 
3. Mitral Endocarditis (Rheumatic Type) 
(a) Early Stages 
In the beginning of a rheumatic heart trouble which the latter 
evidence proves to be “ mitral ” (i.e., more severe there than elsewhere), 
we usually have no signs except a systolic murmur loudest at or near 
the apex of the heart. 
(b) Later Stages 
(a) As time goes on hypertrophy and dilatation of the heart gradu- 
ally develop. It is customary to speak of hypertrophy as an early 
conservative or compensatory process, and of dilatation as a later 
more or less accidental and harmful result. But we usually find 
the two processes combined and have no good reason to call one 
useful and the other harmful. Both sides of the heart increase in 
thickness and in capacity. Predominant hypertrophy and dilatation 
of the right side is, however, the rule in mitral disease. 
The physical evidence of enlargement is shown not to the right of the 
sternum (where the enlarged right auricle might appear), not in the 
epigastrium (where the right ventricle presents), but on the left 
cardiac border. 
The heart’s apex is found normally outside the nipprle line in 
children and as a rule is in the fourth interspace until the child reaches 
the 9th, 10th, or nth year. About that time, or slightly later, it is 
found in the fifth space and in the nipple line—later within it. 
Beyond these limits and especially to the left, the heart of early 
mitral endocarditis gradually extends until it is recognized by palpa- 
tion. Percussion is- rarely needed in examining the thin flexible 
chests of children and young adults in whom mitral disease usually 
begins. 208 
PHYSICAL DIAGNOSIS 
The left auricle also thickens and stretches but presents no physical 
signs.1 
(6) Accentuation of the Pulmonic Second Sound. As a rule there 
is no considerable change in the second sound until mitral endocarditis 
reaches its later or stenotic form. But in a minority of cases the 
second sound on the left side of the sternum becomes louder and 
sharper than normal even in the earlier stages of mitral disease. 
At this prestenotic stage of mitral disease, after the early acute 
infection (with fever, leucocytosis, and anaemia) has passed, and 
before the mitral valve has become notably contracted, we have then 
two physical signs which are fairly constant and one that is inconstant. 
1. Systolic murmur at the apex. 
2. Slight enlargement of the heart, especially to the left. 
3. (In a minority of cases) accentuation of the pulmonic second 
sound. 
These three signs appear in the order just given. For months 
there may be no abnormality except a systolic murmur indistinguish- 
able from those which pass away and do not develop into stenotic 
mitral disease. 
If the murmur persists it is often followed in a few months or 
years by an extension of the apex toward the left, by accentuation of 
the pulmonic second sound and finally by evidence of stenosis. 
The Murmur.—In children the murmur of early mitral disease 
may be among the loudest of all murmurs to be heard in valvular 
disease, but this does not necessarily imply that the lesion is a very 
1st 
1st 
2nd 
2nd 
Fig. 135.—Diagram to Represent Systolic Mitral Murmur. The heavy lines repre- 
sent the normal cardiac sounds and the light lines the murmur, which in this case does 
not replace the first sound and “tapers ” off characteristically at the end. 
severe one. A murmur which grows louder under observation in a 
well-compensated valvular lesion may mean an advance of the disease, 
but if the case is first seen after compensation has failed, a faint, 
variable whiff in the mitral area may mean the severest type of lesion. 
As the patient improves under the influence of rest and cardiac tonics, 
such a murmur may grow very much louder, or a murmur previously 
inaudible may appear. 
1 Except by x-ray or by the electro-cardiogram {vide infra). CARDIO-VASCULAR DISEASES 
209 
The length of the murmur varies in different cases, but as a rule it is 
longer than those which are “functional” in origin. It begins abruptly 
but usually “tails off” at the end of systole (see Fig. 135). The first 
sound of the heart may or may not be replaced by the murmur (see 
Fig. 136). When the sound persists and is heard either with or before 
the murmur, one can infer that the lesion is relatively slight in com- 
parison with cases in which the first sound is wholly obliterated. 
Post-systolic or late systolic murmurs, which are occasionally heard in 
2nd 
2nd 
Fig. 136.—Systolic Mitral Murmur Replacing the First Sound of the Heart. 
early mitral disease, are said to point to a relatively slight amount 
of disease in the valve (see Fig. 137). 
When compensation fails, the murmur may altogether disappear 
for a time, and if the patient is then seen for the first time and dies 
without rallying under treatment, it may be impossible to make the 
diagnosis. 
The murmur of early mitral disease is loud and hence is conducted 
in all directions, but especially toward the axilla and to the back. 
In the latter situation it is usually louder than it is in mid-axilla, and 
1st 
1st 
2nd 
2nd 
Fig. 137.—Late Systolic Murmur. The first sound is clear and an interval intervenes 
between it and the murmur. 
occasionally it is heard as loudly in the back as anywhere else in the 
chest. 
If accentuation of the pulmonic second sound is present, we 
recognize it not because it is louder than the aortic second sound, since 
this is true in the vast majority of cases in healthy individuals under 
thirty years of age. Pathological accentuation of the pulmonic 
second sound means a greater intensity of the sound than we have a right 
to expect at the age of the individual in question. Occasionally the pul- 
monic second sound is loudly reduplicated, but as a rule this points 
to advanced stenosis of the mitral valve, i.e., to the later stages of 
mitral endocarditis. 210 
PHYSICAL DIAGNOSIS 
In children (in whom adhesive pericarditis often complicates the 
disease) a systolic thrill may not infrequently be felt at the apex, 
and the precordia may bulge. 
Pulmonic second 
accented. 
Systolic murmur 
loudest here. 
Fig. 138.—Early Mitral Disease. The murmur is heard over the shaded area as 
well as in the 'back. 
Systolic murmur, 
Fig. 139.—Early Mitral Disease. Murmur heard over the shaded area 
The pulse usually shows nothing characteristic at this stage of the 
disease, although it may be weak when compared to the powerful beat 
at the apex, in case the stenotic element in the lesion is increasing 
rapidly. But arrhythmia at this period is much less common than 
in cases advanced to the stage of stenosis. CARDIO-VASCULAR DISEASES 
211 
Differential Diagnosis 
The murmur of early mitral disease may be confused with: 
(1) Tricuspid regurgitation. 
(2) Functional murmurs. 
(3) Stenosis or roughening of the aorta or aortic valves. 
(1) The post-mortem records of the Massachusetts General 
Hospital show that in the presence of a murmur due to mitral dis- 
ease it is very easy to fail altogether to recognize a tricuspid regur- 
gitant murmur. Only 5 out of 29 cases of tricuspid stenosis and 
regurgitation found at autopsy were recognized during life. Sir Clifford 
Allbutt’s figures from Guy’s Hospital are closely similar. In the 
majority of these cases, “mitral regurgitation” was the diagnosis on 
which attention was concentrated during the patient’s life. This is 
all the more excusable because the tricuspid area is so wide and 
uncertain. Murmurs produced at the tricuspid orifice are sometimes 
heard with maximum intensity just inside the apex impulse, and if we 
have also an apical murmur, it may be impossible under such circum- 
stances to distinguish it from the tricuspid murmur. Sometimes the 
two are of different pitch, but in most cases tricuspid regurgitation 
must be recognized indirectly if at all, i.e., through the evidence given 
by venous pulsation in the jugular veins and in the liver, and through 
the rapid accumulation of ascites and oedema of the legs. 
(2) “Functional” murmurs are usually systolic and may have 
their maximum intensity at the apex of the heart, but in the great 
majority of cases they are heard best over the pulmonic valve or just 
inside or outside the apex beat (Potain). They are faint or inaudible 
at the end of expiration, and are more influenced by position than 
organic murmurs are. In the upright position they are often very 
faint. They are usually short, are rarely transmitted beyond the 
precordia and are unaccompanied by any evidences of enlargement 
of the heart, by any pathological accentuation of the pulmonic second 
sound,1 or any evidences of engorgement of the lungs or general venous 
system. 
Cardio-respiratory murmurs are usually systolic, and as they are 
often heard in and about the mitral area they are frequently mistaken 
for evidence of a mitral lesion. From this they should be distinguished 
1 It must be remembered that in chlorosis, a disease in which functional mur- 
murs are especially prone to occur, the pulmonic second sound is often surprisingly 
loud, owing to a retraction of the left lung, which uncovers the root of the pulmonic 
artery. 212 
PHYSICAL DIAGNOSIS 
by their variation or cessation in certain phases of respiration and 
by the absence of any other evidence of valvular disease. 
(3) Roughening or narrowing of the aortic valves or of the aortic 
arch may produce a systolic murmur with maximum intensity in the 
second right intercostal space, but this murmur is not infrequently 
heard all over the precordia and most plainly at the apex, so that it 
may simulate the murmur of early mitral lesions. The aortic murmur 
may indeed be heard more plainly at or just inside the apex. In such 
cases diagnosis may be impossible, as there may be enlargement of 
the heart as well. Accentuation of the pulmonic second sound is not 
constant enough in early (prestenotic) mitral disease to constitute a 
differential point of much importance. 
The Question of “Mitral Regurgitation" in Early Rheumatic Mitral 
Disease 
Throughout this section on the early or prestetonic stages of 
mitral disease I have refrained from using the classical term “mitral 
regurgitation." I have done so because I know no means by which 
we can recognize with any certainty, either ante-mortem or post-mor- 
tem, that such regurgitation is, or has been, a fact. That there may 
be regurgitation through the mitral at any period of the disease is 
entirely possible. Early coxcomb vegetations may hold the valves 
apart so that they cannot close. Relaxation of the papillary mus- 
cles or shortening of tendinous cords may well permit a reflux. Muscu- 
lar weakness (with or without a demonstrable myocarditis) may 
weaken the sphincteric action of the circular fibers about the base of 
the leaflets so that they do not fill up the mitral orifice. 
Any or all of these events are possible, but we have (so far as I 
know) no way of being even approximately sure that in a given case 
they are happening. On the other hand, we do know that people 
often die with the signs of “mitral regurgitation” when post-mortem 
gives no evidence either of anatomical change in the valves or of an 
increase of the valve circumference. 
Add to this that, when we do find post-mortem an increase in the 
valve circumference, the ante-mortem findings are often widely differ- 
ent from those traditionally associated with “mitral regurgitation." 
So far as I have been able to observe post-mortem the “rheu- 
matic” (streptococcic) lesions of the mitral valve are almost never 
such as one could reasonably expect to produce regurgitation alone, 
i.e., without stenosis as well. One finds vegetations or roughenings CARDIO-VASCULAR DISEASES 
213 
such as might well produce a murmur without any regurgitation. 
One finds at this stage very little predominance of right ventricular 
hypertrophy. 
Later one finds the valves so stiffened and adherent that regurgi- 
tation as well as obstruction is practically certain. But pure regur- 
gitation—before stenosis has occurred—-and in the early stages of 
rheumatic mitral disease, is—so far as I can see—a very rare possibility 
—no more. 
Of its occurrence, or possible occurrence in other types of cardiac 
disease (syphilitic, arteriosclerotic, or nephritic) I shall speak during 
the discussion of those diseases. 
The practical importance of these considerations is, I think, con- 
siderable. Boys with a loud systolic murmur at the apex are fre- 
quently refused permission to enter athletic contests or army life. 
Older men are refused life insurance. This is often wholly wrong. 
Such murmurs are no evidence of disease. I have known boys row a 
four-mile boat race or fight through a war with such a murmur and 
be none the worse for it. It often disappears later in life. 
For practical purposes we should disregard systolic murmurs pro- 
vided the response to exercise is satisfactory, the cardiac sounds, dimen- 
sions and contractions otherwise negative, and a history of rheumatic 
disease absent. 
But it must be remembered that in cases of early mitral stenosis the 
presystolic murmur is often inaudible and only a systolic evident, 
unless we stir up the heart by exercise or amyl nitrite. 
Mitral regurgitation should never he the only or the primary diagnosis 
made. We may rightly diagnose : 
1. Mitral stenosis and regurgitation. 
2. Arteriosclerosis with cardiac hypertrophy and dilatation (and 
possibly relative mitral regurgitation). 
3. Chronic nephritis or pericarditis with the same results. 
4. Hyperthyroidism with the same results. 
5. Syphilitic aortitis with the same results. 
6. Acute rheumatic (streptococcic) myocarditis with the same 
results. 
But in all these cases the mitral regurgitation, if it occurs, is a 
minor result (like congested lungs), never a primary cause. Primary 
mitral regurgitation is the commonest wrong diagnosis in the field of 
the circulation and does the greatest harm to the patient, especially 
when it excludes him from life insurance, from athletics, or from war. 214 
PHYSICAL DIAGNOSIS 
(c) Late Mitral Disease—Stenosis 
In children we often see acute mitral endocarditis with a systolic 
murmur at the apex. But unless they have had previous acute attacks 
so that the total duration of the disease is a year or more, we do not 
Pig. 140.—Diagram to Represent the Position of the Valves in the Normal| iHeart 
during Diastole, the Open Mitral Allowing the Blood to Flow from the Left Auricle, 
the Aortic Closed. 
Fig. 141.—Mitral Stenosis—Period of Diastole. The blood flowing from the left auricle 
is obstructed by the thickened and adherent mitral curtains. 
often get the physical signs presently to be described as those of stenosis. 
Much more often we find the typical signs of stenosis in young adults 
(especially women) or in older persons, who have a history of rheumatic 
arthritis, chorea, or tonsillitis years before. CARDIO-VASCULAR DISEASES 
215 
Since “rheumatic” arthritis and chorea are commoner in girls 
than in boys, it is natural that the commonest late cardiac result of 
these infections (mitral stenosis) should be commoner in women. 
Not infrequently we find advanced stenosis in persons who have no 
remembrance of any previous rheumatism, chorea, tonsillitis, or 
other form of streptococcus infection. But I find no good evidence 
that any of the other assigned causes (such as tuberculosis) plays 
any causative role in mitral disease. 
Post-mortem mitral stenosis is not infrequently the obvious and 
fundamental cause of death. It proved such in 104 of 4000 autopsies 
at the Massachusetts General Hospital. On the other hand there 
was but one case (No. 2825) in which mitral regurgitation seemed the 
cause of death. When an enlarged mitral orifice was demonstrated, 
it was usually as a minor feature—death being due to typhoid fever, 
to arteriosclerosis, or some such cause lying deeper than the stretched 
orifice. 
In typical cases of stenosis the valves are fused together and 
stiffened to form an irregular cone projecting into the ventricle from 
the direction of auricle (see Figs. 142 and 143). 
The orifice is never round but presents an irregular slit (fish 
mouth or button-hole) which may admit one finger (instead of three 
as normally) or may barely admit a probe. It is amazing to see 
such a narrowing in the heart of a person who until a few days before 
death has done active work with but little inconvenience. 
Physical Signs ■ 
Mitral stenosis may probably exist for years without producing 
any physical signs by which it may be recognized and even after 
signs have begun to show themselves they are more fleeting and incon- 
stant than in any other valvular lesion of the heart. In the early 
stages of the disease the heart may appear to be entirely normal if 
the patient is at rest, and especially if examined in the recumbent 
position, characteristic signs being elicited only by exertion. Or again 
a presystolic roll which is audible with the patient in the upright 
position may disappear in the recumbent position; or a murmur may 
be heard at one visit, at the next it may be impossible to elicit it by any 
manoeuvre, while at the third visit it may be easily heard again. 
These characteristics explain to a certain extent the fact that differ- 
ences of opinion so often arise regarding the diagnosis of mitral stenosis, 
and that out of 130 cases in which this lesion was found at autopsy at 216 
PHYSICAL DIAGNOSIS 
the Massachussetts General Hospital, only 73 or 56 per cent, were 
recognized during life. No common lesion has been so frequently 
overlooked in our records. 
In the earliest stage at which the stenosis can be recognized with 
certainty, there are no abnormal signs when the patient is at rest except 
a systolic murmur. This murmur often has a peculiar “explosive” or 
hissing quality like a jet of steam escaping suddenly and under pres- 
sure. Its earliest portion is strongly accented like a sforzando in 
music. It is short, high pitched, and dies away rapidly. 
Pulmonic second 
accented. 
Double-shock ’ 
sound. 
Presystolic murmur 
heard in limited 
area. 
Fig. 142.—Mitral Stenosis. 
Now if by exertion or by the action of amyl nitrite, the heart’s 
contraction is invigorated a low-pitched presystolic role will appear 
faintly, then distinctly, rapidly disappearing again as the heart quiets 
down. With the increase of cardiac activity under amyl nitrite I 
have also seen the presystolic thrill and the double shock sound (pres- 
ently to be mentioned) appear for a few beats and then vanish. 
As a rule the signs just mentioned are those of the very earliest 
stages of the disease; but in some cases they are probably the only 
ones present during the observation period. At any rate no presys- 
tolic murmur was heard at any time in 19 out of 59 cases of pure 
mitral stenosis autopsied at the Massachusetts General Hospital but 
in most of these a systolic murmur was audible. For the most part 
it is probably true that a systolic explosive murmur is the only one 
to be heard in the earliest stages of the stenotic lesion. 
From this point on the symptoms may be divided into three stages 
according to the extent of progress in the case. CARDIO-VASCULAR DISEASES 
217 
I 
In the first stage palpation shows that the apex beat is little if at 
all displaced, and percussion reveals little if any increase in the area 
of cardiac dulness; there is often local tenderness to be elicited near 
the apex. If one lays the hand lightly over the origin of the apex beat, 
one can generally feel the purring presystolic thrill which is so charac- 
teristic of this disease. This thrill is more marked in the second stage 
of the disease, but can generally be appreciated even in the first. 
It runs up to and ceases abruptly with the very sharp first sound, the 
sudden shock of which may be appreciated even by palpation. On 
1st 
1st 
2nd 
2nd 
Fig. 143.-—The Murmur of Mitral Stenosis—First Stage. The place of the murmur 
and its crescendo character indicated by the position of the light lines just before the 
first sound and by their increasing length. 
auscultation one hears, especially after the patient has been exerting 
himself, and particularly if he leans forward and to the left, a short 
low-pitched rumble or roll immediately preceding the systole. The 
murmur seems to be a crescendo, growing louder as it approaches the 
first sound, but phonocardiograms do not show any such crescendo. 
At this stage of the disease the second sound can still be heard at the 
apex. The first sound is often sharply accented or snapping, and 
communicates a very decided shock to the ear. As a rule, the murmur 
is closely confined to the region of the apex beat and not transmitted 
any considerable distance in any direction. I have seen cases in which 
it was to be heard only over an area the size of a half-dollar.1 The 
pulmonic second sound may be accented and is often loudly reduplicated 
(“double-shock sound ”—Sansom) at this stage of the disease, but this 
doubling is more frequent later.2 
Arrhythmia is not infrequently present even in the early stages 
of the affection. The heart may be regular while the patient is at 
rest, but slight exertion is often sufficient to produce marked irregularity. 
1 It may, however, be widely transmitted to the left axilla and audible in the 
back or even over the whole precordia. 
2 This is the opinion of most observers. Sansom has stated that the “double- 
shock sound” may precede all other evidences of mitral stenosis. 218 
PHYSICAL DIAGNOSIS 
II 
In the second stage the murmur and thrill are usually longer and 
may occupy the whole of diastole, beginning with considerable inten- 
sity just after the reduplicated second sound, quickly diminishing 
until barely audible, and then again increasing with a rapid crescendo 
up to the first sound of the next cycle.1 These changes may be 
2nd 
1st 
2nd 
1st 
Fig. 144.—Type of Presystolic Murmur Often Heard in the Second Stage of Mitral 
Stenosis. Here the murmur fills the whole of diastole, with a gradual increase of inten- 
sity as it approaches the first sound. No second sound is audible at the apex. 
graphically represented as in Figs. 144 and 145. Diastole and the 
A-s-V-s interval of the phlebogram (see above, p. 114) are now 
still more prolonged, so that the characteristic rhythm of this lesion 
is even more marked than in the earlier stages of the disease. In 
many cases at this stage no second sound is to be heard at all at the 
apex, although at the pulmonic orifice it is loud and almost invariably 
double. (This is one of the reasons for believing that the second 
sound which we usually hear at the apex is the transmitted aortic 
1st 
2nd 
3rd 
Fig. 145.—Type of Presystolic Murmur Sometimes Heard in the Second Stage of Mitral 
Stenosis. There is a double crescendo. The second sound seems reduplicated. 
second sound. In mitral disease the aortic valves shut feebly owing 
to the relatively small amount of blood that is thrown into the aorta.) 
At this stage of the disease enlargement of the heart begins to make 
itself obvious. The apex impulse is displaced to the left—sometimes 
as far as the mid-axillary line, and often descends to the sixth inter- 
space. 
The instability and fleeting character of the murmur in the earlier 
stages of the disease are much less marked in this, the second stage. 
Some murmurs, presystolic or early-diastolic or mid-diastolic, can 
1 Often one finds a crescendo in the middle of a long presystolic roll with a 
diminuendo as it approaches the first sound. CARDIO-VASCULAR DISEASES 
219 
usually be heard with every beat, but the murmurs vary from instant 
to instant, they can often be heard all over the precordia. The first 
sound at the apex still retains its sharp, thumping quality, and is 
often audible without the murmur in the back. 
The irregularity of the heart is generally greater at this stage 
than in the earlier one, and often becomes “absolute” (auricular 
fibrillation). 
Ill 
The third stage of the affection is marked by the weakening or dis- 
appearance of the characteristic murmur, and is generally synchronous 
with the development of failing compensation. The right ventricle 
becomes dilated sometimes very markedly. Indeed, it may produce 
a visible pulsating tumor below the left costal border and be mistaken 
for cardiac aneurism (Osier). The snapping first sound and the 
“double-shock” sound usually remain audible, but the latter may be 
absent altogether. Diagnosis in this stage rests largely upon the 
peculiar snapping charapter of the first sound, together with the 
prolongation of diastole and the absolute irregularity of the heart, both 
in force and rhythm. But usually a faint early diastolic murmur can 
still be heard along the left sternal border continuously. It is soft 
and high pitched, not at all suggesting the deep rolling presystolic of 
earlier stages. 
As the disease advances, the irregularity of the pulse becomes more 
and more marked, and sometimes presents an amazing contrast with 
the relatively good general condition of the circulation. Even when 
not more than a third of the beats reach the wrist, the patient may be 
able to attend to light work and feel very well. Such cases make us 
feel as if a functioning auricle and a palpable pulse were luxuries rather 
than necessities. 
Under the influence of digitalis the pulse beats are especially apt 
to assume the bigeminal or coupled type. (See above, p. 123.) 
Mitral stenosis is in the great majority of cases combined with 
a systolic mitral murmur, and it often happens that this murmur is 
so much more prominent than anything suggesting stenosis that the 
latter escapes observation altogether, especially in the third stage of 
the disease, when the typical presystolic roll has disappeared. In 
such cases combined stenosis and regurgitation is to be distinguished 
by the sharpness of the first sound. The presence of reduplicated 
second sound, a “double-shock sound” at the outset of the prolonged 
diastolic pause, and the absolute irregularity of the pulse are further 220 
PHYSICAL DIAGNOSIS 
suggestive of mitral stenosis. Moreover, it should be remembered 
that a death from mitral regurgitation is almost unknown and that 
if the patient has a chronic serious mitral disease of the rheumatic type, 
stenosis is almost certainly present whatever the murmur. 
Mitral stenosis is apt to be associated with haemoptysis, with en- 
gorgement of the liver and ascites, and especially with arterial embo- 
lism. No other valve lesion is so frequently found associated with embo- 
lism. This is owing to the very frequent formation of a “ball” or 
pedunculated thrombus in the left auricular appendage. Sudden 
death may result from the impaction of this ‘ ‘ ball ’ ’ in the funnel-like 
cone of the stenosed mitral orifice. More often bits of the thrombus 
break loose and are “heard from” in the brain (hemiplegia). In the 
spleen and kidneys they are usually “silent,” but may cause sudden 
and severe pain. Mesenteric embolism or embolic gangrene of a leg 
are not uncommon and, like hemiplegia, may be the first symptom 
of the disease mitral stenosis. 
Differential Diagnosis 
Other murmurs which may be mistaken for the murmur of mitral 
stenosis are: 
(a) The Austin Flint murmur. 
(b) The murmur of tricuspid stenosis. 
(a) In 1862 Austin Flint studied two cases in which during life a 
typical presystolic roll was audible at the apex of the heart, yet in 
which post mortem the mitral valve proved to be perfectly normal, 
and the only lesion present was aortic insufficiency. This observation 
has since been verified by Osier and other observers. I have had many 
such cases with autopsy. Yet, despite repeated confirmation, Flint’s 
observation still remains unknown to physicians at large. Its impor- 
tance is this: Given a case of aortic regurgitation, or any other cause 
producing marked hypertrophy and dilatation of the left ventricle— 
a presystolic murmur at the apex does not necessarily mean stenosis 
of the mitral valve even though the murmur has the typical rolling 
quality and is accompanied by a palpable thrill. It may be only one 
of the by-effects of the aortic incompetency. How it is that a presys- 
tolic murmur can be produced at the apex in cases with big left ven- 
tricle, has been much debated, but remains unknown. 
Between the “Austin Flint murmur’’ thus defined and the mur- 
mur of mitral stenosis, complicating left-sided hypertrophy, diagnosis 
may be impossible. If there is no dilatation of the mitral orifice. CARDIO-VASCULAR DISEASES 
221 
and no regurgitation, any evidence of engorgement of the pulmonary 
circuit (accentuation of the pulmonic second sound, oedema of the 
lungs, haemoptysis, and cough) speaks in favor of an actual narrowing 
of the mitral valve, while the absence of such signs and the presence 
of a Corrigan pulse, or of predominating hypertrophy of the left ven- 
tricle tend to convince us that the murmur is of the type described 
by Austin Flint, i.e., that it does not point to any stenosis of the mitral 
valve. The sharp, snapping first sound, the thrill and systolic shock 
so characteristic of mitral stenosis are apt to be modified or absent 
in connection with murmurs of the Austin Flint type. A positive 
Wassermann reaction with aortic regurgitation usually means syph- 
ilitic aortitis and no mitral stenosis—since the latter is a rheumatic, 
not a syphilitic, lesion. Hence a presystolic murmur heard in a 
case showing good evidence of syphilis and of aortic regurgitation 
but not rheumatic history is probably of the “Flint” type. 
(6) Tricuspid obstruction. 
Luckily for us as diagnosticians, stenosis of the tricuspid valve is a 
rare lesion. Like mitral stenosis it is manifested by a presystolic 
rolling murmur whose point of maximum intensity is sometimes over 
the traditional tricuspid area, but may be at a point so near the mitral 
area as to be easily confused with stenosis of the later valve. 
The difficulty of distinguishing tricuspid stenosis from mitral 
stenosis is further increased by the fact that the two lesions are both 
of “rheumatic” origin and almost invariably occur in conjunction. 
Hence we have two presystolic murmurs, perhaps with slightly 
different points of maximum intensity and possibly with a difference 
in quality, but often quite undistinguishable from each other. In 
the vast majority of cases, therefore, tricuspid stenosis is first recog- 
nized at the autopsy, and the diagnosis is at best a very difficult one. 
When a mitral stenosis seems to yield to treatment less readily and 
the heart is larger than we should expect, considering the general 
condition of the patient, we may guess that a tricuspid obstruction 
(perhaps also an aortic stenosis) is present as well. 
Broadbent, Rosenbach, and others have noticed in children 
who have just passed through an attack of pericarditis a rumbling 
murmur near the apex of the heart, which suggests the murmur of 
mitral stenosis. It is often distinguished from this, however, by the 
absence of any accentuation of the first sound at the apex, as well as 
by the conditions of its occurrence and by its transiency. Such cases 
are important, since their prognosis is much less favorable than that 
of mitral stenosis. 222 
PHYSICAL DIAGNOSIS 
Phear {Lancet, September 21, 1895) investigated 46 cases in which 
a presystolic murmur was observed during life and no mitral lesion 
found at autopsy. In 17 of these there was aortic regurgitation at 
autopsy. In 20 of these there was adherent pericardium at autopsy, 
in 9 nothing more than dilatation of the left ventricle was found. In none 
of these cases was the snapping first sound, so common in mitral 
stenosis, recorded during life. This finding of presystolic murmurs in 
various conditions involving left ventricular hypertrophy (nephritis, 
arteriosclerosis) is entirely in accord with my own experience and 
tends to show that the Austin Flint murmur is due to the enlarged 
left ventricle characteristic of aortic regurgitation and not to the 
regurgitation itself. 
All this resolves itself for me into the belief that when the heart is 
much enlarged nothing that you hear at the apex is of much importance 
as evidence of valvular disease, except the rare axillary diastolic mur- 
mur of aortic regurgitation. Systolic and presystolic murmurs at the 
apex of a very large heart have little significance. 
It should be remembered that patients suffering from mitral 
stenosis are very frequently unaware of any cardiac trouble, and seek 
advice for anaemia, wasting, debility, gastric or pulmonary complaints. 
This is less often true in other forms of valvular disease. We should 
be especially on our guard in cases of supposed “nervous arrhythmia ” 
or “tobacco heart,” if there has been an attack of rheumatism or 
chorea previously. Such cases may present no complaints except the 
irregularity—yet may turn out to be mitral stenosis. 
4. Aortic Disease (Rheumatic Type) 
Rheumatic endocarditis usually occurs in early life, more commonly 
in women and most often attacks the mitral valve. The commonest 
cause of aortic disease on the other hand—syphilitic aortitis—occurs 
at all ages and attacks men much more often than women. Never- 
theless rheumatic cases do occur at all ages and in both sexes, and 
do not always spare the aortic cusps by any means. 
1. Aortic Regurgitation 
When produced by rheumatic or septic endocarditis, the lesion 
which results in aortic regurgitation is always a thickening, shortening 
and adhesion of the cusps (see Fig. 146). CARDIO-VASCULAR DISEASES 
223 
In the rheumatic type of aortic disease now to be described, 
mitral disease is usually present as well. Hence the signs of the aortic 
lesion may be much modified. I shall describe first the sign in cases 
of rheumatic aortic disease with relatively slight mitral trouble or 
none at all. 
Fig. 146.—Diastole in Aortic Regurgitation. The blood is flowing back through the 
stumpy and incompetent aortic valves. 
Fig. 147-—Position of the Point of Maximum Intensity of the Murmur of Aortic 
Regurgitation. The dots are most thickly congregated where the murmur is oftenest 
heard. 
In rheumatic disease of the aortic valve, the arterial phenomena 
and the cor bovinum seen in syphilitic aortitis are less notable. The 
murmur is the most important evidence that we have. This murmur 
is sometimes difficult to hear. In the majority of cases, however, the 224 
PHYSICAL DIAGNOSIS 
characteristic diastolic murmur is easily heard if one listens in the right 
place, and when heard it is the most distinctive and trustworthy of all 
cardiac murmurs. 
The murmur of aortic regurgitation, as has been already men- 
tioned, is diastolic in time. Its maximum intensity is usually not 
in the conventional aortic area (second right interspace), but on the 
left side of the sternum about the level of the fourth left costal cartilage. 
In about one-fifth of the cases, and especially when the aortic arch 
is much dilated, the murmur is best heard in the conventional aortic 
area. Occasionally there are two points at which it may be loudly 
heard—one in the second right interspace and the other at or outside 
the cardiac apex, while between these points the murmur is faint. 
This is probably due to the fact that the left ventricle, through which 
the murmur is conducted, approaches the surface of the chest only at 
the apex, while the intermediate space is occupied by the right ventri- 
cle, which often fails readily to transmit murmurs produced at the 
aortic orifice. Less frequently the murmur of aortic regurgitation is 
heard with maximum intensity at the second or third left costal carti- 
lage, at the apex, in the left axilla, or in the region of the ensiform 
cartilage. 
From its seat of maximum intensity if.e., usually from the fourth 
left costal cartilage) the murmur is transmitted in all directions, but 
not often beyond the precordia. In about one-third of the cases it is 
transmitted to the left axilla or even to the back. It is sometimes to 
be heard in the subclavian artery and the great vessels of the neck; 
1st 
1st 
2nd 
2nd 
Fig. 148.—Short Diastolic Murmur Not Replacing the Second Sound. 
in other cases two heart sounds are audible in the carotid, but no mur- 
mur. The murmur is usually blowing and relatively high pitched, 
sometimes musical. Its intensity varies much, but is most marked at 
the beginning of the murmur, giving the impression of an accent there. 
It may occupy the whole of diastole or only a small portion of it— 
usually the earlier portion (see Fig. 148). Late diastolic murmurs are 
rare. The murmur may or may not replace the second sound of the 
heart. Broadbent believes that when it does not obliterate the 
second sound, the lesion is usually less severe than when only the 
murmur is to be heard. Allbutt dissents from this opinion. CARDIO-VASCULAR DISEASES 
225 
The position of the patient’s body has but little effect upon the 
murmur—less than upon murmurs produced at the mitral orifice. 
A systolic murmur is almost always present as well—and best 
heard in the second right space. It may be due to the almost in- 
variably accompanying aortic stenosis (see below). 
Differential Diagnosis.—The chief point of difficulty is to distin- 
guish the relatively rare (rheumatic) lesions of the aortic valve alone 
from those accompanying mitral stenosis. For in mitral stenosis we 
may have an early diastolic (not presystolic) murmur soft and blow- 
ing in quality along the left sternal border—in fact a precise imitation 
of the aortic regurgitant murmur (Graham Steele murmur). Differen- 
tial diagnosis from an aortic lesion may then be impossible. True 
aortic disease (rheumatic type) is probable if we have in addition to 
the murmur a jerking or “Corrigan” type of pulse and the other 
arterial phenomena described in detail on page 250. But in rheu- 
matic disease these arterial phenomena are often absent. We are 
then often unable to decide between mitral disease alone and mitral 
plus aortic disease, since the condition of the left ventricle does not 
help us but rather confuses us. 
A loud diastolic murfnur audible without a stethoscope 3 in. 
from the chest occurred in a recent case of “rheumatic” pericarditis 
with adhesions. Autopsy showed no valvular lesion whatever, only 
marked hypertrophy and dilatation. 
2. Aortic Stenosis 
Uncomplicated aortic stenosis, i.e., without aortic regurgitation as 
well, is probably a myth. In the rheumatic type of heart disease the 
two lesions are almost always associated, though it may be impossible 
to find signs of regurgitation during life. It is probably cases of 
this latter type (unautopsied) that have given rise to the conception 
of a “pure” aortic stenosis. At any rate I shall consider it here 
wholly as an accompaniment of (rheumatic) aortic regurgitation. 
Out of two hundred and fifty-two autopsies made at the Massa- 
chusetts General Hospital in cases of valvular disease there was no one 
of uncomplicated arotic stenosis. Thirty cases occurred in combination 
with aortic regurgitation. Of these 19 or 63% were recognized in life 
and 11 or 36% were not recognized. During life the diagnosis of 
aortic stenosis is frequently made, but often on insufficient evidence— 
i.e., upon the evidence of a systolic murmur heard with maximum 
intensity in the second right intercostal space and transmitted into the 226 
PHYSICAL DIAGNOSIS 
vessels of the neck. Such a murmur does indeed occur in aortic 
stenosis, but is by no means peculiar to this condition. Of the other 
diseases which produce a similar murmur more will be said under 
Differential Diagnosis. 
For the diagnosis of aortic stenosis we need the following evidence: 
(1) A systolic murmur heard best in the second right intercostal 
space. 
(2) The characteristic pulse (vide infra). 
(3) A palpable thrill (usually). 
(4) Absence or great enfeeblement of the aortic second sound.1 
Fig. 149.—Aortic Stenosis. The heart is in systole and the blood column is obstructed 
by the narrowed aortic ring. The mitral is closed (as it should be). 
Of these signs the thrill is the most important. The heart may or 
may not be demonstrably enlarged. 
Each of these points will now be described more in detail. 
(a) The Murmur 
(a) The maximum intensity of the murmur, as has already been 
said, is usually in the second right intercostal space near the sternum 
or a little above that point near the sterno-clavicular articulation, but 
it is by no means uncommon to find it lower down, i.e., in the third, 
fourth, or fifth right interspace, and occasionally it is best heard to the 
left of the sternum in the second or third intercostal space. (b) The 
1 Against all reason I have twice seen at autopsy an aortic stenosis despite the 
fact that the “aortic second sound” had been loud in life. CARDIO-VASCULAR DISEASES 
227 
time of the murmur is late systolic; that is, it follows the apex impulse 
at an appreciable interval, contrasting in this respect with the systolic 
murmurs heard loudest at the apex, (c) The murmur is usually 
widely transmitted, often being audible over the whole chest and occa- 
sionally over the skull and the arterial trunks of the extremities (see 
Fig. 150). It is usually heard less well over that portion of the pre- 
cordia occupied by the right ventricle, while, on the other hand, it 
may be loudest in the region of the apex impulse, whither it is trans- 
mitted through the left ventricle. The same line of transmission was 
mentioned above as characteristic of the murmur of aortic regurgita- 
tion in many cases. The murmur is also to be heard over the carotids 
and subclavians, and can often be traced over the thoracic aorta along 
the spine and down the arms. 
Maximum intensity 
of systolic mur- 
mur and thrill. 
Fig. 150. Aortic Stenosis. The murmur is audible over the shaded area and sometimes 
over the whole chest. 
Until compensation fails the murmur is apt to be a very loud one, 
especially in the recumbent position; it is occasionally audible at some 
distance from the chest, and is often rough and vibrating, sometimes 
musical or croaking. Its length is usually great, extending through- 
out the whole of systole, but to this rule there are a good many 
exceptions. 
(2) The Aortic Second Sound 
The diminution or absence of the aortic second sound is an impor- 
tant point in the diagnosis of this lesion. It is true (as already men- 
tioned) that we do not always get this sign. Yet without it diagnosis 
is always uncertain. , a 228 
PHYSICAL DIAGNOSIS 
(b) The Pulse 
Owing to the opposition encountered by the left ventricle in its 
attempt to force blood into the aorta, its contraction is apt to be 
prolonged; hence the pulse wave rises gradually and late, and falls 
away slowly. This is shown very well in sphygmographic tracings 
(see Fig. 151). But further, the blood thrown into the aorta by the 
left ventricle is prevented, by the narrowing of the aortic valves, from 
striking upon and expanding the arteries with its ordinary force; 
hence the pulse wave is not only slow to rise but small in height, 
sometimes contrasting with the powerful apex beat (“ pulsus parvus ”) 
Again, the delay in the emptying of the left ventricle, brought about 
by the obstruction at the aortic valves, may render the contractions 
of the heart relatively infrequent, and hence the pulse is infrequent 
(pulsus rarus) as well as small and slow to rise. The “pulsus rarus, 
Fig. 151.—Sphymographic Tracing of the Pulse in Aortic Stenosis. Compare with 
the normal pulse wave and with that of aortic regurgitation (pages 251 and 252). 
parvus, tardus” is therefore, an important point in diagnosis, 
but unfortunately it is to be felt in perfection only in the cases in 
which aortic stenosis is associated with very little regurgitation, i.e., 
in the extreme cases with excessively narrow aortic orifice. When 
stenosis is combined with free regurgitation, as is usually the case, the 
above-described qualities of the pulse are modified as a result of the 
regurgitation. Indeed, I have in two cases observed a well-marked 
“Corrigan” pulse in life and been confronted post-mortem with a nar- 
rowed, rigid aortic valve! 
The slow, long pulse with a plateau at the summit is seen also 
in some cases of mitral stenosis and renal disease, and is not peculiar 
to aortic stenosis, but taken in connection with the other signs of the 
disease it has great value in diagnosis. 
(c) The Thrill 
In the majority of cases an intense purring systolic vibration may be 
felt if the hand is laid over the upper portion of the sternum, especially 
over the second right intercostal space. This thrill is continued CARDIO-VASCULAR DISEASES 
229 
into the carotids, can occasionally be felt at the apex, and rarely over 
a considerable area of the chest. It is a very important aid in the 
diagnosis of aortic stenosis, but is by no means pathognomonic, since 
aneurism may produce a precisely similar vibration of the chest wall. 
The heart is slightly enlarged to the left and downward as a rule, 
but the apex impulse is unusually indistinct, “a well-defined and 
deliberate push of no great violence” (Broadbent) in some cases. In 
the majority it presents nothing peculiar or characteristic. 
(d) Diagnosis of Aortic Stenosis from the Etiology alone 
Post mortem experience has taught me that in practically all long 
standing cases of “rheumatic” endocarditis affecting the aortic valve, 
stenosis as well as regurgitation is present. Hence if these etiological 
factors can be recognized and if there is clear evidence of aortic 
regurgitaton, it is pretty safe to postulate the existence of aortic 
stenosis as well, whatever the physical signs. 
(e) Differential Diagnosis 
A systolic murmur heard loudest in the second right intercostal 
space is by no means peculiar to aortic stenosis, but may be due to 
any of the following conditions: 
(a) Roughening, stiffness, fenestration, or slight congenital mal- 
formation of the aortic valves. 
(b) Roughening or difEuse dilatation of the arch of the aorta. 
(c) Aneurism of the aorta or innominate artery. 
(d) Functional murmurs. 
(e) Pulmonary stenosis. 
(/) Open ductus arteriosus, and other congenital lesions. 
(a and b) The great majority of systolic murmurs at the base of 
the heart, first appearing after middle life, are due to the causes men- 
tioned above under a, b, and c. They are associated, as a rule, with 
high blood pressure and with evidence of arterio-sclerosis, chronic 
nephritis or syphilis and not with a “rheumatic” history. In such 
cases the murmur is usually combined with accentuation and ringing 
quality of the aortic second sound owing to the arterio-sclerosis and 
high arterial tension associated with the changes which produce the 
murmur. This accentuation of the aortic second sound enables us, 
except in rare cases, to exclude aortic stenosis, in which the intensity 
of the aortic second sound is almost always much reduced. 
Diffuse dilatation of the aorta, which often accompanies arterio- 
sclerosis, is a frequent cause of a systolic murmur loudest in the 230 
PHYSICAL DIAGNOSIS 
second right interspace. This may be recognized in certain cases by 
the characteristic area of dulness on percussion or by x-ray. 
Roughening of the intima of the aorta (endaortitis) is always be to 
suspected in elderly patients with calcified and tortuous peripheral 
arteries, and such a condition of the aorta doubtless favors the occur- 
rence of a murmur, especially when accompanied by a slight degree 
of dilatation. The age, the presence of hypertension, the sharp aortic 
second sound, and the absence of a thrill and rheumatic history serve 
to distinguish such murmurs from those of aortic stenosis. 
(c) Aneurism of the ascending arch of the aorta or of the innomi- 
nate artery may give rise to every sign of aortic stenosis except the 
characteristic pulse and the diminution of the aortic second sound. 
In aneurism we may have a well-marked tactile thrill and a loud sys- 
tolic murmur transmitted into the neck, but there is usually some 
abnormal pulsation to be felt, a characteristic x-ray shadow to be seen, 
and often some difference in the pulses or in the pupils, as well as a 
history of pain and symptoms of pressure upon the trachea and bronchi 
or recurrent laryngeal nerve. In aneurism the aortic second sound is 
usually* loud, and the pulse shows none of the characteristics of aortic 
stenosis. Finally the evidence of syphilis and the absence of a “rheu- 
matic” history may assist our decision. 
(d) Functional murmurs, sometimes known as “hsemic,” are 
occasionally best heard in the aortic area instead of in their usual situa- 
tion (second left intercostal space). They are not accompanied by 
any palpable thrill, any diminution in the aortic second sound, or any 
distinctive abnormalities in the pulse. 
(e) Pulmonary stenosis, a rare lesion, is manifested by a systolic 
murmur and by a thrill whose maximum intensity is usually on the 
left side of the sternum. In the rare cases in which this murmur is 
best heard in the aortic area it may be distinguished from the murmur 
of aortic stenosis by the fact that it is not transmitted into the vessels 
of the neck, has no effect upon the aortic second sound, and is not 
accompanied by the characteristic changes in the pulse. The electro- 
cardiogram should show right sided predominance in pulmonary sten- 
osis, left sided predominance in aortic stenosis. 
if) The murmur due to persistence of the ductus arteriosus may 
last through systole and into diastole; it may be accompanied by a 
thrill, but does not affect the pulse. Most of the other congenital 
lesions can be recognized by their history. 
(g) The systolic murmur of aortic stenosis may be heard loudly at 
the apex, and hence the lesion may be mistaken for mitral disease. CARDIO-VASCULAR DISEASES 
231 
But its association with a thrill and a long, slow pulse should enable 
us usually to differentiate the two lesions. 
By the foregoing differentiae aortic stenosis may be distinguished 
from the other conditions which resemble it, provided it predominates 
over the regurgitation associated with it, but unfortunately this is not 
very common. In many cases it is fairly well balanced or neutralized 
by the accompanying aortic regurgitation, and its characteristic 
signs are therefore obscured or greatly modified by the signs of the 
latter disease. In such cases the thrill and the “rheumatic” history 
are our chief point of support in the more or less reasonable suspicion 
that aortic stenosis is present. 
Occasionally one can watch the development of an aortic stenosis 
out of what was formerly a pure regurgitant lesion, the stenosis gradu- 
ally modifying the characteristics of the previous condition. One 
must be careful, however, to exclude a mitral stenosis which, as has 
been already mentioned above, is very apt to accompany cases of 
aortic disease, and which may modify the characteristic signs of aortic 
regurgitation very much as aortic stenosis does. 
5. Diseases of the Tricuspid and Pulmonary Valves 
1. Tricuspid Regurgitation 
This lesion is in no way peculiar to the rheumatic type of heart 
disease. It occurs in all types as a phenomenon of broken compensa- 
tion, but it is convenient to describe all its forms here along with the 
rarer rheumatic type. 
Rheumatic endocarditis affecting the tricuspid valve is rare in 
post-foetal life; in the foetus it is not so uncommon. In cases of ulcera- 
tive or malignant endocarditis occurring in adult life, the tricus- 
pid valve is occasionally involved, but the majority of cases of tri- 
cuspid disease occur in the following manner: Hypertrophy of the 
right ventricle occurs as a result of the mitral disease, and is followed 
in time by dilation; with this dilatation comes a stretching of the 
ring of insertion of the tricuspid valve, and hence a regurgitation 
through that valve. Tricuspid regurgitation, then, occurs in the 
latest stages of almost every case of mitral disease, and sometimes 
during the earlier attacks of failing compensation. 
Out of 405 autopsies at Guy’s Hospital in which evidence of 
tricuspid regurgitation was found, 271, or two-thirds, resulted from 
mitral disease, 68 from myocardial degeneration, 55 from pulmonary 232 
PHYSICAL DIAGNOSIS 
disease (bronchitis, emphysema, cirrhosis of the lung). Very few of 
these cases had been diagnosed during life, and in all of them the 
valve was itself healthy but insufficient to close the dilated orifice. 
Gibson and some other writers believe that temporary tricuspid 
regurgitation is the commonest of all valve lesions, and results from 
weakening of the right ventricle in connection with states of anae- 
mia, gastric atony, fever, and many other conditions. It is very 
difficult to prove or disprove such an assertion. 
Tricuspid regurgitation is often referred to as serving like the 
opening of a 11 safety valve ” to relieve a temporary pulmonary engorge- 
ment. This “safety-valve” action, however, may be most disastrous 
in its consequences to the organism as a whole, despite the temporary 
relief which it affords to the overfilled lungs. The engorgement is 
simply transferred to the liver and thence to the abdominal organs 
and the lower extremities, so that as a rule the advent of tricuspid 
regurgitation is recognized not as a relief but as a serious and probably 
fatal disaster. 
(a) Physical Signs 
(1) Systolic venous pulsation in the jugulars and in the liver. 
(2) Engorgement of the right auricle producing an area of dulness 
beyond the right sternal margin. 
(3) Intense cyanosis. 
(4) Ascites and oedema of the legs. 
(5) A systolic murmur heard loudest at or near the fifth left 
costal cartilage (a very uncertain and variable sign). 
(1) Of chief importance in diagnosis is the presence of a sys- 
tolic pulsation in the external jugular veins and of the liver, which 
unfortunately is not always present, but which when present is 
pathognomonic. I have already explained (see p. 89) the distinc- 
tion between true systolic jugular pulsation and simple presystolic 
undulation or distention of the same veins, which has no necessary 
relation to this disease. The decisive test is the effort permanently 
to empty the vein by stroking it upward from below. If it instantly 
refills from below and continues to pulsate, tricuspid regurgitation 
is almost certainly present. If, on the other hand, it does not refill 
from below, the cause must be sought elsewhere. 
Pulsation in the liver must be distinguished from the “jogging” 
motion which may be transmitted to it from the abdominal aorta or 
from the right ventricle. To eliminate these transmitted impulses 
one must be able to grasp the liver bimanually, one hand in front and CARDIO-VASCULAR DISEASES 
233 
one resting on the lower ribs behind, and to feel it distinctly expand 
with every systole, or else to take its edge in the hand and to feel it 
enlarge in one’s grasp with every beat of the heart. Pressure upon the 
liver often causes increased distention and pulsation of the external 
jugulars if tricuspid regurgitation is present. 
(2) Enlargement of the heart, both to the right and to the left, as 
well as downward, can usually be demonstrated. In rare cases a 
dilatation of the right auricle may be suggested by a percussion outline 
such as that shown in Fig. 152. 
Dilated right 
auricle. 
Systolic murmur. 
Enlarged and pul- 
sating liver. 
Fig. 152.—Tricuspid Regurgitation. The murmur is heard best over the shaded area 
The pulmonic second sound is usually not accented. The impor- 
tance of this in differential diagnosis will be mentioned presently. If 
a progressive diminution in the intensity of the sound occurs under 
observation, the prognosis is very grave. 
(3) Cyanosis is usually very great, and dyspnoea and general dropsy 
often make the patient’s condition a desperate one. 
(4) The murmur (systolic) is inconstant and usually indistinguish- 
able from those produced at the aortic or mitral orifice. 
(b) Differential Diagnosis 
The cases autopsied at the Massachusetts General Hospital show 
that tricuspid regurgitation with stenosis is less often recognized 
during life than any other valvular lesion. The diagnosis was made 
ante mortem on only five out of twenty-nine cases. This is due to 
the following facts: 234 
PHYSICAL DIAGNOSIS 
(а) Tricuspid regurgitation may be present and yet give rise to no 
physical signs which can be recognized during life. 
(б) Tricuspid regurgitation occurs most frequently in connection 
with mitral disease; hence its signs are frequently masked by those 
of the latter lesion. 
2. Tricuspid Stenosis 
One of the rarest of “rheumatic” valve lesions is narrowing of the 
tricuspid valve. Only 28 cases (none recognized in life) have come 
under my observation, and in 1908, Herrick was able to collect but 
187 cases from the world’s literature. Out of 154 cases, 138, or 90 
per cent., were combined with mitral stenosis, and only 12 times has 
tricuspid stenosis been known to occur alone.1 These observations 
account for the fact that tricuspid stenosis has been recognized during 
life only 10 times since the murmur to which is gives rise is identical 
in time and quality, and nearly identical in position with that of mitral 
stenosis. 
The heart is usually enlarged, especially in its transverse direction; 
the enlargement is greater than that of mitral stenosis, a fact which 
gives aid to our diagnosis. 
The diagnosis is still further complicated in many cases by the 
presence of an aortic stenosis in addition to a similar lesion at the 
tricuspid and mitral valves, so that it seems likely that in the future, 
as in the past, the lesion will usually be discovered first at autopsy. 
When we know we have marked mitral stenosis (perhaps with aortic 
stenosis as well) yet find surprisingly little dyspnoea, no accentuation 
of the pulmonic second sound, distended neck veins with anasarca and 
cyanosis, and when the mitral lesion does not improve as we should 
expect under treatment, and the heart is unusually large, we may be 
led occasionally to suspect tricuspid stenosis. 
3. Pulmonary Regurgitation 
Organic disease of the pulmonary valve is excessively rare in 
post-foetal life, but may occur as part of an acute ulcerative or septic 
endocarditis. A temporary functional regurgitation through the 
1 Out of 87 cases collected from the post-mortem records of Guy’s Hospital, 85, 
or 97 per cent., were associated with still more extensive mitral stenosis. At the 
Mass. General Hospital 26 of the 28 cases of tricuspid stenosis found at autopsy 
were associated with mitral stenosis as well. CARDIOVASCULAR DISEASES 
235 
pulmonary valve may be brought about by any cause producing 
very high pressure in the pulmonary artery. I have known two medical 
students with perfectly healthy hearts who were able, by prolonged 
holding of the breath, to produce a short, high-pitched diastolic 
murmur best heard in the second and third left intercostal spaces and 
ceasing as soon as the breath was let out. Of the occurrence of a 
murmur similarly produced under pathological conditions, especially 
in mitral stenosis, much has been written by Graham Steell. 
From the diastolic murmur of aortic regurgitation we may dis- 
tinguish the diastolic murmur of pulmonary incompetency by the 
fact that the latter is best heard over the pulmonary valve, is never 
transmitted to the apex of the heart nor to the great vessels, and is 
never associated with a Corrigan pulse nor with capillary pulsation. 
The right ventricle is hypertrophied, the pulmonic second sound is 
sharply accented and followed immediately by the murmur. Evi- 
dences of septic embolism of the lungs are frequently present and 
assist us in diagnosis. The regurgitation which may take place 
through the rigid cone of congenital pulmonary stenosis (see p. 274) is 
not recognizable during life. 
6. Combined Valvular Lesions 
It is essential that the student should understand from the first 
that the number of murmurs audible in the precordia is no gauge 
for the number of valve lesions. We may have four distinct murmurs, 
yet every valve sound except one. This is often the ease in aortic 
disease—systolic and disastolic murmurs at the base of the heart, systolic 
and presystolic at the apex, yet no valve injured except the aortic. In 
such a case the systolic aortic murmur is due to roughening of the 
aortic valve. The systolic apex murmur results from relative mitral 
leakage (with a sound valve). The presystolic apex murmur is of 
the “Flint” type. Hence in this case diastolic murmur alone of the 
four audible murmurs is due to a valvular lesion. 
It is a good rule not to multiply causes unnecessarily, and to explain 
as many signs as possible under a single hypothesis. In the above 
example the mitral leak might be due to an old endocarditis, and there 
might be mitral stenosis and aortic stenosis as well, but since we can 
explain all the signs as results—direct and indirect—of one lesion 
(aortic regurgitation) it is better to do so, and post-mortem experience 
shows that our diagnosis is more likely to be right when it is made 
according to this principle. 236 
PHYSICAL DIAGNOSIS 
The most frequent combinations are: 
(1) Mitral regurgitation with mitral stenosis. 
(2) Aortic regurgitation with aortic stenosis, with or without mitral 
disease. 
(3) Mitral and tricuspid stenosis. 
1. Double Mitral Disease 
(a) It very frequently happens that the mitral valve is found to be 
both narrowed and incompetent at autopsy when only one of these 
lesions had been diagnosed during life. In fact mitral stenosis is 
almost never found at autopsy without such a stiffening of the orifice as 
would produce an associated regurgitation, so that it is fairly safe to 
1st 
2nd 
Pig. 153.—Mitral Stenosis and Regurgitation, showing relation of murmur to first 
heart sound. 
assume, whenever one makes the diagnosis of mitral stenosis, that 
mitral regurgitation is present as well, whether it is possible to hear any 
regurgitant murmur or not (see Fig. 153). 
(b) On the other hand, with a double mitral lesion one may have 
only the systolic murmur at the mitral valve and nothing to suggest 
stenosis unless it be a surprising sharpness of the first mitral sound. 
In chronic cases the changeableness of the murmurs, both in type and 
position, is extraordinary. One often finds at one visit evidences of 
mitral stenosis and at another evidences of a systolic mitral murmur 
alone. Either murmur may disappear altogether for a time and 
reappear subsequently. This is peculiarly true of the pre-svstolic 
murmur, which is notoriously one of the most fleeting and uncertain of 
all physical signs. 
As a rule the same inflammatory changes which produce a mitral 
systolic murmur in early life result, as they extend, in a narrowing of 
the mitral valve, so that the signs of stenosis come to predominate in 
later years. Coincidently with this narrowing of the diseased valve 
a certain amount of improvement in the patient’s symptoms may 
take place, and Rosenbach regards the advent of stenosis in such a 
case as an attempt at regenerative or compensatory change. In 
many cases, however, no such amelioration of the symptoms follows. CARDIO-VASCULAR DISEASES 
237 
2. Aortic Regurgitation ivith Mitral Disease 
The signs of mitral disease occurring in combination with aortic 
regurgitation do not differ essentially from those of pure mitral 
disease except that the enlargement of the heart is apt to be more 
Systolic murmur 
over dilated 
aortic arch. 
Maximum intensity 
and diastolic mur- 
mur, conducted 
up and down. 
'Systolic murmur. 
Fig. 154.—Aortic and Mitral Disease. The shaded areas are those in which the 
murmurs are loudest. 
general and correspond less exclusively to the right ventricle (see 
Figs. 154 and 155.) The manifestations of the aortic lesion, on the 
other hand, are considerably modified by their association with the 
mitral disease. The Corrigan pulse is distinctly less sharp at the sum- 
mit and rises and falls less abruptly. Capillary pulse is less likely to 
1st 
1st 
2nd 
2nd 
Fig. 155.—Showing Relation of Murmurs to Heart Sound in Disease of the Aortic 
and Mitral Valves. 
be present, and the throbbing of the peripheral arteries is less often 
visible. 
3. Aortic Regurgitation with Aortic Stenosis 
If the aortic valves are narrowed as well as incompetent, we 
find very much the same modification of the physical signs charac- 
teristic of aortic regurgitation as is produced by the advent of a 238 
PHYSICAL DIAGNOSIS 
mitral lesion; that is to say, the throbbing in the peripheral arteries 
is less violent, the characteristics of the radial pulse are less marked, 
and the capillary pulsation is not always to be obtained at all. Indeed, 
this blunting of all the typical manifestations of aortic regurgitation 
may give us material aid in the diagnosis of aortic stenosis, provided 
always that the mitral valve is still performing its function.1 
(4) The association of mitral disease with tricuspid stenosis has 
been already described on p. 234. 
PERICARDITIS 
Three forms may be recognized clinically: 
(1) Plastic, dry, or fibrinous pericarditis. 
(2) Pericarditis with effusion (serous or purulent). 
(3) Pericardial adhesions or adherent pericardium. 
Fibrinous pericarditis may be fully developed without giving rise 
to any physical signs that can be appreciated during life. In several 
cases of pneumonia in which I suspected that pericarditis might be 
present, I have listened most carefully for evidences of the disease 
and been unable to discover any; yet at autopsy it was found fully 
developed—the typical shaggy heart. We have every reason to 
believe, therefore, that pericarditis is frequently present but unrecog- 
nized, especially in terminal streptococcus sepsis, in pneumonia and 
in the rheumatic attacks of children. On the other hand, it may give 
rise to very marked signs which are the result of— 
(а) The rubbing of the roughened pericardial surfaces against 
one another when set in motion by the cardiac contractions. 
(б) The presence of fluid in the pericardial sac. 
(c) The interference with cardiac contractions brought about by 
obliteration of the pericardial sac together with the results of adhesions 
between the pericardium and the surrounding structures. 
1. Dry and Fibrinous Pericardium 
The diagnosis rests upon a single physical sign—“pericardial 
friction ”—which is usually to be appreciated by auscultation alone, 
but may occasionally be felt as well. Characteristic pericardial fric- 
tion is a rough, irregular, grating or shuffling sound which occurs 
irregularly and interruptedly during the larger part of each cardiac 
cycle. It is almost never accurately synchronous either with systole 
1 Some astonishing exceptions to this rule have been mentioned on pages 229 
and 234. . CARDIO-VASCULAR DISEASES 
239 
or diastole, but overlaps the cardiac sounds, and encroaches upon the 
pauses in the heart cycle. It is seldom exactly the same in any two 
successive cardiac cycles and differs thereby from sounds produced 
within the heart itself. Pericardial friction seems very near to the 
ear and may often be increased by pressure with the stethoscope; it is 
not materially influenced by the respiratory movements. 
It is best heard in the majority of cases in the position shown 
in Fig. 156; that is, over that portion of the heart which lies nearest 
to the chest wall and is not covered by the margins of the lungs; 
but not infrequently it may be heard at the base of the heart along the 
right sternal margin or over the whole precordial region. The sounds 
Pericardial friction. 
Fig. 156.—Showing Most Frequent Site of Audible Pericardial Friction 
are fainter if the patient lies on the right side, and sometimes intensified 
if, while sitting or standing, he leans forward and toward the left, so as 
to bring the heart into closer apposition with the chest wall. 
Pericardial friction sounds often change rapidly from hour to hour, 
and may disappear and reappear in the course of a day. 
In rare cases the friction may occur only during systole or only 
during diastole. In such cases the diagnosis between pericardial 
and intracardial sounds may be very difficult. 
Differential Diagnosis 
(a) Pleuro-pericardial Friction 
Fibrinous inflammation affecting that part of the pleura which 
overlaps the heart may give rise to sounds altogether indistinguishable 
from those of true pericardial friction when the inflamed pleural 240 
PHYSICAL DIAGNOSIS 
surfaces are made to grate against one another by the movements of 
the heart. Such sounds are sometimes increased in intensity during 
forced respiration and disappear at the end of expiration, while true 
pericardial friction is usually best heard if the breath is held at the end 
of expiration. If a friction sound heard in the pericardial region ceases 
altogether when the breath is held, we may be sure that it is produced 
in the pleura and not in the pericardium, but in many cases the 
diagnosis cannot be made correctly. 
(b) Intracardiac Murmurs 
From murmurs due to valvular disease of the heart, pericardial 
friction can usually be distinguished by the fact that the sounds to 
which it gives rise do not accurately correspond either with systole 
or diastole, and do not occupy constantly any one portion of either 
of these periods. Cardiac murmurs are more regular, seem less 
superficial, and vary less with position and from hour to hour. 
(c) Friction Sounds of Unknown origin (dry surfaces?) 
In desiccated patients, e.g. in uraemia with vomiting, friction sounds 
like those of pericarditis may be heard yet no lesion is found post- 
mortem. 
2. Pericardial Effusion 
Following the fibrinous exudation, which roughens the pericar- 
dial surface and produces the friction sounds just described, serum 
may accumulate in the pericardial sac. Its quantity may exceed but 
slightly the amount of fluid normally present in the pericardium, or 
may be so great as to embarrass the cardiac movements and finally 
to arrest them altogether. In chronic (usually tuberculous) cases, 
the pericardium may become stretched so as to hold a quart or more 
without seriously interfering with the heart’s action, while a much 
smaller quantity, if effused so rapidly that the pericardium has no time 
to accommodate itself by stretching, will prove rapidly fatal. 
Hydropericardium denotes a dropsy of the pericardium occurring 
by transudation as part of a general dropsy in cases of renal disease or 
cardial weakness. The physical signs to which it gives rise do not 
differ from those of an inflammatory effusion, and, accordingly, all 
that is said of the latter in the following section may be taken as 
equally an account of the signs of hydropericardium. CARDIO-VASCULAR DISEASES 
241 
Hsemopericardium, or blood in the pericardial sac, due to stabs or 
to ruptures of the heart, is usually so rapidly fatal that no physical 
signs are recognizable. 
Fig. 157.—X-rav of Pericardial Effusion, 
(a) Physical Signs of Pericardial Effusion 
In most cases a pericardial friction rub has been observed prior to 
the time of the fluid accumulation. The presence of fluid in the 
pericardial sac is shown chiefly in four ways: 
(1) By percussion, which demonstrates an area of dulness more or 
less characteristic (see below). 
(2) By auscultation, which may reveal an unexpected feebleness in 
the heart sounds when compared with the power shown in the radial 
pulse. 
(3) By the signs and symptoms of pressure exerted by the peri- 
cardial effusion upon surrounding structures. 
(4) By the x-ray (see Fig. 157). 242 
PHYSICAL DIAGNOSIS 
Bulging of the precordia is occasionally to be seen in children; in 
adults we sometimes observe a flattening of the interspaces just to the 
right of the sternum between the third and sixth ribs. 
(1) The Area of Percussion Dulness.—The extent of the dull area 
depends not only on the size of the effusion and the position of the 
patient, but also on the amount of “give” in the pericardium and in 
the lungs, as well as on the size of the lingula pulmonalis. Allowing 
for these uncertain factors, we may say: (a) One of the most charac- 
teristic points is the unusual1 extension of the percussion dulness a 
considerable distance to the left of the maximum cardiac impulse. 
Tympany 
Dulness. 
Cardiac impulse. 
Liver dulness. 
Fig. 158.—Percussion Dulness in Pericardial Effusion, with Tympanitic Resonance 
Under the Left Clavicle. 
(b) The dullness to the right of the sternum may extend farther than 
in any type of cardiac hypertrophy and dilatation. It is only in peri- 
cardial effusion that we get so wide an area of dulness continuous with 
the heart (see Fig. 158). Rotch has called attention to the impor- 
tance of dulness in the fifth right intercostal space as a sign of pericardial 
effusion, but a similar dulness may be produced by enlargement 
of the liver. 
Except for the two points mentioned above (the unusual extension 
of the dulness to the left of the cardiac impulse, and the wide area to 
the right of the sternum), there seems to me to be nothing characteristic 
about the area of dulness produced by pericardial effusion. Even 
these signs are often unreliable. The sheet anchor for diagnosis in 
pericardial effusion is a good x-ray study. 
1 In health the cardiac dulness extends about % of an inch beyond the maximum 
cardiac impulse, but in pericardial effusion the difference is greater. CARDIOVASCULAR DISEASES 
243 
In some cases the area of dulness may be modified by change in the 
patient’s position. After marking out the area of percussion dulness 
with the patient in the upright position, let him lie upon his right side. 
The right border of the area of dulness will sometimes move consider- 
ably farther to the right. A dilated heart can be made to shift in a 
similar way, but to a lesser extent. Comparatively little change takes 
place if the patient lies on his left side, and no important information 
is elicited by placing him flat on his back or by getting him to lean 
forward. 
Unfortunately, it is only with moderate-sized effusions occurring 
in a pericardial sac free from adhesions to the surrounding parts that 
this shifting can be made out. Large effusions may not shift appre- 
ciably, and less than 150 c.c. of fluid probably cannot be recognized by 
this or by any other method. But with large effusions the lateral 
extension of the area of dulness may be so great as to be almost dis- 
tinctive in itself, i.e., from the middle of the left axilla nearly to the 
right nipple. 
(2) Feebleness of the heart sounds and of the apex impulse is of 
diagnostic importance only when it gradually takes the place of the 
normal phenomena as one watches the heart from day to day. Under 
these conditions they have some confirmatory value in the diagnosis 
or pericardial effusion. 
(3) Tubular breathing with dulness, increased voice sounds and 
tactile fremitus can often be heard near the angle of the left scapula. 
This is usually a result of lung compression, but a patch of pneu- 
monia or a pleural effusion may produce almost identical signs. 
A patch of tympanitic resonance is often to be found below the 
left clavicle, due no doubt to relaxation of the lung. 
Pressure exerted by the pericardial exudation upon surrounding 
structures may also give rise to dyspnoea, especially of a paroxysmal 
type, to dysphagia, to aphonia, and to an irritating cough. The 
“paradoxical pulse,” small and feeble during inspiration, is occasion- 
ally to be seen, but is by no means peculiar to this condition and has 
no considerable diagnosis importance. It is merely an exaggeration 
of pulse variations which often occur in health. 
(4) Inspection and palpation usually helps us very little, but two 
points are occasionally demonstrable by these methods: 
(a) A smoothing out of the intercostal depression in the precordial 
region, especially near the right border of the sternum between the 
third and the sixth ribs. 244 
PHYSICAL DIAGNOSIS 
(b) A progressive diminution of the intensity of the apex impulse 
until it may be altogether lost. If this change occurs while the 
patient is under observation, and especially if the apex impulse 
reappears or becomes more distinct when the patient lies on the right 
side, it is of considerable diagnostic value. In conditions other than 
pericardial effusion, the apex impulse becomes less visible in the right- 
sided decubitus. 
(b) Differential Diagnosis 
(1) Our chief difficulty is to distinguish the disease from hyper- 
trophy and dilatation of the heart. In the latter, which often com- 
plicates acute articular rheumatism with or without plastic pericarditis, 
the apex impulse is often very indistinct to sight and touch as in 
pericardial effusion. But the area of dulness is less likely to extend 
beyond the apex impulse to the left, or far beyond the right sternal 
edge, or to shift, when the patient lies on the right side. Pressure 
symptoms are less marked and there are usually no areas of broncho- 
vesicular breathing with tympanitic resonance under the left clavicle 
or in the back. Yet not infrequently these differentia do not serve us, 
and the diagnosis can be made only by x-ray or by puncture. 
(2) I have twice known cases of encapsulated or interlobular 
empyema to be mistaken for pericardial effusion. In one case a needle 
introduced in the fifth left intercostal space below the nipple drew 
pus from what turned out later to be a localized purulent pleurisy, 
but the diagnosis was not made until a rib had been removed and the 
region thoroughly explored. It is not rare for pleuritic effusions to 
gather first in this situation, viz., just outside the apex impulse in the 
left axilla. 
Such effusions may gravitate very slowly to the bottom of the 
pleural cavity or may become encapsulated and remain in their 
original and very deceptive position. In such cases the signs of 
compression of the left lung are similar to those produced by a peri- 
cardial effusion, and the results of punctures may be equivocal as 
in the case just mentioned. If there is any dulness, even a very narrow 
zone, in the left axilla between the fifth and eighth ribs, though there be 
none in the back, x-ray alone can set us straight. 
As between pleuritic and pericardial effusion the presence of a 
good pulse and the absence of marked dyspnoea favors the former. 
In the two cases above referred to in which interlobar empyema was 
mistaken for pericarditis, the general condition of the patient struck 
me at the time as surprisingly good for pericarditis. CARDIOVASCULAR DISEASES 
245 
If both pleurisy and pericarditis are present, the area of pericardial 
dulness is not characteristic until the pleuritic fluid has been drawn 
off. The persistence of dulness in the cardio-hepatic angle and beyond 
the apex beat after a left pleurisy has been emptied by tapping, and 
after the heart has had time to return to its normal position, should 
make us suspect a pericardial effusion. 
Despite the utmost care and thoroughness in physical examination, 
many cases of pericardial effusion go unrecognized, especially in 
infants, in elderly persons, or when the lung borders are adherent to 
the pericardium or to the chest wall. 
In the rheumatic attacks of children, it should be remembered that 
pericarditis is even more common than endocarditis. 
3. Adherent Pericardium 
In the majority of cases the diagnosis cannot be made during 
life, unless the pericardium is adherent, not only to the heart, but to 
the walls of the chest as well. When this combination of pericarditis 
with chronic mediastinitis is present, the diagnosis may be suggested 
by:— 
(a) A systolic retraction of the chest wall in the region of the apex 
impulse, at the base of the left axilla and in the region of the eleventh 
and twelfth ribs in the left back (Broadbent’s sign). Such retraction 
is more marked during a deep inspiration. (It should be remembered 
that, systolic retraction of the interspaces in the vicinity of the apex 
is very commonly seen in cases of cardiac hypertrophy from any cause, 
owing to the negative pressure produced within the chest by , the 
contraction of a powerful heart.) A quick rebound of the cardiac 
apex at the time of diastole (the diastolic shock) is said to be character- 
istic of pericardial adhesions, but is often absent. 
(b) Collapse of the cervical veins during diastole has been noticed 
by Friedreich, and the paradoxical pulse, above described, is said'to 
be more marked in adherent pericardium than in any other known 
condition. Most recent writers, however, place no reliance upbh it. 
(c) Wm. H. Smith considers that the absence of any shift in dhe 
position of the apex beat wih respiration or change of patientis’pbsit 
tion, is an important point in favor of mediastino-pericarditis; bill 
health and in valvular or parietal disease of the heart, the apek beat 
will swing from one to two inches to the left when the patient lies 
on his left side, and the descent of the diaphragm during-fpll 
inspiration lowers the position of the cardiac impulse considerably 246 
PHYSICAL DIAGNOSIS 
(d) The presence of hypertrophy and dilatation affecting espe- 
cially the left side of the heart, and not accounted for by the existence 
of any disease of the arteries, the cardiac valves, the lung, or of the 
kidney, should make us suspect pericardial and mediastinal adhesions. 
1 In children adherent pericardium is perhaps the commonest 
cause of a corbovinum and in adults the largest hearts that I have seen 
have been due to the same cause. 
(e) X-ray shows a restriction of the up-and-down movement of 
the heart during respiration. This is more marked and more char- 
acteristic than the limitation of lateral swing with change of position. 
Fig. 159.—Adherent Pericardium, Ascites. D D, Dull area; R R, Resonant, 
Inspection of the tissues just below the ensiform cartilage may 
show a complete arrest of the normally slight movements of this part 
of the abdominal wall. 
(0 Adherent pericardium, occurring as a part of a widespread chain 
of fibrous processes involving the pleura, the mediastinum, and the 
peritoneum, may give rise in young persons to a train of symptoms 
and signs suggesting cirrhosis of the liver. Ascites collects, the liver 
is enlarged, yet there are no signs in the heart, kidneys, or blood 
sufficient to explain the condition. In any such case adherent peri- 
cardium should be considered. Fig. 159 shows the appearance in 
cases of this kind in which the diagnosis was verified by autopsy. CARDIOVASCULAR DISEASES 
247 
Summary 
The diagnosis of adherent pericardium with chronic mediastinitis 
is suggested by 
(a) Systolic retraction of the lower intercostal spaces in the left 
axilla and in the left back, followed by a diastolic rebound. 
(b) The absence of any change in the position of the apex impulse 
with respiration or change of position. 
(c) The presence of marked hypertrophy and dilatation of one or 
both ventricles without obvious cause. 
(d) The absence of any respiratory excursion of the heart (v-ray) 
or of the abdominal wall at the costal angle. 
(e) The presence of signs like those of hepatic cirrhosis in a young 
person and without any obvious cause. CHAPTER XIII 
SYPHILITIC HEART DISEASE 
The border lines separating syphilitic infection of the cardio- 
vascular system from the other types of heart disease are not yet 
clearly defined. The painstaking researches of Warthin1 have shown 
that spirochastes can be demonstrated in the heart of many cases of 
“myocarditis” and “arterio-sclerosis” especially if one studies mi- 
nutely the tissues about the blood vessels. From Warthin’s studies 
it appears wise to suspect that the heart is syphilitic in every patient 
showing good evidence of syphilis elsewhere. Cases of myocardial 
weakness or arterio-sclerosis with a positive Wassermann reaction 
may possibly be classed as syphilitic heart disease and doubtless 
a vague but considerable proportion of all the cases described in 
Chapter XV are in fact syphilitic. 
Gumma of the heart wall has often been found post-mortem but 
can rarely be recognized in life. It may be suspected, when in a case 
of florid syphilis there arise sudden and marked evidences of cardiac 
weakness without obvious valve lesions or when extensive heart block 
occurs in a syphilitic. 
The only type of syphilitic cardio-vascular disease now clearly 
recognizable in life is 
I. Syphilitic aortitis with or without Aneurism 
Aortitis can be recognized only when it produces 
(a) Aortic regurgitation. 
(.b) Aneurism. 
In these forms it makes up about 12 per cent, of the hospital cases 
of heart disease. Each of these will now be described in detail. 
1. Aortic Regurgitation (Syphilitic Type) 
Seventy per cent, of my cases have occurred in men, the average 
age being 47. Whenever we find aortic regurgitation in a young or 
middle aged man with no rheumatic history, syphilis is to be sus- 
1 Transactions of the Assoc, of American Physicians, 1914, p. 416. 
248 SYPHILITIC HEART DISEASE 
249 
pected. This type of disease is especially common in negroes. The 
Wassermann reaction is of course a most important aid in diagnosis. 
Since in syphilitic aortitis the regurgitation is due to a primary 
infection of the aortic arch extending down to the aortic valves and 
producing a dilatation of the aortic ring, there is rarely any other 
valve lesion to complicate the picture. The aortic valves rarely, if 
ever, fuse to produce a stenosis (as in “rheumatic” aortic disease), 
and there is no mitral stenosis to limit the amount of blood thrown 
into the aorta. Hence it is in syphilitic aortitis that we get the 
classical picture of aortic regurgitation, full blown and in its typical 
form. In rheumatic disease of the aortic valve the signs are more or 
less masked by other lesions. 
2. Physical Signs 
Inspection reveals more that is important in this disease than in 
any other valvular lesion. In extreme cases the patient’s face or 
hand may blush visibly with every systole. Not infrequently one can 
make the diagnosis across the room or in the street by noting the 
violent throbbing of the carotids, which may be such as to shake the 
person’s whole head and trunk, and even the bed on which he lies. 
No other lesion is so apt to cause a heaving of the whole chest and a 
bobbing of the head, and no other lesion so often causes a bulging of 
the precordia, for in no other lesion is the enlargement of the heart so 
great (cor bovinum or ox-heart). The throbbing of the dilated aorta 
can often be felt and sometimes seen in the suprasternal notch or in 
the second right interspace. Not only in the carotids but the sub- 
clavians, the brachials and radials, the femoral and anterior tibial, and 
even the digital and dorsalis pedis arteries may visibly pulsate, and 
the characteristic jerking quality of the pulse may be seen as well as 
felt. This visible pulsation in the peripheral arteries, while very 
characteristic of aortic regurgitation, is occasionally seen in cases of 
simple hypertrophy and dilatation of the heart from chronic nephritis 
as well as in arteriosclerosis, Graves’ disease, and in severe anaemias. 
If the arteries are extensively calcified, their pulsation may become 
much less marked. 
The peculiar conditions of the circulation whereby it is “changed 
into a series of discontinuous discharges as if from a catapult” (All- 
butt) throws a great tensile strain upon all the arteries, and results, in 
almost every long-standing case, in increasing both their length and 
their diameter. The visible arterial trunks become tortuous and 250 
PHYSICAL DIAGNOSIS 
distended, while the arch of the aorta is diffusely dilated so as to 
resemble an aneurism (see Fig. 160). With each heart beat the 
snaky arteries are often jerked to one side as well as made to throb. 
Inspection of the region of the cardiac impulse almost always 
shows a very marked displacement of the apex beat both downward 
and outward (but especially the former), corresponding to the hyper- 
trophy and still more to the dilatation of the left ventricle, which is 
usually very great, and to the downward sagging of the enlarged aorta. 
Dilatation is in this disease an essentially helpful and compensatory 
Pulsation at the jugulum. 
Pulsating carotids. 
Diastolic murmur. 
Dulness and pul- 
sation > corre-1 
sponding to the 
dilated aortic 
arch. 
Displaced cardiac 
impulse. 
Fig. 160.—Aortic Regurgitation, Showing Position of the Diastolic Murmur and Areas 
of Visible Pulsation. 
process. Not at all infrequently one finds a systolic retraction of the 
interspaces near the apex beat instead of a systolic impulse. This is 
probably due to the negative pressure produced within the chest by 
the powerful contraction of an hypertrophied heart. In the supra- 
sternal notch one often feels, as well as sees, a marked systolic pulsation 
transmitted from the arch of the dilated aorta, and sometimes mis- 
taken for saccular aneurism. 
3. Capillary Pulsation 
If one passes the end of a pencil or other hard substance once or 
twice across the patient’s forehead, and then watches the red mark 
so produced, one can often see a systolic flushing of the hyperasmic 
area with each beat of the heart. This is by far the best method of 
eliciting this phenomenon. It may also be seen if a glass slide is SYPHILITIC HEART DISEASE 
251 
pressed against the mucous membrane of the lip so as partially to 
blanch it, or if one presses upon the finger-nail so as partially to drive 
the blood from under it; but in both these manoeuvres error may result 
from inequality in the pressure made by the observer upon the glass slide 
or upon the nail. Very slight movements of the observer’s fingers, 
even such as are caused by his own pulse, may give rise to changes 
simulating capillary pulsation. Capillary pulsation of normal tissues 
is not often seen in any condition other than aortic1 regurgitation, 
yet occasionally one meets with it in diseases which produce very low 
tension of the pulse, such as Graves’ Diesease, phthisis or typhoid, 
anaemic and neurasthenic conditions, and I have twice seen it in per- 
fectly healthy persons. In such cases the pulsation is usually less 
marked than in aortic regurgitation. 
4. Palpation 
Palpation verifies the position of the cardiac impulse and the heav- 
ing of the whole chest wall suggested by inspection. The shock of 
the heart is very powerful and deliberate unless dilatation is extreme, 
when it becomes wavy and diffuse. In the supraclavicular notch a 
systolic thrill is often to be felt. A diastolic thrill in the precordia is 
very rare. 
Fig. 161.—Sphygmographic Tracing from Normal Pulse. 
The pulse is important, usually characteristic. The wave rises very 
suddenly and to an unusual height, then collapses completely and with 
great rapidity (pulsus celer) (see Figs. 161, 162). 
This type of pulse, which is known as the “Corrigan pulse” or 
“water-hammer pulse,” is exaggerated if one raises the patient’s arm 
above the head so as to make the force of gravity aid in emptying the 
artery. The quality of the pulse in aortic regurgitation is due to the 
fact that a large volume of blood is suddenly and forcibly thrown into 
the aorta by the hypertrophied and dilated left ventricle, thus causing 
1 Jumping toothache and throbbing felon are common examples of capillary 
pulsation in inflamed area. 252 
PHYSICAL DIAGNOSIS 
the characteristically sharp and sudden rise in the peripheral arteries. 
The arteries then empty themselves in two directions at once, forward 
into the capillaries and backward into the heart through the incom- 
petent aortic valves; hence the sudden collapse in the pulse which, 
together with its sharp and sudden rise, are its important character- 
istics. The arteries are large and often elongated so as to be thrown 
into curves. 
Fig. 162.—Sphygmographic Tracing of the “Pulsus Celer” in Aortic Regurgitation. Its 
collapsing character is well shown. 
While compensation lasts, the pulse is usually regular in force and 
rhythm. Irregularity is therefore an especially grave sign, much more 
so than in any other valvular lesion. 
Percussion 
Percussion adds but little to the information obtained by inspec- 
tion and palpation, but verifies the results of these methods of investi- 
gation respecting the increased size of the heart, and especially of the 
left ventricle, which may reach enormous dimensions, especially in 
cases occurring in young persons. The heart may be increased to 
more than four times its normal weight. 
Auscultation 
Unless the free ear is used, the diastolic murmur may be so faint 
as to be easily overlooked. This is especially true in cases, occurring 
in elderly people, and when the patient has been for a considerable 
time at rest. The difficulty of recognizing certain cases of aortic 
regurgitation during life is shown by the fact that out of sixty-eight 
cases of aortic regurgitation demonstrated at autopsy in the Massa- 
chusetts General Hospital, only fifty-seven or 84 per cent, were recog- SYPHILITIC HEART DISEASE 
253 
nized during life. Further description of the aortic regurgitant mur- 
mur of syphilitic disease is unnecessary since it is identical with that 
also described under rheumatic disease of the aortic valve on pages 
223 and 224. 
Over the large peripheral arteries, especially the femoral, one 
hears in most cases a sharp, short, systolic sound (“pistol-shot sound”) 
due to the sudden filling and tautening of a relaxed artery. This 
sound is merely an exaggeration of what may often be heard in health. 
Pressure with the stethoscope will also bring out a systolic mur- 
mur (as in health also) and occasionally a diastolic murmur as well 
(Duroziez’s sign). The last murmur is practically never heard except 
in aortic regurgitation. 
Summary and Differential Diagnosis 
A diastolic murmur heard with the maximum intensity about the 
fourth left costal cartilage (less often in the second right interspace) 
gives us almost complete assurance of the existence of aortic regurgita- 
tion. From mitral stenosis and from pulmonary regurgitation, an 
exceedingly rare lesion, the disease is distinguished by the presence of 
predominating hypertrophy of the left ventricle with a heaving apex 
impulse and by the following arterial phenomena: 
(a) Visible pulsation in the peripheral arteries. 
(h) Capillary pulsation. 
(c) “Corrigan” pulse. 
(d) “Pistol-shot sound’’ in the femoral artery. 
(e) Duroziez’s sign. 
(/) High pulse-pressure (see above, p. 114). 
Cardiopulmonary murmurs (see page 192) are occasionally dias- 
tolic, but are very markedly influenced by position and by respiration, 
while aortic murmurs are but slightly modified. 
The very rare functional diastolic murmur, transmitted from the 
veins of the neck and heard over the base of the heart in cases of 
grave anaemia, may be obliterated by pressure over the bulbus jugu- 
laris. Such pressure has no effect upon the murmur of aortic regur- 
gitation. I have reported (Johns Hopkins Bull., May, 1903) three 
cases of intense anaemia associated with diastolic murmurs exactly 
like those of aortic regurgitation, but proved post mortem to be in- 
dependent of any valvular lesion. The arterial phenomena were 
not marked, but the diagnosis of such cases is very hard. Luck- 254 
PHYSICAL DIAGNOSIS 
ily they are rare. The origin is obscure. It must be remembered 
that aortic regurgitant murmurs are often exceedingly faint, and 
should be listened for with the greatest care and under the most favor- 
able conditions. 
(c) Estimation of the Extent and Gravity of the Lesion 
The extent of the lesion is roughly proportional to— 
(a) The amount of hypertrophy of the left ventricle. 
(b) The degree to which the pulse collapses during diastole (pro- 
vided the radial is not so much calcified as to make collapse 
impossible). 
(c) The degree to which the murmur replaces the second sound as 
heard over the right carotid artery (Broadbent). 
Irregularity of the pulse is a far more serious sign in this disease 
than in lesions of the mitral valve, and indicates the beginning of a 
serious failure of compensation. 
Another grave sign is a diminution in the intensity of the murmur. 
II. Complications 
(1) Aneurism (see p. 256).—Aneurismal dilatation of the aortic 
arch is usually associated with aortic regurgitation and may produce 
a characteristic area of dulness to the right of the sternum (see Fig. 
160). Not infrequently this dilatation is the cause of a systolic mur- 
mur to be heard over the region of the aortic arch and in the great 
vessels of the neck. 
(2) Roughening of the Aortic Valves.—In almost all cases of aortic 
regurgitation the valves are sufficiently roughened to produce a systolic 
murmur as the blood flows over them. This murmur is heard at or 
near the conventional aortic area, and may be transmitted into the 
carotids. (The relation of these murmurs to the diagnosis of aortic 
stenosis has been considered with the latter lesion.) 
(3) The return of arterial blood through the aortic valves into the 
left ventricle produces in time both hypertrophy and dilatation of this 
chamber, and results ultimately in a stretching of the mitral orifice 
which renders the mitral curtains incompetent. The result is a 
“relative mitral insufficiency,” i.e., one in which the mitral valve is 
intact but too short to reach across the orifice which it is intended to 
close. Such an insufficiency of the mitral occurs in most well-marked 
cases, it temporarily relieves the overdistention of the left ventricle SYPHILITIC HEART DISEASE 
255 
and often the accompanying angina, although at the cost of engorging 
the lungs.1 
(4) The Austin Flint Murmur.-—The majority of cases of aortic 
regurgitation are accompanied by a presystolic murmur at the apex. 
(For a fuller discussion of this murmur see above, p. 220). 
(5) Aortic stenosis frequently accompanies cases of aortic regurgi- 
tation, especially in the rheumatic, choreic and tonsillar types occurring 
in young persons. It has the effect of increasing the intensity of the 
diastolic murmur, since the regurgitating stream has to pass through 
a smaller opening. Whether syphilitic aortitis can also produce 
aortic stenosis I am not certain. So far I have not seen a case proved 
post-mortem. 
1 This relative insufficiency of the mitral valve has been termed its “safety- 
valve” action, but the safety is but temporary and dearly bought. CHAPTER XIV 
SYPHILITIC AORTITIS WITH ANEURISM 
For clinical purposes thoracic aneurisms may be divided into the 
diffuse and the saccular. Saccular aneurisms of the ascending or 
descending portion of the arch of the aorta are apt to penetrate the 
chest wall, while aneurism of the transverse aorta or diffuse dilatations 
of the whole aortic arch are more likely to extend within the chest 
without eroding the thoracic bones. Practically any aneurism which 
penetrates the thoracic bones may be inferred to be saccular, but if 
no such penetration takes place, it may be impossible to make out 
whether the dilatation is diffuse or circumscribed. I shall consider: 
I. The signs of the presence of aneurism. 
II. The evidences of its seat. 
I. Inspection and Palpation 
1. Abnormal Pulsation 
Inspection and palpation give us most of the important information 
in the diagnosis of aneurism. The patient should be placed in the 
position shown in Fig. 163, so that the light will strike obliquely across 
the surface of the chest, and the observer should be so placed that his 
eyes are as nearly as possible at the level of that part of the chest at 
which he expects to see pulsation. 
In the majority of cases of aneurism some abnormal pulsation may 
be made out either to the right of the sternum in front, or in the region 
of the left scapula behind. If the aneurism is large, a considerable 
area of the chest wall may be lifted with each beat of the heart; with 
smaller growths the pulsating area may be small and sharply circum- 
scribed. Not infrequently an abnormal pulsation at the sternal 
notch or in the neck may also be observed. Other causes of abnormal 
pulsations in the chest, such as dislocation or uncovering of the heart, 
must of course be excluded. 
Palpation controls the results of inspection, but at times a pulsation 
may be seen better than felt; at others may be felt better than seen. 
256 SYPHILITIC AORTITIS WITH ANEURISM 
257 
2. Tumor 
If the aneurism involves the ascending portion of the aortic arch, 
it is likely sooner or later to erode the right margin of the sternum, 
and adjacent parts of the second or third costal cartilages, and appear 
externally as a round swelling in which a systolic pulsation is to 
be seen and felt. This pulsation is in some cases distinctly expansile 
in character, and differs in this respect from the up-and-down motion 
which may be communicated to a tumor of the chest wall by the beat- 
ing of a normal aorta. The tumor is usually firm, rarely soft, and 
may be as hard as any variety of malignant new growth. Occa- 
sionally the thickness of the lamellated clot within it is so great that 
no pulsations are transmitted to the surface. 
3. Thrill 
Whether the aneurism penetrates the chest or not, it is often possi- 
ble to feel over it a vibration thrill, systolic in time. If the layer of 
lamellated clot in the sac is very thick, the thrill is less apt to be felt. 
Fig. 163.—Position When Looking for Slight Aneurismal Pulsation. 
4. Diastolic Shock 
Of minor value in diagnosis is a diastolic tap which is appreciated 
by laying the palm of the hand lightly over the affected area. This 
diastolic shock is due to the recoil of the blood in the dilated aorta, 
and is felt in a minority of cases. (It also occurs in hypertension 
from any cause.) As the wall of the sac becomes weaker, the inten- 258 
PHYSICAL DIAGNOSIS 
sity of the shock diminishes. It may be appreciated over the tra- 
chea also, and is thought by some to have even more significance 
when felt in this situation. 
Fig. 164.—Aneurismal Tumor (A). The arrow B points to a gummatous swelling 
near the ensiform cartilage. The radiographic appearances of this case are shown below 
(Fig. 167). 
Fig. 165.—Aneurism Tumor Perforating the Sternum at A. At B there is a gummatous 
mass. (See below, Fig. 16.7, a radiograph of this case). 
Of special importance in aneurism of the transverse arch is the sign 
known as the tracheal tug. The arch of the aorta runs over the left SYPHILITIC AORTITIS WITH ANEURISM 
259 
primary bronchus in such a way that when the aorta is dilated, the 
bronchus is pressed upon with each expansile pulsation of the artery. 
5. Tracheal Tug 
This systolic pressure transmitted to the trachea produces a distinct 
downward tug upon it with each systole of the heart. The tug is best 
felt by making the patient throw back his head so as to put the trachea 
upon a stretch. The physician then stands behind him and gently 
presses the tips of the fingers of both hands up under the lower border 
of the cricoid cartilage. In feeling thus for the tracheal tug as trans- 
mitted to the cricoid cartilage certain precautions must be observed: 
(а) One must distinguish the tracheal tug from a simple pulsation 
transmitted to the superficial tissues by the vessels underneath. Such 
pulsation makes the tissues move out and in rather than up and down. 
(■b) A tracheal tug felt only during inspiration has no pathological 
significance and is frequently present in health. 
While preparing to try for the tracheal tug we may notice whether 
there is any dislocation of the trachea, as shown by the displacement of 
Adam’s apple. Stridor, cough, dysphagia, and other symptoms 
are produced by pressure on gullet and windpipe. Other signs of 
aneurism, due to the pressure of the dilated aorta upon the nerves or 
vessels of tlje mediastinum, are: 
(1) Hoarseness or aphonia from pressure on the left recurrent 
laryngeal nerve. 
(2) Inequality of the pupils. 
(3) Inequality of the radial pulses. 
(4) (Edema and cyanosis of one arm or of one side of the neck 
and head. 
(5) Pain in one arm from the pressure of an aneurism involving 
the subclavian artery upon the brachial plexus. 
(б) Evidence of pressure on the lung or on a bronchus. 
Of these pressure signs the commonest and most important are: 
hoarseness, pain, and compression of the lung or bronchus. 
Contraction or dilatation of the pupil is due to a paralytic or irrita- 
tive affection of the sympathetic nerves. This symptom is much 
commoner than the other effect of pressure upon the sympathetic 
nerves; namely, flushing or sweating of one side of the face. 
In comparing the pulses in the two radials we must bear in mind 
the possibility of a congenital difference between them, due to a 
difference either in the size of the arteries or in their position, and also 260 
PHYSICAL DIAGNOSIS 
that a tumor pressing on the subclavian may affect the pulse exactly 
as an aneurism. The pulse wave upon the affected side (most often 
the left) may be either less in volume or later in time than the wave in 
the other radial artery, according as the pulse wave is actually delayed 
in the aneurismal sac or merely diminished by it. In marked cases the 
pulse upon the affected side may be nearly or quite absent. 
Examination of the heart itself may show some dislocation of the 
organ to the left and downward, owing to the direct pressure of the 
aneurismal sac, but no enlargement. 
II. Percussion 
If the aneurism is deep-seated, the results of percussion are nega- 
tive. If, on the other hand, it be situated immediately beneath the 
Aneurismal, 
dulness. 
Heart dulness. 
Liver dulness.' 
Fig. 168.—Diagram of Percussion Dulness in Aortic Aneurism 
sternum or close under the thoracic wall, an area of dulness, not present 
in the normal chest, may be mapped out. The outlines most com- 
monly seen in such cases are shown in Fig. 166. When the aneurism 
involves the descending aorta, an area of dulness may be found in the 
region of the left scapula or below it, and pulsation may be detected 
in the same area. 
III. Auscultation 
The signs revealed by auscultation are not of much diagnostic value 
as a rule. In about one-half of the cases of sacculated aneurism there 
are no sounds or murmurs to be heard over the tumor. In other 
cases a systolic murmur, the audible counterpart of the vibratile thrill, SYPHILITIC AORTITIS WITH ANEURISM 
261 
may be heard over the area of pulsation, tumor, or dulness correspond- 
ing to the aneurismal sac. This systolic murmur may be due to many 
causes other than aneurism, and has nothing characteristic about it. A 
similar systolic sound is sometimes heard over the trachea (Drum- 
mond’s sign) or in the mouth, if the patient closes his lips around the 
pectoral extremity of the stethoscope (Sansom’s sign). 
A loud diastolic murmur is audible in most cases as a result of an 
accompanying aortic regurgitation (see above). 
If a portion of either lung is directly pressed upon by the aneurismal 
sac, we may have the signs of condensation of the lung in the area 
pressed upon (slight dulness, broncho-vesicular breathing, and exag- 
gerated voice sounds). If one of the primary bronchi is pressed upon 
as occasionally happens, atelectasis of the corresponding lung may be 
manifested by the usual signs (dulness, absence of tactile fremitus 
and of respiratory and vocal sounds). 
If the aneurismal sac is of very great size, the pulse wave in the 
femorals may be obliterated, as happened in a case described by Osier. 
IV. Radioscopy 
With the fluoroscope and through radiography one can often make 
out a shadow corresponding to the position of the aneurism. 
From the front. 
From behind. 
Fig. 167.—Radiograph of Case whose Photograph is Reproduced as Figs. 164 and 
165. In the right-hand cut are shown the appearances seen from behind. The left 
hand cut, A, A, aneurismal sac; B, heart displaced; C, liver (not in focus). 
Not infrequently this is the only convincing sign of the disease. 
Hence x-ray examination is of the utmost value. The position of the 
shadow is best explained by reference to Figs. 167, 168, 169, and 170. 262 
PHYSICAL DIAGNOSIS 
Summary 
The most important signs of aneurism are: 
1. Abnormal pulsation—visible or palpable. 
2. Tumor over which (3) a thrill can be felt. 
4. Tracheal tug. 
5. Pressure signs (unequal pulses, pupils, hoarseness, pain, etc.) 
6. Dulness on percussion over the suspected area. 
Fig. 168.—Aortic Aneurism. (From v. Ziemssen’s Atlas.) 
7. Diastolic murmur (aortic regurgitation). 
8. Systolic murmur (least important of all). 
9. Radioscopy may demonstrate a shadow higher up than that 
corresponding to the heart and extending beyond that produced by 
the sternum, spinal column, and great vessels. 
V. Diagnosis 
i. Diagnosis of the Seat of the Lesion 
(a) Aneurism of the ascending arch generally approaches or pene- 
trates the chest wall in the vicinity of the second right intercostal space 
near the sternum. Previous to perforating the thoracic parietes the SYPHILITIC AORTITIS WITH ANEURISM 
263 
growth of the aneurism may give rise to pain, pulsation, and dulness 
and thrill in this region. 
(6) Aneurism of the transverse arch or diffuse dilatation of the 
aorta, which is the most common of all types of aortic aneurism, may 
not give rise to any visible pulsation of the chest wall, and, if deep- 
seated, need not produce any abnormal dulness on percussion. In 
such cases an aneurism is to be recognized, if at all, by x-ray or by 
evidences of pressure on the nerves or vessels of the mediastinum (cough, 
aphonia, inequality of the pupils, tracheal tug, etc.). 
Fig. 169.—Aneurism of the Aorta. (Curschman.) 
(c) Aneurism of the descending aorta gives rise, usually, to severe 
and persistent pain in the back, which radiates along the intercostal 
nerves or downward. Other pressure symptoms are not marked, but 
in advanced cases an area of abnormal dulness and pulsation may be 
found in the region of the left scapula or below it. 
(d) If the innominate artery or one of the carotids is involved, 
we usually find a pulsating lump in the region of one or the other 
claviculo-sternal joint or at the root of the neck, and the trachea may 
be displaced to one side. This form, however, is distinctly rare. The 
violent throbbing and dilated carotid of aortic leakage is often mistaken 
for it. 264 
PHYSICAL DIAGNOSIS 
2. Differential Diagnosis 
(a) It is important to distinguish the diffuse dilatation of the aortic 
arch (not aneurism), which is present in most cases of hypertension 
with nephritis or arterio-sclerosis, from syphilitic aneurism of the 
transverse aorta. Dulness and even slight pulsation, perhaps with 
systolic murmur in the second and third right interspaces near the 
sternum, occur in many cases of chronic hypertension, but though 
the aorta is dilated, its coats are not ruptured and it never breaks. 
Fig. 170.—Aneurism of the Aorta. 
The absence of pressure signs, the negative Wassermann and the shape 
of the x-ray shadow distinguish it from syphilitic aneurism. 
(6) Aneurism is not infrequently mistaken for aortic stenosis, in 
which a systolic murmur and thrill, similar to those occurring in aneu- 
rism, are to be heard over the region of the aortic arch. From aortic 
stenosis aneurism is distinguished by the fact that it does not diminish 
the aortic second sound or produce characteristic changes in the pulse, 
and by the presence of some one of the symptoms above described, such SYPHILITIC AORTITIS WITH ANEURISM 
265 
as tracheal tug, pressure symptoms, etc. The “rheumatic” etiology 
of aortic stenosis, the x-ray, and the syphilitic basis of aneurism may 
often be recognized and help our diagnosis. 
(.c) Simple dynamic throbbing of a normal aortic arch similar 
to that which occurs in the abdominal aorta may lift the chest wall 
so as to simulate aneurism. The other positive symptoms and 
signs of aneurism are, however, absent. 
Fig. i 71.—Aneurism of the Aorta with gumma, 
(d) Pulmonary tuberculosis or cancer of the oesophagus, producing, 
as they may, substernal pain, cough, and aphonia by pressure upon 
mediastinal structures, have been mistaken for aneurism, from which, 
however, they may be distinguished by the absence of the positive 
signs above described, by the more rapid emaciation of the patient, 
and by the positive evidences of cancer or tuberculosis. 
(<e) Empyema necessitatis may produce a pulsating tumor like that 
of aneurism and the area of dulness may be similar, but there is no 
diastolic shock, no tactile thrill or murmur, and the history of the case 
and the x-ray shadow are usually very different from that of aneurism. 
(/) Mediastinal tumors are sometimes mistaken for aneurism during 
life. They may produce a more intense and widespread dulness 
which is usually in the median line, while the dulness of aneurism is 
oftener at one side. The pulsation transmitted to a tumor by the 266 
PHYSICAL DIAGNOSIS 
heart has not the expansile character of aneurismal pulsation. Tumors 
are not associated with any diastolic shock, rarely with a tracheal tug. 
X-ray usually decides. 
The course of most mediastinal tumors is progressive and attended 
by great cachexia, while the symptoms of aneurism are often more or 
less intermittent, and unless pain is severe there is no such emaciation 
Fig. 172.—Neoplasm of mediastinum. Fluid at right base. 
or anaemia as is commonly seen with mediastinal tumors. Pressure 
symptoms may be the same in both diseases, but are usually more 
marked with mediastinal growths. A metastatic nodule over the 
clavicle sometimes betrays the presence of a primary focus within 
the chest. 
The most helpful differential points are the A-ray, the evidence of 
the presence or absence of syphilis, and of a diastolic murmur such as is 
usually present with aneurism and absent with neoplasm. SYPHILITIC AORTITIS WITH ANEURISM 
267 
A'-ray sometimes shows a definite expansile pulsation in the shadow 
corresponding to the sac. But I have found this piece of evidence as 
often wrong as right. 
(g) Retraction of the right lung (fibroid phthisis), with or without 
displacement of the heart toward the diseased side, may uncover 
the heart so as to produce some of the signs of aneurism, i. e., pulsation 
and dulness in the upper right intercostal spaces near the sternum, 
with a loud second sound and sometimes a systolic murmur in the 
dull area. 
The history of the case and a careful examination of the lungs usu- 
ally suffice to set us right. 
(h) Dilatation of the heart may be so extreme that pulsation and 
percussion dulness appear in the characteristic aneurismal area to the 
right of the sternum, especially if there is solidification of the left lung. 
But the pulse is in such cases much weaker and more irregular than 
it is to be expected in uncomplicated cases of aortic aneurism, and the 
history of the case is usually decisive. 
By the same marks we can distinguish the pulsations of a dilated 
heart, which sometimes appear in the left hypochondrium. CHAPTER XV 
HYPERTENSIVE CARDIO-VASCULAR DISEASE 
Whether or not extra-renal arterio-sclerosis causes hypertension 
with cardiac hypertrophy and dilatation, or is the result of a primary 
hypertension (Allbutt’s “Hyperpiesia”), there is a frequent associa- 
tion between them. Indeed, there is no commoner type of cardiac 
enlargement than that associated with arterio-sclerosis and hyper- 
tension. Hence, the term “hypertensive cardio-vascular disease” 
is often used as synonymous with the lesions which I am about to 
describe. “Chronic myocarditis” or “fibrous myocarditis” and 
“fatty heart” are poor terms for clinical use, since we know no 
clinical picture corresponding to them. One recognizes usually in 
this order: 
1. Hypertension. 
2. Enlarged heart (see below). 
3. Disturbances of rhythm, of impulse production or impulse 
conduction. 
4. Sclerosed arteries (especially the brachial). 
5. Dyspnoea, muscular weakness, chronic cough (often miscalled 
“chronic bronchitis,”), and a gradual accumulation of fluid in the legs, 
possibly with angina pectoris. 
I. Physical Signs 
Beside the hypertension and the sclerosed arteries (which need no 
further description here) we have evidence of cardiac hypertrophy 
and dilatation. The apex impulse is displaced downward and to the 
left. Its movement is slow and deliberate (“heaving impulse”) so 
long as compensation remains fair. The aortic second sound is 
usually loud and ringing even in the cases when the systolic blood- 
pressure is not much elevated. 
Diffuse dilatation of the aortic arch can often be made out by 
the x-ray, sometimes by percussion. The x-ray shadow and the 
aortic dullness are often 8 to io cm. wide. 
Systolic murmurs are almost invariably audible at the base of 
the heart and at the apex. Whether one or two systolics are dis- 
268 DISEASES OF THE HEART 
269 
tinguishable it is often impossible to say, but in most cases the basal 
murmur is the louder. When the systolic murmur is loud and rough 
and best heard at the apex, false diagnoses of “mitral regurgitation” 
are often made. The murmur is probably due to sclerotic roughening 
and dilatation of the aortic arch, although it may be loudest at the 
apex. 
When compensation fails, the murmurs often diminish or disappear, 
and we find one or another type of gallop rhythm with short valvular 
sounds. 
Ventricular premature heats (“extrasystoles”) and, with increasing 
decompensation, absolute arrhythmia are often present. Alternation, 
permanent, or more often for a few beats following an extra systole, 
is not at all uncommon. Paroxysmal tachycardia and auricular 
flutter are occasionally seen. 
Delayed A-s-V-s conduction with different degrees of heart block 
are rather rarely encountered. 
For the sure recognition of gross changes in the myocardium our 
present methods of physical examination are always unsatisfactory 
and often wholly inadequate. Extensive degenerations of the heart 
wall are not infrequently found at autopsy when there has been no 
reason to suspect them during life. On the other hand, the autopsy 
often fails to substantiate a diagnosis of degeneration of the heart 
muscle, although all the physical signs traditionally associated with 
this condition were present during life. The following figures from the 
Massachusetts General Hospital illustrate these difficulties: 
Cases of fibrous myocarditis correctly diagnosed.... 
or 
22% 
Cases of fibrous myocarditis diagnosed in life, but 
not found post mortem 
3i 
or 
52% 
Cases of fibrous myocarditis found post mortem, but 
not diagnosed in life 
iS 
or 
26% 
Total attempts 
59 
If therefore we are to attempt a diagnosis of myocarditis this must 
depend upon the history and symptoms of the case; physical exam- 
ination can sometimes supplement these, sometimes not. Symptoms 
of cardiac weakness developing in a man past middle life, especially 
in a patient who shows evidences of arterio-sclerosis or high blood 
pressure, or who has suffered from the effects of alcohol and syphilis, 
suggest parietal disease of the heart. The possibility is increased if 270 
PHYSICAL DIAGNOSIS 
there have been attacks of angina pectoris, Cheyne-Stokes breathing, 
of heart block or of syncope (Stokes-Adams syndrome). 
i. Summary 
1. The causative factors, the history and symptoms of the case and 
the condition of other organs are often of more diagnostic value than 
is the physical examination of the heart itself, which may show 
little that is abnormal. 
2. Among the physical signs, those most reliable are: 
(a) Increased blood pressure. 
(b) Sclerosed arteries. 
(c) Evidences of cardiac hypertrophy and dilatation. 
(d) Weak, irregular heart sounds. 
(e) Reduplication of some of the cardiac sounds (gallop rhythm). 
(/) Murmurs—especially a systolic murmur at the base. 
(g) Evidences of heart block or of alternation. 
2. Differential Diagnosis 
We have to distinguish the weakened heart of hypertensive cardio- 
vascular disease from— 
(a) Uncomplicated valvular lesions. 
(b) Cardiac neuroses. 
(a) It has been already pointed out that valvular lesions do 
not necessarily give rise to any murmurs when compensation has 
failed. Under such circumstances one hears only irregular and weak 
heart sounds, as in myocardial weakness. The age of the patient, 
the history of syphilis or “rheumatism,” the character of the onset, 
the presence or absence of arterio-sclerotic manifestations in the brain, 
kidneys, or extremities, and above all the blood-pressure measurements, 
assist us in diagnosis. High blood-pressure is never found in the 
“rheumatic” type of heart disease, and in syphilitic aortitis only the 
systolic not the diastolic pressure is raised. In arterio-sclerotic disease 
systolic and diastolic pressure are often high. But Allbutt has 
rightly emphasized the fact that there is a senile or “decrescent” type 
of arterio-sclerosis without hypertension or cardiac hypertrophy. 
(■b) Weakness and irregularity of the cardiac sounds, when due to 
“nervous” affection of the heart and unassociated with parietal or 
valvular changes, is usually less marked after slight exertion. The 
heart “rises to the occasion” if the weakness is a functional one. DISEASES of the heart 
271 
On the other hand, if any serious weakening is present, the signs 
and symptoms are much aggravated by any exertion. 
In “neurotic hearts” the arrhythmia is usually of the juvenile 
or sinus type and the evidence of sexual excess or excessive tobacco 
can often be found, also the history and signs of a generalized neurosis 
(see Cardiac signs of Nervousness, p. 277). . 
II. Fatty Degeneration 
There are no physical signs by which fatty degeneration of the 
heart can be distinguished from other pathological changes which 
result in weakening the heart walls. An extensive degree of fatty 
degeneration is often seen post mortem in cases of pernicious anaemia, 
although the heart sounds have been clear, regular, and in all respects 
normal during life. 
III. Senile or “Decrescent” Arterio-sclerosis 
When arterio-sclerosis develops in old age, hypertension and car- 
diac hypertrophy are often absent. This was the case in 58 out of 
166 cases of arterio-sclerosis examined by Ophuls1 (35 %); most of these 
cases were senile. In these cases there may be no complaints at all 
or only those of angina pectoris. Physical examination shows only—- 
1. Rough stiff tortuous arteries (especially the brachials). 
2. Dilated aortic arch (percussion and %-ray). 
3. Loud ringing aortic second sound. 
The heart and circulation may be otherwise normal. 
1 Ophuls: Arch, of Int. Med., 1912, Vol. ix, p. 156. CHAPTER XVI 
NEPHROGENOUS HEART DISEASE. GOITRE 
HEART. CONGENITAL MALFORMATIONS. 
MISCELLANEOUS CARDIAC LESIONS 
I. Nephritic (or Nephrogenous) Heart Disease 
From the point of view of physical diagnosis the cardiac enlarge- 
ment and weakening due to nephritic hypertension presents little to 
distinguish it from hypertensive cardiovascular disease. Indeed the 
two are sometimes indistinguishable or simultaneously present. In 
typical cases, however, we can distinguish nephrogenous heart dis- 
ease by the following criteria. 
1. The age.—In 117 cases of weakened heart due to chronic 
glomerular nephritis (Massachusetts General Hospital) I found the 
average age 36, while in 93 arterio-sclerotic cardiac cases the age 
averaged 59 years. 
2. The condition of the urine (see below, p. 413). 
3. The condition of the arteries.—Nephritic heart disease often 
shows thickened arteries, but not often the roughening of calcifica- 
tion. 
4. Anaemia, retinitis and “uraemia” are commoner in the nephrog- 
enous than in the arterio-sclerotic type. 
The heart itself shows evidences simply of hypertrophy and dila- 
tation as in arterio-sclerosis. There is often gallop rhythm and a 
basal systolic murmur. Delayed A-s-V-s conduction and heart 
block are less common than in any other type of cardiac disease. 
II. Goitre Heart 
Goitres of all sorts, toxic and non-toxic, large or small, are apt to 
be associated sooner or later with high systolic pressure and with some 
hypertrophy and weakening of the heart. The diastolic pressure is 
little if at all elevated. 
Corresponding presumably with this rise of systolic pressure, it 
has long been noticed that simple goitres1 “which produce no other 
1 Balfour: Mayo Clinic Papers, 1914, p. 371. 
272 DISEASES OF THE HEART 
273 
recognizable symptoms, may gradually become associated with marked 
degenerative changes in the cardiovascular system.” The cardiac 
symptoms come on slowly in the simple non-exophthalmic cases (av- 
erage time after the appearance of goitre, 14 years in Plummer’s 
series) while in the toxic and exophthalmic cases, cardiac mischief 
appears within a year. 
The slowly developing cases (‘‘simple goitre”) show the worst 
myocardial weakness, much like that of arterio-sclerotic trouble due 
to syphilis or other causes, while in the acute toxic cases (‘‘exophthal- 
mic goitre”) the cardiac damage is less. 
The heart signs, then, may be divided into two groups: 
1. In toxic (usually exophthalmic) goitre, the heart shows: 
(a) Enlargement: displacement of the apex to the left and down. 
(b) Tachycardia. 
(c) Very loud ‘‘angry” sounds. 
(d) Jumping arteries with bounding then collapsing pulse, often 
a capillary pulse and a large pulse pressure. 
(e) In later stages absolute arrhythmia (auricular fibrillation). 
2. In the “simple” and usually non-toxic group there gradually 
develop signs of myocardial weakness not distinguishable from those 
associated with arterio-sclerosis. We find a large, irregular heart with 
systolic murmurs at all the orifices and usually a high systolic pressure. 
Diastolic pressure may or may not be elevated. The peripheral 
arteries often show sclerosis. 
III. Congenital Heart Disease 
Dr. Maude E. Abbott1 considers pulmonary stenosis as “probably 
the commonest of all (congenital) cardiac anomalies,’’ but the cases 
are reported in so scattered a way that exact summation is difficult. 
Her tables show the following main types among 631 cases analyzed: 
I. 
Stenosis of the descending aortic arch 
(coarctation of the aorta) 
212; 
with other defects in 
119. 
2. 
Defective interventricular septum 
189; 
pulmonary stenosis in 
75- 
other defects in 
68. 
3- 
Patent ductus arteriosus 
166; 
with other defects in 
102. 
4- 
Pulmonaty stenosis 
116; 
with other defects in 
107. 
5- 
Widely patent foramen ovale 
89; 
with other defects in 
7i- 
6. 
Transposition of the arterial trunks 
70; 
with other defects in 
13- 
7- 
Hypoplasia of the aorta 
46; 
with other defects in 
44. 
1 Osier’s Modern Medicine, Vol. IV, p. 323. 274 
PHYSICAL DIAGNOSIS 
These anomalies may be divided into two groups: 
(a) Those with marked cyanosis—pulmonary stenosis, transposi- 
tion of the arterial trunks and in a few cases of septum defect. 
(b) Those with little or no cyanosis-—aortic coarctation, most sep- 
tum defects, patent ductus arteriosus, and hypoplasia of the aorta. 
1. Pulmonary Stenosis 
A harsh systolic murmur (and in 15 per cent, a systolic thrill) is 
recognized at the base of the heart and usually faint or absent at the apex. 
Cyanosis is usually marked. In most cases these signs are best marked 
in the pulmonary area, in or above the second left interspace, but the 
murmur is often audible to some extent all over the chest except in 
the back. 
The heart is enlarged to the right and upwards, and its impulse 
may bulge the precordia and sometimes shakes the head and chest. 
The pulmonic second is usually weak or absent but may be actually 
increased. 
If a thrill is absent there is probably an associated defect in the 
interventricular septum. 
2. Stenosis of the Descending Aortic Arch (Aortic Coarctation) 
There may be no signs or symptoms. In a few cases the blood 
supply to the head and arms is too great, that to the rest of the body, 
too small. Hence there is headache, tinnitus, insomnia, suffusion of 
the head and neck. As a rule, symptoms appear late in life and 
under special strains (e.g., endocarditis). 
Physical Signs.—There may be violent pulsation of the sub- 
clavians and carotids with dilated tortuous vessels over the chest. 
Thus a collateral circulation between the arteries above the stenosis 
and those below it was established in at least 66 of 142 adult cases 
in Dr. Abbott’s collection. The pulse in the abdominal aorta and 
femorals is weak. Hypertrophy and dilatation of the whole heart 
occurred in 87 of 142 cases. 
In some cases no murmur is present. In others a loud systolic 
is heard at the base or apex. 
3. Patent Ductus Arteriosus 
In infants the signs are not distinguishable from those of septal 
defects. Thrill was present in 17 of 64 cases (Abbott’s series), usu- 
ally in the second left space. It is sometimes systolic, sometimes DISEASES OF THE HEART 
275 
continuous through the whole cardiac cycle. The murmur may 
likewise be systolic or continuous—rarely divided into systolic and 
diastolic. Among 46 adult cases it was systolic in 19, continuous in 
14, “double” in 9. 
The murmur is often extraordinarily loud and harsh. 
The second sound may be increased, diminished, or absent. 
Physical signs may be absent and cyanosis is often absent. A 
systolic thrill is present in about one-third of the cases, diffused over 
the precordia or with maximum intensity at the base. There may be 
precordial pulsation and bulging. 
A loud systolic murmur is the commonest sign and is present in 
about two-thirds of the cases. Rarely a diastolic murmur is also 
heard. It is widely diffused but loudest in the pulmonary area or 
just below it. It may last through the entire cardiac cycle with a 
systolic accent as in patent ductus arteriosus. 
4. Defective Interventricular Septum 
5. Defective Inter auricular Septum (.Foramen Ovale) 
Signs are often absent and even cyanosis is rare. When signs 
are present they are like those of ventricular defects, except that the 
murmur is often heard in the left back and is sometimes presystolic 
in time. Both murmur and thrill vary in intensity and in time .with 
the position of the patient (Abbott). 
6. Transposition of the Arterial Trunks 
Marked cyanosis with clubbed fingers may be the only sign in 
uncomplicated cases. Even this may be absent and the only sug- 
gestion of the lesion may be an accented pulmonic second sound with 
evidence of hypertrophied right ventricle. These features plus cyan- 
osis and no murmurs may suggest the diagnosis. 
7. Hypoplasia of the Aorta 
Obstinate anemia in an adolescent with a cardiac hypertrophy and 
dilatation for which no cause is found, are the only known signs of 
the disease. Diagnosis is usually impossible. 
IV. Other Diseases which Weaken the Heart 
The myocardium is seriously, though not incurably, affected in 
all continued fevers, owing less to the fever itself than to the tox- 
i. Acute Myocarditis 276 
PHYSICAL DIAGNOSIS' 
semia associated with it. “Cloudy swelling,’’ or acute degeneration 
of the muscle fibres, is produced by “common colds,’’ tonsilitis and 
other relatively mild infections, while a general septicaemia due to 
pyogenic organisms may produce extensive degeneration of the heart 
within a few days. 
The physical signs are those of cardiac weakness., The most 
significant change is in the quality of the first sound at the apex 
of the heart, which becomes gradually shorter until its quality is 
like that of the second sounds, while in some cases its feebleness 
makes the second sounds seem accented by comparison. Soft blowing 
systolic murmurs may develop at the pulmonary orifice, less often at 
the apex or over the aortic valve. 
The apex impulse becomes progressively feebler and more like 
a tap than a push. Irregularity and increasing rapidity are ominous 
signs which may be appreciated in the radial pulse, but still better by 
auscultation of the heart itself. In most of the acute infections, 
evidence of dilatation of the weakened cardiac chambers is rarely to 
be obtained during life (although at autopsy it is not infrequently 
found), but in acute articular rheumatism an acute dilatation of the 
heart appears to be a frequent complication, independent of the 
existence of any valvular disease. Attention has been especially 
called to this point by Lees and Boynton (British Med. Jour., July 
2, 1898) and by S. West. 
Influenza is also complicated not infrequently by acute cardiac 
dilatation and followed by symptoms of cardiac weakness or by angina 
pectoris. 
V. Miscellaneous Affections of the Heart 
i. Tachycardia (Rapid Heart) 
Simple quickening of the pulse rate, or tachycardia, which may 
pass altogether unnoticed by the patient himself, is to be distinguished 
from palpitation, in which the heart beats, whether rapid or not, 
force themselves upon the patient’s attention. 
The pulse rate may vary a great deal in health. A classmate 
of mine at the Harvard Medical School had a pulse rarely slower 
than ioo, yet his heart and other organs were entirely sound. Such 
cases are not very uncommon, especially in women. Temporarily 
the pulse rate may be greatly increased, not only by exercise and 
emotion, but by the influence of fever, of gastric disturbances, or of 
the menopause. Such a tachycardia is not always of brief duration. DISEASES OF THE HEART 
277 
The effects of a great mental shock may produce an acceleration of 
the pulse which persists for days or even weeks after the shock. 
Among organic diseases associated with tachycardia and weakening 
of the pulse, the commonest are those of the heart itself. Next to 
them, Graves’ disease (thyrotoxicosis) and functional neuroses (some 
of them sexual) are the most frequent causes of tachycardia. 
2. Cardiac Symptoms of Nervousness 
(Effort syndrome, neuro-circulatorv asthenia, irritable heart of soldiers, 
D. A. H.) 
People of nervous temperament (congenital) go to pieces under 
strains which the average person bears without disturbance. War 
brings this defect into prominence—often for the first time. But 
careful questioning usually proves that college examinations, athletic 
stunts and other exciting experiences, have produced symptoms similar 
to those which in the soldier under battle strain prove disabling. (So 
it was in 47 out of 50 cases studied by Friedlander and Freyhof,- 
Arch. of Int. Med., Dec., 1918.) 
Such people may give out with digestive, respiratory or urinary 
symptoms (vomiting, dyspnoea or polyuria), but most often the pa- 
tient’s attention (and that of his physician) is directed to his heart 
by the following symptoms: 
1. Tachycardia and palpitation. 
2. Cardiac pain or distress. 
3. Dyspnoea on emotional or physical strain. 
4. Weakness, vertigo and fainting. 
5. Tremor, flushing and sweating. 
Tobacco often intensifies these symptoms. 
Physical examination shows: 
(a) Very loud, abrupt and rapid heart action without any other 
significant alterations. 
(b) Moderate elevation of systolic blood pressure, while diastolic 
pressure remains normal or nearly so. 
(c) Deficient power of muscular work without exhaustion. 
(d) Trembling, clammy, cyanotic hands. 
(e) Precordial tenderness in 48% (Lewis). 
Systolic murmurs are often heard at the valve-areas. Something 
often taken for a systolic thrill is occasionally felt at the apex. There 
is no enlargement and usually no irregularity of the heart. X-ray 
and electrocardiography show nothing of significance. 278 
PHYSICAL DIAGNOSIS 
The most important duty of the physician is to convince first 
himself and then his patient that the heart is perfectly sound and that 
the only trouble with him is his nervousness. Great harm may be 
done by a doubtful or mistaken diagnosis. Emphatic reassurance 
based on careful examination is the essential. 
Hyperthyroidism is suggested in many of these cases by the tachy- 
cardia, tremor, nervousness and sweating. But the lack of any change 
in the basal metabolism, as shown by the studies of F. W. Peabody, 
makes thyroid involvement very improbable. 
Psychic and physical training improves many cases. Digitalis 
and rest are useless or harmful. 
3. Post Infectious Tachycardia 
A condition almost precisely like that just described sometimes 
occurs during convalescence from pneumonia, typhoid and other in- 
fections. Usually this occurs in those of congenital neurotic type. 
Recovery is more prompt and lasting than in the non-infectious cases. 
4. The Supposed Effect of Tobacco 
The disturbance produced on the heart by tobacco has been greatly 
exaggerated. There is no cardiac abnormality or group of abnor- 
malities that can be referred to the effects of tobacco alone. Persons 
constitutionally subject to tachycardia, palpitation or to occasional 
premature contractions may find these symptoms exaggerated or 
brought into the foreground by the, abuse of tobacco. But almost 
invariably one finds other factors in the background—neurotic tem- 
perament, bad hygiene, sexual excess, convalescence from infectious 
disease. 
• , Physical examination shows either (a) the signs described under 
the “Cardiac Symptoms of Nervousness” (p. 277) or (b) more or less 
frequent premature beats. 
5. “Acute Dilatation of the Heart," “Athlete's Heart" 
If recent acute infections and arterio-sclerosis are excluded, 
we can say that there is no reason to believe that acute dilatation or 
athlete's heart exists. After athletic contests and Marathon races, the 
heart does not dilate. Indeed, x-ray shows that it is generally slightly 
smaller than usual. DISEASES OF THE HEART 
279 
Hypertrophy does not, as far as I can ascertain, result from mus- 
cular exertion, no matter how great and prolonged—when arterio- 
sclerosis and syphilis can be excluded. 
The cases of weak, rapid or irregular heart action, occurring in 
adolescence or later and wrongly supposed to be due to athletics, are 
in fact cases of nervous heart or post infectious weakness, accentuated 
often by the alarm produced by a mistaken diagnosis of heart strain, 
dilatation or athlete’s heart. Of course in cases of organic heart dis- 
ease, valvular or myocardial, compensation may be broken by excessive 
exercise. 
6. Bradycardia (Slow Heart) 
In many healthy adults the heart seldom beats over 50 times a 
minute. 
1. Among the causes which may produce for a short time an 
abnormally slow heart-beat are: 
(а) Exhaustion; for example, after fevers, after parturition, or 
severe muscular exertion. 
(б) Toxcemia; for example, jaundice, uraemia, auto-intoxications in 
dyspepsia. 
(c) In certain hysterical and melancholic states and in neurotic 
children, the pulse may be exceedingly slow. 
(d) An increase of intracranial pressure, as in meningitis, cerebral 
hemorrhage, depressed fracture of the skull. Possibly in this category 
belong the cases of bradycardia sometimes seen in epileptiform or 
during syncopal attacks. Bradycardia from any one of these causes is 
apt to be of comparatively short duration. 
7. Heart Block 
(See above, page 116.) 
8. Palpitation 
Best defined as an “irregular or forcible heart action perceptible 
to the individual.” The essential point is that the individual becomes 
conscious of each beat of his heart, whether or no the heart action is 
in any way abnormal. 
(a) In irritable conditions of the nervous system, such as occur 
at puberty, at climacteric, or in neurasthenic persons, palpitation 
may be very distressing. Temporary disturbances, such as fright, 
may produce a similar and more or less lasting effect. 280 
PHYSICAL DIAGNOSIS 
(b) The effect of high altitudes, or of even a moderate eleva- 
tion (1,500 feet) is sufficient to produce in many healthy persons a 
quickening and strengthening of the heart’s action, so that sleep 
may be prevented. After a few nights this condition usually passes 
off, provided the heart is sound. 
(c) Abuse of tobacco and tea have a similar effect. 
(d) Any marked arrhythmia, with or without organic lesions, may 
be noticed as “palpitation” by the patient. 
(e) Heart block (see p. 116). 
Auscultation of a palpitating heart shows nothing more than 
unusually loud and ringing heart sounds, but since palpitation is 
often associated with arrhythmia of one or another type we must be 
careful to exclude the palpitation symptomatic of acute exhaustion 
of the heart, such as may occur in debilitated persons after violent 
or unusual exertion. In this condition dyspnoea upon slight exertion 
becomes marked. (See above—Cardiac Symptoms of Nervousness.) 
It goes without saying that in almost any case of organic disease of 
the heart, palpitation may be a very marked and distressing symptom. CHAPTER XVII 
DISEASES OF THE LUNGS 
BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
I. Tracheitis 
In connection with bronchitis or as a forerunner thereof, inflam- 
mation of the trachea is not uncommon. It gives rise to no charac- 
teristic physical signs, but is to be suspected when the patient com- 
plains of cough with pain over the upper portion of the sternum. 
II. Bronchitis 
1. Acute Bronchitis 
Inflammation of the larger bronchial tubes is not often the cause 
of any definite physical signs, but with every paroxysm of coughing the 
patient may feel pain in an area corresponding exactly to the anatom- 
ical position of the primary bronchi. I have seen patients indicate 
most accurately the situation of the large tubes when pointing out the 
position of pain produced by coughing. 
In the vast majority of cases of acute bronchitis, foci of broncho- 
pneumonia are also present, but the physical signs are usually those of 
an inflammation of the smaller bronchi, and the swelling of their 
walls, with or without exudation, which is manifested as follows:1 
(1) Diminution in the intensity of vesicular breathing over the 
area affected (rarely in the earliest stages the breath sounds are 
exaggerated and harsh, especially in the upper portions of the chest). 
(2) Rales, fine crackles or squeaks especially in the lower backs 
or axillas in adults. In children the rales are more widely distributed 
and are often musical or squeaking over bronchi which are narrowed 
without any considerable amount of exudation, as is the case in the 
earliest stages of many cases, and bubbling, crackling, or clicking in 
later stages, when watery or viscid exudation is present in the tubes. 
The calibre of the bronchi affected can be estimated from the coarse- 
ness or fineness of the rales. Low-pitched groaning sounds point to a 
1 Bronchitis may exist without r&les, but cannot be diagnosed without them. 
Occasionally they are present only in the early morning. 
281 282 
PHYSICAL DIAGNOSIS 
stenosis of a relatively large bronchus, while squeaking and whistling 
sounds are usually produced in the smaller tubes. Large, bubbling 
rdles are much less often heard than the finer, crackling variety. The 
latter are produced in the smallest tubes, the former in the larger 
variety. 
Simple non-tuberculous bronchitis is almost invariably bilateral 
or symmetrical, and affects most often the lower two-thirds of the 
lungs, leaving the apices relatively free. It is almost never confined 
to an apex. When rales are to be heard on one side of the chest only, 
and when they persist in the same spot for days and weeks, tuberculosis 
is always to be suspected, especially if the rales are localized at the 
summit of one or both lungs. At the base, such a patch is usually 
non-tubereulous. It should never be forgotten that the tubercle 
bacillus is capable of exciting a bronchitis indistinguishable from other 
varieties of bronchitis, except by its tendency to show itself at the 
apex of the lung and on one side only; most cases of pulmonary tuber- 
culosis begin in this way. 
The only other variety of bronchitis which is often unilateral is that 
due to the influenza bacillus. In the course of a case of influenza, a 
unilateral localized bronchitis not infrequently occurs. Over a patch 
of lung, perhaps the size of the palm of the hand, fine, moist rales may 
persist for weeks, finally clearing up only after the patient has resumed 
his ordinary occupation. Doubtless such localized patches of bronchi- 
tis are accompanied by foci of lobular pneumonia too small to be 
detected by our present methods of physical examination. Sometimes 
they can be demonstrated by the x-ray. 
Percussion dulness is absent in bronchitis except near the end of 
fatal cases, when the lung is stuffed with mucus and pus, or when 
atelectasis has occurred owing to extensive plugging of the larger 
bronchi. These events are rarely seen, and in general, the negative 
results of percussion are of great value in excluding solidification or 
fluid exudation. 
Occasionally percussion resonance may be increased owing to a 
slight temporary overdistention of the air vesicles from coughing.1 
Inspection usually shows little or nothing of diagnostic importance 
in acute bronchitis. Long-standing cases, complicated as they almost 
invariably are by emphysema, present changes in the shape of the 
thorax; but these are due to the emphysema rather than to the bron- 
1 In children examined during a crying-spell, a Cracked-pot sound can usually be 
elicited by percussion. This is in no way characteristic of bronchitis and can often 
be obtained in healthy infants. BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
283 
chitis. In children, acute bronchitis sometimes involves so many of 
the smaller bronchi that dyspnoea and use of accessory muscles of 
respiration are notable. But this usually means atelectasis, broncho- 
pneumonia, or laryngeal spasm, in addition to the bronchitis. 
From violent coughing the jugulars may be distended, but no 
systolic pulsation occurs in them. 
Voice sounds and tactile fremitus are sometimes increased owing 
to the coincident broncho-pneumonia. In other cases they are normal 
or decreased. 
(a) Differential Diagnosis 
Oedema of the lung and bronchial asthma are the only pathological 
processes (except hemorrhage into the lung substance) which give 
rise to signs like those of bronchitis. 
(1) In oedema of the lung, or in pulmonary 
apoplexy, one may find, as in simple bron- 
chitis, a diminished vesicular breathing with 
crackling rales, but oedema of the lung is 
almost always best marked in the dependent 
portions; that is, in the posterior parts of the 
lung if the patient has been lying upon the 
back, or in the lower lobes if he has been 
sitting up. Dulness and diminished tactile 
fremitus are usually present, though slight. 
The recognition of a cause for the oedema, for 
example a non-compensated heart lesion, and 
the absence of fever or leucocytosis materially 
aid the diagnosis. 
(2) Bronchial asthma or spasm of the finer 
bronchi gives rise to squeaking and groaning 
sounds similar to those heard in the earlier 
stages of many cases of bronchitis. But in 
bronchial asthma, fever is usually absent, the 
rales are chiefly expiratory, and expiration is 
prolonged and intensified. Moreover, the 
inhalation of a few drops of amyl nitrite 
will temporarily dispel rales due to bronchial 
spasm, while on the rales of dry bronchitis 
it has no effect (Abrams). 
(3) Broncho-pneumonia. In many cases of lobular or broncho- 
pneumonia the physical signs are exclusively those of the coexisting 
Fig. 173.—The Dots are 
Placed over the Area where 
Atelectatic Crepitation is 
Oftenest Heard. 284 
PHYSICAL DIAGNOSIS 
bronchitis. In such cases the diagnosis of bronchitis is not wrong, 
but does not cover the whole ground. Indeed I am doubtful whether 
it ever does. There is, to my mind, no proof that acute bronchitis 
without broncho-pneumonia ever exists. 
(4) Muscle sounds. Under certain circumstances (cold, nervous- 
ness) , the rumbling noises produced by muscular contractions in the 
chest wall may simulate rales so closely that the diagnosis of bronchitis 
may be strongly suggested. The differentiation between rales and 
muscle sounds has already been discussed (see above, p. 150). 
(5) Atelectatic crepitation. Crackling rales heard over the thin 
margins of the lungs at the base of the axilla or along the edges of the 
manubrium are often due to atelectasis (see above). From bronchitis 
they are distinguished by their situation and by the lack of symptoms. 
They are best heard at the point shown in Fig. 173 on page 283. 
2. Chronic Bronchitis 
So far as the bronchitis itself is concerned, there may be no differ- 
ence in the physical signs between the acute and chronic forms of the 
disease; but in the latter, one almost invariably finds associated 
with the bronchitis itself a considerable degree of cardiac weakness 
with emphysema and asthma. Indeed, the foreground of the clinical 
picture and the bulk of the physical signs are made up by these three 
diseases, rather than by the bronchitis itself. The more we study 
bronchitis the more it vanishes from sight as a clinical entity. “Acute 
bronchitis’’ is fast turning into acute broncho-pneumonia; “chronic 
bronchitis’’ is being recognized as chronic pulmonary oedema from weak 
heart action. Lord has analyzed 161 autopsied cases in which the 
history and physical signs were such as are usually attributed to 
‘ ‘ chronic bronchitis ’ ’ and concluded that the correct diagnoses were as 
follows: 
Heart weakness, 103 
Chronic pneumonitis 
or abscess 
Neoplasm of lung, 5 
of the lung, 
15 
Tuberculosis, 31 
Other conditions, 
7 
Total = 161 
It seems very doubtful whether “chronic bronchitis” exists at all 
except as a minor element in other diseases. 
III. Croupous Pneumonia 
In its typical form croupous or fibrinous pneumonia produces 
solidification of one or more lobes, usually the lower, the process being BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
285 
accurately bounded by the interlobular fissures. Although the 
physical signs of the earlier stages differ considerably from those of 
the later ones, there seems to be no sufficient ground for marking off 
stages of engorgement and of red and gray hepatization, for clinically 
these stages cannot be distinguished. 
The solidification may begin in the deeper parts of the lung 
(“ central pneumonia ”), so that no physical signs are obtainable unless 
those shown by v-ray, or unless the process extends to the surface of 
the lung. But in many so-called “central pneumonias” there is really 
no localization or solidification at all. The process is an acute general 
pneumococcus infection which may or may not settle in the lung. 
Massive pneumonia, in which the bronchi as well as the air cells are 
plugged with fibrin and leucocytes, is a relatively rare form of the 
disease, but possesses great clinical importance on account of the 
marked resemblance between its physical signs and those of pleural 
effusion. 
The right lung alone is involved in 54 per cent of cases, the left 
alone in 38 per cent., both lungs in 8 per cent. (Jiirgensen’s analysis 
of 6666 cases quoted by Lord). In 70 per cent, of cases the lower 
lobe is affected. 
i. Physical Signs 
(a) Inspection.—The aspect of the patient frequently suggests the 
diagnosis; the face is anxious, often flushed or slightly cyanosed, the 
flush sometimes affecting most strikingly the side of the face corre- 
sponding to the lung affected.1 Herpetic vesicles (“cold sores”) are 
often to be seen around the mouth or nose. The rapid, difficult 
breathing is at once noticeable, and expiration is often accompanied 
by a grunt. The use of the accessory muscles of respiration and the 
dilatation of the nostrils attract attention. 
The combination of marked dyspnoea with absence of dropsy is 
met with more frequently in pneumonia than in any other disease. 
Both sides of the chest usually move alike, but occasionally the affected 
side shows deficient expansion, especially in the later stages of the 
disease, and the other side of the chest shows increased respiratory 
movements (compensatory). Rarely the pulsations of the heart may 
be transmitted to the chest wall through the affected lung. 
When pneumonia attacks a feeble old man, or follows injuries 
(surgical pneumonia), its onset may be insidious, and none of the 
phenomena just described may be seen. 
1 Probably because the patient is apt to lie upon the affected side. 286 
PHYSICAL DIAGNOSIS 
(6) Palpation.—In the great majority of cases tactile fremitus is 
markedly increased over the affected area,1 but in case the bronchi are 
occluded by secretions or fibrinous exudate, fremitus may be dimin- 
ished or altogether absent. A few hard coughs will sometimes clear 
out the tubes and thus materially assist the diagnosis. Occasionally 
some muscular spasm or an increase in superficial temperature of the 
affected side may be noticed by palpation, and rarely one feels a friction 
rub due to the pleurisy which accompanies the disease. 
(c) Percussion.—Over the area affected, the percussion note is generally 
dull and may he almost flat, except in the earliest and latest stages of 
the disease, in which it may have a tympanitic quality with or without 
slight dulness. More marked tympany is usually present over the 
unaffected lobes of the diseased lung (that is, over the upper lobes in 
most cases) and at the base of the sound lung (Lord). 
The conditions just described represent the great majority of cases, 
but the following exceptions occur: 
(1) In the pneumonias of children, and occasionally in adults, 
dulness may be absent. 
(2) When the lower lobe of the left lung is affected, a distinctly 
tympanitic quality may be transmitted to the consolidated area 
from a distended stomach or colon. 
(3) In central pneumonia there may be no change in the percus- 
sion note, or it may be unusually full and deep so that the sound side 
seems dull by comparison. 
A solidified lobe increases so much in size that the area of dulness 
corresponding to it often seems incredibly large. Thus, although the 
lower lobe reaches in health not more than half-way up the scapula, 
when solidified it produces dulness throughout nearly the whole 
back. 
The right base is the most frequent seat of pneumonic solidifications, 
but the dulness corresponding to it is often first noticeable in the 
posterior axillary line. A dulness appreciable only in the front of the 
chest is almost sure to correspond to the upper lobe, while signs in the 
lower part of the right axilla correspond to the middle lobe. Many 
cases of central pneumonia first appear at the surface in one or the 
other axilla. 
As regards the amount of solidification needed to produce per- 
cussion dulness, Wintrich says that the minimum is a patch 5 cm. 
in diameter, 2 cm. deep, and superficially situated. 
1 By using the edge instead of the flat of the hand the boundaries of solidified 
lobes may often be very accurately marked out by means of the tactile fremitus. BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
287 
Percussion often makes us aware of an increased (perhaps mus- 
cular) resistance or diminished elasticity of the affected side, although 
the resistance is seldom as marked as in large pleural effusions. 
(d) Auscultation.—In the great majority of cases typical tubular 
breathing is to be heard over the affected area. Since a whisper is 
practically a forced expiration, this tubular quality is very well brought 
out if the patient is made to whisper “one, two, three,” or any other 
succession of syllables, and by this method the fatigue and pain of 
deep breathing may be saved. By this use of the whispered voice, one 
may accurately mark out the boundaries of the consolidated area 
without tiring the patient, and may demonstrate in many cases that 
it coincides with the boundaries of one lobe of the lung. 
In the earliest stages of the disease the breathing may be bron- 
cho-vesicular; more often it is feeble or suppressed over the consolidated 
area, and fine crackling rales may be heard at the end of inspiration. 
The crepitant or fine crackling rale is more often heard at the onset 
of broncho-pneumonia than of lobar types.1 
If the smaller bronchi are blocked or if the pleura is much thick- 
ened, as is not infrequently the case, respiration is absent or very 
feeble; such cases may be mistaken for pleuritic effusion. 
In cases of “central pneumonia,” that is, when the area of solidifi- 
cation is in the interior of the organ, there may be no change in the 
breath sounds, or a bronchial element may be faintly audible on auscul- 
tation with the unaided ear, and only by this method. 
The intensity of the spoken or whispered voice is greatly increased 
over the area of consolidation, and sometimes the words can be dis- 
tinguished. The nasal twang known as “egophony” is occasionally 
to be heard. In the majority of cases, as has been already stated, 
the right lower lobe posteriorly is affected, so that the consolidated 
area is immediately in apposition with the spinal column. Under 
these circumstances, it is not at all uncommon to hear bronchial 
breathing transmitted from the consolidated lobe to a narrow zone 
close along the spinal column on the sound side. Such a zone is 
often mistaken for consolidation. 
The signs are usually less marked in the axilla and in the front of 
the lung, but in a minority of cases, and especially when the upper 
lobes are affected, the signs are wholly in the front. When searching 
for evidences of consolidation in persons suspected to have pneumonia, 
1 Crepitant rales are rarely heard in the pneumonias of infancy and old age. 
They are not peculiar to pneumonia, but occur in pulmonary oedema or hemorrhagic 
infarction—conditions easily distinguished from pneumonia. 288 
PHYSICAL DIAGNOSIS 
one should never omit to examine the apices and very summit of the 
armpit, pressing the stethoscope up behind the anterior fold of the 
axilla. 
In examining the posterior lobes, when the patient is too weak 
to sit up and is loath even to turn upon the side, the Bowles stetho- 
scope is a great convenience, owing to the ease with which its flattened 
extremity may be worked in between the patients and the bed-clothes 
without causing any discomfort. A'-ray may be of important service 
in the detection of central pneumonia. The shadow of a solidified 
patch is mottled and ill-defined in comparison with pleural effusion 
or tumor. 
When resolution begins, the signs may almost completely disappear 
within a few hours. More frequently the bronchial breathing is 
Tympany. 
Bronchial breathing 
transmitted by 
spinal column to 
sound lung. 
Solidification. 
Fig. 174.—Diagram of Signs in Pneumonia 
modified to broncho-vesicular, dulness and bronchophony become 
less marked, fine crackling rales (crepitans redux) or coarser moist 
bubbles appear, and the lung gradually returns to its normal condition 
within a period of three to eight days. In the most active stages of 
the disease the entire absence of rales is the rule. In most cases the 
solidification of the lung persists after the fall of the temperature; 
indeed, it may be weeks or even months before it clears up, and yet 
the lung may be perfectly sound in the end. On the other hand, 
abscess or gangrene may develop in the solidified lobe. This was the 
case in 2 per cent, of 500 cases analyzed by Lord. In the 153 autopsies 
of Stone, Bliss & Phillips (see p. 289) pulmonary abscess occurred in 
26 or 16 per cent. Organization or fibrosis of the affected lobe was BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
289 
found in 7.6 per cent, of 210 autopsied cases of pneumonia of the 
Massachusetts General Hospital. Small serous effusions were found 
in 26 per cent, of the same series. Commonest and most important, 
however, is the post-pneumonic empyema (basal or interlobar) which 
is often mistaken for delayed resolution. The latter is rare; empyema 
is discovered in about 4 per cent, (see below, p. 330). 
“ Wandering pneumonia ” is a term applied to cases in which the 
consolidation disappears in one lobe only to reappear in another, 
or spreads gradually from lobe to lobe. The physical signs in such 
cases do not differ essentially from those already described. 
Complications.—Endocarditis is found in about 1 per cent, of all 
cases and 4 to 7 per cent, of fatal cases. Pericarditis is found in from 
13 per cent. (Musser and Norris) to 33 per cent. (Stone, Bliss & Phillips, 
Arch, of Int. Med., Oct., 1918) when autopsied cases only are studied. 
Forty per cent, or more of these cases of pericarditis are not recognized 
in life; acute purulent peritonitis was demonstrated in 5 or 3.2 per cent, 
of 154 cases autopsied at the Massachusetts General Hospital. Stone, 
Bliss & Phillips found it in 24 out of 153 autopsied cases (15 per 
cent.). Meningitis complicated 2.5 per cent, of the same series. 
Otitis media was found in 3.4 per cent., acute arthritis in .4 per cent. 
Peripheral venous thrombosis was seen in 10 of 949 cases (1 per cent.) 
studied by Sears and Larrabee. 
2. Summary 
In a typical case one finds (oftenest at the right base behind) 
1. Dulness on percussion. 
2. Increased tactile fremitus and voice sounds. 
3. Tubular breathing and occasionally crepitant rales. 
These signs occurring in connection with fever, cough, rusty sputa, 
pain in the side, dyspnoea, herpes and leucocytosis are sufficient 
for the diagnosis. 
But many cases are not typical when first seen. The following 
are the commonest anomalies: 
(a) There may be tympany instead of dulness, especially in children 
or when the solidification is at the left base. 
(b) The breathing may be feeble but vesicular in character, or it 
may be absent, in case bronchi are plugged; from the same cause. In 
early stages fine crackles with feeble vesicular breathing and slightly 
increased voice sounds is the commonest combination. 
(c) Tactile fremitus may be diminished. 
19 290 
PHYSICAL DIAGNOSIS 
A hard cough may clear out the bronchi and produce a sudden 
metamorphosis of the physical signs, with a return to the normal type. 
In these atypical cases, we have to fall back upon the symptoms, 
the history, the blood, and sputa for help in the diagnosis. 
Deep-seated pneumonic processes may appear at the surface in 
out-of-the-way places, e.g., at the summit of the axilla, and the area 
of demonstrable physical signs may be no larger than a silver dollar. 
A thorough examination of every inch of the chest and an x-ray study 
are therefore essential in doubtful cases. 
In the later stages of the disease, crepitant or other fine rales often 
appear, and the signs of solidification suddenly or gradually disappear. 
3. Differential Diagnosis 
Pneumonic solidification is to be distinguished from 
(1) Pleuritic effusion, serous or purulent. 
(2) Tuberculosis of the lung. 
(3) Compression of the lung. 
(1) From serous effusion, pneumonia is to be distinguished in the 
great majority of cases by differences in the onset, course, and general 
symptoms of the disease. In pneumonia the patient is far more 
suddenly and violently attacked, the dyspnoea is much greater, cough 
and pain are more distressing and more frequent, the temperature is 
higher, and the sputum often characteristic. In pleuritic effusion the 
dulness is usually more intense than in pneumonia. Tactile fremitus 
and voice sounds are increased in pneumonia (except when the bronchi 
are plugged); decreased or absent in pleuritic effusion. Bronchial 
breathing may be heard in both diseases, but is usually feeble and 
distant when occurring in pleurisy, and loud in pneumonia. If the 
affection be on the left side, the diagnosis is much aided by the presence 
of dislocation of the heart, which is produced by pleuritic effusion and 
never by pneumonia. In cases of pneumonia with occluded bronchi 
one may have every sign of pleuritic effusion—flatness, absent breath- 
ing, voice and fremitus—and in such cases the absence of any disloca- 
tion of the heart, provided the disease is upon the left side, is very 
important. If a similar condition of things occurs upon the right side, 
one may have to fall back upon the symptoms and upon such evidence 
as the blood count, herpes, sputum, etc. The above applies to serous 
pleurisy—tuberculous or streptococcic (“rheumatic”)- Pneumococ- 
cus empyema on the other hand, especially when it accompanies or 
follows pneumonia (as it almost always does), is in its early stages 
almost or quite impossible to distinguish from pneumonia. BRONCHITIS, pneumonia, tuberculosis 
291 
Exploratory puncture is often the only method of diagnosis and should 
be practiced in every doubtful case. Aside from puncture the most 
reliable signs of fluid are: 
1. Flatness (not dulness) on percussion. 
2. Absent tactile fremitus. 
3. Displaced heart (especially in left sided empyema). 
4. X-ray examination. 
(2) Tuberculosis of the lung causing, as it may, a diffuse solidifica- 
tion of the organ, may be indistinguishable from pneumonia if we 
take account only of the physical signs, but the two diseases can usually 
be distinguished without difficulty by the difference in their symptoms 
and course, and by the presence or absence of tubercle bacilli in the 
sputum. 
(3) Compression of the left lung by a pericardial effusion and of 
either lung by some subdiaphragmatic lesion (perinephric abscess, 
hepatic abscess) often simulates pneumonia; indeed the physical signs 
may be indistinguishable. Diagnosis depends mostly on establishing 
the presence or absence of a cause for such compression. The x-ray 
demonstration of an abnormally elevated diaphragm may be of great 
value. 
(4) Pulmonary infarction or thrombosis is often mistaken for pneu- 
monia. Correct diagnosis depends not on physical signs but on 
recognizing a possible cause for such infarction, i.e., typhoid fever, 
failing cardiac compensation, peripheral thrombosis, childbirth with 
or without sepsis, surgical operations. The fever usually appears 
later than in pneumonia. Bloody sputa is commoner in infarction 
than in pneumonia. The signs are 
1. A patch of pleural friction or of crackling rales, often disappear- 
ing without any other signs in 2-3 days. 
2. A small patch of consolidation exactly like pneumonia lasting 
3-4 days. 
3. Signs like those of pleural effusion but with no fluid obtainable 
on tapping. 
In all “queer pneumonias’’ infarct should be suspected. 
Often the causative peripheral venous thrombosis is unsuspected 
until bloody sputa (pulmonary infarct) reveal its results. 
IV. Inhalation Pneumonia. Aspiration Pneumonia 
When food or other foreign substances are drawn into the air 
passages, as may occur, for example, during recovery from ether 
narcosis, a form of broncho-pneumonia may be set up, in which the 292 
PHYSICAL DIAGNOSIS 
solidified patches are not infrequently large enough to be recognized 
by the ordinary methods of physical examination. 
The lesions are usually bilateral and accompanied by a general 
bronchitis. Slight dulness and indistinct bronchial breathing can 
usually be made out over an irregular area in the backs of both lungs. 
The signs are considerably less marked than in croupous pneu- 
monia, and the boundaries of the irregular patches of disease do not 
correspond to those of a lobe of the lung. 
If not rapidly fatal, the disease may be complicated by pulmonary 
gangrene or abscess and large quantities of fetid pus may be spit up. 
V. Broncho-Pneumonia (Catarrhal or Lobular Pneumonia) 
1. Acute Broncho-Pneumonia 
Multiple small areas of solidification scattered through both lungs, 
interspersed with areas of collapse, and usually associated with diffuse 
bronchitis, occur very frequently in children, producing severe 
dyspnoea, cyanosis, cough, and somnolence, and running a very fatal 
course. 
The solidified lobules may fuse so as to form considerable areas of 
hepatized lung, or there may be no lesion larger than a pea. 
This is the usual type of “lung fever” in infants, although ordinary 
lobar pneumonia is fully as common in older children. Of 195 cases 
found at autopsy in Lord’s series only 14 were in children (since the 
hospital receives very few children). Suppurative peritonitis was 
the commonest cause (35 cases). Other infectious diseases and a 
variety of debilitating conditions (cancer, nephritis, brain tumor, 
etc.) make up the other causes. 
The widespread atelectasis of the lower lobes which is associated 
with the disease in most cases owing to the plugging of the bronchi 
with tenacious secretions, is probably as serious in its effects as the 
pneumonic foci themselves. 
The anterior and upper parts of the lungs often become distended 
with air (vicarious emphysema) and render the physical signs very 
confusing and deceptive. Much milder and less widespread types of 
broncho-pneumonia often run their course under the name of “acute 
bronchitis” and are not discovered unless the patient happens to die 
of some other cause. The physical signs are merely those of bronchitis 
and often the patients do not even take to bed. 
(a) Physical Signs 
In the majority of cases there are no physical signs except by x-ray, 
and the diagnosis has to be made largely from the symptoms and BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
293 
course of the disease. The consolidated areas are usually too smalLto 
give rise to any dulness on percussion, or to any change in the voice 
sounds, or fremitus, so that auscultation shows, as a rule, nothing 
more than patches of fine rales occurring at the end of expiration. Care- 
ful listening usually reveals a diminished respiration as well, but this 
is not a “showy” sign and most physicians notice only the rales and 
Fig. 175.—Pneumonia—right lung. Note wedge shaped area with its base in the 
right axilla. 
call the case “bronchitis.” Localized tympanitic resonance is some- 
times present over the diseased area, making the sounder portions of 
the lungs seem dull by comparison. Occasionally, when many lobules 
have fused into a single mass of larger area, the ordinary signs of con- 
solidation may be obtained, although they may disappear within 
twenty-four or forty-eight hours and appear in another situation. As 
above said, the diagnosis is usually to be made, if at all, from the com- 
bination of the physical signs of a localized bronchitis with the symptoms 294 
PHYSICAL DIAGNOSIS 
of pneumonia. “This patient,” we say, “has only the signs of bron- 
chitis, but he is too sick. The cyanosis, dyspnoea, and fever are too 
marked. He is sicker than simple bronchitis will account for, but I 
am in doubt whether there is any such thing as ‘simple bronchitis.’ 
It seems to me probable that what has usually been called ‘simple 
bronchitis’ with patches of rales here and there is, in fact, a relatively 
mild type of broncho-pneumonia with some associated bronchitis.” 
(b) Differential Diagnosis 
(a) Acute pulmonary tuberculosis may be indistinguishable from 
broncho-pneumonia by the physical signs alone. But in the vast 
majority of cases tubercle appear at the apex of the lung and broncho- 
pneumonia does not. The diagnosis is substantiated by the history 
and course of the disease or by the presence of tubercle bacilli in the 
sputa. 
(b) The extensive atelectasis of the lower lobes which may accom- 
pany broncho-pneumonia gives rise to dulness and absence of respira- 
tory and vocal sounds. Thus, the signs of pleuritic effusion are 
simulated, and in children the possibility of empyema should not be 
forgotten. As a rule, broncho-pneumonia gives rise to much greater 
dyspnoea, and is associated with a more extensive bronchitis, than 
usually coexist with pleural effusion. The atelectatic lobules may be 
expanded by coughing or by the cutaneous stimulus of cold water, 
and thus resonance and breath sounds may suddenly return. With 
pleuritic effusions, of course, such a change is impossible. 
(c) Empyema may be indistinguishable from broncho-pneumonia 
except by puncture or surgical operation (see above, p. 291). 
2. Chronic Broncho-Pneumonia 
Pulmonary induration was found in 12 out of 85 cases of broncho- 
pneumonia autopsied at the Massachusetts General Hospital (Lord). 
This corresponds with the clinical type of chronic broncho-pneu- 
monia to which Riesman has recently called attention. It cannot 
be distinguished from the fibroid or chronic interstitial types of pneu- 
monitis but is to be sharply separated from tuberculosis. 
The physical signs are those of solidification with or without rales 
and—in extensive disease of long standing—evidence of contracted 
chest. 
In many cases the disease complicates bronchiectasis or pulmon- 
ary abscess. It is commonest in children. From phthisis it is dis- BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
295 
tinguished by its usually non-apical site, by its history and usually 
by the absence of fever, emaciation and constitutional symptoms. 
The sputum is alone decisive, however. 
VI. Tuberculosis of the Lungs 
i. Incipient Tuberculosis 
In the earlier stages of the disease there may be absolutely no 
recognizable physical signs, and the diagnosis may be established 
only by the positive result of a tuberculin injection or by the combina- 
tion of debility, indigestion or loss of weight with slight fever not other- 
wise to be accounted for. 
In some cases the earliest evidence of the disease is hcemoptyis.1 
When a patient consults a physician on account of haemoptysis, it is 
frequently impossible to find any physical signs of disease in the lungs; 
not until weeks or months later do the characteristic changes recogniz- 
able by physical examination make their appearance. 
The very early hoarseness of the voice in tuberculous patients is of 
great importance and often attracts our attention to the lungs when 
the patient has said nothing about them. Definite physical signs 
in the lungs and tubercle bacilli in the sputa (artificially obtained through 
the use of potassic iodide, see below) may occasionally be demon- 
strated before any cough has appeared. On the other hand, the 
patient may cough for weeks before anything abnormal can be dis- 
covered in the lungs. Occasionally tuberculosis begins with an 
ordinarily bilateral bronchitis or broncho-pneumonia. I have found 
tubercle bacilli in four such cases. More often the earliest physical 
signs are: 
(а) Fine crackling rales at the apex of one lung, heard only with 
or after cough and at the end of inspiration. (More rarely squeaks 
may be heard.) 
(б) A slight diminution in the excursion of the diaphragm on the 
affected side, as shown by x-ray or by Litten’s diaphragm shadow. 
(c) Slight diminution in the intensity of the respiratory murmur, 
with or without a high pitched or interrupted inspiration (“ cog-wheel 
breathing”). 
(a) In examining the apices of the lungs for evidence of early 
tuberculosis one should secure, if possible, perfect quiet in the room, and 
1 Never percuss a patient within forty-eight hours after a hemorrhage, and never 
encourage cough or forced respiration in such a one. There is danger of starting a 
fresh hemorrhage. 296 
PHYSICAL DIAGNOSIS 
have the clothes entirely removed from the patient’s chest. The 
ordinary hard-rubber chest-piece is better than the chest-piece of the 
Bowles instrument, and both the chest-piece and the skin should be 
wetted. After listening during quiet breathing over the apices above 
and below the clavicle in front, and above the spine of the scapula 
behind, the patient should be directed to breathe out and then, at the 
end of expiration, to cough. During this cough and the deep inspira- 
tion which is likely to precede or follow it, one should listen as care- 
fully as possible at the apex of the lung, above and below the clavicle, 
R&les. 
Fig. 176.—Diagram to Show Position of Earliest Signs in Tuberculosis 
concentrating attention especially upon the cough itself and upon 
the last quarter of the inspiration, when rales are most apt to appear. 
Sometimes only one or two crackles may be heard with each inspira- 
tion, and not infrequently they will not be heard at all unless the 
patient is made to cough, but even a single rale, if persistent,1 is impor- 
tant. In children or others who cannot cough at will, one can accom- 
plish nearly the same result by making them count as long as possible 
with one breath and then listening to the immediately succeeding in- 
spiration. When listening over the apex of the lung, one should never 
allow the patient to turn his head sharply in the other direction, since 
such an attitude stretches the skin and muscles on the side on which 
we are listening so as to produce annoying muscle sounds or skin rubs. 
Lowered shoulders and a thoroughly relaxed attitude are essential. 
In cases in which one suspects that incipient tuberculosis is present 
and yet in which no positive evidence can be found, it is a good plan to 
1 R&les heard only during the first few breaths and not found to persist on 
subsequent examinations, may be due to the expansion of atelectatic lobules. BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
297 
give iodide of potassium, (gr. vii, three times a day) for a few days. 
The effect of this drug is often to make rales more distinct, and some- 
times to increase expectoration so that tubercle bacilli can be demon- 
strated when before none were to be obtained.1 
(6) The diminution in the excursion of the diaphragm upon the 
affected side in cases of incipient phthisis has been much insisted upon 
by F. H. Williams and others who have interested themselves in the 
radioscopy of the chest. Litten’s diaphragm shadow gives us a 
method of observing the same phenomenon without the need of a 
fluoroscope. Even very slight tuberculous changes in the lung are 
sufficient to diminish its elasticity and so to restrict its excursion and 
that of the diaphragm. Comparisons must always be made with the 
sound side in such cases. It must be remembered that pleuritic 
adhesions, due to a previous inflammation of the pleura, may diminish 
or altogether abolish the excursion of the diaphragm shadow, inde- 
pendently of any active disease in the lung itself. 
Some radiologists believe that they can detect the presence of 
tuberculosis in the lung by radioscopy at a period at which no other 
method of physical examination shows anything abnormal, but post- 
mortem results rarely in my experience support this belief. In 
incipient tuberculosis the x-ray as often leads us wrong as right. 
Interrupted or cog-wheel respiration, in which the inspiration comes 
in high-pitched irregular jerky puffs not synchronous with the cardiac 
impulse, signifies that the entrance of the air into the alveoli is impeded, 
and such impediment is most likely to be due to tuberculosis when 
present over a considerable period in a localized area of pulmon- 
ary tissue. It has, however, no relation to the activity of the process; 
indeed it may be heard in wholly arrested cases. Only moisture, 
crackles with cough, proves an active process. 
2. Moderately Advanced Cases 
So far I have been speaking of the detection of tuberculosis at a 
stage prior to the production of any considerable amount of solidifica- 
tion. The signs considered have been those of bronchitis localized at 
the apex of the lung, or of a slightly diminished pulmonary elasticity, 
whether due to pleuritic adhesions or to other causes. We have next 
1 Any irritating vapor—for example, creosote vapor—which produces violent 
cough and expectoration, may be used to expel bronchial secretions in doubtful 
cases. Tubercle bacilli may then be found in the sputum of patients who, without 
the irritating inhalation, have no cough and so no sputa, but this is in my opinion a 
dangerous procedure, as it may “light up” a quiescent process in the lung. 298 
PHYSICAL DIAGNOSIS 
to consider the signs in cases in which solidification is present, though 
relatively slight in amount. This condition is comparatively easy to 
recognize when it occurs at the left apex, but more difficult in case 
only the right apex is diseased. Partial solidification of a small 
area of lung tissue at the left apex gives rise to 
(a) Slight dulness on light percussion,1 with increased resistance. 
(b) Slight increase in the intensity of the spoken and whispered 
voice, and of the tactile fremitus (in many cases). 
(c) Some one of the numerous varieties of broncho-vesicular breath- 
ing (true bronchial breathing is a late sign). 
Complete 
solidification. 
Rales. 
Partial 
solidification. 
, RMes. 
Fig. 177.—Diagram of Signs in Phthisis 
(d) Abnormally loud transmission of the heart sounds, especially 
under the clavicle. 
f- In case there is also a certain amount of secretion in the bronchi 
of the affected area or ulceration around them, one often hears rales of a 
peculiar quality to which Skoda has given the name of “ consonating 
rales.” Rales produced in or very near a solidified area are apt to 
have a very sharp, crackling quality, their intensity being increased 
by the same acoustical conditions which increase the intensity of the 
voice sounds over the same area. When such rales are present at the 
apex of either lung, the diagnosis of tuberculosis is almost certain, but 
if, as not infrequently occurs, there are no rales to be heard over the 
suspected area, our diagnosis is clear only in case the signs occur at 
the left apex. Even these signs may mean only a healed tuberculosis, 
1 Other causes of dulness, such as asymmetry of the chest, pleural thickening, 
and tumors, must be excluded. Emphysema of the lobules surrounding the 
tuberculous patch may completely mask the dulness. BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
299 
not an active process, unless rales can be elicited. Precisely the same 
signs, if present at the right apex, leave us in doubt regarding the diag- 
nosis, for the reason that, as has been explained above, we find at 
the apex of the right lung, in health, signs almost exactly identical with 
those of a slight degree of solidification. Hence, if these signs, and 
only these, are discovered at the right apex, we cannot feel sure about 
Fig. 178.—This Patient has Solidification at both Apices and Tubercle Bacilli in the 
Sputa. He feels perfectly well. 
the diagnosis until it is confirmed by the appearance of rales, the 
presence of fever, loss of weight, a positive tuberculin reaction (ocular, 
cutaneous or subcutaneous), by x-ray evidence or by the finding of 
tubercle bacilli in the sputum.1 
A sign characteristic of early tuberculous changes in the lung 
and one which I have frequently observed in the lower and relatively 
1 The natural disparity between the two apices is less marked in the supraspin- 
ous fossa behind than over the clavicle in front, and hence pathological dulness at 
the apex is more often demonstrable behind than in front. 300 
PHYSICAL DIAGNOSIS 
sounder lobes of tuberculous lungs is a raising of the pitch of inspira- 
tion,x without any other change in the quality of the breathing or any 
other physical signs. The importance of this sign in the diagnosis 
of early tuberculosis of the lungs was insisted upon by the elder Flint 
in his work on “The Respiratory Organs” (1866), and has more 
recently been mentioned by Norman Bridge. I have referred to this 
sort of breathing above as broncho-vesicular breathing of the first (i.e., 
earliest) type (see p. 157). 
It must never be forgotten that tuberculosis may take root in the 
most finely formed chests and in persons apparently in blooming health. 
The “phthisical chest” and the sallow, emaciated figure of the classical 
descriptions apply only to very advanced cases. Fig. 178 represents 
a patient with moderately advanced signs of phthisis and abundant 
tubercle bacilli in the sputa. He feels perfectly well and is at work. 
On the other hand, a patient with very slight signs may be utterly 
prostrated by the toxaemia of the disease. 
3. Advanced Phthisis 
Characteristic of the more advanced stages of tuberculosis in the 
lungs is the existence of large areas of solidified and retracted lung, 
and, to a lesser extent, the signs of cavity formation. The patients 
are pale, emaciated, and feverish. The signs of solidification have 
already been enumerated in speaking of pneumonia. They are: 
1. Marked dulness, or even flatness,2 with increased sense of 
resistance. 
2. Great increase of voice sounds or of tactile fremitus. 
3. Tubular breathing, sometimes loud, sometimes feeble. 
4. As a rule, coarse rales, due to breaking down of the caseous 
tissue, are also to be heard over the solidified areas. Sometimes these 
rdles are produced within the pleuritic adhesions, which are almost 
invariably present in such cases. If they disappear just after profuse 
expectoration, one may infer that they are produced within the lung. 
Increase in the intensity of the spoken voice, of the whispered 
voice, or of the tactile fremitus may be marked and yet no tubular 
breathing be audible. Each of these signs may exist and be of im- 
portance as signs of solidification without the others. As a rule, it is 
1 “Sharp breathing’' (Turban). 
2 Unless senile emphysema masks it. Fibroid phthisis (vide infra) may show 
no dulness. Remember that gastric tympany may be transmitted to the left lung 
and mask dulness there. BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
301 
true, they are associated and form a very characteristic group, but 
there are many exceptions to this rule. 
In most advanced cases there is some cardiac displacement usually 
by traction of the adjacent lung and usually to the left. 
Gerald Webb has called attention also to displacement of the trachea 
as felt at the suprasternal notch in many advanced or moderately 
advanced cases. 
One of the common variations from the typical group of signs just 
mentioned occurs in the fibroid cases with pleural thickening. In 
Bronchial breath- 
ing, dulness. 
Rales. 
Increased fremitus. 
Increased voice 
sounds. 
R&les. 
Fig. 179.—To Illustrate Progress of Signs in Pulmonary Tuberculosis, 
these the breathing may be everywhere feeble, though the presence of a 
few rdles with dulness and increased voice sounds makes the diagnosis 
obvious. In any almshouse group of old consumptives one finds 
(a) cases in which one hears much that strikes the novice—loud tubular 
breathing, abundant rales, etc., (b) cases where there is very little to 
hear with the stethoscope and that little not in itself distinctive. Some 
of these cases are probably of the peribronchial type recently discussed 
by Clive Riviere and others. 
The tendency of the spinal column to transmit to the sound lung 
sounds produced in an area of solidification immediately adjacent to 
it on the other side, has been already alluded to in the section on 
pneumonia, and what was then said holds good of tuberculous solidifi- 
cation. But since in tuberculosis both lungs are practically always 
involved whether we find signs or not, spinal transmission is not 
important. 302 
PHYSICAL DIAGNOSIS 
Since solidification is usually accompanied by retraction in the 
affected lung in very advanced cases, the chest falls in to a greater 
or less extent over the affected area, and the respiratory excursion is 
much diminished, as shown by ordinary inspection and by the diminu- 
tion or disappearance of the excursion of the diaphragm shadow. 
The intensity of the tubular breathing depends on the proximity of 
the solidified portions to the chest wall and to the large bronchi, as 
well as on the presence or absence of pleuritic thickening. 
It is rare to find a whole lung solidified. The process, beginning at 
the apex or just below, extends down as far as the fourth rib in front, 
i.e., through the upper lobe, in a relatively short time, but below that 
point its progress is comparatively slow and the lower lobes may be 
but little affected up to the time of death. On the relatively sound 
side, the exaggerated (compensatory) resonance may mask the dulness 
of a beginning solidification there, which sooner or later is sure to 
occur. 
About the time that the tuberculous process appears in the pre- 
viously sound lung it is apt to show itself at the apex of the lower lobe 
of the first affected. Consonating relies appear posteriorly along 
the line which the vertebral border of the scapula makes when the 
arm is raised over the shoulder. These points are illustrated in Fig. 
179. 
(a) Cavity Formation 
Cavities of greater or lesser extent are formed in almost every case 
of advanced phthisis, but very seldom do they attain such size as to be 
recognizable during life. Indeed, the diagnosis of cavity in phthisis 
plays a much larger part in the text-books than it does in the practice 
of medicine, since to be recognizable by physical examination, a cavity 
must not only be of considerable size but its walls must be rigid and 
not subject to collapse,1 it must communicate directly with the 
bronchus and be situated near the surface of the lung, and it must not 
be filled up with secretions. It can readily be appreciated that it is 
but seldom that all these conditions are present at once; even then the 
diagnosis of cavity is a difficult one, and I have often known skilled 
observers to be mistaken on this point. 
The signs upon which most reliance is usually placed are: 
(a) Amhporic or cavernous breathing. 
(b) “Cracked-pot resonance” on percussion. 
(c) Coarse, gurgling rales. 
1 Yet not so rigid as to be uninfluenced by the entrance and exit of air. BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
303 
(a) Cavernous or Amphoric Respiration.—When present, this type 
of breathing is almost pathognomonic of a cavity. It is also to be 
heard in pneumothorax, but the latter disease can usually be dis- 
tinguished by the associated physical signs. Cavernous breathing 
differs from bronchial or tubular breathing in that its pitch is lower and 
its quality hollow. The pitch of expiration is even lower than that of 
inspiration. Since a pulmonary cavity is almost always surrounded 
by a layer of solidified lung tissue, we usually hear around the area 
occupied by the cavity a ring of bronchial breathing with which we 
can compare the quality of the cavernous sounds. 
(b) Percussion sometimes enables us to demonstrate a circum- 
scribed area of tympanitic resonance surrounded by marked dulness. 
More often the ‘ ‘ cracked-pot ’ ’ resonance can be elicited by percussing 
over the suspected area while the chest-piece of the stethoscope is 
held close to the patient’s open mouth. 
Cracked-pot resonance is often absent over cavities; rarely occurs 
in any other condition (e.g., in percussing the chest of a healthy, 
crying baby, and occasionally over solidified lung). 
(c) The voice sounds sometimes have a peculiar hollow quality 
(amphoric voice and whisper). 
(d) Cough or the movements of respiration may bring out over the 
suspected area splashing or gurgling sounds, or occasionally a metallic 
tinkle. Flint has also observed a circumscribed bluging of an inter- 
space during cough. Bruce noted a high-pitched sucking sound 
during the inspiration following a hard cough (“rubber-ball sound”). 
Very important in the diagnosis of cavity is the intermittence of 
all above-mentioned signs, which are present only when the cavity 
is comparatively empty, and disappear when it becomes wholly or 
mostly filled with secretions. For this reason, the signs are very apt 
to be absent in the early morning before the patient has expelled the 
accumulated secretions by coughing. 
Wintrich noticed that the note obtained when percussing over a 
pulmonary cavity may change its pitch if the patient opens his mouth. 
Gerhardt observed that the note obtained over a pulmonary cavity 
changes if the patient shifts from an upright to a recumbent position. 
Neither of these points, however, is of any importance in diagnosis. 
The same is true of metamorphosing breathing (see above, p. 158). 
Tuberculous cavities differ from those produced by pulmonary 
abscess or gangrene in that the latter are usually in the lower two- 
thirds of the lung. Bronchiectasis, if considerable in extent, cannot 
be distinguished by physical signs alone from a tuberculous cavity, 304 
PHYSICAL DIAGNOSIS 
but it is more often disseminated (like abscess or gangrene) in the 
lower part of the lungs especially. 
4. Hilus Tuberculosis (Peribronchial infiltration) 
We are indebted to x-ray work for the recent emergence of a type 
distinctly different from the ordinary apical tuberculosis and probably 
much rarer. Starting in the deep areas about the hilus where child- 
hood infection occurs, a fresh active process may arise in adult life 
and spread outwards in any and all directions towards the surface. 
Though mentioned by occasional German writers since 1911, this form 
of tuberculosis has been practically unrecognized until in 1914-1918 
it was popularized by American Army surgeons through the lessons 
learned by them of Col. Bushnell at Washington and in England by 
Clive Riviere. 
Physical Signs 
1. Retraction and dulness at both apices (narrowing of Kronig’s 
isthmus). 
2. In some cases an area of dulness between the spine of the scapula 
and the vertebral column—and corresponding to one or another lung 
root—can be percussed out. A similar area may be found in front. 
3. The respiratory movements of the lung bases may be impaired 
or abolished. 
4. Auscultation shows practically nothing. 
5. X-ray shows increase of all the normal lung markings and an 
extension of these lines towards and to the surface of the lung. The 
more active and extensive the disease, the more mottling and shading 
of normally light areas around and between the bronchial lines. 
All this might mean nothing but healed tuberculosis unless it is 
coupled with 
6. Constitutional symptoms of active infection—fever, prostation, 
digestive disturbance, loss of weight, etc.—which are essential for 
diagnosis. 
Later, rales may appear as the process reaches out to the lung 
surface, but this may never occur. In that case we have nothing but 
the percussion and v-ray signs of a healed hilus process plus constitu- 
tional signs of activity. Unless tubercle bacilli are to be found (and 
this is often impossible) there is no proof that the process is tubercu- 
lous. Statistical evidence, however, shows that such a process so 
situated is almost always tuberculous. BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
305 
The process is often very slow and chronic in its course. Dyspnoea 
and chest pain are prominent. 
From active apical phthisis this process differs by its scarcity or 
absence of rales, and its lack of unilateral predominance in the evidence 
of disease. 
5. Fibroid Phthisis 
This term applies to slow tuberculous or non-tuberculous processes 
with relatively little ulceration and much fibrous thickening especially 
about the bronchi. 
Fig. 180.—Pneumoconiosis with tuberculosis (right apex). 
In a considerable number of cases the physical signs do not differ 
materially from those of the ordinary ulcerating forms of the disease, 
but occasionally when a slow chronic process at the apex of the lung 
results in the falling-away of the parenchyma of the lung so that we 306 
PHYSICAL DIAGNOSIS 
have left a cluster of bronchi matted together by fibrous tissue, the 
percussion note may be noticeably tympanitic; similar tympany may 
be due to emphysema of the lobules surrounding the diseased portion. 
In such cases rales are usually entirely absent; otherwise, the signs 
Fig. i 8i.—Pneumoconiosis. 
do not differ from those of ordinary phthisis, except that falling-in of 
the chest walls over the retracted lung may be more marked. Quite 
often the heart may be drawn toward the affected lobes, e.g., upward 
and to the right in right-sided phthisis at the apex. In two cases of 
fibroid disease at the left base, Flint found the heart beating near the 
lower angle of the left scapula. 
6. Phthisis with Predominant Pleural Thickening 
Tuberculosis in the lung is in certain cases overshadowed by the 
manifestations of the same disease in the pleura, so that the signs are BRONCHITIS, PNEUMONIA, TUBERCULOSIS 
307 
chiefly those of thickened pleura. To this subject I shall return in the 
section on Diseases of the Pleura (see below, p. 343). 
7. “ Emphysematous ” Form of Phthisis 
Tubercle bacilli are not very infrequently found in the sputa of 
cases in which the history and physical signs point to chronic bron- 
Fig. 182.—Miliary tuberculosis. Pleurisy at right base with adhesions to the 
diaphragm. 
chitis with barrel chest. I have seen two cases within a year. Dulness 
is masked by hyperresonance, tubular breathing is absent, and piping 
and babbling rales are scattered throughout both lungs. The emphy- 
sema may be of the senile or small-lunged type, as in one of my recent 
cases (with autopsy), or it may be associated with huge downy lungs 
and the “barrel chest.” Such cases cannot be identified as phthisis 308 
PHYSICAL DIAGNOSIS 
during life unless we make it an invariable rule to examine for tubercle 
bacilli the sputa of every case in which sputa can be obtained, no 
matter what are the physical signs. 
8. Phthisis with Anomalous Distribution of the Lesions 
I have never known tuberculosis to begin at the base of the lung. 
When the process seems to begin in this way, a healed focus is often 
to be found at one apex surrounded by a shell of healthy lung. 
The summit of the axilla should always be carefully examined, as 
tuberculous foci may be so situated as to produce signs only at that 
point. 
Another point often overlooked in physical examination is the 
lingula pulmonalis or tongue-like projection from the anterior margin 
of the left lung overlapping the heart. Tuberculosis is sometimes 
found further advanced at this point than anywhere else. 
As a rule, cases in which signs like those of phthisis are found at the 
base of the lung turn out to be either empyema, bronchiectasis, abscess, 
or organized pneumonia (cirrhosis of the lung). 
9. Acute Pulmonary Tuberculosis 
No one of the three forms in which acute phthisis occurs, viz.» 
(а) Acute tuberculous pneumonia, 
(б) Acute tuberculous bronchitis and peribronchitis, 
(c) Acute miliary tuberculosis, involving the lungs, can be rec- 
ognized by physical examination of the chest. The first form is 
almost invariably mistaken for ordinary croupous pneumonia, until 
the examination of the sputa establishes the correct diagnosis. In 
the other two forms of the disease, the physical signs are simply those 
of general bronchitis. CHAPTER XVIII 
THE BARREL CHEST, ASTHMA, PULMONARY 
SYPHILIS, ETC. 
I. “The Barrel Chest” and Its Relation to Emphysema 
By pathologists cases of emphysema are divided into two groups. 
(1) Large-lunged emphysema, usually associated with chronic 
cough and asthma. 
(2) Small-lunged, or senile, emphysema. 
In both conditions we have a dilatation and finally a breaking 
down of the alveolar walls until the air spaces are become relatively 
large and inelastic. In both forms, the elasticity of the lung is dim- 
inished; but in the large-lunged form we have an increase in the 
volume of the whole organ in addition to the changes just mentioned. 
Whether there is any clinical picture, or any physical signs are 
recognizable as corresponding with these lesions I am quite uncertain. 
Till 1921 I thought I could recognize emphysema. The following 
facts have disillusioned me. In 12 cases diagnosed as emphysema at 
the Massachusetts General Hospital, only 3 showed any emphysema 
post-mortem. On the other hand, of the 153 cases demonstrated 
post-mortem only 7 were recognized in life. The following description 
refers to a clinical entity which we have been accustomed to call 
emphysema of the lungs. I am now comdnced that this clinical 
entity (barrel chest, hyperresonance, feeble prolonged expiration etc.) 
is not always connected with emphysema and that the pathological 
entity “emphysema” is often present without recognisable physical 
signs. I know today nothing about the physical signs of emphysema. 
The thoracic condition about to be described is very possibly a disease 
or disorder of the chest walls themselves—leading to various changes 
in resonance, respiratory murmur, tactile fremitus, etc. As a guess, I 
will call this condition “The Barrel Chest” and describe under this 
provisional term what is usually described as emphysema. In 
typical cases the antero-posterior diameter of the chest is greatly 
increased, the interspaces are widened, and the costal angle is blunted, 
while the angle of Ludwig1 becomes prominent. The shoulders are 
1 Formed by the junction of the manubrium with the second piece of the 
sternum. 
309 310 
PHYSICAL DIAGNOSIS 
high and stooping and the neck is short (see Fig. 183). The patient is 
often considerably cyanosed, and his breathing rapid and difficult. In- 
spiration is short and harsh; expiration prolonged and difficult. The 
ribs move but little, and, owing to the ossification of their cartilages, 
are apt to rise and fall as if made in one piece (en cuirasse). The 
Fig. 183.—Barrel Chest with Chronic Bronchitis. 
working of the auxiliary muscles of respiration is not infrequently 
seen. The diaphragm shadow (kitten’s sign) begins its excursion one 
or two ribs farther down than usual and moves a much shorter distance 
than in normal cases. 
Palpation shows a diminution in the tactile fremitus, throughout 
the affected portions; that is, usually throughout the whole of both 
lungs. Sometimes it is scarcely to be perceived at all. BARREL CHEST, ASTHMA, PULMONARY SYPHILIS, ETC. 
311 
Percussion yields very interesting information. The disease 
manifests itself— 
(а) By hyperresonance on percussion, with a shade of tympanitic 
quality in the note. 
(б) By the extension of the margins of the lung so that they encroach 
upon portions of the chest not ordinarily resonant. 
The degree of hyper-resonance depends considerably upon the 
thickness of the chest walls. The note is most resonant and has most 
of the tympanitic quality when the disease occurs 
in old persons with relatively thin chest walls. The 
encroachment of the hyperresonant areas upon the 
liver and heart is demonstrated by the lowering of 
the line of liver flatness from its ordinary position at 
the sixth rib to a point one or two interspaces farther 
down or even to the costal margin, while the area of 
cardiac dulness may be altogether obliterated. At 
the apices of the lungs resonance may be obtained 
one or two centimetres higher than normally and 
the quality may be markedly tympanitic. In the 
axillae and in the back the pulmonary resonance 
extends down one inch more below its normal position. 
Auscultation shows in uncomplicated cases no very marked modifi- 
cation of the inspiratory murmur, which, however, may be shortened 
and enfeebled. The most striking change is a great prolongation and 
enfeeblement of expiration, with a lowering of its pitch (see Fig. 184). 
Owing to an accompanying bronchitis or asthma, squeaky rales are 
often heard during expiration, but their high pitch is to be distinguished 
from the low pitch of the accompanying respiratory murmur. 
This type of breathing is like bronchial breathing in one respect; 
namely, that in both of them expiration is made prolonged, but 
“barrel chested’’ breathing is feeble and low-pitched, while bronchial 
breathing is intense and high-pitched. At the bases of the lungs the 
respiration is especially feeble and may be altogether replaced by 
cracking rales. 
Fig. 184.—Dia- 
gram to Illustrate 
“Barrel Chested” 
Breathing with 
Musical Expiratory 
Rales. 
(a) Summary 
1. Hyperresonance on percussion. 
2. Feeble breathing with prolonged expiration. 
3. Diminished fremitus and voice sounds. 
4. Encroachment of the resonant areas on the heart and liver 
dulness. 312 
PHYSICAL DIAGNOSIS 
(h) Differential Diagnosis 
(а) The barrel chest and its results may be confounded with 
pneumothorax, since in both conditions hyperresonance and feeble 
breathing are present. But the former is usually bilateral, does not 
displace neighboring organs, and is not often associated with hydro- 
thorax. The barrel chest is usually associated with cardiac weakness 
and so with squeaking or bubbling rales, while in pneumothorax 
breathing is absent or distant amphoric without rhles. 
(б) The signs of aneurism of the aorta pressing on the trachea 
or on a primary bronchus are sometimes overlooked because the fore- 
ground of the clinical picture is occupied by the signs of a coexisting 
barrel chest with bronchitis. The cough and wheezing which the 
presence of the aneurism produces may then be accounted for as part 
of the long-standing bronchitis, and the dulness and thrill over the 
upper sternum to which the aneurism naturally gives rise may be 
masked by extension of lung borders. But the evidence of pressure 
on mediastinal nerves and vessels (aphonia, unequal pulse or pupils, 
etc.), and the presence of a diastolic shock and tracheal tug are usually 
demonstrable; the danger is that we shall forget to look for them. 
(c) The occurrence of a barrel chested form of phthisis I have 
already mentioned in discussing the latter disease (see p. 307). 
2. Barrel chest with Arterio-sclerosis and Asthma 
In the great majority of cases, the barrel chest is associated with 
weak heart, pulmonary edema, and asthmatic paroxysms.. Such 
association is especially frequent in elderly men who have had a winter 
cough for many years and in whom arterio-sclerosis is more or less well 
marked. In such cases the prolonged and feeble expiration is usually 
accompanied by squeaking and groaning sounds, or by moist rales of 
various sizes and in various parts of the chest. When the asthmatic 
element predominates, dry rales are more noticeable, and occur 
chiefly or wholly during expiration, while inspiration is reduced to a 
short, quick gasp. 
3. Interstitial Emphysema 
In rare cases, violent paroxysms of coughing may rupture the walls 
of the alveoli so as to allow the passage of air into the interstitial 
tissue of the lung, whence it may work through so as to manifest 
itself under the skin, giving rise to a peculiar crackling sensation on 
palpation, and to a similar sound on auscultation. In the influenzal BARREL CHEST, ASTHMA, PULMONARY SYPHILIS, ETC. 
313 
pneumonias of 1918 this complication was often seen. The air appeared 
first under the skin of the neck whence it worked down over the chest 
and sometimes over the entire body and face. It is later absorbed 
and does not increase the gravity of the prognosis. 
4. “Complementary Emphysema" 
When extra work is thrown upon one lung by loss of the function 
of the other, as in pleuritic effusion—a considerable stretching of the 
overworked sound lung may take place. The elasticity of the lung is 
not diminished as in emphysema, but is greatly increased. Hence 
the term complementary emphysema should be dropped and the term 
complementary (or compensatory) hyperresonance substituted. 
Like the barrel chest, this condition leads to encroachment of the 
hyperresonant areas upon the neighboring organs (as shown by a reduc- 
tion in the area of dulness corresponding to them), but the respiratory 
murmur is exaggerated and has none of the characteristics of barrel 
chested breathing. 
A word may here be added regarding the condition described by 
West under the name of 
5. Acute Pulmonary Tympanites 
In fevers and other acute debilitating conditions West has observed 
that the lungs may become hyperresonant and somewhat tympanitic 
on percussion, owing, he believes, to a loss of pulmonary elasticity. 
The tympanitic note, often observable around the solidified tissue in 
pneumonia, is to be accounted for, he believes, in the same way. Like 
the shortening of the first heart sound, acute pulmonary tympanites 
points to the weakening of muscle fibre which toxasmia is so apt to 
produce. Apparently the muscle fibres of the. lung suffer like those 
of the heart. 
II. Bronchial Asthma 
i. Primary Spasm of the Bronchi 
During a paroxysm of bronchial asthma our attention is attracted 
even at a distance by the loud, wfeezing, prolonged expiration 
preceded by an abortive gasping inspiration. The breathing is 
labored, much quickened in rate, and cyanosis is very marked. The 
chest is distended and hyper-resonant, the position of the diaphragm 
low and its excursion much limited, and the cardiac and hepatic dul- 314 
PHYSICAL DIAGNOSIS 
ness obliterated by the resonance of the distended lungs. On ausculta- 
tion, practically no respiratory murmur is to be heard despite the 
violent plunging of the chest walls. We hear squeaks, groans, muscular 
rumbles, and a variety of strange sounds, but amid them all practi- 
cally nothing is to be heard of the breath sounds. “The asthmatic 
storm flits about the chest, now here, now there,’’ the rales appearing 
and disappearing. 
At the extreme base of the lungs there may be dulness due to 
atelectasis of the thin pulmonary margins. 
(a) Differential Diagnosis 
True broncho-spasm due to abnormal sensibility to pollens, horse 
or cat hair, food proteins, bacterial proteins and other irritants is to 
be distinguished from 
(a) Mechanical irritation of the bronchi, by broncho-stenosis, 
aneurism or enlarged glands, may set up a spasm of the neighboring 
bronchioles much resembling that of primary bronchial asthma, but 
thorough examination should reveal other evidence of mediastinal 
pressure, and the history of the case is very different from that of 
asthma. 
(b) Spasm of the glottis produces a noisy dyspnoea, but the diffi- 
culty is with inspiration, instead of with expiration, and the crowing 
or barking sound is not like the long wheeze of asthma. No rales are 
to be heard, and the signs in the lungs are those of collapse instead of 
the distention characteristic of asthma. 
(c) The paroxysmal attacks of dyspnoea, which often occur in 
chronic nephritis, chronic bronchitis, arterio-sclerosis, and other dis- 
eases of the heart and kidney, may be entirely indistinguishable from 
primary bronchial asthma but for the evidence of the underlying 
cardiac of renal disease. 
id) Acute dyspnoea in young infants is sometimes due to enlarged 
thymus (thymic asthma). The diagnosis rests on the elimination of 
all other causes for sudden dyspnoea and the presence (sometimes) of 
increased substernal dulness when the child is put face downward. 
III. Syphilis of the Lung 
The diagnosis cannot be made with certainty from the physical 
signs, and rests entirely (in the rare cases in which it is made at all) 
on the history, the evidence of syphilis elsewhere in the body, and the 
result of treatment. Most cases are mistaken for phthisis. BARREL CHEST, ASTHMA, PULMONARY SYPHILIS, ETC. 
315 
Any case supposed to be phthisis, but in which the examination of 
the sputa for tubercle bacilli is repeatedly negative, should be given 
a course of anti-syphilitic treatment. 
The physical signs, as in phthisis, are those of localized bronchitis 
or of solidification, but the lesions are apt to be extensive in one lung 
and absent in the other. Cavities are not formed. 
i. Bronchostenosis 
Aside from foreign bodies, the usual cause of stenosis in the bron- 
chi is a syphilitic cicatrix at or near the tracheal bifurcation. 
Occasionally an aneurism or a neoplasm may exert narrowing and 
irritative pressure from within or from without. 
The physical signs are: (a) Dyspnoea. (b) Stridor or whistling 
sounds over the affected bronchus, (c) Diminution of resonance, 
breath sounds, and voice over the corresponding lung. 
Syphilitic structures sometimes bleed. Foreign bodies, strange to 
say, may get into a bronchus and lie there forgotten for months or 
years till discovered by x-ray in the course of a search for the cause 
of a chronic couch, a bronchiectasis, lung abscess, or chronic broncho- 
pneumonia. 
IV. Bronchiectasis (Bronchial Dilatation) 
(a) The commonest type is that associated with chronic pneu- 
monitis and recurrent attacks of winter cough. Innumerable small 
bronchioles become dilated and the resulting cavities are repeatedly 
infected—usually with influenza bacilli (Wm. H. Smith). The signs 
may be simply those of a chronic bronchitis with or without emphy- 
sema and asthmatic seizures, but the appearance of profuse purulent 
(not muco-purulent) sputa in rounded masses is distinctive. Foci of 
broncho-pneumonia appear from time to time with acute febrile 
attacks. In summer, the cavities are often dry and uninfected. 
(b) When the disease is further advanced and the cavities are 
larger, a sudden change in the patient’s position (or especially hanging 
head downward over the side of the bed) may cause him to raise large 
amounts of sputa (half a pint or more) within a few minutes. This 
sputum is not usually foul and rarely contains blood or elastic fibres. 
Even at this stage there may be no physical signs of localized cavities— 
but only those of the associated bronchitis, usually more marked at 
one base than at the other and associated with signs of partial 
solidification. 316 
PHYSICAL DIAGNOSIS 
(c) In a small number of cases signs of cavity (see above p. 302) 
may be made out. As a rule the disease is widespread, but 44 per 
cent, of cases are confined to one lung, and 25 per cent, to one lobe. 
In about one-third of the cases there is a chronic fibrous type of 
tuberculosis in the background. Emphysema accompanies one- 
fourth of all cases and there were pleural adhesions in 32 of Lord’s 
42 cases. Haemoptysis occurs in nearly one-half. 
Fig. 185.—Bronchiectasis (bilateral). 
Bronchiectasis is distinguished from abscess of the lung because 
the latter shows elastic tissue in the sputa, more often foul; evidence 
of general infection and of local cavity is oftener obtained in abscess. 
The x-ray helps little when the usual causes of abscess (foreign bodies) 
are absent, but one must remember that a foreign body or a cancerous 
nodule blocking a large bronchus may produce bronchiectasis. In 
such cases x-ray is our main reliance. barrel chest, asthma, pulmonary syphilis, etc. 
317 
The disease may cause marked retraction of the chest on the 
affected side, and neighboring organs may be drawn out of place. 
V. Examination of Sputa 
1. Origin 
Probably the majority of all sputa, excepting tobacco juice, come 
from the nasopharynx, and are hawked, not coughed up. It is rarely 
of value to examine such sputa, although influenza bacilli, diphtheria 
bacilli, pneumococci, and other bacteria may be found. 
What we want in most cases is sputa coughed up from the primary 
bronchi or lower down, and the patient should be accordingly instructed. 
Early morning cough is more likely to bring up sputa from the bronchi. 
Young children do not raise sputum, but when it is important to 
obtain it we may insert the forefinger (covered with a bit of cotton) 
into the. pharynx, so as to excite a spasm of coughing. The sputumi is 
deposited on the cotton before the child has time to swallow it, and 
may then be withdrawn and examined. 
2. Quantity 
If the amount expectorated is large (i.e., one-half a pint or more 
in twenty-four hours), we may be dealing with: 
1. Pulmonary oedema (watery, sometimes pink and frothy). 
2. Advanced phthisis (muco-purulent). 
3. Empyema ruptured into a bronchus (pure pus not separated 
into pellets). 
4. Abscess of the lung (foul smelling). Foul odor also occurs 
rarely in 
5. Bronchiectasis (large amount of pure pus in pellets often expecto- 
rated within a few minutes on change of position). 
3. Odor 
Unless retained in a lung cavity (abscess, gangrene) sputum is 
rarely ill-smelling. In gangrene of the lung the breath as well as 
the sputum is horribly offensive, and the odor soon fills the room 
and the house. 
(a) Bloody sputum (haemoptysis) means pure or nearly pure blood 
in considerable quantity, a teaspoonful or more, not mere streaks of 
4. Gross Appearances 318 
PHYSICAL DIAGNOSIS 
blood in muco-purulent sputum, which comes from an irritated throat 
and is of no importance. 
Haemoptysis thus defined is seen chiefly in the following conditions, 
arranged in the order of frequency: 
1. Phthisis. 
2. Pulmonary congestion with infarction ( mitral disease), typhoid 
fever and other causes of peripheral thrombi. 
3. Pneumonia. 
4. After epistaxis. 
5. Abscess of the lung or bronchiectasis. 
6. Cancer of the lung. 
7. Without known cause (“vicarious menstruation,’’etc.). 
Rare causes are parasites (Distomum Westermanni), aortic aneur- 
ism rupturing into an air tube, ulcer of the trachea or bronchi (usually 
syphilitic). 
The cause of haemoptysis can usually be made out by a thorough 
examination of the chest and a study of the other symptoms in the 
case. In phthisis there are often no physical signs in the lungs at the 
period when the bleeding occurs or for some weeks after it. Blood 
coughed up can usually be distinguished from blood vomited (hcemat- 
emesis) by careful questioning and by examining the blood. Blood 
coughed up often contains bubbles of air and is alkaline in reaction, 
while blood from the stomach is usually mixed with food, not frothy, 
and perhaps acid in reaction. 
(b) Pneumonic Sputum.—The color is most characteristic; it is 
either 
(1) Tawny-yellow or fawn-colored (“rusty”), or 
(2) Orange-juice colored (not orange, but pale straw-colored) 
These colors, associated with great tenacity, so that the sputum 
clings to the lips and does not fall from an inverted sputum-cup, are 
almost pathognomonic of pneumonia—though pneumonia often 
occurs without any such sputa. 
(c) Serous sputum, profuse and watery, is characteristic of pul- 
monary oedema. 
(d) Black or gray sputum is due to carbon, dust, or tobacco smoke 
inhaled. 
(ie) Pure pus—not muco-purulent—is oftenest seen in bronchiec- 
tasis, occasionally in empyema breaking through the lung. 
(/) Muco-purulent sputum occurs in many diseases and is character- 
istic of none. BARREL CHEST, ASTHMA, PULMONARY SYPHILIS, ETC. 
319 
5. Microscopic Examination 
Ninety-nine-one-hundredths of all examinations are for the tubercle 
bacillus. Of the many useful methods of staining for this organism 
the following seems to me the best: 
1. Pick out with forceps the most purulent portion of the sputa 
and smear it thinly over a cover glass. All particles thick enough to be 
opaque should be removed from the cover glass before staining. 
2. Dry the preparation held in the fingers over a Bunsen or alcohol 
flame. Then fix it in Cornet’s forceps and pass it three times through 
the flame, sputum side down. 
3. Flood it with carbolic fuchsin,1 and steam it—do not boil it— 
over the flame for about thirty seconds. Be sure to use enough stain 
so that it does not dry on the cover glass. 
4. Wash in water and decolorize for twenty seconds in twenty- 
per-cent. H2S04. 
5. Wash in water and then in ninety-five-per-cent, alcohol for 
thirty seconds or until the color ceases to come out. 
6. Wash in water and cover with Loffler’s methylene blue2 for 
about thirty seconds. 
7. Wash in water, dry on bottling paper, and mount in Canada 
balsam. 
The whole process need not take more than five minutes, and 
every physician should be familiar with it. 
The bacilli are stained red, everything else blue. They should 
be looked for only with an immersion lens (one-twelfth-inch), a wide- 
open diaphragm, and a good white light. In the vast majority of 
cases the bacilli are found, if at all, within a few minutes and in almost 
every field. Occasionally one has to search longer, but it is better 
to search one well-stained preparation thoroughly than to spend the 
time in preparing and examining several. 
The presence of red-stained bacilli in specimens of sputa so prepared 
is practically pathognomonic of tuberculosis. Other acid-resisting 
bacilli occur in the urine, but almost never in the lung. 
The absence of tubercle bacilli after at least six examinations of 
satisfactory specimens3 obtained several days apart makes it very 
1 Carbolic-acid crystals, 5 gm.; fuchsin (saturated alcoholic solution), 10 gm.; 
water, 100 gm. 
2 Saturated alcoholic solution of methylene blue, 30 c.c.; aqueous solution of 
KOH (1 in 10,000), 100 c.c. 
3 A satisfactory specimen is one prepared without any slips in technique from 
purulent sputa obtained by coughing and not by hawking. 320 
PHYSICAL DIAGNOSIS 
unlikely that phthisis is present. One or two negative examinations 
are of no significance. 
Pneumococcic and Influenza Bacilli.—For both these organisms 
Gram's stain is on the whole the best. This is performed as follows: 
1. Prepare a smear as above directed. 
2. Cover it with aniline-oil-gentian-violet solution1 (freshly 
made each week) and heat to steaming point. 
3. Wash in water and cover with IKI solution2 for thirty seconds. 
4. Wash in ninety-five-per-cent, alcohol until the blue color ceases 
to come out. 
Fig. 186.—Pneumococci in Sputum. (W. H. Smith.) (Gram’s stain.) 
5. Counterstain with Bismarck, brown for thirty seconds. 
6. Wash in water and mount in Canada balsam. 
The pneumococcus with this stain comes out blue-black and its 
morphology is well shown (see Fig. 186). The presence of a few 
pneumococci free in the sputum is not of importance. When the 
organisms are very abundant, and especially when many of them 
are contained within leucocytes, a pneumococcus infection is strongly 
suggested, though it may be a pneumococcus bronchitis without 
1 Saturated alcoholic solution of gentian violet, 13 c.c.; aniline water, 84 c.c. 
aniline water is the clear filtrate from the mixture of aniline, 5 parts, with water, 
25 parts. 
2 Iodine, 1 gm.; potassium iodide, 2 gm.; water, 300 c.c. BARREL CHEST, ASTHMA, PULMONARY SYPHILIS, ETC. 
321 
pneumonia. In the earliest stages of an infection, fewer organisms 
are found within leucocytes than is the case later. Obviously one can 
learn only by practice what is meant by “few” or “many” organisms. 
The influenza bacillus is the smallest organism to be found in the 
sputum. In specimens stained by Gram’s method (as above given) 
the influenza bacilli come out as minute, faintly brown-stained points, 
contrasting with the intense blue-black of pneumococci and other 
organisms. Only when present in large numbers both inside and 
outside the leucocytes of the sputa are they diagnostic of active in- 
fluenzal infection, since the organism is a common inhabitant of the 
upper air passages. 
Although other organisms—actinomyces, micrococcus catarrhalis, 
streptococcus, bacillus mucosus capsulatus—are sometimes found in 
sputa, their importance does not justify an account of them here. 
Indications for Sputum Examination.—Any cough with sputa 
lasting more than a week calls for an examination of sputa. In 
doubtful cases of influenza or pneumonia, and in any case in which 
tuberculosis is suspected an examination is imperative. 
When the symptoms or physical signs suggest tuberculosis but 
no sputa can be obtained, it is well to stimulate the bronchial secre- 
tions with io gr. of potassium iodide after meals for a week. A 
way of getting sputa from young children has already been described 
(page 303). CHAPTER XIX 
DISEASES AFFECTING THE PLEURAL CAVITY 
I. Hydrothorax (Pleural Dropsy) 
In cases of nephritis or of cardiac weakness due to vascular or 
cardiac disease a considerable accumulation of serum may take place in 
both pleural cavities. The physical signs are identical with those of 
pleuritic effusion (see below, page 330) except that the latter is almost 
always unilateral, while hydrothorax is usually bilateral. Exceptions 
to this rule occur, however, especially on the right side or in cases in 
which one pleural cavity has been obliterated by fibrous adhesions, 
the results of an earlier pleurisy.1 The fluid obtained by tapping, in 
cases of hydrothorax, is usually considerably lower in specific gravity 
and poorer in albumin than that exuded in pleuritic inflammation. 
The fluid shifts more readily with change of position than is the 
case with many pleuritic effusions, owing to the absence of adhesions 
in hydrothorax. But shifting of fluid can never be relied upon in the 
diagnosis either of hydrothorax or of pleural exudate. 
Friction sounds, of course, do not occur, as the pleural surfaces 
are not inflamed. 
II. Pneumothorax 
Pneumothorax, or the presence of air in the pleural cavity, may 
result from wounds of the chest wall, but in 78 per cent, of cases it 
is a complication of tuberculosis which weakens the lung until by a 
slight cough or even by the movements of ordinary respiration the 
pulmonary pleura is ruptured and air from within the lung leaks into 
the pleural cavity. Biach (quoted by Fussell in Monographic Medi- 
cine, Vol. V, p. 388) found in 914 cases of pneumothorax the following 
causes: 
Pulmonary tuberculosis 715 cases 
Pulmonary gangrene or abscess 75 cases 
Empyema 45 cases 
Bronchiectasis 10 cases 
Pulmonary infarct 4 cases 
Trauma 35 cases 
’ Other known causes 15 cases 
Unknown cause 14 cases 
(78%) 
134 cases (14.6 %) 
92-7% 
29 or 30% 
1 In about two-thirds of all cases hydrothorax is either confined to the right 
side or more abundant in the right than in the left pleura. Only in about 17 
per cent, of cases is it confined to the left side. 
322 DISEASES AFFECTING THE PLEURAL CAVITY 
323 
Hence disease of the lung or wounds cause 97 per cent, of the cases 
of pneumothorax. 
If the opening is of considerable size, and the air is not hindered 
or encapsulated by adhesions, great and sudden dyspnoea with pain 
and profound “shock” may result. But in about two-thirds of all 
cases the onset is insidious, the air enters the pleural cavity gradually, 
the other lung has time to hypertrophy, and the heart and other organs 
become gradually accustomed to their new situations. 
1. Physical Signs 
1. Inspection.—The affected side may lag behind considerably in 
the movements of respiration. In very marked cases it is almost 
motionless and the interspaces are more or less obliterated. The 
diaphragm is much depressed and kitten’s sign absent. In right- 
sided pneumothorax, which is relatively rare, the liver is depressed 
and its edge can be felt below the ribs. 
The heart is displaced as by pleuritic effusion, but usually to a less: 
extent. With left-sided pneumothorax the cardiac impulse may be 
lowered as well as displaced, owing to the descent of the diaphragm. 
2. Palpation.—Fremitus is usually diminished or absent over the 
lower portions of the chest corresponding to the effused air. At the 
summit of the chest over the retracted lung, fremitus is also diminished 
or absent, as a rule (W. B. James). In rare cases when the lung is 
adherent to the chest wall and cannot retract, fremitus is preserved. 
The positions of the heart and liver are among the most impor- 
tant points determined by palpation. Not infrequently no cardiac 
impulse is to be obtained. Sometimes it may be felt to the right 
of the sternum (see Fig. 188) or in the left axilla, but not infrequently 
it is so fixed by pleuropericardial adhesions that it is drawn upward 
toward the retracted lung or remains near its normal situation. 
The liver is greatly depressed in cases of right sided pneumothorax, 
and may be felt as low as the navel. 
3. Percussion.—Loud tympanitic resonance is the rule through- 
out the affected side. Even a small amount of air is sufficient to ren- 
der the whole side tympanitic and often to obscure the dulness which 
the frequently associated pleural effusion would naturally produce. 
Indeed, it is the rule that small effusions are wholly masked by the 
adjacent tympany. 
In no other disease do we get such clear, intense tympanitic 
resonance over the chest. 324 
PHYSICAL DIAGNOSIS 
The only exception to this rule occurs in cases in which the air 
within the chest is under great tension, making the chest walls so 
taut that, like an over-stretched drum, they cannot vibrate properly. 
Under these conditions the percussion note becomes muffled, at times 
almost dull. 
Areas of dulness corresponding to the displaced organs (heart 
or liver) may sometimes be percussed out. 
4. Auscultation.—Respiration and voice sounds are usually in- 
audible in the lower portions of the chest. At the top of the chest, 
and rarely in the lower parts, a faint amphoric or metallic breathing 
may be heard, but as a rule the amphoric quality is brought out much 
better by cough which is followed by a ringing after-echo. In W. B. 
James’s2 ninety cases the breathing was amphoric in thirty-one, 
diminished or absent in fifty-three, bronchial in six. Or the air in 
the pleura may be set to vibrating and made to give forth its char- 
acteristic, hollow, ringing sound if a piece of metal (e.g., a coin) be 
placed on the back of the chest and struck with another coin, while 
we listen with the stethoscope over the front of the chest opposite the 
point where the coin is. In the combined statistics of Emerson1 and 
James2 the signs were present in forty-five out of sixty cases, or seventy- 
five percent. 
The clear ringing sound heard in this way is quite different from 
the dull chink obtainable over sound lung tissue. 
The “falling-drop sound” or “metallic tinkle,” (see above, p. 170), 
was heard in thirty out of thirty-five of James’s cases. 
On the sound side the breath sounds are exaggerated. At the 
top of the affected side over the collapsed lung the breathing is bron- 
chial and rales are occasionally heard. 
In about 80 per cent, of cases pneumothorax is complicated by 
an effusion of fluid in the affected pleural cavity and we have then 
the signs of 
III. Pneumohydrothorax or Pneumopyothorax 
When both fluid and air are contained in the pleural cavity, the 
patient may himself be able to hear the splashing sounds which 
the movements of his own body produce. These are more readily 
appreciated if the observer puts his ear against the patient’s chest 
and then shakes him briskly. Splashing sounds heard within the 
chest are absolutely pathognomonic and point only to the combina- 
1 Emerson: Pneumothorax, Johns Hopkins Hospital Reports, 1903, Vol. XI. 
2 Osier’s Modern Medicine, Vol. Ill, p. 881. DISEASES AFFECTING THE PLEURAL CAVITY 
325 
tion of fluid and air within the pleural cavity. One must distinguish 
them, however, from similar sounds produced in the stomach. By 
observing the position of maximum intensity of the sounds, this 
distinction may be easily made. Unfortunately the critical condition 
of the patient may make it impossible to try succussion, as in the acute 
cases with great shock it is dangerous to move patients at all. 
The movements of breathing or coughing may bring out a ‘ ‘ metallic 
tinkle” (see above, p. 170). At the base of the chest, over an area 
corresponding to the position of the fluid, an area of dulness may be 
Retracted Lung 
Fluid 
Displaced Heart 
Liver 
Fig. 187.—Left Pneumohydrothorax Seen from Behind. Note the horizontal line at 
the surface of the fluid and the retracted lung just above the inner half of this line. The 
heart is displaced to the right. Compare Fig. 188. (From v. Ziemssen’s Atlas.) 
marked out by percussion, and this area shifts markedly with change 
of position. The shifting dulness of pneumohydrothorax is strongly 
in contrast with the difficulty of obtaining any such shift in ordinary 
pleuritic effusion or in hydrothorax without air. 
(The distinction between “ open pneumothorax, ” in which the rent 
in the lung through which the air escaped in the pleura remains open, 
and “ closed pneumothorax, ” in which the rent has become obliterated— 
is one which cannot be established by physical signs alone. It is 
often said that amphoric breathing, and especially an amphoric ring 
to the voice and cough sounds, denote an open pneumothorax, but 326 
PHYSICAL DIAGNOSIS 
post-mortem evidence does not bear this out. Practically, an open 
pneumothorax is one in which the amount of effused air increases 
and closed pneumothorax is one in which the physical signs remain 
stationary.) 
1. Differential Diagnosis 
The distinction between pneumothorax and emphysema has already 
been discussed. 
(a) When the air in the pleural sac is under such tension that the 
percussion note is dull, the physical signs may simulate pleuritic 
effusion, but real flatness, such as characterizes effusion, has not, so 
Contracted 
lung. 
Tympany, 
breathing 
and voice 
absent or 
faint 
amphoric. 
A ir = 
Displaced 
heart. 1 
Dulness, 
| shifting 
with 
change of 
, position. 
Fluid = 
Liver. 
Fig. 188.—Left Pneumoserothorax with Displaced Heart 
far as I know, been recorded in pneumothorax, and the sense of 
resistance on percussing is much greater over fluid than over air. In 
case of doubt puncture is decisive. 
(b) Acute pneumothorax, coming on as it does with symptoms of 
collapse and great shock may be mistaken for angina pectoris, cardiac 
failure, embolism of the pulmonary artery, or acute pulmonary tym- 
panites (see above, p. 313). 
From all these it can be distinguished by the presence of a displaced 
heart and of amphoric or metallic sounds which are never to be ob- 
tained in the other affections named. 
(c) Hernia of the intestine through the diaphragm (see Fig. 189) 
due to great weakening of the diaphragmatic muscular fibres, allows 
the intestines to encroach upon the thoracic cavity and simulate 
pneumothorax very closely. The history and course of the case, the DISEASES AFFECTING THE PLEURAL CAVITY 
327 
abdominal pain, and vomiting, generally suffice to distinguish the 
condition. The peristalsis of the intestine may go on even in 
the thorax, and gurgling metallic sounds corresponding to it and unlike 
anything produced in the thorax itself may be audible. 
The distinction between open and closed pneumothorax, to which 
I have already alluded, is far less important than the presence or 
absence of 
(a) Pulmonary tuberculosis. 
(b) Encapsulating adhesions in which the air is confined to a 
circumscribed area. 
Fig. 189.—Diaphragmatic Hernia. The outline of the displaced diaphragm visible 
below the left clavicle. Heart displaced to right of sternum. (From v. Ziemssen’s 
Atlas.) 
(a) The examination of the sputa and of the compressed lung may 
yield evidence regarding tuberculosis. On the sound side the com- 
pensatory hypertrophy covers up foci of dulness or rales so that it is 
difficult to make out much. 
(b) Encapsulated pneumothorax gives us practically all the signs 
of a phthisical cavity, from which it is distinguished by the fact that 
with a cavity the nutrition of the patient is almost always much worse. 
Encapsulated pneumothorax needs no treatment. Hence the im- 
portance of distinguishing it from the non-encapsulated form of 
the disease, in which treatment is essential. 328 
PHYSICAL DIAGNOSIS 
IV. Pleurisy 
Clinically, we deal with three types: 
(a) Dry or plastic pleurisy. 
(b) Pleuritic effusion, sero-fibrinous or purulent. 
(c) Pleural thickening (chronic pleurisy). 
1. Dry or Plastic Pleurisy 
Doubtless most cases run their course without being recognized 
The frequency with which pleuritic adhesions are found post-mortem 
would seem to indicate this. 
It is usually the characteristic stitch in the side which suggests 
physical examination. The pain and the physi- 
cal signs resulting from the fibrinous exudation 
are usually situated at the bottom of the axilla 
where the diaphragmatic and costal layers o: 
the pleura are in close apposition. Doubtless 
the pleuritic inflammation is not by any 
means limited to this spot, but it is here that 
the two layers of the pleura make the largest 
excursion while in apposition with each other. 
In the vast majority of cases, then, the physica 
signs are situated at the spot indicated in 
Fig. 190. 
Occasionally pleuritic friction is to be heard 
in the precordial region, and after the absorp- 
tion of a pleuritic effusion evidences of fibrinous 
exudation in the upper parts of the chest are 
sometimes demonstrable. Most rarely of all, 
evidence of plastic pleurisy may be found at 
the apex of the lung in connection with early 
phthisis. In diaphragmatic pleurisy, i.e., when 
the fibrinous exudation is especially marked 
upon the diaphragmatic pleura, friction sounds 
may be heard over the region of the attach- 
ment of the diaphragm in front and behind as 
well as in the axillae. Hiccup often occurs and gives exquisite pain. 
Our diagnosis is based upon a single physical sign, pleuritic friction. 
The nature of this sound has already been described (see above, p. 166), 
and I will here only recapitulate what was there said. During the 
first few deep breaths one hears, while listening over the painful area, a 
Fig. 190.—Showing the 
Point at which Pleural 
Friction is most Often 
Heard. DISEASES AFFECTING THE PLEURAL CAVITY 
329 
grating or nibbing sound usually somewhat jerky and interrupted, 
most marked at the latter part of inspiration, but often audible through- 
out the whole respiratory act. After a few breaths it often disappears, 
but will usually reappear if the patient lies for a short time upon the 
affected side, and then sits up and breathes deeply. In marked cases 
the rubbing of the inflamed pleural surfaces may be felt as well as heard, 
and it is not very rare for the patient to be able to feel and hear it 
himself. Pleuritic friction may be present and loud without giving 
rise to any pain. On the other hand, the pain may be intense, and yet 
the friction-rub barely audible. When heard at the summit of the 
chest, as in cases of incipient phthisis, pleural friction produces only a 
faint grazing sound, much more delicate and elusive than the sounds 
produced at the base of the chest. 
Occasionally the distinctive rubbing or grating sounds are more 
or less commingled with or replaced by crackling sounds indistin- 
guishable from the drier varieties of rales. It is now, I think, gener- 
ally believed that such sounds may originate in the pleura as well as 
within the lung. The greatest care should be taken to prevent any 
shifting or slipping of the stethoscope upon the surface of the chest, 
as by such means sounds exactly like those of pleural friction may be 
transmitted to the ear. In case of doubt one should always wet the 
skin and the stethoscope so that the latter cannot slip. 
Muscle sounds are sometimes taken for pleural friction, but they 
are bilateral, usually low-pitched, sound less superficial than pleu- 
ral friction, and are not increased by pressure. When listening for 
friction at the base of the left axilla, I have once or twice been puzzled 
by some low-pitched rumbling sounds occurring at the end of inspira- 
tion, and due (as afterward appeared) to gas in the stomach which 
shifted its position with each descent of the diaphragm. 
The transmitted shoulder-joint crepitus, audible in the back when 
the patient’s arms are crossed in front (F. T. Lord), has been described 
on p. 151. 
In children, friction sounds and pleuritic pain are much less com- 
mon than in adults, and the signs first recognizable are those of effusion. 
In adults the presence of a very thick layer of fat may make it difficult 
or impossible to feel or hear pleural friction. 
The breath sounds over the affected area are usually absent or 
greatly diminished, owing to the restraint in the respiratory move- 
ments due to pain. Not infrequently pleuritic friction may be heard 
altogether below the level of the lung. 330 
PHYSICAL DIAGNOSIS 
2. Pleuritic Effusion 
Many cases are latent, and the patients consult the physician on 
account of slight cough, weakness, or gastric trouble, so that the 
effusion is first discovered in the course of routine physical examina- 
tion. Since it is usually the results of percussion which first put us on 
the right track, I shall take up first. 
(a) Percussion 
i. A small effusion first shows as an area of dulness 
(a) Just below the angle of the scapula. 
(b) In the left axilla between the fifth and the eighth rib. 
(c) Obliterating Traube’s semilunar area of tympany; or 
(d) In the right front near the angle made by the cardiac and 
hepatic lines of dulness (see Fig. 191). 
Area of cardiac 
dulness. 
Area of dulness 
due to small 
pleural effusion. 
Fig. 191.—Small Pleural Effusion Accumulating (in part) near the Right Border 
of the Heart. 
In the routine percussion of the chest, therefore, one should never 
leave out these areas. A small effusion is most easily detected in 
children or in adults with thin chest walls, provided our percussion is 
not too heavy. An effusion amounting to a pint should always be 
recognizable, and smaller amounts have frequently been diagnosed 
and proved by puncture. 
The amount of a pleuritic effusion is roughly proportional to the 
area of dulness on percussion, but not accurately. It is very common 
to find on puncture an amount of fluid much greater than could have 
been suspected from the percussion outlines; on the other hand the 
dulness may be extensive and intense on account of great inflamma- DISEASES AFFECTING THE PLEURAL CAVITY 
331 
tory thickening of the costal pleura, by the accumulation of layer after 
layer of fibrinous exudate and its organization into fibrous plates, 
while very little fluid remains within. 
The amount of dulness depends also upon the thickness and elas- 
ticity of the chest wall and the degree of collapse of the lung within. 
2. Large Effusions.—When the amount of fluid is large, the dul- 
ness may extend throughout the whole of one side of the chest with 
the exception of a small area above the clavicle or over the primary 
bronchus in front. This area gives a high-pitched tympanitic note, 
provided the bronchi remain open, as they almost always do. This 
tympany is high-pitched and sometimes astonishingly clear. I re- 
cently saw a case in which the note above the clavicle was almost 
indistinguishable, with the eyes shut, from that obtained in the epi- 
gastrium. Occasionally “cracked-pot” resonance may be obtained 
in the tympanitic area. 
Normal resonance 
and vesicular 
breathing. 
Zone of condensed 
lung above the 
fluid. 
Tympany, voice and 
fremitus increased. 
Exaggerated (com- 
pensatory) breath- 
ing and reso- 
nance. 
Flatness, no breath- 
ing, voice sounds, 
or fremitus. 
Fig. 192.—Diagram to Illustrate Physical Signs in Moderate-sized Effusion in the 
Left Pleura. 
The pitch changes if the patient opens and closes his mouth while 
we percuss (“William’s tracheal tone”). 
The dulness over the lower portions of a large effusion is usually 
very marked, and the percussing finger feels a greatly increased resis- 
tance to its blows when compared with the elastic rebound of the 
sound side. 
3. Moderate Effusions.—Three zones of resonance can often be 
mapped out in the back: at the base dulness or flatness, above that a 
zone of mingled dulness and tympany, and at the top normal reso- 
nance. The lowest zone corresponds to the fluid, the middle zone to 332 
PHYSICAL DIAGNOSIS 
the condensed lung immediately above it, and the top zone to the 
relatively unaffected part of the lung (see Fig. 192). Not infrequently 
there is no middle zone but simply dulness below and resonance above, 
as is usually the case in the axilla and front. 
The position of the effusion depends only in part upon the influence 
of gravity, and is greatly influenced by capillarity and the degree of 
retraction of the lungs. Consequently the surface of the fluid is 
hardly ever horizontal. With the patient in an upright position it 
usually reaches a higher level in the axilla than in the back (see Fig. 
193). Near the spine and near the sternum (in right-sided effusions) 
the line corresponding to the level of the fluid may rise sharply. 
Fig. 193.—Left Pleural Effusion. Heart displaced to right of sternum. Note that 
the surface of the fluid slopes outward and upward from the median line. (From v. 
Ziemssen’s Atlas.) 
There is rarely any information of value to be obtained by trying 
to elicit a change in the percussion note with change in the patient’s 
position. First, because in the normal chest there is some change in 
the percussion note if we try it first with the patient upright and then 
bending forward. Next, because even in known pleural effusion it has 
been found that with change in the position of the patient the level of 
the fluid sometimes changes very slowly and irregularly, and some 
times does not change at all. If, for purposes of thorough examina- DISEASES AFFECTING THE PLEURAL CAVITY 
333 
tion, we raise to a sitting posture a patient who has been for some days 
or weeks in bed, we should never begin the examination at once, since 
it may take some minutes for the lungs and the fluid to accommodate 
themselves to the new position. It is well also to get the patient to 
cough and to take a number of full breaths before the examination is 
begun. 
At the base of the sound lung behind the sound side a triangular 
patch of dulness can be percussed out in most cases of pleural effu- 
sion. (Grocco’s (Koranyi’s) Sign—The Paravertebral Triangle.) 
The voice sound and breath sounds are diminished over this triangular 
area. 
I have not found this sign of much value in diagnosis. One can 
rarely percuss out the triangular dull area with any confidence unless 
one previously knows that there is an effusion on the other side. 
When the fluid is absorbed or removed by tapping, one would 
expect an immediate return of the percussion resonance. But in 
fact the resonance returns very slowly and is wholly unreliable as a 
test of the amount of absorption which has occurred. Thickened 
pleura and atelectatic lung may abolish resonance long after the fluid 
is all gone. We depend here far more upon the evidence obtained 
by auscultation and palpation and on the general condition of the 
patient. 
To determine the returning elasticity of the lung and the degree of 
movability of its lower border, percussion is very useful during the 
stage of absorption. After percussing out the lower border of pul- 
monary resonance in the back, the patient is directed to take a long 
breath and hold it. If the lung expands, the area of percussion reso- 
nance will increase downward. 
Percussion aids us in determining whether neighboring organs are 
displaced by the pressure of the accumulated fluid. The liver is often 
pushed down, the spleen very rarely. Dislocation of the heart is one of 
the most important of all the signs of pleural effusion, and is often the 
crucial point in differential diagnosis. It is a very striking and at first 
surprising fact that a left-sided effusion displaces the heart far more 
than a right-sided effusion of the same size. Small or moderate right- 
sided effusions often do not displace the heart at all. 
With left-sided effusions, unless very small, we find the area of 
cardiac dulness shifted toward the right and often projecting beyond 
the right edge of the sternum (see Fig. 193). (Inspection and palpa- 
tion often give us even more valuable information on this point. See 
below, p. 337.) We must be careful to distinguish such an area of 334 
PHYSICAL DIAGNOSIS 
dulness at the right sternal margin from that which may be produced 
in right-sided effusions by the fluid itself (see above). 
As mentioned above, a right pleural effusion may very early show 
itself as an area of dulness along the right sternal margin. Light 
percussion will usually demonstrate that this dulness is continuous 
with a narrow strip of flatness at the base of the axilla (ninth and 
tenth ribs). Such an effusion is late in creeping up the axilla. It 
appears first and disappars first along the right margin of the sternum. 
On the sound side the percussion resonance is often increased, 
owing to compensatory hypertrophy of the sound lung; the diaphragm 
is pushed down and the borders of the heart or of the liver may be 
encroached upon. When the hyperresonance of the sound side is 
present, it should warn us to percuss lightly over the effusion, else we 
may bring out the resonance of the distended lung. 
Summary of Percussion Signs.—(i) Flatness corresponding roughly 
to the position of the fluid. 
(2) Tympany above the level of the fluid over the condensed lung. 
(3) The level of the fluid is almost never horizontal. 
(4) Shifting of the fluid with change of position is rare, slow, and 
has little or no importance in diagnosis. 
Exceptions and Possible Errors.—(a) Great muscular pain and 
spasm may produce an area of dulness which simulates that of pleural 
effusions, especially as the auscultatory signs may be equally mislead- 
ing. A hypodermic of morphine will dispel the dulness along with the 
pain if it is due to muscular cramp. 
(b) Abdominal tumors, ascites, enlarged liver or spleen pushing up 
the diaphragm into the chest may produce all the signs of pleural 
effusion. Study of the belly and A-ray evidence on the position of 
the diaphragm should set us right. 
(c) If the lung on the affected side fails to retract (owing to em- 
physema or adhesions to the chest wall), the area of dulness and its 
intensity will be much diminished. 
(d) It must be remembered that dulness in Traube’s space is sel- 
dom of significance since it may be due to solidification of the lung, to 
situs inversus, to tumors, or to overfilling of the stomach and intestine 
with food, as well as to pleural effusion; also that the size of the tym- 
panitic space varies greatly in health. 
(e) Rarely, percussion may be tympanitic over an effusion at the 
left base owing to distention of the stomach or colon. 
(/) The diagnosis between fluid and thickened pleura will be 
considered later. DISEASES AFFECTING THE PLEURAL CAVITY 
335 
(b) Auscultation 
The auscultatory phenomena vary greatly in different cases, and 
in the same case at different times, because the essential conditions 
are subject to similar variations. Whatever sounds are produced in the 
lungs or in the bronchi may be heard over the fluid unless interfered 
with by inflammatory thickening of the costal pleura. Fluid transmits 
sounds well, but there may be no breath sounds produced and hence none 
audible over the fluid. Or tubular sounds only may be produced 
because only the bronchi remain open, the rest of the lung being 
collapsed. 
Or again, if rales or friction sounds are produced in the lung, they, 
too, may be transmitted to the fluid and may (alas!) deter the timid 
“observer” from tapping. 
In about two-thirds of all large effusions no breathing at all is 
audible over the area of flatness on percussion. In the remaining 
third, and especially in children, tubular breathing, sometimes feeble, 
sometimes very intense, is to be heard. 
In moderate effusions there are often three zones in the back. At 
the bottom we hear nothing, in the middle zone distant bronchial or 
broncho-vesicular breathing, while at the summit of the chest the 
breathing is normal. 
The voice sounds correspond. When breath sounds are absent, 
the voice sounds are likewise absent. When the breathing is tubular, 
the voice, and especially the whisper, is also tubular and intensified. 
That is, whenever the bronchi are open, the lung retracted, and the chest 
walls thin, the breathing, voice, and whisper will correspond to the tracheal 
sounds. Since children have especially thin chest walls, these bron- 
chial sounds are especially frequent and intense in children. 
Near the angle of the scapula and in a corresponding position in 
front, the sound of the spoken voice may have a peculiar high-pitched, 
nasal twang, to which the term egophony is applied. This sign has no 
importance in diagnosis, since it is not constant, and not peculiar to 
fluid accumulations. 
Rales are rarely produced in the retracted lung, and so are rarely 
to be heard over the fluid. 
All these sounds may be diminished or abolished if the costal pleura 
is greatly thickened. 
The influence of cough upon the lung, and so upon the sounds pro- 
duced in it and transmitted through the fluid, may be very great and 
very puzzling. Rales may appear or disappear, breathing change 336 
PHYSICAL DIAGNOSIS 
in quality or intensity. Hence in the differential diagnosis of difficult 
cases the patient should always be made to cough and then breathe 
deeply before the examination is completed. 
In very large effusions, when only the primary bronchi are open, 
there may be signs like those of pulmonary cavity at the site of the 
bronchi in front or behind (amphoric breathing, large metallic rales, 
etc.). Over the sound lung the breathing is exaggerated and extends 
unusually far down in the back and axilla, owing to hypertrophy of the 
lung. 
The heart sounds may be absent at the apex owing to dislocation 
of the heart. In left-sided effusions, the apex sounds are often loudest 
near the ensiform cartilage or beyond the right margin of the sternum. 
Right-sided effusions have much less effect upon the heart, but occa- 
sionally we find the heart sounds loudest at the left of the nipple or in 
the axilla. 
Since most cases of pleural effusion are due to tuberculosis, we 
should never omit to search for evidences of this disease at the apex of 
the lung on the sound side, since experience has shown that phthisis is 
more apt to begin here than on the side of the effusion. 
Summary of Auscultatory Signs 
(1) In most cases, voice and breath sounds are absent or very 
feeble over the area occupied by the fluid. 
(2) In a minority of the cases, the breathing and voice sounds may 
be tubular and intensified, especially in children. 
(3) Over the condensed lung at the summit of the chest, the breath- 
ing is bronchial or broncho-vesicular, according to the degree of con- 
densation. If the amount of fluid is small, the layer of condensed 
lung occupies the middle zone of the chest and the breathing is normal 
at the top of the chest. 
(4) Rales and friction sounds are rarely heard over fluid. 
(5) On the sound side the breathing is exaggerated. 
(6) The heart sounds may be absent at the apex and present in the 
left axilla or to the right of the sternum owing to dislocation of the 
heart. 
(c) Inspection and Palpation 
The most important information given us by inspection and palpa- 
tion relates to the displacement of various organs by the pressure of the 
accumulated fluid. In left-sided pleuritic effusions the heart is usually DISEASES AFFECTING THE PLEURAL CAVITY 
337 
displaced considerably toward the right, even when the level of the 
fluid reaches no higher than the sixth rib in the nipple line. The 
impulse is then to be seen and felt to the right of the sternum, some- 
where between the third and the seventh rib, when a large amount of 
fluid is present. With smaller effusions one may find the apex beat 
lifting the sternum or close to its left border. The position of the heart 
may be confirmed by percussion. 
The spleen is scarcely ever displaced. 
Right-sided effusions are far less likely to displace the heart, and it 
is only when a large amount of fluid is present that the apex of the 
heart is pushed outward beyond the nipple. Moderate right-sided 
effusions often produce no dislocation of the heart whatever. The 
liver may be considerably pushed down by a right-sided pleuritic effu- 
sion, and its edge may be palpable several inches below the costal 
margin. Its upper margin cannot be determined by percussion, as it 
merges into the flatness produced by the fluid accumulation above it. 
Tactile fremitus is almost invariably absent or greatly diminished 
over the areas corresponding to the fluid; just above the level of the 
fluid it is often increased. Spasm of the intercostal muscles near the 
fluid can often be felt and may account for part of the percussion 
dulness. 
Occasionally a slight fulness of the affected side may be recognized 
by inspection, and the interspaces may be less readily visible than upon 
the sound side. Bulging of the interspaces I have never observed. 
When the accumulation of fluid is large the respiratory movements 
upon the affected side are somewhat diminished,1 the shoulder is raised, 
and the spine curved toward the affected side. The diaphragm is 
depressed, and Litteh’s sign therefore absent. 
There are no reliable physical signs for distinguishing purulent 
from serous effusions. The whispered voice may be transmitted 
through either pus or serum. But we know that in children two-thirds 
of all effusions are purulent (pneumococcus or streptococcus infection), 
while in adults three-fourths of them are serous (tuberculosis of the 
pleura). 
Physical Signs During Absorption of Pleural Effusions 
When the fluid begins to disappear, either spontaneously or as a 
result of treatment, the dulness very gradually disappears and the 
11 have purposely made but little of the changes in the shape of the chest 
produced by pleuritic effusions, as it has seemed to me that by far too much stress 
has usually been laid upon such signs. 338 
PHYSICAL DIAGNOSIS 
breath sounds, voice sounds, and fremitus reappear. In case the 
heart has been dislocated, its return to its normal position is often much 
slower than one would anticipate, and indeed all the physical signs are 
disappointingly slow to clear up even after tapping. Pleural friction 
appears when the roughened pleural surfaces, which have been held 
apart by the fluid, are allowed by the disappearance of the latter 
to come into apposition again. Owing to pulmonary atelectasis and 
Fig. 194.—Interlobar Empyema. A, A = Exudate. B = Heart. (Englebach and 
Carman.) 
permanent thickening of the pleura, considerable dulness often remains 
for weeks after the fluid has been absorbed. One need not be dis- 
appointed or believe that the fluid has again accumulated if one 
finds but little change in the physical signs during the first week 
after tapping. A second puncture rarely shows fluid. 
(d) Interlobar Empyema 
In recent years the frequency and importance of empyema limited 
to an interlobar fissure has become impressed upon many clinicians. DISEASES AFFECTING THE PLEURAL CAVITY 
339 
One sees both the post-pneumonic and the tuberculous types, but the 
former is vastly the commoner. In most of the cases so far reported the 
pus has been demonstrated in the fissure which runs along the vertebral 
border of the scapula when that bone is pulled as far forward as possible 
by crossing the arms in front (see Fig. 195). 
This is a region seldom carefully examined. 
In the strip here indicated one finds flatness on percussion with 
(usually) diminished fremitus, and feeble or absent breath-sounds. 
Compressed areas of 
lung, showing in- 
tense tubular 
breathing and 
whisper with dul- 
ness. 
Flatness. 
Diminished or absent 
breathing. 
Diminished or absent 
voice. 
Fig. 195.—Signs in Interlobar Empyema. 
A’-ray examination may bring out in sharp relief a shadow corre- 
sponding to this area and sharply contrasted with the relatively 
normal lung above and below it (see Fig. 194). 
The exploring needle often fails to find the pus, but the search 
should not he given up (if the physical signs are clear) until a rib has 
been excised and the region thoroughly explored under complete ances- 
thesia. Empyema encysted between the diaphragm and lung, between 
the lung and chest wall, and along the right or left cardiac borders are 
not uncommon but can rarely be diagnosed. 
3. Pleural Thickening 
In persons who have previously suffered from pleurisy with 
effusion, and in many who have never to their knowledge had any 
such trouble, a considerable thickening of the pleural membrane with 
adhesion of the costal and visceral layers may be manifested by the 
following signs: 340 
PHYSICAL DIAGNOSIS 
(1) Dulness on percussion, sometimes slight, sometimes marked. 
(2) Diminished vesicular respiration. 
(3) Voice sounds and tactile fremitus diminished or increased. 
(4) Absence of Litten’s phenomenon and diminution in the normal 
respiratory excursion of the chest. 
Fig. 196.—Encapsulated empyema at right base. 
These signs are most apt to be found at the base of the lung behind 
and in the axilla. Occasionally a similar thickening may be demon- 
strated throughout the whole extent of the pleura, and the lung 
failing to expand, the chest may fall in as a result of atmospheric 
pressure. 
The ribs approximate and may overlap, the spine becomes curved, 
the shoulder lowered, the scapula prominent, and the whole side 
shrunken. The heart mav be drawn toward the affected side. DISEASES AFFECTING THE PLEURAL CAVITY 
341 
In the diagnosis of pleural thickening, Rosenbach’s “palpatory 
puncture” is sometimes our only resource. Under antiseptic pre- 
cautions a hollow needle is pushed between the ribs and into the 
pleural cavity. As the needle forces its way through the tough fibrous, 
or perhaps calcified, pleura, the degree and kind of resistance are very 
enlightening. Again, the amount of mobility of the point after the 
chest wall has been pierced tells us whether the needle is free in a 
cavity, entangled in a nest of adhesions, or fixed in a solid “carnified” 
lung. There is no danger if the needle is sterile. 
Diffuse neoplasm spreading over the whole pleura may give all 
the signs of thickened pleura, though usually with rapidly recurring 
effusion. This disease may be mistaken for chronic pleurisy even 
post mortem unless histological examination is expert. 
Haemorrhagic effusions, pain after tapping, and progressive ca- 
chexia may put us on the track of the diagnosis. Occasionally metas- 
tatic glands are found in the brain, neck or axillae. This disease must 
always be remembered in the differential diagnosis of thickened 
pleura. 
4. Encapsulated Pleural Efusion 
Small accumulations of serum or pus may be walled off by adhe- 
sions so that the fluid does not gravitate to the lowest part of the 
pleural cavity or spread itself laterally as it would if free. Such 
localized effusions are not uncommon. Thirty-one per cent of thirty- 
eight empyemata autopsied at the Massachusetts General Hospital 
were encapsulated. They are most apt to be found in the lower 
axillary regions or behind—sometimes between the base of the lung 
and the diaphragm, and more often between the lobes of one of the 
lungs or higher up. The position of the fluid may be almost vertical, 
lying in a shallow pool along the axillary ribs or near the spinal column. 
I have twice seen an encapsulated purulent effusion so close to the 
left margin of the heart that the diagnosis of pericardial effusion was 
made. 
The diagnosis of encapsulated pleural effusion is a difficult one and 
often times cannot be made except by puncture. The signs are those 
of fluid in the pleura, but anomalously placed. Even puncture may 
fail to clear the difficulty, since the needle may pass entirely through 
the pouch of fluid and into some structure behind so that no fluid is 
obtained.- 342 
PHYSICAL DIAGNOSIS 
5. Pulsating Pleurisy 
Under conditions not altogether understood, the movements trans- 
mitted by the heart to pleural effusion (usuallypurulent) maybe visible 
externally as a circumscribed pulsating swelling near the precordial 
region, or as a diffuse undulation of a considerable portion of the 
chest wall. Sometimes this pulsation is visible because the fluid has 
worked its way out through the thoracic wall and is covered only by 
the skin and subcutaneous tissues, but occasionally pulsation in a 
pleural effusion becomes visible, although no such perforation of the 
chest wall has occurred. 
The condition is a rare one (only 12 cases are on record), and is of 
importance only because it may be mistaken for an aneurism, from 
which, however, it should be readily distinguished by the history, the 
absence of a palpable thrill or diastolic shock and by the evidence of 
fluid in the pleura. 
6. Differential Diagnosis of Pleuritic Effusion 
The following conditions are not infrequently mistaken for pleuritic 
effusion: 
(1) Croupous pneumonia with occlusion of the bronchi. 
(2) Pleural thickening with pulmonary atelectasis. 
(3) Subdiaphragmatic abscess of the liver. 
In croupous pneumonia with plugging of the bronchi one may 
have present all the physical signs of pleuritic effusion except displace- 
ment of the neighboring organs. The presence or absence of such 
displacement, together with the history, symptoms, and course of the 
case, is therefore our mainstay in distinguishing the two diseases. 
From ordinary croupous pneumonia (without occlusion of the 
bronchi) pleuritic effusion differs in that it produces a greater degree of 
dulness ' and a diminution of the spoken voice sounds and tactile 
fremitus. Bronchial breathing and bronchial whisper may be heard 
either over solid lung or over fluid accumulation, although the bron- 
chial sounds are usually feeble and distant in the latter condition. The 
displacement of the neighboring organs is of importance here as in all 
diagnoses in which pleuritic effusion is a possibility. A few hard 
coughs may open up an occluded bronchus and so clear up the diagnosis 
at once. In doubtful cases the patient should always be made to 
cough and breathe deeply before the examination is finished. 
It should always be remembered that one may have both pneumonia 
and pleuritic effusion at the same time, and that pneumonia is often DISEASES AFFECTING THE PLEURAL CAVITY 
343 
accompanied by a serous, or followed by a purulent, effusion. In 
children the bronchi are especially prone to become occluded even as a 
result of a simple bronchitis, and we must then differentiate between 
atelectasis and effusion—in the main by puncture and by the use of 
the criteria just described. 
(2) It is sometimes almost impossible to distinguish small fluid 
accumulations in the pleural cavity from pleural thickening with 
pulmonary atelectasis. In both conditions one finds dulness, diminu- 
tion of the voice sounds, respiration, and tactile fremitus, and absence 
Fig. 197.—Area of Dulness in Solitary (tropical) Abscess of the Liver 
of Litten’s phenomenon, but the tactile fremitus is usually more dim- 
inished when fluid is present than in simple pleural thickening and 
atelectasis. The presence of friction sounds over the suspected area 
speaks strongly in favor of pleural thickening, but it is possible to hear 
friction sounds over fluid, probably because they are conducted from 
a point higher up in the chest at which no fluid is present. In doubtful 
cases the diagnosis can and should be cleared up by puncture. 
(3) In several cases I have known subdiaphragmatic abscess or an 
enlargement of the liver due to multiple abscesses to be mistaken for 
empyema. In both conditions, one finds in the right back, dulness 
on percussion as high as mid-scapula, with absence of voice sounds, 
breath sounds, and fremitus. These conditions are due in one case 
to the presence of fluid between the lung and the chest wall, and in 
the other case to the liver or abscess fluid which pushes up the lung 
together with the diaphragm. Without the fluoroscope or a good 
radiograph this diagnosis may be impossible. With the fluoroscope 344 
PHYSICAL DIAGNOSIS 
it should be possible to see that the dome of the diaphragm caps 
the shadow and moves but slightly during inspiration. Some of the 
symptoms, such as chills, sweating, and irregular fever, are common to 
both conditions. A careful consideration of the history and the associ- 
ated signs and symptoms may help us to decide. 
Large solitary abscess of the liver, occurring as it almost invariably 
does in the posterior portions of the right lobe, produces an area of 
flatness or percussion, which rises to a much higher level in the axilla 
and back than in front or near the sternum (see Fig. 198), and may be 
Fig. 198.—Pencil sketch of an x-ray plate showing (see the arrow) a diaphragm domed 
over a subdiaphragmatic abscess. 
in this way distinguished from empyema; but when the liver contains 
many small abscesses, as in suppurative cholangitis, this peculiar line 
of dulness is not present. 
(4) Rare diseases, such as cancer or hydatid of the lung, may be 
mistaken for pleuritic effusion. The history of the case and the results 
of exploratory puncture usually clear up the difficulty. 
7. Carcinoma of the Pleura (Endothelioma) 
About fifty cases are on record. Probably many are falsely diag- 
nosed as a chronic rapidly refilling pleural effusion. The fluid obtained 
by tapping is usually bloody either from the first or later, and con- DISEASES AFFECTING THE PLEURAL CAVITY 
345 
tains a larger proportion of endothelial plaques and a smaller propor- 
tion of lymphocytes than is usual in chronic pleurisy. The cells 
themselves, however, are not characteristic of a neoplasm. 
The physical signs in the chest do not differ from those of any 
ordinary pleural effusion. The points of differential diagnostic value 
are: 
1. The presence of bloody fluid with an endothelial sediment. 
2. Its rapid and repeated reaccumulation. 
3. Metastases (cerebral, supraclavicular, axillary, pectoral and 
along the needle-track). 
4. Pain after tapping. 
Similar signs are obtained in the rare sarcoma of the pleura (four- 
teen cases on record). 
8. Cancer of the Bronchi and Lung 
The condition is almost impossible to diagnose. But 10 of the 90 
cases collected by Weller (Arch, of Int. Med., 1913, XI, 314) were 
recognized in life; 35 of 42 cases in this group had haemoptysis (sputa 
not characteristic). Thirteen per cent, had brain metastasis. The 
other signs are pain, cough dyspnoea and other evidence of bronchial 
obstruction, pressure symptoms due to regional metastases and the 
absence of fever. 
9. Echinoccocus of the Pleura 
This disease is almost unknown in North America. Forty-three 
foreign cases are on record. The signs are those of encysted pleural 
fluid containing eosinophiles and hooklets, remarkable in that it does 
not contain albumen in any considerable quantity. Urticaria often 
follows puncture. 
io. Actinomycosis of the Pleura 
There are no characteristic physical signs. These diseases may be 
suspected if an empyema perforates the chest or is associated with 
chronic pulmonary suppurating. Diagnosis depends on the micro- 
scopic examination of the fluid. 
V. Cyto-Diagnosis of Pleural and Other Fluids 
Only such methods as can be carried out without a thermostat 
will be here described. Hence the examination of diphtheria swabs, 346 
PHYSICAL DIAGNOSIS 
blood cultures, and pus are excluded. We have left the fluids obtained 
by tapping the pleura, the peritoneum, and the spinal cord. The 
first is the most important. 
Pleural Fluids.—A fluid withdrawn from the pleura by puncture 
may be a mechanical transudate (hydrothorax), may be evidence of 
tuberculous pleurisy (primary or associated with phthisis), or, rarely, 
an exudate of septic or cancerous origin. 
Fig. 199.—-Lymphocytosis in Pleural Fluid. Primary tuberculous pleurisy. ( X750 
diameters.) (Musgrave.)' 
To investigate these fluids we note: 
1. Color. Bloody fluids suggest cancer, but occasionally occur in 
pneumonia and tuberculosis. 
2. Weight.1 Dropsical fluid is generally below 1.015 in specific 
gravity. Exudates are usually in the vicinity of 1.020. An ordinary 
specific-gravity bulb is used. 
3. The cells of the sediment (cytodiagnosis). 
i. Technique of Cytodiagnosis 
Pour fluid into tubes of a centrifuge and centrifugalize five minutes. 
2. Pour off the supernatant fluid and stir up the sediment with 
a platinum loop, so as to suspend the sediment in the few remaining 
drops. 
1 The amount of albumin usually runs parallel with the weight of the fluid. DISEASES AFFECTING THE PLEURAL CAVITY 
347 
3. Spread a drop of the mixture on a clean cover glass with the 
platinum loop and let the smear dry without heating it. 
4. Stain like a blood film (see below, page 466) with the following 
mixture:1 Wright’s modification of Leishman’s stain, 3 parts; pure 
methyl alcohol, 1 part.- 
Fig. 200.—Polynuclears and Large Lymphocytes in Pleural Fluid from a Case of Trau- 
matic Acute Infectious Pleurisy. ( X750 diameters.) (Musgrave.) 
5. After staining, wash very gently, using a dropper (else the whole 
film may be pushed off), and dry in the fingers over a Bunsen or alco- 
holic flame. Do not blot the preparation. 
6. Mount in Canada balsam and examine with an oil-immersion 
lens. 
2. Interpretation of Results 
(a) In tuberculous pleurisy, lymphocytes make up from seventy to 
ninety-nine per cent—usually over ninety per cent—all of the cells 
found in the smear2 (see Fig. 199). 
1 Suggested by Musgrave: Boston Med. and Surg. Journ., vol. cli., p. 319, 1904. 
2 This rule, however, does not work both ways. Tuberculosis produces 
lymphocytosis, but so do other chronic irritations. The lymphocytosis is a mark 
of chronicity and only suggests tuberculosis, but there are no other common causes for 
chronic pleural irritation. 348 
PHYSICAL DIAGNOSIS 
(6) In septic cases due to the streptococcus, staphylococcus, or 
pneumococcus the majority of the cells are polynuclear leucocytes 
(see Fig. 200). 
(c) In transudations (dropsical) the predominating cell is a large 
mononuclear type, apparently endothelial in origin and other occur- 
ring in sheets or “plaques ” (see Fig. 201). 
Exceptions occasionally occur, but in the main these rules are 
sufficiently exact to be of value in diagnosis when taken in connection 
with all the facts in the case. 
Fig. 201.—Pleural Fluid in Hydrothorax due to Cardiac Disease. Endothelial plaques 
and cells. ( X750 diameters.) (Musgrave.) 
In peritoneal fluid the use of cytodiagnosis has not as yet furnished 
information of any considerable diagnositic value. 
In cerebrospinal fluid obtained by lumbar puncture the predomi- 
nance of lymphocytes is not so often associated with tuberculosis as 
it is in the pleura, but usually means chronic cerebrospinal irritation 
such as is produced by dementia paralytica and tabes. As excess of 
polynuclear cells is usually due to acute meningitis—epidemic or 
sporadic. CHAPTER XX 
ABSCESS, GANGRENE, AND CANCER OF THE 
LUNG, PULMONARY ATELECTASIS, (EDEMA, 
AND HYPOSTATIC CONGESTION 
I. Abscess and Gangrene of the Lung 
I consider these two affections together, because the physical signs, 
exclusive of the sputa, do not differ materially in the two affections. 
In some cases there may be no physical signs at all, and the diagnosis is 
made from the character of sputa and from a knowledge of the etiology 
and symptomatology of the case. In ioo cases studied by Lord at 
the Massachusetts General Hospital, 22 were due to pneumonia. 
Inhalation of septic material (as during tonsil operations), extension 
from the pleura, bronchi or subdiaphragmatic region, septic emboli 
and trauma are the next most frequent causes. 
The right lower lobe close beneath the pleura is a favorite site. 
In 25 of Lord’s 38 cases there were multiple abscesses. Acute ab- 
scess may be single. Chronic infections are generally multiple. 
The pleura is firmly adherent in only one-third of the cases. The 
symptoms are of sepsis with cough and purulent, foul, sometimes 
bloody sputa, containing elastic tissue. In most cases we find nothing 
more than a patch of coarse rales or a small area of solidification, over 
which distant bronchial breathing, with increased voice sound and 
fremitus, may be appreciated. Usually there is some localized dulness 
on percussion. One may find the signs of cavity (amphoric breathing, 
cracked-pot resonance, and gurgling rales), but this is unusual. 
Pulmonary abscess is often simulated by the breaking of an em- 
pyema into the lung and the emptying of the pus through a bronchus. 
Large quantities of pus are expectorated in such a condition, and ab- 
scess of the lung is suggested, but the other physical signs are those 
of elastic fibres is the crucial point in the diagnosis of intrapulmonary 
abscess, whether due to the tubercle bacillus or to other organisms. 
Tuberculous abscess (cavity) is usually near the summit of the lung, 
and other varieties of abscess are near the base, but often there are no 
physical signs by which we can distinctly localize the process. 
349 350 
PHYSICAL DIAGNOSIS 
II. Neoplasms of the Lung and Mediastinum 
Neoplasms of the lung are usually secondary to tumors of the di- 
gestive tract, bones, uterus or breast, and are recognized chiefly by the 
presence of ill-defined pulmonary symptoms in patients known to have 
previously suffered from neoplasms elsewhere in the body. 
Primary neoplasms, 87 per cent, of which start in the bronchi, 
may be quite without physical signs. The recognizable cases fall 
into two groups: 
1. The lung type. 
2. The mediastinal pressure type. 
In the pulmonary type neoplasms reaching near to the pleural 
surface of the lung may produce a diminution or loss of percussion 
resonance, breath sound, voice, and fremitus. Diagnosis is usually 
made by x-ray alone. The disease is usually mistaken for lung abscess, 
bronchiectasis or tuberculosis. 
In the mediastinal type the diagnosis of mediastinal tumor is 
usually made. Metastatic glandular masses produce pressure signs 
like those of primary mediastinal neoplasms,. 
1. Mediastinal Neoplasms 
According to Christian,1 the mediastinal neoplasms which are 
neither so rare nor so obscure as to make diagnosis practically impos- 
sible are: (1) Sarcoma (including lymphosarcoma, leucaemic growths, 
and Hodgkins’ disease); (2) Teratoma and cyst. 
2. Mediastinal Sarcoma 
Starting in the local lymph nodes, in the thymus or in the connec- 
tive tissue, occurring at any age and chiefly in males, the growths com- 
prise neighboring structures and thus produce dyspnoea, cough, and 
pain, sometimes dysphagia and hoarseness. 
The physical signs are: (a) prominence or bulging of the regions 
near the manubrium; (b) distension of the veins of the neck and upper 
thorax, cyanosis and localized oedema from pressure on the cava or its 
branches; (c) metastatic tumors in the neck which may push the 
trachea to one side; (d) percussion dulness on each side of the manu- 
brium with diminished vocal and tactile fremitus. Auscultation rarely 
yields characteristic results, though there may be noisy strident breath- 
sound from pressure on a bronchus, (e) Evidence of pleural effusion, 
(f) X-ray shadows of characteristic irregular shape. 
1 Christian: Osier’s Modern Medicine, vol. iii, p. 893. ATELECTASIS 
351 
3. Differential Diagnosis 
Our chief business is to exclude aneurism. This is usually possible 
by studying the shape of the x-ray shadow, the course and history 
of the case, the Wassermann reaction, and the pressure symptoms 
which with tumors are far more apt to include venous distension, 
oedema, and cyanosis than is the case with aneurism. 
4. Cysts of the Mediastinum 
Christian (loc. cit.) has collected sixty-four cases of dermoid cyst or 
teratoma of the mediastinum. Most cases occur before the thirtieth 
year. The course is very chronic. The cyst may exist for years with- 
out producing any symptoms and then be accidentally discovered in 
the course of an x-ray examination undertaken for some other pur- 
pose. When it grows large enough to produce pressure symptoms it 
may give rise to dyspnoea, pain, and cough. In eleven of Christian’s 
cases hair was expectorated as a result of communication between the 
cyst and a bronchus. Bulging of the chest wall near the manubrium 
with dulness on percussion, diminished breathing, and vocal sounds, 
and an often characteristically spherical ovoid x-ray shadow, are the 
most constant physical signs. 
III. Atelectasis 
(а) Areas of atelectasis or collapse of pulmonary tissue are often 
present in connection with various pathological processes in the lung 
(such as tuberculosis or lobular pneumonia), but are usually too small 
to give rise to any characteristic physical signs; nevertheless 
(б) In most normal individuals a certain degree of atelectasis of 
the margins of the lungs may be demonstrated in the following way: 
The position of the margins of the lungs in the axillae, in the back, or in 
the precordial region are marked out by percussion at the end of 
expiration. The patient is then directed to take ten full breaths, and 
the pulmonary outlines at the end of expiration are then percussed out 
a second time. The pulmonary resonance will now be found to extend 
nearly an inch beyond its former limits, owing to the distention of 
previously collapsed air vesicles. 
If one auscults the suspected areas during the deep breaths which 
are used to dispel the atelectasis, very fine rales are often to be heard 
at the end of expiration, disappearing after a few breaths in most cases, 352 
PHYSICAL DIAGNOSIS 
but sometimes audible as long as we choose to listen to them. These 
sounds, to which there is given the name of “atelectatic crepitation,” 
are, in my experience, especially frequent at the base of either axilla. 
The same writer has noticed an opacity to the v-rays over such atelecta- 
tic areas. 
Forcible percussion may be sufficient to distend small areas of 
collapsed lung, or at any rate to dispel such dulness as has been 
previously present. 
(c) When one of the large bronchi is compressed, as by an aneu- 
rism, or occluded by a foreign body, collapse of the corresponding area 
of lung may be shown by diminished motion of the affected side, 
dulness on percussion, and absence of breathing, voice sounds, and 
tactile fremitus. 
In new-born babies whose lungs do not fully expand at the time 
of birth, similar physical signs are present over the non-expanded 
lobes. The right lung is especially apt to be affected. 
In the differential diagnosis of extensive pulmonary collapse, the 
etiology, the suddenness of the onset, the absence of fever and of 
displacement of neighboring organs enable us to exclude pneumonia 
and pleuritic effusion. In distinguishing small areas of solidification 
from similar areas of atelectasis fluoroscopic studies may be of value. 
Atelectatic areas brighten up with cough and deep breathing. Solidi- 
fied areas show no change. 
IV. (Edema of the Lungs 
(a) Chronic Form.—In cardiac or renal disease one can often dem- 
onstrate that the lungs have been invaded by transuded serum as a 
part of the general dropsy. More rarely, pulmonary oedema exists 
without much evidence of oedema in other organs or tissues. 
The only physical sign characteristic of this condition is the 
presence of numerous rales in the dependent portions of the lungs; 
that is, throughout their posterior surfaces when the patient has been 
for some time in a recumbent position; or over the lower portions of 
the axillae and the back if the patient has not taken to his bed. 
The rales are always bilateral (unless the patient has been lying for 
a long time on one side), and the individual bubbles appear to be all of 
the same size, or nearly so, differing in this respect from those to be 
heard in bronchitis. Squeaking or groaning sounds are less often 
heard. The respiratory murmur is usually somewhat diminished in 
intensity. ATELECTASIS 
353 
Dulness on percussion and modification of voice sounds are not 
present, unless hydrothorax or hypostatic pneumonia complicate the 
oedema. 
(b) Acute Form.—In brain lesions, comatose conditions, and hyper- 
tensive cardio-vascular disease the lungs may suddenly fill with fluid 
“out of a clear sky” and with such urgency that pinkish frothy serum 
pours from the mouth or is rapidly expectorated. The patient may 
die in the first attack, or often in later attacks. The physical signs 
are coarse bubbling rales throughout the lungs with feeble heart. 
V. Hypostatic Pneumonia 
In long-standing passive congestion, the alveoli of the dependent 
portions of the lungs may become so engorged with blood and alveolar 
cells as to be practically solidified. Under these conditions, examina- 
tion of the posterior portions of the lungs shows usually: 
(a) Slight dulness on percussion reaching usually from the base to 
a point about one-third way up the scapula. At the very base the 
dulness is less marked and becomes mixed with a shade of tympany. 
(b) Feeble or absent tactile fremitus. 
(c) Diminished or suppressed breathing and voice sounds. 
The right lung is apt to be more extensively affected than the left. 
Occasionally the breathing is tubular and the voice sounds are in- 
creased, making the physical signs identical with those of croupous 
pneumonia, but as a rule the bronchi are as much engorged as the alve- 
oli to which they lead, and hence no breath sounds are produced. 
Rales of oedema or of bronchitis may be present in the adjacent 
parts of the lungs. The fact that the dulness is less marked at the 
base of the lung than higher up helps to distinguish the condition from 
hydrothorax. 
The diagnosis is usually easy, owing to the presence of the under- 
lying disease. Fever, pain, and cough such as characterize croupous 
pneumonia are usually absent. CHAPTER XXI 
THE ABDOMEN IN GENERAL, THE BELLY WALLS, 
PERITONEUM, OMENTUM, AND MESENTERY 
I. Examination of the Abdomen in General 
Our methods are crude and inexact compared to those applicable 
to the chest. Auscultation, despite Cannon’s brilliant foundation 
studies,1 is of practically no use. Inspection is helpful in but few 
cases. Palpation, our mainstay, is often rendered almost impossible 
by thickness, muscular spasm, or ticklishness of the abdominal walls. 
Percussion is of great value in some cases, but yields no useful results 
in the majority. 
1. Technique 
The knack of abdominal examination, and especially that part of it 
whereby the skilled diagnostician gets his most valued information, is 
difficult even to demonstrate and almost impossible to describe. 
Hence the account of it in this and other books is very brief when com- 
pared with the space allotted to the methods of examining the chest.2 
The table or bed on which the patient lies during most abdominal 
examinations (excluding gynaecological work) should be at least three 
feet high, narrow, and firm. Most beds are too low, too wide, and too 
soft; but, on the other hand, the patient must not be made uncom- 
fortable by the hardness or coldness of the surface on which he lies. 
A comfortable pillow should be provided. 
(a) Inspection 
We need a tangential light, such as accentuates by shadows 
every unevenness of the surface. If the patient is examined in the 
ordinary dorsal decubitus, the light from any single window, except 
one overhead, is satisfactory. If one inspects the abdomen with 
1 Summarized in his “ Mechanical Factors of Digestion:” Longman’s, 1911. 
21 have heard a physician in a leading American city say that when palpation 
of the spleen in typhoid fever was first introduced, there was but one physician in 
the city who had the knack, and that his colleagues were very sceptical about the 
possibility of accomplishing the feat at all. I have seen a similar uncertainty 
regarding the palpation of the normal but slightly displaced right kidney. 
354 THE ABDOMEN IN GENERAL 
355 
the patient upright, he should stand with his side to the light, not 
facing it. By inspection we seek information on: 
(а) The general contour of the abdomen. 
(б) The surface of the belly walls, especially the skin and the navel. 
(c) Respiratory movements, their limitation or absence. 
(d) Peristaltic movements (gastric or intestinal in origin). 
(e) The presence of local prominence or (rarely) depression. 
Inspection of the Belly Wall.—i. The surface of the belly wall is often 
searched most carefully for the rose spots of typhoid fever, which are 
hyperasmic, very slightly elevated spots, about the diameter of a large 
pin head (2-4 mm.). They disappear on pressure. Pimples are 
usually larger, better defined at the edges, and more highly colored, 
contrasting with the very pale red of most rose spots. They are by no 
means confined to the belly and may be found exclusively on the back. 
Having been at the outset somewhat sceptical of their value in diagno- 
sis, I have become thoroughly convinced by greater experience and 
more careful examination. Richardson1 has shown that they often 
contain bunches of typhoid bacilli. The spots are present in about 
three-fourths of all cases, and, while they also may occur in any dis- 
ease when the blood contains bacteria (e.g., sepsis), they are common- 
est in typhoid. 
2. Distended and tortuous veins on the abdomen are seen in dis- 
eases obstructing the portal circulation (rarely in cirrhotic liver) or 
the inferior cava. 
3. Strise, or linear markings on the skin of the abdomen, follow the 
subsidence of any long-standing trouble that stretches the skin- 
pregnancy, obesity, tumors, etc. They are red, are angry when first 
produced, but later turn white (linece albicantes). 
4. Scars of old wounds or operations may be of great diagnostic 
value in comatose or delirious cases. 
5. Projection or levelling of the normal depression at the navel is 
evidence of distention, usually by fluid, within the belly. 
Respiratory movements of the belly walls are limited or cease in 
painful diseases within the peritoneum (peritonitis, lead colic) or when 
the diaphragm is pushed up by a large tumor, ascites, or meteorism.. 
Peristaltic waves creeping along beneath the belly walls are seen 
with chronic stenosis and obstruction at the pylorus or at some point 
in the colon and occasionally in thin but healthy persons. 
Hernice and local and general prominences will be discussed in 
connection with abdominal tumors. 
1 M. W. Richardson: Pennsylvania Medical Journal, March 3, 1900. 356 
PHYSICAL DIAGNOSIS 
(b) Palpation1 
With the patient on the back upon a suitable bed or table,2 the 
head on a comfortable pillow, and the abdomen exposed, run the palm 
of the hand (warmer) lightly over the whole surface, to accustom the 
muscles to its presence. Then try whether better relaxation of the 
belly walls is obtained when the patient’s knees are drawn up. Some 
patients relax better in this position; others when the legs are extended. 
If the muscles of the abdomen remain contracted and stiff even 
when the patient is comfortable and has become accustomed to the 
presence of the physician’s hand, we may try to induce relaxation: 
(a) By getting the patient to take a series of deep breaths. 
(b) By diverting his attention through conversation or otherwise. 
If these means fail and it is important that we should thoroughly 
investigate the abdomen, we have left two further ways of producing 
relaxation, viz.: 
(c) By putting the patient into a warm bath. 
(d) By anaesthesia (ether or chloroform). 
The movements of the physician’s hand should never be sudden or 
rough. He should avoid digging into the skin with his nails or pressing 
strongly on a small spot with the finger-tips. If any spot be suspected 
to be tender, that should be palpated last, after going over the rest of 
the abdomen. If it is necessary to make deep pressure at any point, 
it is best to lay the fingers of the left hand loosely over the spot and 
then exert pressure upon them with the fingers of the right hand. 
The passive hand is more sensitive. To reach a deep spot, put the 
hands in this position over it, ask the patient to take a long breath, 
and, as the belly falls in expiration, follow it down with the hands. 
Then hold what you have gained, and with the next full expiration 
you may be able to get in still deeper, until after a series of deep breaths 
the desired spot is reached. Naturally this cannot be done if there is 
much tenderness, but pure nervous spasm may sometimes be overcome 
in this way. 
To make use of the relaxation secured by a hot bath, we need an 
unusually long tub, so that the patient can lie almost flat when his 
knees are slightly drawn up. If he is doubled up with his knees and 
1 Special methods of palpating a diseased kidney, spleen, or liver are described in 
the sections on those organs. 
2 It is essential that the physician as well as the patient should be comfortable 
during an abdominal examination, else his attention is not wholly on his work. 
Hence the importance of a high, narrow bed, or table, so that the physician need 
not stretch or stoop to reach the patient. THE ABDOMEN IN GENERAL 
357 
head in close proximity, nothing can be accomplished. The patient 
gets into the tub with the water comfortably warm, and its tempera- 
ture is then raised to between no° and 120° F. by pouring in very hot 
water. The greatest relaxation is usually attained after about ten 
minutes’ immersion. When women are examined the water can be 
rendered opaque by adding milk or soap suds. 
This method is far less inconvenient than etherization, and is 
especially valuable when the recti are well developed and form rounded, 
tumor like masses as soon as ordinary palpation is attempted. If we 
suspect that a tumor-like mass may be one of the bellies of the rectus, 
it is well to grasp the mass with the hand and then ask the patient to 
raise his head. The mass will harden suddenly if it is the rectus. 
2. What can be Felt Beneath the Normal Abdominal Walls 
No part of the normal intestine, including the appendix, can, in 
my opinion, be felt through the abdominal walls. The same is true of 
the stomach, spleen, left kidney, pancreas,1 bladder, and pelvic organs. 
All that we can make out in most normal cases is: 
1. The abdominal aorta. 
2. The spinal column, near and above the umbilicus. 
3. Part of the liver (occasionally, if the costal angle is sharp and the 
belly walls are thin and lax). 
4. The tip of the right kidney (in many young persons). 
5. Gurgling and splashing in the stomach or colon. 
6. The ilio psoas muscle and sometimes the beginning of the iliac 
arteries in thin people. 
The aorta is too deep to be felt at all in some persons, but, on the 
other hand, it is astonishing how close under the belly wall it is in 
others, i.e., in those whose dorsal spine projects sharply forward. In 
such persons the aorta may be almost taken in the hand, and its course, 
calibre, and motions are so startlingly evident that it is often mis- 
takenly supposed to be the seat of an aneurism, especially as a sys- 
tolic murmur and thrill can be appreciated over it if a little pressure 
is exerted, so as to produce an artificial stenosis. 
Behind and beside the aorta we can sometimes feel the bodies of 
the vertebrae, and on them trace the division of the aorta into the 
common iliacs. 
1 Leube believes that in very thin subjects the head of the pancreas may 
occasionally be felt. 358 
PHYSICAL DIAGNOSIS 
The liver cannot be felt at all in the great majority of normal per- 
sons, but occasionally the costal angle is so sharp that a small portion 
of the organ is palpable in the epigastric region. 
Bimanually, (see below, page 407) the tip of the normal right kid- 
ney may often be caught between the hands at the end of a long inspira- 
tion, especially in thin people with lax belly walls. 
If the stomach or colon contains fluids, the palpating hand often 
elicits sounds corresponding to the movement of these fluids. Their 
only importance in diagnosis will be mentioned later. 
Very deceptive often are muscular bundles in the external oblique, 
which seem distinguishable as sausage-shaped tumors, and doubtless 
give rise to some of the legends about feeling the normal appendix. 
3. Palpable Lesion of the Belly Walls 
The occurrence of lesions, to be recognized mainly by inspection 
and percussion, has been discussed (page 355). Besides these we 
search for: 
1. Hernice, epigastric or umbilical (see Fig. 202). The diagnosis 
rests on the presence of an impulse on coughing, with or without a 
reducible tumor. Omental hernise do not bulge with cough. 
Fig. 202.—Epigastric Hernia. 
2. Separation of the Recti.—When the patient, lying on the back, 
lifts his head and shoulders, a longitudinal wedge bulges out along the 
median line of the belly from the gastric to the suprapubic region. 
3. Abscess of the abdominal walls usually represents a stitch abscess 
or the external vent of pus burrowing from the appendix, the pelvis, 
or the prevesical space. But in about one-third of the cases no such 
cause can be found. An infected hasmatoma due to trauma or without 
known cause explains some cases, and occasionally tuberculosis or THE ABDOMEN IN GENERAL 
359 
actinomycosis occurs. The latter conditions are recognized by the 
microscopic examination of the pus and of the abscess wall. 
4. Sarcoma of the belly wall is rather rare, and can be recognized 
with certainty only by microscopic examination; without this I have 
known it to be confused with lipoma and with tuberculosis. 
5. Thickening or inflammation at the navel occurs in some cases of 
cancerous or tuberculous peritonitis. The diagnosis rests on the 
further evidence of cancer or tuberculosis within the peritoneal cavity 
and on the microscopic examination of a piece excised for the purpose. 
Palpation of the Spleen (see page 402). 
Palpation of the Liver (see page 378). 
Palpation of the Kidney (see page 407). 
4. Study of Abdominal Tumors 
One should notice: Size, contour, consistency, mobility with pressure 
and with respiration, tenderness, pulsation, peritoneal crepitus, adherence 
to the skin or to the abdominal wall, relationship to any abdominal organ 
(also dulness or resonance on percussion.) 
Most of these points need no comment. To ascertain whether the 
tumor involves the skin, one lifts up a fold of skin crossing the mass. 
If the skin dimples markedly over the tumor, i.e., fails to rise at that 
point while on all sides of the mass it can easily be picked up, the skin 
is adherent. Tumors in the abdominal wall can usually be gathered 
up along with the latter when we grasp a large fold with both hands. 
To determine the relationship of a tumor with the liver or spleen we 
note: 
(а) Whether a groove or interval can be made out, by palpation 
or percussion, between the mass and either of those organs. 
(б) Whether its respiratory mobility is as great as theirs. 
(■c) Whether there are other facts in the case suggestive of hepatic 
or splenic disease (jaundice, ascites, leukaemic blood). 
(d) The effect of inflation of the colon (see below). Tumors con- 
nected with the spleen are forced forward and do not become resonant 
when the colon is inflated. • 
To determine the degree of respiratory mobility, hold the fingers of one 
hand in contact with the lower edge of the mass and allow them to 
descend with it while the patient takes a full breath. To make sure 
that an actual descent occurs, one must sight the mass (and the hand) 
against some motionless object in the room beyond, else one may be 
deceived bv the movement of the abdominal walls over the tumor, 360 
PHYSICAL DIAGNOSIS 
while the tumor itself remains motionless or nearly so. Tumors con- 
nected with the stomach, omentum, liver or spleen move about two 
inches with a forced inspiration. Kidney tumors move less, seldom 
as much as an inch. Pancreatic and retroperitoneal tumors have 
scarcely any mobility. Those connected with the intestine vary con- 
siderably in respiratory mobility, according to the presence and degree 
of adherence to other parts, but their excursion is rarely an inch. 
Peritoneal crepitus is a grating, rubbing sensation experienced on 
light palpation, and due—supposedly—to the presence of a plastic, 
Fig. 203.—Diastasis recti. 
peritoneal exudate similar to that which produces the friction sounds 
in pericarditis. Over an enlarged spleen (e.g., in leukaemia) peritoneal 
crepitus may be due to local perisplenitis, and in perigastritis, peri- 
hepatitis, and perienteritis similar crepitus occurs. 
Dipping refers to a sudden displacement of the abdominal wall and 
whatever lies close beneath it, by a swift poke of the finger tips, which 
may succeed thereby in touching a solid organ or tumor which gentle, 
gradual palpation misses. Thus one may reach and mark out an 
enlarged liver through a layer of ascites which would prevent ordinary 
palpation. THE ABDOMEN IN GENERAL 
361 
(a) Percussion 
Abdominal percussion is less valuable than thoracic. A lighter 
blow is used, and the distinction between dulness and tympany is easy. 
It is of value chiefly to determine the presence of fluid free in the 
peritoneal cavity, and to ascertain whether a tumor is due to or covered 
by gaseous distention. 
(а) Free fluid (ascites, peritonitis, hasmoperitoneum, ruptured 
cyst) gravitates to the flanks and suprapubic region, while the intes- 
tines float up and occupy the epigastric and umbilical space. Hence 
there is dulness in the flanks and over the pubes, with resonance in the 
epigastric and umbilical regions. But the crucial and ever-necessary 
test is the shifting of this area of dulness when the patient turns on his 
side; then the uppermost flank should become resonant and the lower 
half of the belly—including part of the umbilical region—dull. With- 
out this test the mere marking out of dull areas in the flanks is not 
conclusive evidence of free fluid there. Occasionally one is deceived 
by the shifting of a distended colon or a mass of small intestines con- 
taining fluid. Still less reliable is the “fluctuation wave,” which can 
be transmitted as an impulse palpable to the hand laid flat on one 
flank, by sharply snapping the other flank. Similar impulses can be 
transmitted through the fat of the belly wall, despite all efforts to 
check them by pressure upon the latter. 
(б) Percussion is our final test in the diagnostic procedure that 
begins with inflation of the colon. Air is forced into the rectum with 
an ordinary Davidson syringe, and, as the colon becomes prominent 
and hyperresonant, we note whether its tympany covers up the tumor- 
mass under investigation, or whether the mass lies anterior to and 
remains dull over the inflated colon. Kidney tumors lie behind the 
inflated colon; splenic tumors remain dull in front of it. 
Auscultatory percussion, for identification or demarkation of ab- 
dominal tumors and organs, has never been successful in my hands 
nor in those of most of the observers in whose results I have confidence. 
Hence I omit further description of it. 
Percussion of the stomach and spleen is of very slight value. 
Percussion of Traube's space, the “stomach bubble” (the small area 
bounded on the right by the splenic and on the left by the hepatic 
dulness, above by the free edge of the left lung, and below by the lower 
edge of the ribs) is, in my experience, of very little value in diagnosis. 
This tympanitic area is obliterated in many pleuritic effusions (not 
in all), but many other causes (full stomach or gut, obese omentum) 
may produce similar dulness. 362 
PHYSICAL DIAGNOSIS 
Before describing the signs of the different diseases to which the 
abdominal organs are subject, it seems to me best to introduce here a 
list of the commoner abdominal tumors found in the study of 4876 such 
tumors at the Massachusetts General Hospital. 
Relative Frequency of Abdominal Tumors 
1. Congested liver 1288 
2. Uterine fibromyoma 766 
3. Hernia. . 488 
4. Ovarian cyst 382 
5. Gastric cancer 285 
6. Displaced kidney 227 
7. Cirrhotic liver 153 
8. Cancer of liver 151 
9. Cancer, of colon 90 
10. Abscess of abdominal wall 791 
11. Splenic tumor in cirrhosis of the liver 60 
12. Leuksemic spleen 58 
13. Malignant tumor of the ovary 43 
14. Tuberculous kidney 41 
15. Tumor as part of tuberculous peritonitis 33 
16. Cancer of the pancreas 322 
17. Neoplasm of the kidney 27 
18. Sarcoma of abdominal wall 27 
19. Enlarged spleen of unknown cause 26 
20. Omental cancer 18 
21. Intussusception 17 
II. Diseases of the Peritoneum 
1. Peritonitis—local or general. 
2. Ascites. 
3. Cancer and tuberculosis. 
i. Peritonitis 
1. Local peritonitis gives evidence of its presence by (a) pain, 
(b) tenderness, (c) muscular spasm, (d) tumor, and (e) constitutional 
manifestations. 
The pain may be at first diffuse, later localizing itself at the site of 
the lesion; or it may be felt first where the peritonitis begins and spread 
with the lesion if the general peritoneal cavity becomes involved. The 
character and intensity of the pain vary greatly. 
1 Some of these were so small as hardly to deserve classification as tumors. 
2 Rarely produces a palpable tumor but is here mentioned for convenience. THE ABDOMEN IN GENERAL 
363 
Tenderness is the important sign in diagnosis, and helps us to 
exclude the various colics and other causes of pain which are often 
relieved by pressure. 
Local muscular spasm of the belly muscles to guard the tender le- 
sion beneath is of great value in pointing our attention to the spot 
affected, though the muscles may be so rigid as to prevent palpation 
through them. [Psoas spasm is described in the section on Appendi- 
citis, see page 392.] 
The tumor is apt to consist of intestine or other organs matted 
together by adhesions about the site of the process. 
The constitutional manifestations are those of infection, viz., 
fever, leucocytosis, anorexia, constipation, often albuminuria and 
albumosuria. 
The commonest causes of local peritonitis are: 1. Appendicitis. 
2. Pus tube. 3. Gall-bladder inflammation. 
Less common is cancer or ulcer of the stomach or intestine. 
2. General Peritonitis.—The belly may be generally swollen and 
tympanitic or retracted and hard. General tenderness is the most im- 
portant sign. In advanced cases free fluid in the flanks may be demon- 
strated. No sounds are audible as the intestines are paralyzed. 
Vomiting is the rule, and soon becomes very foul (stercoraceous). 
There is fever, with a rapid, weak pulse. The mind is clear. The 
facial expression may be normal. If there is persistent vomiting the 
face of that condition appears drawn, pinched, anxious, with dark 
circles under the eyes. The rapid loss of fluid by vomiting accounts for 
this. If peritonitis begins in a patient exhausted after operation or 
chronic disease, there may be no signs unless those of free fluid can be 
found. 
The leucocyte count is generally elevated, but in the most viru- 
lent cases remains normal or subnormal. 
2. Ascites 
The commonest causes are: 
(1) Dropsy, from cardiac, pericardial, or renal disease. 
(2) Portal stasis, usually from cirrhosis of the liver. 
(3) Tuberculous peritonitis. 
(4) Cancer of the peritoneum. 
(5) Intestinal obstruction. 
(6) Acute hepatitis (“ yellow atrophy ”). 
(7) Solid ovarian tumors. 364 
PHYSICAL DIAGNOSIS 
The methods of diagnosis of ascites have been explained above. 
I he diagnosis of its cause depends on the history, the results of punc- 
ture, and the general physical examination. The contour of the belly 
is often that pictured in Fig. 204. 
3. Cancer and Tuberculosis of the Peritoneum 
In connection with cancer or tuberculosis of some abdominal or 
pelvic organ, the disease may become spread throughout the perito- 
neum with deposits in the omentum and mesentery. The signs are: 
i. Tumor masses scattered here and there, 
sometimes at the navel. 2. Ascites. 3. 
Emaciation and anasmia. 
The diagnosis of cancer depends on the 
recognition of multiple, hard, nodular 
tumors in the abdomen of a patient known 
to have cancer of some abdominal organ. 
Somewhat similar masses, usually due 
to loops of intestine matted together by 
adhesions, may be felt in tuberculous peri- 
tonitis, but here they are larger, fewer, and 
not so hard. Cancer appears in late life, 
tuberculous peritonitis usually in early 
life. The emaciation and anaemia are less 
marked in tuberculosis, and fever is more 
marked. The history or present evidence 
of tuberculosis elsewhere—lung, pleura, 
glands, pelvis, testis—favors the diagnosis of tuberculous peritonitis. 
Cytodiagnosis and the tuberculin test may be of value in diagnosis. 
Subphrenic Abscess.—There are two common types—the one near 
the liver, the other near the spleen. 
(a) The perihepatic type is recognized, as a rule, chiefly by its 
etiology (perforated gastric ulcer, appendix-abscess), by the constitu- 
tional signs of concealed pus (fever, chills, leucocytosis), and to a less 
extent by physical signs, none of which, however, serves to distinguish 
perihepatic from intrahepatic pus. Pain in the hepatic region, promi- 
nence of the right lower ribs or right hypochondrium, increased area 
of percussion dulness over the lower ribs in front and behind (whence 
empyema or pneumonia is often suspected), and the results of x-ray 
examination are the data from which we must reason. (See Fig. 198.) 
(b) The perisplenic type of abscess follows a general peritonitis, 
which has been treated by drainage and recumbency. The pus 
Fig. 204.—Characteristic Shape 
of Belly in Ascites. THE ABDOMEN IN GENERAL 
365 
becomes pocketed near the spleen instead of gravitating toward the 
pelvis as it does if the patient’s trunk is kept upright. 
Pain, sometimes tenderness, the history of the case and the consti- 
tutional evidence of concealed pus are the facts on which a conjecture 
may be hazarded. 
The Mesentery 
1. Enlarged glands—tuberculous, cancerous, or lymphomatous— 
can occasionally be felt in very thin patients. Their recognition as 
glands would depend on more obvious evidence of their cause in 
other parts of the body. 
2. Mesenteric thrombosis produces all the signs of intestinal 
obstruction (see below, page 393), from which it can rarely be dis- 
tinguished without operation, or autopsy, except when it occurs as a 
complication of mitral stenosis, when we are on the watch for embolism 
of the brain, extremities and mesentery. CHAPTER XXII 
THE STOMACH, LIVER, AND PANCREAS 
I. The Stomach 
The best methods of examining the stomach are: 
1. Inspection and palpation of the epigastrium and the neighbor- 
ing portions of the abdomen. 
2. Bismuth—x-rscy examination. 
3. Examination of the stomach contents: (a) fasting; (b) after a 
test meal. 
By combining the results of these three methods of examination 
with the results of our general examination of the body—emaciation, 
anasmia, etc.—and with the data obtained by a careful history, we 
obtain all the information about the stomach which it is possible for us 
to make use of at the present time. 
1. Inspection and Palpation of the Epigastrium 
(а) Tenderness.-—'The normal stomach cannot be seen or felt, nor 
can anything certain be learned in regard to it by percussion or auscul- 
tation. Tenderness in the epigastrium is so common that we can 
attach no significance to it. In a small portion of cases cutaneous 
tenderness in the back (lower dorsal or upper lumbar region) can be 
elicited in cases of peptic ulcer, but this has no value in diagnosis. 
(б) A tumor in the epigastrium (see Fig. 205) is of far greater impor- 
tance than any other local evidence. If it occurs in an emaciated and 
anaemic person past middle life, is hard and nodular, and does not 
disappear after catharsis, it is almost invariably due to cancer of the 
stomach. Such a tumor may also be due to a mass of adhesions about 
a gastric ulcer. Tumors of the pancreas much less often reach the 
surface in this region; tumors of the liver are generally larger, and 
their connection with this organ can generally be demonstrated by 
percussion, palpation, and by their greater respiratory mobility when 
compared with gastric cancer. 
Epigastric hernia usually shows an impulse on coughing, is soft and 
doughy in feel, and presents none of the other symptoms and signs of 
gastric cancer. 
366 THE STOMACH, LIVER, AND PANCREAS 
367 
Tubercular deposits in the omentum are almost always associated 
with ascites, fever, and other evidences of tuberculosis either in the 
examination of other organs or in the history. 
(c) Visible gastric peristalsis means stenosis of the pylorus (cancer, 
ulcer, adhesions, or muscular spasm). The contraction wave passes 
from left to right across the epigastrium, and is seen by means of the 
shadow cast by a tangential light with the patient in a recumbent 
position. If the peristalsis stops it can sometimes be reexited by 
briskly snapping the epigastric region with the finger. 
Fig. 205.—Epigastric Tumor in Gastric Cancer. 
(d) The normal splash sound can usually be heard if sudden, quick 
pressure is made in the epigastrium within three hours after a meal. 
If splashing can be elicited more than three hours after a meal, and 
especially if it is present before breakfast, it is evidence of gastric stasis 
and usually of dilatation. 
(e) Hypogastric bulging due to dilated stomach is occasionally seen 
in cases of marked dilatation when the patient stands up, and is exam- 
ined in profile (see Fig. 206). 
2. Use of the Stomach Tube 
(a) The passage of the tube. The standard red rubber tube gener- 
ally in use in this country comes in two sizes. Personally I prefer 
the larger, with a lateral as well as a terminal opening at the lower 
end, although the smaller size produces somewhat less discomfort. 
The patient should be covered by a rubber sheet and the clothing 
removed from the abdomen. So prepared, he should sit in a straight- 
backed, wooden chair, with a good-sized foot-tub between his feet 368 
PHYSICAL DIAGNOSIS 
and a towel in his hand ready to wipe away the profuse secretions 
of the mouth and pharynx. He should then be warned that the 
process of passing a tube, although entirely free from danger, is very 
disagreeable, both on account of the nausea which it produces and 
because it often seems to the patient as if he were choking and could 
not get his breath. This, in fact, is not the case, and if the patient will 
persist in drawing long, deep breaths throughout the process of passing 
a tube, the worst of it is over in twenty seconds. 
Fig. 206.—Outline of Abdomen in Dilatation of the Stomach, due to cancer at the 
pylorus. 
The tube is moistened with water and pushed straight down 
through the pharynx without any attempt to direct it, beyond keeping 
the median line. There is no danger of entering the trachea and no 
use in trying to avoid it. On its way down the tube is arrested now 
and then by muscular spasm of the oesophagus, but after a few seconds 
the spasm relaxes and allows us to push the tube on until the twenty- 
two-inch mark reaches the teeth. The lower end of the tube is then 
in the stomach,1 and we are ready to extract the gastric contents (in 
1 Unless there is gastric dilatation or gastroptosis; then the tube must be pushed 
in several inches farther, the distance depending on the position of the lower gastric 
border, as determined in previous examinations. THE STOMACH, LIVER, AND PANCREAS 
369 
case a test meal has been previously given), to wash out the organ, or 
to distend it with air or water. Since the passage of the stomach tube 
is the means whereby we become sure of the existence of such diseases 
as cardio-spasm, diverticulum of the gullet and cancerous stricture of 
the gullet, some account of the diagnosis of these diseases will be given 
here. 
Cardio-spasm with Dilatation of the (Esophagus.—Plummer has 
reported 40 cases seen in the Mayos’ clinic within two and a quarter 
years. Hence the disease cannot be a rare one though there are 
surprisingly few cases on record. The patient complains that food 
sticks, causing discomfort at the lower end of the sternum and later 
regurgitating unmixed with acid juice. The cases usually begin at so 
early an age (29 is the average) and are usually chronic enough when 
seen to exclude a cancerous stricture, but as a rule the first reliable 
evidence on this point is obtained when we find that: 
1. A stomach tube will not pass while a large sound properly 
guided by a thread (see below) passes fairly easily. 
2. Great and long-continuing relief is obtained by dilating the 
stricture a few times with water pressure inside a silk covered rubber 
bag. 
Radiography of a bismuth meal and the use of the oesophagoscope 
are supplementary aids to diagnosis. If there is any difficulty in 
reaching the stomach, a silk thread six yards long is swallowed. 
After the lower end has passd into the gut the upper end can be pulled 
taut and on it as a guide a sound and subsequently a dilator can be 
passed. 
Diverticulum of the (Esophagus.—Most diverticula are so high up in 
the gullet that they are easily recognized by radiography and sounding. 
The rarer diverticula low down in the oesophagus can also be recognized 
in most cases by radiographing a bismuth meal or by the silk thread 
method above described. The thread guides the sound past the 
opening of the diverticulum. 
Cancer of the (Esophagus.—The age of the patient and the duration 
of symptoms usually differentiate cancer of the gullet from cardio- 
spasm. In doubtful cases the fact that sounds even when accurately 
guided do not pass much more easily than the soft rubber tube favors 
the diagnosis of cancer. A'-ray settles it. 
(b) Extracting the Gastric Contents.—One hour after a test meal 
the tube is passed and the patient is then asked to lean forward, press 
with his hands upon his stomach, and strain down as if he were going 
to have a movement of the bowels. In most cases this suffices to force 370 
PHYSICAL DIAGNOSIS 
the gastric contents out through the tube and into a basin, which is 
held ready. If the gastric contents cannot be extracted either in this 
way by having the patient lie down or by moving the tube in the 
pharynx so as to excite nausea, we should make sure first that the eye 
of the tube is not plugged. This may be ascertained by disconnecting 
Fig. 207.—Traumatic Pneumoperitoneum from perforation of an esophageal stricture 
bv a sound. 
the funnel and blowing through the tube, which usually suffices to 
discharge any obstacle from the eye of the tube. If still the gastric 
contents do not flow out, we may use suction by connecting a Politzer 
air-bag with the end of the tube in place of the funnel. 
For the analysis of the contents so obtained, see below. THE STOMACH, LIVER, AND PANCREAS 
371 
(c) Washing the Stomach {Lavage).—Though not of much use 
this procedure may be briefly mentioned here. After introducing the 
tube as above described, about a pint of water is poured in through 
the funnel, and, just before the water disappears in the vortex of the 
funnel, the latter is rapidly lowered so as to empty by siphonage into a 
vessel on the floor. This process is repeated until food and mucus 
cease to come out and the water runs clear. 
To remove the tube at the end of any of the procedures just de- 
scribed, we have only to pinch it tightly just outside of the patient’s 
teeth and pull it rapidly out. 
3. Examination of Gastric Contents 
1. The contents of the fasting stomach are best obtained by passing 
the tube before breakfast, and should consist of no more than a few 
cubic centimetres of clear fluid containing free hydrochloric acid. If 
any food is present, gastric stasis is proven. If more than 50 c.c. of 
fluid without food are present, hypersecretion is indicated. 
2. Gastric Contents after a Test Meal.—The best test meal is that 
of Ewald, and consists of a slice of bread (or its equivalent in crackers 
or cereal) with a glass and a half of water. After this meal not more 
than 100 c.c. should be found in the stomach at the end of an hour. 
Occasionally the stomach has emptied itself even within the hour, and 
we have then to reduce the period. 
After extracting the gastric contents as above described and noting 
the quantity, we should investigate also their color, odor, and general 
appearance.. (a) Small streaks of blood are of no consequence. 
Considerable quantities of blood (fresh) suggest ulcer. Small quanti- 
ties of dark-brown substance resembling blood should be investigated 
by the guaiac test. If this is positive, gastric cancer is suggested. 
The guaiac test is best performed as follows: Chip off the oxidized 
outer shell of a lump of gum guaiac and prepare a fresh tincture by 
shaking a few chips of the inner non-oxidized guaiac with a few cubic 
centimetres of alcohol. Add about 10 drops of this tincture and 2 c.c. 
of hydrogen peroxide to an ethereal solution of the gastric contents 
prepared by extracting 10 c.c. of gastric contents with 2 c.c. of glacial 
acetic acid and 15 c.c. of ether (shake 5 minutes). On adding the 
guaiac to the ethereal solution of gastric contents a blue color indicates 
the presence of blood. 
(b) For acetic and butyric acids we test merely by our sense of 
smell. Whenever stasis or fermentation has occurred, we are apt to 
get a characteristic odor of these acids mingled with that of yeast. 372 
PHYSICAL DIAGNOSIS 
(c) The general appearance of the contents tells us little that is 
important. In cases of marked dilatation they often separate into 
three layers—the upper frothy, the middle a thin, turbid liquid, and 
the lower a flocculent sediment of partially digested food. 
Mucus is not of any considerable clinical significance unless it is so 
abundant that the whole stomach contents will slide in one lump from 
one beaker to another. 
When absolutely no digestion has taken place, as in the rare cases 
of achylia gastrica, the contents consist simply of unaltered bread and 
water. 
(a) Chemical Tests of Gastric Contents 
1. Dip a piece of blue litmus in the contents; if no reddening occurs, 
no further tests need be made. 
2. If the contents are acid to litmus, test with Giinzburg s reagent 
(phloroglucin, 2 gm.; vanillin, 1 gm.; alcohol, 30 gm.), by mixing two 
drops of it with an equal amount of gastric contents (unfiltered) upon 
a white porcelain plate or dish, and evaporating slowly over a flame.1 
If free HC1 is present, a bright rose pink appears. In the absence of 
free HC1, the color is a dirty yellowish-brown. 
If this test is positive, we need make no further tests except the 
following: 
(b) Quantitatiue Estimation of free HCl and of Total Acidity 
To io c.c. of unfiltered gastric contents add four drops (about) of 
Topfer’s reagent (dimethyl-amido-azo-benzol: 0.5 per cent alcoholic 
solution) in a beaker; a carmine-red color results. Fill a graduated 
burette with decinormal NaOH solution, and let it run out into the 
beaker, a few drops at a time, until the carmine-red color disappears. 
While titrating stir the mixture constantly with a glass rod. Note the 
number of cubic centimetres of NaOH that have run out.2 
To estimate the quantity of free HC1, multiply the number of cubic 
centimetres of NaOH used in the titration by 0.0365; the result is the 
1 The same test may be performed on a glass slide which is subsequently put 
upon a piece of white paper to bring out the color. 
2 An ordinary medicine-dropper may be substituted for the burette if we get an 
apothecary to mark with a file upon it the point to which a (previously measured) 
cubic centimetre of water rises when sucked into the dropper. The half-centimetre 
point can be similarly marked. Decinormal NaOH solution is then sucked into 
the dropper and expelled, one-half centimetre at a time, into the beaker containing 
the Topfer’s reagent and gastric contents. THE STOMACH, LIVER, AND PANCREAS 
373 
percentage of free HC1. Normal free HC1 varies from 0.07 to 0.2 
per cent, or from 2 to 6 c.c. of decinormal NaOH for 10 c.c. of gastric 
contents (“gastric acidity = 20 to 60’’). 
The estimation of combined HC1 and of the acid salts is seldom of 
importance. 
Total acidity is determined by adding to the same beaker of contents 
in which the free HC1 has just been neutralized two or three drops of 
a one-per-cent solution (alcoholic) of phenolphthalein, and continuing 
the titration with the NaOH solution (and constant stirring) until a 
permanent red color appears. By multiplying the number of cubic 
centimetres of NaOH used from the beginning of the first titration up 
to the point when the red color reappears by 0.0365, we obtain a figure 
1 representing the percentage of total acidity. The normal range of 
total acidity is from 0.15 to 0.3 per cent, and we usually find that we 
use from 4 to 8 c.c. of NaOH solution in the process of neutralizing 
10 c.c. of gastric contents (“gastric acidity 40 to 80’’). 
Lactic acid is to be tested for only when HCl is absent. The test 
must be made at once, since lactic acid soon develops in stomach 
contents which are kept in a warm place. To perform the test, we 
dilute a solution of FeCl (strong aqueous) with water until a faint 
yellow color barely remains. Then fill the concavities of two test 
tubes with this solution, using one for comparison. If, on adding a 
few drops of stomach contents to the other, a considerable itensifica- 
tion of the yellow color occurs, lactic acid is almost certainly present. 
A negative test rules out lactic acid. 
The sediment need not be examined. It is true that sarcinae and 
various bacteria (Boas-Oppler bacillus and others) are often found in 
cases of gastric stasis, but they add little if anything to the other evi- 
dence of stasis more easily obtained—i.e., the symptoms mentioned on 
page 359, the presence of splashing'more than four hours after a meal, 
the evidence of dilatation or gastroptosis as given above, and the find- 
ing of organic acids. 
In my own practice I have nearly discarded test meals and chemical 
analysis. History, physical examination and x-ray are usually suffi- 
cient for all the diagnosis that we can use. The minor variations in 
the chemistry of the stomach are not in my opinion significant. Still 
I am not prepared yet to omit all description of these methods. 
From two to four ounces of barium sulphate suspended in milk or 
gruel are taken on an empty stomach (say at 5 a. m.). Six hours 
4. X-ray Examination of the Stomach 374 
PHYSICAL DIAGNOSIS 
later the patient is radiographed in the upright position. There should 
be then no bismuth residue in the stomach. The presence of any such 
residue is strong evidence that stasis and, therefore, some of the causes 
of stasis,—gastric cancer, peptic ulcer (gastric or duodenal), adhesions 
or ptosis, are present. 
Immediately after this test for stasis, a second bismuth meal is 
given and the patient is then fluoroscoped at frequent intervals there- 
after in search of departures from the normal shape assumed by the 
Fig. 208a.—Radiograph of Normal Stomach After Bismuth. B. First Portion of 
Duodenum. P. Pyloric Ring. C, C. Normal Contraction Rings. G, G, G, G. Bismuth 
in Gut. 
bismuth shadow under these conditions and corresponding to the 
outline of the stomach’s interior during peristalsis. If the patient is 
fluoroscoped lying down, great care should be taken to avoid pressure 
upon the stomach through the abdominal wall. By such pressure 
the gastric shadow may be so deformed as to simulate hour-glass 
stomach and other abnormalities. The tube is to be focussed in all 
cases upon the third lumbar vertebra, and neither this focus nor the 
patient’s position must change; great distortion of the picture and 
many false inferences result from failure to follow these rules. 
In a satisfactory picture of the stomach one should be able to make 
out the unbroken outline of the organ indented only by one or two 
contraction waves. The pyloric sphincter and portion of bismuth THE STOMACH, LIVER, AND PANCREAS 
375 
just beyond it in the duodenum (the “Bishop’s cap’’) should be visible 
(see Fig. 208a). If these are not to be made out, or if there is a marked 
interruption of the normal outline of the stomach shown in the same 
place in all the plates taken, cancer or ulcer may be suspected (see 
Fig. 208b). 
The changes to be found in peptic ulcer are hyperperistalsis, a 
filling defect or irregularity in outline and a bismuth residue visible 
at the end of six hours. These facts, together with the history and 
physical examination suffice for diagnosis in almost every case. 
Fig. 208b.—Radiograph of Stomach After Bismuth-Meal. P. Pylorus. A. Loss of 
outline proved at operation to be due to cancer of the greater curvature and anterior 
wall. D. Duodenum. 
5. Incidence and Diagnosis of Gastric Diseases 
In the wards of the Massachusetts General Hospital the number of 
cases apparently of gastric disease treated between 1870 and 1905 was 
as follows: 
Cancer 
4«3 
Ulcer 
536 
Dilatation, cause not determined 
170 
Dyspepsia1 
1,002 
T otal 
2,111 
The data at our disposal are as follows: 
1. The history (most important of all). 
2. The local and external examination of the epigastric region. 
3. The examination of the gastric contents. 
4. The x-ray examination. 
11.e., cases of painful digestion including anomalies of motion, sensation, 
secretion “gastritis” and “gastric catarrh,” but without evidence of ulcer or cancer. 376 
PHYSICAL DIAGNOSIS 
(а) In advanced cancer of the stomach we have pain, emaciation, 
anaemia, symptoms of fermentation (see page 371), often dilatation 
and motor insufficiency due to pyloric stenosis, sometimes absence of 
HC1 in the gastric contents (only eighty out of six hundred and fifty 
cases reported from the Mayos’ clinic by Graham and Guthrie showed 
no HC1), and in about two-thirds of the cases the presence of digested 
blood (“coffee grounds”) in the gastric contents and occult blood 
(guaiac) in the faeces. usually shows stasis and a defect in 
the normal outlines. But without the presence of an epigastric 
tumor all these facts are insufficient for diagnosis. Even the tumor 
itself may deceive us, as the adhesions around a gastric ulcer may 
present a similar mass to the palpating hand. 
The age of the patient is of great importance, especially if during 
the earlier decades of life he has been totally free from gastric symp- 
toms. Any type of dyspepsia, any sort of genuine gastric troubled 
. occurring in a person over forty who has never had any such trouble before, 
is strongly suggestive of cancer. 
(б) Peptic Ulcer, gastric or duodenal.—Physical examination usually 
shows us very little. The diagnosis rests upon the history. Contrary 
to the usual belief HC1 is normal or subnormal in nearly three-fourths 
of the cases. Occult blood is occasionally found and the stomach may 
show stasis. The vomiting of blood is infrequent (about twenty-five 
per cent.). X-ray evidence is very helpful. 
(c) Pure functional hyperacidity is not common but may produce 
symptoms indistinguishable from those of ulcer. 
(d) Hypoacidity and achylia gastrica are not characteristic of any 
gastric disease. They are common in alcoholism, in all types of anemia, 
in tuberculosis, diabetes, and nephritis, as well as in gastric cancer. 
(e) Gastric dilatation, when considerable, is almost always secon- 
dary to pyloric obstruction (due to cancer, ulcer, or adhesions). Symp- 
toms suggesting it are the vomiting at one time of a large quantity— 
a quart or more—of stomach contents, often containing fragments of 
food eaten more than eight hours previously. Such attacks of vomit- 
ing occur usually not after every meal, but at longer intervals. It is 
to be positively diagnosed by passing a tube and distending the 
stomach with air or water. 
(/) Gastric stasis occurs in all gastric lesions and in many general 
diseases (tuberculosis, anasmia, general debility). It constitutes 
what is referred to by patients as “dyspepsia,” or “sour stomach.” 
1 We must exclude angina pectoris and nephritis as well as gall stones and their 
effects. THE STOMACH, LIVER, AND PANCREAS 
377 
Fermentation of contents too long retained is the essential. This 
results in a sense of epigastric pressure, eructations (gas, sour or 
burning fluids), anorexia, nausea, and vomiting. Headache, constipa- 
tion and depression of spirits often accompany it. 
(g) Nervous (or better emotional) dyspepsia is the commonest of all 
gastric complaints. Diagnosis rests on the history, the negative 
physical examination and the results of therapy. 
II. The Liver 
The Massachusetts General Hospital records (1870-1905) show the 
following figures bearing on the incidence of diseases of the liver: 
Passive congestion 
1,288 
Portal cirrhosis 
234 
Biliary cirrhosis (Hanot’s) 
0 
Cancer of the liver 
184 
Sarcoma of the liver 
2 
Abscess of the liver 
5i 
Leukaemic infiltration 
46 
Pseudoleuksemic infiltration 
10 
Amyloid infiltration 
9 
Fatty infiltration 
6 
Hydatid cyst 
8 
Syphilis 
8 
“Simple cyst” 
6 
Actinomycosis 
3 
Acute yellow atrophy 
2 
Tuberculosis 
I 
T otal 
1,858 
Cholelithiasis 
457 
Acute cholecystitis 
no 
Catarrhal jaundice 
125 
Cancer of gall-bladder or ducts 
47 
Cholangitis 
9 
T otal 
701 
The evidences of liver disease may be either local or general. 
Local signs include: (a) Pain and tenderness in the hepatic region. 
(b) Enlargement of the organ, symmetrical or irregular, (c) Atrophy 
of the organ. 
The general signs which assist in the diagnosis of liver disease are: 
(d) Portal obstruction, (e) Jaundice, including changes in the color 
of the skin, mucous membranes, and excretions. (/) Loss of flesh and 378 
PHYSICAL DIAGNOSIS 
strength, (g) Evidences of infection (fever, leucocytosis, chills, 
sweats, anorexia), (h) Cerebral symptoms (headache, vomiting, 
depression, delirium, convulsions, coma). 
The various attempts to test the liver functions by chemical 
examination of urine and faeces have not as yet been successful; 
hence all diagnosis of liver disease must be built up of the above 
eight groups of data. 
i. Hepatic Pain 
This forms little or no part of many cases of liver disease, since it 
occurs only when the capsule is stretched or its nerves are involved in a 
perihepatitis. Many cases of hepatic abscess, for example, run their 
course without pain or become painful only when the pus burrows to 
the surface and stretches the capsule. Besides this capsule pain in 
liver disease, we have shoulder pain referred to the right shoulder or 
to the region of the right scapula, less often to other parts of the back. 
Capsule pain is most noticeable in congestion and in cancer of the liver, 
shoulder pain in abscess. 
Tenderness is present in the same cases which are painful, i.e., those 
in which there is perihepatitis or stretching of the capsule by rapidly 
increasing tension from within. The latter condition is commonest in 
passive congestion, but is not characteristic of any single disease. 
2. Enlargement of the Liver 
Tumors behind the liver, pushing it forward and down, are often 
overlooked, because they bring the liver so prominently into the fore- 
ground and fasten our attention on what is mistaken for an enlarge- 
ment of the organ. Wherever the cause of a supposed enlargement 
of the liver is not obvious, retroperitoneal sarcoma or some other deep- 
seated tumor should be suspected. 
I have already alluded to the possibility of mistaking the enlarged 
liver for empyema, and vice versa. 
We are sure of an increase in the size of the liver only when we can 
feel its edge below the ribs and can determine by percussion that its 
upper border is not depressed.1 To feel the edge of the liver, hook the 
fingers of both hands around the margin of the right ribs and ask the 
patient to take a deep breath. At the height of inspiration an edge 
1 A normal liver may be pushed down by air, water, or solid tumors in the lung 
and pleura, so as to be palpable below the ribs; but the evidence of a cause and the 
low position of the upper border usually make diagnosis easy. THE STOMACH, LIVER, AND PANCREAS 
379 
may be felt to descend against the fingers and to push its way beneath 
them. Unless an edge, either sharp or rounded, is felt, one cannot be 
sure of hepatic enlargement, for percussion of the lower edge of the 
liver is notoriously unreliable. Dulness below the costal margin is 
frequently found in cases without hepatic enlargement, and should 
never be relied on unless the liver can be felt. 
The long, smooth edge of the liver descending one or two inches 
with full inspiration is rarely mistaken for anything else, but if the 
edge is irregular and the surface nodular (see below) it may be hard to 
distinguish liver from stomach or possibly kidney. 
If ascites is present, the presence and dimensions of an enlarged 
liver beneath the fluid can sometimes be made out by dipping (see 
above, page 360). If this is impossible, the ascites may be tapped, 
after which it is usually easy to feel any enlargement that is present, 
as the belly walls are very flaccid. 
The causes of hepatic enlargement (in adults1), arranged approxi- 
mately in the order of frequency, are: 
1. Passive congestion (later stages of uncompensated heart dis- 
ease) . 
2. Obstructive jaundice (from any cause). 
3. Cirrhosis. 
4. Fatty liver, including, “infiltration” and “degeneration.” 
5. Malignant disease. 
6. Syphilis of the liver (congenital or acquired). 
7. Abscess of the liver. 
8. Leukaemia and pseudoleukaemia. 
9. Cholangitis. 
10. Amyloid. 
it. Hydatid cysts. 
The largest livers are found in malignant disease, biliary cirrhosis, 
and abscess. 
In passive congestion the liver is very tender, and the presence of 
uncompensated heart disease2 usually makes the diagnosis easy. 
The surface of the organ is smooth and firm. 
In cirrhosis a distinction must be drawn between (a) latent or 
compensated cases, wholly without symptoms, and (b) uncompensated 
cases, in which diagnosis depends on the chronic enlargement without 
1 In infants, rickets, anaemia, and gastrointestinal disturbances often pro- 
duce hepatic enlargement, though the splenic enlargement is usually much 
greater. 
2 Either primary or resulting from arterial disease and hypertension. 380 
PHYSICAL DIAGNOSIS 
any considerable increase under observation, associated with evidence 
of portal or biliary obstruction (or both) and without much pain or 
irregularity of the liver. Eighty per cent of the two hundred and 
thirty-four cases recorded at the Massachusetts General Hospital 
showed enlargement, but only twelve per cent showed pain (cf. 
Malignant Disease, below). 
The fatty liver is soft and smooth in feel. The presence of phthisis 
or alcoholism makes us suspect this diagnosis, which depends largely 
on excluding other causes of enlargement. 
Malignant disease of the liver (cancer or sarcoma) is usually sec- 
ondary to new growth elsewhere. The liver grows rapidly under 
observation, is usually painful (80 per cent of 168 Massachusetts 
Hospital cases) and nodular. Jaundice and irregular fever are present 
in over one-half of the cases (54 and 62 per cent respectively), and the 
loss of flesh and strength is marked. 
Obstructive jaundice (due to stone, catarrh, or tumor of the bile 
ducts, but rarely to any other cause) often produces an enlarged liver. 
Diagnosis depends on the evidence of a cause for the obstruction and 
the absence of hepatic nodules, pain, or a rapid increase in the size of 
the organ. 
Syphilitic liver may be distinguishable from cirrhosis or from 
malignant disease only by the Wassermann test and therapeutic test. 
The history or present evidences of alcoholism or of syphilis are 
important factors in diagnosis, but, since syphilis may simulate the 
nodular liver of malignant disease or the general enlargement and 
portal stasis of cirrhosis, it is essential to give antisyphilitic treatment 
in all doubtful cases of liver disease. 
Abscess of the liver produces enlargement, fever, leucocytosis, 
and chills in typical cases, but any of these symptoms may be absent 
and diagnosis is often difficult. Pain is usually absent. The presence 
of a possible cause (amoebic dysentery, appendicitis) is very important 
evidence. The enlargement is more apt to be upward and to the right 
than in other liver diseases, since the pus usually starts in the right 
lobe and burrows upward. Hence many cases are mistaken for 
empyema (see above, page 343). Should swelling or fluctuation ap- 
pear externally the diagnosis is usually obvious, but in most cases this 
does not occur. Whenever fever, leucocytosis and dulness in the 
right lower back appear after an appendix operation with drainage, 
after a dysentery, or after long continued biliary obstruction (gall 
stone), hepatic abscess should be suspected. As a rule the diagnosis is 
made on the etiology rather than on physical signs. THE STOMACH, LIVER, AND PANCREAS 
381 
Soft new growths and syphilis may be almost indistinguishable 
from abscess by local signs, but jaundice is much commoner in malig- 
nant disease and the liver of syphilis is often irregular. The history 
is of value. 
Suppurative cholangitis, sub phrenic abscess, and pylephlebitis give 
us practically the same symptoms as hepatic abscess. 
Amyloid liver is recognized by the presence of an appropriate 
cause (chronic suppuration or syphilis) and the evidence of amyloid 
in other organs (enlarged spleen, albuminuria, diarrhoea). The liver 
is smooth, not irregular as in hepatic syphilis and cancer. 
The leukcemic liver is recognized by blood examination; the pseudo- 
leuksemic liver by the normal blood and the histological examination 
of the glandular enlargements which always accompany it. 
Hydatid cyst is rarely to be diagnosed by physical signs. The 
history of a residence in Australia, Iceland, certain parts of Germany 
or of the British Isles, is important evidence, since the disease has 
never been known to originate in North America. Physical examina- 
tion may enable us to make out that the heptaic enlargement is due to 
a cystic tumor, tense and elastic, with notable absence of constitutional 
disturbances (Eolleston) and often an eosinophilia. 
3. Atrophy of the Liver 
Diminution in the size of the liver cannot often be demonstrated 
satisfactorily during life, since we must rely upon percussion for our 
evidence, and percussion of the upper and of the lower border of the 
liver may be rendered difficult by distention of the lung (emphysema) 
or of the colon. Atrophy may be recognized in a small proportion of 
the cases of hepatic cirrhosis and in acute yellow atrophy, but is rarely 
recognized in either condition. The rapidly fatal course of the latter 
disease with jaundice and a “typhoidal state” contrasts with the 
prolonged portal stasis characteristic of cirrhosis. 
4. Portal Obstruction 
A characteristic group of signs manifest the presence of an obstacle 
to the flow of blood through the portal system. This group includes: 
1. Haematemesis and dyspepsia. 
2. Ascites1 (see page 361). 
3. Splenic enlargement.1 
1 Ascites and splenic enlargement are not purely mechanical phenomena 
Toxaemia and sometimes chronic peritonitis or cardiac failure contribute. 382 
PHYSICAL DIAGNOSIS 
4. Collateral dilatation of the abdominal veins (rarely seen in life). 
Hcematemesis is usually due to rupture of dilated oesophageal 
veins, occasionally to gastritis. 
Splenic enlargement is more marked in the rare cases associated 
with chronic jaundice (biliary cirrhosis) and without ascites. 
The cause of portal obstruction is: 1. Cirrhosis, in ninety-five per 
cent of the cases. The remaining five per cent is made up of: 2. 
Acute hepatitis and portal compression by thrombosis or tumors. 
5. Jaundice 
The yellow staining of sclera, skin, and mucous membranes, with or 
without changes in the color of the urine and faeces, is known as jaun- 
dice. I have classed it as a general rather than a local sign of liver 
disease, because it may occur from toxaemia and independent of any 
lesion of the liver; for instance, in septicaemia, malaria, yellow fever, 
and pernicious anaemia. It is true, nevertheless, that all jaundice is 
due ultimately to obstruction in the path of the bile stream. In the 
toxaemic cases the obstruction is due to inflammation of some of the 
small ducts within the liver. In the cases due to stone or cancer 
the obstruction is in'the larger bile ducts, usually the common duct. 
Causes of Jaundice.—The four types most often seen are: 
1. Jaundice of the new-born (occurs in from thirty to eighty per 
cent of all children). 
2. Catarrh of the bile ducts (“catarrhal jaundice”). 
3. Gall stones, especially in the common duct. 
4. Cancer (pancreas, glands, liver, gall bladder, or bile ducts). 
Less common are the cases due to 
5. Acute yellow atrophy. 
6. Syphilis of the liver. 
7. Infectious disease or toxaemia. 
Rare causes are: 
8. Cirrhosis of the liver. 
9. Weil’s disease and other types of infectious jaundice. 
10. Congenital obliteration of the bile ducts. 
11. Family hemolytic jaundice. 
The results of jaundice upon the body are chiefly the following: 
(a) Slow pulse (often below 60). (b) Itching of the skin, (c) Mental 
depression. (d) Hemorrhagic tendency (which renders operation 
dangerous). THE STOMACH, LIVER, AND PANCREAS 
383 
In mild cases there is no bile in the urine; in severe cases it is almost 
always present. The stools are gray or clay-colored when the obstruc- 
tion is in the larger bile ducts outside the liver, but in the toxsemic 
forms of jaundice abundance of bile passses into the intestine and the 
stools are of normal color. 
Diagnosis of the cause of jaundice depends on the following con- 
siderations : 
1. If it occurs during the first four days of life without any other 
symptom and passes off within a few weeks, we call it simple jaundice 
of the new-horn. 
2. If the attack is preceded by gastro-intestinal disturbances, 
usually in a young person, if pain and hepatic enlargement are slight 
or absent, and if the jaundice passes off within six weeks, we term it 
“ catarrhal jaundice” (though the pathology of this and of the preceding 
condition is unknown). 
3. If there have been attacks of biliary colic (see below, page 385), 
intermittent fever with intervals of good health, and no considerable 
or progressive enlargement of the liver or gall bladder, stone in the 
common duct is probably the diagnosis. 
4. Cancer of the pancreas, duodenal papilla, gall bladder, bile 
ducts, or of the glands at the hilus of the liver, produces enlargement 
of the gall bladder, and a jaundice usually painless but of the intensest 
type known. Loss of flesh and strength is rapid. Cancer of the liver 
itself gives a rapidly enlarging, nodular liver often with pain, and, 
in fifty per cent of cases, jaundice. 
5. In ordinary portal cirrhosis, the rarely occurring jaundice is less 
intense and permanent, portal stasis is usually evident, and there is 
generally an enlargement of the liver. 
6. Enlargement of the liver with jaundice lasting for years in 
young people is probably due to biliary cirrhosis, or family hemolytic 
jaundice. In some of the cases of this group the red cells can be 
shown to possess an exaggerated vulnerability, and the blood serum 
may have unusual autohemolytic powers. Several such cases may 
occur in a single family. 
7. Hepatic syphilis produces jaundice in a small percentage of 
cases, and under these conditions is so apt to be mistaken for cancer 
that I think in all cases supposed to be cancer in or near the liver a 
Wassermann reaction should be tried and a course of antisyphilitic 
treatment given. Other lesions or symptoms of syphilis will naturally 
influence us. 384 
PHYSICAL DIAGNOSIS 
8. The jaundice secondary to septicaemia, yellow fever, malaria, 
and pernicious anaemia is usually slight and rarely shows in the urine 
or bleaches the stools. The evidence of anaemia or of an infection 
makes clear the nature of the jaundice. 
9. Acute yellow atrophy, when in addition to jaundice and a 
small liver, we have rapid failure of strength and somnolence and 
other mental disturbance leading to death. The urine is rarely char- 
acteristic. 
10. Weil’s disease is a term sometimes applied to the acute 
infections of spirochetal origin which are accompanied by jaundice. 
From catarrhal jaundice it is to be distinguished during life only by 
convincing evidence of general infection. 
6. Loss of Flesh and Strength 
in cases presenting other signs of liver disease is commonest in uncom- 
pensated cirrhosis and in malignant disease, but may occur in gall- 
stone disease, syphilis, or abscess. I have known a physician greatly 
alarmed at his own rapid emaciation, though his symptoms (jaundice 
and colic) pointed to stone in the common duct and operation proved 
this diagnosis correct. 
7. The Infection Group of Symptoms 
These symptoms—viz., fever, chills, sweats, leucocytosis, distur- 
bances of digestion and sleep—are oftenest seen in: i. Cholangitis. 
2. Hepatic abscess.1 3. “Ball-valve” or “floating” stone in the 
common duct. In the last disease jaundice is usually present; in the 
others usually absent. In cancer of the liver, fever and leucocytosis 
are often present, but the other signs of infection are rarely seen. 
8. The Cerebral Symptoms of Liver Disease 
These vary from simple depression and apathy to delirium, con- 
vulsions, and coma. Severe symptoms are oftenest seen at the end of 
uncompensated cirrhotic cases; eighty-two per cent of our fatal cases 
showed during the last days of life symptoms indistinguishable from 
uraemia. Identical disturbance occurs in acute yellow atrophy. 
III. The Gall Bladder and Bile Ducts 
(a) Biliary colic, and (b) enlarged gall bladder, with or without 
tenderness and pain, are the data on which (with the evidence of local 
1 With or without pylephlebitis. THE STOMACH, LIVER, AND PANCREAS 
385 
or general infection, cachexia, intestinal obstruction, and jaundice) 
our knowledge of gall-bladder disease is built up. In some cases 
puzzling digestive symptoms closely resembling those of duodenal 
ulcer are present. 
1. Differential Diagnosis of Biliary Colic 
Biliary colic, due to impaction of a gall stone in the cystic or 
common duct, is a sudden pain in the gastric or hepatic region, radiat- 
ing thence in all directions, but especially to the right shoulder, 
scapula or back, with fever, chills, and vomiting. In most cases the 
attack lasts from three to twelve hours (Rolleston) unless relieved by 
morphine. The pains may be of any degree of severity, and are often 
accompanied and followed by tenderness over the hepatic region and 
right hypochondrium. The liver or gall bladder is seldom palpable. 
Jaundice precedes or follows the attack in about one-half of the cases; 
in about fifty per cent the stone can be visualized by x-ray. 
Renal colic differs in that it usually starts over the kidney (in the 
back) and radiates down the ureter, while the urine is apt to be bloody 
but free from bile. 
Floating kidney with kinked ureter may produce pains which 
cannot in themselves be distinguished from biliary colic. The palpa- 
tion of the floating kidney may be all that makes us suspect that organ 
to be the cause of suffering. 
Peptic ulcer (gastric or duodenal) may produce sharp, paroxysmal 
pain, but this usually comes several hours after a meal, can be relieved 
by food, vomiting, lavage, or alkalies, and produces no fever, chill, or 
sweat. Hyperchlorhydria may produce similar pain at night (the 
commonest time for biliary colic), but is relieved by food or alkali. 
Lead colic is almost always associated with lead dots in the gums 
and stippling of the red corpuscles (see pages 25 and 467). The 
history of work as a painter or plumber and the absence of tenderness 
assist the diagnosis. 
Gastric Crises in tabes are often operated on under a false diag- 
nosis of gall stones. Study of the reflexes prevents such a mistake 
in most cases but lumbar puncture is occasionally necessary for 
diagnosis. 
2. Enlarged Gall Bladder 
An enlarged gall bladder cannot be felt unless it is stretched tight 
by its contents; a very tense gall bladder may be palpable without much 386 
PHYSICAL DIAGNOSIS 
enlargement. Probably most enlarged gall bladders are not tense, 
and so cannot be made out without operation. When palpable the 
organ presents as a smooth, rounded, pear-shaped tumor at the 
margin of the ribs in the nipple line. 
The causes of enlargement are: 
(а) Stone in the cystic duct, at the neck of the gall bladder. 
(б) Cancer of the pancreas or other tumor obstructing the common 
duct from without.1 
(c) Cholecystitis. 
In the first of these jaundice is rarely present (ten to fifteen per 
cent—Riedel2), and colic with or without palpable tumor is our guide 
to diagnosis. 
In cancerous obstruction there is intense and permanent jaundice. 
In cholecystitis there is usually no jaundice, but all the signs of 
local and general infection—pain, tenderness, leucocytosis, and fever— 
are present. In acute cases the symptoms, however, may be indis- 
tinguishable from those of appendicitis, since the pain may be referred 
to the navel or even to the appendix region. Many mistakes of 
diagnosis between appendicitis and acute cholecystitis occur, and 
must occur until our present diagnostic resources are increased. 
3. Results of Cholecystitis 
(a) Adhesions about the gall bladder may involve the duodenum or 
pylorus, and produce kinking and consequent dilatation of the stomach 
and chronic dyspepsia. 
(b) Intestinal obstruction (see below, page 393) is occasionally 
produced by the ulceration of a large gall stone from the gall bladder 
into the intestine, usually the small intestine or duodenum. 
IV. The Pancreas 
Diseases of the pancreas can very rarely be diagnosed by our 
present methods. If greatly enlarged (tumor, cyst, hemorrhage) it 
may become palpable as a deep epigastric tumor, but we are rarely 
1 Courvoisier has shown that if the common duct is obstructed by a gall stone 
the gall bladder is very rarely enlarged. 
2 Riedel: Berlin, klin. Woch., 1901, No. 3. THE STOMACH, LIVER, AND PANCREAS 
387 
able to differentiate such tumors from those of the retroperitoneal 
structures. 
Indirect and uncertain information is afforded by the presence in 
the urine of sugar or fat-splitting ferments1 and in the stools by the 
appearance of an abnormal amount of muscle fibre or of fat not other- 
wise to be accounted for (i.e., in the absence of jaundice, diarrhoea, 
tuberculous peritonitis, or large meals of fat). 
1. Cancer of the pancreas may sometimes be suspected on account of 
its pressure effects. Intense and painless jaundice with enlarged 
(perhaps palpable) gall bladder and liver is often due to the pressure 
of cancer in the head of the pancreas upon the common bile duct. 
Ascites and swelled legs may be produced by compression of the 
inferior vena cava. But the diagnosis can rarely be more than a 
suspicion, for cancer of the gall bladder, ducts, duodenal papilla or 
retroperitoneal sarcoma may produce similar pressure effects. Should 
these pressure effects coincide with a glycosuria and the presence of a 
deep-seated, almost immovable tumor, the suggestion of pancreatic 
disease becomes more plausible. 
2. Acute pancreatic disease, hemorrhagic or suppurative, is not rec- 
ognizable until it is seen at an operation undertaken for the relief of 
some grave, acute lesion of the upper abdomen. Perforated gastric 
ulcer and intestinal obstruction may give identical symptoms, viz., 
sudden, intense, epigastric pain and tenderness, with vomiting and 
collapse. One or two days later a tender epigastric tumor may appear, 
but this presents no characteristic peculiarities. 
3. Pancreatic cyst presents a very slow-growing, possibly elastic, 
deep-seated epigastric tumor, which usually produces little in the way 
of pressure effects, and may be associated with glycosuria and fatty 
stools. 
4. Bronzed Diabetes.—The association of diabetes with bronzing of 
the skin and enlargement of the liver is strongly suggestive of an 
associated chronic fibrous pancreatitis. 
In any doubtful case the possibility of pancreatic disease is in- 
creased: (a) If improvement follows the administration of pancreatic 
preparation; (b) if glycosuria follows the administration of 100 gm. of 
glucose (alimentary glycosuria). 
1 The suspected urine is neutralized with potassium hydroxide and one portion 
of it boiled to destroy any ferment that may be present. To this and to the 
unboiled portion ethyl butyrate is added. In twenty-four hours an acid reaction 
may appear in the unboiled specimen if it contains a ferment, while the other 
specimen shows no considerable change in reaction. 388 
PHYSICAL DIAGNOSIS 
(a) Incidence of Pancreatic Disease 
The following table is from the Massachusetts General Hospital 
records (1870-1905): 
Cases 
Cancer of the pancreas 
35 
Acute pancreatitis 
13 
Chronic pancreatitis 
Cyst of the pancreas 
3 
Total 
61 CHAPTER XXIII 
THE INTESTINE, SPLEEN, KIDNEY 
I. The Intestines 
Incidence of Intestinal Disease (excluding diarrhoea and constipation) 
at the Massachusetts General Hospital, 1870-1905. 
I. 
Appendicitis 
3,314 
2. 
Acute obstruction 
142 
3- 
Cancer (above the rectum) 
155 
4- 
Dilated colon 
6 
5- 
Tuberculosis 
2 
6. 
Fascal impaction (above the rectum) 
2 
Total 
3,621 
1. Data for Diagnosis 
The data on which are based all our conclusions regarding intes- 
tinal disease are obtained from the following sources: 
1. Pain (colicky or steady) and tenderness, tenesmus. 
2. Gaseous distention and the noises and sensations produced by 
gas. 
3. Diarrhoea or constipation. 
4. Muscular rigidity of the belly wall protecting an intestinal lesion. 
5. Tumor, palpable or visible, and believed to be connected with 
the intestines (together with the effects of catharsis on such tumor). 
6. Visible or palpable peristalsis. 
7. Digital or visual examination of the rectum. 
8. Examination of the intestinal contents, fsecal and other. 
9. Inflation of the colon through the rectum. 
10. X-ray after barrina enema. 
11. Constitutional manifestations, such as fevers, vomiting, leu- 
cocytosis, emaciation. 
Some of these data need further comment. 
Intestinal Pain.—Most pains associated with intestinal disease 
(appendicitis, cancer) are due in fact to irritation of the peritoneum. 
Which of the numerous pains referred to the belly should be inter- 
preted as intestinal in origin ? Those especially which (a) shift rapidly 
389 390 
PHYSICAL DIAGNOSIS 
from place to place; (b) accompany the noises and sensations of the 
passage of gas and fasces through the intestine; (c) accompany diar- 
rhoea or constipation; recur rhythmically. 
Tenderness is usually a symptom of peritoneal rather than intes- 
tinal irritation. With true intestinal pain {colic) there is often relief 
by pressure—the precise opposite of 
tenderness. Yet so close is the asso- 
ciation of intestine and peritoneum 
that in appendicitis, intestinal ulcera- 
tion, tumors, and even in simple 
gaseous distention of the gut, there 
is often local or general tenderness. 
When extreme and associated with 
constitutional manifestations—fever, 
leucocytosis, collapse—it always sug- 
gests peritonitis. When there are no 
constitutional manifestations, a purely 
local pain or tenderness has little 
diagnostic value. 
Tenesmus.—The desire to pass 
another stool as soon as one has been 
evacuated, together with local burn- 
ing and straining, means always rectal 
irritation (inflammation, ulcer). It 
is one of the most definite and reliable 
symptoms known. 
Gaseous distention of the intestine 
is proved by an increase of the normal 
tympanitic note over part or all of the 
belly, together with a prominence of 
the overlying belly wall. It is chiefly 
and most frequently the colon that produces distention. 
The significance of distention is vague and depends largely on the 
associated data. In acute gastro-intestinal “catarrh” the diarrhoea 
and absence of severe constitutional manifestations make us put little 
stress on the associated distention. In typhoid fever distention results 
from atony of the intestinal walls and is “to some extent a measure 
of the intensity of the local lesions’’ (Osier). In intestinal obstruction 
distention may be extreme if the stoppage is low down (in the colon), 
less marked if the lesion is high up. 
Fig. 209.—Congenital dilatation 
of colon. THE INTESTINE, SPLEEN, KIDNEY 
391 
Distention which continues despite free purgation is very often due 
to chronic intestinal obstruction. 
In starvation, children often get very large bellies, owing to muscu- 
lar atony of the gut and the resulting gaseous accumulation. But in 
no case is the distention of itself of much diagnostic value. The 
associated symptoms give it significance. 
In congenital dilation of the colon (Hirschsprung’s disease) a huge 
belly is associated with obstinate constipation. The colon can be 
measured and shown to be dilated through the use of bismuth suspen- 
sions (by rectum) and x-ray. (See Fig. 209.) 
Diarrhoea, the passage of more and looser stools than is normal for 
the individual, is, like distention, a result of many causes both within 
and outside the intestine. 
The most important are: 
(a) Indigestion (acute and chronic). 
(b) Ulceration (some cases only). 
(c) Cancer of the colon or rectum. 
(d) Intussusception. 
(e) Infectious diseases (cholera, dysentery, typhoid). 
(/) Intestinal parasites. 
(a) Nervous causes (emotion, Basedow’s disease, etc.). 
(&) General infections (sepsis). 
(e) Cachectic states (anaemias, nephritis, etc.). 
i. Intestinal disease. 
2. Outside influences. 
By a search for these causes, as well as by the use of the data 
obtained by examination of the stools, we arrive at an understanding 
of the diagnostic significance of diarrhoea. 
Aside from symptomatic diarrhoea, constipation, and dysentery, 
which produce no physical signs beyond those described—distention, 
borborygmi, pain, tenderness, tenesmus, and constitutional mani- 
festations—there are but three important1 diseases of the intestines: 
I. Appendicitis. 
II. Intestinal obstruction. 
III. Cancer of the bowel. 
2. Acute Appendicitis 
1. The local signs are pain, tenderness, muscular spasm, and 
tumor. 
2. The general or constitutional signs are fever, chill, rapid pulse, 
vomiting, constipation, frequency or cessation of micturition, and 
leucocytosis. 
1 Tuberculous enteritis and pericaecal tuberculosis will be briefly referred to 
later. 392 
PHYSICAL DIAGNOSIS 
(а) The pain may be at first epigastric (pylorospasm ?) or general, 
later localizing itself in the right iliac fossa, less often near the navel, the 
gall bladder, or in any other part of the belly. 
(б) The tenderness is more important in diagnosis; indeed, without 
tenderness diagnosis is rarely possible. It is usually greatest near a 
point half-way from the anterior iliac spine to the navel. Occasionally 
a tender point in the pelvis may be reached by rectal or vaginal 
examination, but this is not at all a reliable sign. 
(c) Muscular spasm over the appendix region is present in most 
cases, and, while it renders accurate palpation impossible, it is in itself 
so characteristic of the disease that we do not regret it. 
Psoas spasm occurs in a minority of cases. The patient leans his 
body forward and toward the right in walking, or, if recumbent, draws 
up the right thigh to relax the spasm. 
(d) Tumor—about the size and shape of a lemon, ill-defined and 
tender—is felt in the right iliac fossa in many cases. It may be con- 
siderably larger and better defined if abscess has existed for several 
days, or it may be smaller and more sausage-shaped. Fluctuation 
and bulging can sometimes be made out by rectum or vagina. 
(e) The constitutional signs may or may not be marked, according 
to the duration of the process, its virulence, and the degree of infection 
of the peritoneal cavity. The fever is usually moderate, under 102° 
F., with corresponding elevation of the pulse. Vomiting comes at 
the outset if at all, and is usually over by the second day. A leucocyte 
count which rises or remains elevated (above 16,000) accompanies the 
active and advancing stages of the disease. In cases that are very 
mild or tightly walled in by adhesions, and in cases with virulent 
general peritonitis, the leucocytes may be normal or subnormal. 
Diagnosis can hope only to establish the existence of a local inflam- 
matory process in the abdomen; acute cholecystitis and acute pus tube 
may present signs indistinguishable from those of appendicitis, though 
the site of tenderness often sets us right. Non-inflammatory processes, 
such as lead colic, tabes, biliary and renal colic, floating kidney, and 
acute gastro-intestinal upsets, can usually be excluded, since they do 
not show so much local tenderness, fever, and leucocytosis. 
In those who are familiar with the symptoms of appendicitis, a 
vivid imagination may conjure up a set of sensations that are difficult 
for the physician to distinguish from those of the actual disease. Even 
tenderness may be simulated, but, by distracting the patient’s atten- 
tion while we palpate, we may be able to press hard over the appendix 
without eliciting complaint. The absence of leucocytosis, the age and 
sex of the patient, also help us to exclude appendicitis. THE INTESTINE, SPLEEN, KIDNEY 
393 
3. Chronic Appendicitis 
A disease which can be diagnosed by the x-rays alone. There are 
no symptoms or signs characteristic of it and in most cases it repre- 
sents only a harmless historical landmark, a shrivelled appendix. 
4. Intestinal Obstruction 
(a) Acute Obstruction.—A person may have had no faecal discharge 
for a week or even considerably longer and yet present all the evidences 
of good health. It is only when vomiting, severe paroxysms of pain, 
and distention of the belly ensue that we suspect obstruction. In the 
acute cases tumor is noted in only about fifteen per cent. In the 
chronic cases, usually due to stricture or cancer, a faecal tumor can 
often be felt and diarrhoea be the chief symptom or may alternate with 
constipation. 
By physical signs alone I do not believe that general peritonitis 
and acute intestinal obstruction can always be distinguished. Fever 
is not distinctive of general peritonitis, for it occurred in eighty-four 
out of one hundred and twenty-two cases of acute obstruction in the 
Massachusetts Hospital records, and in forty-three of these cases free 
fluid in the peritoneal cavity was demonstrated as well. Stercoraceous 
vomiting may occur in general peritonitis; it was absent in three- 
fourths of the Massachusetts Hospital cases of obstruction. Weak, 
rapid pulse, cold extremities, and a drawn, anxious face are common 
to both diseases. Tenderness is more general and more marked in 
general peritonitis than in simple obstruction, yet some tenderness was 
complained of in fifty-six out of the one hundred and twenty-two cases 
of obstruction just cited. 
On the whole, the differential diagnosis of these two diseases seems 
to depend far more on the history and the etiology than on physical 
signs. 
(b) Chronic Obstruction.—Here the diagnosis is simpler. There is 
usually a history of increasing constipation sometimes interrupted by 
occasional attacks of diarrhoea.1 Tumor is palpable in fifty-eight per 
cent of cases. Visible peristalsis was recorded in seventeen per cent 
of the Massachusetts Hospital cases. Distention is gradual and late, 
but often persists or recurs despite purgation. Cancer, usually at 
the sigmoid or caecum, is the commonest cause. Stricture, except 
cancerous stricture, is rare, but syphilis occasionally produces it. 
(c) Acute Obstruction by a Chronic Lesion.—Cancer of the sigmoid 
often exists for months almost latent, or produces only moderate con- 
1 The latter combination occurred in six per cent of the Massachusetts Hospital 
cases. 394 
PHYSICAL DIAGNOSIS 
stipation, so that the patient considers himself well. Such cancers 
may present an annular growth, hardly bigger than a signet-ring, 
practically an annular stricture. 
This stricture may be suddenly “shut down” during an acute 
gastro-intestinal attack, and we are then confronted with all the signs 
of acute obstruction. Only the seat of the lesion, the age of the 
patient, and possibly the appearance of peristaltic waves can lead us 
aright in our diagnosis of the cause of obstruction. 
5. Cancer of the Bowel 
The signs are those of chronic intestinal obstruction (see last 
section). Occasionally the tumor may not produce much obstruction, 
and we have simply pain and a tumor which we find by examination 
is not attached to the liver, spleen, kidney, or stomach, and usually is 
about the size of a hen’s egg. If faeces have accumulated behind such 
a tumor, we may feel larger masses. In my experience palpable tumors 
due to faecal impaction alone, without organic stricture or cancer, are 
very rare, except in the rectum; if found above this region they are 
almost invariably dependent on stricture or cancer of the bowel. 
6. Examination of Intestinal Contents 
1. Weight.—With the average diet of the adult “Anglo-Saxon,” 
the weight of the daily stool is from ioo to 250 gm. (about 25 to 70 
gm. dry) but Chittenden has shown that with a low proteid diet of 
2,000-2,750 calories value, the weight of the stool may be less than 
half this amount.1 
2. Color.—(a) White or light yellow—milk diet, bread and milk 
diet. 
(b) Black—blood, bismuth or iron (medicinal), blackberries, 
huckleberries, red wine. 
(c) Green; some normal infant’s stools after standing; fermented 
infant’s stool if green when passed; green vegetables, calomel. 
(d) Gray—absence of bile (jaundice), sometimes after cocoa or 
chocolate. 
(e) Bloody red—if in small amount and fresh, usually due to 
hemorrhoids; in large amounts it may also be due to hemorrhoids or 
to any of the causes of intestinal ulceration (typhoid, cancer, dysen- 
tery, etc.). 
3. Odor.—In adults of no great significance. In infants foul stools 
suggest albuminoid decomposition, and strongly sour stools suggest 
acid fermentation. 
1 “Physiological Economy in Nutrition,” 1904, p. 42. THE INTESTINE, SPLEEN, KIDNEY 
395 
4. Abnormal Ingredients.—(a) Undigested food in small quantities 
is present in normal stools, but when digestion is faulty larger quan- 
tities easily recognized by the naked eye may occur. Pieces of meat, 
flakes of casein (especially in typhoid patients overfed with milk), 
fragments of starchy food, and lumps of fat (steatorrhoea) may be seen. 
The natural inference from the presence of these substances is that 
the gastro-intestinal tract is not at present dealing with them satis- 
factorily. Fatty stools are present in jaundice, tuberculosis, or 
amyloid of the intestine, and even in simple catarrh. Though often 
associated with pancreatic disease, fatty stools are by no means char- 
acteristic of it. 
(b) Mucus.—Small shreds of mucus adherent to faeces are of no 
importance and cause much unnecessary worry among anxious 
mothers. Larger amounts, if intimately mixed with the stool, point 
to catarrh of the small intestine; if mucus thickly coats or makes up 
the bulk of the stool, the trouble is in the colon. The latter is by far 
the commonest condition. Anything from a very mild to a severe 
catarrhal condition is accompanied by mucus. Large periodic dis- 
charges of mucus and shreds mean usually the neurosis “colica 
mucosa. ” 
(c) Fresh Blood.—Piles are by far the commonest cause of bloody 
stools, and the amount of blood may be trifling or may be large enough 
to produce in time a severe anaemia. 
Enteritis (the mild follicular or the severe ulcerative form) often 
produces bloody stools. The associated symptoms, diarrhoea, mucus, 
and pain, together with the etiology (dietetic error, typhoid fever, 
amoeba histolytica), must determine the nature of the enteritis. 
In cancer of the rectum or sigmoid (rarely higher up in the bowel), 
small quantities of blood, fresh or altered, are almost always passed 
sooner or later. The infrequent, offensive, and painful stools and the 
results of digital examination usually reveal the source of the blood. 
In intussusception the association of bloody stools with the sudden 
appearance of a painful abdominal tumor (usually in the cascal region), 
vomiting, and severe constitutional manifestations suggest the 
diagnosis. 
In hemorrhagic diseases (purpura, scurvy, acute leukaemia) blood 
may come from the intestine as well as from the other mucous mem- 
branes. Other rare causes for blood in stools are a ruptured aneurism, 
thrombosed mesenteric artery, rectal syphilis, or fissure. 
(d) Altered blood (tarry stools, melaena) follows the pouring out of 
blood—a pint or more—in the upper gastro-intestinal tract, and occurs 396 
PHYSICAL DIAGNOSIS 
in hepatic cirrhosis, gastric or duodenal ulcer, after severe nose-bleed, 
and occasionally from other causes. Occult blood, recognizable by 
the guaiac test, often occurs in cancer or ulcer of the stomach, and 
forms an important link in the chain of evidence on which the diagnosis 
of those diseases is based. 
(1e) Pus is not of great diagnostic value. Large amounts mean the 
breaking of an abscess (appendix, pus tube) into the rectum. Small 
amounts occur in ulcers or even from catarrh. 
(/) Shreds of tissue point to ulceration. 
(g) Gall Stones.—In suspicious cases break up the fasces in a sieve 
with plenty of water. The peculiar, facetted shape of most gall stones 
is easily recognized. 
7. Intestinal Parasites 
Bacteria.—Only the tubercle bacillus can be recognized without 
culture methods, which do not fall within the scope of this book. 
For the identification of tubercle bacilli the following method is to 
be recommended: “Dilute the stool with ten volumes of water, mix 
thoroughly, and let it stand in a wide-mouthed bottle for twenty-four 
hours. The narrow layer between the thin supernatant liquid and 
the solid sediment contains the bacilli. Remove this with a pipette, 
spread it on a cover slip, evaporate slowly to dryness, and proceed as 
with sputum’’ (“Harvard Outlines of Medical Diagnosis, ’’ 1904, p. 29). 
Animal Parasites.—The most important are: 
1. Amoeba histolytica, 
(a) Uncinaria americana. 
I. Serious.... 
2. Hook-worm 
(b) Anchylostoma duodenale. 
3. Bilharzia haematobium. 
4. Balantidium coli. 
5. Tape-worms; the beef-worm (Taenia saginata) is very com- 
mon; the pork-worm (Taenia solium) is rare; the minia- 
ture tapeworm (Taenia nana) and the fish-worm 
(Dibothriocephalus latus1) are fairly common. Several 
other forms occur in foreign countries. 
II. Relatively 
mild. 
6. Strongyloides intestinalis. 
7. Ascaris lumbricoides (round-worm). 
III. Usually 
harmless. 
8. Oxyuris vermicularis (thread-worm; pin-worm). 
9. Trichiuris trichiura (whip-worm). 
10. Trichomonas intestinalis. 
11. Lamblia intestinalis. 
1 Fish tape-worms may produce a severe anaemia, but in probably the great 
majority of all cases they do not do so. Cabot—Physical Diagnosis. 
PLATE I 
Fig. i.—Trichomonas hominis. (Leuckart.) 
Fig. 2.—Balantidium coli. (Leuckart.) Magnified about 150 diameters. 
Fig. 3-—Lamblia intestinalis. (Leuckart ) THE INTESTINE, SPLEEN, KIDNEY 
397 
Tape-worms, round-worms, pin-worms, and the strongyloides are 
to be recognized in their adult form (see Figs. 210, 211, 212, 213, 214). 
They are usually noticed by the patients themselves and brought to 
the physician for examination. If the worm has the look of a common 
earth-worm, but a length of five to nine inches, it is safe to call it the 
“round-worm” (Ascaris lumbricoides); if the worm is about one-hall 
an inch long and as thick as a pin, it is in all probability a “ pin-worm ” 
(Oxyuris vermicularis). 
The Amoeba histolytica is to be searched for in fresh stools passed 
into a warm vessel, after MgS04 has been given. A bit of mucus from 
such stools or a little obtained by 
passing a rectal tube is put upon a 
warmed slide with a drop of water, 
covered with a cover glass, and ex- 
Fig. 210.—a, Head of Taenia saginata, much magnified; b, uterine canal of same. About 
twenty branches on each side. 
amined at once with a high-power dry lens. The organism is rec- 
ognized as an amceba by the presence of distinct amceboid movements. 
When dead it assumes a round shape, but one should not attempt a 
positive diagnosis until live amoeboid parasites are present. 
Apparently there is a harmless variety of amoeba coli to be obtained from the 
stools of many normal persons by purgation. This is distinguished from the amoeba 
histolytica by the following criteria (Vedder). The dysenteric or tissue-destroying 
amoeba is larger, more actively motile, has an easily distinguished refractive ecto- 
plasm which can also be made out in the pseudopods which are themselves relatively 
large and easily seen. 
Especially characteristic of the amoeba histolytica is the presence of the numerous 
vacuoles and usually of ingested red corpuscles which hide the nucleus. 398 
PHYSICAL DIAGNOSIS 
The other parasites are identified, as a rule, by the finding of their 
eggs in the stools. The technique of this operation is described below, 
as exemplified in the search for the egg of uncinaria—at present the egg 
most important for Americans to recognize. 
Eggs of parasites catch the eye in the examination of stools, first 
of all, by the clean-cut, mathematical symmetry of their oval, when com- 
pared with the irregular, shapeless masses which usually appear in 
slide and cover preparations from the faeces. 
Secondly, the size of parasitic eggs is 
greater than that of most of the objects 
seen in the faeces; and, thirdly, they are for 
the most part dark brown, stained with bile 
(the uncinaria is an exception). 
Fig. 21 i.—a, Head of Taenia solium (note crown of hooks); b, uterine canal in two seg- 
ments. Only five to seven branches on each side. 
The differences between individual species will be described later. 
In Plates II. and III. the most important eggs are pictured and 
catalogued. 
The Uncinaria americana or its European equivalent (Anchylos- 
toma duodenale) is recognized most easily by the identification of its 
eggs in the stools. These eggs are characteristic (see Plate II.), and 
“the only thing liable to be confounded with them is the ovum of 
Ascaris lumbricoides stripped of its heavy, bile-stained outer shell 
(see Plate II.); but this has a double contour and contains a shapeless 
mass of granular matter not differentiated” (as most uncinaria eggs Cabot—Physical Diagnosis. 
PLATE II. 
Distoma buski. 
Ascaris lumbricoides. 
Uncinaria americana. 
Anchylostoma duodenale. 
Trichuris trichiura. 
Dibothriocephalus latus. 
Taenia solium. 
Taenia saginata. 
EGGS OF INTESTINAL PARASITES. 
All are magnified 250 diameters. THE INTESTINE, SPLEEN, KIDNEY 
399 
are) “into clear segments.”1 The greater size of the American hook- 
worm’s egg compared to that of the European worm is shown in Plate 
II. “Free embryos are rarely if ever found in intestine. When free 
(worm-like) embryos are seen in the stools, they are generally those 
of the Strongyloides intestinalis ” (see Fig. 214). 
The ova of uncinaria catch the eye in a rapid examination, ‘first, 
because they are “not generally bile-stained, but clear, whereas those 
of the commonly associated intestinal 
parasites are of a yellow to deep amber 
or brown color.” They are dis- 
tributed quite evenly throughout the 
entire faecal mass; hence, in search- 
ing for them, the following method is 
advisable: 
Technique of Microscopic Exami- 
nation.—“A bit of faeces the size of a 
match head is removed with a tooth- 
pick and placed on a glass slide. 
Fig. 212.—Taenia nana (Dwarf Tape-worm), a, Hooklet; b, head, greatly enlarged; c, 
whole worm, magnified about 10 times. 
Upon this is placed a cover glass and pressed down so as to give a 
clear centre to the specimen. Do not add water. Examine with a 
one-third to two-thirds objective, a No. 4 ocular, and a partially closed 
1 All the quotations in this section are from the “Report of the Commission for 
the Study and Treatment of Anaemia in Porto Rico,” by Ashford, King, and Igara- 
videz (December 1st, 1904), a study of 5,490 cases. 400 
PHYSICAL DIAGNOSIS 
diaphragm. If too much light is admitted the delicate ovum will be 
passed over.” 
The following interesting table (from the studies of Ashford, King, 
and Igaravidez in Porto Rico) shows, roughly, the relative frequency 
(in a tropical climate) of the common intestinal parasites recognizable 
Fig. 213.—Segments of the Dibothriocephalus latus (Fish Tape-worm). Note the 
rosette-shaped uterine marking. 
by their eggs. In the examination of the stools of 5,490 cases of uncin- 
ariasis they found as well: 
Ascaris lumbricoides in 1,408 (many others seen but not noted). 
Trichuris trichiura in 326 (many others seen but not noted). 
Strongyloides intestinalis in.. . . 36 (the embryo worms, not eggs). 
Bilharzia haematobium in 21 (frequently no careful search 
was made for this egg). 
Balantidium coli in 14 
Oxyuris vermicularis in 3 
Amoeba coli in 3 
Taenia saginata in 2 
Taenia solium in 2 
Newton Evans (Southern Medical Journal, Nov., 1911) examined 
the stools of 122 children in public institutions of Tennessee and found 
worms in 60 children, or nearly 50%, though no symptoms were 
present. The order of frequency was as fellows: 
1. Hook worm (39 cases). 
2. Round worm. 
3. Whip worm. 
4. Dwarf tape worm. 
5. Pin worm. 
Ascaris lumbricoides has usually a thick, wavy (“ mammillated ”) 
shell; but this is not always seen, and in its absence the egg is dis- Cabot—Physical Diagnosis. 
PLATE III. 
Heterophyes 
heterophyes. 
Distoma 
sinense. 
Fasciola hepatica. 
Distoma buski. 
Dictoccelium 
lanceolatum. 
Taenia solium. 
Taenia 
saginata- 
Diplogonoporus 
grandis. 
Bilharzia 
haematobium. 
Dibothrio- 
cephalus latus. 
Bilharzia 
haematobium. 
Bilharzia 
haematobium. 
Ascaris 
lumbricoides. 
Oxyuris 
vermicularis. 
Paragonimus 
westermani. 
Taenia nana. 
Ascaris 
lumbricoides. 
Anchylostoma 
duodenale. 
Uncinaria 
americana. 
Strongylus 
subtilis. 
Strongyloides 
stercoralis. 
Trichuns 
trichiura. 
DRAWINGS OF EGGS OF INTESTINAL PARASITES. 
All are magnified 250. (After Looss.) THE INTESTINE, SPLEEN, KIDNEY 
401 
tinguishable from Uncinaria americana chiefly by the absence of the 
segmentation usually seen in the egg of the latter (see Plate II., b). 
Trichuris trichiura (also called Triococephalus dispar) has a thick 
shell, very dark-stained, and apparently pointed and perforated at 
each end, instead of curving evenly over as the 
uncinaria egg does (see Plate II., c). 
Bilharzia eggs are not at all uncommon in 
the faeces, though more often described in the 
urine, in connection with haematuria. In the 
urine the terminal spine at one end is their most 
characteristic feature (see Plate III). In the 
faeces the spine is usually at one side (see 
Plate III). 
The other eggs are briefly described in the 
explanatory text accompanying Plate II. 
II. The Spleen 
Diseases of the spleen (abscess, malignant 
disease, cyst) are almost never recognized during 
life. It is for evidence of splenic enlargement 
as a factor in the diagnosis of diseases origi- 
nating elsewhere that we investigate the splenic 
region as part of the routine of abdominal 
examinations. 
Splenic enlargement is detected chiefly by 
palpation. Percussion plays a minor role in the 
determination of the organ’s size, and should 
never be relied on in the absence of palpable 
evidence. Palpation is easy, provided the organ 
is enlarged sufficiently to project beyond the 
ribs without forced respiration, but much prac- 
tice is needed when the enlargement is slight as 
in, for example, most cases of typhoid fever. 
I. Palpation of the Spleen 
Fig. 214. — Strongy- 
loides stercoralis. Mag- 
nified about 250 diame- 
ters. (After Thayer.) 
The co-operative action of both hands is as 
essential as in vaginal examination, and each 
hand must do the right thing at the right moment. The patient 
should be on his back, his head comfortably supported and his knees 
drawn up. The left hand, placed over the normal situation of the 
spleen, (a) draws the whole splenic region downward and inward 402 
PHYSICAL DIAGNOSIS 
toward the expectant finger-tips of the right hand, (b) at the same 
time the left hand should slide the skin and subcutaneous tissues over 
the ribs and toward the right hand (see Fig. 215), so as to leave a 
loose fold of skin along the margin of the ribs and give the palpating 
fingers a slack rather than a taut covering to feel through. 
The right hand lies on the abdominal wall just below the margin 
of the ribs, and the fingers should point straight up the path down 
which the spleen is to move, i.e., obliquely toward the left hypo- 
chondrium. With the hands in this position ask the patient to 
draw a full breath. Keep the hands still and do not expect to feel 
LEFT HAND 
RIGHT HAND 
Fig. 215.—Position of the Hands in Palpation of the Spleen. 
anything until near the end of inspiration. Then draw the hands 
slightly toward each other and dip in a little with the right finger- 
tips, so that if the spleen issues from beneath the ribs its edge will 
meet the finger-tips for an instant and spring over them as they 
rise from diving into the soft tissues (see Fig. 215). 
Some physicians have the patient lie on the right side, and, stand- 
ing behind him, hook their fingers over the ribs in the left hypo- 
chondrium. In this way we may be able to feel the spleen at the 
end of a long inspiration, but I have seldom found this position as 
useful as that described above. 
A hard, fibrous spleen (malaria) is much easier to feel than 
soft one (typhoid). 
2. Percussion of the Spleen 
Only when the edge of the spleen has been felt is it worth while to try 
to define its upper border by percussion. Normally there is dulness in THE INTESTINE, SPLEEN, KIDNEY 
403 
the midaxillary line from the ninth to the eleventh ribs, corresponding 
to that part of the spleen that is most superficial. Its lower and 
posterior borders cannot be defined; its anterior edge is approxi- 
mately in the midaxillary line (see Fig. 59). If this small area of dul- 
ness is enlarged upward and forward, and if the edge has been felt 
below the ribs, it is probable that the increased area of dulness corre- 
sponds to an enlargement of the organ. 
3. Causes of Splenic Enlargement 
Slight enlargement of the spleen can often be detected in: 
1. Rickets and other debilitating conditions of childhood with or 
without anaemia. 
2. Malaria. 
3. Typhoid fever. 
Fig. 2 i6.—Splenic leucaemia. 
In other acute infections slight enlargement can usually be made 
out post mortem, but not during life. 
In a series of ioo cases of marked splenic enlargement studied in 
the Massachusetts General Hospital I found the following types: 404 
PHYSICAL DIAGNOSIS 
1. Leucaemia—35 cases. 
2. Hepatic cirrhosis—30 cases. 
3. Malaria—8 cases. 
4. Hodgkin’s disease—6 cases. 
5. “ Splenic Anaemia ”—4 cases. 
6. Syphilis—2 cases. 
7. Polycythaemia—2 cases. 
8. Amyloid—1 case. 
9. Unknown Cause—13 cases. 
Rarer causes are abscess, tuberculosis, malignant disease, perni- 
cious anaemia, hydatid, and Leishman-Donovan disease. 
Differences Between a Large Spleen and Tumors (of the kidney or 
other organs).-—A large spleen is easily recognized after a little practice. 
As it enlarges it keeps its shape and advances obliquely across the belly 
toward the navel or (in marked cases) beyond it. 
It is always hard and smooth of surface, although the edge nearest 
the epigastrium shows one or more notches which are very char- 
acteristic. The edge is sharp, never rounded, and the whole organ 
is very superficial, being covered only by the belly walls, so that if 
we inflate the colon (by forcing air into the rectum with a Davidson 
syringe), it passes behind the spleen and does not obliterate its dulness. 
Tumors of the kidney fill out the flank, and an impulse can be 
transmitted to the lumbar region by bimanual palpation. They 
have no sharp edge or notches, are often irregular of surface, and 
not so superficial. The inflated colon passes in front of a tumor of 
the kidney and obliterates the dulness due to it. 
All these differences hold for any other tumors likely to be con- 
fused with an enlarged spleen. 
4. Differential Diagnosis of the Various Causes of Splenic 
Enlargement 
In children splenic enlargement without fever or leukaemic blood 
changes is to be classed as a manifestation of general debility. It 
has no special connection with any type of anaemia, though anaemia 
is often seen with it. 
In typhoid the fever with the Widal reaction and blood culture are 
generally sufficient to make clear the cause of the splenic enlargement; 
in active malaria the blood parasites are always demonstrable, and in 
chronic cases the history and the locality are significant. 
Hepatic cirrhosis (and Banti’s disease) should show evidences of 
portal stasis (ascites, jaundice, hasmatemesis). THE INTESTINE, SPLEEN, KIDNEY 
405 
Splenic ancemia means simply an anaemia of unknown origin 
associated with an enlarged spleen. 
Leukcemic enlargement of the spleen is easily recognized by the 
characteristic blood picture. 
Hodgkin s disease (lymphoma) shows enlarged glands in the 
neck, axillae, and groins, with normal blood. Histological examina- 
tion of an excised gland is necessary for diagnosis. 
Amyloid can be suspected if there is a history of syphilis or chronic 
suppuration (hip abscess, etc.). 
III. Diseases of the Kidney 
1. Incidence of Renal Disease (Massachusetts General Hospital, 1870- 
1905) 
Acute nephritis 
200 
Chronic glomerulo-nephritis 
417 
Chronic vascular nephritis 
2501 
Amyloid nephritis 
9 
Floating kidney 
227 
Stone in the kidney 
145 
Malignant disease 
42 
Tuberculous kidney 
4i 
Renal sepsis (pyonephrosis, pyelitis and suppurative nephritis) 
54 
Perinephritic abscess 
35 
Hydronephrosis 
19 
Cystic kidneys 
10 
T otal 
1,449 
We get evidence of diseases of the kidney in six ways: 
1. By study of the constitutional symptoms,—fever, leucocytosis, 
anaemia, uraemia, dropsy, blood pressure and cardiac hypertrophy. 
2. By cystoscopy, the ureteral catheter, and pyelography. 
3. By examination of the urine. 
4. By external examination and radioscopy of the region of the 
kidney. 
5. By study of the non-protein nitrogen and other retention prod- 
ucts in the blood. 
6. By the “Red” test (Phenolsulphonephthalein). 
Local examination acquaints us with the presence of tenderness 
and tumor. 
1 Seven hundred and seventy-five other cases of “nephritis” not further 
specified. 406 
PHYSICAL DIAGNOSIS 
(a) Tenderness is often present in renal abscess (tuberculous or 
non-tuberculous), pyelitis, and perinephritic abscess, less often in 
connection with nephrolithiasis, occasionally in hydronephrosis and 
malignant disease. A floating kidney may have an exquisite and 
peculiar sensitiveness to pressure, which differs from ordinary 
tenderness. 
Fig. 217.—Renal tumor made visible by pneumoperitoneum. Patient lies on' 
his right side. 
{h) Tumor in the kidney region may occur in abscess in or around 
the kidney (including tuberculosis of the kidney and pyonephrosis), 
malignant disease, hydronephrosis, and cystic kidney. The latter 
members of this list afford examples of the largest tumors associated 
with the kidney. 
2. Characteristics Common to Most Tumors of the Kidney 
Renal tumors are best felt bimanually, one hand in the hypo- 
chondrium and the other in the region of the kidney behind, with 
the patient in the recumbent position. In this way the tumor may 
often be grasped and an impulse transmitted from hand to hand. It THE INTESTINE, SPLEEN, KIDNEY 
407 
is usually round and smooth, often very hard, less often fluctuating. 
It descends slightly with inspiration. If the colon is inflated 
by forcing air into the rectum with a Davidson syringe, reso- 
nance appears in front of the tumor; this serves to distinguish it 
from tumors of the spleen which are pushed forward by the inflated 
Fig. 2i8.—Pneumoperitoneum outlining renal tumor. Body seen from behind, 
colon as it passes behind them. Tumors of the kidney never pre- 
sent a thin and sharp edge, like that of the spleen. Occasionally 
they are irregular and nodulated—a condition almost never found 
in the spleen. It must be remembered that an enlarged kidney may 
be the sound kidney hypertrophied in compensation for disease on 
the other side. 
(a) Malignant disease of the kidney, usually a hypernephroma, 
makes up with cystic kidney the great bulk of the large abdominal 
tumors occurring in childhood, but is also not uncommon in adults. 408 
PHYSICAL DIAGNOSIS 
Fig 219.—-Pyelograph of normal renal pelves. 
Fig. 220.—Bilateral hydronephrosis. THE INTESTINE, SPLEEN, KIDNEY 
409 
The characteristics of the tumor are those already described. There 
is usually pain, hasmaturia, emaciation, and anaemia sometimes leuco- 
cytosis, but small tumors at some distance from the renal pelvis are 
symptomless and unrecognizable. Pyelography may show distortion 
of the renal pelvis. Metastases—especially bone metastases—are 
often the first evidence of the disease. 
(b) Hydronephrosis and cystic kidney may be indistinguishable 
from each other unless the hydronephrosis is intermittent and dis- 
appears with a great gush of urine, or unless the cystic kidney is 
Fig. 221.—Pyelograph of hydronephrosis. 
bilateral—as indeed, is usually the case. In both diseases a smooth, 
round rumor forms in the loin and hypochondrium, usually without 
much constitutional disturbance and very frequently with a urine 
like that of contracted kidneys (see below) (see Fig. 222). Pain 
and tenderness are slight. In many cases the tumor is astonish- 
ingly hard and often gives no sign of fluctuation. With cystic kidney 
it may be coarsely lobulated. Like other tumors of the kidney it de- 
scends slightly on inspiration. Cystic kidneys are often congenital, 
but usually produce no symptoms until they have attained a consider- 
able size, and hence are often overlooked or discovered accidentally. 410 
PHYSICAL DIAGNOSIS 
In hydronephrosis the diagnosis may be assisted by etiological hints, 
such as an abnormal degree of mobility of the kidney on the affected 
side, a history of renal colic with or without hasmaturia, or a prostatic 
obstruction. Comparatively slight degrees of dilatation or distortion 
of the renal pelvis and their relation to kinking of the ureter may be 
made out by the use of pyelography. 
This method is of great practical value 
in the diagnosis of hydronephrosis, 
pyonephrosis, pyelitis (which shows 
dilatation of the pelvis), renal tubercu- 
losis and tumors, cystic kidney, hydro- 
ureter and ureteral obstruction, and 
for other purposes. 
(c) Perinephritic abscess usually 
works its way to the surface in the 
back, between the crest of the ilium 
and the twelfth rib. This was the 
situation of the external tumor in 25 
out of 3 5 cases recorded at the Massa- 
chusetts General Hospital. A tender 
swelling appears at the point just de- 
scribed, sometimes with redness and 
heat, and almost always with fever, 
chills, leucocytosis, and some emacia- 
tion. The urine may show nothing abnormal or may show the 
evidence of cystitis, of concomitant nephritis, or, rarely, of an ab- 
scess within the kidney itself. Perinephritic abscess often remains 
latent for weeks or months, and the amount of pus accumulated may 
be a quart or more. 
(d) Abscess of the kidney, including tuberculous, suppurating kid- 
neys and pyonephrosis, may produce a smooth rounded tumor in 
the hypochondrium and loin. It has the characteristics common to 
most renal tumors (see last page), but is usually distinguishable by: 
1. The etiology (cystitis, stone in the kidney, tuberculosis, pyae- 
mia). In acute cases, however, there is often no discoverable cause. 
2. The presence of renal pyuria. 
3. The presence of fever and leucocytosis. Persistent urinary 
frequency, especially nocturnal, in a young adult suggests renal 
tuberculosis. Animal inoculation with the urinary sediment ob- 
tained by ureteral catheter is essential to confirm diagnosis. Bladder 
irritation is usually the first symptom of renal tuberculosis. 
Fig. 222.—Left Hydronephrosis. A, 
Area of dull irregular resistance. THE INTESTINE, SPLEEN, KIDNEY 
411 
(e) Floating Kidney; Displaced and Movable Kidney.—The tip 
of the right kidney is palpable in most thin persons with loose belly 
walls. If the whole organ is palpable but not movable, we speak 
of it as displaced. If the range of mobility is relatively great we 
call it floating; if relatively slight we call it movable. With bimanual 
palpation (as described above) we exert pressure just at the end of 
a deep inspiration and maintain it. During expiration something 
smooth and round may then be felt to slip upward between our 
hands toward the ribs. If the kidney “hides” behind the ribs, have 
the patient sit up, cough, and breathe deeply; then repeat the bimanual 
palpation as he lies on his back. Very movable or floating kidneys 
may be found far from their normal home, and are then recognized by: 
1. Their size, shape, and slippery feel. 2. The sickening pain pro- 
duced by pressure. 3. The possibility of replacing them. 
3. Renal Colic and Other Renal Pain 
Typical renal colic is paroxysmal, like all colics; that is, an attack 
begins suddenly, ends suddenly, and lasts but a few hours or less. 
The pain usually begins in the back, over the kidney, and follows 
the course of the ureter to the groin. During an attack the testicle 
on the affected side may be tender and drawn up tightly by contrac- 
tion of the cremaster. 
When associated with haematuria or pyuria, with or without sud- 
den stoppage of water during an attack and without any general or 
constitutional symptoms between attacks, renal colic is suggestive 
of stone in the pelvis of the kidney; but similar attacks may occur 
with other surgical diseases of the kidney (tuberculosis, neoplasm, 
kinking of the ureter), etc., when blood clot or pus gets wedged into 
the ureter. 
From biliary colic it may be distinguished by the (a) different 
situation of the pain, (6) by the presence of blood or pus in the urine, 
and (c) the absence of jaundice in this or a former attack. 
In intestinal colic the pam shifts its position frequently and is 
associated with noises produced by wind in the bowels, or with diar- 
rhoea or constipation. 
Renal pain, not colic, may occur in almost any disease of the kidney 
except nephritis, and is characterized by its situation over the kidney 
and by the lack of any connection with muscular movements (lum- 
bago), with spinal movements (hypertrophic arthritis), or with the 
sacro-iliac joint. 412 
PHYSICAL DIAGNOSIS 
Fig. 223.—Stone in the kidney. 
Fig. 224.—Stone in the kidney. THE INTESTINE, SPLEEN, KIDNEY 
413 
I have now described what seems to me most important in the 
local external examination for kidney disease, and have mentioned, 
along with the different lesions producing tumor, the general con- 
stitutional manifestations which are of assistance in diagnosis. Aside 
from the local and the constitutional evidence of renal disease (high 
blood pressure and enlarged heart), we have only the evidence afforded 
by the urine, to which I now pass on. 
4. Examination of the Urine 
The urine as passed per urethram is a resultant and reflects the 
influence of many different organs and surfaces. Thus disturb- 
ances of metabolism, such as diabetes, intoxications (lead, arsenic), 
disease of the heart, liver, and intestine, febrile conditions, infec- 
tive or malignant disease of any part of the urinary tract (kidney, 
ureter, bladder, or urethra), as well as the different types of nephritis, 
all affect the urine, though hardly any of them produce pathognomonic 
changes in it. In this section I shall consider the urine as a piece of 
evidence in the diagnosis of kidney disease, and only in contrast with 
this will its characteristics in extrarenal troubles be mentioned briefly. 
The most essential features of the urine in the diagnosis of kid- 
ney disease are: 
1. The amount passed in twenty-four hours, measuring sepa- 
rately the portions passed at night (8 p.m. to 8 a.m.) and in the day- 
time (8 a.m. to 8 p.m.). 
2. The specific gravity. 
3. The looks (optical properties). 
4. The “red test” (see page 418). 
5. The reaction to litmus. 
6. The presence of blood, pus, or tubercle bacilli. 
7. The presence or absence of albumin and sugar. 
Much less important than these is the presence or absence of casts, 
cells, crystals, etc. 
(a) The Amount and Weight of the Urine 
The twenty-four-hour amount concerns us chiefly in diabetes, 
the different types of nephritis, and in cardiac decompensation. 
Polyuria occurs in health after the ingestion of large quantities 
of water, and sometimes in conditions of nervous strain. In dis- 
ease it characterizes both forms of diabetes, contracted kidneys (pri- 414 
PHYSICAL DIAGNOSIS 
mary, secondary, or arterio-sclerotic), and is seen during the con- 
valescence from acute nephritis and from various infectious diseases. 
It also occurs in the early stages of renal tuberculosis or when con- 
tinuous drainage (catheter) is established in cases of prostatic obstruc- 
tion. In diabetes of either form several quarts or even gallons may be 
passed. In contracted kidneys the increase of urine occurs very 
largely at night, so that the amount may be double that passed in 
the day-time, just reversing the conditions of health. 
Oliguria or scanty urine occurs in health when the amount of 
water ingested is small or when water is passed out of the body 
abundantly through the skin or by the bowels (diarrhoea). In dis- 
ease oliguria or absolute suppression of urine (anuria) occurs at the 
beginning of acute nephritis and as a result of occlusion of one or 
both ureters by stone or malignant disease.1 Remarkable examples 
of anuria also occur in hysteria. Infectious fevers and cachectic states 
often diminish the secretion of the urine by one-half or more. 
The specific gravity is usually low with polyuria and high with 
oliguria, but in diabetes mellitus the presence of the sugar gives us 
polyuria with high specific gravity. 
Total Urinary Solids.—By multiplying the last two figures of 
the specific gravity by the number of ounces of urine passed in twenty- 
four hours and the product by i.i, we get a figure representing the 
total urinary solids in grains, with accuracy sufficient for clinical 
diagnosis. Thus if 30 ounces of urine are passed in 24 hours and the 
gravity is 1.020, then 20 X 30 X 1.1 = 660 grains. 
(6) Optical Properties 
Color.—Dilute urines (polyuria) are generally pale, and concen- 
trated urines (oliguria) high in color. A dark or brownish tint in 
the urine is generally produced by bile, by blood pigment, or as a 
result of certain drugs—carbolic acid, coal-tar preparations, and 
salol. If the color is due to bile, a bright canary yellow appears in 
the foam after shaking up a little of the urine in a test tube. No 
other tests for bile are necessary. Urines darkened by blood pig- 
ment show abundant blood corpuscles in the sediment;2 when the 
color is due to drugs we can usually learn this fact from the history. 
1 It is a remarkable but well-attested fact that when one ureter is suddenly 
blocked both kidneys may stop secreting for the time. Yet when one kidney is 
gradually destroyed as in tuberculosis, the other hypertrophies so as to assume the 
function of both. 
2 Except in some cases of hasmoglobinuria. THE INTESTINE, SPLEEN, KIDNEY 
415 
Turbidity in alkaline urine is usually due to the presence of bac- 
teria. In acid urine it is produced in a great majority of cases by 
amorphous urates, and disappears on heating the urine, while the 
turbidity due to bacteria is unaffected by heat. Normal urine may 
be turbid and alkaline, owing to the presence of insoluble carbonates 
and phosphates, but clears on the addition of acetic acid. Hence 
turbidity, not removed by heat or acetic acid, is almost always due to 
bacteria and pus, i.e, to cystitis, pyelonephritis, or both. 
Shreds seen floating in the urine and found to be composed mostly 
of pus are presumptive evidence of urethritis, and practically always 
of gonorrhoea. 
The gross sediment as seen by the naked eye amounts in health 
to nothing more than a slight cloud, which settles in the lower part 
of the vessel containing the urine. This cloud is somewhat denser 
in women than in men, owing to the presence of vaginal detritus. 
When the gross sediment amounts to anything more than this, it is 
almost invariably made up of (a) pus, (b) blood, or (c) urates. The 
latter are dissolved on heating. Pus has usually its ordinary yellow 
color and general appearance. Blood may be somewhat lighter or 
somewhat darker than under ordinary conditions, but is usually 
recognized without difficulty. 
(a) Significance of these Sediments 
A urate sediment means nothing more than a concentrated urine 
standing in a cold room. In the winter-time patients often bring us, 
in great alarm, a bottle of milky or fawn-colored and turbid urine, 
which is not in any way abnormal. The urates have been precipi- 
tated over night by the low temperature of the bedroom. 
Pyuria, or gross pus in the urine, is oftenest seen in cystitis and less 
often in pyelonephritis and renal suppurations, tuberculous or pyogenic. 
The pus occurring in gonorrheal urethritis is usually much less in 
quantity than that coming from the bladder or kidney, and can be 
distinguished by the local signs of gonorrhoea. Leucorrhoeal pus can 
be excluded by withdrawing the urine by catheter. The rupture 
into the urinary passages of an abscess from the prostate or any part 
of the pelvis may produce a profuse but transient pyuria. 
After excluding gonorrhoea, leucorihoea, and abscess, which can usu- 
ally be done with the help of a good history and a catheter, we have left 
cystitis and renal suppurations, which it is very important and some- 
times difficult to differentiate. In both we have the frequent and 416 
PHYSICAL DIAGNOSIS 
painful passage of small quantities of a urine which is in no way remark- 
able except in containing large amounts of pus and bacteria. Cystos- 
copy is often essential. In the vast majority of cases “cystitis” is 
secondary to some other disease above or below the bladder—e.g., 
to prostatic obstruction, renal tuberculosis, etc. 
In many cases the differentiation may be accomplished as follows: 
Have the patient save for twenty-four hours the urine voided at each 
passage in a separate bottle (all of the bottles being of uniform size), 
and mark each bottle with the hour at which it was filled. Then arrange 
the specimens in a row, beginning with that passed earliest and ending 
with that passed last. Now if the case is one of cystitis without 
involvement of the kidney, the amount of pus that settles is practically 
the same in each bottle (allowing for differences in the amount of urine 
in the different bottles). But if the pus comes from the kidney, it is 
almost always discharged intermittently, and hence some of the bottles 
will be almost free from sediment, while in a group of the others the 
amount of pus increases as we pass along the line, reaches a maximum 
in one or two bottles, and decreases again in those representing the 
later acts of micturition. 
Pus from the bladder is generally alkaline, although in tubercu- 
losis it may be acid; pus from the kidney is generally acid. When 
both organs are involved, as is frequently the case, we have a mixture 
of the characteristics of both types of pyuria, and cystoscopic examina- 
oion with or without catheterization of the ureters is usually necessary. 
5. Pyuria 
In renal pyuria we often have local signs in the renal region (tumor 
and tenderness), a history of renal colic, and decided constitutional 
symptoms. 
In vesical pyuria we have vesical pain, often tenesmus, no renal 
pain or tumor, and usually slighter constitutional symptoms. The 
amount of squamous epithelium (see below) is sometimes larger in 
cystitis than in renal suppurations, but no reliable inferences can be 
drawn from the size or shape of the cells. 
To determine whether pus from the bladder or the kidney is tuber- 
culous or non-tuberculous in origin, we usually inject the sediment 
into a guinea-pig, which develops tuberculosis or not according 
to the nature of the pus injected. This method is much more reliable 
than the bacteriological examination of the sediment, for besides 
the tubercle bacillus other bacilli which retain fuchsin and resist THE INTESTINE, SPLEEN, KIDNEY 
417 
decolorization by strong acid and by alcohol occasionally occur in the 
urine. 
6. Hcematuria 
In searching for the source of the blood we must be sure to exclude 
the female genital organs. Menstrual blood and uterine bleeding 
from various other causes often contaminate the urine, and must be 
excluded by using a catheter. 
The causes of true haematuria, arranged approximately in the order 
of frequency, are: 
1. Prostatic congestion or irritation. 
2. Stone in the kidney (less often vesical stone). 
3. Tumors of the kidney or bladder. 
4. Acute nephritis and acute hemorrhage in chronic nephritis. 
5. Tuberculosis of the kidney or bladder. 
Less common causes are: floating kidney, hydronephrosis and 
cystic kidneys, animal parasites in the urinary passages, poisons 
(turpentine, carbolic acid, cantharides), hemorrhagic diseases (pur- 
pura, scurvy, leuksemia), trauma and renal infarction. In nearly 
one-fourth of all cases no cause can be found. 
In cystitis there are bladder symptoms—pain, tenesmus, fre- 
quent and painful micturition. The blood is mixed with pus and 
epithelium, and is especially abundant in the urine passed near the 
end of the act of micturition. If the bladder is irrigated it is 
hard [to get the wash-water clear. Cystoscopy demonstrates or 
upsets the diagnosis and also serves to show some other disease to 
which the cystitis is secondary. Distrust all diagnoses of “primary 
cystitis.” 
In renal stone there are no bladder symptoms to speak of, the 
blood is pure and thoroughly mixed with the urine, and if the bladder 
is washed out the final wash-water is clear. There is often renal 
colic (see p. 411) and sometimes the passage of stones or gravel by 
urethra. X-ray evidence is usually conclusive. 
In acute nephritis the blood is rarely fresh, generally dark choco- 
late in color. The twenty-four-hour amount of urine is small, and 
albumin and casts (see below) are abundant. General oedema is 
common. Local symptoms in the kidney or bladder are absent. 
Most cases of “acute nephritis” in adults turn out, on careful study, to 
represent acute exacerbations of chronic nephritis. 
In renal tumor and especially in renal tuberculosis we have often 
pyuria and the local and constitutional evidences above described 418 
PHYSICAL DIAGNOSIS 
(page 410), with marked and early bladder symptoms (even when the 
bladder is not diseased). 
Tumors of the-bladder need cystoscopy for diagnosis. 
In the diagnosis of the rarer forms of hasmaturia we rely chiefly 
on the history (trauma, poisons ingested) and on the evidences afforded 
by cystoscopy and general physical examination. 
7. The “Red Test" (.Phenolsulphonephthalein) for Renal Function 
Of the many “functional” kidney tests introduced in recent 
years that of Rowntree and Geraghty is by far the most useful for 
clinical purposes. One cubic centimeter of the standard sterilized 
solution of phenolsulphonephthalein1 is injected subcutaneously into 
the back or thigh. Two hours later the patient passes urine which 
is then made alkaline with sodic hydrate and diluted up to i liter. 
The degree of red color in the resulting fluid is then compared in a 
test tube with a scale of standard test tubes representing 90 per cent., 
80 per cent., 70 per cent., etc., of the amount of coloring matter 
originally injected. Such a scale of test tubes can be cheaply made 
by any one who has access to a Dubose colorimeter. The scale can 
also be bought for a few dollars from Joseph Godsoe, Massachusetts 
General Hospital, Boston. If there is prostatic obstruction or urethral 
stricture the patient should be catheterized when the “red” is injected 
and at the end of two hours. 
Normal young adults excrete 65 per cent, to 90 per cent, of the 
color injected within 2 hours. In nephritis and decompensated 
heart disease the color output may fall to 5 per cent, or to zero. In 
elderly people confined to bed 20 to 40 per cent, may be considered 
normal and does not indicate nephritis. Allowing for age and activ- 
ity the test is a valuable measure of the kidney’s general excretory 
function. 
8. Chemical Examination of the Urine 
(a) The Reaction of the Urine 
The reaction of normal urine is acid to litmus, except temporarily 
after large meals. Its acidity becomes excessive in fevers or occa- 
sionally without any known cause. 
Alkaline urine has generally an ammoniacal odor and suggests 
cystitis. As a result of decomposition and bacterial fermentation all 
1 Any dealer in medical supplies can furnish it. THE INTESTINE, SPLEEN, KIDNEY 
419 
urine becomes alkaline (ammoniacal) on standing exposed to air.1 
Occasionally we find urine alkaline from fixed alkali and without 
known cause. 
The value of the litmus test is chiefly as prima-facie evidence of 
stasis in the bladder and cystitis. Occasionally tuberculous cystitis 
and the first stages of any variety of cystitis are associated with 
acid urine, but in most cases lasting over a week 
ammoniacal fermentation and alkalinity appear. 
(b) Albuminuria and the Tests for It 
Serum albumin is the only variety of clinical impor- 
tance, and for this but two tests are necessary: (i) Nitric- 
acid test; (2) test by boiling. 
The nitric-acid test is best performed in a small wine- 
glass. After filling this half full of urine, insert a small 
glass funnel to the bottom of the urine and gently pour 
in concentrated nitric acid. If albumin is present, a 
white ring forms at the junction of the acid with the 
urine, either immediately or in the course of ten 
minutes. If carefully performed this test is delicate 
enough for all clinical purposes, but since some of the 
albumoses give a similar precipitate, th‘e boiling test 
should be used as a control whenever a positive reac- 
tion is obtained with nitric acid. None of the other 
rings, observable above or below but not at the junc- 
tion of the acid with the urine, is of any clinical 
importance. 
The Boiling Test.—To half a test tube full of urine 
add three or four drops of dilute acetic acid, and boil the 
upper three-quarter inch of the urine. If albumin is 
present a white cloud appears. If the Bence-Jones 
body is present, a white cloud appears on heating, disap- 
pears on boiling, and reappears on cooling. In performing 
this test the addition of acetic acid as above described 
is absolutely necessary to prevent error. 
For the detection of albumin no other tests are needed. For its 
approximate quantitative estimation, Esbach’s method is the best. 
Fig. 225.— 
Esbach’s Albu- 
menometer. 
1 Simultaneously a dark-brown color rarely appears: alkaptonuria, a fact at 
present of no clinical significance except that such urines reduce Fehling’s solution 
and may be mistakenly supposed to contain sugar. 420 
PHYSICAL DIAGNOSIS 
Esbach’s Method.—A special tube (see Fig. 225) is employed. 
Urine is poured in up to the mark “U,” and then Esbach’s reagent1 
up to the mark “R.’ The tube is then corked, inverted about half 
a dozen times, and set aside for twenty-four hours. A precipitate 
falls and the amount per mille is then read off on the scale etched 
upon the tube. If the urine is not acid it must be made so with 
dilute acetic acid, and unless its specific gravity is already very low 
it should be diluted once or twice with water so as to bring the gravity 
below 1.008. After such a dilution we must, of course, multiply the 
result obtained by a figure corresponding to the dilution. The method 
is not accurate, but is probably accurate enough for practical pur- 
poses, if all tests are made at approximately the same temperature. 
(c) Significance of Albuminuria 
It is important to realize that albuminuria very often occurs with- 
out nephritis and that nephritis occasionally occurs without albu- 
minuria. Among the more important types not due to kidney disease 
are the following: (i) Juvenile albuminuria; (2) febrile albuminuria; 
(3) albuminuria from renal stasis; (4) albuminuria due to pus, blood, 
bile, or sugar in the urine; (5) toxic albuminuria. 
Besides these, there are a good many cases of albuminuria occur- 
ring in diseases of the blood, after violent exertion, after epileptic 
attacks, and without known cause. Many of the juvenile group 
occur only when the patient is on his feet and are absent as long as 
the patient lies down (orthostatic albuminuria); others occur irregu- 
larly or at regular intervals (cyclic albuminuria). Most of these 
cases appear at adolescence and all pass off without nephritis ever 
developing. Nearly one in ten college freshmen shows this harmless 
albuminuria. 
Exclude the juvenile cases, fever, circulatory disturbance, anemia, 
poisons—such as cantharides, turpentine, carbolic acid—and deposits 
of blood or pus in the urine, before deciding that any case of albuminu- 
ria is due to nephritis. In general, it is a good rule not to attribute 
albuminuria to nephritis unless there is other and more convincing 
evidence in the physical characteristics of the urine and in the other 
organs of the patient. If the 2-hour amount and the gravity are 
approximately normal, and if there is no oedema, no increased blood 
pressure, no cardiac hypertrophy, no uraemic manifestations, and 
1 Esbach’s reagent: Picric acid, io gm.; citric acid, 20 gm.; distilled water, 
x,ooo c.c. THE INTESTINE, SPLEEN, KIDNEY 
421 
nothing alarming in the sediment of the urine, we should not diag- 
nose nephritis. I shall discuss this point further in the section on 
the examination of the sediment (see page 423). It will be noted 
that practically all the types of albuminuria not due to nephritis are 
transient, while, with the exception of certain stages of chronic nephritis, 
the albuminuria of nephritis is as permanent as the nephritis itself. 
On the other hand, many cases of nephritis (so proved by autopsy) 
show no albuminuria for long periods. They are then to be recognized 
by the low fixed gravity, the evidence of high blood-pressure and by 
its results. 
(d) Significance of Albumosuria 
The Bence-Jones body is very constantly present in the urine of 
cases of multiple myeloma. It has no known importance in any 
other disease. Deuteroalbumoses have no clinical significance. 
(e) Glucosuria and Its Significance 
For glucose in the urine we need but one qualitative and one 
quantitative test, viz., Fehling’s test and the fermentation test. 
1. Fehlings Test.—Mix in a test tube equal parts of a standard 
solution of copper sulphate1 and a standard solution of alkaline tar- 
trates,2 and add to this mixture an equal amount of urine. Mix 
and heat nearly to boiling. The amount of error entailed by boil- 
ing is slight and unimportant, but the only advantage of boiling is 
a slight saving of time. If sugar is present a yellow or reddish- 
yellow precipitate occurs, either at once or (if the amount of sugar 
is very small) after the urine has cooled. Fehling’s solution may 
also be used for quantitative estimation of sugar, but it is more con- 
venient to use: 
2. The Fermentation Test.—Take the specific gravity of the urine 
as carefully as possible, and acidify it if necessary with acetic acid. 
Pour six or eight ounces of urine into a wide-mouthed vessel and 
crumb into it half a cake of fresh Fleischmann’s yeast. Set the flask 
aside in a warm place, and after twenty-four hours test the super- 
natant fluid with Fehling’s solution as above; if sugar is still present 
fermentation must be allowed to go on twenty-four hours longer. As 
1 Made by dissolving 34.64 gm. pure CUSO4 in water and then adding enough 
water to make 500 c.c. 
2 Made by dissolving 173 gm. Rochelle salts and 60 gm. sodic hydrate each in 
200 c.c. of water, mixing the two solutions, and adding water to make 500 c.c. 422 
PHYSICAL DIAGNOSIS 
soon as a negative reaction to Fehling’s has been secured (whether 
in twenty-four or forty-eight hours), the specific gravity of the fil- 
tered urine is again taken.1 It will be found lower than before the 
fermentation, and for every degree of specific gravity lost we may 
reckon that 0.23 per cent of sugar has been fermented out of the 
urine. Thus if the reading was 1.040 before fermentation and 1.020 
afterward, we multiply the difference between these readings, 20, by 
0.23, giving 4.6 per cent—the percentage of sugar. 
Fehling's test should be applied to every urine examined; it takes 
but a minute or two. When it shows a yellow or red precipitate, the 
fermentation test should also be tried; and if both tests are positive we 
shall run but a negligible risk in saying that glucose is present. From 
the result of the fermentation test and the twenty-four-hour amount 
of urine, we can estimate the daily output of sugar through the urine. 
Permanent glucosuria means diabetes mellitus. Transitory glu- 
cosuria may be due to a great many causes, among which are: (r) 
Diseases of the liver; (2) diseases of the brain, organic or functional, 
especially the latter; (3) infectious fevers; (4) poisons, especially 
narcotics (alcohol, chloral, morphine); (5) pregnancy; (6) exoph- 
thalmic goitre. 
Experimental (“alimentary”) glucosuria or levulosuria can be 
produced in many of these same diseases by giving the patient 100 gm. 
of glucose or levulose in solution. 
The differential diagnosis of the cause of glucosuria depends on 
the recognition of one of the above conditions. The other sugars 
occasionally found in the urine (levulose, lactose, pentose, etc.), are of 
no clinical importance. 
(/) The Acetone Bodies 
Acetone, Diacetic and Beta-0xybutyric Acids 
1. Test for Acetone.—To about one-sixth of a test tube of urine 
add a crystal of sodium nitroprusside, and then NaOH to strong 
alkalinity. Shake and add to the foam a few drops of glacial acetic 
acid. A purple color shows acetone. 
2. Test for Diacetic Acid.—A Burgundy red color when a strong 
aqueous solution of ferric chloride is added to fresh urine (not pre- 
viously boiled) in a test tube. If this reaction is well marked beta- 
1 The room temperature must be approximately the same as at the time of the 
previous reading. THE INTESTINE, SPLEEN, KIDNEY 
423 
oxybutyric acid is probably also present, but we possess no clinical 
test for the latter substance. 
Significance of the Acetone Bodies.—Diminished utilization of 
carbohydrate food by the body is usually the cause of the appear- 
ance of these bodies in the urine. This may occur: (a) Because suf- 
ficient carbohydrates are not eaten (starvation, rectal alimentation, 
fevers, etc.). (b) Because they are not absorbed (vomiting, diar- 
rhoea, etc.), (c) Because they are not assimilated (diabetes), and 
rarely for other reasons. 
(g) Other Chemical Tests 
The information to be derived from testing for indican, for the 
amounts of urea, uric acid, chlorides, phosphates, and sulphates, 
does not seem to me sufficient to justify the time spent. The same 
is true of the diazo reaction. The guaiac test for blood, described 
above (see p. 371) in connection with the examination of gastric 
contents and fevers, is also of value in the urinary examination. 
Simon’s lucid arguments for the value of the indican test have 
not been borne out by my experience with it in diagnostic puzzles. 
The tests for urea and uric acid are of value only when we possess 
a knowledge of all the factors governing their excretion, knowledge 
which in clinical work we almost never have. Diminution or ab- 
sence of the urinary chlorides in pneumonia is not constant, and 
occurs in many other infections (typhoid, scarlet fever, etc.). The 
diazo reaction is nearly constant in typhoid, but is occasionally 
found in so many other febrile and cachectic states that most clini- 
cians have ceased to rely on it. Its value in the prognosis of phthisis 
is slight. I believe that the general abandonment of the tests for 
the sulphates and phosphates have now led to the abandonment of 
the tests for urea, uric acid, indican, and the chlorides. The use of 
these tests gives the appearance of accuracy and scientific method in 
diagnosis—the appearance, but not the reality. 
9. Microscopic Examination of Urinary Sediments 
Methods.—A centrifuge is convenient, but not necessary. The 
sediment should be allowed to settle in a conical glass (see Fig. 226), 
whence a drop of it can be transferred to a slide by means of a pointed 
glass pipette. Close the upper end of this with the forefinger and 
introduce the pointed end into the densest portion of the sediment; 
next very slightly relax the pressure of the forefinger until urine and 424 
PHYSICAL DIAGNOSIS 
sediment flow into the lower one-half or three-fourths inch of the 
pipette. Then resume firm pressure with the forefinger, withdraw 
the pipette, wipe the outside of it dry, put its point upon a microscopic 
slide, and again slightly relax the pressure of the forefinger so as to let a 
small drop of urine and sediment run out upon the slide. 
Cover this drop with a seven-eighths inch cover glass, and 
examine it with a Leitz objective No. 5 or Zeiss DD. 
The arrangement of the light is most important. 
The iris diaphragm should be closed until one can just 
distinguish the outlines of the cells and other objects in 
the field. If more light is admitted the pure hyaline 
casts will be invisible. 
Results.—The objects most often sought for in the 
sediment are: (a) Casts; (b) cells; (c) crystals; (d) animal 
parasites or their eggs. 
1. Casts.1—Casts, or moulds of the renal tubules, may be homo- 
geneous and transparent (hyaline, Fig. 227, 1) or may have attached 
to this matrix a variety of granules, cells, crystals, or fat drops. 
According to the variety of passengers carried down from the kidney on 
the casts, we call them 
granular, hr own-granular, 
cellular, blood, fatty, or 
crystal-bearing casts (see 
Fig. 227, 2 and 3, and Fig. 
228, 1, 2, 3 and 4). 
Dense or highly refrac- 
tile casts, colorless or straw 
colored, are occasionally 
seen, and are often given a 
variety of names quite 
unjustified by any knowl- 
edge of their composition 
(e.g., “waxy,”2 “fibrin- 
ous,” etc.). 
From strands of mucus, foreign bodies, and other sources of error, 
true casts may be distinguished by the following traits: 
Fig. 226.— 
Conical Glass 
for Urinary 
Sediments. 
Fig. 227.—Casts. 1, Hyaline casts; 2 and 3, 
hyaline casts with cells and blood adherent; 4, 
“cylindroids.” 
1 Though I have here described casts first I believe that the finding of blood or 
pus in the sediment is of far more frequent and more considerable importance. 
2 Some dense, refractile casts give the amyloid reaction, but this does not indi- 
cate amyloid kidneys and has no known clinical significance. THE INTESTINE, SPLEEN, KIDNEY 
425 
(а) Their sides are parallel. 
(б) One end is rounded; sometimes both ends. 
Red corpuscles and other cells upon casts are to be recognized—the 
former by the size, shape, and, if fresh, by their color (pale straw); 
the latter by the presence of a 
nucleus. 
Fat drops are spherical and 
very highly refractile, so that 
they seem to have a black line at 
their periphery. 
Crystals can be recognized 
by their angles. They are very 
rarely of importance. When 
showers of oxalate crystals in 
large masses are associated with 
attacks of hsematuria not other- 
wise explained, the crystals 
may be of some etiological sig- 
nificance. 
Other bodies on casts are called granules. 
Significance Of Casts.—Casts may occur in health (unless we 
choose to class muscular fatigue as disease) as well as under any of the 
conditions giving rise to albuminuria (see page 420). They are usually 
more numerous in acute nephritis and in the acute exacerbations of 
chronic nephritis than in most other conditions. 
Any type of cast may occur in any type of nephri- 
tis, but 
Cellular,1 blood, and brown-granular casts are 
most often found in acute nephritis. 
Fatty, highly refracting, or dense casts most often 
predominate in chronic glomerular nephritis (“dif- 
fuse” or “parenchymatous” nephritis). 
Hyaline and granular casts may occur in any 
type of nephritis and in many other conditions 
(fatigue, renal stasis, etc.). In the urine of persons over fifty 
years of age the presence of a few hyaline and granular casts has 
no known clinical significance, and may probably be considered 
physiological. 
Fig. 228.—Casts, i, Blood-casts; 2, fatty 
casts; 3, granular casts; 4, cellular casts. 
Fig. 229. 
Spermatozoa. 
1 “Cellular” is a better term than “epithelial,” since we have no marks for 
recognizing renal epithelium or for distinguishing a renal cell from a lymphocyte. 426 
PHYSICAL DIAGNOSIS 
Periods occur in the course of many cases of chronic contracted 
kidney when no casts can be found. If any occur they are usually of 
the hyaline and fine granular types. 
2. Free Cells in Urinary Sediment. A. Recognition.—The presence 
of macroscopic pus or blood already alluded to may be verified by the 
microscope. 
(a) Fresh red cells, lately freed from the blood-vessels, preserve their 
straw-yellow color. Their presence points to the recent effusion of 
blood, probably from the bladder, urethra, or renal pelvis. 
Fig. 230.—Crystals of Triple Phosphate 
(prisms) and Ammonium Urate (small 
spheres with spines.) 
Fig. 231.—Crystals of Uric Acid (whet- 
stone-shaped) writh Calcic Oxalate (small 
octahedral) and Amorphous Urates. 
(ib) Abnormal blood, decolorized and shadowy red discs, can be 
recognized with practice by their size and shape. We may infer 
that they have remained some time in the urine and have probably 
come from the kidney. 
(c) Pus is easily recognized as a rule by the presence of the familiar 
polymorphous nucleus in most of the cells. Should doubt arise, a 
drop of dilute acetic acid allowed to run under the cover glass will 
sharpen the outlines of the nuclei and facilitate their recognition. 
(d) Spermatozoa (see Fig. 229) are often seen in the urine after 
coitus or nocturnal emissions. They are of no importance, except 
that when appearing in the urine of females they may afford valuable 
medico-legal evidence. They are easily recognized by their size and 
shape. 
(e) Other varieties of cells need not be differentiated, since almost 
any of the varieties usually described (squamous, spindle-shaped, THE INTESTINE, SPLEEN, KIDNEY 
427 
caudate, etc.) may come from any part of the urinary tract. Renal 
cells are not .recognizable by our present methods of examination. 
Any of the urinary cells may contain fat drops, but these have 
no special diagnostic significance. 
B. Interpretation.—The significance of large quantities of blood 
or of pus in the urine has already been discussed (page 417). When 
recognizable only by the microscope they have no diagnostic value. 
The presence of large numbers of cells not coming from the 
blood-vessels (squamous, spindle-shaped, etc.) is usually associated 
with cystitis, provided the acci- 
dental admixture of vaginal detritus 
is excluded. Pyelitis and renal 
suppurations may fill the sedi- 
ment with similar cells, and only 
by other methods of examination 
(cystoscopy, ureteral catheteriza- 
tion) and by taking account of all 
the facts in the case can the differ- 
entiation be made. 
3. Crystals in Urinary Sedi- 
ments (see Figs. 230, 231 and 232). 
The varieties oftenest seen are: (a) Triple phosphate (ammoniacal 
urine, cystitis); (b) ammonium urate; (c) uric acid; (d) calcic oxalate. 
All of these varieties are colorless except the uric-acid crystals, 
which are usually light or dark yellow or yellowish-brown. 
None of these have much significance in diagnosis. The first 
two merely confirm the evidence of urinary decomposition (usually 
from cystitis), afforded by the reaction, turbidity, and odor of the 
urine. 
Uric-acid crystals, if present in great numbers in the urine 
when passed, suggest the search for macroscopic masses (gravel) 
and for other evidence of renal stone, but as a rule they are of no 
importance. 
The same may be said of calcium oxalate. Oxaluria is one of the 
most persistent bugbears of the medical profession, but it is utterly 
harmless except in the rare cases in which it accompanies hasmaturia 
(see above) or gravel. 
4. Animal parasites or their eggs are occasionally found in the 
urine, with or without haematuria and evidence of cystitis (see Figs. 
233 and 234). 
Fig. 232.—Calcic Oxalate Crystals. 428 
PHYSICAL DIAGNOSIS 
10. Summary of the Urinary Pictures Most Useful in Diagnosis 
Aside from polyuria, oliguria, hcematuria, and pyuria, which 
have already been discussed, the most important conditions in which 
the urine gives valuable diagnostic evidence are: 
Fig. 233.—Vinegar Eels in Urine. (Billings.) a, Protruded hooks of male; b, top- 
shaped oesophageal enlargement. The Strongyloides stercoralis (see above, Fig. 214, 
page 401) has also been found in the urine. 
1. Cystitis.—Urine passed frequently, painfully, and in small 
amounts. Turbid, ammoniacal, and offensive (after the earliest 
stages). Much pus and many other cells are found in the sediment, 
with bacteria, triple phosphate crystals, and amorphous debris. It 
must be remembered that cystitis is usually but one element in the 
diagnosis; bladder stone, obstructing prostate, tuberculous kidney, or 
other diseases may be its cause. 
2. Acute Nephritis (or acute exacerbations in chronic cases).— 
Scanty, heavy, highly albuminous urine, often bloody and containing THE INTESTINE, SPLEEN, KIDNEY 
429 
in the sediment much blood and many cells, free or on casts. Other 
varieties of casts occur, but are not characteristic. In convalescence 
the urine becomes abundant and of light weight, and the other 
abnormalities gradually disappear. 
3. Chronic Nephritis (“parenchymatous” or “diffuse”).—The 
urine is rather scanty, pale, and light (1.012-1.018), with a varying 
amount of albumin and, in the sediment, much fat— free, in cells, and 
on casts. Also found, but not characteristic, are all the other varieties 
Fig. 234.—Bilharzia Eggs in the Urine, with Blood, Calcic Oxalate, and a Hyaline Cast 
(O’Neil.) 
of casts. If death does not ensue within eighteen months, the urine 
is apt to assume the different characteristics: 
4. The later stages of chronic nephritis show often polyuria (often 
several quarts; urine especially abundant at night), low specific 
gravity (1.014 or less ). Traces of albumin and a few hyaline and 
granular casts occur steadily or intermittently. High blood pressure 
is nearly constant. 
5. Pyelitis and acute hcematogenous renal suppurations are dis- 
eases much more commonly recognized since 1904 than previously. 
The presence of bacteria (usually colon bacilli) and pus without many 
cells of other types in acid urine should always lead to bacteriological 430 
PHYSICAL DIAGNOSIS 
and cystoscopic examinations. This condition of the urine may 
at times be the only sign of the disease. The presence of pain, tender- 
ness, or tumor in the region of the kidney (usually the right kidney) 
and the occurrence of fever and leucocytosis support the diagnosis, 
especially in little girls and in women near parturition. To dis- 
tinguish pure pyelitis from pyelitis complicating a renal infection is 
impossible. 
This disease should be borne in mind: 
(a) In all cases of unexplained fever without obvious local cause— 
especially in girl babies and in women a short time before or after 
parturition (subacute or chronic renal infection). 
(b) In acute abdominal emergencies when appendicitis, chole- 
cystitis, intestinal obstruction, perforating peptic ulcer, and pan- 
creatitis are being considered. With these consider also acute infection 
of the kidney, for in some cases the pain is in the right hypochondrium 
and no complaints suggesting the kidney are uttered. CHAPTER XXIV 
THE BLADDER, RECTUM, AND GENITAL ORGANS 
I. The Bladder 
1. Incidence of Bladder Disease 
(Massachusetts General Hospital, 1870-1905.) 
Cystitis 829 cases. 
Stone 538 cases. 
Cancer ,. 57 cases. 
Papilloma 20 cases. 
Tuberculosis 43 cases. 
(a) Data 
Distention, tumor, the urine, and the results obtained by cystos- 
copy, by catheterization, by rectal and vaginal examination, and by the 
x-ray, furnish most of our direct evidence in bladder disease. Pain 
in the bladder or near the end of the penis, and frequent, painful 
micturition with vesical tenesmus or straining, are common symptoms 
in various lesions of the organ, and direct our attention to it, though 
they do not indicate the nature of the trouble. 
2. Distention of the Bladder 
In both sexes, distention is often wholly unknown to the patient, 
and may be accompanied by frequent acts of urination, especially 
in prostatic obstruction, in acute infections, and after operations. A 
distended bladder is readily recognized by palpation as a smooth, 
round, firm, symmetrical tumor in the median line, above the pubes. 
The tumor is dull on percussion, and in slight degrees of distention 
this dulness above the pubes may be the only physical sign obtainable. 
In well-marked cases, which are most common in males, the distended 
bladder may reach to the navel or even above it, and the beginner is 
usually astonished at its dimensions and its firm, resistant surface (see 
431 432 
PHYSICAL DIAGNOSIS 
Fig. 235). Diagnosis rests on the infrequency of other tumors of 
this region in men and on the result of catheterization or suprapubic 
aspiration. In females a history of failure to pass urine almost 
invariably makes the diagnosis obvious, though occasionally after 
operations distention of the bladder and dribbling of urine may go 
together in women, as they so frequently do in men. 
The commonest causes of distended bladder are: 
(1) Prostatic obstruction. 
(2) Old strictures of the urethra. 
Less common are: 
(3) Spasm of the urethra in gonorrhoea. 
(4) Acute prostatitis. 
Fig. 235.—Distended Bladder Reaching Above the Navel. 
(5) Paralysis of the bladder, from disease or injury, after opera- 
tion, and in fevers. 
(6) Tumor or stone near the neck of the bladder. 
The diagnosis of the cause of distention rests on the history, the 
result of attempts at catheterization, the rectal examination, the 
condition of the urine, and the physical signs in other parts of the 
body. A long history of frequent micturition, especially at night, in 
an old man, an obvious enlargement of the prostate felt by rectum, THE BLADDER, RECTUM, AND GENITAL ORGANS 
433 
and the passage of ammoniacal urine suggest prostatic obstruction. 
The information obtained during the passage of a catheter usually 
clinches the diagnosis. 
Acute retention, with no previous history of frequent micturition or 
foul-smelling urine in a young or middle-aged man, who has had 
gonorrhoea and may or may not have noticed a diminution in the 
size of the stream of urine passed, suggests a urethral stricture. The 
catheter decides. 
Spasm of the urethra may occur in acute gonorrhoea, and pro- 
duces a retention which may often be overcome by hot poultices and 
enemata. The history and the effects of treatment suggest the 
cause of the retention. 
Acute prostatitis, as a cause of retention following gonorrhoea, 
is suggested by pain and tenderness in the perineum, painful defe- 
cation, fever, perhaps chills, and a hot, tender prostate felt by rectum. 
Abscess may form and discharge by urethra or rectum. 
Paralysis of the bladder, as a cause of retention, is usually obvi- 
ous from the history and from the evidence of disease of the spinal 
cord, or of operation and semicomatose states (as in fevers and shock). 
3. The Urine as Evidence of Bladder Disease 
This has been described above (page 427). Cystitis, acute or 
chronic, usually gives characteristic evidence of itself in the urine, 
and suggests as its cause the possibility of gonorrhoea, of vesical stone, 
of prostatic or other obstruction to the outflow, and of vesical or 
renal tuberculosis. When a urine like that described in chronic 
nephritis occurs with chronic prostatic obstruction the relief of the 
obstruction is necessary if we are to prevent progressive development 
of cirrhotic kidney from back pressure. 
Frequent micturition is much commoner and less significant in 
women than in men. All sorts of “nervousness” and emotional 
strain produce this symptom in women, independent of any demon- 
strable source of irritation in the urinary tract. Aside from these 
conditions the symptom is oftenest met with in: 
(a) Cystitis, from any cause, including stone and renal tuberculosis, 
or without known cause, with characteristic changes in the urine. 
(b) Prostatic obstruction, with evidence of retention. 
(c) Gonorrhoea, with evidence of this disease. 
(d) Paralysis of the bladder (see above). 
(e) Overconcentration of the urine (estimated by the color and 
specific gravity). 434 
PHYSICAL DIAGNOSIS 
III. Stone in the Bladder.—Pain near the end of the penis, espe- 
cially at the end of micturition and aggravated by jolting or active 
motion, frequent urination, especially in the daytime, sudden inter- 
ruption of the stream of urine, and hasmaturia at the end of micturi- 
tion, are the most frequent symptoms of stone, especially if they 
occur in boys. In old men stone may be wholly without character- 
Fig. 236.—X-ray of stone in the bladder. 
istic symptoms, and at any age the symptoms can never do more 
than suggest the possibility of stone and the advisability of search- 
ing for it systematically with a cystoscope. 
IV. Tuberculosis of the Bladder.—Cystoscopy and the recogni- 
tion of tubercle bacilli by animal inoculation are the only reliable 
means of diagnosis. A chronic cystitis in a young or middle-aged 
person, especially with an acid urine, is suggestive. 
V. Tumors of the bladder are suggested by intermittent hema- 
turia with vesical irritation, and confirmed by cystoscopic examination. THE BLADDER, RECTUM, AND GENITAL ORGANS 
435 
II. The Rectum 
1. Symptoms 
It is not and should not be a part of routine physical examina- 
tion to examine the rectum. The commonest conditions which call 
for such investigation are: 
(а) Hemorrhage at stool. 
(б) The protrusion after defecation of something which is not 
easily returned (“piles”)- 
Fig. 237.—X-ray of stone in the bladder. 
(c) Painful defecation or pain in the region of the rectum at 
other times. 
(id) The presence of an ulcer or sinus near the rectum. 
(e) Habitual constipation, not explained by lesions elsewhere. 
(/) Intestinal obstruction. 
(g) All subacute diarrhoeas of elderly persons (cancer). 436 
PHYSICAL DIAGNOSIS 
(h) Suspected appendicitis, prostatitis, prostatic cancer or ob- 
struction, or diseases of the seminal vesicles. 
(i) Pelvic symptoms in women with tight hymen. 
The diseases of the rectum which we are especially on the look- 
out for are: (1) Hemorrhoids; (2) fissure of the anus; (3) ischio- 
rectal abscess; (4) fistula in ano; (5) cancer of the rectum. Less 
common are: (6) pruritus ani; (7) prolapse of the rectum; (8) ulcera- 
tion or stricture of the rectum. 
2. Methods 
For most examinations the finger suffices. It should be covered 
by a thin, rubber finger-cot, greased with vaseline, and should be 
introduced slowly and gently while the patient strains down as dur- 
ing defecation. 
The examining finger should note the presence of abnormal promi- 
nences or resistance (piles, tumors) in any part of the rectum, of tender 
spots (ulcer, abscess), and strictures. The shape and size of the pros- 
tate gland, its consistence, and the presence or absence of tenderness 
in it are of importance. The normal seminal vesicles can be felt if 
distended. If they are hard and nodular, tuberculosis should be sus- 
pected. By milking the vesicles and massaging the prostate, pus con- 
taining gonococci may be pressed out through the urethra. This 
process is often of value both in diagnosis and in treatment. 
High up on the right one may touch a tender spot if an inflamed 
appendix is near the pelvic brim (often a fallacious sign). 
In women the uterus, especially if retroverted, may be easily 
felt, and most of the other details of pelvic examination (see below, 
page 440), can be more or less clearly made out. 
For higher and more thorough examination a cylindrical speculum 
and a head mirror should be used. 
Hemorrhoids.—The diagnosis of external hemorrhoids, which can 
easily be brought outside the anus, is made at a glance. Internal 
hemorrhoids are best seen with a rectal speculum, and may resemble 
the external or may consist of “bright red, spongy, granular tumors, 
rarely larger than a ten-cent piece, and situated high up in the 
rectum.” 
Fissure of the anus is often connected with a small ulcer and with 
oedematous folds, which resemble an external pile but are much 
more tender. On separating these folds the fissure comes into sight. 
It usually produces severe pain during and after defecation. THE BLADDER, RECTUM, AND GENITAL ORGANS 
437 
Ischio-rectal abscess presents near the anus the ordinary signs of 
abscess with pain radiating through the pelvis, but may open either 
within or outside the rectum and results in 
Fistula in ano, a sinus beside the rectum, opening internally, 
externally, or in both directions. It may be very tortuous. Tubercu- 
losis is to be suspected in such fistulae. 
Cancer of the rectum is suggested by the occurrence of rectal pain 
during defecation, with blood in the stools and either diarrhoea or 
constipation, usually with some pallor and emaciation, in persons past 
middle life. Owing to neglect of a thorough examination many cases 
are at first mistaken for piles. 
The examining finger reaches a hard, ulcerating mass high up, 
as a rule, in the rectum. It may be easier to reach if the patient 
stands or squats and strains down during examination. 
From tuberculous or syphilitic stricture with or without ulcera- 
tion, and from benign villous growths, it may be impossible to dis- 
tinguish cancer without histological examination of an excised piece. 
Cancer of the prostate is felt on the anterior wall of the rectum and 
makes the prostate hard, fixed, sometimes nodular. It is often very 
difficult to recognize. 
III. The Male Genitals 
Routine examination of the male genitals includes investigation 
of the penis for the presence of: 
(a) Urethral discharge and its consequences. 
(b) Chancre. 
(c) Chancroid. 
(d) Balanitis. 
(e) Phimosis or paraphimosis. 
(/) Periurethral abscess. 
(g) Malformations. 
(h) Cancer. 
In the testes and scrotum we look for: 
(a) Epididymitis (gonorrhoeal or tuberculous). 
(b) Orchitis (traumatic, syphilitic, tuberculous, after mumps and 
other infections). 
(c) Tumors of the testis (cancer or sarcoma). 
(d) Hydrocele and haematocele. 
(e) Varicocele. 
(/) Scrotal hernia. 
(g) Absence of one or both testes. 438 
PHYSICAL DIAGNOSIS 
i. The Penis 
Urethral discharge, if not obvious, may often be brought to light 
by “stripping” the urethra forward from the prostatic region to the 
meatus. If Gram’s stain brings out an intracellular, decolorizing 
diplococcus in the exudate, there is no reasonable doubt of the pres- 
ence of gonorrhoea. 
Chancre (“hard sore”),'the primary syphilitic lesion, is a super- 
ficial, painless, indolent ulcer with an indurated base and a scanty 
serous discharge. It is usually round or oval and sharply demarked 
from the surrounding tissue by elevated edges. It is rarely multi- 
ple. Painless, hard, non-suppurating buboes accompany it. The 
glans and the inner surface of the prepuce are the commonest sites. 
The Treponema pallidum can often be identified in stained smears 
or by the dark field illumination. In a certain percentage of cases 
a positive Wassermann reaction may be obtained. 
Chancroid (“soft sore”) is like any other painful, superficial 
ulcer without induration, irregular in shape, often multiple, and 
with abundant discharge. A single, painful bubo accompanies it in 
about one-third of all cases. 
Balanitis (inflammation of the surface of the glans penis), usu- 
ally gonorrhoeal, has the ordinary signs of inflammation; it often 
spreads to the inner surface of the prepuce. 
Phimosis is a contraction of the orifice of the prepuce, so that it 
cannot be retracted to uncover the glans. May be hereditary or the 
result of gonorrhoea. 
In paraphimosis the prepuce is caught behind the glans penis so 
that it cannot be brought forward. Great oedema of the neighbor- 
ing parts usually results. 
Peri-urethral abscess, usually a complication of gonorrhoea, appears 
as a small, tender swelling on the under surface of the urethra. 
Malformations are chiefly hypospadias or congenital deficiency of 
some portion of the lower wall of the urethra, and epispadias (rare), 
a similar deficiency in the upper wall. A short, downward curved 
penis is often associated with hypospadias. 
Cancer of the penis attacks the foreskin or the glans, and has the 
usual characteristics of epithelioma elsewhere. 
2. The Testes and Scrotum 
Acute epididymitis, usually a complication of gonorrhoea, appears 
as a hot and tender swelling behind the testis, often preceded by THE BLADDER, RECTUM, AND GENITAL ORGANS 
439 
tenderness along the spermatic cord. Acute hydrocele may accom- 
pany it. 
Chronic epididymitis, usually tuberculous, is painless and insid- 
ious in onset, and produces a hard, irregular enlargement low down 
behind one or both testes, to which, however, the process is apt soon 
to spread. Caseation and involvement of the skin later produce a 
suppurating sinus, which is often the first thing to bring the patient 
to a physician. 
Acute orchitis is often due to a blow, to gonorrhoea, or to mumps. 
The testis is symmetrically swollen and tender, but suppuration 
rarely follows. 
Chronic orchitis, often syphilitic, is slow, painless, and may be 
accidentally discovered as a slightly irregular induration of the testes 
with little if any increase in size. Ulceration and fistulse are rare in 
the syphilitic form, common in the tuberculous. 
Cancer of the testis may appear at any age. It is soft, almost 
fluctuating, and grows very rapidly, soon involving and perforat- 
ing the skin, so as to produce an offensive, fungous, granulating out- 
growth which easily bleeds. The inguinal glands are involved. 
Sarcoma of the testis, commonest at puberty, produces a painless, 
uniform enlargement, and may reach great size. It may resemble 
hydrocele or hsematocele and be mistaken for the latter, especially 
for an old effusion in a thickened sac (see below). 
Diagnosis depends on rapid growth, the entire absence of trans- 
lucency, the tendency to adhere to the skin and to present unequal 
resistance in different portions (Jacobson). Incision should be made 
in all doubtful cases. 
Hydrocele, an accumulation of serous fluid in the tunica vagi- 
nalis, may depend on trauma or on an acute epididymitis or orchitis, 
but is usually chronic and of unknown cause. It may be congenital 
and communicate with the peritoneal cavity or form part of a general 
dropsy in heart or kidney disease. 
Examination shows a smooth, tense, fluctuating tumor, without 
impulse on cough, usually without pain, tenderness, or any sign of 
inflammation, and, above all, translucent if examined with a hydro- 
scope tube or in a dark room with a candle. 
If the fluid is opaque or bloody, or if the tunica is thickened, there 
may be no translucency and diagnosis may be impossible without 
puncture. The testis lies behind the effusion and near its lower end. 
Hcematocele usually follows injury and produces a heavy, opaque, 
non-fluctuating tumor, which may closely resemble sarcoma unless 440 
physical diagnosis 
the history and evidence of trauma are clear. Incision or puncture 
should decide. 
Varicocele, a usually harmless enlargement of the veins about the 
spermatic cord, is easily recognized as a mass of tortuous vessels, 
generally in the left side. It often complicates hypernephroma. 
Scrotal hernia is usually reducible, tympanitic on percussion 
and gives an impulse on coughing. If it consists largely of omen- 
tum it will be dull on percussion. The history of the ease and the 
progression of the tumor from above downward usually make its 
origin clear. 
Absence of one or both testes from the scrotum should direct our 
search upward to the inguinal canal, since a retained testis may be 
the seat of troublesome inflammation or of malignant disease. (For 
examination of the seminal vesicles, see the Rectum, page 436.) 
IV. The Female Genitals 
1. Methods 
Inspection of the external genitals is easy if the parts are properly 
exposed by a satisfactory position and a good light. Intravaginal 
inspection needs a speculum (Sims’ or bivalve) and usually an assistant 
to hold it. 
Palpation should always be bimanual, the left forefinger in the 
vagina (or in the rectum if the hymen is narrow), the right hand 
above the symphysis pubis. The proper co-operation of the hands 
is hard to describe and depends on practice. The pressure oflthe 
external hand helps to bring the pelvic organs within reach of|the 
examining finger in the vagina. Unless the organs can be thus 
grasped or balanced between the outer and inner hands, no satisfac- 
tory examination is possible. Tenderness may prevent this or render 
an anaesthetic necessary, but gentleness and the avoidance of any 
sudden or rapid motions do much to facilitate the examination. 
The left hand, in making its way into the upper parts of the vaginal 
vault, should press only on the perineum, avoiding the region of 
the clitoris. It is astonishing how much pressure can be borne 
without pain, provided it is exerted gradually and upon the peri- 
neum only. Many examiners find it advantageous to rest the left 
foot upon a stool, with the left elbow on the knee. 
2. Lesions 
I. In the External Genitals one looks for some of the same 
lesions already described on page 438, viz., chancre, chancroid, local THE BLADDER, RECTUM, AND GENITAL ORGANS 
441 
inflammations, and tumors. Only the commonest and most impor- 
tant lesions will be mentioned here. 
(a) In young children a suppurating vulvo-vaginitis, usually 
gonorrhoeal, but often non-venereal, is easily recognized by the abun- 
dant purulent discharge. 
ib) Local eczema, often red and angry, is commonly the result 
of the irritation of diabetic urine or a leueorrhoeal discharge. 
(r) Varicose veins and oedema of the vulva are common in preg- 
nancy and occasionally result from large pelvic tumors. 
(d) Ruptured perineum, with more or less protrusion of the vaginal 
walls, carrying with it the bladder (cystocele or rectum (rectocele), 
is readily recognized if the normal anatomy of the parts is familiar. 
(<?) The hymen may be imperforate with retention of menstrual 
fluid, or tender, irritated remains of it after rupture may cause pain 
and need removal. 
(/) Urethral caruncle (a small vascular papilloma at the entrance 
of the urethra) is a bright red excrescence, usually the size of a split 
pea or smaller. It may cause no symptoms or may produce irritation, 
especially during micturition. 
(g) Small abscesses of the glands within or around the urethra 
may cause pain in coitus or during micturition. 
II. The Uterus.—Only the commonest lesions will be dealt 
with here, viz.: 
1. Laceration and “erosion” of the cervix. 
2. Malpositions of the organ. 
3. Endometritis. 
4. Cancer of the uterus. 
5. Fibor-myoma of the uterus. 
1. (a) Lacerations of the cervix following childbirth are very common 
and frequently produce no symptoms. They are readily recognized 
by inspection and palpation, and are often combined with: 
ib) “Erosions,” an ulcerated, raw surface at and around the os 
uteri with or without the formation of small cysts. At times the 
os assumes a warty, irregular appearance, suggesting cancer, from 
which it can be distinguished only by histological examination of an 
excised piece. 
2. (a) “Malpositions” (backward or forward) may involve the 
whole organ (ante- or retroversion) or represent a bending of the 
organ upon itself (ante- or retroflexion). These lesions may be 
variously combined and frequently exist without producing any symp- 
toms. Indeed, it is doubtful whether there is any single “normal” 442 
PHYSICAL DIAGNOSIS 
position for the uterus. Its position is recognized by bimanual pal- 
pation, which should also determine whether the uterus is freely 
movable or whether it is bound in place by adhesions, such as are 
very often found with backward displacements. 
(b) Prolapse of the uterus toward the vaginal outlet is often a 
result of pelvic lacerations unrepaired. When the uterus is outside 
the vaginal outlet, we call the condition procidentia. 
(c) Lateral displacement of the uterus by pressure of tumors or 
traction by old adhesions is less common. 
3. Endometritis may present no definite physical signs except a 
muco-purulent discharge (leucorrhcea, “whites”) and perhaps un- 
duly frequent, profuse, or prolonged menstruation. The slightest 
touch of a uterine sound may produce bleeding. It often accom- 
panies disturbances of digestion and neurasthenic conditions, usually 
as part of a general prostration. 
4. Cancer of the uterus usually attacks the cervix, and in marked 
cases is easily recognized by sight and touch as a “ cauliflower ”- 
like, fungating mass on the cervix. In its early stages it may be 
confounded with “erosions” and papillomatous growths, and only 
microscopic examination can satisfactorily determine its nature. 
Profuse hemorrhage, especially in a woman about the period of the 
menopause, and the offensive odor of the discharge suggest the diag- 
nosis. The vaginal wall is soon involved in the growth, and irrita- 
bility or obstruction in bladder or rectum may result. Cancer of the 
fundus is suspected from the finding of enlargement or a suspicious 
discharge, but confirmed only by the histological examination of bits 
removed by curetting. 
5. Fibro-myoma of the uterus is by far the commonest tumor of 
that organ. It produces hemorrhages at or between the menstrual 
periods, and anaemia results. Otherwise its effects are those of 
pressure on the bladder and rectum, or on neighboring nerves or 
vessels (pain, oedema). 
Bimanual palpation determines, first of all, the fact that the 
growth is connected and moves with the uterus. This determined 
and cancer excluded by the absence of any involvement of the cervix 
or of the' vaginal wall, the chief difficulty may be in distinguishing 
the growth from a pregnant uterus. Usually its irregular shape, 
the persistence of menses, and the lapse of time settle the question. 
Lengthening of the uterine canal is an important confirmatory 
sign of fibromyoma, but sounds should never be passed to determine 
this pregnancy is definitely impossible. THE BLADDER, RECTUM, AND GENITAL ORGANS 
443 
III. Fallopian Tubes.—Salpingitis (acute or chronic) and tubal 
pregnancy are the most important diseases of the tubes. 
(а) Salpingitis is usually gonorrhoeal, occasionally tuberculous, 
sometimes of unknown origin. A painful, tender swelling or in- 
duration in the region of the tube, with or without fever, chill, or 
leucocytosis, constitutes the evidence for diagnosis. From pelvic 
peritonitis of the tubal region diagnosis is impossible. 
From tubal pregnancy diagnosis may be very difficult, and sus- 
picions are rarely aroused until rupture' occurs (vide infra). If the 
signs and symptoms of pregnancy are absent and tenderness is marked 
the condition is usually called salpingitis; but even then mistakes 
often occur, as the menses may persist in tubal pregnancy and the 
foetal tumor may be tender. Only when pregnancy can absolutely 
be excluded is diagnosis sure. 
(б) Tubal pregnancy, as just explained, is rarely to be diagnosed 
until the growth of the foetus ruptures the tube—an event which 
usually occurs between the third and the twelfth week of pregnancy.1 
Sudden pelvic pain with tenderness, vomiting, and evidence of internal 
hemorrhage (i.e., pallor, fainting, weak, rapid pulse, thirst, air hunger) 
suggest the diagnosis, especially if a tumor in the tubal region can be 
detected bimanually. 
IV. Ovaries.—A prolapsed ovary is often felt during a vaginal 
examination, being recognized by its size, shape, and relation to the 
uterus. 
Ovaritis, enlargement, and tenderness of one or both ovaries is 
usually part of tubal disease and not sharply to be distinguished 
from it before operation. In other cases it is associated with cyst for- 
mation, and the cysts may be palpated bimanually. Abscess of the 
ovary is not commonly diagnosed, but is met with in operations for 
pus tubes. 
Ovarian Tumors 
(a) Small Tumor.—In their earlier stages these growths pro- 
duce symptoms only when complications arise, i.e., suppuration or 
twisting of the pedicle. Small, suppurating cysts give practically 
the same signs as those of a pus tube, and are recognized only at 
operation or autopsy. 
1 If disturbances of menstruation, morning nausea, changes in the breasts, and 
cyanosis of the vagina are combined with an extra-uterine tumor and an unusually 
slight uterine enlargement, the diagnosis of tubal gestation may be suspected prior 
to rupture. 444 
PHYSICAL DIAGNOSIS 
Twisted pedicle gives rise to symptoms and signs often indistin- 
guishable from those of perforative peritonitis or intestinal obstruction. 
Only the recognition of the tumor as ovarian can suggest that the acute 
symptoms may be due to twisting of its pedicle. 
(b) Large ovarian tumors have been confused in my experience 
with pregnancy, fibroid of the uterus, ascites, and tuberculous peri- 
tonitis. From these we may usually distinguish an ovarian tumor by 
Fig. 238.—Huge Ovarian Cyst. 
its history, its origin from one side of the belly, by the shape of the 
belly, the area of percussion dulness, and the pelvic examination. 
By the history we should attempt to exclude disease of the heart, 
kidney, and liver, and tuberculosis of any organ, should inquire 
into the position of the tumor in the earlier stages of its growth, 
and establish the presence or absence of the ordinary signs of preg- 
nancy and of uterine hemorrhages such as occur with fibroids. 
In ascites or tuberculous peritonitis the flanks often bulge (see 
Fig. 204, page 364), whereas in ovarian disease the bulging is central 
and greatest just below the navel (see Fig. 238). THE BLADDER, RECTUM, AND GENITAL ORGANS 
445 
If by the history or by palpation and percussion we can deter- 
mine that the tumor is fluctuant and springs from one side of the 
abdomen, it is in all probability ovarian. High psoas abscess some- 
times presents identical signs, but is associated with evidence of 
spinal tuberculosis (see below, p. 482). Moderate ascites or tuber- 
culous peritonitis leaves an oval, resonant area about the navel, 
which is absent with large ovarian tumors; but if the amount of 
free fluid is large, percussion and palpation may give results identical 
with those found in ovarian disease. 
Vaginal examination may exclude fibroid by showing that the 
uterus is not directly connected with the tumor and by demonstrating 
with a uterine sound that the uterine canal is not elongated. 
Solid tumors of the ovary, carcinoma, sarcoma, or fibroma are 
rarely recognizable before operation and are often mistaken for pedun- 
culated uterine fibroids. They are apt to be associated with ascites. CHAPTER XXV 
THE LEGS AND FEET 
I. The Legs 
1. Hips 
The examination of the hip will be discussed later (see page 482). 
2. Groin 
In the groin we look for evidences of: 
1. Enlarged or inflamed lymphatic glands and scars of previous 
inflammation. 
2. Hernia and hydrocele of the cord. 
3. Psoas abscess. 
Less common are: 
4. Retained testis. 
5. Filarial lymphatic varix. 
1. Inguinal Glands.—Two sets of inguinal glands are distin- 
guished—one arranged along the lower half of Poupart’s ligament; 
the other lower down, around the saphenous opening. 
(a) The “Poupart’s group” are acutely enlarged in lesions of 
the genitals (“bubo” or gonorrhoea,1 syphilis, chancroid) and peri- 
neum; chronically enlarged in malignant disease of the penis, uterus 
(late), and other genitalia. 
(b) The saphenous group is enlarged in response to lesions of the 
thigh, leg, and foot (cuts, wounds, ulcers, eczema, etc.). 
(c) Either or both groups may be enlarged in leukaemia, Hodg- 
kin’s disease (see above, page 32), infectious arthritis, and various 
obscure fevers. In many cases no cause for enlargement can be found. 
2. Hernia is diagnosed by the presence of a soft, resonant, fluc- 
tuating, usually reducible tumor with an impulse on coughing. 
Hydrocele of the cord gives also an impulse on coughing, but usually 
shows a distinct limit above. On pulling the cord the swelling moves 
too. 
1 The bubo of gonorrhoea often suppurates; that of syphilis rarely. Hence a 
scar in the inguinal region suggests an old gonorrhoea. 
446 THE LEGS AND FEET 
447 
3. Psoas abscess (see Fig. 239) is associated with vertebral tubercu- 
losis. Don’t cut into it without excluding aneurism! 
4. Retained testis should be suspected whenever an inguinal tumor 
is present and only one testis is found in the scrotum. 
5. Filarial lymphangiectasis is generally mistaken for hernia and 
operated on as such, although it gi-ves no impulse on coughing and 
cannot be completely reduced. 
The history of residence in the 
tropics should always suggest an 
examination of the blood (at 
night) for filariae. 
3. The Thigh 
The records of the Massa- 
chusetts General Hospital show 
that (i) epiphysitis and osteo- 
myelitis (septic or tuberculous) 
are almost ten times as common 
as any other serious lesion of 
the thigh, except fracture. The 
cases are to be divided into 
acute septic cases and chronic, 
usually tuberculous, cases. 
The acute septic cases begin 
with severe pain, tenderness, 
fever, chill, and leucocytosis. Later an induration and finally fluc- 
tuation appear, and the abscess, if not incised, will break externally. 
General, sometimes fatal, septicaemia may take place. 
The chronic tuberculous cases first consult the physician, as a 
rule, for sinus, which proves when explored to lead to dead bone, 
as do most of the sinuses from septic cases. 
The diagnosis of the acute cases depends chiefly on excluding 
arthritis of any type. Careful examination with testing of joint 
motions will usually demonstrate that the pain and tenderness are 
in the bone and not in the joint. The leucocyte count is but slightly 
elevated in most cases of arthritis, but is decidedly high, 20,000 or 
more, in most cases of acute osteomyelitis. The same is true of the 
temperature. Monarticular arthritis—the only variety likely to be 
considered in such a diagnosis—is rare in youth, when most cases of 
acute osteomyelitis and epiphysitis occur. 
Fig. 239.—Psoas Abscess. (Bradford 
and Lovett.) 448 
PHYSICAL DIAGNOSIS 
Whether the disease starts in the shaft of the bone or in the epiphy- 
sis is to be determined by the seat of pain and tenderness. 
Tuberculous cases can be recognized only by the histological 
examination. Old cases may be suspected by the presence of a scar, 
but 
(2) Multiple white scars should always suggest, though they are 
far from proving, syphilis, for chronic ulcer above the knee is often 
due to gumma. 
(a) Tumors of the Thigh 
(i) Sarcoma of the femur is the commonest and largest tumor 
of the thigh. Among one hundred and thirty-three tumors of the 
thigh recorded at the Massa- 
chusetts General Hospital, 
sixty-six were sarcoma. A 
hard, spindle-shaped growth 
encircles the femur; the lower 
end is the commonest site, 
but any part of the bone may 
be affected (see Fig. 240). 
(2) Osteoma, or exostosis, 
occurred eleven times in the 
one hundred and thirty-three 
cases just mentioned. It is 
much smaller and of slower 
growth. The last trait usually 
serves to distinguish it from 
sarcoma; should decide. 
(3) Metastatic cancer of the upper half of the femur may occur 
after cancer of the breast, but rarely gives rise to symptoms unless 
spontaneous fracture occurs—an event which always should suggest 
cancer. Epithelioma of the thigh is not very rare (twelve cases in 
the one hundred and thirty-three above referred to). Its traits are 
those of epithelioma elsewhere. 
Tuberculosis of the knee may simulate sarcoma of the lower end of 
the femur, but sarcoma grows more rapidly. The tuberculin test 
or an exploratory incision may be necessary to decide the diagnosis. 
(4) Psoas abscess or kip-joint abscess (see Fig. 239) may burrow 
down so as to point on the thigh. The evidence of disease in the hip 
or vertebrae is usually sufficient to make clear the diagnosis. 
Fig. 240.—Sarcoma of the Femur. THE LEGS AND FEET 
449 
i. Sciatic pain and tenderness more or less clearly confined to the 
distribution of the sciatic nerve may be due to 
(a) Sacroiliac disease (strain, looseness, displacement). 
(b) Spondylitis. 
(c) Unknown cause (neuritis). 
(d) Prostatitis, prostatic abscess or neoplasm. 
(e) Pelvic tumors or abscess (including psoas abscess). 
Right 
Left 
Fig. 241.—Paget’s disease. X-ray of tibiae. Right much more extensively diseased 
(b) Miscellaneous Lesions of the Thigh 
(2) Phlebitis with thrombosis of a vein, usually the saphenous, 
is a common cause for swollen thigh (and leg) with pain and tender- 
ness, especially over the inflamed vein, where a cordy induration can 
often be felt. Typhoid fever and the puerperal state are the usual 450 
PHYSICAL DIAGNOSIS 
causes, but it also occurs after tonsillitis and other infections, and 
sometimes without any known cause. Diagnosis depends on the 
presence of these signs and causes and the absence of any other demon- 
strable cause for inflammation. 
(3) Meralgia parcesthetica means the presence of a patch of anaes- 
thesia, parassthesia, or hyperaesthesia (tenderness), with or without 
pain, on the anterior and upper 
surface of both thighs (the area of 
the external cutaneous nerve). 
(4) Paget's disease (osteitis de- 
formans) presents usually its most 
marked lesions in the legs and 
head, though most of the other 
bones are also affected. In the 
leg the most characteristic lesions 
are forward bowing of the femur 
and tibia with outward rotation of 
the whole limb (see Fig. 242). 
The x-ray shows marked thicken- 
ing of some areas, with thinning 
of others. 
(5) Intermittent Claudication 
and 11 Cramps." Insufficient circu- 
lation through the arteries of the 
legs may give rise to sudden “giv- 
ing way” of one or both during 
running or wralking, the power 
returning after a short rest. In 
patients at rest the frequent re- 
currence of painful cramps in the 
muscles may be the only manifestation of the disease. In other 
cases there are various forms of parassthesia such as numbness, 
prickling, and “hot feet at night.” 
Obliteration of the dorsalis pedis (or larger arteries) by arterio- 
sclerosis is often found, but there is reason to believe that local anaemia, 
due to vasomotor disturbances or other causes, may produce similar 
cramps (e.g., those seen in football players during a hard run and in 
pregnant women). 
Fig. 242.—Paget’s Disease (Osteitis 
Deformans). Note the outward and for- 
ward bowing of legs and arms. (Robin.) 
(c) Paralyses 
(i) Paralysis of one leg, occurring in children, is usually due to 
anterior poliomyelitis; in adults it usually forms part of a hemiplegia or THE LEGS AND FEET 
451 
is of hysterical origin. Neuritis, due to alcohol, lead, arsenic, or 
diphtheria, may affect one leg predominantly, but both are usually 
involved. Cerebral monoplegias, due to cortical lesions of the leg area, 
are rare. Chorea may be associated with a limp, half-paralyzed condi- 
tion in one leg, usually with some involvement of the arm on the same 
side, and the characteristic motions (see above, page 48) make the 
diagnosis clear. 
The differential diagnosis of the other varieties of monoplegia is 
usually easily made with the aid of a careful history and a thorough 
examination of the other parts of the body. 
(2) Complete paralysis of both legs (paraplegia) is commonest in 
diffuse or transverse myelitis (e.g., in spinal tuberculosis or metastatic 
cancer with pressure on the cord), in multiple sclerosis, spastic para- 
plegia (hereditary or acquired), pernicious anemia and tabes. Hysteria 
also may produce a spastic paraplegia, though monoplegia is commoner 
in this disease. 
(3) Partial paralysis of both legs is oftenest due to neuritis, resulting 
from the causes mentioned above. The extensors of the foot are 
especially affected and toe-drop results, so that in walking “the entire 
foot is slapped upon the ground like a flail ’ ’ (Osier). 
Differential Diagnosis.—(a) In diffuse or transverse myelitis, 
whether or not the trouble be due to pressure, there are increased 
reflexes, anaesthesia, usually loss of control of the sphincters (involun- 
tary urine and faeces), and often bed-sores. 
(6) In spastic paraplegia of any type the legs are stiff and the 
reflexes increased, but sensation and the sphincters are normal and 
there is no atrophy or bed-sore formation. 
(c) In multiple sclerosis there are usually no disturbances of sensa- 
tion or of the sphincters, and the paralysis is associated with nys- 
tagmus, intention tremor, and slow, staccato speech. 
(d) Tabes dorsalis shows ataxia but no paralysis until late in its 
course. The paralytic stage is preceded by a long period characterized 
by lightning pains, bladder symptoms, Argyll-Robertson pupil (see 
page 16), and loss of knee-jerks. 
(e) Hysteria may take on almost any type of paralysis and may 
deceive the very elect, but as a rule the other evidences of hysteria 
guide the diagnosis. 
4. The Knee 
(a) Tuberculosis, atrophic, hypertrophic, and infectious arthritis, 
and traumatic synovitis are the commonest diseases, but will be 
described with other diseases of the joints (see page 480). 452 
PHYSICAL DIAGNOSIS 
(6) Housemaid’s knee is a bursitis of the prepatellar bursa (see 
Fig. 243). Fluctuation, with or without heat and tenderness, and 
limited to the prepatellar space, is diagnostic. 
(c) Bow-legs and knock-knee are so easy of diagnosis that I shall 
simply mention them here. 
Fig. 243.—Prepatellar Bursitis (“Housemaid’s Knee 
5. The Lower Leg 
1. Varicose veins, with their results (eczema and ulcer), are the 
commonest lesions of the lower leg. The soft, twisted, purplish 
eminences are easily recognized. Hardness in such a vein usually 
means thrombosis. It should be remembered that pregnancy and 
pelvic tumors may produce varicose veins in the legs. 
2. Chronic ulcers of the lower leg, especially those in front, are 
usually due to varicose veins and the resulting malnutrition of the 
tissues. They leave a brown scar after healing. Syphilitic ulcers THE LEGS AND FEET 
453 
usually leave a white scar; they may occur in the same situation, 
but are more common above the knee or on the calf. 
3. Syphilitic periostitis is common on the shaft of the tibia, and 
gives rise to pain (worse at night) with tenderness and some swelling. 
Later bony nodes are sometimes formed, similar to those already 
pictured on the frontal bone. In doubtful cases of syphilis in other 
parts of the body we may sometimes secure convincing evidence by 
radiography of the tibiae. Periosteal thickening, not otherwise 
Fig. 244.—Syphilitic Periostitis (“Saber Shins”), 
recognizable, may be thus brought to light and may help our diagnosis 
of a cardiac arthritis or hepatic lesion. 
4. Osteomyelitis (septic, tuberculous) often starts on the head of 
the tibia, with intense pain, tenderness, fever, and leucocytosis (if 
acute); ‘ ‘ rheumatism ’ ’ is often falsely diagnosed; there results a 
genereal septicaemia or a local sinus leading to dead bone. 
5. Sarcoma not infrequently attacks the upper end of the tibia or 
fibula, producing lesions similar to those described in the femur. 
Secondary or metastatic tumors are often to be detected in the thigh 
bones and_ pelvic bones (set Figs. 246, 247, 248). 454 
PHYSICAL DIAGNOSIS 
6. CEdema of the legs1 isoftenest due to: 
(а) Uncompensated heart lesions, primary or secondary from 
lung disease. 
(б) Nephritis. 
Fig. 245.—Angioneurotic (Edema of One Leg. 
(c) Cirrhotic Liver. 
(d) Anaemia. 
(e) Neuritis (alcoholic, beri-beri, etc.). 
(/) Varicose veins. 
(g) Obesity, flat-foot, and other causes of deficient local circu- 
lation. 
In some cases no cause can be found (“angioneurotic” oedema, 
“essential” and “hereditary” oedema). Diagnosis of the cause of 
oedema depends on the history and the examination of the rest of 
the body. 
1 It is notable that oedema is usually greatest in the front of the leg and in the 
back of the thigh. THE LEGS AND FEET 
455 
Fig. 246.—Metastatic bony tumors of the head of the right femur. 
Fig. 247.—Metastatic bony tumors of the ischium pubic bone. 456 
PHYSICAL DIAGNOSIS 
In one leg oedema may be due to thrombosis of a vein (see page 
449), to pressure oi tumors in the pelvis (pregnancy, etc.), to hemi- 
plegia, elephantiasis (see Figs. 249 and 250) or to inflammation. 
7. Tenderness in the lower legs frequently accompanies oedema 
from any cause. It may also be due to neuritis or trichiniasis, and, 
of course, to any local inflammation. 
Fig. 248.—Metastatic bony tumors of upper one-half of both femora 
II. The Feet 
i. The variaties of club-foot are: (a) Equinus, the heel drawn 
up. (6) Varus, the ankle bent outward, (c) Valgus, the ankle 
bent inward and the foot outward, (d) Calcaneus, the foot turned 
outward and upward. 
The affection is usually congenital. THE LEGS AND FEET 
457 
2. Flat-foot is a breaking down or weakening of the normal arch 
of the foot. There may or may not be changes, in the sole-print. 
There may be pain and tenderness near the attachment of the liga- 
ments and often higher up on the leg, but many cases are symptom- 
less and should not be treated. 
Fig. 249.—Sporadic elephantiasis. (Non-filarial.) 
3- Tenosynovitis of the Achilles tendon often produces pain in the 
tendon, increased by use and sometimes associated with palpable 
creaking or crepitus over it. 
4. Enlarged (rachitic) epiphyses are seen at the lower end of the 
tibia and fibula just above the ankle-joint in about forty per cent of 
rachitic cases. There may also be bending of the bones (see Fig. 252). 
The other signs of rickets in the child make diagnosis easy. 458 
PHYSICAL DIAGNOSIS 
Fig. 250.—Elephantiasis. 
Fig. 251.—Flat-foot. (Bradford and Lovett.) THE LEGS AND FEET 
459 
5. Tuberculosis is especially apt to attack the ankle bones in 
young persons. It is recognized by the usual evidences of joint 
tuberculosis (see below, page 483). 
6. Epithelioma of the ankle has the characteristics of epithelioma 
elsewhere. 
Fig. 252.—Rachitic deformity of leg bones. 
7. Erythromelalgia, or red neuralgia of the extremities, is common- 
est in the feet. The toes (or fingers) are red, hot, tender, and painful. 
In Raynaud’s disease the digits are cold and painless or ansesthetic. 
The attacks are aggravated by heat and not (like those of Raynaud’s 
disease) by cold. Such attacks are probably akin to the condition of 
“hot feet” often seen in the arteriosclerosis of elderly people. The 
patient kicks off the bed clothes from his feet at night on account of 460 
PHYSICAL DIAGNOSIS 
the burning sensations in them. Other evidence of insufficient 
arterial blood supply (e.g., clubbing, intermittent claudication, 
cramps, gangrene) may coexist. 
8. “Judaische Krankheit,” an obliterating thrombosis of veins 
and arteries in the extremities, chiefly the feet, confined practically 
to the Jewish race, and usually resulting, after months of pain, in 
gangrene. 
Pig. 253.—Arteriosclerotic gangrene. 
i. The Toes 
Many of the lesions already mentioned in the fingers are found also 
in the toes (e.g., atrophic and hypertrophic arthritis, acromegaly, 
pulmonary osteoarthropathy, tuberculous or syphilitic dactylitis, 
tremors, spasms, and choreiform movements). Other lesions, such 
as ingrowing toe-nail, bunion, hallux valgus, policeman’s heel, are 
too purely local to deserve description here. Excluding these we 
have left: THE LEGS AND FEET 
461 
1. Gout, which is especially prone to attack the metatarso-phalan- 
geal joint of the great toe, producing all the classical signs of inflamma- 
tion and in chronic cases tophi (see page 494). 
2. Gangrene is usually the result of arteriosclerosis (see Fig. 253) 
with or without diabetes mellitus, but may result (as in the fingers) 
from arterial spasm or local asphyxia (Raynaud’s disease). 
3. Perforating Ulcer.—In diabetes and sometimes in tabes a 
trophic or nutritional ulcer may develop in the toe or tarsus as a 
result of nerve influences similar to those which produce Charcot’s 
joint or herpes zoster in the disease just mentioned. It is called 
11 perforating ulcer ” because of its stubborn progression despite a plan 
of treatment that checks ordinary infectious abscesses. Actual per- 
foration is not often seen. 
4. “ Tender toes ” after typhoid fever result from an infectious 
neuritis. 
5. “Morton's disease” (metatarsalgia) means pain in the tarsus at 
a small spot near the distal end of one of the three outer toes, always 
associated with compression of the foot by tight boots and probably 
due to pinching of the external plantar nerves between the metatarsal 
bones. It is relieved by proper shoes. CHAPTER XXVI 
THE BLOOD 
I. Examination of the Blood 
The essentials of blood examination as a part of physical diagnosis 
are as follows: 
I. Hemoglobin test (Tallqvist) in all cases. 
II. Study of a stained blood film in most cases. 
III. Total leucocyte count (Thoma-Zeiss) in many cases. 
IV. Count of red corpuscles and Widal reaction in a few cases. 
I will now give a brief account of each of these methods and of the 
interpretation of the data obtained by them. 
1. Hcemoglobin 
(a) The Tallqvist scale consists of ten strips of red-tinted paper 
corresponding to the tint of a filter paper of standard quality when 
saturated with blood containing ten per cent, twenty per cent, thirty 
per cent, etc., hcemoglobin up to one hundred per cent. To perform 
the test we puncture the lobe of the ear with a glover’s needle (not with 
sewing needle), saturate a strip of the filter paper which is bound up 
with the scale, in the blood of the patient to be examined, and compare 
the tint of this strip with the different standard tints in the scale. 
Let the blood dry until the gloss has disappeared. Hold the blood 
spot beside not behind the scale. Ignore the perforation in the latter. 
Do not blot the blood spot, and do not delay in making the comparison 
after the humid gloss has disappeared. Stand with the light behind 
you or at one side of you; use daylight always. 
The test is not accurate within ten degrees, but a degree of accuracy 
greater than this is very rarely required for any purpose of diagnosis, 
prognosis, or treatment. In rare cases, when a more accurate reading 
is needed, we may use the instrument of Gowers as modified by Sahli. 
(b) Sahli’s instrument (see Fig. 254) would supplant all others 
but for the unfortunate fact that the standard solution is likely to 
become inaccurate in color. To use the instrument we first put a few 
462 THE BLOOD 
463 
drops of decinormal HC1 solution into the empty tube (Fig. 254, B), so 
as to fill it to the mark 10; then suck up blood with the pipette (Fig. 
254, C), until the mark 1 is reached. Wipe the point of the pipette 
and immediately blow out the blood into the solution at the bottom 
of the tube (B). Suck this mixture of blood and water back into the 
pipette and blow it out again twice to cleanse the pipette. Next add 
water from the dropper (D), a few drops at a time, until the tint of the 
mixture of the blood and water is the same as that of the standard 
solution, when both are looked at 
with transmitted light. After each 
addition of water close the end of 
the tube with the thumb and invert 
it twice, then scrape the thumb on 
the edge of the tube so as to rub off 
any moisture deposited there during 
the process of inversion. As the 
tint of the mixture of blood and 
water approaches that of the 
standard solution, add the water 
two drops at a time,' and close the 
eyes for a few seconds between 
each two attempts at reading. When the colors in the two tubes 
seem to be identical, read off the figure corresponding with the 
meniscus of the column of fluid in the tube. The resulting figure 
represents the percentage of haemoglobin. 
(c) The Color Index.—The data to be obtained by these instru- 
ments stand for the amount of the coloring matter in a given unit of 
blood when compared with the amount in a similar unit 6f normal 
blood. When the haemoglobin percentage is low, anaemia is always 
present, and the degree of anaemia is measured by the amount of 
reduction in the haemoglobin per cent. But the percentage of haemo- 
globin is not a measure of the number of corpuscles present in a given 
unit of blood, for if the corpuscles are large and contain each of them 
a relatively large amount of haemoglobin, they may be considerably 
diminished in number and yet furnish a normal bulk of haemoglobin, 
as tested by either of the instruments described. Thus in pernicious 
anaemia the corpuscles are often so large that they contain nearly one- 
third as much again as a normal corpuscle, so that even though their 
number is considerably diminished they may carry a normal amount of 
haemoglobin. This condition is known as a “high color index.” On 
the other hand, the number of red corpuscles may be normal, yet each 
Fig. 254.—Sahli’s Haemoglobinometer. B, 
Diluting tube; C, pipette; D, dropper. 464 
PHYSICAL DIAGNOSIS 
corpuscle so deficient in haemoglobin that the haemoglobin in a given 
quantity of blood is as low as forty or fifty per cent. This state of 
things is often found in chlorosis or in any form of secondary anaemia 
(see below, page 472). When the diminution in the number of red 
corpuscles is greater than the diminution of haemoglobin, we say,that 
the color index is high, meaning that each corpuscle carries more haemo- 
globin than normal. Thus if we have a red count of two millions and a 
half of red cells, and each cell contained the normal amount of haemo- 
globin, the haemoglobin percentage would be fifty, representing a reduc- 
tion in haemoglobin proportional to the reduction in the red cells; 
but if with the same count we had a haemoglobin percentage of seventy- 
five, this would mean that each corpuscle contained half as much again 
as compared with the haemoglobin in normal red cells. Here we should 
say that the color index is 1.5 Five million red cells and one hundred 
per cent, of haemoglobin give a color index of 1. Four million red 
cells with forty per cent, haemoglobin, represents a color index of 0.5; 
three million red cells with 40 per cent, haemoglobin, represents a 
color index of 0.58. 
The diagnostic significance of the color index is briefly this: Any 
diminution in hoemoglobin means anoemia, but a diminution in hoemoglo- 
bin with a high color index suggests, though it does not prove, pernicious 
anaemia, while a low color index points to chlorosis or secondary anosmia 
of any type. Normal color index, despite anaemia, is most often found 
immediately after hemorrhage. 
Achromia shown in the stained film is the best obtainable evidence 
of low color index. When the film contradicts the hemoglobin 
measurement always believe the film. 
2. Study of the Stained Blood Film 
To recognize the presence and the degree of anaemia one needs only 
the hoemoglobin test, but to determine the kind of anaemia, to study the 
leucocytes, or to search for parasites we need the stained blood film. 
Two processes are now to be described: 
1. Preparing the film. 
2. Staining. 
i. Blood films may be spread on slides or on cover glasses. The 
first method is the easier; the second gives better preparations. To 
prepare blood films on slides, dip two slides in water and rub them 
clean with a towel or handkerchief. Puncture the lobe of the ear 
(not the finger) with a bayonet pointed Glover’s needle or surgical THE BLOOD 
465 
needle. Put a drop of blood near one end of one slide, put the other 
slide against the drop, and rest it evenly upon the first, as shown in 
Fig. 255, so that the drop will spread laterally across the face of the 
“spreader.” Next draw the upper slide along horizontally, so as to 
spread the drop over the whole surface of the lower slide. The process 
may then be repeated, reversing the slides and using as a “spreader” 
the one on which the film has already been prepared. Both slides 
are then allowed to dry in the air without touching each other. This 
method is so simple that one can usually succeed with it at the first 
attempt, but the corpuscles are not spread quite so evenly as in cover- 
glass preparations and it is somewhat more difficult to get a perfect 
stain. 
The cover-glass method requires a much greater degree of cleanliness 
and manual dexterity than the slide method. Cover glasses must be 
washed in water and then thoroughly polished with a silk (not cotton 
Fig. 255.—Method of Spreading 
Blood Films. 
Fig. 256.—Proper Method of Holding 
a Cover Glass. 
or linen) handkerchief. The success of the whole process depends 
upon the thoroughness of the polishing. Every part of the glass 
must be thoroughly gone over, taking care not to omit the corners. 
This is rather tedious and often drives us to use slides, which can be 
much more quickly prepared. With cover glasses we must remove 
not only all dirt and grease, but also every speck of dust or lint which 
may settle upon them. The use of silk as a polisher reduces this 
difficulty to a minimum. 
Having prepared the cover glasses in this way, the next point is to 
keep them both clean and dry during the process of spreading the 
blood. We must always hold them as in Fig. 256, and never touch 
any part of their surfaces with the fingers. Any one whose fingers 
tend to get moist must handle the cover glasses with forceps, but most 
of us will always use our fingers, despite the warnings of our Teutonic 
brethern. Holding a cover glass as in Fig. 256, touch the centre of it 466 
PHYSICAL DIAGNOSIS 
with the tip of a drop of blood as it issues from a puncture, taking care 
not to touch the skin of the ear itself; then drop this cover glass (blood 
side downward) upon a second cover glass in such a position that their 
corners do not match. If the covers are quite clean and free from 
dust, the blood drop will at once spread so as to cover the whole surface 
of the glasses. The instant it stops spreading, take hold of the upper 
cover glass by one corner and slide it rapidly off without lifting it or 
tilting it at all. This needs some practice, and some men never learn 
it; hence the use of slides. 
Films so prepared will keep for a long time without deteriorating, 
especially if the air is excluded. 
2. Staining.—The introduction of the Romanowsky method of 
staining (Nocht’s, Ziemann’s, Jenner’s, Leishman’s, Wright’s) enables 
us to dispense with all other blood stains and greatly shortens the time 
of the process. Wright’s stain is identical with Leishman’s except in 
the method of preparation, which Wright has considerably simplified, 
and as either of these mixtures can be obtained ready made of any of 
the larger dealers in physicians’ supplies, I shall not describe the 
method of making it. Reliable stains can always be obtained from 
the Massachusetts General Hospital in Boston. An ounce bottle will 
stain hundreds of specimens. 
To stain a cover-glass film, grasp it with Cornets’s forceps, rest the 
forceps on the sink so that the film side is upward and is approximately 
horizontal. Draw a little of Wright’s or Leishman’s stain into a 
clean medicine-dropper and squeeze out upon the film enough to 
flood its surface. 
(a) Allow the stain to act for one minute; during this time the 
methylic alcohol contained in it fixes the film upon the cover glass. 
(b) Next add distilled water from a clean medicine-dropper until 
a greenish metallic lustre appears like a scum upon the surface of the 
stain. Usually about six or eight drops of water are needed if we are 
using a seven-eighths-inch cover glass. The stain, so diluted with 
water, should remain upon the cover glass about two minutes. The 
exact time does not matter. 
(c) Next wash off the stain with water cautiously and let the film 
remain in clean water for about a minute more or until it takes on a 
light pink color. Dry gently with blotting paper and mount in 
Canada balsam. 
This whole process can be completed inside of five minutes, and I 
know of no other staining method at once so rapid, so reliable, and so 
widely applicable. It brings out all the minutiae of the red corpuscles, THE BLOOD 
467 
leucocytes, and blood parasites and for clinical work no other stain is 
needed. 
Appearance of Films so Stained.—i. The normal red corpuscles 
appear as round discs with pale centres. Their color depends upon 
the length of time that we continue the washing with clear water after 
the staining mixture has been poured off, and varies from brown 
through pink to golden yellow. 
(a) Poikilocytosis means the appearance in the blood of red cells 
variously deformed, sausage 
shaped, battledore shaped, oblong, 
pear shaped, etc. It is always 
associated with abnormalities in the 
size of the corpuscles, so that dwarf 
forms and giant forms appear. 
(b) Polychromasia (or poly- 
chromatophilia) refers to abnormal 
staining reactions in the red cor- 
puscles, whereby isolated indi- 
viduals take on a brownish or 
purplish tint, sharply contrasted 
with the pink or yellow of the 
corpuscles around. If this brown- 
ish or purplish tint occurs in all 
the corpuscles, it has no patho- 
logical significance, but merely means that the staining has been in- 
correctly performed. 
(c) “Stippling” refers to fine, dark-blue dots scattered over the 
pink surface of a red corpuscle, as if a charge of fine shot had been 
fired into it. 
All the abnormalities just described are to be found in any of 
the types of severe aneemia, whether primary or secondary, but 
stippling may also be found without ancemia in some cases of lead 
poisoning, and is therefore useful as a confirmatory sign in cases of 
this disease. 
Nucleated red corpuscles are divided into two main varieties: (i) 
normoblasts, which are of the size of normal corpuscles; and (2) mega- 
loblasts, which are larger than normal corpuscles (see Fig. 257). The 
nucleus of the normoblast is generally small and deeply stained, navy 
blue. In the megaloblast the nucleus may have the same character- 
istics or may be much larger and paler, with a distinct intranuclear net- 
work. The protoplasm of both varieties is often discolored, murky, 
Fig. 257.—Nucleated Red Cells, m, m, 
Megaloblasts; n, normoblast; 5, stippled 
cell. 468 
PHYSICAL DIAGNOSIS 
gray, or even blue, and sometimes stippled, so that by beginners the 
cell may be mistaken for a leucocyte. The mistake may be avoided, 
however, after some experience. In the protoplasm of nucleated cells 
there are often concentric rings like the layers in an oyster shell, and 
their outline is usually more irregular than that of any leucocyte. 
Further points of differentiation must be learned bv practice. 
2. Leucocytes.—In normal blood four main varieties may be dis- 
tinguished : 
(a) Polynuclears or polymorphonuclear neutrophiles. 
(■b) Lymphocytes (including endothelial cells). 
(c) Eosinophiles. 
(d) Mast cells. 
(a) Polynuclears.—The deeply stained, markedly contorted nucleus 
assumes a great variety of shapes in different cells, and is surrounded 
Fig. 258.—a, Leucocytosis (40,000); sixteen polynuclears in a field, b, Lymphatic 
leukaemia, p, Polynuclear; m, megaloblast; e, eosinophile. Twenty-one lymphocytes 
in this field. 
by a pinkish protoplasm studded with spots or granules just large 
enough to be distinguished under the oil immersion and slightly deeper 
in tint than the protoplasm around them. These cells make up about 
two-thirds (fifty to seventy per cent) of all the leucocytes present in the 
blood (see Fig. 258, a). 
(b) Lymphocytes.—The smallest variety is about the size of a red 
cell, and consists of a round nucleus stained deep blue and surrounded 
by a very narrow rim of pale, bluish-green protoplasm. In the larger 
forms (endothelial cells) the nucleus occupies less space, is often less 
deeply stained, and may be indented. The latter variety is sometimes 
burdened with the useless name of “transitional cell,’’ a term which in THE BLOOD 
469 
my opinion should be given up, since all lymphocytes are transitional. 
In the protoplasm of the larger varieties of lymphocyte one often sees 
a sprinkling of fine pink granules. From thirty to fifty per cent 
(or about one-third) of all leucocytes belong to the lymphocyte group 
-—classing’all sizes together (see Fig. 258, b). 
(■c) Eosinophiles.—The nucleus is irregularly contorted and attracts 
very little notice, owing to the very brilliant pink color and relatively 
large size of the granules in which it is immersed. The outline of the 
cell is more irregular than that of any other leucocyte, and its granules 
often become broken away and scattered in the technique of spreading 
the blood. The eosinophiles make up approximately one per cent of 
the leucocytes of normal blood. 
(d) Mast Cells ~—The shape of the nucleus can rarely be made out, 
and the main characteristic of the cell is the presence of large dark 
granules, stained bluish black or plum color, and arranged most thickly 
about the margin of the cell. Mast cells are very scanty in normal 
blood and make up not more than one-half of one per cent of the 
leucocytes. 
Other varieties of leucocytes which appear in the blood only in 
disease will be mentioned later. 
3. Blood Plates.—In the normal blood film, stained as directed 
above, one finds, beside the red corpuscles and the different varieties 
of leucocytes, a varying number of bodies, usually about one-third the 
diameter of a red corpuscle, irregularly oval in shape, staining dark red 
or blue and tending to cohere in bunches. Occasionally larger forms 
occur, and in these a vague network and some hints of a nucleus may 
be traced. 
These bodies which are probably derived from one or more species 
of leucocytes have at present no considerable importance in medicine, 
although they not infrequently lead to mistakes, because, when lying 
on top of a red corpuscle, they bear a slight resemblance to a malarial 
parasite. They are usually increased in secondary anaemia and dimin- 
ished in pernicious anaemia. 
(a) The Differential Count of Leucocytes 
A film stained as above directed is moved past the objective of 
the microscope either with a mechanical stage or with the fingers, and 
every leucocyte seen is classified under one of the heads just described 
until from 200-400 leucocytes have been thus differentiated. The 
percentages are then reckoned out. 470 
PHYSICAL DIAGNOSIS 
The points most often looked for are: 
1. Increase in the per cent of polynuclears. 
2. Increase of eosinophiles. 
3. Increase of lymphocytes. 
4. Presence of myelocytes and other abnormal forms (see below). 
5. Changes in the red cells noted simultaneously. 
The instrument used all over the world at the present day is the 
pipette of Thoma-Zeiss, in which the blood is diluted either ten or 
twenty times. The diluting solution is one-half of one per cent glacial 
acetic acid in water. This diluting solution often accumulates spores 
and becomes cloudy. As 
soon as this happens a fresh 
bottle should be prepared. 
After a rather deep puncture 
blood is sucked up to the 
point marked .5 on the pipette, 
which is then immersed in the 
diluting solution and suction 
exerted until the mixture is 
drawn up to the point marked 
11. This gives a dilution of 
one to twenty. By drawing 
blood up to the point marked 
1, instead of to the point 
marked .5, we obtain a dilu- 
tion of one to ten. After this 
the ends of the pipette can 
be closed with a rubber band, and the blood, so shut in, can be kept or 
transported without loss or change. 
When we are ready to make the count, the rubber band is removed 
and the pipette rolled in the fingers rapidly back and forth for about 
one minute, to mix up the contents of the bulb thoroughly and evenly. 
Next blow out three drops, in order to get rid of the pure diluting 
solution which is in the shank of the pipette. Then put upon the 
circular disc of the counting chamber a drop of the mixture from the 
bulb of the pipette. This drop must be of such a size that when the 
cover glass (see Fig. 260, B) is let down upon it1 the drop will cover at 
3. Counting the White Corpuscles 
Fig. 259.—Indicating an Order in which the 
Squares may be Counted. 
1 To avoid air bubbles lower the cover glass with aid of a needle as in mounting 
microscopic specimens. This must be done as quickly as possible after the drop 
has been adjusted on the counting disc. THE BLOOD 
471 
least nine-tenths of the circular disc and not spill into the moat around 
it. The size of this drop can only be learned by practice. After 
about five minutes the leucocytes will have settled upon the ruled 
space which occupies the centre of the floor of the counting chamber, 
and the count can then be begun, using preferably a No. 5 objective 
of Leitz or a DD of Zeiss. The whole ruled space should be counted, 
and after a little practice this takes not more than five minutes. I 
usually begin my count in the left upper corner of the ruled space and 
proceed in the direction indicated by the serpentine arrow in Fig. 259. 
In normal blood one finds from thirty to fifty leucocytes in the whole 
ruled space. The number of leucocytes per cubic millimetre is 
obtained by multiplying this figure by 200. Thus if the number of 
Fig. 260.—Thoma-Zeiss Counting Slide. A. Ruled disc; B, cover-glass; C, moat. 
leucocytes counted is 35, the number in a cubic millimetre of blood is 
35 X 200 = 7,000. If great accuracy is needed, a second count with a 
fresh drop should be made and the average of the two taken; but in 
ordinary clinical work this does not seem to me necessary, for the 
amount of error, although considerable, is not such as to affect our 
diagnostic inferences. 
4. Counting the Red Corpuscles 
Perhaps once in every twenty-five or fifty cases that one sees it is 
well to know the number of red corpuscles. They can then be counted 
with the Thoma-Zeiss pipette which is made for the purpose, and so 
arranged that the blood may be diluted one to two hundred. The 
technique is exactly that described in the last section, except that we 
need less blood and use a different diluting solution. I am accustomed 
to use a mixture suggested by Gowers, made up as follows: 
Sodium sulphate gr. cxii. 
Dilute acetic acid Si- 
Water 5iv. 
Blood is sucked up to the mark 0.5 and then Gowers’ solution to 
the mark 101. After the drop has been adjusted in the counting 
chamber and the corpuscles have settled upon the ruled space, we 
usually count a field of twenty-five small squares at each of the four 
corners of the whole ruled space. The figure so obtained is multiplied 
by 8,000. The result is the number of corpuscles per cubic millimetre. 472 
PHYSICAL DIAGNOSIS 
II. Interpretation of the Results so Obtained 
1. Secondary Anaemia 
The haemoglobin is usually reduced more than the count of red 
corpuscles giving a low color index. In mild cases the haemoglobin 
may fall as low as forty per cent before the red corpuscles show any 
considerable diminution. In severe cases the red cells fall to 3,000,000, 
2,000,000, and occasionally even to 1,000,000 or below it; but the haemo- 
globin usually suffers even more severely. 
The leucocytes may be normal, increased, or diminished, depending 
on the cause of the anaemia. Thus in anaemia due to chronic suppura- 
tive hip-disease the leucocytes are often increased to 20,000 or 30,000, 
while in malarial anaemia the leucocytes are often subnormal. There 
are no characteristic changes in the differential count, which varies 
with the underlying disease. 
The changes seen in the red cells in the stained blood film are 
briefly: Achromia; sometimes polychromasia, stippling, poikilocy- 
tosis, and the presence of nuclei either in normal-sized corpuscles 
(normoblasts) or in giant corpuscles (megaloblasts). Achromia or 
abnormally great pallor of the centres of the cells is the most important 
point in the recognition of secondary anaemia and the exclusion of perni- 
cious anaemia. An occasional normoblast or rarely a megaloblast can 
be found. 
The commonest causes for secondary or symptomatic anasmia in 
adults are as follows: 
(a) Hemorrhage—gastric, hemorrhoidal, traumatic, puerperal, etc. 
(b) Malaria, more rarely sepsis or other infections. 
(c) Malignant disease. 
(d) Chronic suppurations. 
(e) Chronic nephritis. 
(/) Cirrhosis of the liver. 
(g) Poisons, especially lead. 
(h) Chronic dysentery. 
(i) Intestinal parasites. 
It is important to remember that insufficient food or even starva- 
tion does not produce anasmia, and so far as we know no form of bad 
hygiene has any notable effect upon the blood. Persons may grow 
very pale under bad hygienic conditions, but their blood is usually not 
affected unless one of the diseased conditions mentioned above is 
present. THE BLOOD 
473 
2. Chlorosis 
The blood is practically identical with that just described, though 
the color index is sometimes lower, poikilocytosis less marked, and 
nucleated red cells fewer. The pallor of the centres of the cells 
(“achromia”) is often very marked. The leucocytes are generally 
normal and the differential count practically so, although the percent- 
age of polynuclear cells is often low with a corresponding relative 
increase of lymphocytes. 
3. Pernicious Anoemia 
The number of red cells is usually below 2,000,000 when the case 
is first seen. The color index is high and the leucocyte count sub- 
normal. In the stained specimen the essential point is the prevalence 
of big non-achromic red cells; there are also very marked deformities 
and abnormal staining reactions in the red cells. A few of the large 
reds contain nuclei (“megaloblasts”), and a number of normal-sized 
cells also contain nuclei (“normoblasts”). 
The polynuclears are absolutely diminished, with a corresponding 
relative increase in the lymphocytes. 
In the remissions which form so important a feature of the course 
of pernicious anasfnia, the blood is generally transformed until it con- 
tains approximately 100 per cent, of haemoglobin, although the red cells 
seldom get above 4,000,000. The abnormally large and deeply stained 
red cells still prevail in most cases and make diagnosis possible though 
difficult. 
(a) Interpretation of the Results of the Leucocyte Count and 
Differential Count 
By combining the facts obtained by the total white count and the 
differential count, we can estimate the number of each variety of 
leucocyte contained in a cubic millimetre of blood. Thus with 10,000 
white corpuscles, 70 per cent, of which are polynuclear (as seen in the 
stained film), we have 7,000 polynuclear cells per cubic millimetre, 
which may be considered the upper normal limit. Any number greater 
than this should be considered as a leucocytosis. In a similar way 
we can say that any number greater than 3,500 is above the normal 
limit for lymphocytes and constitutes a lymphocytosis, while eosino- 
philia is present whenever the number of eosinophiles is more than 400 474 
PHYSICAL DIAGNOSIS 
per cubic millimetre. It is much better to use these absolute numbers 
than to rely upon percentages. If we say, for example, that 3 per cent 
of eosinophiles is within normal limits, we shall make an error now and 
then in cases of myelogenous leukaemia, in which, with a total count of 
500,000 leucocytes, 3 per cent of eosinophiles would amount to a total 
of 15,000 per cubic millimetre, or nearly thirty times the normal number. 
Errors are also common in the opposite direction. For example, in 
typhoid, with a total leucocyte count of 3,000, the lymphocytes may 
reach 60 per cent and yet be well within the normal limits, for 60 per 
cent of 3,000 is only 1,800. In this case the apparent lymphocytosis 
is due to an absolute decrease in polynuclear cells. 
For the reasons here given it seems to me best to use the following 
definitions: 
1. Leucocytosis is an increase in the polynuclear cells beyond the 
normal—7,000. 
2. Lymphocytosis is an increase of lymphocytes beyond the normal 
upper limit—3,500. 
3. Eosinophilia is an increase of eosinophiles beyond the normal 
upper limit—500 per cubic millimetre. 
4. Occurrence of Leucocytosis 
Leucocytosis, like fever, occurs in a great variety of conditions, of 
which the following are the most important: 
1. In infectious diseases—-except typhoid, typhus, malaria, uncom- 
plicated tuberculosis, measles, smallpox (prior to the pustular stage), 
mumps, German measles, and influenza (most cases). 
2. In a variety of toxaemic conditions, such as ursemia, hepatic 
toxaemia, diabetic coma, rickets, and poisoning by illuminating gas. 
3. In a minority of cases of nialignant disease, especially sarcoma. 
4. After violent muscular exertion, including parturition, after cold 
baths or massage, haemorrhage and apoplectic seizures. 
There is in all probability no constant leucocytosis in pregnancy or 
during digestion. 
Leucocytosis is most often of value in the differential diagnosis 
between typhoid fever or malaria on the one hand, and pyogenic 
infections (meningitis, appendicitis, sepsis, pneumonia) on the other. 
A leucocyte-chart is often of value in judging whether a local suppura- 
tive process, such as appendicitis, is advancing or receding, or whether 
pus-pocketing has taken place. By a leucocyte-chart is meant 
series of leucocyte counts at short intervals—twelve, twenty-four, or THE BLOOD 
475 
forty-eight hours. When taken in connection with the other clinical 
data, a leucocyte chart is often of the greatest value, especially in 
following the course of any disease; to a less extent in diagnosis. Son- 
dern {Med. Record, N. Y., March 25,1905) considers that the higher the 
per cent of polynuclears, the severer the infection, while the body’s 
resistance is mirrored in the height of the total leucocyte count. By 
noting both these facts, therefore, we have a prognostic guide of some 
importance. Most subsequent observations have tended to verify 
Sondern’s theory. In internal medicine leucocyte counts are especially 
useful in febrile conditions, in the great majority of which they assist the 
diagnosis. 
Certain exceptions to the rules above given must be remembered: 
1. Quiescent, thickly encapsulated collections of pus, in which the 
bacteria have died or lost their virulence, usually produce no leucocyto- 
sis. In this group come some of the abscesses of the liver or about the 
kidney, and a few cases of appendicitis. 
2. The most virulent and overwhelming infections are apt not to be 
accompanied by leucocytosis. Thus, for example, the most virulent 
cases of pneumonia, diphtheria, or general peritonitis often run their 
course without leucocytosis. 
5. Lymphocytosis 
Only in three diseases does well-marked lymphocytosis often occur: 
1. Lymphatic leukaemia. 2. Whooping-cough and its complications 
(many cases). 3. Acute sepsis especially tonsillitis with or without 
glandular enlargement may produce a lymphocytosis which, but for 
the etiological factor, would be alarmingly like lymphoid leukaemia. 
Occasionally lymphocytosis occurs in rickets, hereditary syphilis, 
and anything that produces debility in children. Lymphocytosis is 
of value chiefly in the differentiation of lymphatic leukaemia from 
other causes of chronic glandular enlargement. 
6. Eosinophilia 
The eosinophiles are increased chiefly in: 
1. Bronchial asthma. 
2. Chronic skin diseases. 
3. Diseases due to animal parasites (trichiniasis, uncinariasis, 
filariasis, hydatid disease, Bilharzia disease, trypanosomiasis, and with 
most of the intestinal worms). 
4. Myelogenous leukaemia. 476 
PHYSICAL DIAGNOSIS 
There seems to be also some vague connection between eosinophilia 
and disease of the female genital tract (except cancer and fibromyoma 
of the uterus). 
Leukcemia 
Two forms are distinguished, though the distinction is chiefly a 
clinical one: (a) Myeloid and (b) lymphoid. 
(a) Myeloid Leukcemia 
The leucocytes are usually about 250,000 per cubic millimetre when 
the case is first seen, but often run much higher, and sometimes lower. 
There is no anasmia in the earliest 
stages; later moderate secondary 
anaemia develops. 
The differential count shows 
an extraordinary variety of types, 
including many not seen in normal 
blood (see Fig. 261). The majority 
of the leucocytes are polynuclears, 
but many of these are atypical in 
size or in the shape of their nucleus. 
From 20 to 40 per cent of the leuco- 
cytes are myelocytes (or mononu- 
clear neutrophiles), the “infantile” 
form of the polynuclear cell. Lym- 
phocytes are absolutely normal or 
increased, but their percentage is 
low, on account of the greater increase of the other forms. 
Eosinophiles are absolutely much increased, though the percentage is 
not much above normal. Mast cells are more numerous than in any 
other disease (1 to 12 per cent, out of an enormous total increase). 
Normoblasts are usually very numerous; megaloblasts scanty. 
Under the influence of intercurrent infections or after x-ray treat- 
ment the blood may return to normal. 
Fig. 261.—Myelogenous Leukaemia. 
m. Myelocytes; p, polynuclear; b, mast 
cell; n, normoblast. 
(b) Lymphoid Leukcemia 
The total increase of leucocytes is usually much less than in the 
other type of leukaemia—40,000 or 80,000—or less in average cases. 
The differential count shows an overwhelming proportion of lymph- Cabot—Physical Diagnosis. 
PLATE IV. 
Fig. i.—Young Tertian Parasites. (Stained with Wright’s modification of Leishman’s 
stain.) 
Fig. 2.—Mature Tertian Parasites. (Eosin and methylene blue.) 
Fig. 3.—Segmenting Tertian Parasites. (Eosin and methylene blue.) THE BLOOD 
477 
ocytes—90 to 99.9 per cent as a rule. In the acute forms of the disease 
the large lymphocytes predominate; in chronic cases the small forms. 
Tonsillar infections and whooping-cough must be excluded before 
diagnosing lymphoid leukaemia from the blood film. 
III. The Widal Reaction 
(a) Technique. Among the numerous agglutinative reactions 
between the serum of a given disease and the micro-organism producing 
that disease, only one has yet attained wide use in clinical medicine, 
viz., the so-called Widal reaction in typhoid fever. 
There are many ways of performing this reaction, but in my 
opinion the following is the best: 
Measure out in two small test tubes ten drops and fifty drops 
respectively of a highly motile twelve- to twenty-four-hour bouillon 
culture of typhoid bacilli, in which the bacilli have no tendency to 
adhere spontaneously to each other. Carry these tubes and a micro- 
scope to the bedside, puncture the patient’s ear as usual, and draw a 
little blood into a medicine-dropper of the same size as that used in 
measuring out the typhoid culture. Expel one drop of blood into each 
of the tubes containing typhoid culture, and examine a drop of each 
mixture between a slide and cover glass with a high-power dry lens. 
If within fifteen minutes clumping has taken place in the i :io mixture, 
or if within one hour clumping has taken place in the i '.50 mixture, 
the reaction may be considered positive. By clumping I mean an 
agglutination of the bacilli into large groups and the complete or nearly 
complete cessation of motility. 
If it is inconvenient to carry the culture and the microscope to the 
bedside, ten or twenty drops of blood may be milked out of the ear 
and collected in a test tube (a three-inch test tube of small calibre is 
best). After clotting has taken place, if the edges of the clot are 
separated from the glass with a needle or a wire, a few drops of serum 
will exude, and this serum can be mixed with the bouillon culture in 
the manner already described. 
Less reliable, in my opinion, is the use of blood dried upon glass or 
glazed paper in large drops and subsequently dissolved in the culture 
itself. 
(■b) Interpretation. A positive reaction occurs at some period in 
the course of ninety-five per cent of all cases of typhoid fever, but the 
proportion of cases in which the reaction occurs early enough to be of 
diagnostic value varies greatly in different epidemics. In most 478 
PHYSICAL DIAGNOSIS 
epidemics about two-thirds of the cases show a positive Widal reaction 
by the time the patient is sick enough to consult a physician. In 
the early days of the fever the Widal is often used but it is just at this 
period that we so often find typhoid bacilli by blood culture. Thus 
the two tests supplement each other. 
IV. The Wassermann Reaction 
I shall attempt no description of the technique of this most valuable 
and important test, because its performance is so difficult and delicate 
Fig. 262.—Trypanosoma in Human Blood. (By permission of Dr. J. Everett Dutton 
and the London Lancet.) 
that only one who is constantly doing it is reliable. A positive reaction 
reliably done is important but not conclusive evidence of syphilis. 
Negative reactions do not exclude syphilis. The reaction is of especial 
value in cases of aneurism, aortic regurgitation, visceral and cerebral 
syphilis, doubtful cutaneous and arthritic and osseous lesions. Also in 
tabes and dementia paralytica. 
V. Blood Parasites 
i. The Malarial Parasite (see Plates IV. and V.) 
In films stained as above directed the malarial parasite appears 
blue against the pink background of the corpuscle. A crimson- 
stained dot should appear in some portion of the blue-stained organism; Cabot—Physical Diagnosis. 
PLATE V. 
Fig. i.—Two Young Parasites. (Wright’s modification of Leishman’s 
stain.) 
Fig. 2.—/Estivo-autumnal Parasites. Ring body at the left; crescent at the right. Stained 
like Fig. i. 
Fig. 3.—Ovoid in 
autumnal Malaria. 
Fig. 4.—Crescent in Malaria. THE BLOOD 
479 
the protoplasm of the red corpuscle around it is often studded with 
pink dots. 
The stained specimen is preferable to the fresh blood in the search 
for malarial parasites, for the young, ring-shaped, or “hyaline” forms 
often escape notice altogether in fresh specimens. 
Tertian organisms are distinguished from the asstivo-autumnal 
variety by the following tests: 
Fig. 263.—The Filaria Sanguinis Hominis. The head, curled up, is seen to the right 
ofTthe cut, the tail to the left. Instantanepus photomicrograph. Four hundred 
diameters magnification. 
(а) Tertian parasites make the corpuscle to which they are 
attached larger than its uninfected neighbors. 
(б) Segmenting forms are rare in the peripheral blood of sestivo- 
autumnal fevers. 
(c) “Crescents” (see Plate V.) never occur except in aestivo- 
autumnal fevers. 
2. The Trypanosomiasis 
In Central Africa (and presumably in other tropical countries) the 
blood or gland juice of many persons contains the organism shown 
in Fig. 262, which has long been known as a parasite of the blood of 
horses and of many of the lower animals. Human trypanosomiasis— 
a chronic debilitating malady—becomes “sleeping sickness” when the 
trypanosoma enters the cerebrospinal canal. 
3. Filariasis 
In the blood of many inhabitants of tropical countries there is 
found (with or without symptoms) the parasite shown in Fig. 263. 
The species most often found is present in the peripheral blood only 
at night; hence the blood should be examined after 8 p. m. A fresh 
drop is spread between side and cover and examined with a low-power 
lens (No. 5 objective Leitz). CHAPTER XXVII 
THE JOINTS 
I. Examination of the joints 
1. Methods and Data 
I. By inspection and palpation we detect: 
1. Pain, tenderness, and heat in, near, or at a distance from the 
joint. 
2. Enlargement: 
(a) Hard, probably bony. 
(b) Boggy, probably infiltration or thickening of capsule and 
periarticular structures. 
(c) Fluctuating, probably fluid in the joint. 
3. Irregularities in contour: 
(a) Osteophytes or “lipping” (attached to the bone). 
(b) Gouty tophi (not attached to the bone). 
(c) Constriction-line opposite the articulation. 
(d) Protrusion of joint-pockets in large effusions, filling out of 
natural depressions. 
4. Limitation of motion: 
(a) Due to pain and effusion. 
(b) Due to muscular spasm. 
(c) Due to thickening or adhesions in the capsular and periarticular 
structures. 
(d) Due to obstruction by bony outgrowths or gouty tophi. 
(e) Due to ankylosis. 
5. Excess of motion (subluxation). 
6. Crepitus and creaking. 
7. Free bodies in the joint. 
8. Trophic lesions over or near a joint (cold, sweaty, mottled, 
cyanosed, white, or glossy skin, muscular atrophy). 
9. Sinus formation, the sinus leading to necrosed bone, to gouty 
tophi, or absence in or near the joint. 
10. Distortion and malposition, due to contractures in the muscles 
near the joint, to necrosis, to exudation, or to subluxation. 
480 THE JOINTS 
481 
ii. Telescoping of the joint with shortening (limb, toe, finger, or 
trunk). 
II. By radioscopy we investigate: 
1. Bony outgrowths, their shape, extent, and position. 
2. Necroses and atrophies of bone, their extent and position. 
3. The structure of the bones in and near the joints. 
4. The presence of lesions in the articular cartilages. 
5. Free joint bodies, their presence and position. 
III. Indirectly we may gain valuable information about the joints 
by noting: 
1. General constitutional symptoms, their presence or absence. 
These include fever, chills, leucocytosis, glandular enlargement, 
albuminuria, and emaciation. 
2. Tuberculin reaction and Wassermann reaction, perhaps gono- 
coccus fixation test,-—their presence or absence. 
3. Disease of other organs, their presence or absence, i.e., syphilis, 
tuberculosis, tabes, and other chronic spinal-cord lesions, endocarditis, 
haemophilia, various acute infections (gonorrhoea, influenza, scarlatina, 
septicaemia), and skin lesions (psoriasis, purpura, hives). 
4. The course of the disease and the results of treatment. 
2. Technique of Joint Examination 
(a) Enlargement is generally unmistakable, but when there is 
much muscular atrophy between the joints the latter may seem en- 
larged by contrast, when in fact they are not. 
(b) Fluctuation is obtained in most joints, as in any part of the 
body, by pressing a finger on each of two slightly separated spots 
in the suspected area, and endeavoring to transmit through the inter- 
vening space an impulse from one finger to the other. Fat or muscle 
will also transmit an impulse, but less perfectly than fluid. 
In the knee we test for “floating of the patella” over an effusion 
by surrounding the joint with the hands, which are pressed slightly 
toward each other to limit the escape of fluid in either direction, and 
then suddenly making quick pressure on the patella with one finger. 
If we feel or hear the patella knock against the bone below and rebound 
as we release the pressure, fluid in abnormal quantity is present. 
(c) Irregularities of contour are easily recognized, provided the 
normal contour is familiar. 
{d) Bony outgrowths may be obvious (as in Heberden’s nodes), but 
if within the joint they may be recognized only by the sudden arrest of 482 
PHYSICAL DIAGNOSIS 
an otherwise f ree joint motion at a certain point. In many cases radio- 
scopy is necessary. 
(e) Gouty tophi are identified positively by transferring a minute 
piece to a glass slide, teasing it in a drop of water, covering with a cover 
glass, and examining with a high-power dry lens and a partly closed 
diaphragm. The sodium biurate crystals are characteristic. 
Fluid or semi-fluid exudates in joints may fill up and smooth out 
the natural depressions around the joint, or, if the exudate is large, 
Fig. 264.—Testing for Psoas Spasm. (Bradford and Lovett.) 
may bulge the joint pockets; in the knee-joint four eminences may 
take the place of the natural depressions, two above and two below 
the patella. 
(/) Limitations of motion due to muscular spasm are seen with 
especial frequency in tuberculous joint disease, but may occur in 
almost any form of joint trouble, particularly in the larger joints. 
(i) Hip-joint, two forms of spasm are important: (i) That which 
is due to irritation of the psoas alone (psoas spasm); (2) that in which 
all the muscles moving the joint are more or less contracted. 
In pure psoas spasm the thigh is usually somewhat flexed on' the 
trunk, though this may be concealed by forward bending of the latter. 
Very slight degrees of psoas spasm may be appreciable only when, 
with the patient lying on his face, we attempt hyperextension (see 
Fig. 264). 
The other motions of the hip-—rotation, adduction, abduction, and 
flexion—are not impeded. 
General spasm of the hip muscles is tested with the patient on the 
back upon a table or bed (a child may be tested on its mother’s lap) 
and the leg flexed to a. right angle, both at the knee and at the hip. THE JOINTS 
483 
Using the sound leg as a standard of comparison, we may then draw 
the knee away from the middle line (abduction), toward and past the 
middle line (adduction), and toward the patient’s chest (flexion). 
Rotation is tested by holding the knee still and moving the foot away 
from the median line of the body or toward and across it. 
(2) Spinal column. Muscular spasm of the muscles guarding 
motion in the vertebral joints can be tested by watching the body 
attitude (a stiff, “military” carriage in most cases), and by efforts to 
bend the spine forward, backward, and to the sides. 
In most cases we can make out limitation of these motions by 
asking the patient to stand with knees and hips stiff and then bend 
Fig. 265.—Rigidity of Spine in Pott’s Disease. 
his trunk (of course, naked) as far as he can in each of the four direc- 
tions. If we are familiar with the average range of motility in each 
direction and at the different ages, this test is usually easy and rapid. 
Backward bending is the least satisfactory, and in doubtful cases the 
patient should be on his face, while the physician, standing above him, 
lifts the whole body by the feet (see Fig. 265). 
(3) In the joints of the shoulder, knee, elbow, wrist, ankle, toes, 
and fingers, there is usually no difficulty in testing for muscular spasm, 
and no special directions are needed. 
To distinguish muscular spasm from bony outgrowth as a cause of 
limited joint motion, we should notice that bony outgrowths (e.g., in 
the hip) allow perfectly free motion up to a certain point; then motion 
is arrested suddenly, completely, and without great pain. Muscular 484 
PHYSICAL DIAGNOSIS 
spasm, on the contrary, checks motion a little from the outset, the 
resistance and pain gradually increasing until our efforts are arrested 
at some point, vaguely determined by our strength and hard-hearted- 
ness and by the patient’s ability to bear the pain. 
Motions limited by capsular thickening and adhesions are not, as 
a ride, so painful after the first limbering-up process is over. There 
is no sudden arrest after a space of free mobility, but motion is limited 
from the first and usually in all directions, though the muscles around 
the joint are not rigid. The possibility of more or less limbering-out 
after active exercise (or passive motion) distinguishes this type of 
limitation. 
In true ankylosis there is no motility whatever. 
(g) Excessive motion in a joint is recognized simply by contrast 
with the limits furnished us by our knowledge of anatomy and of the 
physiology of joint motion at different ages. When the bone and 
cartilage appear normal or are not grossly injured, we call the excessive 
motility of the joint a subluxation, but excessive motility may also be 
due (as in Charcot’s joint) to destruction of bone and other essentials 
of the joint. 
(h) To detect crepitus and creaking we simply rest one hand on the 
suspected joint, and with the other put it through its normal motions, 
while the patient remains passive. 
(i) Most free joint bodies are not palpable externally, and are rec- 
ognized only by their symptoms, by the v-ray, and by operation. 
(;) Shortening of a limb as evidence of joint lesions is tested by 
careful measurements. The vast majority of such measurements are 
made with reference to the hip-joint. The tip of each anterior superior 
iliac spine is marked with a skin-pencil, and likewise the tip of each 
inner malleolus. Then, with the patient lying at full length on a flat 
table, the distance from anterior superior spine to inner malleolus is 
measured with a tape on each side. 
The method of obtaining the other data tabulated on page 480 
needs no explanation, except the radioscopic technique—a subject 
which I am not competent to discuss. 
II. Joint Diseases 
I shall use the classification proposed by Goldthwait and divide 
joint diseases as follows: 
1. Infectious arthritis: (a) Tuberculosis. (b) Other infections. 
2. Atrophic arthritis: (a) Primary. (b) Secondary to organic 
nerve lesions (Charcot’s joint). THE JOINTS 
485 
3. Hypertrophic arthritis. 
4. Gouty arthritis. 
5. Hasmophilic arthritis. 
1. Infectious Arthritis 
Under infectious arthritis are included all varieties of articular 
“rheumatism” and the joint troubles symptomatic of gonorrhoea, of 
streptococcus infections (including scarlet fever), influenza, syphilis, 
typhoid, and other fevers. As tuberculosis is an infection we must 
include it in this group, although the disease begins usually as an 
osteitis and involves the joint secondarily by extension. 
I. Tuberculous Arthritis.—The characteristics of joint tuberculosis 
are: 
(a) Slow progress, with gradual enlargement and disabling of the 
joint. 
(b) Muscular spasm, especially in disease of the hip or vertebras. 
(c) Evidences of low-grade inflammation (moderate heat, swelling, 
pain, and tenderness). 
(1d) Abscess and sinus formation. 
(ie) Malpositions (e.g., shortening of one leg in hip-joint disease, 
angular backward projection in spinal disease, subluxations in the 
knee-joint). 
(/) Bone necrosis, as shown by x-ray. 
The order of frequency in the different joints is as follows: spine, hip, 
knee, wrist, shoulder (tuberculous dactylitis is described on page 56). 
In the deep-seated hip-joint, diagnosis has to depend largely on 
shortening and on the presence of limitation of all the hip motions by 
muscular spasm (see above, page 482), unless the disease is of long 
standing and manifests itself by abscesses burrowing to the surface. 
Usually these abscesses point in the upper anterior thigh, but they 
may open behind the great trochanter, below the gluteus maximus, or 
at any point in the vicinity of the hip. 
Besides muscular spasm, shortening, and abscess formation, we 
get some aid from the general and vague joint symptoms present in 
this as in many other joint lesions. Such are enlargement (felt as 
thickening about the great trochanter), muscular atrophy, pain, ten- 
derness, and crepitus. 
In spinal tuberculosis (Pott's disease) the distortion of the bones 
with formation of a knuckle in the back is often obvious and practically 
diagnostic. In other cases we depend on muscular spasm or abscess 
formation. The muscular spasm gives a stiff back and often psoas 486 
PHYSICAL DIAGNOSIS 
contraction (see below). The abscess is peculiar, in that it usually 
works along in the sheath of the psoas and points in the groin below 
Poupart’s ligament (see Fig. 239); less often it appears in the back or in 
the gluteal region, and rarely it may invade almost any part of the body,' 
lung, gullet, gut, peritoneum, rectum, hip-joint, etc.). 
Psoas spasm, which is common both in hip and spinal tuberculosis, 
is by no means peculiar to these diseases, and it is worth remembering 
that it may be due to various other lesions, such as: 
(а) Hypertrophic arthritis of the spine. 
(б) Appendix abscess. 
(c) Perinephritic abscess. 
In the peripheral joints (shoulder, elbow, wrist, finger, knee, 
ankle) the diagnosis of tuberculosis rests on the chronic enlargement 
and disability, with abscess and sinus formation. 
Hysterical or acute traumatic lesions (with or without neurosis) 
may present symptoms and signs identical with those of tuberculosis. 
Decision is aided most by: (a) The lapse of time and the effects of 
treatment. (6) X-ray examination, (c) The predominance in func- 
tional and traumatic cases of pain and tenderness rather than muscular 
spasm or malposition. 
II. Acute Infectious Arthritis.—All varieties are distinguished from 
the other types of arthritis by: (a) The absence of any marked bone 
lesions1 in most cases, (b) The tendency to recovery in the great 
majority of cases. 
The milder forms, whose cause is unknown, we have hitherto 
designated as “ rheumatism.” The others are distinguished as gonor- 
rhoeal, pneumococcic, syphilitic, influenzal, dysenteric, etc., according 
to the organism producing them. 
Between this group and those known as “rheumatism,” there is 
no clear pathologic distinction. Mild infection with streptococci 
may leave a sound joint. Virulent infections may lead to crippling 
through fibrous adhesions. On the other hand, arthrtitis of “rheu- 
matic” (i.e., of streptococcic) origin may end in suppuration, crippling 
the joint with adhesions, though in most cases it leaves a sound joint. 
All the members of the infectous group of joint lesions present 
the local signs of inflammation and the constitutional signs of infection. 
All may be complicated by endocarditis, but in those of streptococcic 
origin (“rheumatic”) this complication is especially common. Therp 
is no hypertrophy, bone destruction,1 sinus formation, or marked 
1 Exceptionally, virulent infections (especially those due to pneumococci or 
gonococci) may destroy cartilage and bone and end in true bony ankylosis. THE JOINTS 
487 
irregularities of contour. A general enlargement (more or less spindle 
shaped, owing to periarticular thickening and muscular atrophy) is 
Fig. 266.—X-ray, showing Hands in Atrophic Arthritis. 
the rule. The joint motions are limited chiefly by pain and effusion; 
muscular spasm is not prominent. 488 
PHYSICAL DIAGNOSIS 
One or many large or small joints may be affected in any of the 
varieties of infectious arthrtitis, though the gonorrhoeal virus is apt to 
lodge in few joints (oftenest the knee or ankle) and the ‘‘rheumatic” 
virus in many joints, while the typhoid poison has a predilection for 
the spine. 
2. Atrophic Arthritis 
Two types must be recognized: (a) A monarticular form, secon- 
dary usually to tabes or syringomyelia (‘‘ Charcot’s joint,” ‘‘neuropathic 
Fig. 267.-0, Charcot’s Joint with Loose Bodies; b, Pulmonary Osteo-arthropathy. 
(v. Ziemssen’s Atlas.) 
joint”), and other diseases of the spinal cord. (b) A polyarticular 
primary form (‘‘rheumatoid arthritis” or ‘‘ankylosing arthritis”). 
In both, the distinguishing characteristic is atrophy and destruc- 
tion of cartilage, bone, and joint membranes—a process which in the 
early stages can be identified only by the x-ray (see Fig. 266). Later 
the disintegration of the joint is usually evident, and is followed by 
notably painless distortions, contractures, and ankylosis. 
(a) The monarticular form is generally easy to recognize on account 
of its rapid, painless course, with semifluctuant swelling, secondary to 
a well-marked cord lesion, such as locomotor ataxia. A large joint is 
almost always affected, oftenest the knee, less often the hip, shoulder, 
or elbow. The joint shows abnormal mobility and the bones can often 
be felt to grate (see Fig. 267). THE JOINTS 
489 
Fig. 268.—Atrophic Atrophic. Early stage. 
Fig. 269.—Atrophic Arthritis. (Goldthwait.) 490 
PHYSICAL DIAGNOSIS 
(6) The primary polyarticular form usually begins in ,the fingers, 
and is very apt to occur symmetrically, i.e., in corresponding joints of 
both hands at the same time (see Fig. 268). The joints are enlarged, 
boggy, spindle shaped (owing to the rapid atrophy of the interossei), 
often abnormally white, apparently fluctuant, and show trophic skin 
lesions (glossy skin, sweating, mottling) (see Fig. 269). The terminal 
finger-joints are rarely swollen. Late in the course of the disease a 
ring of constriction often marks the line of articulation (see Fig. 270). 
Pain is not severe until motion is attempted or unless the joint is 
jarred and stirred up by some traumatism. 
Fig. 270.—Atrophic Arthritis. Late stage with constriction ring at the joint line 
(Goldthwait.) 
The changes progress slowly and attack new and larger joints, 
moving centrally from the periphery. At any stage the process may 
become arrested, but usually not until ankylosis or contractures have 
occurred in one or many joints. Some of the “ossified men” of dime 
museums are in the ankylosed stage of this terrible malady. Flexion 
of fingers with hyperextension of the terminal joints, and deflection to 
the ulnar side are common deformities. 
3. Hypertrophic Arthritis 
This is degenerative type of disease in which osteophytic spurs 
are the distinguishing feature. It occurs mostly in elderly persons. 
The new bone is deposited round the edges of the articular cartilage, 
forming an irregular ring (“ring bone” in horses) or “lip” near the THE JOINTS 
491 
joint. The attachments of the ligaments {e.g., the anterior lateral 
ligament of the spine, or the cotyloid ligament in the hip-joint) furnish 
another favorite site for the bony deposits. There is no ankylosis and 
motion is limited only by the collision of bony spurs in joint margins. 
(a) In the terminal finger-joints (“Heberden’s nodes") the process 
may remain for years without extending to any other articulation and 
without producing any discomfort (Figs. 54 and 271). 
(b) The disease may be limited to the hip-joint (“morbus coxae 
senilis”) or to any other single joint, producing purely mechanical 
Fig. 271.—Hypertrophic Arthritis with Heberden’s Nodes 
disturbances by limitation of motion. There is no considerable 
muscular spasm, and motion is quite free up to a certain point, at 
which it is suddenly “locked” by the interference of the bony out- 
growths. The situation, size, and shape of these outgrowths can be 
shown, as a rule, by the x-ray alone. Pain and swelling are slight or 
absent, unless traumatism (internal or external) stirs up the joint and 
produces a synovitis. The chief complaint is of stiffness. 
(c) Several joints may be affected, and there may result much pain 
because nerves pass through or over the new-formed -bone and are 
compressed by it. This form is most often seen in the spine (“spon- 492 
PHYSICAL DIAGNOSIS 
dylitis deformans,” “osteoarthritis”), where a portion of the front 
and side of the vertebral column is “plastered over” with new- 
formed bone (see Fig. 272), which later invades the intervertebral 
cartilage and produces (see Fig. 273) finally either a straight “ramrod” 
spine or a forward curved spine. 
Fig. 272.—Hypertrophic Arthritis of Spine. (Goldthwait.) 
Non-tuberculous disease of the sacro iliac joint has already been 
referred to on* page 59. 
In the early stages the disease is recognized by: THE JOINTS 
493 
(a) Nerve pain, running round the body or down the legs,1 as the 
intercostal and spinal nerves are pressed on. 
Fig. 273.—Hypertrophic Arthritis (Spine) of Spine with Ankylosis. (Goldthwait.) 
Fig. 274.—Showing Normal Flexibility of Spine. (Goldthwait.) 
(6) Limitation of Motion.—The process is usually unilateral, wholly 
or predominantly; hence the patient can usually bend much better to 
one side (see Figs. 274 and 275) than to the other. Motion is also 
more or less limited in other directions, but forward bending is fairly 
1 Many neuralgias and sciaticas are due to this disease. 494 
PHYSICAL DIAGNOSIS 
well performed as a rule, in sharp contrast with “lumbago,” which 
renders forward bending and the subsequent recovery almost 
impossible. 
Fig. 275.—Hypertrophic Arthritis of Spine. Motion to left limited. (Goldthwait.) 
Fig. 276.—Gouty Tophus in the Ear. 
(c) Coughing or sneezing often gives great pain, probably because 
the costo-vertebral joints are involved in the new growth; if ankylosis 
of these joints occurs later the respiratory movements of the chest are 
interfered with. THE JOINTS 
495 
Fig. 277.—Gouty Arthritis. 
Fig. 278.—X-ray of Hand in Gouty Arthritis. (Goldthwait.) 496 
PHYSICAL DIAGNOSIS 
4. Gouty Arthritis 
The deposits of urate of sodium in the soft structures around 
the joint are, like those in the ear (see Fig. 276), close beneath the 
skin or perforate it, and hence are recognizable (as above explained) 
by microscopic examination. 
They somewhat resemble the nodes of hypertrophic arthritis, but 
are not attached to the bone and can be moved about in the soft 
structures over it. X-ray examination shows that there is often con- 
siderable destruction of bone in the vicinity of the tophi (see Figs. 
277 and 278). 
5. Hcemophilic Arthritis 
A chronic stiffening and enlargement of the joint resembling in 
many respects the joint of hypertrophic arthritis, but often accom- 
panied by the formation of fibrous adhesions, ensures in some cases of 
haemophilia, presumably as a result of frequent hemorrhages and serous 
oozings on the joint. The diagnosis depends on the evidence of 
haemophilia, the youth of the patient, and the absence of infection 
as a causative factor. 
6. Relative Frequency of the Various Joint Lesions1 
The following table was prepared by Dr. Vickery2 from the records 
of the Massachusetts General Hospital (1893-1903): 
Acute rheumatic arthritis 591 
Subacute rheumatic arthritis 193 
Gonorrhoeal arthritis 86 
Typhoid arthritis (spine) 3 
Infectious arthritis. 
•873 
Hypertrophic and atrophic arthritis 43 
Gout 9 
1 Chronic villous arthritis (“dry joint”) is a purely local process and therefore 
receives no further mention. 
2 Boston Med. and Surg. Jour., November 17, 1904. CHAPTER XVIII 
THE NERVOUS SYSTEM 
I. Examination of the Nervous System 
The outlines of neurological diagnosis depend on knowledge of: 
I. Disturbances of motion. 
II. Disturbances of sensation. 
III. Disturbances of reflexes (including sphincteric and sexual 
reflexes). 
IV. Disturbances of electrical excitability. 
V. Disturbances of speech and handwriting. 
VI. Disturbances of nutrition (“trophic”). 
VII. Psychic disorders. 
VIII. Changes in the spinal fluid. 
I shall attempt no topical diagnosis of nerve lesions, no diagnosis, 
that is, depending on memorizing the brain areas, cord levels, or skin- 
and-muscle areas corresponding to particular nerve lesions. The 
general practitioner for whom this book is intended will not attempt 
to carry such points in his head, but will refer to specialists or special 
text-books when the case confronts him. The general methods most 
often employed are all that I attempt to describe. 
1. Gaits. 
2. Paralyses. 
3. Spasms and tremors. 
4. Ataxia. 
i. Gaits.—The most important gaits are: 
(a) The spastic 
(b) The ataxic. 
(c) The gait of paralysis agitans. 
(d) The toe-drop gait 
(e) The gait of simple weakness. 
With the spastic gait there is rigidity of the legs, making it difficult 
to lift the feet; hence the patient scuffs along, usually with bent knees 
and as if his feet were fastened to the ground.1 
i. Disorders of Motion 
1 The cross-legged gait is a spastic gait in which the adductors of the thighs are so 
contracted that the feet tend to be crossed. This gait is oftenest seen in the 
congenital spastic paralysis. 
497 498 
PHYSICAL DIAGNOSIS 
The ataxia gait is difficult to describe. The patient is not muscu- 
larly weak, but does not know where his feet are or where the ground 
is; hence he flounders and throws his feet about irregularly. 
The gait of paralysis agitans is an exaggeration of the old man’s 
gait, such as we often see on the stage. The whole body is bent for- 
ward and rigid (see Fig. 279), and, 
if progress is accelerated by a push 
given from behind, the patient maj 
be unable to stop himself. 
In the toe-drop gait the foot is 
raised high and slapped down upon 
the ground with a flail-like motion, 
2. Paralysis or Paresis.—Nc 
detailed account can be given here 
of the method of testing individua 
muscles for loss or impairment o: 
power. In . general, a knowledge 
of the origins and attachments o: 
muscles enables us to work out foi 
ourselves a series of tests that wil 
bring any desired group into con- 
traction. It is convenient to class 
paralyses according to their origir 
as follows: 
(a) Brain paralysis: usually 
hemiplegia (arm and leg on same 
side, with or without the face). 
(b) Cord paralysis: usually 
paraplegia (both legs, rarely both 
arms) or monoplegia (one ex- 
tremity) . 
(c) Cranial nerve paralysis 
usually one or more eye muscles. 
(d) Peripheral nerve paralysis 
special muscle groups, oftenest the extensors of the wrist or foot, the 
shoulder muscles, and those supplied by the facial nerve. 
(e) Hysterical paralysis: no strict anatomical* distribution, oftenes' 
monoplegia (one extremity). 
Peripheral nerve paralyses are especially apt to be accompanied b> 
sensory symptoms, electrical changes, and wasting. Brain paralyses 
have relatively few sensory symptoms (sometimes paraesthesise, see 
Fig. 279.—Attitude Characteristic of 
Paralysis Agitans. THE NERVOUS SYSTEM 
499 
below, page 501) and relatively slight wasting. Mental changes, coma, 
or convulsions often precede or follow them. Cord paralyses may or 
may not show these associations, but are often accompanied by 
disorders of the bladder and rectum. 
3. Spasm, Tremor, and Fibrillary Twitching.—(a) Spasm means 
involuntary muscular contraction. The familiar “cramp” is a good 
example of the type of spasm known aS tonic spasm. In contrast with 
this is the clonic spasm, in which flexors and extensors contract alter- 
nately to produce a motion like that of our forearm when we shake up 
a fluid in a test tube, or like the ankle clonus (see below). 
Spasms may be general or local, i.e., involve few or many muscles. 
In strychnine poisoning the whole body may be thrown into rigidity 
or general tonic spasm. At the beginning of an epileptic seizure the 
body stiffens out (tonic spasm), then becomes “convulsed” (general 
clonic spasm). Local tonic spasm is exemplified in the ordinary 
“cramp." The spastic gait, above described, is another common 
example of tonic spasm limited mainly to one group of muscles. The 
contractures which so often affect the sound muscles in a partially 
paralyzed limb (see above, page 482) are also examples of local tonic 
spasms. 
Athetosis, a special variety of local tonic spasm, has been described 
on page 47. 
Local clonic spasm is not common. It may be due to irritation of 
a small portion of the cerebral cortex by various lesions (“Jacksonian 
epilepsy”), and sometimes precedes or alternates with the general 
spasms of ordinary epilepsy. It also occurs in hysteria. 
Artificially a momentary or prolonged clonic spasm of the foot 
muscles is often produced in testing for the ankle clonus (see below, 
page 504). 
(b) Tremor may be defined as a clonic spasm of short excursion. 
Its causes and varieties have already been discussed (see page 46). 
(c) Fibrillary twitchings means the brief repeated contraction of 
small bundles of muscle fibres. It is seen in patients who are cold or 
nervous, in many debilitated and neurasthenic conditions and often 
in muscles affected by progressive muscular atrophy. 
(d) Choreic and choreiform movements occur in true chorea, in 
encephalitis lethargica, and after hemiplegia. 
4. Ataxia.—Inco-ordination of the various muscles which normally 
act together to produce a well-directed movement is called ataxia. All 
young infants exhibit ataxia in their more or less unsuccessful grasping 
movements. Alcoholic intoxication often produces typical ataxia, 500 
PHYSICAL DIAGNOSIS 
and it is also exemplified in the gait of tabes dorsalis. There is no lack 
of muscular contraction—often too much—but it is disorderly and 
ill-directed. 
Deficiency in the power to balance in standing or walking is perhaps 
the commonest type of ataxia, and may be due not only to the causes 
just mentioned, but also to cerebellar disease and ear disease. In these 
types there is often a tendency to stagger in one particular direction, 
e.g., to the right, and the ataxia is associated with vertigo and with 
other evidences of brain tumor or of ear disease. 
In tabes dorsalis and other diseases we test the power to balance 
by asking the patient to bring his feet together (toe to toe and heel to 
heel) and to close his eyes. If he is unable to preserve his balance his 
failure is known as 11 Romberg’s sign.” 
2. Disorders of Sensation 
The following are the most important types: 
1. Ancesthesia (or insensibility to pain, to touch, to heat and cold, 
and to muscle sensation). 
2. Hyperesthesia (or oversensitiveness). 
3. Paresthesia (abnormal, false, or disordered sensation). 
4. Pain. 
5- Disorders of special sense. 
These disturbances may all be seen in different stages or types of 
lesions of the spinal cord or peripheral nerves. They are less common 
in brain lesions. 
1. Tests of anesthesia are time-consuming and difficult, because 
we depend for our data on the patient’s intelligent answer to the 
question, “Do you feel that?” As a rule, we cover the patient’s 
eyes and then touch the suspected parts—first lightly, then more 
strongly—questioning him to see if he feels the touch, can judge the 
nature of the touching object (finger, pencil, pin), and tell where he is 
touched. A pin-prick is oftenest used to test pain sense, and test 
tubes filled, one with hot, one with cold water, are convenient for 
trying the temperature sense. Finally, we try whether the patient 
can recognize familiar objects placed in his hand and can tell the 
position in which you may put his arms or legs. Failure to make these 
discriminations is known as astereognosis, and occurs oftenest in brain 
lesions affecting the temporal lobes. 
Dissociation of sensation—the preservation, for example, of sensa- 
tions of touch with loss of those of pain and temperature—occurs 
oftenest in syringomyelia. THE NERVOUS SYSTEM 
501 
Delayed sensation and mistakes regarding the point touched in 
testing are commonest in tabes dorsalis, which disease presents a 
great variety of sensory disorders not here catalogued. 
The distribution of anaesthesia depends, like the distribution of 
paralysis, on the lesion. Hemiancesthesia is seen oftenest in hysteria 
and organic brain lesions. Cord lesions, such as transverse myelitis or 
compression of the cord, usually produce anaesthesia in the area supplied 
by the spinal nerves below the lesion. Peripheral nerve lesions may 
produce anaesthesia of the skin areas supplied by the nerve in question. 
Areas of hysterical ancesthesia (with hyperaesthesia and paraesthesia) 
usually do not correspond to the distribution of any set of nerves or 
centres, and are distinguished by this fact. 
2. Hyperaesthesia is most often recognized as hyperaesthesia for 
pain (tenderness) or in the special senses (sensitiveness to light or 
noise). It is commonest in peripheral nerve lesions and in hysteria. 
The tests are the same as those for anaesthesia. 
3. Paraesthesia is commonest in the form of the familiar prickling 
and tingling felt when one’s arm or leg has “gone to sleep.” Sensa- 
tions as of crawling insects are not uncommon, the “hot feet” of 
many elderly persons (with arterio-sclerosis) and the “ burning hands” 
of many washerwomen are other familiar examples. 
Local paraesthesia is not uncommon in lesions of the cerebral cortex, 
and constitutes the preliminary “aura” with which many attacks of 
epilepsy are ushered in. Well-developed tabes dorsalis shows many 
curious or distressing varieties of paraesthesia, as do many other varie- 
ties of peripheral neuritis. 
3. Reflexes 
We may distinguish: 
1. Pupil reflexes. 
2. Deep reflexes (tendon reflexes). 
3. Superficial reflexes (skin reflexes). 
4. Sphincteric reflexes. 
5. Sexual reflexes. 
1. Pupil reflexes have been described on page 16. 
2. Tendon Reflexes.—Among the most important of these is the 
knee-jerk (quadriceps tendon); less important are the ankle-jerk 
(Achilles tendon) and ankle clonus, the wrist, elbow, and jaw reflexes. 
To test the knee-jerk many methods are used; the following seems 
to me the best: The patient sits with his knees flexed at a blunt angle. 502 
PHYSICAL DIAGNOSIS 
The physician lays his left hand on the front of the thigh and strikes 
the tendon of the quadriceps, just below the patella, with the finger 
tips of the right hand or with a rubber hammer. The left hand feels 
the sudden contraction of the quadriceps whether the foot jerks or not. 
If no contraction is obtained we should try what is known as “reen- 
forcement of the knee-jerk.” The essence of this is concentration of 
the patient’s attention on a voluntary muscular contraction in another 
part of the body. We may accomplish this by asking the patient to 
hook the fingers of his hands together, and at a given signal to give a 
quick pull upon them and then let go. The physician gives the 
signal (often the word “now”) and strikes the patella tendon at the 
same moment. 
The knee-jerk is often wanting or feeble in young infants and in 
pneumonia. It varies a great deal in persons of different temperament; 
in high-strung or oversensitive persons and in the Jewish race very 
lively knee-jerks are often seen without disease. 
Absence of knee-jerk is oftenest found in: 
(a) Peripheral neuritis (alcoholic, diphtheritic, lead, etc.). 
(b) Tabes dorsalis. 
(c) Anterior poliomyelitis (on the paralyzed side). 
(d) In the deepest coma from any cause. 
(e) In complete severing of the spinal cord. 
Given a case without knee-jerks: 
Neuritis is suggested by the history (alcohol), by the presence of 
marked sensory symptoms (pain, tenderness), and the absence of 
symptoms pointing to the brain or cord. 
In tabes the Argyll-Robertson pupil, the disturbance of the sphinc- 
ters and sexual power, the ‘‘lightning pains,” here and there, the 
changes in the spinal fluid (see page 510), and later the ataxic gait 
are important confirmatory signs. 
Anterior poliomyelitis presents a flaccid paralysis, usually of one 
extremity, coming on suddenly in a young child and wholly without 
sensory symptoms. 
Comatose patients, if the coma is due to cerebral hemorrhage and 
is not of the profoundest type, often show increased knee-jerks on the 
paralyzed side; but in very profound unconsciousness all reflexes are 
lost. 
Partial destruction of the cord often increases the reflexes, but total 
division usually abolishes them. THE NERVOUS SYSTEM 
503 
Increased knee-jerk is found in: 
(a) Cerebral paralyses (infantile, apoplectic, dementia paralytica 
etc.). 
(b) Spastic paraplegia and the amyotrophic forms of lateral 
sclerosis. 
(c) Many cord lesions, localized above the lumbar enlargement 
(transverse of pressure myelitis). 
(d) The earliest stages of peripheral neuritis. 
(e) Multiple sclerosis. 
(/) Some forms of chronic arthritis. 
Differential Diagnosis of cases with increased knee-jerks: 
Cerebral paralyses usualy manifest their place of origin by the 
presence of psychic symptoms (coma idiocy, dementia) and by con- 
vulsions. The paralysis is usually hemiplegic and involves no wasting 
beyond the atrophy of disuse. 
Spastic paraplegia is readily recognized by the gait (see page 497) 
and the absence of marked sensory or sphincteric symptoms. Its 
pathology is not known. If marked wasting of the muscles ocurs it 
is termed “ amyotrophic lateral sclerosis.” 
Transverse or diffuse cord lesions above the lumbar enlargement 
produce usually anesthesia below the level of the lesion and relaxation 
of the sphincters. Such cases are often syphilitic. 
The earliest stages of peripheral neuritis are usually recognizable, 
despite a lively knee-jerk, by the predominant sensory symptoms 
and the etiology. 
Multiple sclerosis presents, in typical cases, intention tremor (see 
above, page 46), nystagmus (page 17), and staccato speech. In 
atypical cases diagnosis is difficult and cases are often mistaken for 
hysteria. 
Almost any chronic joint disease, except tuberculosis, may be 
associated with increased reflexes. Diagnosis depends on the absence 
of other causes for the increase. 
Other Deep Reflexes.—The Achilles reflex is best obtained by 
having the patient kneel on the seat of a well-padded chair, with 
his feet unsupported, while we strike the Achilles tendon. The 
significance of its absence or increase is practically the same as that 
just given for the knee-jerk, but, since it represents a slightly lower 
position in the spinal cord, it may be affected earlier than the knee- 
jerk in any cord disease which begins at the bottom of the cord and 
travels up. Thus in tabes I have known the Achilles reflex absent 
when the knee-jerk still persisted. 504 
PHYSICAL DIAGNOSIS 
Ankle clonus occurs in spastic conditions of the legs or in any 
disease which increases the other leg reflexes. It is obtained by 
supporting the patient’s leg in a state of such relaxation as can be 
obtained, then suddenly and quickly forcing the foot up as far as it 
will go toward the shin, and holding it in this position. A clonic 
spasm results, which in true ankle clonus persists as long as we choose 
to hold the foot in this position. Spurious clonus is obtained when 
only a few contractions occur, the muscle then relaxing. This spurious 
clonus can often be obtained in neurasthenic and hysterical states, 
and has not the significance of true clonus. 
Kernig’s sign is a reflex hypertension of the ham-string muscles, 
when we flex the thigh on the trunk at a right angle (as in the sitting 
position) and then try to extend and lower leg. Its motion is arrested 
about half way between the right angle and full extension. 
This reflex is of some value in the diagnosis of meningitis, though 
allowance must be made for the stiffness of old age. The sign is by 
no means pathognomonic, but is of some confirmatory value. 
The precise opposite of Kernig’s sign, viz: a great slackness of 
the hamstrings (hypotonus) is often a valuable confirmatory sign in 
tabes dorsalis. 
The deep reflexes oi the arms (wrist, biceps, and triceps tendon) 
are obtained by snapping these tendons sharply with the finger. 
Decreased reflexes we can rarely perceive, as a rule they are obtainable 
only when increased. Such increase may occur in the diseases which 
increase leg reflexes; also in chronic joint troubles. 
The jaw-jerk is obtained by asking the patient to let the lower 
jaw drop fully, placing a finger on the chin and percussing that finger 
as in percussion of the chest. It can be elicited only when increased. 
3. Superficial Reflexes.—A “ticklish” person is one whose super- 
ficial reflexes (skin and muscles) are very lively. Among pathological 
reflexes of this type: 
(a) The Babinski reflex is the most important. It is a modification 
or reverse of the normal reflex, which crumples up the toes toward the 
sole of the foot if the skin of the foot is tickled. 
To obtain the Babinski reflex, bare the patients foot and draw 
the blunt end of a pencil along the inner side of the sole from heel to toe 
with moderate pressure. If the great toe cocks up toward the shin, 
Babinski’s reflex is present. Sometimes several other toes spread 
laterally and follow the great toe. Squeezing the calf or drawing the 
finger along the outer tibial surface of various other ways to irritating THE NERVOUS SYSTEM 
505 
the lower leg may also bring out the Babinski reflex (Gordon’s sign, 
Oppenheim’s sign, etc.). 
This reflex is obtained on the affected side in hemiplegia and other 
lesions involving the upper motor neuron. 
(b) The cremasteric reflex draws the testis tight up against the 
body (as after a cold bath) when the skin and muscles on the inner 
side of the thigh are gathered up and firmly grasped in the hand. 
(■c) The abdominal and epigastric “tickle reflexes” are excited 
by lightly and quickly stroking the skin of these parts with a pencil 
point or something of the sort. 
The presence of cremasteric, abdominal, and epigastric reflexes 
indicates that the portion of the spinal cord in which they are rep- 
resented (upper lumbar and lower dorsal regions) is functionally 
sound. The absence of these reflexes, however, signifies nothing, 
for in many healthy persons they cannot be excited. 
(d) The reflex of winking excited by the ordinary stimuli signifies 
the approximately normal conductivity of the fifth and seventh nerves 
(trigeminal and facial). 
4. Sphincteric Reflexes.—The sphincters of the bladder and rectum 
are kept closed in the normal adult by reflex contraction, normally 
of moderate degree, but excited by the presence of urine and fasces. 
If there is no awareness of faeces at the anus or of urine at the neck of 
the bladder, owing to destruction of the conducting nerves or spinal 
nerve-centres, involuntary urination and defecation occur. 
This is the case in transverse, diffuse, or compression myelitis 
above the segment (fourth and fifth sacral) where the centres for 
bladder and rectum are represented;1 also in tabes dorsalis, dementia 
paralytica, and less often in other chronic spinal-diseases. Periph- 
eral neuritis rarely affects the sphincters. 
In deep coma from any cause (epilepsy, cerebral hemorrhage) 
the sphincters may be relaxed, owing to the abolition of sensation. 
5. Sexual Power.—Sexual power may be regarded as a reflex in 
the presence of a particular stimulus, and is diminished or lost in 
chronic cord diseases involving the first and second sacral segments 
(lumbar enlargement) or the nerves leading to them, e.g., in tabes, 
some cases of myelitis and dementia paralytica, etc. Temporary 
increase of power may precede the diminution. 
1 It must be remembered that these nerves arise from the cord at the level of 
the first lumbar vertebra, though they do not issue from the spinal column till the 
fourth and fifth sacral foramina are reached. 506 
PHYSICAL DIAGNOSIS 
4. Electrical Reactions 
In health, a sharp contraction occurs if a faradic current is applied 
to a nerve or over a muscle, and a similar contraction can be obtained 
with the galvanic current just when the circuit is closed or broken, 
but not when the current is passing. 
In contrast with these conditions is the reaction of degeneration. 
When this is present we obtain no muscular twitching with the 
faradic current and none over the nerve with the galvanic; but 
with the galvanic over the muscle a slow, worm-like contraction occurs, 
and the response to the positive pole is as good as to the negative, 
or better, whereas normally there is far better response to the negative. 
This is the complete reaction of degeneration; in partial reactions of 
degeneration all the normal reactions may be present, but diminished 
in intensity. 
Reaction of degeneration occurs in all diseases affecting the anterior 
motor horns of the cord or their prolongations downward in the per- 
ipheral nerves; for example, in anterior poliomyelitis, progressive 
muscular atrophy, transverse or pressure myelitis, and all severe 
forms of peripheral neuritis. In brain lesions this reaction rarely 
occurs. 
In prognosis a reaction of degeneration persisting after six to 
twelve weeks is unfavorable for recovery of the use of the muscles 
in which it occurs. If reaction of degeneration is absent or partial 
from the start, the prognosis is for relatively speedy recovery, i.e., in 
weeks rather than months. 
5. Speech and Handwriting 
Aphasia, the loss of the power to speak or understand speech, 
despite normal hearing and muscular powers, occurs in lesions affecting 
the third left frontal and first left temporal convolutions of the brain.1 
The lesions producing aphasia may be permanent anatomical 
changes following hemorrhage or tumor, or they may be transitory, 
as in uraemia and migraine. 
The power to write or read letters is lost (agraphia) when the 
angular and supramarginal convolutions are destroyed. 
Degeneration of the handwriting, as compared with the standard 
of former years, is often a helpful bit of evidence in the diagnosis 
of dementia paralytica, but may occur temporarily in various fatigue 
states. 
1 In some left-handed persons the centres are on the right side of the brain. THE NERVOUS SYSTEM 
507 
6. Trophic or Vasomotor Disorders 
Trophic lesions of the joints, muscles (atrophy), skin, and nails 
have already been exemplified (pages 490 and 58). They blend with, 
and are by some explained as the results of vascular changes (vaso- 
motor). Herpes labialis (“cold sore”) and herpes zoster (“shingles”) 
certainly seem to give every evidence of being due to nutritive dis- 
orders in the ganglia and not to vascular changes. The acute bedsores 
which form in myelitis, the “angioneurotic” local swellings which 
appear here and there in certain persons, and the local syncope or 
asphyxia which sometimes lead to Raynaud’s form of gangrene, 
seem to need both nerve and vessel changes to explain them. 
In brain lesions these trophic and vasomotor changes are much 
rarer than in disease of the cord and peripheral nerves. 
7. The Examination of Psychic Functions 
The diagnosis of the mental factors of disease forms an important 
part of the study not only of neurology, but of all diseases wherever 
situated; but as it cannot be called physical diagnosis, it falls outside 
the scope of this book, except in so far as loss of consciousness, coma, 
may be considered under this heading. 
(a) Coma 
The causes of coma are nearly identical with the causes of con- 
vulsions. Almost every disease which causes the one may cause the 
other; hence all that is here said on the diagnisis of coma applies 
equally well to the diagnosis of convulsions. Either or both may 
result from: 
1. Cerebral compression (skull fractures). 
2. Apoplexy (including cerebral hemorrhage, embolism, and acute 
softening thrombosis). 
3. Alcohol. 
/ 4. Epilepsy. 
5. Cerebral concussion (stun). 
6. Uraemia and hepatic toxaemia. 
7. Diabetes. 
8. Syncope (fainting). 
9. Opium. 
10. Hysteria. 
11. Gas poisoning. 508 
PHYSICAL DIAGNOSIS 
12. Sunstroke. 
13. Stokes-Adams’ syndrome. 
Apoplexy is the probable diagnosis when an elderly person who 
has shown no previous signs of ill-health becomes suddenly and 
deeply comatose within a few seconds or minutes. If hemiplegia is 
present (with or without aphasia ) and if we can exclude the other 
causes above mentioned, the probability of apoplexy is increased. 
To determine hemiplegia in a comatose patient, try the following 
tests: 
(a) Lift the arm and then the leg, first on one side and then on 
the other, and let go. The supported member falls more limply on 
the paralyzed side. 
(b) Pinch or prick the limbs alternately. The sound limb may 
be moved, while the other remains motionless. Pressure over the 
supraorbital notch may bring out a similar difference in the response 
of the two sides. 
(c) Try the knee-jerks. On the paralyzed side the jerk may be 
increased. 
(d) Try Babinski’s reaction. It may be present on the paralyzed 
side or on both sides. 
Urcemia.—The diagnosis between apoplexy and uraemia is some- 
times impossible, since uraemia may produce hemiplegia, and the 
urine in the two conditions (as obtained by catheter) may be iden- 
tical. In practically all cases, however, the uraemic patient has pre- 
viously shown obvious signs of nephritis—oedema, headache and 
vomiting, hypertrophy, oliguria, or polyuria with albuminuria. 
“Acute uraemia” suddenly appearing in a person apparently healthy 
is almost always a false diagnosis. The cases turn out to be skull 
fracture, apoplexy, arterio-sclerosis, etc. Convulsions more often 
precede or follow the coma of uraemia than that of apoplexy. Retinal 
hemorrhages or albuminuric retinitis, if recognized by ophthalmo- 
scopic examination, point to uraemia. 
The hepatic toxaemia in which many cases of cirrhosis and acute 
yellow atrophy die is distinguishable from uraemia only if the previous 
history of the case is known to us and the signs of liver disease 
(ascites, jaundice, and enlarged spleen) are evident. 
Diabetic coma is usually recognized with ease, because the evidences 
of advancing diabetes lead gradually up to it. Like uraemia and unlike 
apoplexy it very rarely appears “out of a clear sky.” The emaciation 
of the patient, the sweetish odor of the breath, the presencel4of 
sugar, and especially the evidences of acetone and diacetic acid in THE NERVOUS SYSTEM 
509 
the catheter-urine, are the essential factors in diagnosis. Dyspnoea 
(“air hunger”) precedes the coma in about one-third of the cases. 
Concussion (or stun) after a blow usually clears up in a few minutes 
and so presents no difficulty in diagnosis. If the coma lasts on for 
hours or days (as it sometimes does) the suspicion arises that we are 
dealing with 
Compression. For this the evidences are: Focal symptoms, con- 
vulsions, slowing of the pulse, and signs of depressed fracture. To 
determine the latter fact may be impossible even with v-ray, since 
the inner table of the skull may be broken, while the outer is intact. 
The focal signs to be looked for are paralyses (ocular or peripheral). 
Syncope (or fainting) is usually over in a few minutes and so betrays 
its nature, but it must not be forgotten that a slight convulsion may 
occur just as the patient comes out of coma. No suspicions of epilepsy 
need be aroused thereby, but if there have previously been signs of 
hysteria we may be in doubt whether the fainting fit is not of hysterical 
origin. The history of the case, the circumstances at the onset of the 
attack, and the presence or absence of hysterical behavior during it 
usually guide us aright. 
Opium poisoning produces a coma from which the patient can 
usually be more or less aroused. Contracted pupils and slow respi- 
ration are the most characteristic signs. A laudanum bottle or a 
subcutaneous syringe found near the patient often assist the diagnosis. 
Alcoholic coma is rarely complete. The patient can be aroused. 
The circumstances under which he is found, the odor of alcohol on 
the breath, the absence of paralysis, fever, small pupils, or urinary 
abnormalities are the main supports in diagnosis. There is no char- 
acteristic pulse and the pupils show no constant changes, though in 
many cases they are dilated. 
Hysterical coma usually occurs in young women who have pre- 
viously shown signs of hysteria. In falling they never hurt them- 
selves. The eyelids are contracted, often tremulous, and when 
forcibly pulled open often expose eyeballs rolled up so that the whites 
alone are seen. The hands are apt to make grasping motions, and 
there are irregular, semipurposive movements of various parts of the 
body. A startling word may arouse the patient, but anaesthesia to 
pain (over one-half or all the body) is often complete. 
Postepileptic coma is usually recognized with ease, because of the 
convulsions wffiich precede it and which are usually known to have 
occurred at intervals before. The scar of previous falls may be found 
on the head. 510 
PHYSICAL DIAGNOSIS 
Gas poisoning rarely presents any diagnostic difficulties, because 
the circumstances under which the patient is found make clear the 
cause of his condition. An odor of gas may hang about his breath for 
some hours. 
Sunstroke is recognized by the state of the weather and the presence 
of a very high temperature (106°, 1 io°, 1150 F., or even more). There 
is no other characteristic sign. This condition is to be distinguished 
from heat exhaustion in which there is no fever and no coma. 
The Stokes-Adams’ Syndrome (see above p. 114) produces coma and 
convulsions with a very slow radial pulse and a quicker venous pulse 
(visible or traceable polygraphically) in the neck. 
8. Examination of the Cerebro-Spinal Fluid 
In cerebro-spinal syphilis (including tabes and paresis), in lethargic 
encephalitis and in all types of meningitis, the character of the fluid 
obtained by lumbar puncture is of great diagnostic value. In all 
comatose and paralytic states it may be useful. 
To obtain spinal fluid, a hollow needle is inserted between the 
spines of the vertebras in the median line at the level of a line carried 
round the back from the crest of one iliac bone to the other. The 
needle is pushed straight on until fluid begins to flow through it. 
This usually occurs when the needle point is about two inches from 
the surface. If the spinal fluid is under tension it may spurt through 
the tube but usually it falls drop by drop into the test tube, which 
is held in position to receive it. 
The most important tests are: i. The cell count. 2. The differ- 
ential cell count. 3. The WasSermann test. 4. The Lange colloidal 
gold test. 5. The quantitative test of sugar. 
To count the cells one puts a drop of the well shaken fluid on the 
counting disc of the Thoma-Zeiss blood counter and proceeds ex- 
actly as in dealing with blood. Normal cerebro-spinal fluid contains 
from 1 to 10 (usually 1 to 5) cells per cm. In syphilis from 20 to 
200 or more cells are often found. In meningitis and pneumonia 
there are often several hundred. In leucaemia the count rises into 
the thousands. 
The differential count shows in most chronic inflammations of 
the canal, i.e. in tabes, paresis, and tuberculous meningitis, go to 
100 per cent, of lymphocytes. In acute irritations such as epidemic 
meningitis and pneumonia the cells are largely polynuclear. In 
poliomyelitis the polynuclears range from o to 60 per cent. The rest THE NERVOUS SYSTEM 
511 
are lymphocytes. There is also a considerable lymphocytic increase 
in lethargic encephalitis but in this disease an increase of the sugar in 
the spinal fluid is the most characteristic point, especially when this in- 
crease reaches as high as .07 to .09 per cent, (normal 0.4 to .06 percent). 
The Wassermann reaction is often positive in the spinal fluid when 
it is negative in the blood, e.g. in tabes. Its value is therefore obvious. 
The Lange gold test depends on a color change produced by certain 
spinal fluids in a solution of colloidal gold. It is valuable chiefly in the 
recognition of dementia paralytica. Bacteriologic examination by cul- 
ture or more often by cover. INDEX 
Abbott, Maud E., 273 
Abdomen, contour of, 355 
distended and tortuous veins of, 
355 
examination of, 354-359 
free fluid in, 361 
inspection of, 355 
organs palpable in, 357 
palpation of, 356 
projection or levelling of navel, 
355 
respiratory movements of, 355 
rose spots on, 355 
striae of, 355 
tumors of, 359 
tumors of, frequency of, 362 
tumors of, respiratory mobility 
in, 359 
Abdominal distention, 391 
reflexes, 505 
wall, abscess of, 358 
wall, inflammation of, 359 
wall, lesions of, 358 
wall, movements of, 355 
wall, sarcoma of, 359 
wall, thickening of, 359 
Abscess, alveolar, 26 
axillary, 41 
cervical, caries in, 33 
cervical in Pott’s disease, 33 
cold, 61 
glandular, 33 
in tuberculous arthritis, 483 
ischiorectal, 437 
of abdominal wall, 358 
of hip-joint, 59 
of liver, 380 
of lung, breath in, 23 
of urethra, 438 
peri-urethral, 438 
Abscess, perihepatic, 381 
perinephritic, 410 
psoas, 447 
pulmonary, 316 
pulmonary, sputa in, 317 
retropharyngeal, 29 
subphrenic, 357 
tonsillar, 29 
tuberculous, 61 
Acetone breath, 23 
Achilles reflex, 503 
Achromia of red cells in chlorosis, 473 
Achylia gastrica, stomach contents in, 
372 
Acne rosacea, nose in, 19 
Acromegalia, 9 
arm in, 44 
hands in, 53 
nose in, 9, 18 
“whopper jaw” in, 9 
Actinomycosis, 61 
of belly-wall, 358 
of neck, 36 
Addison’s disease, 113 
disease, buccal patches in, 27 
Adenitis, 30 
Adenoid growths, 67 
growths, nose in, 19 
Adenoids, 12 
lips in, 20 
Adherent pericardium, 86, 245 
Albuminuria, 419 
significance of, 420 
with nephritis, 429 
without nephritis, 420 
Albumosuria, significance of, 421 
Alcoholism, 502 
breath in, 23 
coma in, 507 
face in, 13 
513 INDEX 
514 
Alcoholism, hands in, 46 
nose in, 18 
pharyngeal reflexes in, 30 
skin in, 102 
tongue in, 23 
Alkaline urine, 419 
Alternation, 123 
Amoeba coli, 397 
histolytica in feces, 397 
Amyloid disease, of liver, 381 
Anaesthesia, hysterial, 501 
tests of, 500 
Anatomy of chest, 63 
Anemia, capillary pulsation in, 92 
functional heart murmurs in, 190 
haemoglobin test in, 462 
interpretation of blood count in, 
472 
lips in, 20 
murmurs in, 190 
nails in, 58 
oedema of lids in, 15 
pernicious, 473 
retinal hemorrhage in, 18 
splenic, 405 
secondary causes of, 472 
Aneurism, 256-267 
aortic, 256-267 
auscultation in, 260 
diagnosis of, 262 
diffuse and saccular, 256 
distinguished from aortic steno- 
sis, 264 
distinguished from diffuse dilata- 
tion of the arch, without 
rupture of coats, 264 
distinguished from empyema 
necessitatis, 265 
distinguished from mediastinal 
tumors, 265 
location of, 262 
of aorta, 256 
percussion signs in, 260 
pulsation in, 256 
pupils in, 259 
radial pulse in, 256 
radioscopy in, 261 
saccular, 256 
Aneurism, seat of, 262 
thrill in, 257 
tracheal tug in, 259 
tumor of, 257 
Angioneurotic oedema, 15, 21 
Ankle clonus, spasm in, 499 
clonus, test for, 504 
Anterior poliomyelitis, 502 
Aorta, hypoplasia of, 275 
Aortic aneurism, see Aneurism 
Aortic arch, roughening of, 230 
coarcuation, 274 
dilatation, 229 
insufficiency, 222 
obstruction, see Stenosis 
regurgitation, see Regurgitation 
second sound, 176-178 
stenosis, see Stenosis aortic 
valves, roughening of, 229-254 
Aortitis, syphilitic, 248 
with aneurism, 256-267 
Aphasia, 406 
Aphonia, 259 
Apoplexy, coma in, 507 
distinguished from uraemia, 507 
Appendicitis, 391 
local and constitutional signs, 
392 
muscular spasm in, 392 
psoas spasm in, 392 
simulated, 392 
tenderness in, 392 
tumor in, 392 
Arcus senilis, 17 
Argyll-Robertson pupil, 17, 502 
Argyria, 16 
Arms, atrophy of, 40 
contractures of, 40 
contractures of, in cerebral lesion, 
40 
contractures of, in hysteria, 
40 
deep reflexes of, 501 
in acromegalia, 44 
in acute anterior poliomyelitis, 
39. 40 
in osteoarthropathy, 44 
in Paget’s disease, 43 INDEX 
515 
Arms, in rickets, 43 
oedema of, 41 
oedema of, causes of, 41 
oedema of, in aneurism, 41 
oedema of, in cancer, 41 
oedema of, in Hodgkin’s disease, 
4i 
oedema of, in nephritis, 41 
oedema of, in sarcoma of medi- 
astinum, 41 
oedema of, in sarcoma of lung, 
4i 
oedema of, in thrombosis, 41 
pain in, 36 
paralysis of, 38 
sarcoma of bone of, 41 
tuberculosis of bone of, 42 
tuberculous lesions of, 42 
Arrhythmia, 116 
absolute, 119 
causes of, x 16-124 
sinus type, 124 
Arterial murmurs, 181 
phenomena, 90 
pressure, 109 
tension, 106 
walls, calcification of, 108 
walls, condition of, 108 
Arteries, calcification of, 108 
changes in, 41 
in nephritic heart disease, 272 
inspection of, 90 
position of, 107 
pulsation in, see Pulsation 
stiffening of, 108 
Arteriograms, 116 
Arterio-sclerosis, 88, 108, 116, 193 
cornea in, 17 
decrescent, 271 
gangrene of toes in, 460 
heart sounds in, 178 
hypertrophy in, 197 
Anterio-sclerosis, pulse in, 105 
senile, 271 
Arterio-sclerotic heart disease, 268, 
271 
Arthritis, 485 
acute, 485 
Arthritis, acute infectious, distinguished 
from other types, 4.85 
acute infectious, endocarditis in, 
485 
atrophic, 488 
atrophic, monarticular form, 488 
atrophic, primary polyarticular 
form, 488 
atrophic, symmetrical involve- 
ment of joints in, 488 
atrophic, X-ray of hand in, 488 
gouty, 496 
hsemophilic, 496 
hypertrophic, features of, 490 
hypertrophic, Heberden’s nodes 
in, 490 
hypertrophic, limitation of mo- 
tion in, 480 
hypertrophic, nerve pain in, 480 
infectious, 485 
rheumatic, 207 
tuberculous, characteristics of* 
485 
Ascaris lumbricoides, 396 
Ascites, causes of, 363 
Astereognosis, 500 
Asthma, 313 
bronchial, 313 
bronchial, eosinopnilia in, 473 
Ataxia, 497 
Romberg’s sign in, 498 
Atelectasis, crepitant r&les in, 164 
Athetosis, 51 
Atrophic arthritis, see Arthritis 
Atrophy, acute yellow, 381 
following fracture or dislocation, 4 
of disuse, 40 
in hysteria, 40 
muscular, claw hand in, 52 
muscular, reaction of degenera- 
tion in, 506 
progressive muscular, fibrillary 
twitching in, 498 
Auricle, dilatation of, 202 
hypertrophy of, 202 
Auricular fibrillation, 119 
Auscultation, differences between two 
sides of chest, 158 516 
INDEX 
Auscultation, in aneurism, 260 
in aortic regurgitation, 224 
in croupous pneumonia, 287 
in mitral stenosis, 214 
mediate versus immediate, 142 
of heart, 171 
of lungs, 152 
of muscle sounds, 150 
of voice sounds, see Vocal Frem- 
itus 
see also Breathing, Murmurs, Rdles, 
Heart sounds 
sources of error in, 151 
technique of, 142 
Austin Flint murmur, 220, 222 
Babinski reflex, test for, 506 
Bacilli tubercle, identification of, 319 
Back, 58-61 
aneurism pointing in, 60 
dermoid cyst of, 61 
epithelioma of, 60 
in lumbago, 58 
nodes in, 60 
spina bifida of, 61 
stiffness of, 58 
tumors of, 60, 61 
Balanitis, 438 
Baldness, 8 
patchy, in alopecia areata, 8 
Basedow’s disease, 272 
Bilharzia disease, eggs, 396 
Biliary colic, 385 
Bismuth line, 25 
X-ray examination of stomach, 373 
Bladder disease, incidence of, 431 
disease, percussion in, 431 
disease, urine in, 433 
distention of, 431 
pus in, 416 
stone of, 434 
tuberculosis of, 434 
tumor of, 431 
Blood, color, index of, 472 
counting red corpuscles of, 
method of, 471 
counting white corpuscles, 
method of, 470 
Blsod, cover-glass preparation of, 465 
eosinophilia in, 475 
examination of, 462 
filaria in, 479 
films, appearance of stains, 466 
films, preparation of, 465 
haemoglobin tests, 462 
in chlorosis, 473 
in filariasis, 479 
in hydatid disease, 479 
in lymphoid leukaemia, 476 
in myeloid leukaemia, 476 
in pernicious anemia, 476 
in secondary anemia, 472 
interpretation of result of leuco- 
cyte count and differential 
count, 473 
in trichiniasis, 479 
in trypanosomiasis, 479 
in uncinariasis, 479 
in urine, 417 
leucocytes in, 416 
lymphocytes in, 475 
normoblast distinguished from 
megaloblasts in, 467 
nucleated red cells in, 467 
parasites in, 478 
plates, 469 
poikilocytosis, 467 
polychromasia, 467 
polynuclears in, 468 
pressure, see Pressure 
stippled red cells in, 467 
trypanosoma in, 479 
Wassermann reaction, 478 
Widal reaction, 477 
see also Anemia 
Body, as a whole, 1 
Bowel, cancer of, 394 
Bradycardia, 279 
Brain, abscess of, optic neuritis in, 18 
defects, spasms in, 15 
lesions, astereognosis in, 500 
lesions, hemianassthesia in, 501 
lesions, nystagmus in, 17 
tumor, optic neuritis in, 18 
Breast, funnel, 66 
pigeon, 60 INDEX 
517 
Breath, 23 
acetone, 23 
alcoholic, 23 
cause of foul, 23 
Breathing, amphoric, 158 
asthmatic, 157 
bronchial, 157 
bronchial or tracheal, 157 
broncho-vesicular, 157 
cavernous, 158 
Cheyne-Stokes, 76 
cog-wheel, 157 
compensatory, 159 
differences between two sides of 
chest, 158 
difficult, 72 
exaggerated vesicular, 159 
in asthma, 157 
in hysteria, 78 
interrupted, 157 
metamorphosing, 158 
normal, 71 
rapid, 74 
shallow, 77 
“sharp,” 296 
sighing, 77 
stertorous, 77 
stridulous, 77 
tubular, 157 
types of, 154 
vesicular, 156 
see also Respiration 
Bronchi, cancer of, 350 
dilatation of, see Bronchiectasis 
spasm of, 313 
Bronchial asthma, see Asthma 
breathing, see Breathing 
pneumonia, see Pneumonia 
Bronchiectasis, 315 
sputa in, 316 
Bronchitis, acute, 281 
chronic, 284 
tuberculous, acute, 308 
Bronchophony, 168 
Broncho-stenosis, 314 
Buccal cavity, see Mouth 
Bulbar paralysis, see Paralysis 
Bundle of His, 116 
Cachexia, of old age, i 
Cancer, anemia in, 472 
gastric, advanced, symptoms, 
375 
gastric, bismuth X-ray examina- 
tion in, 373 
gastric, statistics of, 375 
gastric, tumor in, 266 
metastatic, of femur, 455 
oedema of arm in, 41 
of bowel, 394 
of bronchi, 350 
of esophagus, 369 
of lip, 21 
of liver, 381 
of lung, 350 
of pancreas, jaundice in, 387 
of peritoneum, 364 
of pleural, 344 
of rectum, 436 
of sigmoid, 394 
of stomach, 375 
of tongue, 23 
of tonsil, 29 
of uterus, 441 
of vertebrae, 58 
tongue in, 24 
“ Canker sores” 21 
Cardiac compensation, see Compen- 
sation 
cycle, see Heart cycle 
disease, diuresis in, 1 
disease, sweating in, 1 
disease, weight in, 1 
disease, see also Heart 
dulness, 134 
impulse, 96 
impulse, maximum, 96 
incompetence, 195 
insufficiency, 195 
murmurs, see Murmurs 
neuroses, 277 
Cardio-spasm, 369 
Cardio-vascular disease, 204-279 
hypertensive, 268 
Casts in urine, 423 
Catarrhal pneumonia, see Pneu- 
monia 518 
INDEX 
Cavity, pulmonary, 300 
Cerebro-spinal fluid, examination of, 
5io 
Cervical rib, an accessory, 36, 40 
Charcot’s joint, atrophic arthritis in, 
486 
Chest, abnormal pulsation in, 256 
anatomy of, 62 
barrel shaped, 67 
diminished expansion of, 72 
examination of, 62 
flattening of, 69 
in adenoid disease, 66 
increased expansion of, 72 
in phthisis, 66 
inspection of, 65 
landmarks of, 63, 64 
local prominences, 70 
palpation of, 96 
percussion of, 125 
prominence of one side, 71 
rachitic, 66 
shape of, 65 
size of, 65 
tenderness in, 101 
tumor of, 71 
wall, nutrition of, 68 
Chill, cause of, 4 
true, cause of, 5 
Chilliness distinguished from chill, 5 
Chlorosis, blood in, 473 
Cholangitis, 383 
Cholecystitis, signs of, 386 
results of, 386 
Chorea, 205 
hands in, 48 
spasms in, 14 
Sydenham’s, 48, 205 
true, to differentiate, 15 
Cirrhosis of liver, see Liver 
of lung, see Pneumonia, chronic 
interstitial 
portal, jaundice in, 375 
Claudication, intermittent, 450 
Coarctation, aortic, 274 
Colic, biliary, 385 
lead, 385 
renal, 285 
Collargol radiographs in kidney dis- 
ease, 408 
Colon, palpation of fluid in, 361 
Coma, alcoholic, 507 
causes of, 507 
in Stokes-A dams syndrome, 
507 
lumbar puncture in, 511 
postepileptic, 507 
Compensation, cardiac, establishment 
and failure of, 194-202 
failing, 195 
Compression, coma in, symptoms of, 
507 
Concussion, coma in, 507 
Conjunctivitis, causes of, 15, 16 
following arsenic, 14 
following iodide of potash, 15 
with hay fever, 15 
with measles, 15 
with yellow fever, 15 
Constipation, 393 
in intestinal obstruction, 394 
tongue in, 24 
Contractures following atrophic ar- 
thritis, 487 
hemiplegic, hand in, 52 
of arm, 40 
of the interossei and lumbricales. 
claw.hand in, 52 
Cor bovinum, 249 
Cornea, 67 
Corrigan pulse, 252 
Cranium, size and shape, 6 
Crepitation, atelectatic, 284 
Cretinism, 12 
lips in, 20, 21 
teeth in, 23 
tongue in, 25 
Cyanosis, causes of, 92 
of intestinal origin, 20 
of lips, 20 
of tongue, 24 
Cyst, branchial, 35, 26 
hydatid, 381 
Cystitis, 433 
urine in, 433 INDEX 
519 
Dactylitis, syphilitic, 56 
tuberculous, 56 
Deformities, congenital, of heart, 253 
of chest, 68 
of hands, 52 
Dextrocardia, 85 
Diabetes, acetone breath in, 23 
coma in, 507 
dyspncea in, 74 
optic neuritis in, 18 
retinal hemorrhage in, 18 
Diaphragm, movements of, 71-78 
Diarrhoea, causes of, 389 
Dilatation cardiac, 182 
of aortic arch, 223 
of heart, 182, 268 
Diphtheria, tonsils in, 28 
with nasal discharge, 20 
Displacement of cardiac impulse, see 
Cardiac impulse 
Diverticulum of esophagus, 368 
Dropsy, 1, 
in cardiac disease, 197 
Ductus arteriosus, persistence of, 274 
Duodenal ulcer, 375 
Dupuytren’s contraction, 57 
Duroziez’s sign, 251 
Dyspepsia, clean tongue in, 24 
Dysphagia, 259 
Dyspncea, 75, 92 
nose in, 19 
varieties of, 73-75 
see also Breathing 
Dystrophy, muscular lordosis in, 60 
Ear, gouty tophi of, 496 
Echinococcus of pleura, 345 
Egophony, 169 
Electrical reactions, 506 
Electrocardiograms, 116-124 
Emaciation, 2 
Embolism, in mitral stenosis, 220 
Emphysema, complementary, 313 
interstitial, 312 
subcutaneous, see Interstitial 
vicarious, 313 
with asthma, 313 
Empyema, 338 
Empyema, interlobar, 338 
necessitatis, 267, 342 
tuberculous, 339 
Endocarditis, 204-238 
acute, 206 
and pericarditis, 206 
malignant, 206 
rheumatic, 205 
ulcerative, 206 
Endometritis, 442 
Eosinophilia, 473 
Epididymitis, 438 
Epigastrium, hernia in, 358 
inspection and palpation of, 358 
Epithelioma, 25 
of nose, 20, 21 
Epulis, 26 
Erysipelas, oedema of lids in, 15 
Erythromelalgia, 460 
Esbach’s test for albumin, 419 
Esophagus, cancer of, 361 
cardio-spasm with dilatation of, 
368 
dilatation of, 368 
diverticulum of, 368 
Ewald’s test meal, 369 
Exophthalmic goitre, see Graves’ 
disease 
Extrasystoles, 121 
Eyes, 15 
circles under, 15 
cedema of lids, causes of, 15 
Face, 9-14 
after vomiting, 13 
in acromegalia, 9 
in adenoids, 12 
in alcoholism, 13 
in cretinism, 12 
in Graves’ disease, 13 
in leprosy, 13 
in myxoedema, 9, 11 
in nephritis, 14 
in paralysis agitans, 12 
in phthisis, 13 
“mask-like,” 12 
oedematous, 14 
spasms of, cause of, 14 520 
INDEX 
Face, swelling of, 26 
Fallopian tubes, 443 
Faradic reaction in disease, 506 
Feces, abnormal ingredients in, 394 
blood in, 394 
color of, 394 
gall-stones in, 396 
microscopic examination of, 395 
parasites’ eggs in, diagnosis of, 
396 
parasites in, types of, 396 
pus in, 394 
Feet, hot, in myocarditis in arterio- 
sclerosis, 460 
Fever, 2 
causes of, 2, 3 
“continued,” 3 
crisis in, 3 
determination of, 3 
dilatation of pupils in, 17 
emaciation in, 2 
“intermittent,” 3 
in tonsillar abscess, 29 
lysis in, 3 
sordes in, 25 
tongue in, 24 
typhoid, see Typhoid fever 
types of, 3 
Fibrillary twitchings, 497 
Fibro-myoma of uterus, 441 
Filariasis, blood in, 479 
parasites in, 479 
Finger-ends, tender, 58 
Fingers, clubbed, 44-55 
in heart disease, 44 
in lung disease, 44 
in pleural disease, 44 
Fistulas, branchial congenital, 36 
Flipper-hand in atrophic arthritis, 
52| 
Fluid, examination of cerebro-spinal, 
5io 
free in abdomen, tests for, 354 
in pleurisy, 330 
Fontanels, 7 
bulging, 7 
delayed closure of, 7 
depressed, 7 
Forehead, bony nodes of, 9 
eruptions of, 8 
scars of, 8 
Foot, 456 
club-, varieties of, 458 
flat-, 458 
Fremitus, tactile, see Tactile fre- 
mitus 
Friction, pericardial, 238 
pleural, see Pleural 
Foramen ovale, 275 
Frontal sinusitis, 9 
Funnel breast, 67 
Gait, ataxic, 497 
in paralysis agitans, 497 
spastic, 497 
toe-drop, 497 
Gall bladder, 384 
bladder, enlarged, 385 
bladder, incidence of diseases of, 
377 
-stones in feces, 395 
Galvanic reaction in disease, 506 
Gangrene, local, in Raynaud’s disease, 
57 
of lung, 349 
of mouth, 27 
of toes, 460 
Gas, poisoning by, coma in, 507 
Gastric cancer, see Cancer 
contents, see Stomach contents 
crises, 385 
diseases, incidence and diagnosis 
of, 375 
fermentation, breath in, 23 
fermentation, tongue in, 24 
peristalsis, 266) 
stasis, 376 
ulcer, 375 
ulcer, malnutrition in, 3 
ulcer, toungue in, 24 
Genitals female inspection of, 440 
female, lesions of, 440 
female, palpation of, 440 
male, 437 
Gland, atrophy of thyroid, 34 
cancer of thyroid, 34 INDEX 
521 
Gland, cervical, in malignant disease, 32 
cervical, in syphilis, 31 
cervical, in tuberculosis, 31 
enlarged, causes of, 31 
in cancer, 31 
in German measles, 31 
inguinal, in syphilis, 446 
in Hodgkin’s disease, 31 
in lymphatic leukaemia, 31 
in mumps, 31 
in tonsillitis, 31 
sarcoma of, 31, 32 
see also Adenitis 
Glanders, 60 
Glottis, obstruction of, 74 
Glucosuria, 421 
experimental, 422 
permanent, 422 
Goitre, exophthalmic, see Grave’s dis- 
ease 
simple, 33 
with exophthalmus, 13 
Gold test, 510 
Gonorrhoea, arthritis in, 485 
balanitis in, 438 
distended bladder in spasm of 
urethra in, 431 
inguinal glands in, 446 
orchitis in, 438 
with epididvmitis. 428 
Gout, toes in, 460 
tophi in arm, 42 
tophi in ear, 496 
tophi in joints, 496 
Gouty arthritis, 496 
arthritis, destruction of bone in, 
496 
arthritis, X-ray of hand in, 496 
Graves’ disease, 13, 33, 46, 272 
disease, capillary pulsation in, 91 
disease, expression in, 13 
disease, hands in, 46 
disease, heart sounds in, 197, 
Groin, 446 
glands in, 446 
hernia in, 446 
psoas abscess in, 447 
Guaiac test stomach contents, 372 
Gumboil, 26 
Gums, 25 
bismuth line in, 25 
bleeding, 26 
in lead poisoning, 25 
in poisoning by mercury, 25 
in poisoning by potassic iodide, 
25 
in scurvy, 26 
sordes of, 25 
spongy, 26 
suppuration of, 26 
Giinzburg’s reagent, 372 
in portal obstruction, 
381 
Hasmaturia, 417 
Haemoglobin, tests for, 462 
Haemopericardium, 241 
Haemophilia, nosebleed in, 19 
Haemophilic arthritis, 496 
Haemoptysis, 295 
causes of, in mitral stenosis, 215 
Hair, abnormal loss of, 8 
in myxcedema, 9 
in rachitis, 7 
in syphilis, 8 
parasites in, 8 
Hands, 44 
choreiform movements of, 48 
deformities of, 52 
evidence of occupation, 44 
examination of, 44 
in alcoholism, 45 
in atrophic arthritis, 54 
in cardiac weakness, 45 
in carphologia, 45 
in contractures following hemi- 
plegia, 52 
in Graves’ disease, 45 
in Jacksonian epilepsy, 47 
in myxoedema, 52 
in paralysis of median or ulnar 
nerves, 52 
in progressive muscular atrophy, 
52 
moisture of, 45 
spasms of, 48 522 
INDEX 
Hands, temperature of, 45 
tremor of, 45 
Handwriting, degeneration of, 306 
Hang-nails, 57 
Hare-lip, 22 
Harrison’s groove, 66 
Hay fever with conjunctivitis, 15 
Head, abnormalities of, 6 
open areas of, 6 
shaking of, 14 
Heart, see also Cardiac, Murmurs. 
Regurgitation, Stenosis. 
Breathing. 
hypertensive diseases of, 268 
“athlete’s,” 278 
auscultation of, 171-193 
block, 116 
cycle, systole and diastole, 184 
dilatation of, 196 
disease, classification of, 204 
disease, congenital, 273 
disease, nephritic, 272 
disease, rheumatic, 204 
disease, syphilitic, 248 
goitre, 272 
hypertrophy and dilatation of, 196 
irregular action of, 116-125 
253 
murmurs, see Murmurs 
percussion of, 134 
rapid, see Tachycardia 
situation of apex impulse, 96 
slow, see Bradycardia 
“valve areas,” 64 
valvular lesions of, 204 
Heberden’s nodes, 55, 488 
Hemianaesthesia, 500 
Hemiplegia, 497 
Hemorrhage, anemia in, 472 
in retina, 18 
pulmonary, 295 
Hepatic abscess, sy imptomsn, 378 
Hernia, epigastric, 358 
of intestine, 326 
of scrotum, 439 
umbilical, 358 
Herpes labialis, 21, 507 
zoster, 507 
Hip-joint, hypertrophic arthritis morbus 
coxae senilis, 491 
limitation of motion of, 482 
psoas-spasm of, 48; 
Hodgkin’s disease, 350, 404 
disease, glands in, 31, 94 
disease, oedema of arm in, 41 
Hook-worm, 398 
Housemaid’s knee, 352 
Hydatid disease, liver in, 381 
Hydrocele, 439 
of scrotum, 426 
Hydrocephalus, head in, 6 
Hydronephrosis, 409 
Hydropericardium, 240 
Hydrothorax, 322 
Hyperacidity, gastric, 376 
Hyperaesthesia, tests, of, 500 
Hyperchlorhydria, pain in, 385 
Hypernephroma, 409 
Hyperresonance, 305 
Hypertension, vascular, hi, 268 
nosebleed in, 19 
See also Pressure, blood 
Hypertrophic arthritis, see Arthritis 
Hypertrophy, cardiac impulse in, 84, 
86 
cardiac, causes of, 197 
cardiac, results, 197 
Hypertrophy of left ventricle, 201 
of right ventricle, 202 
Hypostatic pneumonia, 353 
Hypotonus, 505 
Hysteria, anaesthesia in, 500 
atrophy in, 40 
breathing in, 78 ' 
coma in, 507 
contractures of arm in, 40 
hemianaesthesia in, 500 
hyperaesthesia in, 500 
paralysis in, 437, 498 
ptosis in, 17 
spasms in, 15 
temperature in, 3 
Idiocy, mouth in, 19 
Infections, 195, 205, 248 
acute chills in, 4 INDEX 
523 
Infections, leucocytosis in, 473 
lymphocytosis in, 473 
pulse in, 106 
Inspection in aneurism, 256 
in aortic regurgitation, 222 
in croupous pneumonia, 285 
of abnormal thoracic pulsations, 
66 
of apex beat, 81 
of cardiac movements, 81 
deformities of chest, 68 
of head and face, 6 
of peripheral vessels, 88 
of respiratory movements, 72 
of skin and mucous membranes, 
92 
of thorax, 66 
Insufficiency, aortic, 222 
Interlobar empyema, see Empyema 
Intestinal colic, 411 
contents, examination of, 396 
obstruction, acute and chronic, 
393 
obstruction by gall-stones, 394 
obstruction, causes of, 393 
obstruction, physical signs in, 
393 
parasites, 396 
parasites, diagnosis of eggs of, 
398 
parasites, eosinophilia due to, 
473 
parasites, relative frequency of, 
400 
Intestines diseases of, 389 
diseases of, constitutional mani- 
festations, 389 
gaseous distention in, 389 
Iritis with irregular outline of pupil, 
17 
Itching in jaundice, 16 
Jacksonian epilepsy, 47 
epilepsy, spasms of hand, causes, 
47 
Jaundice, 
catarrhal, 382 
causes of, 382 
Jaundice, congenital, 383 
diagnosis of cause, 383 
mental depression in, 16 
of tongue, 24 
slow pulse in, 16 
with toxaemia, 382 
Jaw, in acromegalia, 9 
-jerk, test for, 505 
Joints, ankylosis of, 484 
chronic diseases of, knee-jerks in, 
501 
creaking in, 480 
diseases of, 480 
enlarged, 480 
examination of, 480 
excessive motion in, 480 
fluctuation in, 480 
free bodies in, 480 
gouty deposits in, 496 
inspection of, 480 
lesions of, relative frequency of, 496 
neuropathic, 488 
pain in, 480 
sacro-iliac, hypertrophic arthritis 
of, 58 
sacro-iliac, tuberculosis of, 58 
tests of limitation of motion, 480 
see also Arthritis, Hip-joint 
Keratitis, syphilitic, cornea in, 17 
Kernig’s sign, 505 
Kidney, abscess of, 410 
cyst of, 409 
diseases of, 405 
diseases, urine in, 413 
displaced, movable, 411 
malignant disease of, 409 
see also Renal 
Knee, tuberculosis of, distinguished 
from sarcoma, 451 
-jerk, 501 
-jerk, absence of, 502 
-jerk, increased, 502 
Koplik’s spots in measles, 26 
Kyphosis, 59 
in Paget’s disease, 59 
in Pott’s disease, 59 
in rickets, 59 524 
INDEX 
Lactic acid in gastric contents, 369 
Lavage of stomach, 367 
Lead colic, pain in, 385 
line, 25 
poisoning, see Plumbism 
Legs, bowed, 452 
chronic ulcers of, 453 
in spastic paraplegia, 452 
oedema of, causes of, 455 
osteomyelitis in, 455 
paralysis of, causes of, 452 
paralysis of, differential diagnosis 
in, 452 
syphilitic periostitis of, 453 
tenderness, in trichiniasis, 456 
varicose veins of, 452 
Leprosy, 57 
face in, 13 
Leucocyte chart, 470 
count, 470 
Leucocytosis, 473 
diagnostic value of, 468 
Leukasmia, 476 
lymphatic, blood in, 476 
myelogenous, blood in, 476 
spleen in, 404 
Line, mid-axillary, 63 
Lips, 20 
angioneurotic oedema of, 21, 22 
cancer of, 21 
chancre of, 21 
cracks or fissures in, 20 
in cretinism, 20, 22 
in heart disease, 20 
in myxoedema, 20, 22 
pallor of, 20 
parted, 20 
Litten’s sign, 77 
Liver, 377 
abscess of, 378 
abscess of, distinguished from 
syphilis or malignant dis- 
ease, 378 
acute yellow atrophy of, 381 
amyloid, 381 
atrophy of, 381 
cancer of, 372, 378 
cirrhosis of, 378 
Liver, disease, incidence of, 377 
disease, portal obstruction in, 
381 
enlargement, 378 
enlargement, causes of, 379 
hydatid disease of, 380 
leukaemic, 378 
syphilis of, distinguished from 
cirrhosis or malignant dis- 
ease, 378 
see also Gall bladder, Jaundice 
Lordosis, 60 
in muscular dystrophy, 60 
in tuberculosis, 60 
with abdominal tumors, 60 
with pregnancy, 60 
Lumbago, 58 
Lumbar puncture, 510 
Lung, abscess of, 315 
adhesions of, 192 
adventitious sounds, see Rales 
anatomy of, 62 
atelectasis of, 343 
cancer of, 350 
cirrhosis of, 305 
collapse of, see Atelectasis 
congestion of, see (Edema 
consolidation of, see Solidification 
fibroid disease of, 305 
gangrene of, 345 
hilus tuberculosis, 304 
malignant disease of, 350 
miliary tuberculosis of, 305 
oedema of, 284 
phthisis, 295; see also Tuberculosis 
of the lungs 
pneumonia, 285 
retraction of, 86 
syphilis of, 314 
tuberculosis of, 295 
Lymphatic leukaemia, blood in, 
476 
leukaemia, glands in, 32 
Lymphocytosis, 473 
in inflammations of spinal canal, 
511 
Malaria, chills in, 4 INDEX 
525 
Malaria, jaundice in, 16, 382 
parasites in, 478 
splenic, enlargement in, 403 
Malignant disease, anemia in, 472 
disease, glands in, 32 
disease, toxemia in, 474 
disease, see also Cancer, Epithe- 
lioma, Sarcoma, Myelomata 
Malnutrition, 3 
emaciation in, 3 
in anorexia nervosa, 3 
in chronic diarrhoea, 3 
in chronic dyspepsia, 3 
in diabetes, 3 
in gastric cancer, 3 
in gastric dilatation, 3 
in gastric ulcer, 3 
in infantile atrophies, 3 
in oesophageal stricture, 3 
Massage, leucocytosis in, 473 
Measles, conjunctivitis in, 14, 15 
German, glands in, 33 
Koplik’s spots in, 26 
mouth eruption in, 26 
oedema of face in, n, 15 
Mediastinitis, chronic, 245 
Mediastino-pericarditis, 245 
Mediastinum, cysts of, 350 
neoplasms of, 343, 350 
sarcoma of, 350 
Melasna, 395 
Meningitis, bulging of fontanels in, 7 
cytodiagnosis in, 347 
lumbar puncture in, 511 
tuberculous, optic neuritis in, 
18 
Mensuration, 62 
Mental depression in jaundice, 16 
Meralgia paraesthetica, 447 
Mesentery, enlarged glands of, 365 
thrombosis of, 365 
Metallic tinkle, 170 
Metatarsalgia, 460 
Methaemoglobinaemia, lips in, 20 
Microcephalia, 7 
Migraine, aphasia in, 507 
Mitral disease, 207 
stenosis, see Stenosis, mitral 
Monoplegia, 498 
Morbus coxae senilis, 491 
Morvan’s disease, 57 
Motion, disorders of, 497 
Mouth, eruptions of, 26 
fissures of, 20 
gangrene of, 27 
herpes of, 21 
in Addison’s disease, 27 
in adenoids, 20 
in cretinism, 20, 21 
in dyspnoea, 20 
in idiocy, 20 
mucous patches in, 26 
pigmentations of, 27 
syphilitic ulcers of, 21 
Movements, respiratory, 72 
Mucus in feces, 397 
Multiple sclerosis, 499 
sclerosis, knee-jerk in, 500 
sclerosis, nystagmus in, 17 
sclerosis, spastic gait in, 46 
sclerosis, speech in, 46 
sclerosis, tremor in, 46 
Mumps, glands in, 32 
orchitis in, 438 
Murmurs, areas of propagation, 185 
arterial, 193 
cardiac, 182 
cardio-respiratory, 192 
diastolic, 222, 249 
disappearance of, 190 
functional, 190 
haemic, see Functional 
in aortic aneurism, 260 
in mitral stenosis, 214 
localization of, 185 
metamorphosis of, 190 
mode of production, 182 
musical, 188 
organic, 190 
presystolic, 214 
quality of, 188 
relation to normal sounds, 188 
significance of, 188 
terminology of, 182 
time of, 184 
transmission of, 185 526 
INDEX 
Murmurs, venous, 193 
Muscle sounds, 150 
Muscular dystrophy, lordosis in, 
16 
Myelitis, acute, bedsores in, 507 
knee-jerks in, 502 
reaction of degeneration in, 
506 
sexual power in, 505 
transverse or diffuse, paraplegia 
in, 45i 
Myelomata of skull, 6, 7 
Myocardial weakness, 268 
Myocarditis, 275 
acute, 275 
Myoma of uterus, 442 
Myxoedema, 9, 12 
face in, 9, 12 
hands in, 52 
increase in weight in, 1 
infantile form, 12 
lips in, 20, 22 
loss of hair in, 8 
nose in, 18 
tongue in,25 
Nails, 57 
capillary pulse, 92 
changes, in hemiplegia, 57 
changes, in myxoedema, 57 
changes, in neuritis, 57 
changes, in syringomyelia, 57 
grooved, 57 
in anemia, 58 
incurvation of, 58 
indolent sores around, 57 
Neck, 30 
abscess in, 33 
actinomycosis of, 36 
diseases of, 30 
in paralysis agitans, 12 
oedema of, 37 
scars of, 33 
Nephritic heart disease, 272 
Nephritis, 272, 428 
acute, 419 1 
acute, urine in, 429 
albuminuria in, 430 
Nephritis, chronic glomerular, urine in, 
429 
coma in, 507 
face in, 14 
heart sounds in, 178 
oedema of legs in, 454 
oedema of lids in, 15 
retinal hemorrhage in, 18 
Nervous system, 497 
Nervousness, cardiac symptoms of, 277 
Neuralgia, intercostal, 78 
Neuritis after anaesthesia, 38 
alcoholic, 39 
atrophy of arm in, 40 
due to pressure, 38 
lead, 39 
multiple, 40 
oedema of legs in, 452 
obstetrical, paralysis in, 39 
optic, 18 
paralysis of arm in, 38 
paralysis of leg in, 452 
peripheral, knee-jerk in, 501 
postdiphtheritic, pharyngeal re- 
flexes in, 36 
pressure, test for, 38 
toxic, paralysis in, 39 
Nodes, Heber den’s, 55 
in back, 60 
in gouty arthritis, 496 
on forehead, 9 
syphilitic, 41 
Noma, 27 
Normoblasts in blood, 467 
Nose, 18 
discharge from, 19 
epithelioma of, 20 
falling in of bridge of, 19 
hemorrhage of mucous mem- 
branes, 19 
in acne rosacea, 19 
in acromegalia, 18 
in adenoid growths, 19 
in alcoholism, 19 
in lupus erythematosus, 19 
in myxoedema, 18 
in syphilis, 19 
in tuberculosis, 20 INDEX 
527 
Nose, local disease of, 20 
size and shape of, 18 
Nosebleed, 19 
Nostrils, 19 
Nystagmus, 17 
Obesity, i 
Obstruction, intestinal, see Intestinal 
laryngeal, 78 
portal, 381 
Ocular motions, 17 
CEdema, 195 
angioneurotic, 15 
angioneurotic of lips, 21 
in anaemia, 455 
in deficient local circulation, 456 
in flat-foot, 456 
in heart disease, 198 
in hemiplegia, 456 
in inflammation, 456 
in nephritis, 456 
in neuritis, 456 
in obesity, 456 
in pressure, 456 
in thrombosis, 456 
in varicose veins, 441 
of arm, 41 
of eyelids, causes of, 15 
of face, 14 
of legs, causes of, 456 
of lungs, 284 
of neck, 37 
Oliguria, 413 
Opium-poisoning, coma in, 507 
-poisoning, shaking of head in, 14 
Oppenheim’s sign, 501 
Optic atrophy, 18 
Orchitis acute, 438 
Osteitis deformans, 6 
Osteoarthritis, 490 
Osteo-arthropathy, 44, 53, 
arm in, 44 
Osteoma or exostosis of thigh, 447 
Osteomyelitis, acute, septic, 447 
chronic, tuberculous, 447 
Ovarian disease, diagnosis of, 443 
Ovaries, cyst of, with twisted pedicle, 
443 
Ovaries, tumors of, 443 
Ovaritis, 443 
Oxyuris vermicularis, 396 
“Pace-maker,” 116 
Paget’s disease, 6, 60, 450 
disease, arm in, 43 
Pain, hepatic, 378 
in appendicitis, 391 
in intestinal disease, 391 
in joints, 482 
in sacro-iliac joint, 58 
in tonsillar abscess, 29 
nerve, in hypertrophic arthritis, 
493 
over sternum, 278 
precordial, 199 
Palate, perforation of soft, 30 
Pallor, 93 
causes of, 93 
in phthisis, 13 
Palpation, 96 
and friction, 100 
Palpitation of heart, 279 
Pancarditis, rheumatic, of children, 
206 
Pancreas, cancer of, diagnosis of, 386 
cyst of, 386 
diseases of, 386 
diseases of, diabetes in, 387 
diseases of, incidence of, 387 
diseases of, stools in, 386 
diseases of, urine in, 386 
Parsesthesia, 500 
in neuritis, 39 
Paralysis agitans, 12, 46 
agitans, gait in, 498 
agitans, shaking head in, 14 
bulbar, 24 
cerebral, knee-jerk in, 501 
congenital, choreiform move- 
ments in, 51 
facial, tongue in, 24 
in acute anterior poliomyelitis, 
38, 451 
in chorea, 451 
in diseases of spinal cord, 451 
infantile cerebral, athetosis in. 51 528 
INDEX 
Paralysis in hemiplegia, 50, 451 
in hysteria, 40, 451 
in lead-poisoning, 38, 451 
in myelitis, 451 
in neuritis, 38, 451 
in tabes, 451 
in toxic neuritis, 451 
in traumatic neurosis, 40 
of arm, 38 
of brain, 497 
of cord, 497 
of cranial nerve, 497 
of dorsal or abdominal muscles, 
60 
of legs, 451 
of interossei and lumbricales, 
claw-hand in, 52 
of muscles of respiration, 160 
of peripheral nerve, 497 
pharyngeal reflexes in, 30 
pupils in, 17 
serratus, scapula in, 61 
with contraction of pupil, 16 
Paraphimosis, 438 
Paraplegia, 497 
paralysis of leg in, 497 
spastic, 497 
Parasites, animal, diseases due to, 473 
in feces, 396 
in hair, 8 
intestinal, eggs of, 398 
malarial, 478 
Paravertebral triangle, 333 
Paresis, 497 
lumbar puncture in, 510 
Paronychia, 57 
Parotid gland, cancer of, 32 
gland, enlargement of, 32 
Patent ductus arteriosus, 274 
Pectus carinatum, 66 
Pediculi in hair, 8 
Penis, 438 
cancer of, 439 
chancre of, 438 
chancroid of, 439 
discharge from, 438 
inflammation of glands of, 439 
malformations of, 439 
Peptic ulcer, 375 
Percussion, auscultatory, 132 
dull areas in, 133 
force of, 128 
note, modifications of, 133 
resonance, amphoric, 139 
resonance, cracked-pot, 139 
resonance, dull, 133 
resonance of chest, 133 
resonance, tympanitic, 136 
resonance, varieties of, 133 
technique of, 125 
Peribronchitis, tuberculous, acute, 
304 
Pericardial friction, see Pericarditis 
Pericarditis, 238 
acute, 238 
dry, 238 
effusion, 240 
effusion, distinguished from pleu- 
ritic, 244 
fibrinous, 238 
friction in, 238 
distinguished from hypertrophy 
and dilatation of heart, 244 
Pericardium adherent, 245 
diseases of, 238 
Perihepatitis, 378 
Perinephritic abscess, 410 
Perineum, ruptured, 441 
Periostitis, syphilitic, 454 
Peripheral nerve lesions, hemianass- 
thesia in, 500 
nerve lesions, hyperassthesia in, 
500 
neuritis, reaction of degenera- 
tion in, 506 
Peristalsis, visible gastric, 366 
visible, in intestinal obstructions 
393 
Peritoneum, cancer of, 364 
diseases of, 362 
tuberculosis of, 364 
Peritonitis, causes of, 363 
general, 363 
local, 362 
respiratory movements of belly 
in, 355 INDEX 
529 
Peritonitis, with thickening or inflam- 
mation of navel, 359 
Peri-urethral abscess, 438 
Pernicious anemia, see Anemia 
Pharyngeal reflexes in alcoholism, 30 
reflexes in paralysis, 30 
reflexes in postdiphtheritic neuri- 
tis, 30 
Pharyngitis, 28 
Pharynx, 28 
eruptions of, 28 
examination of, 28 
Phenolsulphonephthalein test for 
renal function, 418 
Phimosis, 438 
Phlebitis, 450 
Phlebograms, 116 
Photophobia, 17 
Phrenic wave, 77 
Phthisis, 295 
advanced, 300 
chest in, 66, 68 
cracked-pot resonance in, 139 
face in, 13 
fibroid, 305 
fibroid with pleural thickening, 
306 
hilus, 304 
pupils in, 17 
sweating in, 5 
with pleural thickening, 306 
see also Tuberculosis of lung 
Pigmentation in Addison’s disease, 27 
in negroes, 27 
Pin-worm, in feces, 396 
Pleura, actinomycosis of, 345 
cancer of, 344 
diseases of, 322 
echinococcus of, 345 
Pleural adhesions, 78 
effusion, 330 
effusion, cytodiagnosis in, 345 
effusion, distinguished from peri- 
cardial, 244 
effusion, distinguished from pneu- 
monia, 342 
effusion, encapsulated, 341 
fluid, examination of, 345 
Pleural friction, 328 
thickening, 339 
Pleurisy, 328 
auscultatory signs in, 335 
breathing in, 78 
clubbed fingers with, 54 
dry, 328 
Grocco’s sign in, 333 
pulsating, 342 
Plumbism, 40 
anemia in, 472 
lead line in, 25 
paralysis in, 38, 449 
Pneumonia, 285 
aspiration, 292 
broncho-pneumonia, chronic, 292 
chronic interstitial, 315 
complications of, 290 
croupous (or lobar), 284 
distinguished from tuberculosis, 
290 
hypostatic, 353 
inhalation, 292 
lobar, 285 
lumbar puncture in, 510 
nostrils in, 19 
tuberculous, 308 
wandering, 290 
Pneumohydrothorax, 324 
Pneumopyothorax, 324 
Pneumoserothorax, 324 
Pneumothorax, 322 
Poisoning by gas, coma in, 507 
by illuminating gas, breath in, 23 
by mercury, gums in, 24 
by potassic iodide, gums in, 26 
lead, see Plumbism 
silver nitrate, 16 
opium, coma in, 507 
Poliomyelitis, (acute) anterior, 37 
reaction of degeneration in, 40 
atrophy in, 40 
chronic, hands in, 52 
Polynuclear cells in blood, 466 
Polyuria, 413 
Portal cirrhosis, jaundice in, 381 
obstruction, causes of, 381 
stasis, ascites in, 381 530 
INDEX 
Postepileptic coma, 507 
Pregnancy, choreiform movements in. 
48, 51 
glucosuria in, 421 
lordosis in, 60 
spasm in, 14 
tubal, 443 
Pressure, arterial, 109 
arterial, methods of measuring, 109 
blood-, 109, see also Hypertension 
by pericardial exudation, 243 
in aneurism, 259 
diastolic, 112 
high systolic blood-, 109 
normal blood-, 109 
systolic, 109 
Presystolic murmur, see Murmurs 
Procidentia, 441 
Progressive muscular atrophy, fibril- 
lary twitchings in, 499 
muscular atrophy, reaction of 
degeneration in, 506 
Prostate, hypertrophy of, distended 
bladder in, 435 
Prostatitis, acute retention of urine 
in, 435 
Psoas abscess, 446 
Psychic functions, examinations of, 
507 
Ptosis, 17 
Pulmonary abscess, 349 
Pulmonary disease, see Lung 
hemorrhage, 317 
regurgitation, 234 
osteoarthropathy, 43, 48 
stenosis, see Stenosis 
tuberculosis, see Tuberculosis of- 
lung 
Pulmonic area, 171 
second sound, 175 
sound in mitral stenosis, 219 
Pulsation, capillary, 237, 250 
Pulse, 96 
alternating, 123 
bigeminal, 123 
capillary, 250 
compressibility of, see Arterial 
pressure 
Pulse, Corrigan, 105 
coupling of, 123 
in aortic stenosis, 230 
in misplaced artery, 107 
in mitral stenosis, 217 
irregular, 116-125 
method of feeling, 104 
paradoxical, 243 
rapid (tachycardia), 277 
rhythm or regularity, 116 
slow (bradycardia), 279 
tension, 106 
value of, 102 
value of tracings, 116 
waterhammer, 251 
wave, dicrotic, 105 
wave recording of, 116 
wave, size and shape of, 105 
see also Arrhythmia, Artery walls, 
Pressure, arterial 
Pulsus celer, 251 
rarus, parvus, tardus, 227 
Pupil, 16 
Argyll-Robertson, 17 
contraction of, 17 
dilatation of, 17 
reflexes, 16 
value of, in diagnosis, 16 
Purpura, nosebleed in, 19 
Pus in feces, 394 
in kidney, 416 
in urine, 416 
tube, cause of peritonitis, 363 
Pyelitis, urine in, 430 
Pylephlebitis, 381 
Pyonephrosis, 410 
Pyorrhoea alveolaris, 26 
Pyuria, 416 
vesical, 417 
Quinsy, sore throat, 29 
Rachitic rosary, 66 
Rachitis, 59, 65 
arm in, 43 
epiphyses in, 43 
hair in, 7 
head in, 6 
teeth in, 23 INDEX 
531 
Radioscopy, 36, 62, 262, 264 
examination in spinal tuberuc- 
losis, 486 
examination of stomach, bismuth, 
372 
in aneurism, 261 
in bismuth X-ray examination 
of stomach, 372 
in diaphragmatic movements, 
78 
in interlobar empyema, 338 
of joints, 480 
Rales, 163, 165 
Raynaud’s disease, 56 
Reaction of degeneration, 506 
Rectum, cancer of, 435 
fissure of, 435 
fistula of, 435 
hemorrhoids of, 435 
methods of examination, 435 
symptoms which suggest exami- 
nation, 435 
Red test for renal function, 418 
Reflex Achilles, 501 
Babinski, 502 
Reflexes, 501 
deep, 501 
of pupil, 16, 501 
pharyngeal, 30 
pharyngeal, in post-diphtheritic 
neuritis, 30 
sexual, 505 
sphincteric, 505 
superficial, 488, 504 
tendon, 501 
Regurgitation, 222 
aortic, 248 
Renal calculus, 41 x 
disease, diuresis in, 1 
disease, sweating in, 1 
pyuria, 416 
suppuration, 416 
tuberculosis, 417 
tumor, 417 
see also Kidney 
Resonance, see Percussion resonance, 
hyper-, 394 
Respiration, see Breathing, 71 
Retina, 18 
hemorrhage of, 18 
see also Neuritis, optic, and 
Atrophy, optic 
Retraction of thorax, 72, 73 
systolic, 245 
Retropharyngeal abscess, 29 
Rheumatism, 204 
Rheumatoid arthritis, 488 
Rhythm, disturbances of, 116, 125 
Rib, cervical, 37, 40 
Rickets, see Rachitis 
Romberg’s sign, 501 
Rosary, rachitic, 66 
Round-worm in feces, 396 
Sacro-iliac joint, see Hip-joint, 59 
Sahli’s test for haemoglobin, 462 
Salpingitis, 443 
Sarcoma, glands in, 32 
of abdominal wall, 359 
of arm, 41 
of legs, 455 
of lung, oedema of arm in, 41 
of mediastinum, 350 
of mediastinum, oedema of arm 
in, 41 
of scapula, 60 
of testis, 438 
of thigh, 447 
of tonsil, 29 
Scapula, prominent, 60 
sarcoma of, 60 
Scarlet fever, pharynx in, 28 
fever, tonsils in, 28 
Scars, 94 
from syphilitic ulcers on leg, 
45i 
of forehead, 8 
Sciatica, 59 
Sclerosis, multiple, nystagmus in, 17 
multiple, paraplegia in, 451 
Scoliosis with twisting of spine, 60 
Scrotum, hernia of, 438 
hydrocele of, 438 
“Scurvy” in gums, 26 
Senility, tremor of hands in, 46 
Sensation, delayed, 500 532 
INDEX 
Sensation, disorders of, 500 
dissociation of, 500 
Sepsis, leucocytosis in, 473 
lymphocytosis in, 473 
Septum, defects in, 275 
Serratus paralysis, scapula in, 61 
Sexual power, 506 
Sigmoid, cancer of, 394 
Silver nitrate poisoning, 16 
Situs inversus, 84 
Skin diseases, chronic, blood in, 473 
in leprosy, 13 
in myxcedema, 9 
in phthisis, 13 
inspection of, 91 
lesions of, trophic, in atrophic 
arthritis, 489 
Skull, enlargement of, 6 
Sleep, loss of, 3 
Small-pox, eruptions on forehead in, 7 
throat in, 28 
Snuffles, syphilitic, 19 
Sordes, 25 
Sound, falling drop, 170 
lung-fistula, 170 
splashing, 169 
succussion, 169 
see also Heart sounds 
Spade-hand, 92 
Spasm, cardio-, 368 
psoas, 58 
psoas, in appendicitis, 392 
clonic, 499 
habit, 15, 48 
Spasms, in chorea, 14 
in hereditary brain defects, 15 
in hysterical conditions, 15 
in torticollis, 34 
of bronchi, 313 
of face, causes of, 14 
of glottis, 77 
of hands, 48 
of hip, 482 
tonic, 499 
Speech, loss of, 506 
Sphincteric reflexes, 505 
Sphygmograph, 116 
Sphygmomanometer, 109 
Spina bifidia, 61 
Spinal cord, paralysis of arms in diseases 
of, 40 
curvature, 35, 59 
curvature, cardiac impulse in, 84 
myosis, 17 
twisting, 69 
Spine, chronic diseases of, sphincteric 
reflexes in, 505 
hypertrophic arthritis, 490 
tuberculosis of, 59 
Spirometer, 79 
Spleen, abscess of, 403 
diseases of, 403 
enlarged, distinguished from 
tumors, 403 
enlarged, types of, 403 
Spondylitis deformans, 491 
Sputa, artificially obtained, 296 
appearance of, 317 
bloody, 317 
examination of, 317 
staining of, 318 
obtained from children, 317 
odor of, 317 
origin of, 317 
pneumonic, 318 
qualities of, 318 
quantity of, 317 
Squint, 17 
Starvation, acetone breath in, 23 
intestinal distention in, 389 
Statistics on bladder, 431 
on gall-bladder and bile-ducts, 
384 
on diseases of the intestine, 389 
on diseases of liver, 377 
on gastric diseases, 366 
on joint lesions, 496 
on kidney, 405 
on pancreatic disease, 386 
Stenosis, aortic, 225 
mitral, 214 
of a bronchus, 314 
pulmonary, 234, 273 
tricuspid, 234 
Stethoscope, selection of, 143 
use of, 147 INDEX 
533 
Stokes-Adams syndrome, 116 
syndrome, coma in, 507 
Stomach, bismuth X-ray examina- 
tion of, 373 
cancer of, 375 
cancer of, glands in, 32 
contents, acetic acid in, 372 
contents, acidity of, 372 
contents, blood in, 372 
contents, examination of, 372 
contents, free hydrochloric acid 
in, tests for, 372 
contents, in hyperacidity, 372 
contents, in stasis, 372 
contents, lactic acid in, 372 
contents, mucus in, 369 
dilatation of, 369 
hypoacidity, 372 
inspection and palpation, 366 
lavage of, 367 
methods of examination, 366 
tube, passing of, 367 
washing of, method, 367 
see also Gastric 
Stomatitis, breath in, 23 
gangrenous, 27 
herpetic, 21 
Stools in jaundice, 16, 382 
in pancreatic disease, 387 
Strabismus, 17 
in meningitis, 17 
in syphilis, 17 
in tumors, 17 
Stridor, 260 
Subphrenic abscess, 364 
Succussion, 169 
Sugar, see Glucosuria 
Sunstroke, 3, 509 
Suppurations, chronic, anemia in, 472 
of gums, 26 
renal, 416 
Sweating in jaundice, 16 
in phthisis, 5 
night and day, causes of, 5 
Syncope, 507 
local, in Raynaud’s disease, 57 
Syphilis, 248 , 
breath in, 23 
Syphilis, chancre of penis in, 437 
(congenital), teeth in, 23 
cornea in, 17 
coryza in, 19 
dactylitis in, 56 
enlarged glands in, 94 
eruptions on forehead in, 8 
glands of neck in, 31 
hereditary, delayed closure of 
fontanels in, 7 
inguinal glands in, 446 
keratitis in, 17 
lip chancre, 21 
lip scars in, 20 
loss of hair in, 8 
lumbar puncture in, 510 
mucous patches in, 20, 26 
nose in, 19 
of lung, 314 
orchitis in, 438 
palate in, 30 
ptosis in, 17 
strabismus in, 17 
teeth in, 23 
tongue in, 24 
ulcerations of tonsils in, 28, 29 
Wassermann reaction in, 478 
Syphilitic aortitis, 248-268 
aortitis, with aneurism, 256 
heart disease, 248 
liver, 381 
periostitis, 453 
Syringomyelia, changes of nails in, 
5i 
claw-hand in, 52 
felons in, 57 
Morvan’s disease in, 57 
with atrophic arthritis, 488 
Systolic murmur, see Murmurs 
Tabes dorsalis, ataxia in, 499 
dorsalis, hypotonus in, 504 
dorsalis, knee-jerk in, 502 
dorsalis, lumbar puncture in, 510 
dorsalis, optic atrophy, 18 
dorsalis, parsesthesia in, 501 
dorsalis, paraplegia in, 451 
reaction of pupil in, 17 534 
INDEX 
Tables dorsalis, Romberg’s'sign, 500,520 
dorsalis, sexual power in, 505 
dorsalis, sphincteric reflexes in, 
505 
dorsalis, ulcer of toe in, 461 
dorsalis with atrophic arthritis, 
488 
Tachycardia, 276 
paroxysmal, 120 
Tactile fremitus, 98 
Taenia nana, 396 
saginata, 396 
solium, 396 
Tallqvist’s test for haemoglobin, 20, 
462 
Tape-worm in feces, 396 
Teeth, 22 
carious, 26 
grinding of, 23 
in congenital syphilis, 23 
in cretinism, 23 
in rickets, 23 
order of appearance, 22 
second, 22 
Temperature, 2 
in hysterical patients, 2 
method of taking, 2 
significance of, 2 
sub-normal, 3 
Tenderness in general peritonitis, 362 
in intestinal diseases, 362 
Tenosynovitis, 44 
of Achilles tendon, 458 
Tension of pulse, 106 
Test, Lange colloidal gold, 510 
“red” (phenolsulphoneph- 
thalein), 418 
tuberculin, 25, 42, 59 
Wassermann, 478 
Widal, 477 
Testes, 438 
absence of one or both, 439 
cancer of, 439 
haematocele of, 439 
sarcoma of, 437 
Tetany, spasm in, 51 
Thigh, 447 
cancer of, metastatic, 448 
Thigh, diseases of, statistics on, 447 
intermittent claudication of, 447 
meralgia, paraesthesia of, 447 
osteoma t>r exostosis of, 447 
sarcoma of, 447 
tumors of, statistics, 447 
Thoma-Zeiss blood counter, 468 
Thoracic aneurism, see Aneurism 
deformities, 68-71 
Thorax, paralytic, 66 
tender points on, 100 
Thrill, 97, 256 
in aneurism, 257 
in aortic stenosis, 228 
in mitral stenosis, 220 
in patent ductus arteriosus, 274 
in pulmonary stenosis, 273 
presystolic, 220 
systolic, 228, 257 
Thrombosis, mesenteric, 365 
oedema of arm in, 41 
venous, 37 
with cervical rib, 36 
Thrush, 28 
Thyroid gland, see Glands 
tumor, causes of, 33 
Toes, 460 
lesions of, 461 
perforating ulcer of, 461 
tender, after typhoid fever, 462 
Tongue, 22-25 • 
cancer of, 24 
cyanosis of, 24 
geographic, 25 
herpes of, 24 
hypertrophy of, 25 
in fever, 24 
leukoplakia buccalis, 25 
“simple ulcers” of, 25 
syphilis of, 25 
tremor of, 24 
Tonsillitis, acute, septic, 205 
follicular, 23, 28, 205 
glands in, 31 
Tonsils, 28 
abscess of, 28 
enlargement of, 28 
examination of, 28 INDEX 
535 
Tonsils, in adenoids, 29 
in diphtheria, 28 
inflammation of, 28 
in leukaemia or pseudo-leukaemia, 
28 
in pharyngitis, 28 
in scarlet fever, 29 
in streptococcus infection, 28 
malignant disease of, 25 
membrane on, 28 
sarcoma of glands in, 31, 32 
swollen, 29 
ulcerations of, 28 
yellowish-white-spots on, 28 
Tophi, gouty, diagnosis of, 42, 496 
Torticollis, 34 
Toxemia, cause of jaundice, 16 
fever in, 3 
in hepatic cirrhosis, 3 
in tuberculosis, 3 
in typhoid, 3 
leucocytosis in, 473 
lymphocytosis in, 473 
shaking head in, 14 
tremor of hands in, 46 
Tracheal tug, in aneurism, 259 
Tracheitis, 281 
Tremor, 499 
Tremors, intention, 46 
Trichiniasis, blood in, 473 
oedema of lids in, 15 
tenderness of leg in, 453 
Tricuspid stenosis, see Stenosis 
regurgitation, see Regurgitation 
Trophic disorders, 507 
disturbances, 55 
Trypanosomiasis, blood in, 479 
Tuberculin, 25, 42, 59 
Tuberculosis, 295-304 
Tug, tracheal, 260 
Tympanites, pulmonary, 313 
Typhoid fever, breath in, 23 
fever, distinguished from malaria, 
473 
fever, distinguished from pyo- 
genic infections, 473 j 
fever, hands in, 45 
fever, nosebleed in, 19 
Typhoid fever, rose spots in, 355 
fever, splenic enlargement in, 403 
fever, tender toes after, 461 
fever, tongue in, 23 
fever, toxaemia in, 3 
fever, Widal reaction in, 477 
Ulcer, peptic, bismuth X-ray examina- 
tion in, 372 
perforating, of toe, 460 
“simple,” of tongue, 25 
of tonsils, 28, 29 
Uncinaria americana, 396 
Urethra, abscess of, 438 
caruncle of, 441 
Urine, 406, 430 
Uterus, cancer of, 442 
endometritis of, 442 
erosions of cervix, 441 
fibro-myoma of, 442 
laceration of cervix, 441 
malpositions of, 441 
prolapse of, 441 
Uvula, 30 
Valve areas, 63 
Valvular heart lesions, 204, 248 
Varicocele, 439 
Vascular phenomena, 87, 507 
tension, 106 
Vaso-motor disorders, 507 
Veins, abdominal, 354 
cervical, 116 
inspection of, 87 
pulsations in, see Pulsation 
varicose, 452 
Ventricle, dilatation of, 201 
hypertrophy of, 202 
Ventricular preponderance, 124 
Vertebrae, cervical, dislocation of, 
35 
deviations of, 35 
Vocal fremitus, 167, 169 
Voice sounds, see Vocal fremitus 
Vomiting, face after, 13 
in appendicitis, 391 
in gastric cancer, 375 
in gastric ulcer, 375 536 
INDEX 
Vomiting, in general peritonitis, 362 
in intestinal obstruction, 393 
Vomitus, “coffee-ground,” 375 
Vulva, eczema of, 440 
oedema of, 440 
varicose veins, 440 
Vulvo-vaginitis, 440 
Wassermann reaction, 478 
Weeping sinew, 44 
Weight, gain in, 1 
in infectious fevers, 2 
in insomnia, 2 
in malnutrition, 1, 2 
in myxoedema, I 
in old age, 1 
Weight, in toxaemic states, i 
loss of, i 
physiological changes in, 2 
Whooping-cough, 77 
lymphocytosis in, 473 
oedema of lids in, 15 
Widal reaction, interpretation of, 
477 
reaction, technique of, 477 
Winking reflex, 501 
-drop, in lead poisoning, 39 
Wry-neck, 34 
X-ray, see Radioscopy 
Yellow fever with conjunctivitis, 15