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Cabot — Physical Diagnosis 

Silver Nitrate Poisoning, with Slaty Blue Color of Skin 

{Painted from Life) 





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Digitized by tine internet Archive 

in 2011 with funding from 

Open Knowledge Commons and Harvard Medical School 


This book has been revised and reset throughout and twenty- 
three new illustrations added. The most important additions are the 
sections on the Phlebogram and the Arteriogram, the recasting of the 
section on Blood Pressure and the Arryhthmias, as well as those on 
Neoplasms of the Lung and Pleura, on Subphrenic Abscess and Peptic 
Ulcer. Bismuth X-ray examination of the stomach receives more 
adequate notice in this edition. 

I am under particular obligations to Dr. Thomas Lewis and to his 
publishers, Messrs. Shaw & Sons, London, for permission to use a cut 
from his invaluable monograph on ' ' The Mechanism of the Heart 
Beat"; also to Drs. Englebach and Carman and to Messrs. Lea & 
Febiger, for the use of a cut of Interlobar Empyema published in the 
American Journal of Medical Sciences for December 191 1. Dr. 
Walter Dodd and Mr. Lewis S. Brown of the Massachusetts General 
Hospital have helped me very kindly with some of the X-ray pictures. 

100 Marlborough Street, 
Boston, August 1, 1912. 


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 Button, 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. 




i. Weight, i 

(a) Causes of Gain in Weight, i 

(b) Causes of Loss in Weight, i 

2. Temperature — Technique and Sources of Error, 2 

(a) Causes of Fever, 2 

(b) Types of Fever, 2 

(c) Subnormal Temperature, 3 

(d) Chills and Their Causes, 3,4 



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 

(a) Ocular Motion, 16 

(b) The Retina, 17 

VI. The Nose, 17 

VII. The Lips, 19 

VIII. The Teeth, 21 

IX. The Breath, 22 

X. The Tongue, 22 

XL The Gums, 24 

XII. The Buccal Cavity, 25 

XIII. The Tonsils and Pharynx, , 27 

XIV. The Neck, 29 

Glands, . 29 

Abscess or Scars, , 32 

Tumors and Cysts, 32 

Torticollis 33 

Vertebral Tuberculosis, 34 

Bronchial Cysts and Fistulas 34 

Actinomycosis, 35 

Cervical Rib, 35 

Inflammatory or Dropsical Swelling of Neck 36 




The Arms. 

I. Paralysis, 37 

II. Wasting of One Arm, 39 

III. Contractures, -.,.... 39 

IV. (Edema, 4° 

V. Tumors, 4° 

VI. Miscellaneous Lesions of the Forearm, 42 

The Hands. 

I. Evidence of Occupation, 43 

II. Temperature and Moisture, 44 

III. Movements, 44 

IV. Deformities, 51 

The Nails .- 56 

The BAck. 

I. Stiff Back, 57 

II. Sacro-iliac Disease, 57 

III. Spinal Curvature, 58 

IV. Tumors of the Back, 59 

V. Prominent Scapula, 59 

VI. Spina Bifida, 60 





I. Methods of Examining the Thoracic Organs, .61 

II. Regional Anatomy of the Chest, 61 


I. Size, 64 

II. Shape, 64 

(a) The Rachitic Chest, 65 

(b) The Paralytic Chest, 65 

(c) The Barrel Chest, 66 

III. Deformities, 67 

(a) Curvature of the Spine, 67 

(6) Flattening of One Side of the Chest 68 

(c) Prominence of One Side of the Chest, 69 

(d) Local Prominences, 69 



IV. Respiratory Movements, 70 

(a) Normal Respiration, 70 

(b) Anomalies of Expansion, 71 

1. Diminished Expansion, 71 

2. Increased Expansion, 72 

(c) Dyspnoea, 72 

V. The Respiratory Rhythm, 74 

(a) Asthmatic Breathing, 74 

(b) Cheyne-Stokes Breathing, 75 

(c) Restrained Breathing, 76 

(d) Stridulous Breathing, 76 

VI. Diaphragmatic Movements (Litten's Phenomenon), 77 

VII. The Cardiac Movements, 79 

1. Normal Cardiac Impulse, 79 

2. Displacement of the Cardiac Impulse, 82 

3. Apex Retraction, 83 

4. Epigastric Pulsation, 84 

5. Uncovering of the Heart, 84 

VIII. Aneurism and Other Causes of Abnormal Pulsations of the 

Chest Wall, 85 

IX. The Peripheral Vessels, 86 

(a) Venous Phenomena, 86 

(b) Arterial Phenomena, 88 

(c) Capillary Phenomena, 90 

X. The Skin and Mucous Membranes, 90 

1. Cyanosis, 90 

2. CEdema, 91 

3. Pallor, 92 

4. Jaundice, 92 

5. Scars and Eruptions, 92 

XI. Enlarged Glands, 92 


I. Palpation, 94 

1. The Cardiac Impulse, 94 

2. Thrills, 95 

3. Tactile Fremitus, 96 

4. Friction, Pleural or Pericardial, 98 

5. Palpable Rales, 99 

6. Tender Points, 99 

II. The Pulse 100 

1. The Rate, 10 1 

2. Rhythm, 102 

3. Compressibility, 102 



4. Size and Shape of Pulse Wave, 102 

5. Tension, 103 

6. Size and Position of Artery, 105 

7. Condition of Artery Walls, 106 

III. Arterial Pressure and the Instruments for Measuring it, . 107 

1. Systolic or Maximum Pressure, 108 

2. Diastolic Pressure, ■ no 

3. Normal Readings, no 

4. Use of Data, , in 



I. Heart Block, 113 

II. Auricular Fibrillation, 115 

III. Paroxysmal Tachycardia, 116 

IV. Premature Beats (Extrasystoles), 118 

V. Coupling op Heart Beats and Alternation, 119 



I. Technique, 120 

( \ J Mediate Percussion, 1 

^ Immediate Percussion, J 

(b) Auscultatory Percussion, 126 

(c) Palpatory Percussion, 127 

II. Percussion-Resonance of the Normal Chest, 128 

(a) Vesicular Resonance, 128 

(b) Dulness and Flatness, 129 

(c) Tympanitic Resonance, 131 

(d) Cracked-pot Resonance, 134 

(e) Amphoric Resonance, 135 

if) The Lung Reflex, 135 

III. Sense of Resistance, 136 


1. Mediate and Immediate Auscultation, 137 

2. Selection of a Stethoscope, 138 

3. The Use of ihe Stethoscope, 142 

A. Selective Attention and What to Disregard, 142 

B. Muscle Sounds, 145 

C. Other Sources of Error, 146 

4. Auscultation of the Lungs, 147 

I. Respiratory Types, 148 

(a) Vesicular Breathing, 148 



(b) Tubular Breathing, 150 

(c) Broncho-vesicular Breathing, 152 

(d) Emphysematous Breathing, 152 

(e) Asthmatic Breathing, 153 

(/) Cog-wheel Breathing, 153 

(g) Amphoric Breathing, 154 

(h) Metamorphosing Breathing, • I 54 

II. Differences between the Right and the Left Chest, 154 

III. Pathological Modifications of Vesicular Breathing, 154 

(a) Exaggerated Vesicular Breathing, 155 

(b) Diminished Vesicular Breathing, 155 

IV. Bronchial Breathing in Disease, 157 

V. Broncho-vesicular Breathing in Disease, 157 

VI. Amphoric Breathing, 158 

VII. Rales, 158 

(a) Moist, 158 

(b) Dry, 159 

(c) Musical, 161 

VIII. Cough. Effects on Respiratory Sounds, ..161 

IX. Pleural Friction, 161 

X. Auscultation of the Voice Sound, 163 

(a) The Whispered Voice 163 

(b) The Spoken Voice, 164 

(c) Egophony, 164 

XI. Phenomena Peculiar to Pneumo-hydrothorax, 165 

(a) Succussion, 165 

(6) Metallic Tinkle, 165 

(c) The Lung Fistula Sound, 166 


1. The Valve Areas, ' 167 

2. Normal Heart Sounds, 168 

3. Modifications in the Intensity of the Heart Sounds, 170 

(a) Mitral First Sound 170 

1. Lengthening, , 170 

2. Shortening, 171 

3. Doubling, ■. ... 171 

(b) The Second Sounds at the Base of the Heart 171 

1. Physiological Variations, 171 

2. Pathological Variations, 174 

(a) Accentuation of Pulmonic Second Sound, 174 

(b) Weakening of Pulmonic Second Sound 174 

(c) Accentuation of the Aortic Second Sound, 174 

(d) Weakening of the Aortic Second Sound, 174 

(c) Modifications in Rhythm of Cardiac Sounds and Doubling of 

Second Sounds, 175 



(d) Metallic Quality of the Heart Sounds, 176 

0) "Muffled" Heart Sounds, 176 

4. Sounds Audible Over the Peripheral Vessels, 177 


(Auscultation of the Heart, Continued.) 


I. Terminology, 178 

1. Mode of Production, 178 

2. Place of Murmurs in the Cardiac Cycle, 181 

3. Area of Transmission, 181 

4. Intensity, Quality, and Length, 183 

5. Relation to Heart Sounds, 184 

6. Effects of Respiration, Exertion, and Position, 185 

7. Metamorphosis of Murmurs, 186 

II. Functional Murmurs, 186 

III. Cardio-Respiratory Murmurs, 188 

IV. Venous Murmurs, 189 

V. Arterial Murmurs, 189 



1. Valvular and Parietal Disease 191 

2. The Establishment and Failure of Compensation, 194 

3. Hypertrophy and Dilatation, 196 

4. Valvular Disease, 201 

I. Mitral Regurgitation, 202 

(a) Pre-compensatory Stage, 203 

(b) Stage of Compensation, 203 

(c) Stage of Failing Compensation, 207 

(d) Differential Diagnosis, 208 

II. Mitral Stenosis, 209 

1. First Stage, 212 

2. Second Stage, 213 

3. Third Stage, 214 

4. Differential Diagnosis, 215 

III. Aortic Regurgitation, 218 

1. Inspection, 219 

(a) Arterial Jerking, 219 

(b) Capillary Pulsation, 220 

2. Palpation, 221 

3. Percussion, 222 



4. Auscultation, 222 

5. Summary and Differential Diagnosis 225 

6. Prognosis, 225 

7. Complications, 226 

IV. Aortic Stenosis, 227 

1. (a) The Murmur, 228 

(6) The Pulse, . 229 

(c) The Thrill, 230 

2. Differential Diagnosis, 230 

V. Tricuspid Regurgitation, 232 

1. (a) The Murmur, 233 

(b) Venous Pulsation, 234 

(c) Cardiac Dilatation, 235 

(d) Feeble Pulmonic Second Sound, 235 

2. Differential Diagnosis, 235 

VI. Tricuspid Stenosis, 237 

VII. Pulmonary Regurgitation, 237 

VIII. Pulmonary Stenosis, 238 

IX. Combined Valvular Lesions, 239 

(a) Double Mitral Disease, 240 

(b) Aortic and Mitral Regurgitation, 241 

(c) Aortic Stenosis and Regurgitation, 242 



I. Parietal Disease of the Heart, 243 

1. Acute Myocarditis, 243 

2. Chronic Myocarditis, 244 

3. Fatty Overgrowth, 246 

4. Fatty Degeneration, 246 

II. Disturbances of Rhythm, 247 

1. Tachycardia, 247 

2. Bradycardia, 248 

3. Arrhythmia, 248 

4. Palpitation, 249 

III. Congenital Heart Disease, 250 


I. Pericarditis, 253 

(a) Dry or Fibrinous, 253 

(b) Pericardial Effusion, 255 

1. The Area of Dulness, 256 

2. The Cardiac Impulse and the Pulse, 258 

3. Pressure Signs, 258 


(c) Adherent Pericardium, . . 260 

1. Retraction of Interspaces, .260 

2. Limitation of Respiratory Movements, 260 

3. Absence of Cardiac Displacement with Change of Position, . 260 

4. Hypertrophy and Dilatation not Otherwise Explained, . . 261 

5. Capsular Cirrhosis of the Liver, 261 



x. Inspection and Palpation. 

(a) Abnormal Pulsation, 263 

(b) Tumor, 264 

(c) Thrill, 264 

(d) Diastolic Shock, 264 

0) Tracheal Tug, 265 

(/) Pressure Signs, 266 

2. Percussion Dulness, 267 

3. Auscultation, 267 

(a) Murmurs 267 

(b) Diastolic Shock Sound, 267 

4. Radioscopy, 268 

5. Diagnosis 269 



1. Tracheitis, 274 

2. Bronchitis, 274 

(a) Physical Signs, 274 

(b) Differential Diagnosis, 276 

3. Croupous Pneumonia, 277 

(a) Inspection, 278 

(b) Palpation, 278 

(c) Percussion, 278 

(d) Auscultation, 279 

(e) Differential Diagnosis, 282 

4- Inhalation Pneumonia, 283 

5. Broncho-Pneumonia, 283 

6. Pulmonary Tuberculosis, 285 

(a) Incipient Tuberculosis, 285 

(b) Moderately Advanced Cases, 288 

(c) Advanced Phthisis, 290 

(d) Anomalous Forms of Pulmonary Tuberculosis, 294 



(Diseases of the Lungs, Continued.) 


i. Emphysema, 296 

(a) Small- Lunged Emphysema, 296 

(b) Large- Lunged Emphysema, 296 

(c) Emphysema with Bronchitis and Asthma, ......... 299 

(d) Interstitial Emphysema, 299 

(e) Complementary Emphysema, 300 

(/) Acute Pulmonary Tympanites, 300 

2. Bronchial Asthma, 300 

3. Syphilis of the Lung, 301 

4. Bronchiectasis, 302 

5. Cirrhosis of the Lung, 302 

6. Examination of Sputa, 303 

(a) Origin, 303 

(b) Odor and Appearances, 303 

(c) Staining, 305 

(d) Microscopic Examination, 305 

(e) Description of Commoner Organism, 307 



I. Hydrothorax, 308 

II. Pneumothorax, 308 

III. Pneumoserothorax and Pneumopyothorax, 310 

Differential Diagnosis of Pneumothorax and Pneumohydrothorax, . 312 

IV. Pleurisy, 313 

1. Dry Pleurisy, 314 

2. Pleuritic Effusion, 315 

(a) Percussion, 316 

(b) Auscultation, 320 

(c) Inspection and Palpation, 323 

3. Pleural Thickening, 325 

4. Encapsulated Pleural Effusions, 326 

5. Pulsating Pleurisy and Empyema Necessitatis, . .' 327 

6. Differential Diagnosis of Pleural Effusions, . 327 

V. Cyto-Diagnosis of Pleural and Other Fluids, 330 

(a) Technique, 330 

(b) Interpretation of Results, 331 




i. Abscess and Gangrene of the Lung, 333 

2. Cancer of the Lung, 334 

3. Atelectasis, 335 

4. GEdema and Hypostatic Congestion, . . . . 336 



Examination op the Abdomen in General, 338 

1. The Omentum, Mesentery, and Peritoneum, 338 

2. Technique, 338 

3. Inspection, 338 

4. Palpation, 340 

5. What can be felt Beneath the Normal Abdominal Walls, . . . 341 

6. Palpable Lesions of the Belly Walls, 342 

7. Abdominal Tumors, , 343 

8. Percussion, 345 

Diseases op the Peritoneum, 346 

1. Peritonitis, Local or General, 346 



3. Cancer and Tuberculosis, 348 

The Mesentery, 


1. Glands, 349 

2. Thrombosis, 349 


The Stomach, 350 

1. Inspection and Palpation, 350 

2. Estimation of the Size, Position, Secretory and Motor Power, . 351 

3. Examination of Contents, 355 

(a) Qualitative Tests, 356 

(b) Quantitative Estimation of Free HC1 and of Total Acidity . .357 

4. Incidence and Diagnosis of Gastric Diseases, 360 

The Liver 361 

(a) Pain, 3 6 2 

(b) Enlargement, 362 

(c) Atrophy, 365 

(d) Portal Obstruction, 366 

(e) Jaundice, 367 

(/) Loss of Flesh and Strength, 368 



(g) The Infection Group of Symptoms, 368 

(h) Cerebral Symptoms of Liver Disease, 369 

The Gall Bladder and Bile Ducts, 369 

1. Differential Diagnosis of Biliary Colic, 369 

2. Enlarged Gall Bladder, 369 

3. Cholecystitis, 370 

The Pancreas, 371 

1. Cancer, 371 

2. Acute Pancreatic Disease, 371 

3- Cyst, . 371 

4. Bronzed Diabetes, 372 


The Intestines, ■ 373 

1. Data for Diagnosis, 373 

2. Appendicitis, 375 

3. Obstruction, 377 

4. Cancer, 378 

5. Examination of Contents, 378 

6. Parasites, 380 

The Spleen, 385 

1. Palpation, 385 

2. Percussion, 386 

3. Causes of Enlargement, 387 

4. Differential Diagnosis of the Various Causes of Enlargement, . .388 
The Kidney, 389 

1. Incidence and Data, 389 

2. Characteristics Common to Most Tumors of the Kidney,- . . . .390 

(a) Malignant Disease, 390 

(6) Hydronephrosis and Cystic Kidney, 390 

(c) Perinephritic Abscess, 391 

(d) Abscess of the Kidney, 391 

(e) Floating Kidney, 392 

3. Renal Colic and Other Renal Pain, 392 

4. Examination of the Urine, 393 

(a) Amount and Weight, 394 

(b) Optical Properties, 394 

(c) Significance of Sediments (Gross), 395 

5. Pyuria, • - • 395 

6. Haematuria, 397 

7. Chemical Examination of the Urine, 398 

(a) Reaction of Normal Urine, 398 

(6) Tests for Albuminuria, 398 

8. Significance of Albuminuria, 399 

9. Glucosuria and Its Significance, 400 



io. The Acetone Bodies 402 

11. Other Constituents, 402 

12. Microscopic Examination of Urinary Sediments, 403 

13. Summary of the Urinary Pictures Most Useful in Diagnosis, . .408 


The Bladder, 410 

1. Incidence and Data, , 410 

2. Distention, 410 

3. The Urine as Evidence of Bladder Disease, 412 

The Rectum, 413 

1. Symptoms which should Suggest an Examination, 413 

2. Methods, ." . 413 

3. Results, 414 

The Male Genitals, 415 

1. The Penis, 415 

2. The Testes and Scrotum, 416 

The Female Genitals, 418 

1. Methods 418 

2. The External Genitals, 418 

3. The Uterus, 419 

4. The Fallopian Tubes, 420 

5. The Ovaries, 421 



The Legs, 424 

I. Hip, 424 

II. Groin, 424 

III. Thigh, 425 

IV. Knee, 


V. (a) Lower Leg, 430 

(b) The Feet, 433 

(c) The Toes, 434 


Examination of the Blood, 437 

1. Haemoglobin 437 

2. Study of the Stained Blood Film, 439 

3. Counting the White Corpuscles, 445 

4. Counting the Red Corpuscles, 446 

5. Interpretation of These Data, 447 

(a) Secondary Anaemia, 447 

(b) Chlorosis, 448 



(c) Pernicious Anaemia, 448 

(d) Leucocytosis, 449 

(e) Lymphocytosis, 450 

(f) Eosinophilia, 450 

(g) Leukaemia, 451 

6. The Widal Reaction, 452 

7. The Wasserman Reaction, 453 

8. Blood Parasites, lb 453 

(a) Malaria, 453 

(6) Trypanosoma, 455 

(c) Filaria, 455 


Examination of the Joints, 456 

1. Methods and Data, . . * 456 

2. Technique, 457 

Joint Diseases, 460 

1. Infectious Arthritis, 461 

2. Atrophic Arthritis, 464 

3. Hypertrophic Arthritis, 466 

4. Gouty Arthritis, 472 

5. Hemophilic Arthritis, 472 

6. Relative Frequency of the Various Joint Lesions, 472 



Examination of the Nervous System, 470 

I. Disorders of Motion, 473 

II. Disorders of Sensation, 476 

III. Reflexes, 477 

IV. Electrical Reactions, 481 

V. Speech and Handwriting, 482 

VI. Trophic Vasomotor Disorders, 482 

VII. The Examination of Psychic Functions; Coma, 483 





To weigh the patient should be part of every physical examina- 
tion, and every physician's office should contain a good set of scales. 

i. 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 
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. 

(c) Myx oedema is occasionally a cause of increased weight, i.e., when 
the myxedematous infiltration is widespread (see below, page 8). 

2. Loss of Weight. — The aging process is so often associated with 
loss of weight that some writers speak of the "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 toxaemic states. 

Under the head of malnutrition come the cases of oesophageal 



stricture, chronic dyspepsia (with or without gastric ulcer or dil- 
atation) and gastric cancer, chronic diarrhoea, the atrophies of in- 
fancy, 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. 

Toxcemia is, I suppose, accountable for part at least of the ema- 
ciation in 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. Unless the patient takes 
more than his normal share of food he loses weight steadily. 


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 dyspnceic 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 99 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. Graves' disease is an example. 

(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 

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. 


For such causes we search when the thermometer indicates fever. 

Types of fever often referred to are : 

(a) " 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. 

(6) ''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 — 
are usually due (in the temperate zone) to one of three causes: — 
Typhoid, tuberculosis, sepsis. 

In 1,000 "long fevers" (as above denned) the following causes 
were found in the medical records of the Massachusetts General 
Hospital : 

Typhoid Fever 586 ] 

Tuberculosis 192 j- 926, or 92 . 6 per cent. 

Pyogenic Infections 148 J 

Epidemic Meningitis 27 

"Influenza" 10 

Infectious Arthritis ("rheumatism") 9 

Leucaemia 5 

Cancer 4 

Syphilis 2 

Miscellaneous 17 

Since the 7.4 per cent, just listed represent fevers whose cause is 
usually obvious, it is substantially true to say that any long obscure 
fever arising in the temperate zones is due to typhoid, tuberculosis or 
sepsis. Under sepsis I include vegetative endocarditis ("benign" 
or "malignant"), all local inflammatory 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 myx oedema. It 
is rarely of diagnostic value, but is a rough measure of the degree 
of prostration. 

3. Chills (due usually to a sudden rise in temperature) are seen 
chiefly in: (a) Sepsis of any type; (b) Malaria; (c) Onset of acute 
infections; (d) "Nervous" states. 

74, or 7.4 per cent. 


After the passage of a catheter, after or during labor, and after 
infusion of saline solution, a chill is often seen, but not easily ex- 

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 ex- 
amination (leucocytosis, malarial parasites) and by the general 
physical examination. 

4. Night Sweats and Day Sweats. 

Sweating in disease seems to be conditioned by: (a) Fever (infec- 
tion) ; (b) 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 ty- 
phoid fever and pneumonia sweating often begins in convalescence 
when the temperature is nearly or quite normal. In alcoholism, 
hyperthyroidism, and neurasthenic states we sometimes see sweating 
without fever. 

Sepsis, acute rheumatism, and tuberculosis are the infections 
most often accompanied by sweating. In rickets the head sweats 



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. Other methods — percussion, x-ray, palpation — ' 
yield but little. I shall begin at the top. 

I. The Cranial Vault. 
i. 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, 
especially if the sutures are closed. 

(b) An abnormally large head is seen 
in hydrocephalus (see Fig. i), asso- 
ciated with enormous "open" areas 
uncovered by bone and a peculiar 
downward inclination 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 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). 

(e) Myelomata of the skull may or may not be accompanied by a 


Fig. 1. — Hydrocephalus. 


leuksemic blood and a greenish staining of the tumor tissues. They 
are recognized by the concurrent presence of albumosuria, by the 
x-ray, the negative Wasserman 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. 

a b c 

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 with- 
out dyspnoea) . (b) Depressed fontanels are seen in severe diarrhoea, 
wasting diseases, collapsed states, and acute dyspnceic 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 


alopecia areata, and occasionally over the painful area in trigeminal 

(b) 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 myxoedema; but in both these diseases the 
hair usually grows again in convalescence. 









' % 

IKte. ^^L 

Fig. 3. — Multiple Myelomata. 

Fig. 4. — Multiple Myelomata. 

(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 often results. 

II. The Forehead. 

Scars, eruptions, and bony nodes are important. 

(a) Scars may be due to trauma or to old syphilitic periostitis. 
The epileptic often cuts his forehead in falling. 

(b) 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.) . 


(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). 

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. 6 and 8). The huge, bony "whopper jaw" is the 

^ijW : 

1 ■ 



Fig. 5. — Syphilis of the Frontal Bone. (Curschmann.) 

most striking item, then the prominent cheek bones, and the ridge 
above the eyes. The nose and chin are very large. 

(b) Myxcedema (see Fig. 10) 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, make us suspect the disease, especially at or near the meno- 


Fig. 6. — Acromegalia. 

Fig 7. — Gumma Involving Frontal Bone. 



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II ■ 

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Fig. 8. — Typical Face in Acromegaly. 

Fig. 9. — Frontal Sinusitis. 

Fig. 10. — Myxoedema. 



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 myxoedema — can generally 
be recognized by sight alone (see Figs, n and 12). Here the tongue 
is often protruded, and there 

are often pot-belly and deformed 

(d) In adenoids of the naso- 
pharynx 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 

Figs, ii and 12. — Cretinism. 

snoring, with frequent "colds," a high-arched palate, and perhaps 

(e) In paralysis agitans 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 characteristics just mentioned 
are then of great importance in diagnosis. 

(/) In Graves' disease (exophthalmic goitre) the startled or fright- 
ened 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. 15). 

■J % 

Fig. 13. — Adenoid Face. (Schadle.) 

(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. 

(1) 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 do not recognize any single expression as charac- 
teristic of peritoneal lesions. 

00 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 (edematous 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, and sometimes (especially in the morning) without 
any known cause. When combined with anaemia, the puffy face 
gives a peculiar "pasty" look (chronic diffuse nephritis). 

Fig. 14. — Exophthalmic Goitre. (Meltzer.) 

Fig. 15. — Face in Leprosy. 

IV. Movements of the Head and Face. 

1. 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: 

(a) As a matter of habit without other disease. 

(b) As a part of the disease chorea, associated with similar " rest- 


less" motions of the hands and feet. We often see these spasms in 
school-children; occasionally in pregnant women. 

(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 460), 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 472). 

V. The Eyes. 

I shall not attempt to deal with lesions essentially local (such 
as a "sty"), and shall confine myself to data that have diagnostic 
value in relation to the rest of the body. 

1. (Edema 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) Ancemia (prove by blood examination). 

(c) Measles and whooping-cough (eruption, paroxysms of cough). 
Rarer causes are 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 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. 

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, yellow fever, 
and some cases of influenza. It may also occur 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. 

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, %tching, x and mental depression. Lack 
of bile in the gut leads to flatulence and clay-colored stools. 

The commonest causes are: (a) Biliary obstruction (catarrh, 
stone or tumors obstructing the bile ducts, hepatic cirrhosis, or 
syphilis constricting them). 

(b) Toxaemia (malaria, sepsis, icterus of the new-born, pernicious 
anaemia) . 

5. The Pupils. 

The normal reflexes to light and distance are tested as follows: 
Let the patient face the light and cover one eye with the hard. On 
withdrawing the hand, the pupil contracts. Then 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, in fact, comparatively few conditions 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. 

1 In gall-stone cases one often finds itching without jaundice. 


(a) The Argyll-Robertson 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 deficient 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 

(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 myosis) by paralyzing 
the sympathetic dilators. Aortic aneurism may produce in the same 
way contraction of one pupil (see below, page 266). 

(d) Contraction with irregular outline and sluggish reactions 
is often seen in iritis as a result of adhesions to the lens (posterior 
synechiae) . 

6. 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. 

(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. 

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 syphilis. The eye is usually drawn out by the action of the 
unparalyzed external rectus. Moderate, bilateral ptosis is common 
in hysterical and neurasthenic conditions. 

(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 many 
other brain lesions. Rarely the oscillation is vertical. 



The Retina. 

The lesions which are of greatest interest in general medicine 
are: Retinal hemorrhage, optic neuritis, and optic atrophy. 

(a) Retinal hemorrhages , with or without other retinal changes, 
are important signs of nephritis, grave anaemias, and diabetes. 

* (6) Optic neuritis (usually bilateral) is of great value in the 
diagnosis of brain tumors, tuberculous meningitis, and brain abscess. 
It also forms part of the lesions in many cases of nephritis and diabetes. 

(c) Optic atrophy may be the end result of any of the types of 
optic neuritis just mentioned, or in a primary form is important 
evidence of tabes dorsalis. Many cases occur without any known 

Fig. i 6.- — Syphilitic Depression of the Nasal Bones. 

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 
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. 

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 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. 

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. 470.) 

VII. The Lips. 

1. Pallor of the mucous membrane of the lips suggests, though it 
never proves, anaemia. No diagnosis of anaemia should be made with- 
out at least testing the haemoglobin (Tallqvist's scale). One minute 

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 emphysema 
and pneumonia). — (c) Poisoning by acetanilid or other coal-tar anti- 
pyretics, producing methaemoglobinaemia. 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 

1 Cyanosis of intestinal origin occurs in connection with certain diseases involving 
excessive intestinal decomposition. (See Gibson, Quarterly Journal of Medicine, Oct., 
1907, p. 29.) 



of the skin with the labial mucous membrane, especially at the corners 
of the mouth. 

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 
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 elsewhere. It may be connected with a 
"cold" (which is often a disease of the trigeminus), with pneumonia, 
malaria or meningitis, but it frequently occurs without any discover- 
able cause. Herpetic stomatitis (" canker sores ") may accompany it. 

Fig. 18. — Epithelioma of the Lip. 

Fig. 19. — Chancre of the Lip. 

6. Epithelioma 1 of the lip and chancre should be suspected whenever 
a long-standing sore is discovered there. Epithelioma occurs almost 
always on the lower lip in a man past middle life (see Fig. iS). It 
lasts longer than chancre, is slower in producing glandular enlargement 
at the angle of the jaw, and is not associated with other syphilitic 

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 

1 It does harm to call this lesion "cancer" because this term is so firmly associated 
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." 



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 else- 
where) 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. 

Fig. 20. — Angioneurotic (Edema of 
Lower Lip. 

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. 21. — Diagram Showing the 
Month at which Each Tooth (of the 
First Set) Should Appear. 

Fig. 22. — Notched Incisors in Con- 
genital 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. 

2. Congenital syphilis may be associated with deformities of the 
central incisors (permanent). The most constant is that shown in 
Fig. 22. 

3. Teeth- grinding. — Nervous,- delicate, oversensitive children often 
grind their teeth in their sleep. There is no foundation for the popular 
superstition that this act indicates "worms." 

IX. The Breath. 

Foul breath is oftenest due to: 

(a) Foul teeth and gums (neglect, Riggs' Disease) . 

(b) Stomatitis of any variety. 

(c) Follicular Tonsillitis with cheesy deposits in the crypts. 

(d) Gastric fermentation (with or without constipation) . 

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 

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 urczmia 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. 

(a) The hesitating, tremulous tongue of typhoidal states is very 
characteristic. Simple tremor is seen in alcoholism, dementia par- 

1 See Taylor: "Studies on an Ash-free Diet." University of California Publication. 
July 30th, 1904. 



alytica, and weakness. A tongue protruded very far means usually a 
neurasthenic individual who is in the habit of examining it in a looking 

(b) 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 gastric fermentation, constipation, or fevers. 

A clean tongue in a dyspeptic suggests hyperacidity or 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 serious 
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 vesi- 
cles, 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 
Wasserman reaction, and the therapeutic test (see Fig. 23). Cancer 
and tuberculosis should be diagnosed by microscopic examination, 
though cancer is more commonly found in men (especially smokers) 

Fig. 23. — Syphilis of the Tongue. 


past middle life and on the side of the tongue. A local reaction after 
the injection of tuberculin may be of decisive importance. 

ih) "Simple ulcers" are due to irritation from a tooth or to trauma, 
and heal readily if their cause is removed. 

(i) Fissures of the tongue are usually due to syphilis, which is 
recognized in other lesions. 

(j) Leukoplakia buccalis (lingual corns) refers to whitish, smooth, 
hard patches of thickened epithelium, usually on the dorsum of the 
tongue in smokers, running a chronic course without pain or ulceration, 
but important because epithelioma has been known (and not very 
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. 

(/) Hypertrophy of the tongue has already been mentioned in 
connection with myx oedema and cretinism. It may occur independ- 
ently 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 and about one millimetre from it. 
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 arrange- 
ment of the deposit very clearly (see Fig. 24). It is unfortunate 
that the term "blue line" has become attached to these gray-black 

(b) A bismuth line — 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. 



(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 neglected mouths, and seems in some cases to injure 
digestion, but in most cases its effects appear to be wholly local. 

-Mm £ 

Fig. 24. — Lead-dots in the Gums. 

(/) Gumboil (alveolar abscess), originating in a carious tooth, is 
easily recognized by the familiar signs of abscess associated with a 
diseased tooth and sometimes with a surprising amount of swelling 
of the face. 

(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. 
1. Eruptions. 

(a) 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. 

(b) The syphilitic mucous patch (see above) should be looked for 
in suspicious cases, not only in easily accessible parts of the mouth, 


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 swell- 

Fig. 25. 

ing of the whole cheek, especially under the eye. The odor of gan- 
grene 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. 


XIII. The Tonsils and Pharynx. 

Method of Examination. — Place the patient facing a good light, 
natural or artificial. 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 : 

i. Inflammations (redness, eruptions, spots, or membranes). 

2. Ulcerations. 

3. Swellings. 

4. Reflexes. 

1. Inflammations. 

(a) General redness means a mild or early pharyngitis, but may 
precede severe diseases like diphtheria and scarlet fever. 

(6) 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 ulcerations of the tonsils or soft palate are oftenest due 
to syphilis. Improvement under potassium iodide and the manifesta- 
tions of syphilis elsewhere make the diagnosis possible. 

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 coaeulum axe sometimes mistaken for a membrane. 


(b) Tuberculosis may produce similar deep ulcerations, recognized 
by their association with obvious 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 
tender, syphilitic lesions almost free from tenderness. The chronic 
course of pharyngeal tuberculosis and the presence of other tuber- 
culous lesions identify it. 

(c) Malignant disease (oftenest sarcoma) may attack the tonsil, 
and forms a rapidly growing 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 tonsil (unilateral or bilateral) without fever or 
constitutional symptoms represents usually the residual hypertrophy 
following many acute attacks of tonsillitis or may be part of the general 
adenoid hypertrophy so common in children's throats. Rarely it 
forms part of the leukasmic or pseudo-leuksemic process. 

(6) 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) Tonsillar 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 tons'llitis. 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 vertebras occurs not infrequently during the first 
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 cervical caries 
(see below, page 32). 

(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 

(a) 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 nervous persons and in many alcoholics without 
nervousness. It is this condition, combined with a smoker's pharyn- 
gitis, that leads to many cases of morning vomiting in alcoholics. 

(b) 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 
paralysis the whole palate is still. 


Long, thin necks are often seen in phthisical individuals, and short 
necks in the emphysematous, but nothing more than a bare hint can 
be derived from such facts. The lesions oftenest searched for in the 
neck are: 1. Enlarged glands (cervical adenitis). 2. Abscesses and 
scars. 3. Thyroid tumors. 4. Pulsations (see below, page 86). 
5. Torticollis and other lesions simulating it. (6) Tuberculosis of the 
cervical vertebrae. 

Rarer lesions will be mentioned below. 

/. 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- 
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, 

Fig. 26. — Tubercular Glands. 

is usually due to this cause. Certain diagnosis depends on microscopic 
examination, animal inoculation, and the tuberculin test. 

(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 

(d) Hodgkin's disease; chronic, large, rarely suppurating glands in 
the neck, axillae, and groins, with slight splenic enlargement and nor- 
mal blood, suggest Hodgkin's disease, but microscopic examination is 


necessary to exclude tuberculosis. A superficial gland can be excised 
under cocaine, with very little pain. 

(e) Lymphatic Leukcemia. 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, and the leukaemic 
blood changes are 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, 

Fig. 27. — Hodgkin's Disease, Six Months Duration. 

and, among distant lesions, cancer of the stomach and sarcoma of the 
lung have caused enlargement of these glands in cases under my 

(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 may also 
attack the parotid. 

(h) German measles may be accompanied by swelling of the pos- 
terior cervical or occipital glands without the involvement of any 



II. 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 (car- 
buncle) and superficial boils are 
common. High Pott's disease 
may be complicated by abscess 
(see Figs. 28 an 29). 

Figs. 28 and 29. — Cervical Abscess in Pott's Disease. (Bradford and Lovett.) 

III. Thyroid Tumors 

occur chiefly in two diseases: 

(a) Simple goitre (unilateral or bilateral). 

(6) Goitre with exophthalmos, tachycardia, and tremor (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 



Fig. 30. — Simple Goitre. 

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 at- 
tached 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 myxcedema) is un- 

Cancer or sarcoma have oc- 
curred in the thyroid and may 
be difficult to distinguish from 
goitre. Malignant tumors are 
usually painful, grow fast, are accompanied by emaciation and 
anaemia, are often harder and more nodulated than benign goitres, 

and invade the neighboring 
tissues and lymphatics. His- 
tological examination should 
decide in doubtful cases. 

IV. Torticollis (Wry-neck) and 
Other Lesions Resembling It. 

(a) Spasm (tonic, rarely 
clonic) of the sterno-mastoid 
and trapezius may be due to 
irritation of the spinal acces- 
sory 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. 

(b) 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. 



-Dislocation of the Cervical Vertebrae. 


(c) Dislocation of the upper cervical vertebras, causes a distortion of 
the neck much like that of torticollis (see Fig. 31). The diagnosis 
depends on the history of injury, the absence of true muscular spasm, 
and the x-ray picture. 

(d) Compensatory cervical deviations: (1) 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 resemble torticollis. 
The diagnosis depends on the other evidences of intracranial disease. 

V. 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 32). 

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. 

VI. Branchial Cysts and Fistulas. 

These, due to persistence of parts of the fcetal 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,, 
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 unknown. Some 
such cysts may be emptied by external pressure. 1 

Branchial cysts may contain serous, mucous, or sero-sanguineous 
fluid, or hair and sebaceous material, according as their lining wall 

1 A patient of mine can produce a gush of foul fluid in the mouth by pressure over a 
small cyst in the neck. 



on the 

is derived from ectoderm or entoderm. Diagnosis depends 
position and consistency of the growth and on the results of 

Branchial fistulas (congen- 
ital) may open externally in 
the neck, and occasionally 
are complete from neck to 
pharynx. They may become 
occluded and suppuration 

VII. Actinomycosis. 

Actinomycosis, though it 
usually arises in the lower jaw 
bone, may appear externally 
in the neck. A dense infiltration with bluish-colored, semifluctuat- 

Fig. 32. — Branchial Cyst. 

ing areas in it, but without any distinct lumps or sharp outlines, is 
strongly suggestive of actinomycosis, and should always lead to a 

microscopic examination of 
excised portions or of the dis- 

Fistulae may form, but are less 
common than in tuberculosis. 

VIII. A Cervical Rib, 

springing from the seventh cer- 
vical vertebra and ending free 
or 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 symp- 
toms and is generally encoun- 
tered when percussing the apex 
of the lung. The bone can be 
felt behind the artery by careful 
palpation and demonstrated by 

Fig. 33. — Mediastinal Neoplasm with Cervical 
Metastases and Obstructed Vena Cava. 

radiography. Pain or wasting in the arm, and occasionally throm- 
bosis may occur. 



IX. Inflammatory or Dropsical Swelling of Neck. 

Venous thrombosis, mediastinal tumors and inflammatory 
exudates (see Fig. 33a) may produce oedema in the neck. 

Fig. 33a. — Anthrax Infection of the Neck. 


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. 

/. Paralysis of One Arm. 

Paralysis of most or all the muscles of one arm occurs of tenest in : 
(a) Hemiplegia — with paralysis of the leg and often of the face on 
the same side, (b) 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 

Pressure Neuritis. — The history of the case is of the greatest im- 
portance. During surgical anaesthesia the brachial plexus or the 
musculo-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 hanging over a 
bench or doubled under the body, the nerves may be injured. Pres- 
sure 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. 

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 
affected, but also the supinator longus, while in the toxic paralyses, 
especially lead, the supinator longus is spared. To test the function 
of this muscle, grasp the patient's wrist with the thumb side upper- 
most, and resist while he attempts to flex the arm at the elbow. If 
the supinator is intact it will spring into relief on the thumb side of the 

1 Less common are paralyses due to lesions of the arm centre in the cerebral cortex 
(tumor, softening, cyst, abscess, hemorrhage, thromboses, or embolism). 




Obstetrical Neuritis. — In instrumental deliveries or when forcible 
traction on the child's arm has been necessary, with or without 
fractures, a paralysis of the arm often results, and, what is important, 
is often not noticed till some years later, and then thought to have 
just arisen; thus it may be mistaken for anterior poliomyelitis or other 

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 

Fig. 34. — Wrist Drop, following Lead Neuritis. 

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 by pain, 
anaesthesia, or paresthesia, 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 
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. 

(a) Rapid atrophy occurs in all the types of neuritis mentioned 
above, as well as in poliomyelitis and progressive muscular atrophy. 
In the latter it occurs without complete paralysis, though the wasted 
muscles are, of course, 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 all the atrophies just mentioned a lack of the trophic or nourish- 
ing functions which should flow down the nerve is assumed to ex- 
plain the wasting {"trophic atrophy"). From this we distinguish the 
atrophy due simply to disuse of the muscles without nerve lesions. 

(b) 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- 
tures have in themselves little or no diagnostic value, but indicate a 
late and stubborn stage of whatever lesion is present. 


IV. (Edema of the Arm. 1 

Causes.— i. Thrombosis of axillary or brachial vein, usually the 
result of heart disease. 2. Pressure of tumors — aneurism, cancer of 
axillary glands, Hodgkin's disease, sarcoma of lung or mediastinum. 
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 88) and for the evidence given by 
their pulsations as to the work of the heart (see page 100). 

V . Tumors of the Upper Arm. 

In the upper arm we have: 1. 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 

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 tumor 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. 

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 

1 Distinguished, like all cedema, by the fact that a dent made by pressing with the 
finger does not at once disappear when the pressure is removed. 



characteristic lesion of syphilis or a Wassermann reaction may be 
necessary for diagnosis. 

Tuberculous lesions 1 are much more common on the forearm bones, 
but are occasionally seen on the humerus near the epiphyseal ends. 
They usually involve and perforate the skin, leaving an indolent, sup- 
purating sinus leading to necrosed bone. The evidence of tuberculosis 

Fig. 35. — Sarcoma of Humerus. 

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 tubercu in may be of distinct value. Pain, tenderness, 
oedema, redness and heat may appear or may be increased if already 

Gouty tophi are sometimes seen along the fasciae covering the triceps 
tendon. They are hard and painless. The diagnosis depends upon 

1 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 other Californian physicians. 



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. 229). The lesions in the other parts of the body make the 

diagnosis clear- 
Local lesions of the bones of the forearm are chiefly tuberculous 

and syphilitic, both of which have been sufficiently described in the 

last section. 

Fig. 36. — Rachitic Epiphysitis. 

Fig. 37. — Sarcoma of Ulna. 

In the wrist bones we find : 

1. Rachitic enlargement of the epiphyses. In rickets the terminal 
epiphyses at the wrists take part in the general epiphyseal enlargement 
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 

1 Bursitis over the olecranon ("miner's elbow") produces a tender fluctuating swelling 
over the tip of the elbow. 



of the fingers (see below, page 53), is recognized by its association with 
pulmonary or pleural diseases of many years' duration (bronchiectasis, 
phthisis, empyema). 

3. Acromegalia (see page 8) affects chiefly the bones and soft tissues 
of the hand. 

4. Hypertrophic, atrophic, or tuberculous disease of the wrist-joint 
will be described below (see Examinations of the joints, page 456). 

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 tubercu- 
lous, in which case the sac is generally divided into several parts 
("compound ganglion") ; bacilli may occasionally be demonstrated in 
the exudate. 

6. Neoplasms (see Fig. 37). 

Fig. 38. — Hypertrophic Pulmonary Osteo-arthropathy. (Thayer.) 


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 information 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 

(6) 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 Graves' disease (exophthalmic 
goitre), and if the warmth and 
moisture are present most of the 
time and not only as a temporary 
phase — e.g., after violent exercise 
— this disease is strongly suggested, 
and a search for tremor, rapid 
heart, goitre, and bulging eyes 
should be made. 

III. 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 -opened 
hand, which never really grasps 
and gets away as soon as possible; 
the firm, hearty grasp; the limp, 
"wilted" hand — furnish hints of 
character that every physician 
must take account of. 
In fevers or toxaemic states (typhoid, alcoholism) there are two 

sets of movements which recur so often that names have been given 

them, viz.: i. Carphologta — picking and fumbling at the bed clothes. 

2. Subsultus tendinum — involuntary twitching and jerking of the ten- 

Fig. 39. — Radiographs of the Hand 
and Arm of a Case of Hypertrophic Pul- 
monary Osteoarthropathy (the left figure) 
compared with the hand and arm of a 
normal individual of the same height (the 
right figure). Note especially the thick- 
ening of the radius and ulna. (Thayer.) 



dons in the wrist and on the back of the hand, usually associated with 
tremor and carphologia. 

(6) 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 tox- 
aemia. 3. Alcohol (less often lead, tobacco, morphine, or other drugs) . 
4. Graves' disease. 5. Paralysis agitans. 6. Multiple sclerosis. 7. 

Fig. 40. — Radiograph of the Wrists in Hypertrophic Pulmonary Osteo-arthropathy. 

(v. Ziemssen's Atlas.) 

Most of these tremors need no comment. The intention tremor 
of multiple sclerosis (sometimes seen also in hysteria) is exaggerated 
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 16), a spastic 
gait (see page 473), and a slow, staccato speech. This group of symp- 
toms suggests multiple (or insular) sclerosis. 



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 474) . 

FlG. 41. — Athetosis. Successive positions of the hands. (Curschmann.) 

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 : 
1. Jacksonian epilepsy — convulsive attacks which begin in and 
may remain confined to one set of muscles, often preceded by prick- 
ling or other paresthesia 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, softening, 
chronic meningitis, etc.) , but may also occur in uraemia and dementia 
paralytica. Coma and general spasms may follow. 

2. Professional Spasm. — Writers, violin- players, and others who 
use one set of muscles continually are often attacked with painful 

cramps in the muscles used 
("writer's cramp"). Weakness or 
semi-paralysis of the muscles may 

3 . Chorea and Choreiform Move- 
ments. — 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 

Ftg. 42. — Tetany (Masland.) 

Fig. 43. — Tetany. (Masland.) 

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 are not. At first sight 
one would surely think the child was simply fidgety. 

Similar movements occur in pregnant women or somet'mes after 
parturition, but the type is much severer and is apt to be associated 
with maniacal symptoms. 

Habit spasms or tics are much commoner in the face, throat and 
shoulders but also reach the hands occasionally. They constitute an 



Fig. 44. — Tetany. (Masland.) 

Fig. 45. — Tetany. (Masland.) 



independent chronic neurosis and may or may not be associated with 
mental or emotional disturbances. Winking and nodding movements 
are commonest. They have no relation to infectious chorea, to the 
joints or the heart. 

Fig. 46. — Tetany. (Masland.) 

Fig. 47. — Atrophic Arthritis with "Flipper Hand." 

Post-hemiplegic chorea refers to similar movements in the paralyzed 
hands of hemiplegic cases (children or adults). 

In hysteria or by a sort 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 n the rarer congenital 
forms of paralysis with or without idiocy. 

4. Athetosis (see Fig. 41) means slow twisting and bending move- 

Fig. 48. — Spade Hand in Myxoedema. 

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), occuring in the course of diseases 
of the stomach and intestine in children, in nursing women, after 



gastric lavage, and after thyroidectomy, 1 usually lasting minutes or 
hours — rarely days. 

IV. Deformities of the Hands. 

i. "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. 

Fig. 49. — a, Acromegalic Hand, b, Normal Hand. 

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 (see below, page 472). 

3. " Hemiplegic hand," a result of the contractures following hemi- 
plegia from any cause. 

4. Myxoedema 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 

1 When the parathyroid glands are accidentally removed. 



it rapidly develop in connection with other myxedematous lesions 
before it can have diagnostic significance. (The same is true of the 
myxcedematous face.) (See Fig. 48.) 

Fig. 50. — Atrophic Arthritb. 

Fig. 51. — Clubbed Fingers. 

5. Acromegalia produces general enlargement of the bones and 
other tissues of the hands and feet. 

6. Pulmonary Osteo-arthropathy. — Any long-standing disease of 



the heart, lungs, or pleura may be followed by this peculiar hyper- 
trophic change in all the tissues of the extremities. Mild forms 
produce " clubbed fingers," a bulbous enlargement of the finger-tips 

Fig. 52. — Clubbed Fingers. 

Fig. 53. — Raynaud's Disease. 

with double curvation of the nails, lateral and antero-posterior 1 (see 
Fig. 51). In severer forms the bones of the hand and wrist are also 
considerably enlarged (see Figs. 39 and 40). 

1 Clubbed fingers are occasionally seen in a variety of other diseases: e.g., hepatic 
abscess, nephritis; and even in apparently healthy persons. 



7. Heber den's nodes, later described under the head of hypertrophic 
arthritis, are here pictured (Fig. 54). The distinction from gout has 
already been referred to (page 472). 

8. Atrophic arthritis (Fig. 47) (further described on page 460) 

Fig. 54. — Heberden's Nodes. 

Fig. 55. — Tuberculous Dactylitis. 

presents its most typical lesions in the hands and wrists. The con- 
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 rc-ray examination is necessary to 



establish the diagnosis which is important because of the unfavorable 
prognosis which it involves. 

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 Wasser- 
man reaction, the results of giving tuberculin or potassic iodide, and 

Fig. 56. — Morvan's Disease. 

the evidence of syphilitic or tuberculous lesions elsewhere. In either 
disease we have a chronic, almost painless, boggy, red enlargement 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. 

10. Raynaud's disease attacks the fingers more often than any 



other part. Osier distinguishes three grades of intensity: A. Loca 
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. 434.) 

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: 

12. Leprosy, in which there is likewise anaesthetic 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 

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. 

1 . The nutrition of the nails suffers 
in chronic skin diseases, in myxoe- 
dema, in many nerve lesions (neuritis, 
hemiplegia, syringomyelia, etc.), de- 
mentia paralytica; also in atrophic 

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. 
They 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. 

Fig. 57. — Grooved Nails after Acute 


5. (a) Cyanosis, the slatey or purplish-blue color of venous con- 
gestion, can be well seen in the nails, (b) Ancemia, 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 52). 

7. Capillary pulse (see below, page 90). 

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, 


The evidences of spinal tuberculosis, spinal curvature, and of the 
spinal form of infectious and of hypertrophic arthritis will be described 
later (pages 459 and 466). 

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 
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 spinal arthritis or tuberculosis. 

Metastatic cancer of the vertebras often follows cancer of the breast 
producing a stiff, painful spine. The x-ray picture is usually charac- 

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. 

Goldthwait 1 has recently shown that the sacro-iliac joint is subject 
to most of the diseases of other joints, and that some (e.g., hypertro- 
phic 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 
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 rc-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. 

77/. 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 an- 
gular, means Pott's disease (tuberculosis) . If the curve is gentle and 
gradual it may be due to "round shoulders," to hypertrophic arthritis, 
to emphysema, 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 emphysema 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 
1 Goldthwait: Bostoh Medical and Surgical Journal, March 9th, 1905. 


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 270). 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 391). 

(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. 

if) 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 re- 
sistance (" an gel- wing " scapula). 

VI. 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 

Fig. 58. — Spina Bifida With Meningocele. 

spinal column. There is no other congenital tumor in this position 
communicating with the spinal canal. 

In the sacral region there are other congenital tumors, dermoid 
cysts, lipomata, and others. Their nature can be learned only by 
incision, but they are all distinguished from spina bifida by the lack 
of communication with the spinal canal. 



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 the movements 
of the chest ("mensuration") is often mentioned 
as co-ordinate with the above methods, but it 
yields very little information of practical value, 
and is at present very little used. 

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 recall- 
ing 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 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 


Fig. 59.— The Mid- 
axillary Line. 


more exactly what part of the axilla anteroposteriorly is affected, 
we may refer to the " mid-axillary line " (see Fig. 57) ; 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 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 measure- 
ments from mid-sternum. 

/ (T Y/' (f ^^C '"-. •' r^^ ;v\ ^\ ) V-- Upper lobe of left 

Right auricle. — <- 1~(I^<^/7V ^^^^T'k Left ventricle - 

\ vj&5^' < // ^\^*$^7M I Lower lobe of left 

Fig. 60. — 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 continu- 
ous lines. The ribs are numbered. 

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 
"valve areas" of the heart, which do not correspond to the actual 
position of the valves, for reasons to be explained later on, and (6) 



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 
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 

Upper lobe. 


Lower lobe. 



_ Liver. 

Fig. 61. — Position of the Left Lung from the Fig. 62. — Position of the Right Lung from 
Side, and of the Spleen. the Side, and of the Liver. 

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. 

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 120). 




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, and 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: 

i. 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 are seen chiefly in emphysema. 
Of course the chests of healthy individuals vary a great deal in size at 
any given age, and I have been referring in the last sentences only to 
variations greater than those normally found. 

II. Shape. 

I I 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 
diameter is nearly as great as the lateral. The adult's chest is dis- 
tinctly flattened from before backward, although individual variations 
in this respect are considerable, as Woods Hutchinson has shown. 
In childhood the commonest pathological modifications are due 
to adenoids or to rickets; in middle and later life to emphysema, 
phthisis, or old pleuritic disease. 

(a) 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 depres- 
sion or groove is to be seen running 
downward and outward to the 
axilla and corresponding nearly to 
the attachment of the diaphragm. 
This is sometimes spoken of as 
"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 articulation there is to be 
felt, and sometimes seen, a line of 
eminences or swellings, to which the name of "rachitic rosary" has 
been given. 

(b) 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 

1 In some cases this condition appears to be congenital. 

Fig. 63. — Funnel Breast. 



such persons are spoken of as "flat-chested." The clavicles are very 
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 

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. 186, page 289.) 

(c) The "Barrel Chest." 

Nothing is less like a barrel than the "barrel chest." 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 


respiratory movements of the barrel chest will be spoken of later (see 
Figs. 68 and 69). 

Nutrition of the Chest Walls. 

Emaciation is readily appreciated by inspection. The ribs are 
unusually prominent, the scapulae stand out, and the clavicles project. 
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. 

Fig. 65. — Pigeon Breast. 

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. 

(a) Spinal Curvatures and Twists. 1 

Slight degrees of deformity are best seen by marking with a skin- 
pencil the position of the spinous processes (see Fig. 71). The more 

1 See also page 58. The lesions are referred to here only in relation to their effects 
on heart and lungs. 



marked cases of lateral curvature, which are usually accompanied by a 
certain amount of twisting, give rise to considerable displacement of 
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 

Fig. 66. — Pigeon Breast. 

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 
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. 

(b) 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 jt>)- The shrinkage of the 
affected side is made more obvious by contrast with the compensatory 



hypertrophy of the sound lung, which makes the sound side unusually 
full and prominent. 

(c) Prominence of One Side of the Chest. 
In pneumothorax or pleural effusions, and sometimes in malignant 
disease of the lung or pleura, there 
is a marked increase in the size of 
the affected side of the chest. 
Very rarely emphysema may affect 
one lung predominantly. In pneu- 
mothorax or pleuritic effusion we 
usually see, in addition to the 
above enlargement of the affected 
side, a smoothing out of the inter- 

Fig. 67. — The Paralytic Thorax. 

Fig. 68. — Barrel Chest in a Case of 
Bronchial Asthma (aet. 13). 

costal depressions so that the surface of that side is much more 
uniform than the other side. Bulging of the interspaces from great 
pressure within the chest rarely occurs. I have never seen it. 

(d) 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 outward 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: 
i. Aneurism of the arch of the aorta. 

2. Tumor of the chest wall (lipoma, sarcoma, gumma) or of the 
lung, mediastinum, or of the thoracic glands pressing their way 

3. " Cold abscess" (tuberculosis, actinomycosis) of a rib or of the 

4. Empyema perforating the chest wall, the so-called "empyema 

IV. The Respiratory Movements. 
(a) 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, diaphragmatic > 
breathing is more marked, while itir' 
women breathing is mostly of pie 
"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. In emphysema, 
for example, and in some cases of 
asthma, the ribs move very little, and 
most of the work of respiration is 
performed by the diaphragm, whose 
pull upon the lower ribs can some- 
times be distinctly seen during in- 
spiration. On the other hand, when 
the movements of the diaphragm are impeded by the presence of fluid 
or a solid tumor, as in cirrhosis of the liver or leukaemia, the breath- 
ing has largely to be performed by the ribs, and becomes, as we say, 
costal in type (see below, p. 73). 

Fig. 69. — Barrel Chest. Chronic 
Bronchitis and Emphysema. 

(b) 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. 
We may see: (i) Diminished expansion of one side (as a whole, or at 
the apex). (2) Increased expansion of one 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 

Fig. 70. — Scoliosis. 

Fig. 71. — Scoliosis. 

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, occlusion of the bronchus, or from the pressure of an aneurism, 
we have immobility combined with a retraction of the affected side. 
In tuberculous 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 diaphragm. 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. Occasionally a hemiplegia or a 
unilateral 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-standing pleurisy with contraction, 
or other causes. 

(c) Dyspnoea. 

This term is often used rather loosely to include: (1) Difficult 
breathing, whether rapid or slow. (2) Unusually deep breathing, 

whether difficult or not. (3) 
Rapid breathing. 

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, per- 
formed with difficulty, and 
unusual muscles, not ordinar- 
ily 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, emphysema, asthma, 
and phthisis. 

Dyspnoea may affect especially inspiration, as, for example, when 

Fig. 72. — Lateral Curvature. Scoliosis. 



a foreign body lodges in the larynx, or in ordinary " croup." In such 
cases we speak of "inspiratory dyspnoea," distinguishing it from 
"expiratory dyspnoea" such as occurs in asthma and emphysema. 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 noisy. 

Combined types in which both respiratory acts are difficult are 
more common. 

Fig. 73. — Contraction of Left Chest. Empyema. 

Abnormally deep and full respiration, without any appearance of 
difficulty in the process, is sometimes seen near the fatal termination 
of cases of diabetes, the so-called diabetic dyspnoea. 

Simple rapidity of breathing should be distinguished from dyspnoea 
of any type. 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. 

Fig. 74. — Prominence of Right Side. Pleural Effusion. 

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 

V. Changes in the Respiratory Rhythm. 
(a) Asthmatic Breathing. 
In asthma the normal rhythm is reversed; audible expiration be- 
comes longer, instead of shorter, than inspiration. Inspiration may 

1 Slight retraction of the lower interspaces in the axilla during inspiration is often 
seenjn health. In disease this phenomenon is greatly exaggerated. 



be represented only by a short gasp, while expiration becomes a pro- 
longed wheeze lasting several times as long as inspiration. Dyspnoea 
is usually very marked. In emphysema we get very much the same 
type of breathing so far as rhythm is concerned, but the dyspnoea is 
not usually so extreme and the auxiliary muscles of respiration are not 
so apt to be called into use. In many cases of emphysema one sees 
the thorax move all as one piece, "en ciiirasse," owing to a senile fixa- 
tion of the bones of the thorax from ossification of the cartilaginous 
portions. In hereditary syphilis or phthisis this fixation may occur in 
youth or early middle age. 

(b) 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 (apnoea) . If we represent the normal respiratory 
movement by an up-and-down line, as seen in Fig. 75, the Cheyne- 
Stokes type of breathing would appear as in Fig. 76. The period of 



-Diagram to Represent Normal Breathing-Rhythm. 

apnoea may last from one to ten seconds ; then short, shallow respira- 
tions 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 

Fig. 76. — Cheyne-Stokes Respiration. 

asleep for a few seconds and the pupils may become contracted. When 
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 
the phenomenon also occur, in which there is a rhythmic increase and 


decrease in the depth and rapidity of respiration but without any 
intervening period of apnoea. This type of breathing is most often 
seen in severe cases of cardiac, renal, or cerebral disease. Conner has 
recorded many varieties in tuberculous meningitis. Respiratory 
arrhythmias are generally more marked at night and may occur only 
at that time. In children they appear sometimes to be physiological 
during sleep. As a rule, 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. 

(c) Restrained or "Catchy" Breathing. 

When the patient has a "stitch in the side," due to dry pleurisy, 
intercostal neuralgia, or to other causes, the inspiration may be sud- 
denly 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 expiration is often accompanied by a little moan or grunt of 

Shallow and irregular breathing is often seen in states of pro- 
found unconsciousness from any cause, such as apoplexy or poison- 
ing. A few deep respirations may be followed by a number of shallow 
and irregular ones. 

Stemo-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. 

After severe hemorrhage the breathing may be of a sighing type 
as well as very shallow. 

(d) 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, or 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. 73). 

VI. Diaphragmatic Movements. 

The Phrenic Wave. 

The normal movements of the diaphragm may be rendered visible 
by the following procedure, suggested by Litten in 1892: The patient 
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 contain 1 (see Fig. jj) . 
The observer stands at the patient's side. As the ribs rise with the 
movement of inspiration, a short, narrow shadow moves down the 

Fig. 77. — Litten's Diaphragm Shadow. Proper position of patient and of observer. The 
shadow is best seen near L. 

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, and 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. 

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. 



In normal chests, the excursion of the shadow is about two and a 
half inches; with very forced breathing three and a half inches. 
The mechanism of this phenomenon is best understood by imagining 
a coronal section of the thorax as seen from the front or back (see Fig. 
78). At the end of expiration, the diaphragm lies flat against the 
thorax from its attachment up to about the sixth rib. During inspira- 
tion it " peels off" 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 advanced cases of emphysema, the shadow is 
absent. This is explained by the fact that in pneumonia, pleuritic 
effusion, and emphysema the diaphragm is held off from the chest wall 
so that its. movements communicate no shadow. In pleuritic adhe- 
sions 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 affected 
lung and in part probably to 
pleuritic adhesions. On the 
other hand, fluid or solid 
tumors below the diaphragm, 
unless very large, do not pre- 
vent the descent of that 
muscle, and so do not abolish the diaphragm shadow. In cases in 
which the diagnosis is in doubt between fluid in the right pleural 
cavity and an enlargement of the liver upward or a subdiaphragmatic 
abscess, the preservation 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. 

The use of this method of examination tends, to a certain extent, 
to free us from the necessity of using the *-rays, inasmuch as it 
furnishes us with the means of observing the diaphragmatic movements, 
on the importance of which so much stress has been laid by F. H. 

Fig. 78. — Excursion of the Diaphragm during 
Forced Respiration. R, Ribs; E, position of the 
diaphragm at end of expiration; /, position of 
diaphragm at end of inspiration. 


Williams and others, much more easily and cheaply than with the 

It also frees us to a considerable extent from the need of using the 
spirometer to determine the capacity of the lungs. By measuring 
the excursion of the phrenic shadow and taking account of the thoracic 
movement, we obtain a very fair idea of the respiratory capacity of the 

VII. 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 
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 
the fourth interspace or behind the fifth rib ; while in persons of ad- 
vanced age it often descends as low as the sixth interspace. In adults 
it is occasionally absent even in perfect health and under certain patho- 
logical 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. 79). 
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 the impulse brought about by disease, I shall speak 
in a later paragraph. 

1 For a more detailed description of the normal position of the cardiac impulse, see 
next page. 



(b) Relation of the maximum cardiac impulse to the apex of the 
heart. — I mentioned above that the maximum cardiac impulse is not 
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 import 
ance 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 


Fig. 79. — 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. 

found three-fourths of an inch or more farther to the left (see Fig. 80). 
This may be proved by percussion (vide infra, p. 63), and by fluoros- 
copy. The true position of the cardiac apex thus determined corres- 
ponds usually not with the maximum impulse, but with the point 
farthest out and farthest down at which any rise and fall synchronous 
with the heart beat can be felt (for further discussion of this point see 
below, p. 256). 

(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 " Herzenstoss " of the Germans, with which the " Spitzenstoss " 
or apex impulse is contrasted. A variable amount of "Herzenstoss" 
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 or in 
cases in which the heart is hypertrophied and in which there is more 
or less stiffening of the ribs with loss of their natural elasticity. At 

Fig. 80. — The Inner Dot is the Maximum Cardiac Impulse. That to the right is the true 
apex of the heart, as obtained by percussion. The ribs are numbered. 

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 

(d) 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 less often in 
the opposite direction. 

(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. 

(a) 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, or downward. As a rule, it is 
displaced in both these directions at once. I shall return to this 
subject 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. 

(b) 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 or by solid tumors of large size, we may 
see the apex beat of the normal heart in the fourth interspace and 
often an inch or more inside the nipple line. 

(c) Of nearly equal frequency is displacement of the heart due to 
pleuritic effusion or to pneumothorax (see below, p. 313). 

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 as far as 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 down- 
ward 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 men past forty-five the 
whole heart sinks considerably, so that a marked systolic 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 likely, 
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. 


The apex impulse is displaced by: 

(a) Hypertrophy and dilatation of the heart, 

(b) 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. 


(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 mediastinitis 1 
(see below, pages 260 and 262.) 

(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 autopsy 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. 

(a) It is in chlorosis, perhaps, that we most frequently see such 
pulsations. 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. 

(b) A rarer cause of retraction of the lungs is fibroid phthisis or 
chronic interstitial pneumonia. In these diseases a very large area of 

1 Or more often as a result of simple cardiac hypertrophy. More cases of aortic 
regurgitation in thin young patients show this systolic retraction in the left lower back. 



pulsation may be seen in the precordial region owing to the entire un- 
covering of the heart by the retracted lung, even when the heart is not 
drawn out of its normal position. 

VIII. Aneurism, Dilated Aorta, 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 or a dilated aorta may transmit to the chest wall pulsa- 
tions which it is exceedingly important for us to recognize and properly 
to interpret. 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 recog- 
nize the disease while it is confined within the thorax. In such cases, 

Fig. 8i. — Position When Looking for Slight Aneurismal Pulsation. 

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. 81, 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. 


Pulsations due to a dilated aorta or 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. 264). 

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 

IX. 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 phenomena; (b) Arterial 
phenomena; (c) Capillary phenomena. 

(a) Inspection of the Veins. 

1 . 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 



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 muscles. 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 one of the most 
common valvular diseases of the heart — tricuspid regurgitation, 1 

Fig. 82. — -Tortuous Veins on Chest and Abdomen. (Autopsy showed obliteration of the 

vena cava inferior.) 

as well as in a good many other conditions. 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 regurgitation, it is well to 

1 A pulsating carotid may transmit an up-and-down motion to the veins overlying 
it. In such cases, if the veins be emptied by "milking" them upward, they will not 
refill from below. 


try the experiment of emptying the vein by stroking 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 variations in the cervical 
venous pressure are recognized by phlebograms traced by MacKenzie's 
instrument or in some similar way. 

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. 114.) 

Fig. 83. — Enlarged Tortuous Brachial Arteries ( Arterio-sclerosis) . 

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. 83). * 

(b) Arterial Phenomena. 

1 . In thin or nervous persons pulsations are not infrequently to be 
seen in the carotids independent of any abnormal condition of the 

1 Enlarged veins about the navel, the so-called "caput Medusae," are commonly found 
in text-books, but rarely in cirrhosis of the liver. 


2. Very violent throbbing of the carotids, more noticeable than 
the normal, often occurs in severe anaemias and occasionally in simple 
hypertrophy of the heart without any valvular 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. 

I lately examined a blacksmith whose heart was considerably 
enlarged by hard work, but without any valvular disease. Pulsation 
was violent in all the peripheral arteries which I have just named. 

3. In arterio-sclerosis occurring in spare, elderly men, with or 
without aortic regurgitation, one often notices a lateral excursion of 

Fig. 84. — Enlarged and Tortuous Brachial Artery (Arterio-sclerosis). 

the tortuous brachial arteries synchronous with every heart beat. 
An up-and-down pulsation may occur at the same time. Not infre- 
quently the arteries which are stiffened by deposition of lime salts 
(see below, page 105) stand out visibly as enlarged, tortuous cords 
upon the temple and along the inner sides of the biceps muscle, (see 
Figs. 83 and 84) 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. 


(c) Capillary Pulsation. 

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 
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 drawing a pencil or other hard substance across the 
forehead so as to cause a line of hypersemia, at the edge of which the 
systolic flushing occurs. 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, and occurs 
occasionally in health, in anaemia, in exophthalmic goitre, and in 
conditions associated with low tension in the peripheral arteries, as 
well as in any area of inflammatory hyperemia (jumping toothache, 
throbbing felon, etc.). 

X. 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 : 

(i) Cyanosis. 

(2) (Edema. 

(3) Pallor. 

(4) Jaundice. 

(5) Scars and eruptions. 

(1) 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) Emphysema. 

(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) Methemoglobinemia, such as occurs after the excessive use 
of coal-tar analgesics (antifebrine, 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 polycythaemia 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 palpa- 
tion 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 


(3) Pallor. 

Pallor suggests, though it does not in any way prove, anaemia. 
Pallor of the mucous membranes, as seen in the lips and conjunctivas, 
is much more apt to be a sign of real anaemia than is pallor of the 
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 anaemia 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 and of trauma 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 

XI. 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 pulmonary 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. 85), 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 
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 

Fig. 85. — Sarcoma of Sternum and Cervical Glands. (Curschmann.) 

account for a well-marked dyspnoea. Axillary adenitis means most 
often peripheral sepsis, next tuberculosis, then metastatic cancer, 
leucaemia and Hodgkin's disease. Inguinal adenitis (suppurative) is 
most often a result of gonorrhoea. If non-suppurative, it is usually 
due to sepsis in the leg, syphilis, leucaemia and 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. 



I. Palpation. 

The most important points to be determined by palpation — that 
is, by laying the hand upon the surface of the chest — are : 

(i) The position and character of the apex beat 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 pericardial friction. 

Other less important data furnished by palpation will be mentioned 

(1) The Apex Beat. 

(a) 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 
movements 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, whether the beats are 
unequal in force or whether some are skipped; 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 diffuse slap often felt in 
dilatation of the right ventricle, the sudden tap characteristic of 
mitral stenosis, may be thus appreciated. 

(b) 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. 80). 



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. 

The results obtained by palpation and inspection of the apex 
region give us the most reliable data that we have regarding the size 
of the heart. Percussion may be 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, consider- 
ing 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 influ- 
ences 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 centimetres 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. 

(2) " Thrills." 

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 diseases 
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 also distinguish a purring thrill from the slight shudder 
or jarring which often accompanies the cardiac impulse in functional 
neuroses of the heart or in conditions of mental excitement. 



As a rule we can appreciate a thrill more easily if we lay the palm 
very lightly upon the chest, using as 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. 

(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 fremitus is to ask the patient to count "one, two, 
three," or to repeat the words "ninety-nine" while the palm of the 
hand is laid flat upon the chest. The amount of fremitus to be ob- 
tained over a given part of the thorax varies, of course, according 
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. 
86 will help us to realize this. The parts shaded darkest communi- 
cate 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 intermediate 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 lung in front, (b) that it is 
greater in the upper part of the chest than in the lower, and some- 
what greater throughout the right chest than in corresponding parts 

Fig. 86. — Distribution of Tactile Fremiti!?. 



of the left. This natural inequality 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 
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 

Fig. 87. — Showing Point at Which Pleural Friction is Most Often Heard. 

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. 

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. 

(&) Increase or absence of fremitus. 

(a) 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. 

(b) Solidification of the lung due to phthisis or pneumonia is the 
commonest cause of an increase -in tactile fremitus. Further details 
as to the variations in amount of fremitus in different diseases may 
be found in later chapters of 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 move- 
ments of respiration, and 
especially at the end of in- 
spiration. 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. 87, p. 97). 

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 
heart's movements. Such friction is most often to be felt in the region 
of the fourth left costal cartilage (see Fig. 88). 

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 

Fig. 88.— Showing Point (P) at Which Peri 
cardial Friction is Most Often Heard. 



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) 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 it is the parts near the 
apex impulse that are sore. The 
position of the tender points in 
intercostal neuralgia generally 
corresponds with the point of 
exit of the intercostal nerves. 
These points are shown in Fig. 89. 

The tenderness in phthisis is 
most apt to be in the upper and 
front portions of the chest. In 
neurotic individuals we some- 
times 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. 

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. 

Fluctuation or elasticity in any tumor or projection from the 
chest is a very important piece of information which palpation may 
give us. 

Fig. 89. — Showing Points of Exit of the 
Intercostal Nerves. 


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 elas- 
ticity 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 in- 
formation 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 sub- 
sequent examination are guided. In emergencies or accidents 
the pulse gives us our bearings and tells us whether or not 
the patient's condition is one demanding immediate succor — e.g., 
hypodermic stimulation — and whether the outlook is 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 
important 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 radial pulse when taken in 
connection with other signs may furnish decisive evidence of aneu- 
rism of the aortic arch; aortic stenosis is a lesion which cannot be 
diagnosed unless the pulse shows certain characteristic features; 
arterial degeneration may betray its presence chiefly in the periph- 
eral 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 most 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 bra- 
chial arteries should always be palpated. 

(b) Both radials should always 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 : 

i. 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. 

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 


ioo. 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 
100 or more in a normal adult (see below, p. 247). Exercise or emo- 
tion quickens the pulse very markedly, and after food it is somewhat 
accelerated. Some account of the causes of pathological quicken- 
ing or slowing of the pulse will be found on pages 247 and 24S. 

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, and form part of that absolute type of arrhy- 
thmia which is now known to be associated with auricular fibrillation 
(see below, p. 115). Intermittence or irregularity in rhythm alone 
is usually 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 myocarditis. 

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. 

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). 

(6) The tightness or looseness of the artery {tension, or diastolic 


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 contractions 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 ora '' 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 221) and in many 
cases of arteriosclerosis. 

(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 2 2 9). 

(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 
"anacrotic pulse." 

(d) The shape of the high-tension pulse wave will be described 
in^the next paragraph. 

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. 
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. 90.- — Sphygmographic Tracing of Low 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, and 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. 90). 

Fig. 91. — Sphygmographic Tracing of High Tension Pulse. 

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 
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. 91). 


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 contracted 
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 

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. 

7. The Condition of the Artery Walls. 

Arterio-sclerosis 1 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. 

(c) Calcification. 

Simple stiffening without calcification is due to fibrous thickening 
of the intima and produces a condition of the arteries not manually 

1 "Arterio-sclerosis" is here used to mean any anatomical change in the arterial walls 
that permanently diminishes their elasticity. No single histological entity is referred to. 


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 vast 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 no" pulse 
can be felt. 

Such are the points to be observed in the preliminary 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 Addison's disease, tuberculosis, pernicious anaemia, and 
many infectious fevers. 

High tension is produced by cold (e.g., cold bathing, malarial 
chills). As a rule, the tension of the pulse increases with age and is 
high after the fiftieth year. Hysteria and migraine are said to be 
associated with increased vascular tension, and it is almost always 
high during and before eclamptic spasms. Increase of intracranial 
pressure (as by cerebral hemorrhage or trauma) has a similar but more 
lasting effect. Most frequent among pathological conditions as causes 
of high tension are chronic nephritis and arteriosclerosis with the 

1 Tortuosity in the temporal artery, however, is normal. 


various diseases in which arterio-sclerosis is a factor (gout, lead poison- 
ing, diabetes of fat old people) . 

In valvular heart disease without nephritis or arterio-sclerosis 
the tension is usually normal or slightly lowered. 

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 accu- 
racy the lateral pressure in the peripheral arteries. We have long 
attempted to estimate this pressure, by simple digital compression 
and palpation, and no doubt these methods in the hands of skilled 
observers will always have a field of usefulness; but it seems to me 
clear that by the instruments about to be described we can obtain 
data in regard to the force of the heart's contractions and the tension 
of the peripheral arteries more accurate and more reliable than those 
furnished by digital examination. This is especially true of com- 
parative records, as, for example, if one attempts to compare the 
tension of the pulse to-day with what it was yesterday, when one has 
felt many pulses in the interim. Another objection to estimates 
of pulse pressure based on digital examination results from the fact 
that the size of the artery itself is apt to be a confusing factor. 

Among the many instruments introduced within the past decade 
we may distinguish (i) those which aim to estimate the amount of 
compression which has to be exerted upon a given artery in order to 
arrest the onward flow of blood in it, and (2) those which seek to 
estimate also the amount of pressure in a given artery at the moment 
when its wall makes the widest excursion or oscillation. 

Instruments of the first type are said to measure systolic pressure, 
and those of the second type to measure also diastolic pressure. Here 
as elsewhere in this book I shall describe only such instruments and 
methods as are clinically available and only such 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 I have found the instruments of the Riva-Rocci 
type by far the best {i.e., Faught's, Stanton's and Mercur's). Despite 
the inconveniences of transporting a mercury column it remains the 
most reliable method. Instruments 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. Gaertner's tonometer is very inaccurate. 



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, 
and an air-pump (see Figs. 90 and 91). The air forced from the pump 


Fig. 92 — Mercur's Type of Riva-Rocci Sphygmomanometer. 

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 

1 . Measurement of Systolic or Maximum Pressure. 

To use the instrument for measuring systolic blood pressure we 
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. 



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 arterio- 

Fig. 93. : — Faught's Type of Riva Rocci Sphygmomanometer. 

sclerosis is present, it has been estimated by Herringham that the 
artery may oppose a resistance of 15 to 20 mm. Hg. The more care- 
fully conducted experiments of Janeway, however, convince me that 
Herringham is wrong and that sclerosed arteries offer a direct resist- 
ance 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 
importance, provided the compressing armlet is at least 12 cm. wide. 
A huge arm gives no higher reading than a shrivelled one, as has been 
shown by Janeway in a patient one of whose arms was congenitally 
atrophied while the other was enormous. 

The instrument is a very simple and quick one to use, needing 
very little practice and not more than a minute or a minute and a 
half for a single reading. The chief objection to it is its bulk and 

Systolic pressure may also be measured by listening with the 
stethoscope over the brachial artery just peripheral to the cuff, and 
noting when the tapping systolic sound disappears. 

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, becomes loud, and remains so 
until we reach a point 30-45 mm. below the systolic reading. Then 
the sound rapidly disappears. Its point of disappearance or of very 
marked weakening corresponds within 5 mm. to the diastolic pressure 
as estimated by the most accurate and complicated instruments, such 
as Erlanger's. 

3. Normal Readings. 

With any of the various types of Riva-Rocci instrument mentioned 
on p. 107, the readings in healthy adults at rest are approximately as 
follows: Systolic, 1 10-135 mm. Hg. Diastolic, 60-90 mm. Hg. 

The "pulse pressure," i.e., the difference between any individual's 
systolic and diastolic pressure, averages 30-45 mm. Hg. 

In women all the figures run about 10 mm. lower than in men. 
Children under 2 years, 75-90 mm. In older children, 90-110 mm. 
Excitement or exercise raise the pressure temporarily but considerably. 
It is 5-10 mm. lower in recumbency than in the sitting position. 

The instrument devised by Erlanger (Johns Hopkins Hospital 
Reports, 1904, Vol. XII.) gives very accurate readings both for 
systolic and for diastolic pressure. Its bulk, delicacy, the difficulty 
of keeping it in good order, and the amount of time needed to secure 
a reading will prevent its general use in clinical work. 


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 more I 
use the instrument, the more firmly I am convinced that digital 
measures of blood pressure are often ludicrously wrong. The Riva- 
Rocci instrument as modified by Faught, Janeway or Stanton has 
now secured a firm position in the routine work of good clinicians 
all over this country. 

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 
associated 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 causes of high blood pressure are : 

1. Chronic nephritis. 1 

2. Arteriosclerosis. 2 

3. Acute compression of the brain (as by apoplexy, skull fractures, 
meningitis, and other rapidly advancing intracranial lesions). 

4. Puerperal eclampsia. 

Less important are the transitory effects of acute pain (as in gout, 
tabetic crises, lead colic, biliary colic and during child birth). 

Neurasthenia and insanity are often mentioned as causes of hyper- 
tension, but I suspect other causes in the background. 

Clinically it is easy to exclude in most cases all the causes of 
hypertension just listed except two: chronic nephritis, and arterio- 
sclerosis. Hence vascular hypertension and high blood pressure should 
always make us suspect these diseases 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 raises a presumption against the existence of arteriosclerosis. 

1 Especially if the thoracic, aortic or splanchnic arteries are extensively diseased. 

2 i.e., any nephritis of more than a few months duration. 


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.), in per- 
nicious anaemia, infectious fevers (tuberculosis, pneumonia, typhoid) 
and surgical "shock." Occasionally the diagnosis of tuberculosis 
may be assisted or confirmed if hypertension is marked. 

Diastolic Pressure. 

There is very seldom any need of measuring diastolic pressure. 
Very little information of clinical value is obtained from it. It is 
relatively low (i.e., the pulse pressure relatively high) in aortic regur- 
gitation and in some cases of arteriosclerosis, anaemia, and Graves' 
disease; but no diagnostic or prognostic value attaches to it in my 
experience though it has been measured along with the systolic 
pressure as a matter of routine in my wards for a considerable period. 
The general practitioner may safely disregard it, bearing in mind 
that in acute aortic regurgitation the high systolic pressure is balanced 
by a low diastolic pressure. 



In the last edition 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 in- 
vestigators in the field of phlebographic and electrocardiographic 
work, is able to state, in his recent monograph 1 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.'' 1 

We may come back to the sphygmograph and to the results of 
auscultation, 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 others' 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 seem to consist of a better knowledge of : 
i. Heart block, partial or total. 

Auricular fibrillation and absolute irregularity of the pulse. 

Paroxysmal tachycardia. 

Premature contractions of auricle or ventricle. 

Coupling of heart beats and alternation. 

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 

1 Thomas Lewis: "The Mechanism of the Heart Beat," Shaw & Sons, London, 1911, 
a work to which I am profoundly indebted. 

8 113 


cavo-auricular junction, spreads through the bundle of His in the 
membranous 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 origination 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," normally 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. 

(c) Regularly recurring "dropped beats" every tenth beat or 

(d) The establishment of a 3:1 or 2:1 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 As — 
Vs 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 must be far more frequent. 

When the As — Vs interval is already increased, the act of swallowing, 
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 or 3:1 
rhythm, or to complete dissociation of auricle and ventricle, always a 
very serious condition. 

To establish the presence of heart block we need 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 cal- 
culate 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 stethoscope 1 something corresponding to the auricular move- 
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 generally recognize and 
treat the disease underlying heart block with about the same measure 
of success whether the heart block itself escapes us or not; while in 
heart block itself there is no effective treatment and no more definite 
prognosis than one could give from a knowledge of the underlying 

Auricular Fibrillation. 

The researches of MacKenzie in 1904-5 brought out the fact 
that when a beat 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, inco- 

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." Hirschf elder 
describes them as "very soft distant sounds like the ticking of a watch" and "best heard 
along the left sternal margin." 


ordinate 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 experimentation, 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 escape" 1 along the bundle and 
produce the absolutely irregular pulse. 

Auricular fibrillation thus defined produces the majority of all the 
arrhythmias clinically observed. The irregular pulse of most cases 
of rheumatic endocarditis and of myocardial insufficiency (the fa- 
miliar arteriosclerotic or cardiorenal types) is generally of this kind. 
For the classification of arrhythmias see p. 248. 

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. 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 insurrection 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 
following diagram from Lewis (loc. cit. ? p. 191). 

This diagram suggests the "close relation" of paroxysmal tachy- 

1 Lewis, loc. tit., p. 247. 



K^dJ^-NMj^-^U JUA? /uJU/V ^ 






Fig. 94. — (after Lewis). 

I. Occasional premature beats, ("auricular extras ystoles") 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. 


cardia to the more serious auricular fibrillation just described and 
to the commoner and less serious form of arrhythmia next to be 

Histologically nothing definite is known about the cause of par- 
oxysmal tachycardia. 

Premature Beats (Extrasystoles). 

i. Ventricular. — Except when the auricle is fibrillating, premature 
beats of -ventricular origin are rare; they occur occasionally in heart 
block and in other conditions involving a tardy impulse from 
the auricle. The ventricle "escapes" with a spontaneous contrac- 
tion, as if impatient of waiting longer for the delayed signal. We 
may assume that the chemical stimulus-material accumulates during 
the prolonged pause and finally discharges itself in a contraction inde- 
pendent of the ordinary signal from above. 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. 

(6) 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. 

2. Auricular. — Premature contractions arising in the auricle and 
leading to a similarly premature ventricular beat are more commonly 
seen than "ventricular extrasystoles." The pause following such a 
beat may be compensatory in the sense explained above, but usually 
it is not so. This fact and the presence in the phlebogram of one 
auricular wave preceding each ventricular wave enable us to recognize 
the premature beat as auricular in origin. 

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 
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. 

Coupling of the Heart Beats and Alternation. 

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. 

Alternation. — In the healthy but overtaxed and rapidly beating 
heart, in many cases of paroxysmal tachycardia, and in the myocardial 
insufficiency 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 electrocardiogram is of the normal type. 

The weak beat may appear faintly or not at all in the arterio- 
gram; a powerful apex impulse may correspond either with the strong 
or the weak pulse beat in the alternation. It is always a serious 
symptom and means that "the heart muscle is in a precarious condi- 
tion, be it structural or functional." (Lewis, loc. cit., p. 278). 



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- 

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 fin- 
gers; in Germany instruments are still used to a considerable extent. 

(a) 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 


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 
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 

Fig. 95. — Position of the Hands When Percussing the Right Apex. 

forward and his muscles must be thoroughly relaxed. Many pa- 
tients, when stripped for examination, swell out their chests and 
sit up with a military erectness. The muscular tension thus pro- 
duced modifies the percussion note and causes an embarrassing 
multitude of muscle sounds which greatly disturb auscultation. 

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 



Fig. 96. — Position of the Hands When Percussing the Left Apex. 

Fig. 97. — The Right Way to Percuss — i.e., From the Wrist. 



chest with the second finger of the left hand 1 on the dorsum of which 
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 finger 2 of the right hand upon the second finger of the 
left just behind the nail, imitating as far as possible with the right 


-The Wrong Way to Percuss — i.e., From the Elbow. 

hand the action of a piano-hammer. The quicker the percussing 
finger gets away again after striking, the clearer will be the note 

(3) Let all the blows struck in any one part of the chest be uni- 
form in force. 

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. 95 and 96) 
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. 



(4) Strike from the wrist and not from the elbow (see Figs. 97 
and 98) . The wrist must be held perfectly loose. 

(5) Keep the percussing finger bent at a right angle as in Fig. 99. 
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 
that part of the chest. For example, it is necessary to percuss very 
strongly when examining the back of a muscular man, where an 

Fig. 99. — Proper Position of the Right Hand During Percussion. 

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 suffices. In children or 
emaciated patients, or in any case in which the muscular develop- 
ment 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 rela- 
tively large area of the chest and does not therefore give us infor- 
mation about the condition of any sharply localized area. If a car- 



penter, 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 percussion is always inaccurate. 1 
It may be necessary where the muscles are very thick, but its value 
is then proportionately diminished. On the other hand, it is pos- 
sible to strike so lightly that no recognizable sound is elicited at 

Fig. ioo. — Proper Position of the Patient During Percussion of the Back. 

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. 

The position of the patient above described applies to percus- 
sion of the front. When we desire to percuss the back, it is im- 
portant to get the scapulae out of the way as far as possible, since 
we cannot get an accurate idea of sounds transmitted through them. 
To accomplish this, we put the patient in the position shown in 
Fig. ioo, the arms crossed upon the chest and each hand upon the 
opposite shoulder. The patient should be made to bend forward; 
1 See also below, page 135, the lung reflex. 



otherwise the left hand of the percussor will be uncomfortably bent 
backward and his attention thereby distracted (see Fig. 101). 

When the axillae are to be percussed, the patient should put the 
hands upon the top of the head. 

(b) 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 

Fig. ioi. — Wrong Position for Percussing the Back. The patient should be bent forward. 

patient or an assistant to hold it there, the sounds produced by 
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. 


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 
centre is the chest piece of the stethoscope (see Fig. 102). 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 

Percussion arc. 

Chest piece of 

Fig. 102. — Auscultatory Percussion, Showing the Arc along which such Percussion should 

be made. 

straight line must bring the point percussed either closer to the 
stethoscope 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 a very 
important one, among serviceable methods of physical examination. 

(c) 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- 
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. 

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. 

Normal dulness of 
the right apex. ---. J V^ s Deep cardiac 

*' dulness. 

Superficial cardiac 

Liver dulness. 

Traube's semilunar 

tympanitic space. 

Liver flatness. 

Fig. 103. — Percussion Outlines in the Normal Chest. 

II. Percussion Resonance of the Normal Chest. 

The note obtained by percussing the normal chest varies a great 
deal in different areas. In Fig. 103, 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. 

(a) 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. 
This short, feeble, high-pitched sound is known technically as a "</»//" 



or "flat" sound, flatness designating the extreme of the qualities that 
characterize dulness. Over the parts shaded dark in Fig. 103, 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 occupied by the liver, or rather by that part of it which is in 
immediate contact with the chest wall. The upper portion of the 
liver is overlapped by the right lung (see 
Fig. 103), and hence at this point we get 
a certain amount of resonance on percus- 
sion, 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 point. As we go toward the axilla, 
the line of lung resonance slopes down, as 
is seen in Fig. 104. In the back resonance 
extends to the ninth or tenth ribs. 

(b) Normal Dull Areas. 

On the left side, the main dull area 
corresponds 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 portion of the heart 
which is overlapped by the margin of the 
right and left lungs. 

Over the portion of the heart not over- 
lapped by the lung (see Fig. 103, p. 128) 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 corresponding 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 of the heart wall comes in contact with the chest wall. 

Fig. 104. — Position of the Left 
Lung in the Axilla. 


Accordingly, either the superficial or the deep dulness may be mapped 
out as a means of estimating the size of the heart. Each method 
has its advantages and its advocates. The superficial dulness is 
easier to map out, but varies not only with the size of the heart, 
but with the degree to which the lungs are distended with air, or 
adherent to the pericardium or chest wall. What we are percussing 
is in fact the borders of the lungs at this point. 

On the other hand, the deep cardiac dulness is much more satis- 
factory as a means of estimating the size of the heart, but much 
more difficult to map out. It needs a trained ear and long practice 
to percuss out correctly the borders of the heart itself, especially 
the right and the upper borders, since here we have to percuss over 
the sternum where differences of resonance are very deceptive and 
difficult to perceive. 

It is a disputed point whether light or forcible percussion should 
be used when we attempt to map out the deep cardiac dulness. 
Heavy percussion is believed by its advocates to penetrate through 
the overlapping lung margins and bring out the note corresponding 
to the heart beneath, a note which, they say, is missed altogether 
by light percussion. On the other hand, those who employ light 
percussion contend that heavy percussion sets in vibration so large 
an area of lung superficially that fine distinctions of note are made 
impossible (see above, p. 124). 

Good observers are to be found on each side of this question, 
and I have no doubt that either method works well in skilled hands. 
Personally I have found light percussion preferable. 

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. Thus, if we 
wish to percuss out the upper border of the liver, we strike successive 
points along a line running parallel to the sternum and about an 
inch to the right of it. 1 When a change of note is perceived, the 
point should be marked with a skin pencil; then we percuss along a 
line parallel to the first one, and perhaps an inch farther out, and 
again mark with a dot the point at which the note first changes. A 
line connecting the points so marked upon the skin represents the 
border of the organ to be outlined. 

If now we look at the upper part of the chest in Fig. 103, we notice 
at once that the two sides are not shaded alike: the left apex is dis- 

1 Or we may reverse the procedure; percuss first over the liver and then work toward 
the lung above until the note becomes more resonant. 


tinctly lighter colored than the right. This is a very important 
point and 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 position. 

In percussing at the bottom of the left axilla, we come upon a 
small oval area of dulness corresponding to that outlined in Fig. 104. 
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 
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. 

(c) Tympanitic Resonance. 

Tympanitic resonance is that obtained over a hollow body, 
like the stomach when moderately distended with air. 1 It is usu- 
ally 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 appre- 
ciate 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 more or less 
distended with air. 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 dul- 
ness, and below by the resonance 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. 103.) 

1 Extreme distention here, as in a snare drum, is associated with a dull percussion note 
(see below p. 309). 


In the back, when the scapulae are drawn forward, as shown in Fig. 
ioo, page 125, 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 corresponding 
portion of the left, on account of the presence of the liver on the right. 

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 of Percussing Symmetrical Points. — Since we depend 
for our standard of resonance upon comparison with a similar spot 
on the outside of the chest, it is all-important that in making such 
comparisons we should percuss symmetrical points, and not, for 
example, compare 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 patho- 
logically 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 accumulates 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 
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 two 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 

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 and 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 lungs are almost always more or less emphyse- 
matous, a shade of tympanitic quality is added to the normal vesicular 
resonance. The distention of the colon with gas may obliterate 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. 

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 

1 There is also a shade of tympany associated with the dulness of the feebly expanded 
lung of the lower side. 


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 lung. In the axilla Litten'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. 

( d) 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 
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 
pulmonary cavity (as in advanced phthisis) from which the air is 
suddenly and forcibly 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. 


(e) Amphoric Resonance. 

A low-pitched hollow sound approximating in quality to tym- 
panitic resonance, and sometimes 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. 

Summary . 

The varieties of resonance to be obtained by percussing the normal 
thorax are: 

(i) Vesicular resonance, to be obtained over normal lung tissue. 

(2) Tympanitic resonance, to be obtained in Traube's semilunar 

(3) Diminished resonance or dulness, such as is present over the 
scapulae, 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. Tympanitic resonance is 
normal at the bottom of the left front and axilla, but not elsewhere. 
Dulness or flatness is normal over the areas corresponding to the 
heart, liver, and spleen, and over the scapulae, but not elsewhere 
unless the muscular covering of the chest is enormously thick. Vesic- 
ular resonance is normal over the areas corresponding to the lungs, 
but becomes evidence of disease if found over the cardiac or hepatic 

Cracked-pot resonance may be normal if produced while percussing 
the chest of a child, but under all other conditions, so far as is known, 
denotes disease. 

Amphoric resonance always means disease, usually pulmonary 
cavity or pneumothorax, if found elsewhere than over the trachea. 

(/) The Lung Reflex. 

It must also be remembered, when percussing, that in some cases 
every forcible percussion blow increases the resonance to be obtained 
by subsequent blows. Any one who has demonstrated an area of 


percussion dulness to many students in succession must have noticed 
occasionally that the more we percuss the dull area, the more resonant 
it becomes, so that to those who last listen to the demonstration the 
difference which we wish to bring out is much less obvious than to 
those who heard the earliest percussion strokes. Abrams has referred 
to this fact under the name of the "lung reflex," believing, partly 
on the evidence of fluoroscopic examination, that if an irritant such 
as cold or mustard is applied to any part of the skin covering the 
thorax, the lung expands so that a localized temporary emphysema 
is produced in response to the irritation. Apparently percussion has 
a similar effect. 

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 resist- 
ance felt underneath the finger. Normally the elasticity of the 
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.). In some physicians this sense of resistance is very 
highly developed and as much information is obtained thereby as 
through the sounds elicited. As a rule, however, it is only by long 
practice that the sense of resistance is cultivated to a point where it 
becomes of distinct use in diagnosis. 


Auscultation may be practised 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 lung — 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: 

(a) On grounds of delicacy (when examining persons of the oppo- 
site sex). 

(b) 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 

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 most 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. 

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. 

i. Selection of a Stethoscope. 

(i) 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 ordi- 
nary 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 stetho- 
scope with too large rather than 
too small ends. 

(2) The binaural stethoscope, 
which is now almost exclusively 
used 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. 105) 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 

Fig. 106. — Cam- 
man Stethoscope 
With Stiff Tubing 
and Rubber Strap. 

Fig. 105. — Stetho- 
scope Fitted with 
Long Flexible 
Tubes, Especially 
Useful When Ex- 
amining Children. 



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. 105). Stiff tubing (see Fig. 106) makes it necessary for the aus- 

cultator to move his head and 

body from place to place as 

the examination 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 stetho- 
scopes are especially incon- 
venient when examining the 


(4) Jointed stethoscopes 

which fold up or take apart 

should be scrupulously avoid- 
ed. 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 producing 

in this way sounds which may 

be easily mistaken for rales. 

Such an instrument is no 

more portable nor compact 

than the ordinary form with 

flexible tubes. It has, there- 
fore, no advantages over stethoscopes made in 
one piece and possesses disadvantages which 
are peculiarly annoying. 

(5) The Chest Piece. — The majority of the stethoscopes now in 
use have a chest piece of hard-rubber or wood with a diameter of 
about seven-eighths of an inch. Chest pieces of larger diameter than 
this are to be avoided as they are very difficult to maintain 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. 107 and 108). Within 
recent years there has been introduced an instrument which, for 

Fig. 107.- 

Fig. 108. — Combination 
Bowles' Stethoscope. 


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. 109) over the 
mouth of which a thin metal plate or a bit of pigskin is fastened. 
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 
stethoscope may be distinctly heard with this. Especially is this 
true of low-pitched murmurs due to aortic regurgitation. Yet it is 
useful for examination not merely of the heart, but of the lungs as well. 

Fig. iog. — Chest Piece of Bowles' Stethoscope. On the right the shallow cup communi- 
cating with the ear tubes. On the left the diaphragm which covers the cup, and the 
ring which holds it in place. 

For any one who has difficulty in hearing the ordinary cardiac or respir- 
atory 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 prevent the instru- 
ment from slipping on the skin. The flat chest piece makes the 
instrument very useful in listening to the posterior portions 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- 
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 found the Bowles stetho- 
scope inferior to the ordinary 
stethoscope : 

(i) For listening over the apex 
of the lung for fine rales, e.g., in 
incipient phthisis. 

(2) For listening for superficial 
sounds, such as a friction 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 separate the 
chest piece of the Bowles stetho- 
scope 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 giyes us infor- 
mation similar in some respects 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 condition 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 

Fig. iio.- 

-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 



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. 1 10 and 1 1 1, and 
the method of its use in Fig. 112. In the teaching of auscultation this 
instrument is of great 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. 

II. The Use of the 

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 
squnds 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 attention is concen- 
trated upon them. 

Fig. hi. — Bowles' Multiple Stethoscope for 
Twelve Students. 

A. 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 

Among the sounds which we must learn to disregard are the 
following : 

(i) 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 

Fig. 112. — Bowies' Multiple Stethoscope in Use. Twelve students listening at once. 

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, 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 
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 
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 

B. Muscle Sounds. 

Patients who hold themselves very erect while being exam- 
ined, or who for any reason contract the muscles of that portion of 
the chest over which we are listening, produce in these muscles a 
very peculiar and 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 muscle sounds during forced inspiration, owing to the 
contraction of voluntary muscles during that portion of the respira- 
tory 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 muscular 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 contractions. The adjectives 
"muffled" and "distant" give us an inkling as to the qualities which 
distinguish muscular sounds from rales. Rales 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. 
I have made no attempt exhaustively to describe all the sounds 
due to muscular contractions and conducted to the ear by the stetho- 
scope, but have intended simply to call attention to the importance 
of studying them carefully. 

C. 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 attribute 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 stethoscope upside down, so that the ear pieces point downward 
instead of upward (see Figs. 113 and 114). 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 steth- 
oscope 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 sounds themselves have grown louder as we 
continue to listen, especially 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 attention successively upon each of the different elements 
in the sounds under consideration. In difficult cases we should use 

¥ * i IT ^ w rjfir 1 

Fig. 113. — Stethoscope Held 
Right Side Up. 

Fig. 114. — Stethoscope Held 
Wrong Side Up. 

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 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 profitably. 

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 

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 simply 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. 

I. Respiratory Types. 

In the normal chest two types of breathing are to be heard : 

(i) Tracheal, bronchial, or tubular breathing. 

(2) Vesicular breathing. 

Tracheal, bronchial, or tubular breathing is to be heard in normal 
cases if the stethoscope is pressed against the trachea, and as a rule it 
can also be heard over the situation of the primary bronchi, in front or 
behind (see Figs. 115 and 116). 

Vesicular breathing is to be heard over the remaining portions 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 where the 
presence of the scapulae obscures it, and throughout both axillae. 

(1) 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 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. 117. 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. 117). 

Fig. 115. — Situation of the Trachea and 
Primary Bronchi. 

Fig. 116. — Situation of the Trachea and 
Primary Bronchi. 

(2) The length of the up-stroke as compared with that of the 
down-stroke corresponds to the length of inspiration compared with 

(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 
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. 117 we see that when compared with 
expiration (the down-stroke) , the inspiration is — ■ 



(a) More intense. 

(&) Longer. 

(c) Higher pitched. 

Our comparison is invariably made between inspiration and ex- 
piration, 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 
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 

Fig. 117. — Vesicular 

Fig. 1.18. — Distant 
Vesicular Breathing. 

JtiG. 119. — Exaggerated 
Vesicular Breathing. 

vesicular breathing graphically we have only to draw its symbol on a 
smaller scale (see Fig. 118). 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. 119. 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. 

(2) Bronchial or Tracheal Breathing in Health. 
Bronchial breathing may be symbolically represented as in Fig. 1 20, 
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, it will be noticed, slightly exceeds inspiration both in inten- 
sity and pitch, and considerably exceeds it in duration, while as 
compared 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. 115), but 
practically one hardly ever listens over the trachea and bronchi except 
by mistake, and the importance of familiarizing one's self with the 

FiG. 120. — Bronchial Breath- Fig. 121. — Distant Bronchial Fig. 122. — Very Loud 
ing of Moderate Intensity. Breathing. Bronchial Breathing. 

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 repre- 
sented in Fig. 121, and is to be heard over the back of the neck 
opposite the position of the trachea and bronchi. Fig. 122 repre- 
sents very loud bronchial breathing such as is sometimes heard in 



(3) 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. 123. 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 one of the nipples. In the course of this journey one passes 
over points at which the breathing has, in varying degrees, the charac- 
teristics intermediate between the bronchial type from which we 

Fig. 123. — Two Common Types of 
Broncho-Vesicular Breathing. 


Fig. 124. — Distant Broncho-Vesicular 

started and the vesicular type toward which we are moving. Expira- 
tion 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 
convenience (see below, page 290), I have called the first type of broncho- 
vesicular breathing (see Figs. 123, a, and 124, a) and the second type of 
broncho-vesicular breathing (Figs. 123, b, and 124, 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"). 

(4) The Breathing in Emphysema. 

A glance at Fig. 125 will call up the most important features of this 
type of respiration. The inspiration is short and somewhat feeble, 
but not otherwise remarkable. The expiration is long, feeble, and low 
pitched. This type of breathing is the rule in elderly persons, particu- 
larly those of the male sex. 



(5) The Breathing in Asthma. 

Fig. 126 differs from emphysematous only in the greater intensity 
of the inspiration. In this type of breathing, however, both sounds 
are usually obscured to a great extent by the presence of piping and 
squeaking rales (see below) . 

Fig. 125. — Emphysematous Breathing. Fig. 

126. — Asthmatic Breathing, 
squeaking (musical) rales. 

(6) Interrupted or ''Cogwheel" Breathing. 

As a rule, only the inspiration is interrupted, being transformed 
into a series of short, jerky puffs as shown in Fig. 128. 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 then disappears. If, on the other hand, cog- 
wheel respiration is confined to a relatively small portion of the chest, 
and remains present despite the exclusion of fatigue, nervousness, or 

Fig. 127. — Cogwheel Breathing. 

Fig. 1 28. — Metamorphosing Breathing. 

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 diagnosis of early phthisis, a significance similar to 
that of rales or other signs of localized bronchitis (see below) . Cog- 
wheel breathing must be distinguished from cardio-respiratory mur- 
murs which have the qualities of breath sounds, but occur only with the 
systole of the heart. Such murmurs are very often heard at the left 
base behind, but have, so far as I know, no clinical importance. 


(7) Amphoric or Cavernous Breathing (see below, p. 158). 
(8) 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. 128), or the intensity of the breath sounds may suddenly 
be increased without other change. These metamorphoses are usu- 
ally 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. 

II. 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 
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 in the corresponding 
portion of the right lung. 1 

III. 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 

1 If the patient lies on the side, that side shows a slightly more tubular respiration 
with increased voice, whisper, and fremitus. This must be allowed for in all comparisons 
made in this position. 


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 "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 
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) Emphysema of the lung, by destroying its elasticity and reducing 
the extent of its movements, makes the breath sounds relatively 
feeble, but seldom, if ever, abolishes them altogether. 

(c) 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 bronchial secretions, distract our notice to 
such an extent that we find it difficult to concentrate attention upcn 
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, espe- 
cially over the lower two-thirds of the chest. (Edema of the lung may 
diminish the breath sounds in a similar way. 

(d) 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 
respiratory movements or because the lung is mechanically hindered 
by the presence of pleuritic adhesions, the breath sounds are propor- 
tionately feeble. 

(e) Occlusion of the upper air passages, as by spasm or oedema of the 
glottis, renders the breathing very feeble on both sides of the chest. 
If one of the primary bronchi is occluded, as by a foreign body or by 
pressure of a tumor or enlarged gland from without, we may get a 
unilateral enfeeblement of the breathing over the corresponding lung. 

(/) 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. 

It should be remembered, when estimating the intensity of the 
breathing, that the sounds heard over the right base are, as a rule, 
slightly more feeble than those heard over the left base in the normal 


IV. Bronchial or Tubular Breathing in Disease. 

(a) I 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 commonly in phthisis 
(see below, p. 285). 

(6) 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. 277. 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 
an accumulation of fluid there is often a layer of bronchial or broncho- 
vesicular breathing a little higher up near the root of the lung which is 
compressed by the fluid outside or below it. (See also changes associ- 
ated with pericardial effusion, p. 258.) 

(d) Rarer causes of bronchial breathing are hemorrhagic infarction 
of the lung, syphilis, or malignant disease, any one of which may cause 
a solidification of a portion of the lung. 

V. 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 heard in 
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 pneumonia. 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. 

VI. Amphoric Breathing (Amphora = A Jar). 

Respirations have a hollow, empty sound like that produced by 
blowing across the top of a bottle, are occasionally heard in disease 
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 


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: 

(i) Bubbling rales, including (a) coarse, (b) medium, and (c) fine 

(2) Crackling rales (large, medium, or fine) . 

The smallest varieties of this type are known as "crepitant" or 
" subcrepitant " rales. 

(3) Musical rales (high or low pitched) . 

Each of these varieties will now be described more in detail. 

(1) Bubbling Rales. 

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 

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.) 


stethoscope. In catarrh of the larger 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. 290). The finer grades of rales correspond to the finer 

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. 129, 
using large dots for coarse rales and small dots for fine rales. Musical 
rales can be symbolized by the letter S (squeaks) . 

(2) 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 bronchitis in which the secretions are unusually tenacious and viscid. 
They are especially apt to come at the end of inspiration, a large 
number being evolved in a very short space of time, so that one often 
speaks of an "explosion of fine crackling rales" at the 
end of inspiration. Crackling rales are to be heard in 
any one of the conditions in which bubbling rales occur, 
but are more frequent in tuberculosis than in simple 
bronchitis. There is some doubt whether or not fine j 

crackles can be produced in a pleural exudate, old or 

new, but personally I am convinced that they are not 
. ' f , Fig. 129 — 

infrequently so produced. Explosion of 

Crepitant rales, which represent the finest sounds of p me Rales at 
this type, are very much like the noise which is heard End of Inspi- 
when one takes a lock of hair between the thumb and ration, 
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 
sound, but with practice the component parts may be distinguished. 
This type of rales is especially apt to occur during inspiration alone, 
but not very infrequently they are heard during expiration as well. 
From subcrepitant rales they are distinguished merely by their being 
still finer than the latter. 1 Subcrepitant rales are often mixed with 

1 A distinction was formerly drawn between crepitant and subcrepitant rales, on the 
ground that the latter were heard both during both respiratory sounds and the former 
only during inspiration, but this distinction cannot be maintained and is gradually being 
given up. 


sounds of a somewhat coarser type, while crepitant rales are usually- 
all of a size. If the chest is covered with hair, sounds precisely like 
these two varieties of rales may be heard when the stethoscope is 
placed upon the hairy portions. To avoid mistaking these sounds for 
rales one must thoroughly wet or grease the hair. 

Crepitant Rales in Atelectasis. 

Crepitant and subcrepitant rales 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 patient who is breathing superficially first begins 
to take deep breaths. In such cases, they usually disappear after 
the few first respirations, and are then to be explained by the tearing 
apart of the slightly agglutinated surfaces of the finer bronchioles. 

It is by no means invariably the case, however, that such subcrep- 
itant rales are merely transitory in their occurrence. In a large number 
of cases they persist despite deep breathing. The frequency of 
subcrepitant 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 axillae 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 This explanation would agree 
with the observations of Abrams, to which I shall refer later (see below, 

P- 335)- 

(b) Crepitant or subcrepitant rales are also to be heard in a certain 
portion of cases of pneumonia, in the very earliest stages and when 
resolution is taking place ("crepitans redux ") . More rarely this type 
of rale may be heard in connection with tuberculosis, infarction, or 
oedema of the lung. 

1 So as to expand the lung and produce the "entfaltungsgeriiusch" of the Germans. 


In certain cases of dry pleurisy there occur fine crackling sounds 
which can scarcely be differentiated from subcrepitant rales. I shall 
return to the description of them in speaking of pleural friction (see 
below, p. 314). 

(3) Musical Rales. 

The passage of air through bronchial tubes narrowed by inflam- 
matory swelling of their lining membrane (bronchitis), by dropsical 
effusions or by spasmodic contraction (asthma), gives rise not infre- 
quently to a multitude of musical sounds. Such a stenosis occurring 
in relatively large bronchial tubes produces a deep-toned groaning 
sound, 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 the "bubbling rales" 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 rales are of all adven- 
titious 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 short time. This is to some extent true of all 
varieties of rales, but especially of the squeaking and groaning 

Musical rales are heard, as a rule, more distinctly during expiration, 
especially when they occur in connection with asthma or emphysema. 
In these diseases one may hear quite complicated chords from the 
combinations of rales which vary in pitch. 

VIII. 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. Lateral decubitus multiplies and 
intensifies rales on the lower side. Other effects of coughing upon 
physical signs will be mentioned later (pp. 278, 285). 

IX. 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 abnorm- 
ally dry, as in Asiatic cholera, 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. 87) . 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. Very rarely 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, ir- 
regular 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. 
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 pleuritic friction can be felt 
if the palm of the hand is laid over the suspected area; occasionally the 
sound is so loud that it can be heard by the patient himself or by those 


around him. F. T. Lord 1 has recently called attention to 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 apparently 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. 

X. Auscultation of the Spoken or Whispered Voice Sounds. 
The more important of these is: 

(a) 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 
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 exact boundaries 
of a solidified area is very great, especially when we desire 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. 

1 F. T. Lord: Boston Med. & Surg. Journal, Oct. 21, 1909. 


(6) 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 
transmission of audible words, and not merely of diffuse, unrecogniz- 
able voice sounds, is considerably commoner in the solidifications 
due to pneumonia than in those due to phthisis; it occurs in some 
cases of pneumothorax and pulmonary cavity. 

(c) Ego phony. 

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. 


XI. Phenomena Peculiar to Pneumohydrothorax and Pneumo- 


(i) Succussion Sounds. 

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 ruptured diaphragm. In accident cases this 
possibility must be remembered. 

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 succussion 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 

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. 


probably to rales 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 

(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. " Valve Areas." 

In the routine examination of the heart, most observers listen in 
four places: 

(i) 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." 

Aortic area.r 

Tricuspid area. 

Pulmonic area. 

Mitral area. 

Fig. 130. — The Valve Areas. 

(4) At the bottom of the sternum near the ensiform cartilage, 
the "tricuspid area." 

These points are represented in Fig. 130 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 sounds heard best 
at the apex can be proved (by post-mortem examination or otherwise) 
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; those which 
are loudest at the second right intercostal space to be produced at the 
aortic orifice; 1 while those which are most distinct near the origin of 
the ensiform cartilage are produced at the tricuspid orifice. 

II. The Normal Heart Sounds. 

A glance at Fig. 131, 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 "mitral 
area," that is, in the region of the apex impulse of the heart, keeping 
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 admitted to be 
due to the closure of the semilunar valves. The cause of the first 
sound has been a most fruitful source of discussion, and no one expla- 
nation of it can be said to be generally received. Perhaps the most 
commonly accepted view attributes the first or systolic sound of the 
heart to a combination of two elements — 

(a) 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. 

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 
"snapping" 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 

1 For the exceptions to this rule, see below, page 214. 

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. 


appreciation of the rhythm alone for the identification of the systolic 
sound. This is, however, an unsafe practice and leads to many errors. 
Our impression as to which of the two 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 synchronous 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. 

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 listen 

„-- Pulmonic valve. 

•" Aortic valve. 

Tricuspid valve. — " """ /\ \^E^V\ /v^C^ A Mitral valve 

Fig. 131. — Anatomical Position of the Cardiac Valves. 

over the pulmonary area (in the second left intercostal space) , we find 
that the rhythm of the heart sounds has 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. 

Over the aortic area (i.e., in the second right interspace) 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. 172). 

1 When the cardiac impulse can be neither seen nor felt, the pulsation of the carotid 
will generally guide us. The radial pulse is not a safe guide. 


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 and during conditions of 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 stiffer. 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 

(i) 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 bodily or mental 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, but less 

1 A third heart sound (or reduplication of the second sound) is audible on careful 
auscultation in a considerable proportion of healthy young individuals — especially if they he 
on the left side. Barie described it in 1893 (Semaine med., 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. 


often than one would suppose, while dilatation 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 " thump- 
ing first sound" or as a "sharp slap." 

(6) 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. Chronic myocarditis, or any 
other change in the heart wall which tends to enfeeble it, produces a 
weakening and shortening of the first sound similar to that just de- 
scribed. 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. Among valvular diseases 
of the heart the one most likely to be associated with a diminution in 
intensity of the first apex sound is mitral regurgitation. 

(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, however, to be 
unusually frequent in the weakened heart of nephritis and arterio- 

(2) Modifications in the Second Sounds as Heard at the Base of the 


Physiological Variations. — The relative intensity of the pulmonic 
second sound, when compared with the second sound heard in the 
conventional aortic area, varies a great deal at different periods of life. 



Attention was first 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 


70/o— - 




30-39 J40-49 





— 90% 

— 80% 


— - 30*/ 










Fig. 132. — Showing the Per Cent, of Accentuated Pulmonic Second Sound in Each Decade. 

Based on 1,000 cases. 

cases, between the ages of twenty and twenty-nine, showed an accen- 
tuation of the pulmonic second, while after the thirtieth year 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. 132 and 133, and appear to show 

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" (1900); Allbutt, "System of Medicine." 



that the relative intensity of the two sounds in the aortic and pulmonic 
arteries depends primarily upon the age of the individual, the pulmonic 
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 





30-39 40-49 




— Mxtf 



— «r. 









10% - 

Fig. 133. — Showing the Per Cent, of Accentuated Aortic Second Sound in Each Decade. 

Based on 1,000 cases. 

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 
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. 


Pathological Variations. 

A. 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 
in stenosis or insufficiency of the mitral valve, or in obstructive disease 
of the lungs (emphysema, bronchitis, phthisis, chronic interstitial 
pneumonia). Indirectly accentuation of the pulmonic second sound 
points to hypertrophy of the right ventricle, since without such hyper- 
trophy the work of driving the 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. 

B. Weakening or Absence of the Pulmonic Second Sound. 

Weakening of the pulmonic second sound is a very serious symp- 
tom, sometimes to be observed in cases of pneumonia or cardiac dis- 
ease near death. It is thus a very important indication for prognosis. 

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 is 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. 

C. 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 intensity of the aortic second sound 
occurs in aneurism or diffuse dilatation of the aortic arch. 

D. 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 to a lesser degree in mitral regurgitation, 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, such as fibrous myocarditis, fatty degeneration, and 
cloudy swelling. Relaxation of the peripheral arteries has the 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 hypertrophy 
and dilatation of the left ventricle, and among valvular diseases espe- 
cially by mitral stenosis. It is weakened or reduplicated by parietal 
disease of the heart. Any of these changes may occur temporarily 
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, emphysema, 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 aortic and pulmonic sounds have little practical 

(3) Modifications in the Rhythm of the Cardiac Sounds. 

(1) 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 heart, the name of "embryocardia" is sometimes applied to 
it. The "tick-tack" rhythm may be heard in any form of cardiac 
disease after compensation has failed, or in any condition leading to 

(2) A less common change of rhythm is that produced by a short- 
ening of the interval between the two heart sounds owing to an incom- 
pleteness of the contraction of the ventricle. This change may occur 
in any disease of the heart when compensation fails. 

(a) The commoner type is the presystolic gallop rhythm in which an 
extra sound occurs j ust 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 probably identical with 
the so-called "third heart sound" referred to on page 170, and most 
constantly heard in the early stages of mitral stenosis. 

At the end of a long inspiration this change may be observed in 
almost any healthy person if one listens at the base of the heart. It 
is still better brought out after muscular exertion or by holding the 

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. 
(5) ''Muffling," "Prolongation" or " 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 
chiefly an un clearness 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. 

(i) 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, 
lead poisoning, and other diseases, a similar arterial sound is to be 
heard much more frequently than in health. 




Cardiac Murmurs. 
(a) 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 

(b) 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, or by a stretching of the orifice into which the valves 
are inserted. 

Diseases of the valves themselves may lead to the production of 
murmurs : 

(a) When the valves fail to close at the proper time (incompetence, 
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 
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 

Fig. 134. — 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. 

blood current and thereby to the abnormal sounds to which we give 
the name murmurs. 1 (See Figs. 134, 135 and 136.) 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, 


Fig. 135. — Diagram to Illustrate the Production of a Cardiac Murmur Through Stenosis 

of a Valve-Orifice. 

for example, the aortic valves fail to close after the left ventricle has 
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," 

Fig. 136. — Diagram to Illustrate the Production of Cardiac Murmurs Through Roughening 

of a Valve. 

and of the murmur so produced as an aortic regurgitant murmur or a 
murmur of aortic regurgitation. A similar regurgitation from the 
left ventricle into the left auricle takes place in case the mitral valve 

1 The method by which functional murmurs are produced will be discussed later. 
(See page 186.) 


fails to close at the beginning of systole. If, on the other hand, 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 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 (tri- 
cuspid 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 : 

(i) 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 when 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 
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 vast 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 car- 
diac 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 
almost invariably produced at the pulmonic orifice or just above it in 
the conus arteriosus. 

Murmurs whose maximum intensity is at the root of the ensiform 
cartilage or within a radius of an inch and a half from this point are 
usually produced at the tricuspid orifice. Murmurs produced at the 
aortic orifice may be heard best in the aortic area, but in a large propor- 
tion of cases are loudest on the other side of the sternum at or about 
the situation of the fourth left costal cartilage. Occasionally they are 
best heard at the apex of the heart in the axilla or over the lower part 
of the sternum (see below, Fig. 159). 

(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 tricuspid regions, how are we to know 
whether the sound is simple or compound, whether produced at one 
valve orifice or at several? 

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 : 

(i) 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 in- 
tensity which regularly diminishes as we recede from a maximum 
whose seat corresponds with some one of the valve areas just de- 
scribed. These areas of propagation are shown in Figs. 147, 148, 151, 
and 156. 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 tricuspid area, we may get an impression best 
expressed by Fig. 137. That is, a systolic murmur heard loudly at the 
apex may fade away as we move toward the ensiform, until at the point 
x (Fig. 137) it is almost inaudible. But as we go on in the same direc- 
tion the murmur may begin to grow louder (and perhaps to change in 
pitch and quality as well) until a maximum is reached at the tricuspid 
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 tricuspid orifice, 
and may be confirmed by the discovery of other evidences of a double 
lesion. • No diagnosis is satisfactory which rests on the evidence of mur- 
murs alone. Changes in the size of the heart's chambers or in the pulmo- 



nary 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. 137, generally means two-valve lesions. A similar 
"hour-glass " may be found to represent the auditory facts as we move 
from the mitral to the pulmonic or to the aortic areas (see Fig. 138) 
and, as in the previous case, arouses our suspicion that more than one 
valve is diseased. 

It must not be forgotten, however, that "a murmur may travel 
some distance underground and emerge with a change of quality" 


Fig. 137. Fig. 138. 

Fig. 137. — Mitral and Tricuspid Regurgitation. The intensity of the systolic murmur 
is least at the "waist" of the shaded area and increases as one approaches either end of it. 

Fig. 138. — Mitral Regurgitation and Aortic Stenosis. The systolic murmur is 
loudest at the extremities of the shaded area and faintest at its "waist." 

(Allbutt). This is especially true of aortic murmurs, which are 
often heard well at the apex and at the aortic area, and faintly in the in- 
tervening space, probably owing to the interposition of the right 

In such cases we must fall back upon the condition of the heart 
itself, as shown by inspection, palpation, and percussion, and upon the 
condition of the pulmonary and peripheral circulation, as shown in 
the other symptoms and signs of the cases (dropsy, cough, etc.). 

(4) Intensity of Murmurs. — Sometimes murmurs are so loud 
that they are audible to the patient himself or even at some dis- 
tance 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 functional murmurs, see below, p. 188.) 

A loud murmur means a powerful heart driving the blood strongly 
over the diseased valve. 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 
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 
murmur is its increase or decrease while under observation, and not 
its loudness at any one time. 

(5) 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 "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 
rasping murmurs are associated either with the calcareous deposit 
upon a valve or very marked narrowing of the valve orifice. 

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. Almost all murmurs are of the latter type except those 
associated with mitral or tricuspid obstruction. 

(6) 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. 

(7) 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. 

(8) 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 entirely disappear 
when he lies down. Diastolic murmurs are relatively little affected 

1 Rosenbach holds that they may be produced by adhesive pericarditis. 


by the position of the patient, but in the majority of cases are some- 
what 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 (see above, p. 184). 

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 
valve, and is in marked contrast with the variations of functional mur- 
murs which are heard chiefly or exclusively at the end of inspiration. 

(9) 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 

' ' 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 oc- 
cur, although with exceeding rarity, are probably due to stretching of 

1 For exception to this see below, page 205. 


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 vast majority of them are heard best over the pulmonic 
valve in the second left intercostal space. From this point they are 
transmitted in all directions, and are frequently to be heard, although 
with less intensity, in the aortic and mitral areas. Occasionally 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. 

(4) They are not associated with any 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 and not 
transmitted to the left axilla or to the back. 

(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 ancemia, 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 It should 
not be forgotten that a real, though temporary, leakage through the 
mitral or tricuspid valve may be associated with anaemia or debilitated 
conditions owing to weakening of the papillary muscles or of the mitral 
sphincter. In such cases we find not the signs of a functional murmur, 
as above described, but the evidence of an organic valve lesion here- 
after to be described. 

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. 


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. 
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; never musical. The very rare 
diastolic functional murmur occurs exclusively, so far as I am aware, 
in conditions of profound anaemia; i.e., when the haemoglobin is twenty- 
five per cent, or less. It can sometimes be abolished by pressing the 
jugular bulb and can then be observed, if followed to the neck, to pass 
over gradually into a continuous venous hum with a diastolic accent. 

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 of the chest. 

Cardio-respiratory murmurs may be either systolic or diastolic, 
but the vast majority of 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 murmur, and sound like an inspiration 
interrupted by each diastole 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- 
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 i-s not the case. 

Murmurs of Venous Origin. 

I have already mentioned that the venous hum so often heard in 
the neck in cases of anaemia may be transmitted to the region of the 
base of the heart and heard there as a diastolic murmur owing to the 
acceleration of the venous current by the aspiration of the right 
ventricle during diastole. Such murmurs are very rare and may 
usually be obliterated by pressure upon the bulbous jugularis, or even 
by the compression brought to bear upon the veins of the neck when 
the head is sharply turned to one side. They are heard better in the 
upright position and during inspiration. 

Arterial Murmurs. 

(i) Roughening or slight dilatation of the arch of the aorta, due to 
chronic endaortitis, is a frequent cause in elderly men of a systolic 
murmur, heard best at the base of the heart and transmitted into the 
vessels of the neck. Such a murmur is very rarely accompanied by a 
palpable thrill. From cardiac murmurs it is distinguished by the lack 

*For the distinction from cog-wheel breathing, see above, page 153. 


of any other evidence of cardiac disease and the presence of marked 
arterio-sclerosis in the peripheral vessels (see further discussion under 
Aortic Stenosis, p. 227, and under Aneurism, p. 264). 

(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 

(3) Pressure exerted upon any of the superficial arteries (carotid, 
femoral, etc.) produces a systolic murmur (see below, p. 224). Dias- 
tolic arterial murmurs are peculiar to aortic regurgitation. 

(4) Over the anterior fontanelle 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. 



Clinically it is convenient to divide the ills which befall the heart 
into three classes: 

(i) Those which deform the cardiac valves (valvular lesions). 

(2) Those which weaken the heart wall (parietal disease). 

(3) Congenital malformations. 

Lesions which affect the cardiac valves without deforming them 
are not often recognizable during life. The vegetations of acute 
endocarditis often do not produce any peculiar physical signs until 
they have so far deformed or obstructed the valves as to prevent their 
opening or closing properly. 

The murmurs which are often heard over the heart in cases of acute 
articular rheumatism cannot be considered as evidence of vegetative 
endocarditis unless an access of fever and leucocytosis, some evidence 
of embolism or some valvular deformities, with their results in valvu- 
lar obstruction or incompetency, ensue. The chordae tendineae may 
be ruptured or shortened, thickened, and welded together into shape- 
less masses, but if these deformities do not affect the action of the 
valves we have no means of recognizing them during life. Congenital 
malformations are practically unrecognizable as such. If they do not 
affect the valves, we cannot with any certainty make out what is 

For physical diagnosis, then, heart disease means either deformed 
valves or weakened walls. I include here, under the results of weak- 
ened walls, all the disorders of conduction and rhythm described on 
pages 244 to 250. Whatever else may exist, we are none the wiser 
for it unless the autopsy enlightens us. 

In this chapter I shall confine myself to the discussion of valvular 
lesions and their results. 

Valvular lesions are of two types : 

(a) Those which produce partial obstruction of a valve orifice or 
prevent its opening fully ("stenosis"). 




(6) Those which produce leakage through a valve orifice or prevent 
its closing effectively {"regurgitation," "insufficiency," "incompetency"). 

Stenosis results always from the stiffening, thickening, and con- 
traction of a valve. 

Regurgitation, on the other hand, may be the result either of — 

(a) Deformity of a valve, or 

(6) Weakening of the heart muscle. 

Valvals semilunaris 
BiaiStrn a. pfhrnsmalis " , 

,„,„:, „„„.., J. J 

Fig. 139. — The Base of the Contracted Heart Showing Sphincteric Action of the Mus- 
cular 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.) 

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. 139) and the contraction 
of the papillary muscles (Fig. 140). 

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, 



so that the valve-flaps swing back into the auricle and permit 
regurgitation of blood from the ventricle. 

Valvular incompetence, then, differs from valvular obstruction 
in that the latter always involves deformity and stiffening of valves, 
while incompetence or leakage is often the result of deficient muscular 
action on the part of the heart wall. An obstructed valve is almost 
always leaky as well, since the same deformities which prevent a 
valve from opening usually prevent its closure; but this rule does not 
work backward. A leaky valve is often not obstructed. It is leaky 

Mitral curtains. 




Fig. 140. — The Mitral Valve Closed, Showing the Action of the Papillary Muscles. 



but not obstructed if the valve curtain has been practically destroyed 
by endocarditis; or, again, it is leaky but not obstructed if the leak 
represents muscular weakening of the mitral sphincter or of the papil- 
lary muscles. Pure stenosis is very rare. Pure regurgitation is very 
common, especially at the mitral. 

When valves are so deformed that their orifice is both leaky and 
obstructed, we have what is known as a "combined" or "double" 
valve lesion. 

Since valvular lesions are recognized largely by their results, first 
upon the walls of the heart itself and then upon the other organs of 
the body, it seems best to give some account of these results before 
passing on to the description of the individual lesions in the heart 



The results of valvular lesions are first conservative and later de- 
structive. The conservative results are known as: 

The establishment of compensation through hypertrophy. 
The destructive or degenerative results are known as: 
The failure of compensation through (or without) dilatation. 
I shall consider, then, 

(a) The establishment and the failure of compensation. 

(b) Cardiac hypertrophy. 

(c) Cardiac dilatation. 

Establishment and Failure of Compensation in Valvular 
Disease of the Heart. 

We may discriminate three periods in the progress of a case of 
valvular heart disease : 

(i) The period before the establishment of compensation. 

(2) The period of compensation. 

(3) The period of failing or ruptured compensation. 

(1) Compensation Not Yet Established. 

In most cases of acute valvular 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 regurgitation due to 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 de 
absolutely no evidence of the valve lesion except the characteristic 
diastolic murmur. 

(2) 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 affects especially 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 
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 hypertrophy of the right ventricle. 

On the other hand, it is obvious that obstruction at the aortic 
valves or in the peripheral arteries (arterio-sclerosis, nephritis) 
demands an increase in power in the left ventricle, in order that the 
requisite amount of blood may be forced through arteries 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 that 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 

(3) 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 stretching of the heart's walls. Not 
infrequently recurrent attacks of "failing compensation" represent a 
flare-up of a smouldering endocarditis as the accompanying leucocytosis 
{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 statis; 
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, 

1 Rosenbach brings forward evidence to show that the arteries, the lungs, and other 
organs actively assist in maintaining compensation. 


liver, and the serous cavities. Engorgement of the lungs is especially 
marked in cases of mitral disease with weakening of the right ventricle, 
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. 

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 different 
lesions with which they are associated. 


i. Vascular hypertension (nephritis, arterio-sclerosis) . 

2. Valvular disease (mostly "rheumatic"). 

3. Syphilitic aortitis (with or without aneurism). 

4. Adherent pericardium. 

5. Beer drinking. 

6. Severe and prolonged muscular exertion (athlete's heart). 
Moderate hypertrophy and dilatation are often found in Graves' 

disease and in severe anaemias. 

W. T. Howard's classification of 108 cases of cardiac hypertrophy 
post mortem (Johns Hopkins Bull., 1894, iii, 266), is entirely in accord 
with my own experience : 



Valvular heart disease 

Adherent pericardium 

Hard work 






Per c 























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 cause, both sides of the heart 
are affected, but we may distinguish cases in which one or the other 
ventricle is predominantly affected. 

(i) Cardiac hypertrophy affecting especially the left ventricle. 

(a) High systolic blood pressure is the most constant and reliable 
of all the 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. 

,(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. 2 

(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. A very loud 
first sound is much more characteristic of a cardiac weakness or 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 

1 This is due partly to a stretching of the aorta, produced by the increased weight 
of the heart. 

2 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. 


subclavians, 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, anaemia, or muscular work. I have 
frequently observed it in healthy athletes. 

The radial pulse wave has no constant characteristics, but depends 
rather upon the cause which has produced the hypertrophy than upon 
the hypertrophy itself. 
(2) 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 
two 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 right and left 
borders of the heart; and 

(b) Accentuation of the pulmonic second sound, which is often 
palpable as well as audible. 

The apex beat is displaced both to the left and downward, but 
especially to the left. In cases of long-standing mitral disease, the 
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 almost 
invariably present in hypertrophy of the right ventricle, though it is 
not peculiar to that condition. It may be heard, for example, in cases 
of pneumonia when no such hypertrophy is present, but in the vast 
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 

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. 



Dilatation of the Heart. 

Dilatation cannot be considered as an unmixed evil. In aortic 
regurgitation and most other types of cardiac disease it is inseparably 
linked with hypertrophy and is present long before compensation 
fails. Probably it is the predominance of dilatation over hypertrophy 
that causes stasis and the other abnormalities next to be described. 

(i) 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 
is said to occur occasionally. In debilitated or poorly nourished 

Fig. 141. — Dilated Heart. From v. Ziemssen's Atlas. 

subjects or when the heart has been previously weakened by disease 
such an acute dilatation may be serious or even fatal in its results. I 
have never seen this in healthy persons, but Hornung (Berl. klin. 
Woch., xlv, 1769) believes that with the fmoroscope he has identified 
cases of acute dilatation in healthy persons after fright, sexual excite- 
ment, high altitude, and other strains. 

(2) Chronic dilatation comes on gradually as a result of valvular 
disease or other cause, and gives rise to practically the same physical 
signs as those of acute dilatation, from which it differs chiefly as regards 
the accompanying physical phenomena and the prognosis. 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; (b) enlargement of the heart, as indicated by inspection, 


palpation, and percussion, and (sometimes) (c) murmurs indicative 
of stretching of one or another of the valvular orifices; (d) often 
presystolic gallop rhythm (see above, p. 176); (e) evidence of stasis 
at the periphery. 

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 and sometimes shows an unusually blunt or rounded 
outline at the apex of the heart. 

On auscultation, the first sound is usually very short and sharp, but 
not feeble unless it is accompanied by a murmur. In case the mitral 
orifice is so stretched as to render the valve incompetent, or in case 
the muscles of the heart are so fatigued and weakened that they do 
not assist in closing the mitral orifice, a systolic murmur is to be heard 
at the apex of the heart. This murmur is transmitted to the axilla 
and back, but does not usually replace the first sound of the heart. 
The aortic second sound, as heard in the aortic area and at the apex, 
is feeble. Peripheral blood-pressure falls. 

Predominant Dilatation of the Right Ventricle. 

The failure of muscular tone is shown by an increase in the area 
of cardiac dulness to the right of the sternum (corresponding to the 
position of the right auricle), by feebleness of the pulmonic second 
sound together with signs of congestion and engorgement of the lungs, 
and often by a systolic murmur at the tricuspid valve; i.e., at or near 
the root of the ensiform cartilage. When this latter event occurs, 
one may have also systolic pulsation in the jugular veins and in the 
liver (see below, p. 234). 

In cases of acute dilatation, such as occur in infectious fevers or 
in chronic latent myocardial disease, there is often to be heard a systolic 
murmur loudest in the pulmonary area and due very possibly to a 
dilatation of the conus arteriosus. 

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. 


(4) Chronic Valvular Disease. 

I. Mitral Regurgitation. 

The commonest and probably one of the least serious of valvular 
lesions is incompetency of the mitral. It results in most cases from 

Fig. 142. — Normal Heart during Systole. Mitral valve closed; blood flowing through the 
open aortic valves into the aorta. 


Fig. 143. — Mitral Regurgitation. The heart is in systole and the arrows show the current 
flowing back in the left auricle as well as forward into the aorta. 

the shortening, stiffening, and thickening of the valve produced by 
rheumatic endocarditis in early life. It is the lesion present in most 
cases of chorea (see Figs. 142 and 143). 


Temporary and curable mitral regurgitation may result from weak- 
ening of the heart muscle, which normally assists in closing the mitral 
orifice through the sphincter-like contraction of its circular fibres. 
- Great muscular fatigue, such as is produced by a hard boat race, 
may result in a temporary relaxation of the mitral sphincter or of the 
papillary muscles sufficient to allow of genuine but temporary and 
curable regurgitation through the mitral orifice. In conditions of 
profound nervous debility, excitement, or exhaustion, similar weak- 
ening of the cardiac muscles may allow of a leakage through the mitral, 
which ceases with the removal of its cause. Stress has been laid upon 
these points by DaCosta, by Prince, and recently by Arnold. 

Mitral insufficiency due to stretching of the ring into which the 
valve is inserted occurs not infrequently as a result of dilatation of the 
left ventricle, and is commonly known as relative insufficiency of the 
mitral valve. The valve orifice can enlarge, the valve cannot, and 
hence its curtains are insufficient to fill up the dilated orifice. This 
type of mitral insufficiency frequently results from aortic regurgitation 
with the dilatation of the left ventricle which that lesion produces, 
and from chronic nephritis and arterio-sclerosis, which weaken the 
heart wall until it dilates and widens the mitral orifice. 

The results of any form of mitral leakage occur in this order: 

( i ) Dilatation and hypertrophy of the left auricle, which has to receive 
blood both from the lungs and through the leaky mitral from the left 

(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 the tricuspid valve 
gives way and tricuspid leakage occurs. 

(4) The capacity for hypertrophy possessed by the right auricle 
is soon exhausted, and we get then — 

(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 some vestige of sphincter action at the leaky mitral orifice, 


as well as by the labor of contracting upon the extra quantity of blood 
delivered to it by the enlarged left auricle. 

At last the circle is complete. Every chamber in the heart is 
enlarged, overworked, and failure is imminent. 

Returning now to the signs of mitral regurgitation, we shall find 
it most convenient to consider first the type of regurgitation produced 
by rheumatism and resulting in thickening, stiffening, and retraction 
of the valve. 

Physical Signs. 
(a) First Stage — Prior to the Establishment of Compensation. 

We have but one characteristic physical sign : 

A systolic murmur heard loudest at the apex of the heart, trans- 
mitted to the back (below or inside the left scapula) and to the left 
axilla. The murmur is usually long and sometimes musical in char- 
acter; when this is the case diagnosis is much easier. Systolic musical 
murmurs widely transmitted do not occur without valvular leakage. 
Rosenbach believes that adherent pericardium is capable of producing 
such a murmur, but only, if I understand him rightly, in case there is a 
genuine mitral leakage due to the embarrassing embrace of the peri- 
cardium which prevents the mitral orifice from closing. 

"Functional" or "haemic" murmurs are usually short, are rarely 
heard in the back, and very rarely, if ever, have a musical quality. 

Cases of mitral regurgitation are not very often seen at this stage, 
but in acute endocarditis after the fever and anaemia have subsided, 
or in chorea, such a murmur may exist for days or weeks before any 
accentuation of the pulmonic second sound or any enlargement of 
the heart appears. I have had the opportunity of verifying the 
diagnosis at autopsy in many such cases. 

(b) Second Stage — Compensation Established. 

As long as compensation remains perfect, the only evidence of 
regurgitation may be that obtained by auscultation, and I shall ac- 
cordingly begin with this rather than in the traditional way with 
inspection, palpation, and percussion. 

The distinguishing auscultatory phenomena in cases of well-com- 
pensated mitral insufficiency are: 

(a) A systolic murmur whose maximum intensity is at or near the 
apex impulse of the heart, but which is also to be heard in the left 


axilla and in the back below or inside the angle of the left scapula 
(so far the signs are those of the first stage, above described). 

(b) A pathological accentuation of the pulmonic second sound. 
This is the minimum of evidence upon which it is justifiable to 

make the diagnosis of compensated mitral regurgitation. In the vast 
majority of cases, however, our diagnosis is confirmed by the following 
additional data: 

(c) Enlargement of the heart as shown by inspection, palpation, 
and percussion. 

The pulse in well-compensated cases shows no considerable ab- 
normality. When compensation begins to fail, or sometimes before 
that time, the most characteristic thing about the pulse is its marked 
irregularity both in force and rhythm. Such irregularity, though 
usually of the " absolute" type and associated with auricular fibrillation, 
is at once more common and less serious in mitral disease than in that 
of any other valve; it may continue for years and be compatible with 
very tolerable health. 

Returning now to the details of the sketch just given, we will take 
up first — 

(a) The Murmur.— -In children the murmur of mitral regurgitation 
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 




Fig. 144. — Diagram to Represent Systolic Mitral Murmur. The heavy lines represent 
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. 

The length of the murmur varies in different cases, but as a rule it is 
longer than those which are "functional" in origin. It rarely ends 
abruptly, but usually "tails off" at the end of stystole (see Fig. 144). 
Musical murmurs are heard more often in mitral regurgitation than 


in any other valve lesion. The first sound of the heart may or may 
not be replaced by the murmur (see Fig. 145). When" the sound 
persists and is heard either with or before the murmur, one can infer 
that the lesion is relatively slight in comparison with cases in which 
the first sound is wholly obliterated. Post-systolic or late systolic 
murmurs, which are occasionally heard in mitral regurgitation, are 
said to point to a relatively slight amount of disease in the valve 
(see Fig. 144). Rosenbach claims that the late systolic murmur 

2nd ,.. 2nd 

Jllim.. I : ilUllHlni i , I 

Fig. 145. — Systolic Mitral Murmur Replacing the First Sound of the Heart. 

is always due to organic disease of the valves and never occurs as a 
functional murmur. 

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 mitral regurgitation is conducted in all directions, 
but especially toward the axilla and to the back (not around the chest, 
but directly) . In the latter situation it is usually louder than it is in 
mid-axilla, and occasionally it is heard as loudly in the back as any- 

11, 2nd I 

IIHlliiiiii I I 



Fig. 146. — Late Systolic Murmur. The first sound is clear and an interval intervenes 
between it and the murmur. 

where else. This is no doubt owing to the position of the left auricle 
and the direction of the regurgitant stream (see Figs. 147 and 148). 

(b) After compensation is established and as long as it lasts an 
accentuation of the pulmonic second sound is almost invariably to be 
made out, and may be so marked that we can feel and see it, as well 
as hear it. Not infrequently one can also see and feel the pulsation 
of the conus arteriosus — not the left auricle — in the second and 
third left intercostal space. (It may be well to mention again here 
that by accentuation of the pulmonic second sound one does not 
mean merely that it is louder or sharper in quality 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.) 

Pulmonic second 

Systolic murmur 
loudest here. 



-Mitral Regurgitation. The murmur is heard over the shaded area as well as 
in the back. 

Systolic murmur. -~ 

Fig. 148. — Mitral Regurgitation. Murmur heard over the shaded area. 

Occasionally the pulmonic second sound is loudly reduplicated, but 
as a rule this points to an accompanying stenosis of the mitral valve. 
At the apex the second sound {i.e., the transmitted aortic second) 
is feeble or even wanting altogether, owing to the relatively small 
amount of blood which recoils upon the aortic valves. 


(c) Enlargement of the heart, and more especially of the right 
ventricle, is generally to be made out, and in the majority of cases this 
enlargement is manifested by displacement of the apex impulse both 
downward and toward the left, but more especially to the left. Per- 
cussion confirms the results of inspection and palpation regarding the 
position of the cardiac impulse. The normal substernal dulness is 
increased in intensity, and we can sometimes demonstrate an enlarge- 
ment of the heart toward the right (see Fig. 145). 

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 be bulged, and even in adults such a systolic 
thrill is not so rare as some writers would have us suppose. 

(d) The pulse, as said above, shows nothing characteristic at any 
stage of the disease. While compensation lasts, there is usually noth- 
ing abnormal about the pulse, although it may be somewhat irregular 
in force and rhythm, and may be weak when compared to the powerful 
beat at the apex in case the regurgitant stream is a very large one. 
Irregularity at this period is less common in pure mitral regurgitation 
than in cases complicated by stenosis. 

(c) Third Stage — Failing Compensation. 

When compensation begins to fail, the pulse becomes weak and 
irregular, and many heart beats fail to reach the wrist, but there is 
still nothing characteristic about the pulse, which differs in no respect 
from that of any case of cardiac weakness of whatever nature. 

(e) Evidence of venous stasis, first in the lungs and later in the 
liver, lower extremities, and serous cavities, does not show itself so 
long as compensation is sufficient, but when the heart begins to fail the 
patient begins to complain not only of palpitation and cardiac distress, 
but of dyspnoea, orthopnoea, and cough, and examination reveals a 
greater or lesser degree of cyanosis with pulmonary oedema manifested 
by crackling rales at the base of the lungs posteriorly, and possibly 
also by haemoptysis or by evidences of hydrothorax (see below, p. 308). 
If compensation is not re-established, the right ventricle dilates, the 
tricuspid becomes incompetent, the liver becomes enlarged and 
tender, dropsy becomes general, the heart and pulse become more and 
more rapid and irregular, the heart murmur disappears and is replaced 
by a confusion of short valvular sounds, " gallop rhythm" or "delirium 
cordis," often considerably obscured by the noisy, labored breathing 


with numerous moist rales. In a patient seen for the first time in such 
a condition diagnosis may be impossible, yet mitral disease of some 
type may usually be suspected, since murmurs produced at the aortic 
valve are not so apt to disappear when compensation fails. The 
relative tricuspid insufficiency which often occurs is likely to manifest 
itself by an enlargement of the right auricle, sometimes demonstrable 
by percussion and later by venous pulsation in the neck and in the liver. 

(d) Differential Diagnosis. 

The murmur of mitral regurgitation may be confused with 
(i) Tricuspid regurgitation. 

(2) Functional murmurs. 

(3) Stenosis or roughening of the aortic valves. 

(4) Dilatation or aneurism of the aortic arch. 

(1) The post-mortem records of the Massachusetts General 
Hospital show that in the presence of a murmur due to mitral regur- 
gitation it is very easy to fail altogether to recognize a tricuspid 
regurgitant murmur. Only 5 out of 29 cases of tricuspid regurgitation 
found at autopsy were recognized by the presence of a murmur during 
life. Allbutt's figures from Guy's Hospital are similar. In the major- 
ity of these cases, mitral regurgitation was the lesion on which atten- 
tion was concentrated during the patient's life. This is all the more 
excusable because the tricuspid area is so wide and uncertain. Mur- 
murs produced at the tricuspid orifice are sometimes heard with maxi- 
mum intensity just inside the apex impulse, and if we have also a 
mitral regurgitant 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 j ugular veins and in the liver, and through 
the rapid accumulation of ascites and oedema of the leg. 

(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 and 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 

Cardiorespiratory 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 leak. From this they should be distinguished 
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 may produce a 
systolic murmur with maximum intensity in the second right inter- 
costal space, but this murmur is not infrequently heard all over the 
precordia and very plainly at the apex, so that it may simulate the 
murmur of mitral regurgitation. The aortic murmur may indeed be 
heard more plainly at the apex than at any other point except the 
second right intercostal space, owing to the fact that the right ventricle, 
which occupies most of the precordial region between the aortic and 
mitral areas, does not lend itself well to the propagation of certain 
types of cardiac murmurs. Under these circumstances " a loud, rough 
aortic murmur may be heard at the apex as a smooth murmur of a 
different tone" (Broadbent). Such a murmur is not, however, likely 
to be conducted to the axilla or heard beneath the left scapula, nor 
to be accompanied by accentuation of the pulmonic second sound 
nor evidences of engorgement of the lungs and general venous system. 

(4) Dilated aorta with or without aneurism may produce all the 
signs described in the last section. The evidences of such dilatation 
are, however, obvious in most cases and the points of distinction from 
mitral disease identical with those mentioned in the last paragraph. 

II. Mitral Stenosis. 

Narrowing or obstruction of the mitral orifice is the result of a 
chronic endocarditis which gradually glues together the two flaps of 
the valve until only a funnel-shaped opening or a slit like a button- 
hole is left (see Figs. 149 and 150). As we examine post-mortem the 
tiny slit which may be all that is left of the mitral orifice in a case of 
long standing, it is difficult to conceive how sufficient blood to carry on 
the needs of the circulation could be forced through such an insig- 
nificant opening. 

Usually a slow and gradually developed lesion, mitral stenosis 

1 It must be remembered that in chlorosis, a disease in which functional murmurs 
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. 



often represents the later stages of a process which in its earlier 
phases produced pure mitral regurgitation. By some observers the 
advent of stenosis is regarded as representing an attempt at com- 

■J/e&ar/ g/ie/i 

Fig. 149. — Diagram to Represent the Position of the Valves in the Normal Heart 
during Diastole, the Open Mitral Allowing the Blood to Flow from the Left Auricle, 
the Aortic Closed. 

/, <r/ea/rtfjf//£(z/. 

Fig. 150. — Mitral Stenosis — Period of Diastole. The blood flowing from the left auricle 
is obstructed by the thickened and adherent mitral curtains. 

pensation for a reduction of the previous mitral leakage. Others 
consider that the stenosis simply increases the damage which the 
valve has suffered. 



A remarkable fact never satisfactorily explained is the predilec- 
tion of mitral stenosis for the female sex. 1 A large proportion of the 
cases — seventy-six per cent, in my series — occur in women. 

Physical Signs. 

Mitral stenosis may exist for many years without giving rise to 
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 murmur which is easily 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 

Pulmonic second 

" Double-shock " 

Presystolic murmur 
heard in limited 

Fig. 151. — Mitral Stenosis. 

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 differences of opinion so often arise regarding the diagnosis of 
mitral stenosis, and that out of seventy-one cases in which this 
lesion was found at autopsy at the Massachusetts General Hospital, 
only forty-nine were recognized during life. No common lesion 

1 Fenwick's explanation, viz., that the sedentary life of women favors the slow adhesive 
inflammation of the valve and its curtains, resulting in stenosis, does not seem to me 
to be satisfactory. 


(with the exception of tricuspid regurgitation) has been so fre- 
quently overlooked in our records. 

I shall follow Broadbent in dividing the smyptoms into three 
stages, according to the extent to which the lesion has progressed. 

In the first stage inspection and palpation show that the apex 
beat is little if at all displaced, and percussion reveals no 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 characteristic cf 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 

lst 1st 

2nd Hlllli I 2nd 


Fig. 152. — 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. 

by palpation. The thrill is sometimes palpable even when no murmur 
can be heard, and often the thrill is transmitted to the axilla when the 
murmur is confined to the apex region. On 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 and increasing in intensity as it 
approaches the first sound. At this stage of the disease the second 
sound can still be heard at the apex. The first sound is very sharply 
accented on snapping, and communicates a very decided shock to the 
ear when a rigid stethoscope is used. As a rule, the murmur is closely 
confined to the region of the apex beat and not transmitted any con- 
siderable 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 Very charac- 

1 It may, however, be widely transmitted to the left axilla and audible in the back or 
even over the whole of the left chest, especially when the stenosis is combined with 


teristic of mitral stenosis is a prolongation of the diastolic pause so 
that the interval between the second sound of one cycle and the first 
sound of the next is unduly long. The pulmonic second sound is 
accented and often loudly reduplicated ("double-shock sound" — 
Sansom) at this stage of the disease, but this doubling is much more 
frequent later. 1 

Irregularity of the heart beat both in force and rhythm is very 
frequently 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. 


In the second stage the murmur and thrill are usually longer and 
may occupy the whole of diastole, beginning with considerable in- 
tensity 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. 2 These changes may be 

1st 1st 

ni I I I I I II lllllllllllltllllllllilll |_LL 

Fig. 153. — 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 intensity 
as it approaches the first sound. No second sound is audible at the apex. 

graphically represented as in Figs. 152 and 153. Diastole and the 
As-Vs interval of the phlebegram (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 

1 This is the opinion of most observers. Sansom has stated that the "double-shock 
sound" may precede all other evidences of mitral stenosis, but this opinion was given 
before the discovery by Barie and Thayer that a "third heart sound" probably identical 
with one of the beats of the "double shock sound" is often heard in healthy young 

2 Rarely one finds a crescendo in the middle of a long presystolic roll with a diminuendo 
as it approaches the first sound. (See Fig. 154.) 


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 manifest. The apex impulse is displaced to the left — sometimes 
as far as the mid-axillary line, and often descends to the sixth inter- 
space. Occasionally the cardiac dulness is increased to the right of 
the sternum (right auricle) . 

The instability and fleeting character of the murmur in the earlier 
stages of the disease are much less marked in this, the second stage. 


II. Mil lilllllllll llllllll ll I 




Fig. 154.; — Type of Presystolic Murmur Sometimes Heard in the Second Stage of Mitral 
Stenosis. There is a double crescendo. The second sound seems reduplicated. 

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) . 


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 tricuspid regurgitation. 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 character of the first sound, together with the 
prolongation of diastole and the absolute irregularity of the heart, both 
in force and rhythm. At times a presystolic thrill may be felt even 
when no murmur is to be heard. 

The pulse shows nothing characteristic in many cases except that 
early and persistent irregularity which has been already alluded to. 

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 functionary auricle and a palpable pulse were luxuries 
rather than necessities. 

Under the influence of digitalis the pulse is especially apt to assume 
the bigeminal or coupled type in mitral stenosis. Every other beat is 
then so abortive that it fails to send a wave to the wrist, and the weak 
beat is succeeded by a pause. See above ; p. 119. 

Mitral stenosis is in the great majority of cases combined with 
mitral regurgitation, and it often happens that the signs of regurgita- 
tion are so much more prominent than those of stenosis that the 
latter escape 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 
from pure regurgitation by the sharpness of the first sound, which 
would be very unusual at this stage of a case of pure mitral regurgita- 
tion. 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 suggestive of mitral stenosis. 

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. 

Differential Diagnosis. 

I have already discussed the difficulty of distinguishing a double 
lesion at the mitral valve from a simple mitral regurgitation (see 
above, p. 205). 

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) The Austin Flint murmur. 


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, Bramwell, Gairdner, and other com- 
petent observers. At the Massachusetts General Hospital we have 
had many such cases with autopsy. Yet, despite repeated confirma- 
tion, Flint's observation has remained for nearly forty years unknown 
to physicians at large. Its importance is this: Given a case of aortic 
regurgitation — 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 presystolic murmur can be produced at the apex in cases of 
aortic regurgitation has been much debated. Some believe it is due 
to the impact of the aortic regurgitant stream upon the ventricular side 
of the mitral valve, floating it out from the wall of the ventricle so as 
to bring it into contact with the stream of blood descending from the 
left auricle. Others suppose that the mingling of the two currents of 
blood, that from the mitral and that from the aortic orifice, is sufficient 
to produce the murmur. 

Between the "Austin Flint murmur" thus defined and the mur- 
mur of true mitral stenosis, complicating aortic regurgitation, diagno- 
sis may be impossible. If there is no dilatation of the mitral orifice, 
and no regurgitation, either from this cause or from deformities of the 
mitral valve itself, 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 predominating hypertrophy of the left ventricle 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, snap- 
ping first sound, the thrill and systolic shock so characteristic of 
mitral stenosis are said to be modified or absent in connection with 
murmurs of the Austin Flint type. 

(b) Tricuspid obstruction. 

Luckily for us as diagnosticians, stenosis of the tricuspid valve is a 
very 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 latter valve. 


The difficulty of distinguishing tricuspid stenosis from mitral 
stenosis is further increased by the fact that the two lesions 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 undistinguish- 
able from each other. In the vast majority of cases, therefore, tri- 
cuspid stenosis is first recognized at the autopsy, and the diagnosis 
is at best a very difficult one. When a mitral stenosis seems to 
yield to treatment much less readily and satisfactorily than we should 
suspect, considering the age and general condition of the patient, we 
may guess that a tricuspid obstruction (perhaps also an aortic 
stenosis) is present as well. 

(c) 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 distinguished from the latter, 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 more favorable than that 
of mitral stenosis. 

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 end is of much importance 
as evidence of valvular disease, except the rare axillary diastolic 
murmur 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 signs of disease except 
the irregularity — yet may turn out to be mitral stenosis. 

IV. Aortic Regurgitation. 

Rheumatic endocarditis usually occurs in early life 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. Nevertheless cases occur at all 
ages and in both sexes, and rheumatic endocarditis does not spare the 
aortic cusps altogether by any means. 

7./tfitta/ (fwy 

Fig. 155. — Diastole in Aortic Regurgitation. The blood is flowing back through the 
stumpy and incompetent aortic valves. 

Whether produced by syphilitic aortitis extending down from the 
aorta, or by rheumatic or septic endocarditis, the lesion which results 
in aortic regurgitation is usually a thickening and shortening of the 
cusps (see Fig. 155). In rare cases it is said that an aortic cusp may 
be ruptured as a result of violent muscular effort, and the signs and 
symptoms of regurgitation may then appear suddenly. I have never 
seen such a case ; as a rule the lesion comes on slowly and insidiously, 
and unless discovered accidentally or in the course of routine physical 
examination it may exist unnoticed for years. Dropsy and cyanosis 
are relatively late and rare, and the symptoms which first appear are 
usually those of dyspnoea and precordial distress. 

It is a disputed point whether relative and temporary aortic in- 
sufficiency due to stretching of the aortic orifice ever occurs. If it 


does occur, it is certainly exceedingly rare, as the aortic ring is very 
tough and inelastic. 

Dilatation of the aortic arch — resembling diffuse aneurism — occurs 
in almost every case of aortitis and aortic regurgitation, and produces 
several important physical signs. This complication is a very well- 
known one, but has not, I think, been sufficiently insisted on in text- 
books of physical diagnosis. It forms part of that general enlarge- 
ment of the arterial tree which is so characteristic of the disease. 

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 the carotids but the sub- 
clavian, 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 of the heart from hard muscular work {e.g., in 
athletes) 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 
distended, while the arch of the aorta is diffusely dilated so as to 
resemble an aneurism (see Fig. 156). 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 
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 

Pulsation at the jugulum. 
I /( >- Pulsating carotids. 

^^^'ftV_^^t -Tafc* V|i -— "1 — Diastolic murmur. 

D ulness and pul- J,-' \ AVp ^/str**. 5|Fv v /~wYA ft 

sation corre- -"" A \\V^3-T ^/Ar^^ r^i/ /\ 

sponding to the \ ^Vj/xf/V \0>vs<l / _ _ Displaced cardiac 

dilated aortic Hv^?// \V^^T impulse, 

arch. WX<„V YinXTI 

Fig. 156. — Aortic Regurgitation, Showing Position of the Diastolic Murmur and Areas 

of Visible Pulsation. 

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. 

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 hyperaemic 
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 
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 aortic 1 regurgitation, 
yet occasionally one meets with it in diseases which produce very low 
tension of the pulse, such as Graves' Disease, 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. 


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. 157. — 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. 157, 158). 

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 the 
characteristically sharp and sudden rise in the peripheral arteries. 
The arteries then empty themselves in two directions at once, forward 

1 Jumping toothache and throbbing felon are common examples of capillary pulsation 
in inflammed area. 


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. 158. — 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 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. 


In rare cases there may be absolutely no murmur and the diag- 
nosis may be impossible during life, though it may be suspected by 
reason of the above-mentioned signs in the peripheral arteries. Un- 
less the free ear is used the murmur is often 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 Massachusetts General 
Hospital, only fifty-seven or 84% were recognized during life. 



In the majority of cases, however, the 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. 
It almost invariably points to aortic regurgitation and to nothing else. 

The murmur of aortic regurgitation, as has been already men- 
tioned, is diastolic in time. 1 Its, maximum intensity is usually not 
in the conventional aortic area {second right interspace), but on the 

Fig. 159. — Position of the Point of Maximum Intensity of the 'Murmur of Aortic 
Regurgitation. The dots are most thickly congregated where the < murmur is oftenest 

left side of the sternum about the level of the fourth left ostal 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- 

1 Another murmur, systolic in time, which almost always accompanies the diastolic 
murmur, is usually due to roughening of the edges of the aortic valves or to dilatation of 
the aortic arch. This murmur must not be assumed to mean aortic stenosis (see below, 
p. 230). 


lage at the apex, in the left axilla, or in the region of the ensiform car- 
tilage (see Fig. 159). 

From its seat of maximum intensity (i.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; 
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. 160) . Late diastolic murmurs are 

1st 1st 



Fig. 160. — Short Diastolic Murmur Xot Replacing the Second Sound. 

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. 

The position of the patient's body has but little effect upon the 
murmur — less than upon murmurs produced at the mitral orifice. 

The first sound at the apex is generally dull and long. There is no 
accentuation of the pulmonic second. 

Over the larger peripheral arteries, especially over the femoral 
artery, one hears in most cases a sharp, short systolic sound ("pis- 
tol-shot sound") due to the sudden filling of the unusually empty 
artery; this sound is merely an exaggeration of what may be heard 
in health. Pressure with the stethoscope will usually bring out a 
systolic murmur (as also in health) , and occasionally a diastolic mur- 
mur as well (Duroziez's sign) . This diastolic murmur in the peripheral 
arteries, obtained on pressure with the stethoscope, is practically 
never heard except in aortic regurgitation. It is thought by some 
to be due to the regurgitant current in the great vessels which in very 
marked cases may extend as far as the femoral artery. Duroziez's 
sign is a comparatively rare one, not present in most cases of aortic 
regurgitation, and usually disappears when compensation fails. 


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. 

(b) Capillary pulsation. 

(c) "Corrigan" pulse. 

(d) "Pistol-shot sound" in the femoral artery. 

(e) Duroziez's sign. 

if) High pulse-pressure (see above, p. in). 

Cardiopulmonary murmurs (see page 188) 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 arotic regur- 
gitation. I have recently reported (Johns Hopkins Bull., May, 
1903) three cases of intense anaemia associated with diastolic mur- 
murs exactly like those of aortic regurgitation, but proved post mortem 
to be independent of any valvular lesion. The arterial phenomena 
were not marked, but the diagnosis of such cases is very hard. Luck- 
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. 

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. 

(&) The degree to which the pulse collapses during diastole 
(provided 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. 


(i) Dilatation of the Aorta. — Diffuse 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. 
156). 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 will be 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 
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. 215.) 

(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. 

The excessive arterial pulsation may be less marked if stenosis 
accompanies regurgitation, but this is not always the case (see below, 
p. 230). 

1 This relative insufficiency of the mitral valve has been termed its " safety-valve '* 
action, but the safety is but temporary and dearly bought. 



Aortic Stenosis. 

Uncomplicated aortic stenosis is by far the rarest of the valvular 
lesions of the left side of the heart, as well as the most difficult to recog- 
nize. Out of two hundred and fifty-two autopsies made at the Massa- 
chusetts General Hospital in cases of valvular disease there was not one 
of uncomplicated aortic 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 
vessels of the neck. Such a murmur does indeed occur in aortic 

r /c&Jfi/, . 

Fig. 161. — 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) . 

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 and transmitted to the neck. 

(2) The characteristic pulse (vide infra) . 

(3) A palpable thrill (usually) . 

(4) Absence or great enfeeblement of the aortic second sound. 1 

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. 


Of these signs the characteristic pulse is the most important. The 
heart may or may not be enlarged. 

Each of these points will now be described more in detail. 

(i) 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. (6) The 
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 

Maximum intensity 
of systolic mur- 
mur and thrill. 

Fig. 162. — Aortic Stenosis. The murmur is audible over the shaded area and sometimes 

over the whole chest. 

murmur usually to be heard in mitral regurgitation, (c) The mur- 
mur is usually widely transmitted, often being audible over the whole 
chest and occasionally over the skull and the arterial trunks of the 
extremities (see Fig. 162). It is usually heard less well over that por- 
tion of the precordia occupied by the right ventricle, while, on the 
other hand, it is relatively loud in the region of the apex impulse, 
whither it is transmitted through the left ventricle. The same line of 
transmission was mentioned above as characteristic of the murmur of 
aortic regurgitation 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. 


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 unusually great, extending through- 
out the whole of systole, but to this rule there are occasional exceptions. 
The first sound in the aortic region is altogether obliterated, as a rule, 
and the second sound is usually either absent or very feeble. 1 

(2) 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. 163). 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; 

Fig. 163. — Sphygmographic Tracing of the Pulse in Uncomplicated Aortic Stenosis. 
Compare with the normal pulse wave and with that of aortic regurgitation (pages 221 and 

hence the pulse wave is not only slow to rise but small in height, con- 
trasting strongly 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, renders 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, parvus, 
tardus" is, therefore, a most constant and important point in diagnosis, 
but unfortunately it is to be felt in perfection only in the very rare 
cases in which aortic stenosis occurs uncomplicated. When stenosis 
is combined with regurgitation, as is almost always the case, the 
above-described qualities of the pulse are usually modified as a result 
of the regurgitation. But I have in two cases observed a well marked 

1 " Occasionally, as noted by W. H. Dickinson, there is a muscial murmur of great 
intensity in the region of the apex, probably due to a slight regurgitation at high pressure 
through the mitral valve." — Oslee. 


"Corrigan" pulse in life and been confronted post mortem with a 
narrowed, rigid aortic valve! 

The slow, long pulse with a long 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. 

(3) The Thrill. 

In the majority of cases an intense purring 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 
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) . Corresponding to 
the protracted sustained systole the first sound at the apex is dull and 
long, but not very loud. 

Diagnosis of Aortic Stenosis from the Etiology. 

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 
regurgitation, it is pretty safe to postulate the existence of aortic 
stenosis as well, whatever the physical signs. 

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 diffuse 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. 


(g) Mitral regurgitation. 

(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. 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, such as often accompanies aortic 
regurgitation, is a frequent cause of a systolic murmur loudest in the 
second right interspace. This may be recognized in certain cases by 
the characteristic area of pulsation and of dulness on percussion ; by its 
association with aortic regurgitation of long standing (see Fig. 153). 

Roughening of the intima of the aorta (endaortitis) is always to be 
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 absence of a thrill and a long, slow pulse with a 
low maximum serves to distinguish such murmurs from those of 
aortic stenosis. 

(c) Aneurism of the ascending arch of the aorta or of the innomin- 
ate 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 ^c-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 accompanied by a shock, and the pulse 
shows none of the characteristics of aortic stenosis. 

(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 occur especially in young, 
anaemic persons, are not accompanied by any cardiac enlargement, 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 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 aortic second sound nor 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 regurgitation. 
But the maximum intensity of the murmur of aortic stenosis is almost 
invariably in the aortic area, and its association with a thrill and a 
long, slow pulse should enable us easily to differentiate the two lesions. 

By the foregoing differentiae aortic stenosis may be distin- 
guished from the other conditions which resemble it, provided it 
predominates over the regurgitation associated with it, but unfortunately 
this is not very common. As a rule, it is fairly well balanced or 
neutralized by the accompanying aortic regurgitation, and its char- 
acteristic signs are therefore obscured or greatly modified by the signs 
of the latter disease. We may suspect stenosis: (a) In all young 
(rheumatic) patients with long-standing aortic regurgitation. 1 (6) 
In older (syphilitic or arterio-sclerotic) patients who show, besides 
the signs of aortic regurgitation, palpable thrill in the aortic area 
transmitted into the great vessels, a modification of the Corrigan pulse 
in the direction of the "pulsus tardus, rarus, parvus," and less visible 
arterial pulsation than is to be expected in pure aortic regurgitation. 

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 relative mitral insufficiency 
which, as has been already mentioned above, is very apt to supervene 
in cases of aortic disease, owing to dilatation of the mitral orifice, and 
which may modify the characteristic signs of aortic regurgitation 
very much as aortic stenosis does. 

Tricuspid Regurgitation. 

Endocarditis affecting the tricuspid valve is rare in post-fcetal life; 
in the foetus it is not so uncommon. In cases of ulcerative or malig- 

1 Because post-mortem experience shows that in cases of this type stenosis and insuffi- 
ciency are usually combined. 


nant endocarditis occurring in adult life, the tricuspid valve is occa- 
sionally involved, but the majority of cases of tricuspid disease occur 
as a result of disease of the mitral valve and in the following manner : 
Hypertrophy of the right ventricle occurs as a result of the mitral 
disease, and is followed in time by dilatation; 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 
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 " safety valve" to relieve a temporary pulmonary en- 
gorgement. 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. 

Physical Signs. 

(1) A systolic murmur heard loudest at or near the fifth left 
costal cartilage. 

(2) Systolic venous pulsation in the jugulars and in the liver. 

(3) Engorgement of the right auricle producing an area of dulness 
beyond the right sternal margin. 

(4) Intense cyanosis. 

(5) Ascites and oedema of the legs. 

(1) The Murmur. — The maximum intensity of the systolic mur- 
mur of tricuspid regurgitation is usually near the junction of the fifth 


or sixth left costal cartilages with the sternum. Leube finds the 
murmur a rib higher up, but it is generally agreed that the tricuspid 
area is a large one, so that the murmur may be heard anywhere 
over the lower part of the sternum or even to the right of it. On the 
other hand, there are some tricuspid murmurs which are best heard 
at a point midway between the apex impulse and the ensiform carti- 
lage. The murmur is not widely transmitted and is usually inaudi- 
ble in the back; at the end of expiration its intensity is increased. 

In some cases we have no evidence of tricuspid regurgitation 
other than the murmur just described, but — 

(2) Of more 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. 86) the distinc- 

Systolic murmur. "' 

Enlarged and pul- 
sating liver. 

Fig. 164. — Tricuspid Regurgitation. The murmur is heard best over the shaded area. 

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 


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. 

(3) 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. 164. 

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. 

(4) Cyanosis is usually very great, and dyspnoea and general dropsy 
often make the patient's condition a desperate one. 

Differential Diagnosis. 

The statistics of the cases autopsied at the Massachusetts General 
Hospital show that tricuspid regurgitation 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 : 

(a) Tricuspid regurgitation may be present and yet give rise to no 
physical signs which can be recognized during life. 

(b) Tricuspid regurgitation occurs most frequently in connection 
with mitral regurgitation; hence its signs are frequently masked by 
those of the latter lesion. It is, therefore, a matter of great importance 
as well as of great difficulty to distinguish tricuspid regurgitation from 

(1) Mitral Regurgitation. 

The difficulties are obvious. The murmur of mitral regurgitation 
has its maximum intensity not more than an inch or two from the 
point at which the tricuspid murmur is best heard. Both are systolic 
in time. They are, therefore, to be distinguished only — 

(a) In case we can demonstrate that there are two areas in which 
a systolic murmur is heard with relatively great intensity, with an 
intervening space over which the murmur is less clearly to be heard 
(see Fig. 165). 

(6) Occasionally the two systolic murmurs are of different pitch 
or of different quality, and may be thus distinguished. 


(c) Tricuspid murmurs are not transmitted into the left axilla 
and are rarely audible in the back, and this fact is of value in case we 
have to distinguish between uncomplicated tricuspid regurgitation 
and uncomplicated mitral regurgitation. Unfortunately these le- 
sions are very apt to occur simultaneously, so that in practice our 
efforts are generally directed toward distinguishing between a pure 
mitral regurgitation and one complicated by tricuspid regurgitation. 

id) In cases of -doubt the phenomena of venous pulsation in the 
jugulars and in the liver are decisive if present, but their absence 
proves nothing. 

(e) Accentuation of the pulmonic second sound is almost inva- 
riably present in uncomplicated mitral disease and is apt to disap- 
pear in case the tricuspid begins to leak, since engorgement of the 

Fig. 165. — Two Systolic Murmurs (Mitral and Tricuspid) with a "Vanishing Point" 


lungs is thereby for the time relieved, but in many cases the pul- 
monic second sound remains most unaccountably strong even when 
the tricuspid is obviously leaking. 

(2) From "functional" systolic murmurs tricuspid insufficiency 
may generally be distinguished by the fact that its murmur is best 
heard in the neighborhood of the ensiform cartilage, and not in the 
second right intercostal space where most functional murmurs have 
their seat of maximum intensity. Functional murmurs are unac- 
companied by venous pulsation, cardiac dilatation, or cyanosis. 

(3) Occasionally a pericardial friction rub simulates the mur- 
mur of tricuspid insufficiency, but, as a rule, pericardial friction is 


much more irregular in the time of its occurrence and is not regularly 
synchronous with any definite portion of the cardiac cycle. 

Tricuspid Stenosis. 

One of the rarest of valve lesions is narrowing of the tricuspid 
valve. Only 8 cases (none recognized in life) have come under my 
observation, and in 1898, Herrick was able to collect but 154 cases 
from the world's literature. Out of these 154 cases, 138, or 90 per 
cent., were combined with mitral stenosis, and only 12 times has tri- 
cuspid stenosis been known to occur alone. 1 These observations ac- 
count for the fact that tricuspid stenosis has hardly ever been recog- 
nized during life, since the murmur to which it gives rise is identical 
in time and quality and nearly identical in position with that of mitral 
stenosis. Narrowing of the tricuspid valve is to be diagnosed, there- 
fore, only by the recognition of a presystolic murmur best heard in 
the tricuspid area and distinguished either by its pitch, quality, or 
position from the other presystolic murmur due to the mitral stenosis 
which is almost certain to accompany it. 

The heart is usually enlarged, especially in its transverse direc- 
tion, but the enlargement is just such as mitral stenosis produces, 
and does not aid our diagnosis at all. 

The diagnosis is still further complicated in many cases by the 
presence of an aortic stenosis in addition to a similar lesion a h . the 
tricuspid and mitral valves, so that it seems likely that in the future 
as in the past the lesion will be discovered first at autopsy. 

One may be led occasionally to suspect the hidden presence of 
tricuspid stenosis, if a case of supposedly pure mitral stenosis does 
not yield to treatment in the usual way. 

Pulmonary Regurgitation. 

Organic disease of the pulmonary valve is excessively rare in 
post-fcetal life, but may occur as part of an acute ulcerative or septic 
endocarditis. A temporary functional regurgitation through the 
pulmonary valve may be brought about by any cause producing 
very high pressure in the pulmonary artery. I have known two 

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 all of the 8 cases of tricuspid stenosis found at autopsy were associated 
with mitral stenosis as well. 


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 occur- 
rence of a murmur similarly produced under pathological condi- 
tions, especially in mitral stenosis, much has been written by Graham 

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. 1 
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 is not recog- 
nizable during life. 

Pulmonary Stenosis. 

Among the rare congenital lesions of the heart valves this is prob- 
ably the commonest. The heart, and particularly the right ventricle, 
is usually much enlarged. There is a history of cyanosis and dyspnoea 
since birth. Pulmonary tuberculosis complicates from one-fourth 
to one-third of all cases. A systolic thrill is usually to be felt in the 
second left intercostal space, and a loud systolic murmur is heard 
in the same area. The pulmonic second sound is weak. 

The region in which this murmur is best heard has been happily 
termed the ''region of romance" on account of the multiplicity of 
mysterious murmurs which have been heard there. The systolic 
murmur of pulmonary stenosis must be distinguished from 

(a) Functional murmurs due to anaemia and debility or to severe 
muscular exertion, and possibly associated with a dilatation of the 
conus arteriosus. 

(&) Uncovering of the conus arteriosus through lack of expansion 
of the lung. 

(c) Aortic stenosis. 

1 By registering the variations of pressure in the tracheal column of air Gerhardt has 
shown graphically that a systolic pulsation of the pulmonary capillaries may occur in 
pulmonary regurgitation. With the stethoscope a systolic whiff may be heard all over the 


(d) Mitral regurgitation. 

(e) Aneurism. 

(/) Roughening of the intima of the aortic arch. 

(g) Other congenital lesions such as septum defects. 

(a and b) Functional murmurs, and those produced in the conus 
arteriosus, are rarely if ever accompanied by a thrill, are rarely so 
loud as the murmur of pulmonary stenosis, and are not associated 
with dyspnoea, cyanosis, and enlargement of the right ventricle. 

(c) The murmur of aortic stenosis is usually upon the right side 
of the sternum and is transmitted to the neck, whereas the murmur 
of pulmonary stenosis is never so transmitted and is not associated 
with characteristic changes in the pulse (see above, p. 229). 

(d) The murmur of mitral regurgitation is occasionally loudest 
in the region of the pulmonary valve, but differs from the murmur 
of pulmonary stenosis in being, as a rule, transmitted to the back 
and axilla and associated with an accentuation of the pulmonary 
second sound. 

(e) Aneurism may present a systolic murmur and thrill similar 
to those found in pulmonary stenosis, but may usually be distin- 
guished from the latter by the presence of the positive signs of aneur- 
ism, viz. — pulsation, and dulness in the region of the murmur, and 
signs of pressure on the trachea or on other structures in the 

(/) Roughening of the aortic arch occurs after middle life, while 
pulmonary stenosis is usually congenital. The murmur due to rough- 
ening may be transmitted into the carotids; that of pulmonary 
stenosis never. Enlargement of the right ventricle is characteristic 
of pulmonary stenosis, but not of aortic roughening. 

(g) It is practically impossible to distinguish pulmonary stenosis 
from septum defects, especially as the two are often combined. 

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 case in aortic 
regurgitation — systolic and diastolic 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 the diastolic 
murmur alone of the four audible murmurs is due to a valvular 

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 endocar- 
ditis, 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. 

The most frequent combinations are: 

(i) Mitral regurgitation with mitral stenosis. 

(2) Aortic regurgitation with mitral regurgitation (with or with- 
out stenosis). 

(3) Aortic regurgitation with aortic stenosis, with or without 
mitral disease. 

(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 steno- 
sis is almost never found at autopsy without such a stiffening of the 
orifice as would produce an associated regurgitation, so that it is 



Fig. 166. — Mitral Stenosis and Regurgitation, showing relation of murmur to 
first heart sound. 

fairly safe to 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. 166). 

(b) On the other hand, with a double mitral lesion one may 
have only the regurgitant 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 mitral 



regurgitation alone. Either murmur may disappear altogether for 
a time and reappear subsequently. This is peculiarly true of the pre- 
systolic murmur, which is notoriously one of the most fleeting and 
uncertain of all physical signs. 

As a rule the same inflammatory changes which produce mitral 
regurgitation 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 a regenerative or compensatory change. In 
many cases, however, no such amelioration of the symptoms follows. 

(2) Aortic Regurgitation with 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. 167. 

-Aortic and Mitral Regurgitation. The shaded areas are those in which the 
murmurs are loudest. 

general and correspond less exclusively to the right ventricle (see 
Figs. 167 and 168) . 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 summit 
and rises and falls less abruptly. Capillary pulse is less likely to be 
present, and the throbbing of the peripheral arteries is less often 



(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 
mitral lesion; that is to say, the throbbing in the peripheral arteries 
is less violent, the characteristics of the radial pulse are less marked, 

1st 1st 

I 2nd lllh. 2nd 

Fig. 168. — Showing Relation of Murmurs to Heart Sound in Regurgitation at the Aortic 

and Mitral Valves. 

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 insufficiency 
has been already described on p. 208. 

1 Some astonishing exceptions to this rule have been mentioned on pages 227 and 230. 





Parietal Disease of the Heart. 

Acute Myocarditis. 

The myocardium is seriously, though not incurably, affected in 
all continued fevers, owing less to the fever itself than to the tox- 
aemia associated with it. "Cloudy swelling," or acute degenera- 
tion of the muscle fibres, is produced by relatively mild infections, 
while a general septicaemia due to pyogenic organisms may produce 
extensive fatty 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 blow- 
ing 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), 1 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 

1 Henchen's recent monograph on this subject," Ueber die acute Herzdilatation bei 
acuten Infectionskrankheiten," Jena, 1899, does not seem to me convincing. 



Weakened Heart ("Chronic Myocarditis"). 

Fatty or fibroid changes in the heart wall occurring in chronic 
disease may result from coronary sclerosis and imperfect nutrition 
of the myocardium, but in many cases no lesions are found post 
mortem in the heart, whose muscle weakens as a result of long-con- 
tinued overwork against an increased arterial resistance (nephritis, 
arterio-sclerosis) . 

Whether definite myocardial changes are present or not, the signs 
are the same. 

Physical Signs of Weakened Heart. 

For the sure recognition of changes in the myocardium our pres- 
ent 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. ... 13 or 22 % 
Cases of fibrous myocarditis diagnosed in life, but 

not found post mortem 31 or 52 % 

Cases of fibrous myocarditis found post mortem, but 

not diagnosed in life 15 or 26 % 

Total attempts 59 

To a considerable extent, therefore, our diagnosis of myocarditis must 
depend upon the history and symptoms of the case; physical ex- 
amination can sometimes supplement these, sometimes not. Symp- 
toms of cardiac weakness developing in a man past middle life, espe- 
cially 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, fatty or fibroid. The 
probability is increased if there have been attacks of angina pectoris, 
Cheyne-Stokes breathing, or of syncope. 


Inspection and palpation may reveal nothing abnormal, or there 
may be an unusually diffuse, slapping cardiac impulse associated 
perhaps with a displacement of the apex beat to the left and down- 
ward. Marked irregularity of the heart beat, both in force and in 
rhythm, is sometimes demonstrable by these methods, and an in- 
crease in the area of cardiac dulness may be demonstrable in case 
dilatation has followed the weakening of the heart wall. Ausculta- 
tion may reveal nothing abnormal except that the aortic second 
sound is unusually sharp ; in some cases feeble and irregular heart 
sounds are heard, although the first sound at the apex is not infre- 
quently sharp. Blood pressure is often much increased. The 
sounds may be reduplicated and "gallop rhythm" is not infrequent. 
If the mitral sphincter is dilated, or the papillary muscles are weak- 
ened, as not infrequently happens, we may have evidences of mitral 
regurgitation, a systolic murmur at the apex heard in the left axilla 
and back with accentuation of the pulmonic second sound. 


i . 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 
nothing abnormal. 

2. Among the rather unreliable physical signs, those most often 
mentioned are: 

(a) Weakness and irregularity of the heart sounds. 

(b) Increased blood pressure. 

(c) A diffuse slapping cardiac impulse. 

(d) Reduplication of some of the cardiac sounds (gallop rhythm). 

(e) Evidences of cardiac dilatation. 

(/) Murmurs — especially the murmur of mitral insufficiency 
which often occurs as a result of dilatation of the valve orifices and 
weakening of the cardiac muscle. 

Differential Diagnosis. 

We have to distinguish the weakened heart from — 
(a) Uncomplicated valvular lesions. 
(&) 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 history of a long- 
standing valvular trouble, a knowledge of the previous history of the 
case, the age, method of onset, and the blood pressure measurements 
may assist us in the diagnosis. Cases of weakened heart are less often 
associated with extensive dropsy than are cases of valvular disease 
whose compensation has been ruptured. 

(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. 
On the other hand, if any serious weakening is present, the signs 
and symptoms are much aggravated by any exertion. 

In some cases of myocarditis the pulse is excessively slow and 
shows no signs of weakness. This point will be referred to again 
in the chapter on Bradycardia. 

Fatty Overgrowth. 

An abnormally large accumulation of fat about the heart may 
be suspected if, in a very obese person, signs of cardiac embarrass- 
ment (dyspnoea, palpitation) are present, and if on examination we 
find that the heart sounds are feeble and distant but preserve the 
normal difference from each other. When the heart wall is seri- 
ously weakened (as in the later weeks of typhoid), the heart sounds 
become more alike owing to the shortening of the first sound. 

In fatty overgrowth this is not the case. 

The diagnosis, however, cannot be positively made. We sus- 
pect it under the conditions above described, but no greater cer- 
tainty can be attained. 

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 re- 
spects normal during life. The little we know of the physical signs 
common to fatty degeneration and to other forms of parietal dis- 
ease of the heart has been included in the section on Weakened 
Heart (see p. 243). 


Disturbances of Rhythm. 
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. 
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, 
exophthalmic goitre, functional neuroses (some of them sexual) are the 
most frequent causes of tachycardia. 

The only form of tachycardia which is worthy to be considered 
as a more or less independent malady is 

Paroxysmal Tachycardia. 

As indicated in the name, the attacks of this disease are apt to 
begin and to cease suddenly. They may last a few hours or several 
days. The pulse becomes frightfully rapid, often 200 per minute or 
more. Bristowe records a case with a pulse of 308 per minute. 
In the radial artery the pulse beat may be impalpable. The heart 
sounds are regular and clear, but the diastolic pause is shortened and 
the first sound becomes short and "valvular," resembling the second 
(" tic-tac heart"). Paroxysms may begin and end with absolute sud- 
denness, the heart doubling or halving its rate within a few beats. 
Phlebograms and electrocardiograms show that the heart beats origi- 
nate in the auricle, but not in the pace-maker (see above, p. 1 14) . The 
paroxysm may be associated with aphasia and abnormal sensations 
in the left arm. Occasionally the heart becomes dilated, and oedema 
of the lungs, albuminuria, and other manifestations of stasis appear. 
Usually, however, the paroxysm has no serious results. It can be 
distinguished in most cases from the tachycardia of cardiac dilatation 
by the fact that the heart remains perfectly regular. This same fact 


also assists us in excluding the cardiac neuroses due to tobacco, tea, 
and other poisons. From the tachycardia of Graves' disease the affec- 
tion now in consideration differs by its paroxysmal and intermittent 

Bradycardia (Slow Heart). 

In many healthy adults the heart seldom beats over 50 times a 

I. Among the causes which may produce for a short time an 
abnormally slow heart-beat are : 

(a) Exhaustion; for example, after fevers, after parturition, or 
severe muscular exertion. 

(b) Toxcemia; for example, jaundice, uraemia, auto-intoxications in 

(c) In certain hysterical and melancholic states and in neurotic 
children, the pulse may be exceedingly slow. Pain has also a tendency 
to retard the pulse. 

(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. 

II. Stokes- Adams' disease (due to a lesion of the bundle of His) 
refers especially to a paroxysmal bradycardia with syncope, yet the 
pulse may remain below 40 for months, though strong and regular, 
and the patient may be free from symptoms of any kind. The rate 
of the heart-beat cannot be estimated by counting the radial pulse. 
Careful study of the jugular motions, especially with a polygraph, 
usually shows that some auricular beats do not reach the ventricle 
(heart block) so that there are 2 or 3 beats in the jugular for every 1 
in the radial (see above, p. 114). 


1. Physiological or " Youthful" Arrhythmia. — Arrhythmia, or 
irregularity in the force or rhythm of the heart-beat, is to a certain 
extent physiological. The heart normally beats a little faster and a 
little more strongly during inspiration than during expiration, espe- 
cially during childhood and youth. Any psychical disturbance or 
muscular exertion may produce irregularity as well as a quickening of 
the heart-beat. 


In children the pulse is especially apt to be irregular, and during 
sleep some children show that modification of rhythm known as the 
" paradoxical pulse," which consists in a quickening of the pulse with 
diminution in volume during inspiration. 

2. Arrhythmia from Premature Contractions (" Extrasystoles ") .■ — 
Isolated, occasional or regularly recurrent interruptions of the ordinary 
cardiac rhythm by premature contractions followed by a compensatory 
pause are not uncommon in healthy persons. In the absence of all 
other evidence of cardio-vascular disease, they have no known signifi- 
cance and may continue throughout life. They may also accompany 
various types of heart disease. Many of them represent very inefficient 
ventricular contractions and are not transmitted to the wrist. This 
fact together with the compensatory pause and the presence of normal 
beats before and after them, makes them recognizable in most cases 
(see also p. 1 18). 

3. If we leave on one side diseases of the heart itself, pathological 
arrhythmia is most frequently seen in persons who have used tobacco or 
tea to excess, or in dyspepsia. In these conditions it is often combined 
with palpitation and becomes thereby very distressing to the patient. 
In connection with cardiac disease the following types of arrhythmia 
may be distinguished : 

(a) Paradoxical Pulse. — Any cause which leads to weakening of 
the heart's action may occasionally be associated with paradoxical 
pulse. Fibrous pericarditis has been supposed to be frequently 
associated with this type of arrhythmia, but if so it is by no means its 
only cause. 

(6) The bigeminal pulse is seen most frequently in cases of uncom- 
pensated heart disease (particularly mitral stenosis) after the adminis- 
tration of digitalis. Every other beat is weak or abortive and is suc- 
ceeded by an unusually long pause. Sometimes every third beat is of 
the abortive type, or an unusually long interval may divide the heart- 
beats into groups of three (" trigeminal pulse") . 

(c) Delirium cordis or absolute irregularity is a term used to express 
great irregularity and rapidity of the heart-beats which cannot be 
reduced to a single type or rhythm. It is seen in the gravest stages 
of uncompensated heart disease from any cause and is associated with 
auricular fibrillation. See above, p. 116. 


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. 

(6) 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) Heart block, complete or partial (see above, p 113). 

(e) Gallop rhythm is not strictly an arrhythmia but an auscultatory 
anomaly. It is described on p. 176. 

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 dilatation 
of the heart, such as may occur in debilitated persons after violent 
or unusual exertion. In this condition the area of cardiac dulness 
is increased and dyspnoea upon slight exertion becomes marked. It 
goes without saying that in almost any case of organic disease of the 
heart palpitation may be a very marked and distressing symptom. 

Congenital Heart Disease. 

From the time of birth it is noticed in some cases that the child 
is markedly cyanosed, hence the term "blue baby." Dyspnoea is 
often, though not always, present, and may interfere with sucking. 
The cyanosis, if present, is practically sufficient in itself for the 
diagnosis, though incomplete expansion of the lungs may simulate it. 

Among congenital diseases of the heart the commonest and the 
most important (because it is less likely than any of the others to prove 
immediately fatal) is : 

1. Pulmonary Stenosis. 

This lesion is usually the result of foetal endocarditis, and is often 
associated with malformations and defects, such as patency of the 
foramen ovale and persistence of the ductus arteriosus. The physical 
signs of pulmonary stenosis are: 


(a) A palpable systolic thrill most distinct in the pulmonary area. 

(b) A loud systolic murmur (often rough or musical) heard best in 
the same region, but transmitted to all parts of the chest. 

(c) A weak or absent pulmonic second sound. 

(d) An increased area of cardiac dulness corresponding to the right 

Unlike most other varieties of congenital heart disease, pulmonary 
stenosis is compatible with life for many years, and "blue babies" 
with this lesion may grow up and enjoy good health, although usually 
subject to pulmonary disorders (pneumonia or tuberculosis). For a 
discussion of the differential diagnosis of this lesion, see above, p. 238. 

2. Defects in the Auricular or Ventricular Septum. 

The loud systolic murmur produced by the rush of blood through an 
opening between the auricles or ventricles is heard, as a rule, over the 
whole precordia. Its point of maximum intensity differs in different 
cases, but is hardly ever near the apex of the heart. The most im- 
portant diagnostic point (which however cannot be relied upon) is the 
absence of a palpable thrill. With almost every other form of con- 
genital heart disease in which a loud murmur is audible, there is a 
thrill as well, and even in septum defects a thrill does sometimes occur, 
especially if the auricular septum is at fault ; but thrills are nevertheless 
rarer in this than in most other congenital lesions. Hypertrophy of 
both ventricles may be present, but is seldom marked in uncomplicated 

(Patency of the foramen ovale, if unassociated with other defects, 
does not usually produce any murmur or other signs by which it can 
be recognized during life, and causes no symptoms of any kind.) 

3. Persistence of the Ductus Arteriosus. 

The most characteristic sign is a loud, vibratory systolic murmur 
with its greatest intensity at the base of the heart and unassociated with 
hypertrophy of either ventricle. If complicated with stenosis at or close 
above the pulmonary valves, persistence of the ductus arteriosus 
cannot be diagnosed, as the murmur produced by it cannot with 
certainty be distinguished from that of the pulmonary stenosis, and 
the presence of hypertrophy of the right ventricle deprives us of the 
one relatively characteristic mark of a patent arterial duct. 

Gibson considers that a murmur persisting through systole and into 


diastole is diagnostic of an open arterial duct, but this supposition is 
not borne out in all cases by post-mortem evidence. 

The signs produced by the other varieties of congenital heart 
disease, such as aortic stenosis and tricuspid or mitral lesions, do not 
differ materially from those characterizing those lesions in adults. 
Excluding these, we may summarize the signs of the other lesions as 
follows : 

(a) Practically all cases of congenital heart disease, which produce 
any physical signs beyond cyanosis and dyspnoea, manifest themselves 
by a loud systolic murmur heard all over the precordia and often 
throughout the chest. Its maximum intensity is usually at or near 
the base of the heart. 

(b) If there is no thrill and no hypertrophy, the lesion is probably a 
defect in the ventricular septum. 

(c) If there is a thrill but no hypertrophy, the lesion is probably a 
patent ductus arteriosus. 

(d) If there is a thrill and hypertrophy of the right ventricle, the 
lesion is probably pulmonic stenosis, especially if the pulmonic second 
sound is feeble. 


I. Pericarditis. 

Three forms may be recognized clinically : 
(i) 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 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 — 

(a) The rubbing of the roughened pericardial surfaces against 
one another when set in motion by the cardiac contractions. 

(b) 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 or Fibrinous Pericarditis. 

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 friction 
is a rough, irregular, grating or shuffling sound which occurs irregu- 
larly and interruptedly during the larger part of each cardiac cycle. 
It is almost never accurately synchronous either with systole 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. 169; 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. 169. — 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 
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. 

(6) 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. Pres- 
sure with the stethoscope does not increase so strikingly the intensity 
of intracardiac murmurs. When endocarditis and pericarditis occur 
simultaneously, it may be very difficult to distinguish the two sets 
of sounds thus produced. The pericardial friction is usually recognized 
with comparatively little difficulty, but it is hard to make sure whether 
in addition we hear endocardial murmurs as well. 

(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. 



Haemopericardium, 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. 170. — Pericardial Effusion, Cardio-hepatic Angle obtuse. (From v. Ziemssen's Atlas.) 

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 three 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 

(3) By the signs and symptoms of pressure exerted by the peri- 
cardial effusion upon surrounding structures. 

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 unusual 1 extension of the percussion dulness a 
considerable distance to the left of the maximum cardiac impulse. 
(b) Next to this, it is important to notice a change in the angle made 
by the junction of the horizontal line corresponding to the upper limit 
of hepatic dulness and the nearly perpendicular line corresponding to 
the right border of the heart. In health this cardio-hepatic angle is 
approximately a right angle; in pericardial effusion it is much more 
obtuse (see Fig. 171). Rotch has called attention to the importance 

_,. Tympany. 

..,- Dulness. 

Cardiac impulse. 

Liver dulness. 

Fig. 171. — Percussion Dulness in Pericardial Effusion, with Tympanitic Resonance Under 

the Left Clavicle. 

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 

Except for the two points mentioned above (the unusual extension 
of the dulness to the left of the cardiac impulse and the blunting of the 
cardio-hepatic angle), there seems to me to be nothing characteristic 
about the area of dulness produced by pericardial effusion. The 
"pear-shaped" or triangular area of percussion dulness mentioned by 
many writers has not been present in cases which have come under 
my observation. 

1 In health the cardiac dulness extends about f of an inch beyond the maximum cardiac 
impulse, but in pericardial effusion the difference is greater. 


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 

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 
of 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 compression of the lung, but a patch of 
pneumonia or a pleural effusion may be present and 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 dyspncea, 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 diagnostic importance. 

(4) Inspection and palpation usually help 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. 

(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. 

Differential Diagnosis. 

(i) 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 impiilse to the left, or to modify the cardio-hepatic 
angle, 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 differentiae do not serve 
us, and the diagnosis can be made only by puncture. 

(2) I have twice known cases of encapsulated or interlobar em- 
pyema 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, the likelihood of empyema should be suggested. 

As between pleuritic and pericardial effusion the presence of a 
good pulse and the absence of marked dyspncea 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. 


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. 

Adherent Pericadium. 

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 

(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 upon it. 

(c) Broadbent considers that the absence of any shift in the 
position of the apex beat with respiration or change of patient's 
position, is an important point in favor of mediastino-pericarditis. 
In health and in valvular or parietal disease of the heart, the apex 
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 full 
nspiration lowers the position of the cardiac impulse considerably. 



(d) The presence of hypertrophy or dilatation affecting especially 
the right 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. 
Such adhesions embarrass especially the right ventricle, because it is 
the right ventricle far more than the left which becomes attached to 
the chest wall. The left ventricle is more nearly free. 

(e) Since the space enclosed by the divergent costal cartilage 
just below the ensiform is but loosely associated with the central ten- 
don of the diaphragm, Broadbent looks especially at this point for 

Fig. 172. — Adherent Pericardium, Ascites. 

evidence of mediastinal or pericardial adhesions, the effect of which 
is to arrest completely the slight respiratory movements of this part 
of the abdominal wall. 

(/) Adherent pericardium, occurring as a part of a widespread hain 
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. 172 shows the appearance in 
cases of this kind in which the diagnosis was verified by autopsy. 


Summary . 

The diagnosis of adherent pericardium with chronic mediastini- 
tis 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 hypertrophy and dilatation of one or both 
ventricles without obvious cause. 

(d) The absence of any respiratory excursion 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. 



Aneurism of the Thoracic Aorta. 

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. 

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. 170, 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 at 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 cir- 
cumscribed. Not infrequently an abnormal pulsation at the sternal 
notch or in the neck may also be observed. Other causes of ab- 
normal 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. 


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 
the 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. 

Whether the aneurism penetrates the chest or not, it is often possi- 
ble to feel over it a vibrating thrill, systolic in time. If the layer of 
lamellated clot in the sac is very thick, the thrill is less apt to be felt. 

-' ft j 

3^ * 

Fig. 173. — Position When Looking for Slight Aneurysmal Pulsation. 

Diastolic Shock. 

• "■ More important in diagnosis is a diastolic shock or 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 one of the important and characteristic signs in 
aneurism. As the wall of the sac becomes weaker, the intensity of 
this shock diminishes. This diastolic shock may be appreciated over 
the trachea also, and is thought by some to have even more signifi- 
cance when felt in this situation. 

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 



primary bronchus in such a way that when the aorta is dilated, the 
bronchus is pressed upon with each expansile pulsation of the artery. 

Fig. 174. — Aneurismal Tumor (.4). The arrow B points to a gummatous swelling 
near the ensiform cartilage. The radiographic appearances of this case are shown below 
(Fig. 177). 

Fig. 175. — Aneurism Tumor Perforating the Sternum at A. At B there is a gummatous 
mass. (See below, Fig. 177, a radiograph of this case). 

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: 

(a) 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. Aphonia, 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 the mediastinum, are: 

(i) Inequality of the pupils. 

(2) Inequality of the radial pulses. 

(3) (Edema and cyanosis of one arm or of one side of the neck 
and head. 

(4) Pain in one arm from the pressure of an aneurism involving 
the subclavian artery upon the brachial plexus. 

(5) Clubbing of the fingers of one hand (rare). 

(6) Prominence of one eye (rare). 

(7) Flushing or sweating of one side of the face (very rare). 

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 
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 
sternum on 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. 176. When the aneurism 


-Heart dulness. 

Liver dulness.'' / ^^ 3/ I 

/ U I 

Fig. 176. — Diagram of Percussion Dulness in Aortic 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, 
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, low-pitched diastolic sound, corresponding to the palpable 
diastolic shock, is generally to be heard in the aortic region. 

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 
exaggerated 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) . 

Since aneurism is frequently associated with regurgitation at the 
aortic valve, a diastolic murmur is not infrequently to be heard. 

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 fiuoroscope and through radiography one can often 
make out a shadow corresponding to the position of the aneurism. 

From the front. 

From behind. 

Fig. 177. — Radiograph of Case whose Photograph is Reproduced as Figs. 174 and 175. 
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). 

The position of the shadow is best explained by reference to Figs. 
177, 178, 179, and 180. 


The most important signs of aneurism are: 

1. Abnormal pulsation — visible or palpable 

2. Tumor over which a 

3. Thrill and a 



Diastolic shock may be felt. 

Tracheal tug. 

Pressure signs (unequal pulses, pupils, hoarseness, pain, etc.), 

Dulness on percussion over the suspected area. 

Loud, low-pitched aortic second sound. 

Systolic murmur (least important of all) . 

Fig. 178. — Aortic Aneurism. (From v. Ziemssen's Atlas.) 

10. 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. 

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 
growth of the aneurism may give rise to pain, pulsation, and dulness 
and thrill in this region. 

(b) 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 evidences of 
pressure on the nerves or vessels of the mediastinum (cough, aphonia, 
inequality of the pupils, tracheal tug, etc.) . 

(c) Aneurism of the descending aorta gives rise usually to severe 
and persistent pain in the back, which raidates 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. 

Fig. 170. — Aneurism of the Aorta. (Curschman.) 

(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. 

Differential Diagnosis. 

(a) It is important to distinguish the diffuse dilatation of the 
aortic arch, which sooner or later complicates almost every case of 
incompetency of the aortic valves, from saccular aneurism of the 



transverse aorta. Dulness and pulsation, perhaps with systolic mur- 
mur and thrill in the second and third right interspaces near the 
sternum, occur in many cases of aortic. regurgitation, but though the 
aorta is dilated, its coats are not ruptured and it never breaks. The 
absence of pressure signs (pain, aphonia, etc.) and the shape of the 
x-ray shadow distinguish it from true aneurism. 

(b) Aneurism is not infrequently mistaken for aortic stenosis, in 
which a systolic murmur and thrill, similar to those occurring in aneu- 

Fig. 180. — Aneurism of the Aorta. (Curschman.) 

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 
as tracheal tug, pressure symptoms, abnormal area of percussion dul- 
ness, x-ray shadow, etc. 

(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. 

(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 

Fig. 181. — Aneurism of the Aorta with gumma. 

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 almost indistinguishable 
from aneurism during life. They may produce a more intense and 
widespread dulness which is usually in the median line, while the dul- 
ness of aneurism is oftener at one side. The pulsation transmitted to 
a tumor by the heart has not the expansile character of aneurismal 
pulsation. Tumors are not associated with any diastolic shock, 
rarely with a tracheal tug. 

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 
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. 

(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. 




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. 

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 

(i) 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, squeaking or piping 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 
stenosis of a relatively large bronchus, while squeaking and whistling 
sounds are usually produced in the smaller tubes. Large, bubbling 

1 Bronchitis may exist without rales, but cannot be diagnosed without them. Occa- 
sionally they are present only in the early morning. 



rales are much less often heard than the finer, crackling variety. The 
latter are produced in the smallest tubes, the former in the larger 

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. 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 
tuberculosis 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 often accompanied by foci of lobular pneumonia too small to be 
detected by our present methods of physical examination. 

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- 
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. 

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. 



From violent coughing the jugulars may be distended, but no 
systolic pulsation occurs in them. 

Voice sounds and tactile fremitus are normal. 

Differential Diagnosis. 

(Edema 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. 

(i) In oedema of the lung, or in pulmonary apoplexy, one may find, 
as in simple bronchitis, 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. The 
rales of oedema are mostly bubbles, and are 
more uniform in size when compared to those 
of bronchitis. 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 produces dry 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 

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 bronchopneumonia ever exists. 

(4) Muscle sounds. Under certain circumstances (cold, nervous- 

FiG. 182.— The Dots are 
Placed over the Area where 
Atelectatic Crepitation is 
Oftenest Heard. 


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. 145). 

(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. 182. 

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 emphysema, of 
asthma, and of bronchiectasis. 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. Accordingly, I shall not 
discuss chronic bronchitis any further at this point, but will return to 
the subject in the chapters on Emphysema and on Bronchiectasis. 
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 bronchiectasis 
or as chronic pulmonary cedema from weak heart action. 

Croupous Pneumonia. 

In its typical form croupous or fibrinous pneumonia produces 
solidification of one or more lobes, usually the lower, the process being 
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, 
later in the course of the disease, 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 later 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 

The frequency of endocarditis and pericarditis in connection with 
lobar pneumonias, especially with those of the left side, should be 
borne in mind. 

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 corres- 
ponding 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 dila- 
tation 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. 

(b) Palpation. — In the great majority of cases tactile fremitus is 
markedly increased over the affected area, 2 but in case the bronchi are 
occluded by secretions or fibrinous exudate, fremitus may be diminished 
or altogether absent. A few hard coughs will sometimes clear out the 
tubes and thus materially assist the diagnosis. Occasionally an increase 
in superficial temperature of the affected side may be noticed by palpa- 
tion, and rarely one feels a friction rub due to the fibrinous pleurisy 
which almost invariably accompanies the disease. 

(c) Percussion. — Over the area affected the percussion note is generally 
dull and may be almost flat, except in the earliest and latest stages of 
the disease, in which it may have a tympanitic quality with or without 

1 Perhaps because the patient is apt to lie upon the affected side. 

2 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. 


an element of slight dulness. More marked tympany is usually present 
over the unaffected lobes of the diseased lung (that is, over the upper 
lobes in the great majority of cases.) 

The conditions just described represent the great majority of cases, 
but the following exceptions occur: 

(i) 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. 

Percussion often makes us aware of an increased 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 "crepitant rales," that is, very fine crackling sounds, may 
be heard at the end of inspiration, but these are much more common 
in the stage of resolution 1 ("crepitans redux"). 

If some of the smaller bronchi are blocked, as is not infrequently 
the case, respiration is absent or very feeble, and such cases are often 
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. 

„- Tympany. 

Bronchial breathing 
•transmitted by 
spinal column to 
sound lung. 


Fig. 183. — Diagram of Signs in Pneumonia. 

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. It 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 (see Fig. 183). 

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 

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 distinguised from pneumonia. 


lobes are affected, the signs are wholly in the front. When searching 
for evidences of consolidation in persons suspected to have pneumonia, 
one should never omit to examine the apices and very summit of the 
armpit, pressing the stethoscope up behind the anterior fold of the 

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 patient and the bed-clothes 
without causing any discomfort. 

When resolution begins, the signs may almost completely disappear 
within a few hours. More frequently the bronchial breathing is 
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 active stages of the 
disease the entire absence of rales is very characteristic. In most 
cases the solidification of the lung persists after the fall of the tem- 
perature; 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 or fibrosis may develop in the solidified 
lobe. Commonest and most important, however, is the post- pneu- 
monic empyema (basal or interlobar) which is often mistaken far delayed 
resolution. The latter is rare; empyema, common (see below, p. 324). 

"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. 


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. 


(6) The breathing may be feeble but vesicular in character, or it 
may be absent, in case bronchi are plugged; from the same cause, 

(c) Tactile fremitus may be diminished. 

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 is 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. 

Differential Diagnosis. 

Pneumonic solidification is to be distinguished from 
(i) Pleuritic effusion, serous or purulent. 

(2) Tuberculosis of the lung. 

(3) Compression of the lung. 

(1) From pleuritic 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. 


(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 

(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. 

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 
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. 


(Catarrhal or Lobular 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 

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. 

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 wide spread 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 

Physical Signs. 

In the majority of cases there are no characteristic physical signs, 
and the diagnosis has to be made largely from the symptoms and 
course of the disease. The consolidated areas are usually too small to 
give rise to any dulness on percussion, or to any change in the breath 
sounds, voice sounds, or fremitus, so that auscultation shows, as a rule, 
nothing more than patches of fine rales occurring at the end of expira- 
tion. Localized tympanitic resonance is sometimes 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 consolidation may be 
obtained, although they are apt to 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 combination of the 
physical signs of a localized bronchitis with the symptoms of pneumonia. 
"This patient," we say, "has only the signs of bronchitis, 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." 

Differential Diagnosis . 

(a) Acute pulmonary tuberculosis may be indistinguishable from 
broncho-pneumonia by the physical signs alone. The diagnosis 
must be made from the history and course of the disease or from the 
presence of tubercle bacilli in the sputa. 

(6) 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 
dyspncea, 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. 

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 haemoptysis} 
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. I have found tubercle bacilli in four 
such cases. More often the earliest physical signs are: 

(a) 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.) (See Fig. 184). 

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 



(b) A slight diminution in the excursion of the diaphragm on the 
affected side, as shown 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 

(a) In examining the apices of the lungs for evidence of early 
tuberculosis one should secure if possible perfect quiet in the room, and 
have the clothes entirely removed from the patient's chest. The 
ordinary hard-rubber chest-piece is better than the chest-piece of the 

Rales. » 

Fig. 184. — Diagram to Show Position of Earliest Signs in Tuberculosis. 

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 to follow it, one should listen as care- 
fully as possible at the apex of the lung, above and below the clavicle, 
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 who cannot cough at will, one can accomplish 
nearly the same result by making them count as long as possible with 

1 Rales heard only during the first few breaths and not found to persist on subsequent 
examinations, may be due to the expansion of atelectatic lobules. 


one breath and then listening to the immediately succeeding inspira- 
tion. 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. 

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 
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, as individuals differ very much in the extent 
with which they are capable of depressing the diaphragm. 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, independently of any active disease in the lung 

Those who are expert in the use of the fluoroscope 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. 

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 im- 
peded, 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. 

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. 


(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 
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 

^^ Complete 
^>"" solidification. 
Rales. _ 

-\~~ solidification. 

1— Rales. 

Fig. 185. — Diagram of Signs in Phthisis. 

(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). 

(d) Abnormally loud transmission of the heart sounds, especially 
under the clavicle. 

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 

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. 



have a very sharp, crackling quality, their intensity being increased 
by the same acoustical conditions with 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 in clear only in case the signs occur at 
the left apex. Precisely the same signs, if present at the right apex, 
leave us in doubt regarding the diagnosis, for the reason that, as has 

Fig. i 86. — This Patient has Solidification at both Apices and Tubercle Bacilli in the Sputa. 

He feels perfectly well. 

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 solidifica- 
tion. Hence, if these signs, and only these, are discovered at the right 
apex, we cannot feel sure about 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), 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 
sounder lobes of tuberculous lungs is a raising of the pitch of inspi- 
ration, 2 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 re- 
cently 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. 152). 

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. 186 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, 3 with increased sense of 

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 
rales are produced within the pleuritic adhesions, which are almost 

1 The natural disparity between the two apices is less marked in the supraspinous fossa 
behind than over the clavicle in front, and hence pathological dulness at the apex is 
more often demonstrable behind than in front. 

2 "Sharp breathing" (Turban). 

3 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 



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 
true, they are associated and form a very characteristic group, but 
there are many exceptions to this rule. 

One of the common variations from the typical group of signs just 
mentioned occurs in the fibroid cases with pleural thickening. In 
these the breathing may be everywhere feeble, though the presence of a 
few rales 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 

Bronchial breath- 
ing, dulness. 

Increased fremitus. 

Increased voice 


■ Rales. 

Fig. 187. — To Illustrate Progress of Signs in Pulmonary Tuberculosis. 

tubular breathing, abundant rales, etc., (b) cases where there is very 
little to hear with the stethoscope and that little not in itself distinctive. 

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 
solidification. Owing to this it is easy to be misled into diagnosing 
solidification at both apices when only one is affected. 

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 almost sure 
to occur. It is exceedingly rare for the disease to extend far in one 
lung without involving the other. 

About the time that the tuberculous process invades the previously 
sound lung it is apt to show itself at the apex of the lower lobe of the 
lung first affected. Consonating rales 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. 187. 

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) Amphoric or cavernous breathing. 

(b) " Cracked-pot resonance " on percussion. 

(c) Coarse, gurgling rales. 

(a) Cavernous or Amphoric Respiration. — When present, this type 
of breathing is almost pathognomonic of a cavity. It is also to be 
1 Yet not so rigid as to be uninfluenced by the entrance and exit of air. 


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 bulging 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 ' inter mittence 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 much importance in diagnosis. 
The same is true of metamorphosing breathing (see above, p. 154). 

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, 
but it is more often disseminated (like abscess or gangrene) in the 
lower part of the lungs especially. 


Fibroid Phthisis. 

This term applies to slow tuberculous processes with relatively 
little ulceration and much fibrous thickening. 

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 
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 
do not differ from those of ordinary phthisis, except that falling-in of 
the chest walls over the retracted lung may be more marked. Occa- 
sionally 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. 

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 
chiefly those of thickened pleura. To this subject I shall return in the 
section of Diseases on the Pleura (see below, p. 308). 

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- 
chitis with emphysema. I have seen two cases within a year. Dulness 
is wholly masked by emphysema, tubular breathing is absent, and 
piping and babbling rales are scattered throughout both lungs. The 
emphysema 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 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. 

Phthisis with Anomalous Distribution of the Lesions. 

Very rarely a tuberculous process may 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 

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, or abscess, or unre- 
solved pneumonia (cirrhosis of the lung) . 

Acute Pulmonary Tuberculosis. 

No one of the three forms in which acute phthisis occurs, viz., 

(a) Acute tuberculous pneumonia, 

(b) 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. 



I. Emphysema. 

For clinical purposes, the great majority of cases of emphysema 
may be divided into two groups. 

(i) Large-lunged emphysema, usually associated with chronic 
bronchitis and asthma. 

(2) Small-lunged, or senile, emphysema. 

Although the second of these forms is exceedingly common, it 
is so much less likely than the first form to give rise to distressing 
symptoms that it is chiefly the large-lunged emphysema which is seen 
by the physician. 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 diminished; but in the large-lunged form we have an increase 
in the volume of the whole organ in addition to the changes just 

Large-Lunged Emphysema. 

The diagnosis can usually be made by inspection alone. In typical 
cases the antero-posterior diameter of the chest is greatly increased, 
the in-spaces are widened, and the costal angle is blunted, while the 
angle of Ludwig 1 becomes prominent. The shoulders are high and 
stooping and the neck is short (see Fig. 188). 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 
working of the auxiliary muscles of respiration is not infrequently 
seen. The diaphragm shadow (Litten's sign) begins its excursion one 
or two ribs farther down than usual and moves a much shorter distance 
than in normal cases. 

1 Formed by the junction of the manubrium with the second piece of the sternum. 



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. 

Percussion yields very interesting information. The disease 
manifests itself — 

Fig 188. — Barrel Chest due to Chronic Bronchitis and Emphysema. 

(a) By hyper-resonance on percussion, with a shade of tympanitic 
quality in the note. 

(6) By the extension of the margins of the lung so that they en- 
croach upon portions of the chest not ordinarily resonant. 

The degree of hyper-resonance depends not only upon the degree 
of emphysema but 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 over- voluminous lungs 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, the lungs completely closing 
over the surface of the heart. 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 
or more below its normal position. 

Auscultation shows in uncomplicated cases no 
very marked modification of the inspiratory mur- 
mur, which, however, may be shortened and enfee- 
bled. The most striking change is a great pro- 
longation and enfeeblement of expiration, with a 
Fig. 189.— Dia- i owe ring of its pitch (see Fig. 189). 

gram o us ra e This type of breathing is like bronchial breath- 

Lmphysematous J ■*■ ° 

Breathing with Musi- ' m S in one respect; namely, that in both of them 
cal Expiratory Rales, expiration is made prolonged, but emphysematous 
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 
crackling rales. 

In "small-lunged emphysema" we have precisely the same physical 
signs, except that the boundaries of the lung are not extended, expira- 
tion is less prolonged and less difficult, and inspiration is normal. 
It does not tend to be complicated by bronchitis and asthma; indeed 
the small-lunged emphysema rarely gives rise to any symptoms, 
and is discovered as a matter of routine physical examination. 


1. Hyper-resonance on percussion. 

2. Feeble breathing with prolonged expiration. 

3. Diminished fremitus and voice sounds. 

4. Encroachment of the resonant lungs on the heart and liver 
dulness (in the large-lunged form). 

Differential Diagnosis. 

(a) Emphysema may be confounded with pneumothorax, since in 
both conditions hyper-resonance and feeble breathing are present. 


But emphysema is usually bilateral, encroaches upon but does not 
displace neighboring organs, and is not often associated with hydro- 
thorax. Emphysema, if extensive, is usually associated with chronic 
bronchitis and so with squeaking or bubbling rales, while in pneumo- 
thorax breathing is absent or distant amphoric without rales. 

(b) 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 
bronchitis with emphysema. 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 pulses 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) Uncompensated mitral stenosis may produce dyspnoea and 
cyanosis and weak rapid heart action somewhat similar to that seen in 
emphysema, and may not be associated with any cardiac murmur, but 
the dyspnoea is not of the expiratory type, and the irregularity of the 
heart, with evidence of dropsy and general venous stasis, should make 
it evident that something more than simple emphysema is present. 

(d) The occurrence of an emphysematous form of phthisis I have 
already mentioned in discussing the latter disease (see p. 294). 

Emphysema with Bronchiectasis , Bronchitis or Asthma. 

In the great majority of cases, emphysema of the lungs is associated 
with chronic bronchitis, bronchiectasis, 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. 

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, from whence it may work through and manifest 
itself under the skin, giving rise to a peculiar crackling sensation on 
palpation, and to a similar sound on auscultation. More frequently the 
trouble arises in connection with a tracheotomy wound, the air pene- 
trating under the skin and producing a downy, crepitating swelling. 

" 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) hyper-resonance substituted. 

Like emphysema, this condition leads to hyper-resonance on per- 
cussion and to encroachment of the pulmonary margins upon the 
neighboring organs (as shown by a reduction in the area of dulness 
corresponding to them) , but the respiratory murmur is exaggerated and 
has none of the characteristics of emphysematous breathing. 

A word may here be added regarding the condition described by 
West under the name of 

Acute Pulmonary Tympanites. 

In fevers and other acute debilitating conditions West has observed 
that the lungs may become hyper-resonant 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 toxaemia is so apt to 
produce. Apparently the muscle fibres of the lung suffer like those 
of the heart. 

(Primary Spasm of the Bronchi.) 

During a paroxysm of bronchial asthma our attention is attracted 
even at a distance by the loud, wheezing, 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- 
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 
practically nothing is to be heard of the breath sounds. "The asth- 
matic 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. 

Differential Diagnosis. 

(a) Mechanical irritation of the bronchi, as by the pressure of an 
aneurism or enlarged gland, 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 

(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, myocarditis, and other diseases of the heart and 
kidney, may be entirely indistinguishable from primary bronchial 
asthma but for the evidence of the underlying cardiac or renal disease. 

(d) 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 downwards. 


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. 

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 not at the apex but usually 
about the root of the lung or lower down. Cavities are not formed. 
Stenosis of a bronchus may occur with resulting atelectasis of the 
corresponding lobules. 

Bronchiectasis (Bronchial Dilatation). 

(a) The commonest type is that associated with chronic bronchitis 
and recurrent attacks of winter cough. Innumerable small bron- 
chioles become dilated and the resulting cavity is repeatedly infected — 
usually with influenza bacilli (Wm. H. Smith). The signs may be 
simply those of a chronic bronchitis with or without emphysema 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 

(c) In a small number of cases signs of cavity (see above, p. 292) 
may be made out. 

From pulmonary abscess the disease may usually be distinguished 
by the history, the sputa, and the fact that local signs of cavity sur- 
rounded by solidification and bronchitis can usually be demonstrated 
in abscess. 

The disease may cause marked retraction of the chest on the 
affected side, and neighboring organs may be drawn out of place. 

Cirrhosis of the Lung. 
(Chronic Interstitial Pneumonia.) 

As an end stage of unresolved croupous pneumonia, or as a result 
of chronic irritation from mineral or vegetable dust, a shrinkage of a 
part or the whole of the lung may occur, which progresses until the 
pulmonary tissue is transformed into a fibrous mass enclosing bronchi. 


The side of the chest corresponding to the affected lung becomes 
shrunken and concave; fremitus is increased, percussion resonance 
diminished or lost, respiration tubular with coarse rales. 

From tuberculosis the condition is to be distinguished solely by 
the history, the absence of bacilli in the sputa, and the comparative 
mildness of the constitutional symptoms. 

The right ventricle of the heart may become hypertrophied and 
later dilated with resulting tricuspid insufficiency. 


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 in- 
structed. Early morning cough is most 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 sputum is 
deposited on the cotton before the child has time to swallow it, and 
may then be withdrawn and examined. 

II. Quantity. — If the amount expectorated is large (i.e., one-half 
a pint or more in twenty-four hours) , we may be dealing with : 

i. Pulmonary oedema (watery, sometimes pnk 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). 

5. Bronchiectasis (large amount of pure pus in pellets often ex- 
pectorated within a few minutes on change of position) . 

III. 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. 

IV. Gross Appearances. — (a) Bloody sputum (haemoptysis) means 
pure or nearly pure blood in considerable quantity, a teaspoonful or 
more, not mere streaks of blood in muco-purulent sputum, which 
usually comes from an irritated throat. 


Haemoptysis thus defined is seen chiefly in the following conditions, 
arranged in the order of frequency: 
i. Phthisis. 

2. Pulmonary congestion with infarction (mitral disease). 

3. Pneumonia. 

4. After epistaxis. 

5. Abscess or gangrene of the lung. 

6. Without known cause ("vicarious menstruation," etc.). 
Rare causes are new growths of the lung, parasites (Distomum 

Westermanni) , aortic aneurism rupturing into an air tube, ulcer of the 
trachea or bronchi. 

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 

(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) Serotis sputum, profuse and watery, is characteristic of pul- 
monary oedema. 

(d) Black or gray sputum is due to carbon, dust, or tobacco smoke 

(e) Pure pus — not muco-purulent — is oftenest seen in influenza 
and bronchiectasis, occasionally in empyema breaking through the 

(/) Muco-purulent sputum occurs in many diseases and is character- 
istic of none. 

IV. 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: 


i. 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. H 2 S0 4 . 

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 blue 2 for 
about thirty seconds. 

7. Wash in water, dry on blotting paper, and mount in Canada 

The whole process need not take more than five minutes, and it is 
absolutely essential that 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 specimens 3 obtained several days apart makes it very 
unlikely that phthisis is present. One or two negative examinations 
are of no signifiance. 

Pneumococcic and Influenza Bacilli. — For both these organisms 
Gram's stain is on the whole the best. This is performed as follows: 

1 Carbolic-acid crystals, 5 gm.; fuchsin (saturated alcoholic solution), 10 gm.; water, 
100 gm. 

9 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. 



i. Prepare a smear as above directed. 

2. Cover it with anikne-oil-gentian-violet solution 1 (freshly 
made each week) and heat to steaming point. 

3. Wash in water and cover with IKI solution 2 for thirty seconds. 

4. Wash in ninety-five-per-cent. alcohol until the blue color ceases 
to come out. 

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. 190). The presence of a few 

Fig. iqo. — Pneumococci in Sputum. (W. H. Smith.) (Gram's stain.) 

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 
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. 

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. 


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 10 gr. of potassium iodide after meals for a week. A 
way of getting sputa from young children has already been described 
(page 303). 



I. Hydrothorax. 

In cases of nephritis or of cardiac weakness due to valvular heart 
disease a considerable accumulation of serum may take place in both 
pleural cavities. The physical signs are identical with those of pleu- 
ritic effusion (see below, page 315) 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. 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. 

Friction sounds, of course, do not occur, as the pleural surfaces 
are not inflamed. A few grains of potassium iodide by mouth soon 
produce a reaction for iodine in the fluid of hydrothorax and not in 
pleuritic effusion. 

II. Pneumothorax. 

Pneumothorax, or the presence of air in the pleural cavity, may 
result from stabs or wounds of the chest wall, but is usually a com- 
plication of pulmonary 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. 

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. More commonly the onset of 
symptoms 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. 



Physical Signs. 

i. 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 l ess obliterated. The 
diaphragm is much depressed and Litten's sign absent. In right- 
sided pneumothorax, which is relatively rare, the liver is depressed 
and the 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. 191) 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. 

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's 1 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 satistics of Emerson 2 and 
James 1 the signs were present in forty- five out of sixty cases, or seventy- 
five per cent. 

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. 165), 
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 the great majority 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- 
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 "metal- 
lic tinkle" (see above, p. 165). At the base of the chest, over an 

1 Osier's Modern Medicine, Vol. Ill, p. 881. 

2 Emerson: Pneumothorax, Johns Hopkins Hospital Reports, 1903, Vol. XI. 


area corresponding to the position of the fluid, an area of dulness may 
be easily marked out by percussion, and this area shifts very markedly 
with change of position. The shifting dulness of pneumohydro thorax 
is strongly in contrast with the difficulty of obtaining any such shift 
in ordinary pleuritic effusion (see Fig. 192). 

(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 

Fig. 191. — 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. 197. (From v. Ziemssen's Alfas.) 

to the voice and cough sounds, denote an open pneumothorax, but 
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 

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 
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 pucture 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. 294). 

f Tympany, 

I breathing 

a • J and voice 

' 1 absent or 


Displaced I / / /(V"^- 15 ^^ ' )\ \ \ \ ^ amphoric 

heart. ' I— — — 

Fluid = 
Liver. — — — — 

Fig. 192. — Left Pneumoserothorax with Displaced Heart. 

From all these it can be distinguished by the presence of amphoric 
or metallic sounds, which are never to be obtained in the other affec- 
tions named. 

(c) Hernia of the intestine through the diaphragm (see Fig. 193) 
or great weakening of the diaphragmatic muscular fibres, may allow 
the intestines to encroach upon the thoracic cavity and simulate 
pneumothorax very closely. The history and course of the case, the 
abdominal pain, vomiting, and indicanuria, generally suffice to dis- 
tinguish 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. 

(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. 

Fig. 193. — Diaphragmatic Hernia. The outline of the displaced diaphragm visible below 
the left clavicle. Heart displaced to right of sternum. (From v. Ziemssen's Atlas.) 

(6) 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 
importance of distinguishing it from the non-encapsulated form of 
the disease, in which treatment is essential. 


Clinically, we deal with three types: 
(a) Dry or plastic pleurisy. 
(6) Pleuritic effusion, serous or purulent, 
(c) Pleural thickening. 



(a) Dry or Plastic Pleurisy. 

Doubtless many 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 physical signs resulting from 
the fibrinous exudation are usually situated at the bottom of the axilla 
where the diaphragmatic and costal layers of the pleura are in close 
apposition. Doubtless the pleuritic inflam- 
mation 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 physical signs are 
situated at the spot indicated in Fig. 194. 

Occasionally pleuritic friction is to be 
heard in the precordial region, and after the 
absorption 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 connec- 
tion with early phthisis. In diaphragmatic 
pleurisy, when the fibrinous exudation is 
especially marked upon the diaphragmatic 
pleura, friction sounds may be heard over 
the region of the attachment of the dia- 
phragm in front and behind as well as in the 
axillae. Hiccup often occurs and gives exquisite 

Our diagnosis is based upon a single physi- 
cal sign, pleuritic friction. The nature of this 
sound has already been described (see above, 
p. 162), and I will here only recapitulate 
During the first few deep breaths one hears, 
while listening over the painful area, a grating or rubbing sound 
usually somewhat jerky and interrupted, most marked at the latter 
part of inspiration, but often audible throughout 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 

Fig. 194. — Showing the 
Point at which Pleural 
Friction is most Often 

what was there said. 


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. 163. 

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. 

(b) 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 


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. 195). 

In the routine percussion of the chest, therefore, one should never 
leave out these areas. A small effusion is most easily detected in 

Area of dulness I ' AVT '^^5il I III (ctmlnE=j--^A— ^--' i Area of cardiac 

due to small -_--| i-l^^^--^1llllll!nW]lllfflfc^r . \ dulness. 

pleural effusion. 

Fig. 195. — Small Pleural Effusion Accumulating (in part) near the Right Border of the 


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- 
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 elasti- 
city 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. 

Normol resonance 
and vesicular 

Tympany, voice and ._ 
fremitus increased. 

Flatness, no breath- 
ing, voice sounds, 
or fremitus. 

Zone of condensed 
lung above the 

Exaggerated (com- 
pensatory) breath- 
ing and reso- 

Fig. 196. — Diagram to Illustrate Physical Signs in Moderate-Sized Effusion in the Left 


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 resist- 
ance 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 
the condensed lung immediately above it, and the top zone to the 
relatively unaffected part of the lung (see Fig. 196) . 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. 
197). Near the spine and near the sternum (in right-sided effusions) 
the line corresponding to the level of the fluid may rise sharply. 

Fig. 197. — 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- 
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 

Grocco's (Koranyi's) Sign — The Paravertebral Triangle. 

On the sound side in the position shown in Fig. 196 (p. 317) a 
triangular patch of dulness can be percussed out in most cases of 
pleural effusion. 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 reson- 
ance 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. 197). (Inspection and palpa- 
tion often give us even more valuable information on this point. See 
below, p. 323.) We must be careful to distinguish such an area of 


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 disappears 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 hyper-resonance 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) If the lung on the affected side fails to retract (owing to 
emphysema or adhesions to the chest wall) , the area of dulness and its 
intensity will be much diminished. 

(c) 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. 

(d) Rarely percussion may be tympanitic over an effusion at the 
left base owing to distention of the stomach or colon. 

(e) The diagnosis between fluid and thickened pleura will be 
considered later. 


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 

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 bronchial sounds are especially frequent and intense in 
children. 1 

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 
in quality or intensity, and in the differential diagnosis of difficult 

^acelli's theory — that the whispered voice is conducted through serum but not through 
pus — is not borne out by facts. 



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 

Fig. 198. Interlobar A, A=Exudate 

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. 

(i) 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 

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 
displaced considerably toward the right, even when the level of the 
fluid reaches no higher than the sixth rib in the nipple line. The im- 
pulse is then to be seen and felt to the right of the sternum, somewhere 
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. 

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, l the shoulder is raised, 
and the spine curved toward the affected side. The diaphragm is 
depressed, and Litten'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, while in adults three-fourths of them are 
serous. The presence of leucocytosis in empyema and its absence 
in most cases of serous {i.e., tuberculous) pleurisy is of more value 
in diagnosis. 

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 
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 
permanent thickening of the pleura, considerable dulness often 
remains for weeks after the fluid has been absorbed. One need not 
be disappointed 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. 

Interlobar Empyema. 

In recent years the frequency and importance of empyema lim- 
ited to an interlobar fissure has become impressed upon many 

1 1 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. 



clinicians. I have seen both the post-pneumonic and the tuberculous 
types, but the former is much 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. 199). 

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- 

Diminished or absent 

Diminished or absent 


XtAA 1 ^y 
Fig. 199. — Signs in Interlobar Empyema. 

X-ray examination may bring out in sharp relief a shadow corres- 
ponding to this area and sharply contrasted with the relatively 
normal lung above and below it. 

The exploring needle often fails to find the pus, but the search 
should not be given up (if the physical signs are clear) until a rib has 
been excised and the region thoroughly explored under complete 
anaesthesia. Empyema encysted between the diaphragm and lung or 
between the lung and chest wall are not uncommon but can rarely be 

(c) 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 : 


(i) 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. 

These signs are most apt to be found at the base of the lung be- 
hind and in the axilla. Occasionally a similar thickening may be 
demonstrated throughout the whole extent of the pleura, and the 
lung failing to expand, the chest may fall in as a result of atmospheric 
pressure (see Fig. 73). 

The ribs approximate and may overlap, the spine becomes curved, 
the shoulder lowered, the scapula prominent, and the whole side 
shrunken. The heart may be drawn over toward the affected side. 

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. 

Encapsulated Pleural Effusion. 

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 autopsies 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 

The diagnosis of encapsulated pleural effusion is a difficult one and 
oftentimes cannot be made except by puncture. The signs are those 
of fluid in the pleura, but anomalously placed. Even puncture may 


fail to clear up the difficulty, since the needle may pass entirely 
through the pouch of fluid and into some structure behind so that no 
fluid is obtained. 

Pulsating Pleurisy. 

Under conditions not altogether understood the movements trans- 
mitted by the heart to a pleural effusion (usually purulent) may be 
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 absence of a 
palpable thrill or diastolic shock and by the evidence of fluid in the 

Differential Diagnosis of Pleuritic Effusion. 

The following conditions are not infrequently mistaken for pleuritic 
effusion : 

(1) Croupous pneumonia with occlusion of the bronchi. 

(2) Pleura thickening, with pulmonary atelectasis. 

(3) Subdiaphragmatic abscess or abscess of the liver. 

In croupous pneumonia with plugging of the bronchi one may 
have present all the physical signs of pleuritic effusion except dis- 
placement 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 usuallv 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 pneu- 
monia and pleuritic effusion at the same time, and that pneumonia is 
often 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 the use of the criteria just 

(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. 200. — Area of Dulness in Solitary (tropical) Abscess of the Liver. 

of Litten's phenomenon, but the tactile fremitus is usually more 
diminished 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 two cases I have known 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 which pushes 


up the lung together with the diaphragm. Without the fluoroscope or 
a good radiograph this diagnosis may be impossible. With the fluoro- 
scope it should be possible to see that the dome of the diaphragm caps 
the shadow and moves down with it 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 on percussion, which rises to a much higher level in the axilla 
and back than in front or near the sternum (see Fig. 200) , and may be 
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. 

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- 
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 

1. The presence of bloody fluid with any endothelial sediment. 

2. Its rapid and repeated reaccumulation. 

3. Metastases (supraclavicular, axillary, pectoral) and along the 

Similar signs are obtained in the rare sarcoma of the pleura (four- 
teen cases on record) . 

Echinococcus 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 with eosinophiles and hooklets in the tap fluid, which is remark- 
able in that it does not contain albumen in any considerable quantity. 
Urticaria often follows puncture. 


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. 

Examination of Exudates and Transudates. 

Only such methods as can be carried out without a thermostat 
will be here described. Hence the examination of diphtheria swabs, 
blood cultures, and pus are excluded. We have left the fluids obtained 


Fig. 201. — Lymphocytosis in Pleural Fluid. Primary tuberculous pleurisy. (X750 

diameters.) (Musgrave.) 

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. 

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. Exuates are usually in the vicinity of 1.020. An ordinary 
specific-gravity bulb is used. 

3 . The cells of the sediment (cytodiagnosis) . 

Technique of Cytodiagnosis. — 1. Pour fluid into tubes of a cen- 
trifuge and centrifugalize five minutes. 


Fig. 202. — Polynuclears and Large Lymphocytes in Pleural Fluid from a Case of Trau- 
matic Acute Infecdous Pleurisy. (X 750 diameters.) (Musgrave.) 

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 

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 441) with the following 
mixture: 2 Wright's modification of Leishman's stain, 3 parts; pure 
methyl alcohol, 1 part. 

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. 
Interpretation of Results. — (a) In tuberculous pleurisy, lymphocytes 

1 The amount of albumin usually runs parallel with the weight of the fluid. 

2 Suggested by Musgrave: Boston Med. and Surg. Journ., vol. cli., p. 319, 1904. 



make up from seventy to ninety-nine per cent — usually over ninety 
per cent — of all the cells found in the smear 1 (see Fig. 201). 

(6) In septic cases due to the streptococcus, staphylococcus, or 
pneumococcus the majority of the cells are polynuclear leucocytes 
(see Fig. 202). 

(c) In transudations (dropsical) the predominating cell is a large 
mononuclear type, apparently endothelial in origin and often occur- 
ring in sheets or "plaques" (see Fig. 203). 

Fig. 203. — Pleural Fluid in Hydrolhorax due to Cardiac Disease. Endothelial plaques 
and cells. (X 750 diameters.) (Musgrave.) 

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. 

In peritoneal fluid the use of cytodiagnosis has not as yet furnished 
information of any considerable diagnostic value. 

In cerebrospinal fluid obtained by lumbar puncture the predom- 
inance 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 

1 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. 





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. Lobar pneumonia, inhalation of 
foreign bodies and suppuration elsewhere are the commonest causes. 
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. 

Gangrene of the lung is not a common disease. The diagnosis 
usually rests altogether upon the smell and appearance of the sputa. 
In fetid bronchitis one may have sputa of equal foulness, but the odor is 
different. The finding of elastic tissue in the sputa proves the exist- 
ence of something more than bronchitis. X-ray examination may 
help in diagnosis. Often it reveals areas other than those previously 

Pulmonary abscess, which, like gangrene, is a rare affection, is 
often simulated by the breaking of an empyema into the lung and the 
emptying of the pus through a bronchus. Large quantities of pus are 
expectorated in such a condition, and abscess of the lung is suggested, 
but the other physical signs are those of empyema and should be easily 
recognized as such. The finding 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. 



Neoplasms of the Lung and Mediastinum. 

(a) Neoplasms of the lung are usually secondary to tumors of the 
digestive 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 may be quite without physical signs or may 
present some of those of solidification not explained by any of the 
ordinary causes. Fremitus is often absent. Pleural effusion may 
overshadow all other signs. Supraclavicular or axillary metastases 
may put us on the right track or if the superior cava or its branches are 
compressed by glandular metastases, the resulting venous distension 
and oedema is suggestive. 

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: (i) Sarcoma (including lymphosarcoma, leucaemic growths, 
and Hodgkins' disease; (2) Teratoma and cyst. 

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.. 

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 

Christian: Osier's Modern Medicine, vol. iii, p. 893. 


which with tumors are far more apt to include venous distension, 
oedema, and cyanosis than is the case with aneurism (see also p. 272). 
Tumors of the lung itself may produce mediastinal metastases, and 
are then indistinguishable from primary mediastinal disease. 

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. 


(a) 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 

(b) 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, 
but sometimes audible as long as we choose to listen to them. These 
sounds, to which Abrams has given the name of "atelectatic crepita- 
tion," are in my experience especially frequent at the base of either 


axilla. The same writer has noticed an opacity to the #-rays over 
such atelectatic areas. 

Forcible percussion may be sufficient to distend small areas of 
collapsed lung, or at any rate to dispel the dulness previously present 
(see above, p. 135, the lung reflex). 

(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, Abrams finds the "lung-reflex" (see 
page 135) of value. Atelectatic areas expand if the skin overlying 
them is irritated. Solidified areas show no change. 

(Edema of the Lungs. 

In cardiac or renal disease one can often demonstrate 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 

Dulness on percussion and modification of voice sounds are not 
present, unless hydrothorax or hypostatic pneumonia complicate the 


Hypostatic Pneumonia. 

In long, debilitating illness, such as typhoid fever, 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 condi- 
tions examination 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 

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. 





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. 

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 compared with the space allotted to the methods of exam- 
ining 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^rra. 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. 

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 

1 Summarized in his "Mechanical Factors of Digestion:" Longman's, 191 1. 

2 1 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 accom- 
plishing the feat at all. I have seen a similar uncertainty regarding the palpation of the 
normal but slightly displaced right kidney. 



with the patient upright, he should stand with his side to the light, 
not facing it. By inspection we seek information on: 

(a) The general contour of the abdomen. 

(b) 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 
hyperaemic, 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. Richardson 1 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 (see Fig. 82). 

3. Striae, 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 {linea 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 (page 343). 

1 M. W. Richardson: Pennsylvania Medical Journal, March 3, 1900.. 


Palpation. 1 — 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 (warm) 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 impor- 
tance of a high, narrow bed, or table, so that the physician need not stretch or stoop to 
reach the patient. 


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. 

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 (see above, page 263), 
especially as a systolic 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 com- 
mon 'iliacs. 

The liver cannot be felt at all in the great majority of normal per- 

1 Leube believes that in very thin subjects the head of the pancreas may occasionally be 



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 390) 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 young, 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 on page 35 1 . 

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. 

Palpable Lesion of the Belly Walls. 

The occurrence of lesions, to be recognized mainly by inspection 
and percussion, has been discussed (page 338). Besides these we 
search for: 

1. Herniae, epigastric or umbilical (see Fig. 204). The diagnosis 
rests on the presence of an impulse on coughing, with or without a 
reducible tumor. Omental herniae do not bulge with cough. 

Fig. 204. — 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 haematoma due to trauma or without 
known cause explains some cases, and occasionally tuberculosis or 


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 386). 
Palpation of the Liver (see page 362). 
Palpation of the Kidney (see page 390) . 

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, see below, page 345). 

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 

(a) Whether a groove or interval can be made out, by palpation 
or percussion, between the mass and either of those organs. 

(b) 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, leukeemic 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 by the movement of the abdominal walls over the tumor, 



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, 
peritoneal exudate similar to that which produces the friction sounds 

Fig. 205. — Diastasis recti. 

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 


Percussion. — Abdominal percussion is less valuable than tho- 
racic. 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. 

(a) Free fluid (ascites, peritonitis, hsemoperitoneum, ruptured 
cyst) gravitates to the flanks and suprapublic 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. 

(b) 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 (see below, pages 354 and 385). 

Percussion of Traube's semilunar tympanitic space (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. 

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 79 x 

1 1 . Splenic tumor in cirrhosis of the liver 60 

12. Leukemic spleen 58 

13. Malignant tumor of the ovary 43 

14. Tuberculous kidney 41 

15. Tumor as part of tuberculous peritonitis ^3 

16. Cancer of the pancreas 32 s 

17. Neoplasm of the kidney 27 

18. Sarcoma of abdominal wall 27 

19. Enlarged spleen of unknown cause 26 

20. Omental cancer 18 

2 1 . Intussusception 17 

Diseases of the Peritoneum. 

1. Peritonitis — local or general. 

2. Ascites. 

3. Cancer and tuberculosis. 

/. Peritonitis. 

1. Local peritonitis gives evidence of its presence by (a) pain, 
(&) tenderness, (c) muscular spasm, (d) tumor, and (c) constitutional 

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. 


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 376.] 

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 

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, as explained on page 345. Faeces and even gas cease to move, 
as the intestines are paralyzed. Vomiting is the rule, and soon be- 
comes very foul (stercoraceous) . There is fever, with a rapid and 
very weak pulse. The mind is clear, alert. The facial expression is 
not peculiar and may be normal. If there is persistent vomiting the 
facies of that condition appears, viz., a drawn, pinched, anxious look, 
with dark circles under the eyes. The nausea and the rapid loss of 
fluid by vomiting account for these appearances. 

The leucocyte count is generally elevated, but in the most viru- 
lent cases remains normal or subnormal. 

II. 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) Solid ovarian tumors. 

The methods of diagnosis of ascites have been explained above. 



The 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. 206. 

III. 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: 

1 . Tumor masses scattered here and there, 
sometimes at the navel. 2. Ascites. 3. 
Emaciation and anaemia. 

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 *-ray 
examination are the data from which we must reason. 

(b) The perisplenic type of abscess follows a general peritonitis, 

Fig. 206. — Characteristic Shape 
of Belly in Ascites. 


which has been treated by drainage and recumbency. The pus 
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. 

i . Enlarged glands — tuberculous, cancerous, or as part of Hodgkin's 
disease — 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 ph- 
struction (see below, page 377), from which it can rarely if ever be 
distinguished without operation or autopsy. 



The Stomach. 

The best methods of examining the stomach are: 
i. Inspection and palpation of the epigastrium and the neighbor- 
ing portions of the abdomen. 

2. Estimation of the size and position of the organ after distending 
it with air or water. 

3. Examination of the stomach contents: (a) fasting;, (b) after 
a test meal. 

4. Bismuth — x-ray examination. 

By combining the results of these four methods of examination 
with the results of our general examination of the body — emaciation, 
anaemia, 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. 

(a) 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 unless it is extreme and sharply localized 
in a small area. In a small proportion of cases cutaneous tenderness 
in the back (lower dorsal or upper lumbar region) can be elicited in 
cases, of peptic ulcer. 

(6) A tumor in the epigastrium (see Fig. 207) 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. 

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, 
cicatrix, adhesions, simple thickening, or muscular spasm). The 

Fig. 207. — Epigastric Tumor in Gastric Cancer. 

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 some- 
times be reexcited by briskly snapping the epigastric region with the 

(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. 208). 

2. Estimation of the Size, Position, Secretory and Motor Power of the 


Whenever we cannot arrive at a satisfactory diagnosis by means 
of the above methods of external examination when taken in connec- 
tion with the history and the general condition of nutrition, we must 



undertake a more direct investigation of the organ, which begins with 
(a) the passage of the stomach tube. The standard red rubber tube 
generally 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 discom- 
fort. The patient should be covered by a rubber sheet and the cloth- 
ing removed from his abdomen. So prepared, he should sit in a 
straight-backed, wooden chair, with a good-sized foot-tub between 

Fig. 208. — Outline of Abdomen in Dilatation of the Stomach. 

his feet and a towel in his hand ready to wipe away the profuse secre- 
tions 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. 

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 cesophagus, 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 
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 diagnos is of these diseases will be given 

Cardiospasm 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 less 
than 200 more 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 passes fairly 

2. Great and long-continuing relief is obtained by dilating the 
stricture a few times with water pressure inside a silk covered rubber 

Radiography of a bismuth meal and the use of the esophagoscope 
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 passed into the gut the upper end can be pulled 
taut and on it as a guide a sound and subsequently a dilator can be 

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 esophagus can also be recognized 
in most cases by radiographing a bismuth meal or 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- 

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. 


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. 

(b) Extracting the Gastric Contents. — One hour after a test meal 1 
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 
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 
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, page 355. 

(c) Distending the Stomach. — We may use either air or water. The 
first is more comfortable, the second rather more accurate. To 
distend the stomach with air, disconnect the funnel and attach a 
Davidson syringe. Then have the patient — still with the tube in his 
stomach — lie down upon a bed with the abdomen exposed, and pump 
air rapidly in with the Davidson syringe. The rapid entrance of air 
causes a reflex closure of the pylorus and allows us to distend the 
stomach. While an assistant pumps in the air, we inspect and percuss 
the epigastric region, which soon begins to bulge out and assume on 
percussion a tympanitic note differing clearly in pitch and quality 
from that obtained in other portions of the abdomen. Auscultation 
is also of value for the note produced by the puff of air entering the 
stomach is much louder, sharper, and more metallic when one's 
stethoscope is over the stomach than when one has moved the instru- 
ment beyond the gastric limits. After a certain amount of air has 
been pumped in, the lower border of the stomach (as shown by percus- 
sion) ceases to descend, and about this time the patient begins either to 
complain of pain or to belch up wind around the tube, showing that 
the organ is fully distended. We then mark upon the abdominal wall 
the position of the lower border of the stomach, and if possible of the 
upper, which can usually be obtained by percussion. 

Position of the Normal Stomach. — The lower border of the normal 
stomach after air distention rarely descends below the level of the 
1 A slice of bread and a glass and a half of water is a good lest meal. 


umbilicus ; hence any stomach whose lower border descends lower than 
this should be considered dilated, provided that the upper border is 
approximately in the normal situation. If the upper border is 
lowered as much as the fundus, we are probably dealing with a case 
of gastro ptosis or dropping of the whole organ. 

To distend the stomach with water, we simply pour it in through 
the funnel until the patient complains of decided discomfort and ful- 
ness. We then note the amount poured in, let the funnel empty into 
a large foot-tub on the floor, allow the water to siphon out, and 
measure the amount so obtained. The normal stomach will hold 
about 1,500 c.c. (or three pints). Anything over this amount is 
pathological. A difficulty of the method of distention by water is that 
it is sometimes impossible to get out of the stomach all of the water 
that we have put into it, whereas with distention with air there is no 
difficulty in forcing out the air through and around the tube by pres- 
sure on the epigastrium. 

(d) Washing the Stomach (Lavage). — Though not of much use in 
diagnosis, this procedure may be briefly mentioned here. After intro- 
ducing 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. 

(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 

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 

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. 


Quantitative Estimation of free HCl and of Total Acidity. 

To 10 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. 1 

To estimate the quantity of free HCl, multiply the number of cubic 
centimetres of NaOH used in the titration by 0.0365 ; the result is the 
percentage of free HCl. Normal free HCl 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 

The estimation of combined HCl and of the acid salts is seldom of 

Totol acidity is determined by adding to the same beaker of contents 
in which the free HCl 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 presenting 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 
have used from 4 to 8 c.c. of the NaOH solution in the process of 
neutralizing 10 c.c. of gastric contents. 

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 intensifica- 
tion of the yellow color occurs, lactic acid is almost certainly present. 
A negative test rules out lactic acid. 

1 An ordinary medicine-dropper may be substituted for the burette if we get an apothe- 
cary 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 



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 361, 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. 

4. Bismuth X-ray Examination of the Stomach. 

From two to four ounces of bismuth subcarbonate suspended in 
milk or mucilage of acacia are taken on an empty stomach (say at 
5 a. m.). Six hours later the patient is radiographed in the upright 


Fig. 209a. — Radiograph of Normal Stomach After Bismuth. B. First portion of 
Duodenal. P. Pyloric Ring. C, C. Normal Contraction Rings. G, G, G, G. Bismuth 
in Gut. 

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 radiographed at frequent intervals there- 



after in search of departures from the normal shape assumed by the 
bismuth shadow under these conditions and corresponding to the 
outline of the stomach's interior during peristalsis. If the patient is 
radiographed 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 


Fig. 209b. — Radiograph of Stomach After Bismuth- Meal, 
outline due to score and exudate from chronic ulcer. 

P. Pylorus. A. Loss of 
D. Duodenum. 

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 
just beyond it in the duodenum (the "Bishop's cap") should be visible 
(see Fig. 209a) . 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. 209b. 

The changes to be found in peptic ulcer are not yet thoroughly 
worked out though in most cases a bismuth residue is visible at the 
end of six hours, and this fact, together with the history and the other 
data of physical and chemical examination may be of value. The 
radiographs supposed to show bismuth deposited in the floor of an 
ulcer are doubted by some of the best experts. 


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 403 

Ulcer 536 

Dilatation '. : . 170 

Dyspepsia 1 1,002 

Total 2,111 m 

The data at our disposal are as follows: 

1 . The history. 

2. The local and external examination of the epigastric region. 

3. The estimation of the size and motor power of the stomach. 

4. The examination of the gastric contents. 

(a) In advanced cancer of the stomach we have pain, emaciation, 
anaemia, symptoms of fermentation (see page 361), 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. 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 trouble,' 
occurring in a person over forty who has never had any such trouble before, 
is strongly suggestive of cancer. 

(b) 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). 

(c) Pure functional hyperacidity is not common but may produce 
symptoms indistinguishable from those of ulcer. 

1 I.e., cases of painful digestion including anomalies of motion, sensation, secretion, 
"gastritis" and "gastric catarrh," but without evidence of ulcer, cancer, or dilatation. 

2 We must be careful to exclude angina pectoris as well as gall stones and their effects. 


(d) Hypoacidity and achylia gastrica are not characteristic of any 
gastric disease. They are common in alcoholism, in all types of anaemia, 
in tuberculosis, diabetes, and nephritis, as well as in gastric cancer. 

(e) Gastric dilatation, when considerable, is almost always second- 
ary to pyloric obstruction (due to cancer, cicatrix, or adhesions) . 
Symptoms suggesting it are the vomiting at one time of a large quan- 
tity — a quart or more — of stomach contents, often containing frag- 
ments of food eaten more than eight hours previously. Such attacks 
of vomiting 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 with more or less constancy in almost 
every disease of the stomach and in many general constitutional 
diseases (tuberculosis, anaemia, general debility) . It constitutes what 
is usually referred to by patients as "indigestion," "dyspepsia," or 
"sour stomach." Fermentation of stomach contents too long retained 
is the essential point. This results in a sense of weight and pressure 
in the epigastrium, eructations of gas and of sour or burning fluids, 
loss of appetite, nausea, and vomiting. The tongue is generally 
furred and the bowels are constipated. Headache, vertigo, and depres- 
sion of spirits often accompany it. 

The Liver. 

The Massachusetts General Hospital records (i 870-1 905) show the 
following figures bearing on the incidence of diseases of the liver : 

Passive congestion 1,288 

Portal cirrhosis 234 

Biliary cirrhosis (Hanot's) o 

Cancer of the liver 184 

Sarcoma of the liver 2 

Abscess of the liver 51 

Leuksemic infiltration 46 

Pseudoleukaemic infiltration 10 

Amyloid infiltration 9 

Fatty infiltration 6 

Hydatid cyst 8 

Syphilis 8 

" Simple cyst" 6 

Actinomycosis 3 

Acute yellow atrophy 2 

Tuberculosis 1 

Total 1,858 


Diseases of the Gall Bladder and Bile Ducts. 

Cholelithiasis 457 

Acute cholecystitis no 

Catarrhal jaundice 125 

Cancer of gall-bladder or ducts 47 

Cholangitis 9 

Total 701 

The evidences of liver disease may be either local or general. 

Local signs include : (a) Pain and tenderness in the hepatic region. 
(6) 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 
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 (e.g., alimentary levulosuria) have not 
as yet been successful; hence all diagnoses of liver disease must be 
built up of the above eight groups of data. 

(a) 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 region of the right 
scapula, less often to other parts of the back. Capsule pain is most 
noticeable 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. 

(6) 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 (see above, page 329). 

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 
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 to 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 344). 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 adults 2 ), 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) . 

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. 

2 In infants, rickets, anaemia, and gastro-intestinal disturbances often produce hepatic 
enlargement, though the splenic enlargement is usually much greater. (The infant's liver 
is normally \ inch below the ribs in the nipple line.) 


7. Abscess of the liver. 

8. Leukaemia and pseudoleukaemia. 

9. Cholangitis. 

10. Amyloid. 

11. 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 disease 1 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 
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, and 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, stricture, catarrh, or tumor of 
the bile ducts, or 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 antisy philitic treatment 
in all doubtful cases of liver disease. 

1 Either primary or resulting from chronic bronchitis and emphysema. 


Abscess of the liver produces enlargement, pain, 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 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 329). 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. 

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, subphrenic 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. 

The leuk&mic liver is recognized by blood examination ; the pseudo- 
leukaemic 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 hepatic enlargement is due to 
a cystic tumor, tense and elastic, with notable absence of constitutional 
disturbances (Rolleston) . 

(c) Atrophy of the Liver. 

Diminution in the size of the liver can hardly ever 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. 

(d) 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: 
i. Haematemesis and dyspepsia. 

2. Ascites 1 (see page 347). 

3. Splenic enlargement. 1 

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. 
Obliterations of the portal vein, usually by thrombosis or tumors. 

(e) Jaundice. 

The yellew 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). 

1 Ascites and splenic enlargement are not purely mechanical phenomena. Tox;emia 
and sometimes chronic peritonitis or cardiac failure contribute. 


Less common are the cases due to - 

5. Cirrhosis of the liver. 

6. Syphilis of the liver. 

7. Infectious disease or toxaemia. 
Rare causes are: 

8. Acute yellow atrophy, with or without phosphorus poisoning. 

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: 
(d) Slow pulse (often below 60). (b) Itching of the skin, (c) Mental 
depression, (d) Hemorrhagic tendency (which renders operation 
dangerous) . 

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 passes 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-born. 

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 369), 
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 with steady pain, and, 
in fifty per cent of cases, jaundice. 

5. In ordinary portal cirrhosis the jaundice is less intense and 
permanent, portal stasis is usually evident, and there is generally a 
moderate 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 

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 
Wasserman reaction should be tried and a course of antisyphilitic treat- 
ment given. Other lesions or symptoms of syphilis will naturally 
influence us. 

8. The jaundice secondary to septicaemia, yellow fever, malaria, 
and pernicious anaemia is usaully slight and rarely shows in the urine 
or bleaches the stools. The evidence of the anaemia or of an infection 
makes evident the nature of the jaundice. 

9. Acute yellow atrophy cannot be determined without autopsy. 
Its chief symptoms are given in its name. 

10. Weil's disease is the term applied to some or all of the groups 
of infections of unknown origin which are accompanied by jaundice. 
From catarrhal jaundice it is to be distinguished during life only by 
convincing evidence of general infection. 

Congenital obliteration of the biliary ducts is suggested by the 
occurrence of congenital, intense, and permanent jaundice with 
hemorrhage and enlargement of the liver and spleen. In some of the 
cases of this group the red cells can be shown to possess an exag- 
gerated vulnerability, and the blood serum may have unusual auto- 
hemolytic powers. Several such cases may occur in a single family. 

(/) 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. 

(g) The Infection Group of Symptoms. 

These symptoms — viz., fever, chills, sweats, leucocytosis, disturb- 
ances of digestion and sleep — are oftenest seen in: 1. Cholangitis. 
2. Hepatic abscess. 1 3. "Ball-valve" or "floating" stone in the 

1 With or without pylephlebitis. 


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. 

(h) 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 
those of uraemia. 

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 
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. 

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. 

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) produces 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 24 and 442). The 
history of work as a painter or plumber and the absence of tenderness 
assist the diagnosis. 

Gastric Crises in Tabes are not infrequently operated on under a 
false diagnosis of gall stones. Study of the reflexes should prevent 
such a mistake. 

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 
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 : 

(a) Stone in the cystic duct, at the neck of the gall bladder. 

(b) 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 — Riedel 2 ) , 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. 

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. 

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. 


(&) Intestinal obstruction (see below, page 377) is occasionally 
produced by the ulceration of a large gall stone from the gall bladder 
into the intestine, usually the small intestine or duodenum. 

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 
able to differentiate such tumors from those of the retroperitoneal 

Indirect and uncertain information is afforded by the presence in 
the urine of sugar or fat-splitting ferments 1 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) . 

Cancer of the pancreas may sometimes be suspected on account of 
its pressure effects. Intense and permanent jaundice with enlarged 
(perhaps palpable) gall bladder and liver may be 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. 

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. 

Pancreatic cyst presents a very slow-growing, possibly elastic, deep- 
seated epigastric tumor, which usually produces little in the way of 

J 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 


pressure effects, and may be associated with glycosuria and fatty 

Bronzed Diabetes. — The association of diabetes with bronzing of the 
skin and enlargement of the liver is strongly suggestive of chronic 
fibrous pancreatitis. 

In any doubtful case the possibility of pancreatic disease is in- 
creased: (a) If improvement follows the adminstration of pancreatic 
preparation; (b) if glycosuria follows the administration of ioo gm. of 
glucose (alimentary glycosuria) . 

Incidence of Pancreatic Disease. 

The following table is from the Massachusetts General Hospital 
records (1870-1905): 


Cancer of the pancreas 35 

Acute pancreatitis 13 

Chronic pancreatitis 10 

Cyst of the pancreas 3 

Total 61 


The Intestines. 

Incidence of Intestinal Disease (excluding diarrhoea and constipation) 
at the Massachusetts General Hospital, 1870- 1905. 

1. Appendicitis 3,3 14 

2. Acute obstruction 142 

3. Cancer (above the rectum) 155 

4. Dilated colon 6 

5. Tuberculosis 2 

6. Fsecal impaction (above the rectum) : 2 

Total 3.62 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 

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 effect of catharsis on such tumor). 

6. Visible or palpable peristalsis (see page 339). 

7. Digital or visual examination of the rectum (see page 413). 

8. Examination of the intestinal contents, faecal and other (see page 

9. Inflation of the colon through the rectum (see page 345). 

10. Indicanuria — rarely of value. 

1 1 . Constitutional manifestations , such as fevers, vomiting, leu- 
cocytosis, emaciation. 

Some of these data need further comment. 

Intestinal Pain. — Many 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 
from place to place; (b) accompany the noises and sensations of the 
passage of gas and faeces through the intestine; (c) accompany diar- 
rhoea or constipation. 

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 
burning 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. 210. — Congenital dilatation 
of colon. 

i. Intestinal disease. 


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. 210.) 

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). 
(6) Ulceration (some cases only). 

(c) Cancer of the colon or rectum. 

(d) Intussusception. 

(e) Infectious diseases (cholera, dysentery, typhoid). 
{ (f) Intestinal parasites. 

r (a) Nervous causes (emotion, Basedow's disease, etc.). 
2. Outside influences, -j (b) General infections (sepsis). 

I (c) Cachectic states (anaemias, nephritis, etc.). 

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 diarrhoea, constipation, and dysentery, which produce 
no physical signs beyond those described — distention, borborygmi, 
pain, tenderness, tenesmus, and constitutional manifestations — there 
are but three important 1 diseases of the intestines : 

I. Appendicitis. 

II. Intestinal obstruction. 

III. Cancer of the bowel. 

/. Appendicitis. 

1. The local signs are pain, tenderness, muscular spasm, and 

2. The general or constitutional signs are fever, chill, rapid pulse, 
vomiting, constipation, frequency or cessation of micturition, and 

1 Tuberculous enteritis and pericaecal tuberculosis will be briefly referred to later. 


(a) 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. 

(b) 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 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 
considerably 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 

(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. 2° 
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. 

II. 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 

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 

(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 despite purgation. Cachexia is frequently present. 
Cancer of the colon, usually at the sigmoid or caecum, is the commonest 
cause. Stricture, except cancerous stricture, is rare. 

(c) Acute Obstruction by a Chronic Lesion. — Cancer of the sigmoid 
often exists for months almost latent, or produces only moderate con- 
stipation, so that the patient considers himself well. Such cancers 

1 The latter combination occurred in six per cent, of the Massachusetts Hospital cases. 


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. 

III. 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 or lower sigmoid ; if found 
above this region they are almost invariably dependent on stricture or 
cancer of the bowel. 

Examination of Intestinal Contents. 

i. 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 infants' stools after standing; fermented 
infant's stool if green when passed; green vegetables, calomel. 

(d) Gray — absence of bile (jaundice), sometimes after cocoa or 

(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. 


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 
satisfactorily. 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 
discharges of mucus and shreds mean usually the neurosis "colica 

(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 coli) , 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 caecal region) , 
vomiting, and severe constitutional manifestations suggest the 

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 


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. 

(e) 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 faeces in a sieve 
with plenty of water. The peculiar, facetted shape of most gall stones 
is easily recognized. 

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: 

f 1. Amoeba histolytica. 

I. Serious < TT , f (a) Uncinaria americana. 

2. Hook-worm <,,».,, , , , 

1 (0) Anchylostoma duodenale. 

(" 3. Bilharzia haematobium. 
I 4. Balanlidium coli. 

5. Tape-worms; the beef-worm (Taenia saginata) is very common; 

II. Relatively the pork-worm (Taenia solium) is rare; the miniature tape- 

mild, worm (Taenia nana) and the fish-worm (Dibothriocephalus 

latus 1 ) are fairly common. Several other forms occur in 
foreign countries. 
i 6. Strongyloides intestinalis. 

7. Ascaris lumbricoides (round-worm). 

TTT TT ,, [ 8. Oxyuris vermicularis (thread-worm; pin-worm). 

III. Usually / 

, , 0- rnchiuns tnchiura (whip- worm), 

harmless. _ . , . ... 

I 10. 1 nchomonas intestinalis. 

[ ii. 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. 


Fig. i. — Trichomonas hominis. (Leuckart.) 

Fig. 2. — Balantidium coli. (Leuckart.) Magnified about 150 diameters. 

Fig. 3. — Lamblia intestinalis. (Leuckart.) 



Tape-worms, round-worms, pin-worms, and the strongyloides are 
to be recognized in their adult form (see Figs. 211, 212, 213, 214, 215). 
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-half 
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 MgS0 4 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. 2ir. — a, Head of Taenia saginata, much magnified; b, uterine canal of same, 
twenty branches on each side. 


amined at once with a high-power dry lens. The organism is rec- 
ognized as an amoeba by the presence of distinct amoeboid 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 ectoplasm 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 numerous vacuoles 
and usually of ingested red corpuscles which hide the nucleus. 



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. 212. — a, Head of Ttenia solium (note crown of hooks) ; b, uterine canal in two segments' 
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 

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. 


' '. 



Ti f'Tiff 

k * 


Distoma buski. 

Ascaris lumbricoides. 

Uncinaria americana. 

Anchylostoma duodenale. 


• "-*■ 

i •.••> , "'^_j 


■ ; >q £^Z 

JU %$ 




W T'-»* 

■ "i®^( 

*BL ■/■? 

WA/> «i 

YF. i J 

v ■**^$»*: 

y<* r ■ 

>^V ;Jpr 

^' k 

Trichuris trichiura. Dibothriocephalus latus. Taenia solium. 

All are magnified 250 diameters. 

Taenia saginata. 



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. 215). 

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 searching 
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. 

& f 

Fig. 21 : 

-Taenia nana (Dwarf Tape-worm), a, Hooklet; b, head, greatly enlarged; c, 
whole worm, magnified about 10 dmes. 

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 Igaravidez 
(December 1st, 1904), a study of 5,490 cases. 



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. 214. — 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 i,4°S (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. 191 1) 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 follows : 

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. 




Fasciola hepatica. 

Distoma buski. 



Taenia solium 


Bilharzia Diplogonoporus Bilharzia Dibothrio- Bilharzia 

haematobium. grandis. haematobium, cephalus latus. haematobium. 

Ascaris Oxyur's 

lumbricoides. vermicularis. 


Taenia nana. 





All are magnified 250. (After Looss). 



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 Tricocephalus 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 hsematuria. 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. 

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 

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. 

■ ■ 

.,"•'; Kill 

. ^K%Jb*> 





W A 

1 II 

I I 

Fig. 215. — Strongy- 
loides stercoralis. Mag- 
nified about 250 diame 
ters. (After Thayer.) 

Palpation of the Spleen. 

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 



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. 216), 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 

Fig. 216. — 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. 216). 

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 a 
soft one (typhoid) . 

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 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. 

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. 217. — Splenic leuaemia. 

In other acute infections slight enlargement can usually be made 
out post mortem, but not during life. 

In a series of 100 cases of marked splenic enlargement studied in 
the Massachusetts General Hospital I found the following types 


i. 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 near- 
est 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. 

Differential Diagnosis of the Various Causes of Splenic 

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 "1 
portal stasis (ascites, jaundice, haematemesis) . 


Splenic anxmia means simply an anaemia of unknown origin 
associated with an enlarged spleen. 

Leukemic enlargement of the spleen is easily recognized by the 
characteristic blood picture. 

Hodgkin's disease shows glandular enlargements in the neck, 
axillae, and groins, with normal blood. Histological examination 
of an excised gland is necessary for diagnosis. 

Amyloid can be suspected (never positively diagnosed) as the 
cause of an enlarged spleen, if there is a history of syphilis or chronic 
suppuration (hip abscess, phthisis, etc.) . 

Diseases of the Kidney. 
Incidence of Renal Disease {Massachusetts General Hospital, 1870-1905). 

Acute nephritis 200 

Chronic glomerulonephritis 417 

Chronic interstitial nephritis 250 1 

Amyloid nephritis 9 

Floating kidney 227 

Stone in the kidney 145 

Malignant disease 42 

Tuberculous kidney 41 

Pyonephrosis and abscess 54 2 

Perinephritic abscess 35 

Hydronephrosis 19 

Cystic kidneys -. 10 

Total 1 ,449 

We get evidence of diseases of the kidney in four ways : 

1. By external examination of the region of the kidney. 

2. By examination of the urine. 

P3. By cystoscopy and the ureteral catheter. 
4. By study of the constitutional symptoms — fever, leucocytosis, 
anaemia, uraemia, dropsy, blood pressure and cardiac hypertrophy. 

Local examination acquaints us with the presence of tenderness 
and tumor. 

(a) Tenderness is often present in abscess of the kidney (tuber- 
culous or non-tuberculous) and in perinephritic abscess, less often in 
connection with nephrolithiasis, occasionally in hydronephrosis and 
malignant disease. A floating kidney may have an exquisite and 

1 Seven hundred and seventy-five other cases of "nephritis" not further specified. 

2 Including acute haematogenous cases and pyelitis. 


peculiar sensitiveness to pressure, which differs from ordinary 

(b) 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. 

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 is usually round and smooth, often very hard, less often fluctu- 
ating. It descends slightly with inspiration. If the colon is in- 
flated by forcing air into the rectum with a Davidson syringe, res- 
onance appears in front of the tumor; this serves to distinguish it 
from tumors of the spleen which are pushed forward by the inflated 
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, sarcoma, or hypernephroma, 
makes up with cystic kidney the great bulk of the large abdominal 
tumors occurring in childhood, but is also not uncommon in adults. 
The characteristics of the tumor are those already described, except 
that in advanced stages the tumor pushes forward from its position in 
the loin until it may reach the umbilicus or even fill the abdomen. 
Nodular irregularities can usually be felt. There is usually pain, 
haematuria, emaciation, and anaemia, sometimes leucocytosis, but 
small tumors at some distance from the renal pelvis are symptomless 
and unrecognizable. 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 
bilateral — as, indeed, is usually the case. In both diseases a smooth, 
round tumor forms in the loin and hypochondrium, usually without 



much constitutional disturbance and very frequently with a urine 
like that of chronic interstitial nephritis (see below) (see Fig. 218). 
Pain and tenderness are slight. The tumor may be astonishingly 
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 consid- 
erable size, and hence are often overlooked or discovered accident- 
ally. In hydronephrosis the diag- 
nosis 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 haematuria, 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 collargol-radio- 
graphic plates. Braasch, from the 
Mayos' clinic, considers this method 
of practical value in the diagnosis of 
hydronephrosis, pyonephrosis, pyelitis 
(which shows dilatation of the pelvis), 
renal tuberculosis and tumors, cystic 
kidney, hydro-ureter and ureteral ob- 
struction, and for other purposes. I 
have no experience with this method, but it sounds promising. 

(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 35 cases recorded at the 
Massachusetts General Hospital. A tender swelling appears at the 
point just described, sometimes with redness and heat, and almost 
always with fever, chills, leucocytosis, and some emaciation. The 
urine may show nothing abnormal or may show the evidence of cys- 
titis, of concomitant nephritis, or, rarely, of an abscess within the 
kidney itself. Perinephritic abscess often remains latent for weeks 
or months, and the amount of pus accumulated may be a quart or 

(d) Abscess of the kidney, including tuberculous, suppurating kid- 
neys and pyonephrosis, usually produces a smooth, round tumor in 

Fig. 218. — Left Hydronephrosis. 


the hypochondrium and loin. It has the characteristics common to 
most renal tumors (see last page), but is usually distinguishable by: 
i. 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 (see below, page 395). 

3. The presence of fever, leucocytosis, and the usual constitu- 
tional signs of an infectious process. Persistent urinary frequency, es- 
pecially nocturnal, in a young adult suggests renal tuberculosis. 
Bladder irritation is usually the first symptom of renal tuberculosis, 
even though the bladder itself is apparently normal. 

(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. 

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 strongly sug- 
gestive of stone in the pelvis of the kidney; but similar attacks may 
occur with other surgical diseases of the kidney, with tuberculosis, 
neoplasm, with kinking of the ureter, and very often without any 
cause discoverable at operation. 

From biliary colic it may be distinguished by the (a) different 


situation of the pain, (b) 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 pain 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, occurs in almost any disease of the kidney 
except nephritis, and is characterized by its situation over the ana- 
tomical seat of the kidney and by the lack of any connection with 
muscular movements (lumbago), with spinal movements (hypertro- 
phic arthritis), or with the sacro-iliac joint. 

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. 

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), 
diseases 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 : 

i. 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 reaction to litmus. 

5. The presence of blood, pus, or tubercle bacilli. 

6. The presence or absence of albumin and sugar. 

Much less important than these is the presence or absence of casts, 
cells, crystals, etc. 


The Amount and Weight of the Urine. 

The twenty-four-hour amount concerns us chiefly in diabetes and 
the different types of nephritis. 

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, cirrhotic kidney (pri- 
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 cirrhotic kidney 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} 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 20X30X1.1 =660 grains. The significance 
of this figure will be discussed later (see page 400) . 

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 

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. 


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; 1 when the 
color is due to drugs we can usually learn this fact from the history. 

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 carbon- 
ates 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. 

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 precipitated 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 

1 Except in some cases of haemoglobinuria. 


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, leucorrhcea, and abscess, which can 
usually 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 sometimes difficult to differentiate. In both we have the fre- 
quent and painful passage of small quantities of a urine which is in 
no way remarkable except in containing large amounts of pus and 
bacteria. Cystoscopy 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 fol- 
lows: Have the patient save for twenty-four hours the urine voided 
at each passage in a separate bottle (all of the bottles being of uni- 
form 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 differ- 
ences in the amount of urine in the different bottles). But if the 
pus comes from the kidney, it is almost always discharged inter- 
mittently, 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 ex- 
amination with or without catheterization of the ureters is usually 

In renal pyuria we often have local signs in the renal region 
(tumor and tenderness), a history of renal colic, and decided con- 
stitutional 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 
decolorization by strong mineral acid and by alcohol occasionally 
occur in the urine. 

Hematuria. — 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: 

i. Acute nephritis and acute hemorrhage in chronic nephritis. 

2. Stone in the kidney (less often vesical stone). 

3. Tumors of the kidney or bladder. 

4. Tuberculosis of the kidney or bladder. 

5. Early cystitis. 

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, leukaemia), 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. 392) 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 
(page 390) , 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 hematuria we rely chiefly 
on the history (trauma, poisons ingested) and on the evidences 
afforded by cystoscopy and general physical examination. 

Chemical Examination of the Urine. 
/. 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 occasionally 
without any known cause. 

Alkaline urine has generally an ammoniacal odor and suggests 
cystitis. As a result of decomposition and bacterial fermentation all 
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 fer- 
mentation and alkalinity appear. 

II. Albuminuria and the Tests for It. 

Serum albumin is the only variety of clinical importance, and 
for this but two tests are necessary: (1) Nitric-acid test; (2) test 
by boiling. 

The nitric-acid test is best performed in a small wineglass. 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 care- 
fully performed this test is delicate enough for all clinical purposes, 
but since some of the albumoses give a similar precipitate, the boiling 
test should be used as a control whenever a positive reaction is 

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 mis- 
takenly supposed to contain sugar. 



obtained with nitric acid. None of the other rings, observable above 
or below but not at the junction 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, disappears 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. 

Esbach's Method. — A special tube (see Fig. 219) is 
employed. Urine is poured in up to the mark "U," 
and then Esbach's reagent 1 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 cor- 
responding to the dilution. The method is not accurate, 
but is probably accurate enough for practical purposes, 
if all tests are made at approximately the same temper- 

** if 

777. Significance of Albuminuria. FlG - 2I 9- — 

Esbach's Albu- 
It is important to realize that albuminuria very men ometer. 

often occurs without nephritis and that nephritis occa- 
sionally occurs without albuminuria. Among the more important 
types not due to kidney disease are the following: (1) Febrile albu- 
minuria; (2) albuminuria from renal stasis; (3) albuminuria due to 
pus, blood, bile, or sugar in the urine; (4) toxic albuminuria. 

Besides these, there are a good many cases of albuminuria occur- 
ring in diseases of the blood, after violent exertion, after epileptic 
1 Esbach's reagent: Picric acid, 10 gm.; citric acid, 20 gm.; distilled water, 1,000 c.c. 


attacks, and without any known cause. Many of the latter group 
occur only in the daytime when the patient is in an upright position, 
and are absent as long as the patient lies down {orthostatic albuminuria) ; 
others occur intermittently and sometimes at regular intervals (cyclic 
albuminuria). Most of these cases appear at adolescence and pass 
off without any signs of nephritis ever developing. 

Exclude fever, circulatory disturbance, anaemia, poisons — such as 
cantharides, turpentine, carbolic acid, and arsenic — and deposits of 
blood or pus in the urine, before deciding that a case of albuminuria 
is due to nephritis. In general, however, 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 24-hour amount and the 
gravity are approximately normal, and if there is no cedema, no 
increased blood pressure, no cardiac hypertrophy, no uraemic mani- 
festations, and nothing alarming in the sediment of the urine, we 
should not diagnose nephritis. I shall discuss this point further in 
the section on the examination of the sediment (see page 403). It will 
be noted that practically all the types of albuminuria not due to neph- 
ritis are transient, while, with the exception of certain stages of 
chronic interstitial nephritis, the albuminuria of nephritis is as per- 
manent 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 evidence and the result of high 
blood pressure. 

IV. Significance of Albumosuria. 

The Bence-Jones body is very constantly present in the urine of 
cases of multiple myeloma. So far it has not been reported in any 
other disease. Deuteroalbumoses have no clinical significance. 

V. 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. Fehling's Test. — Mix in a test tube equal parts of a standard 
solution of copper sulphate 1 and a standard solution of alkaline tar- 
trates,- and add to this mixture an equal amount of urine. Mix 

1 Made by dissolving 34.64 gm. pure CuSO, in water and then adding enough water to 
make 500 c.c. 

2 Made by dissolving [73 gm. Rochelle salts and do gm. sodic hydrate each in 200 c.c. 
of water, mixing the two solutions, and adding water to make 500 c.c. 


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 hah 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 
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 
p.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: (1) 
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 gin. 
of glucose or levulose in solution. 

The differential diagnosis of the cause of glucosuria depends on 
the recognit on of one of the above conditions. The other sugars 

1 The room temperature must be approximately the same as at the time of the previous 


occasionally found in the urine (levulose, lactose, pentose, etc.), are of 
no clinical importance. 

VI. The Acetone Bodies. 
Acetone, Diacetic and Beta-Oxybutyric Acids. 

i. 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- 
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 carbodydrates 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. 

VII. 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. 356) 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 

Fig. 220. 


the sulphates and phosphates will soon be followed by the abandon- 
ment 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. 

VIII. Microscopic Examination of Urinary Sediments. 

Methods. — A centrifuge is convenient, but not necessary, 
sediment should be allowed to settle in a conical glass (see Fig. 
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 sedi- 
ment 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 
, . ., . . . ,. , , . Conical Glass 

dry, put its point upon a microscopic slide, and again . 

slightly relax the pressure of the forefinger so as to let a Sediments. 

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 dia- 
phragm 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 ; (6) 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. 221, 1) or may have attached 
to this matrix a variety of granules, cells, crystals, or fat drops. Ac- 
cording to the variety of passengers carried down from the kidney on 
the casts, we call them granular, brown- granular, cellular, blood, fatty, or 
crystal-bearing casts (see Fig. 221, 2 and 3, and Fig. 222, 1, 2, 3, and 4). 

Dense or highly refraclile casts, colorless or straw colored, are 
occasionally seen, and are often given a variety of names quite un- 
justified by any knowledge of their composition (e.g., "waxy," 2 
"fibrinous," etc.). 

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 indicate 
amyloid kidneys and has no known clinical significance. 



Fig. 22i. — Casts, i, Hyaline casts; 2 and 3, 
hyaline casts with cells and blood adherent; 4, 

From strands of mucus, foreign bodies, and other sources of error, 
true casts may be distinguished by the following traits : 
(a) Their sides are parallel. 

(6) 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 per- 

Crystals can be recog- 
nized by their angles. They 
are very rarely of importance. When showers of oxalate crystals in 
large masses are associated with attacks of hgematuria not otherwise 
explained, the crystals may be 
of some etiological significance. 

Other bodies on casts are 
called granules. 

Significance of Casts. — 
Casts may occur in health (un- 
less we choose to class muscular 
fatigue as disease) as well as 
under any of the conditions giv- 
ing rise to albuminuria (see page 
399). 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 nephritis, but 

Cellular, 1 blood, and brown- granular casts are most often found 
in acute nephritis. t 

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. 

Fig. 222. — Casts. 1, Blood-casts; 2, fatty 
casts; 3, granular casts; 4, cellular casts. 





Fig. 223. 

Fatty, highly refracting, or dense casts most often predominate 
in chronic glomerular nephritis ("diffuse" 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. 

Periods occur in the course of many cases of \r 
chronic interstitial nephritis when no casts can be irr^o' ( 
found. If any occur they are usually of the hyaline 
and fine granular types. 

2. Free Cells in Urinary Sediment. A. Recogni- 
tion. — 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 effu- 
sion of blood, probably from the bladder, urethra, or renal pelvis. 

(b) 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 proba- 
bly come from the kidney. 

(c) Pus is easily recognized as 
a rule by the presence of the fa- 
miliar 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 recog- 

(d) Spermatozoa (see Fig. 223). 
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 

Fig. 224. — Crystals of Triple Phosphate 
(prisms) and Ammonium Urate (small 
spheres with spines.) 



Fig. 225. — Crystals of Uric Acid 
stone-shaped) with Calcic Oxalate 
octahedral) and Amorphous Urates. 


(e) Other varieties of cells need not be differentiated, since almost 
any of the varieties usually described (squamous, spindle-shaped, 
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 sig- 
nificance of large quantities of 
blood or of pus in the urine has 
already been discussed (page 
395). When recognizable only 
by the microscope they have no 
diagnostic value. 

The presence of large num- 
bers of cells not coming from the 
blood-vessels (squamous, spin- 
dle-shaped, etc.) is usually asso- 
ciated with cystitis, provided the 
accidental admixture of vaginal 
detritus is excluded. Pyelitis 
and renal suppurations may fill the sediment with similar cells, 
and only by other methods of examination (cystoscopy, ureteral 
catheterization) and by taking account of all the facts in the case 
can the differentiation be made. 

3. Crystals in Urinary Sedi- 
ments (see Figs. 224, 225, and 226). 
— The varieties oftenest seen are: 
(a) Triple phosphate (ammoniacal 
urine, cystitis) ; (b) ammonium 
urate; (c) uric acid; (d) calcic 

All of these varieties are color- 
less 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 

Uric-acid crystals, if present in great numbers in the urine 

Calcic Oxalate Crystals. 



when passed, suggest the search for macroscopic masses (gravel) 
and for other evidence of renal stone, but as a rule they are of no 

The same may be said of calcium oxalate. Oxaluria is one of the 
most persistent bugbears of the medical profession, but it is utterly 

Fig. 227. — Vinegar Eels in Urine. (Billings.) a, Protruded hooks of male; b, top- 
shaped oesophageal enlargement. The Strongyloides stercoralis (see above, Fig. 215, page 
385) has also been found in the urine. 

harmless except in the rare cases in which it accompanies haematuria 
(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. 
227 and 228). 



Summary of the Urinary Pictures Most Useftd 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: 

i. 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 

Fig. 228. — Bilharzia Eggs in the Urine, with Blood, Calcic Oxalate, and a Hyaline Cast. 


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 
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 Glomerular Nephritis {" parenchymatous"). — The urine 
is rather scanty, pale, and of light weight (1.012-1.018), with a 


large 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 of casts. If death does not ensue within eighteen 
months, the urine is apt to assume the characteristics of the : 

4. Contracted kidney (primary, secondary, or arterio-sclerotic) , 
with polyuria (often several quarts; urine especially abundant at 
night), low specific gravity (1.010 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 hematogenous 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 
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 children and in women near parturition. To distinguish 
pure pyelitis from pyelitis complicating a renal infection is at present 

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. 




The Bladder. 

Incidence of Bladder Disease. 

(Massachusetts General Hospital, 1870- 1905.) 

Cystitis 829 cases. 

Stone 538 cases. 

Cancer 57 cases. 

Papilloma 20 cases. 

Tuberculosis 43 cases. 


Distention, tumor, the urine, and the results obtained by cystos- 
copy, by catheterization, by rectal and vaginal examination, by the 
x-ray, and by sounding for stone 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 

/. 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 



Fig. 229). 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 hypertrophy, alone or combined with 

(2) Old strictures of the urethra. 
Less common are: 

(3) Spasm of the urethra in gonorrhoea. 

(4) Acute prostatitis. 

Fig. 229. — 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, 


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). 

Tumors of the bladder are suggested by intermittent hematuria 
with vesical irritation, and confirmed by cystoscopic examination. 

//. The Urine as Evidence of Bladder Disease. 

This has been described above (page 408). 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 of chronic interstitial 
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 of tenest 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) Over concentration of the urine (estimated by the color and 
specific gravity) . 

777. 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 hematuria 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- 
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 proper sound. 

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. 

The Rectum. 

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 : 

(a) Hemorrhage at stool. 

(b) The protrusion after defecation of something which is not 
easily returned ("piles"). 

(c) Painful defecation or pain in the region of the rectum at 
other times. 

(d) 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) . 

(h) Suspected appendicitis, prostatitis, prostatic tumor 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: (i) 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. 


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 
prominences or resistance (piles, tumors) in any part of the rectum, 
of tender spots (ulcer, abscess), and strictures. The shape and size 
of the prostate 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 suspected. 

High up on the right side the finger may touch a tender spot if 
an inflamed appendix is near the pelvic brim. 

In women the uterus, especially if retroverted, may be easily 
felt, and most of the other details of pelvic examination (see below, 
page 419) can be more or less clearly made out. 

For higher and more thorough examination a cylindrical specu- 
lum and a head mirror should be used, with the patient in the knee- 
chest position. 

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 " 
{ncevoid piles). 

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 produces severe pain during and after defecation. 

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 and need 
examination with speculum and probe. Tuberculosis is always 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 diarrhcea 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 benign stricture with or without ulceration, 
and from benign villous growths, it may be impossible to distin- 
guish cancer without histological examination of an excised piece. 
Tumors of the prostate are felt on the anterior wall of the rectum 
and practically never ulcerate. They are often very difficult to 

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 hematocele. 

(e) Varicocele. 

(/) Scrotal hernia. 

(g) Absence of one or both testes. 

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- 


pie. 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 
connot 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, ap- 
pears 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. 

The Testes and Scrotum. 

Acute epididymitis, usually a complication of gonorrhoea, appears 
as a hot and tender swelling behind the testis, often preceded by 
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 hematocele 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 
the history and evidence of trauma are clear. Incision or puncture 
should decide. 

Varicocele, an enlargement of the veins about the spermatic cord 
and vas deferens, 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 case 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 413.) 

The Female Genitals. 


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 of the 
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. 


I. In the external genitals one looks for some of the same 
lesions already described on page 415, viz., chancre, chancroid, local 
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 non-venereal, is easily recognized by the abundant 
purulent discharge. 

(b) Local eczema, often red and angry, is commonly the result 
of the irritation of diabetic urine or a leucorrhceal discharge. 

(c) Varicose veins and oedema of the vulva are common in preg- 
nancy and occasionally result from large pelvic tumors. 


(J) 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. 

(e) The hymen may be imperforate with retention of menstrual 
fluid, or tender, irritated remains of it after rupture may cause pain 
and need removal. 

if) 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. : 

i. Laceration and "erosion" of the cervix. 

2. Malpositions of the organ. 

3. Endometritis. 

4. Cancer of the uterus. 

5. Fibro-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 : 

(b) "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" 
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 
mucopurulent discharge (leucorrhoea, "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, prob- 
ably as part of a general prostration rather than as its cause. 

4. Cancer of the uterus usually attacks the cervix, and in marked 
cases is easily recognized by sight and touch as a " cauliflower "- 
like, /ungating mass on the cervix. In its early stages it may be 
confounded with "erosions" and inflammatory conditions, 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 curretting. 

.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 fact unless pregnancy can be definitely excluded. 

III. Fallopian Tubes. — Salpingitis (acute or chronic) and tubal 
pregnancy are the most important diseases of the tubes. 

(a) 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. 

(6) Tubal pregnancy, as just explained, is rarely to be diag- 
nosed 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 

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. 

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. 

(6) 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 
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. 

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. 



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. 206, page 348) , whereas in ovarian disease the bulging is central 
and greatest just below the naval (see Fig. 230). 

Fig. 230. — Huge Ovarian Cyst. 

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. 458). 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. 


The Legs. 

, mp. 

The examination of the hip will be discussed later (see page 458). 

II. Groin. 

In the groin we look for evidences of : 

1. Enlarged or inflamed lymphatic glands and scars of previous 

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" of gonorrhoea, 1 syphilis, chancroid) and peri- 
neum; chronically enlarged in malignant disease of the penis, uterus 
(late) , and other genitalia. 

(6) 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 30), 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. Hy- 
drocele of the cord gives also an impulse on coughing, but usually 
shows a distinct limit above. On pulling the cord the swelling moves 

1 The bubo of gonorrhoea often suppurates; that of syphilis rarely. Hence a scar in the 
in guinal region suggests an old gonorrhoea. 




3. Psoas abscess (see Fig. 231) presents the ordinary signs of pus 
and is associated with vertebral tuberculosis (dorsal or lumbar) . 

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 gives no impulse on coughing and 
cannot be completely reduced. The history of residence in the tropics 
should always suggest an exami- 
nation of the blood (at night) 
for filariae. 

777. The Thigh, 

The records of the Massa- 
chusetts General Hospital show 
that (1) 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 

fluctuation appear, and the abscess, if not incised, will break ex- 
ternally. 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. 231. 

-Psoas Abscess, 
and Lovett.) 




Whether the disease starts in the shaft of the bone or in the 
epiphysis is to be determined by the seat of pain and tenderness. 

Tuberculous cases can be recognized only by the histological ex- 
amination. Old cases may be suspected by the presence of a scar, 

(2) Multiple white scars should always suggest, though they are 
far -frem-pro-ving, syphilis, for chronic ulcer above the knee is often 
due to gumma. 

Tumors of the Thigh. 

(1) 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. 232). 

(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. X-ray 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 hip-joint abscess (see Fig. 231) 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. 232. — Sarcoma of the Femur. 



Miscellaneous Lesions of the Thigh. 

(i) 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 
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 de- 
monstrable cause for inflammation. 

(2) Meralgia paresthetica means 
the presence of a patch of anaes- 
thesia, paresthesia, or hyperes- 
thesia (tenderness) , with or without 
pain, on the anterior and upper 
surface of one or both thighs (the 
area of the external cutaneous 
nerve) . 

(3) 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. 233). The 
#-ray shows marked thickening of 

some areas, with thinning of „ _, _. fr . L ... ^ 

tiG. 233. — Paget s Disease (Osteitis De- 

Otners. formans). Note the outward and forward 

(4) Intermittent Claudication and bowing of legs and arms. (Robin.) 
"Cramps." — Insufficient circula- 
tion through the arteries of the legs may give rise to sudden "giving 
way" of one or both during running or walking, the power returning 
after a short rest. In patients at rest the frequent recurrence of 
painful cramps in the muscles may be the only manifestation of the 
disease. In other cases there are various forms of paresthesia 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). 


(i) Paralysis of one leg, occurring in children, is usually due to 
anterior poliomyelitis ; in adults it usually forms part of a hemiplegia or 
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 47) 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), and in late tabes. Hysteria also may 
produce a spastic paraplegia, though monoplegia is commoner in this 

(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 fasces), and often bed-sores. 

(b) 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. 

IV. 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 456). 




HV \ 



Fig. 234. — Prepatellar Bursitis ("Housemaid's Knee' 

(b) Housemaid's knee is a bursitis of the prepatellar bursa (see 
Fig. 234). 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. 



V. The Lower Leg. 

i. 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 

Fig. 235. — Syphilitic Periostitis ("Salve Shins"). 

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 



recognizable, may be thus brought to light and may help our diagnosis 
of a cardiac arthritis or hepatic lesion. 

4. Osteomyelitis (acute septic or chronic tuberculous) often starts 
on the head of the tibia, with intense pain, tenderness, fever, and 
leucocytosis (if acute or septic) ; there results a general septicaemia or 
a local sinus leading to dead bone. 

Fig. 236. — Angioneurotic oedema of legs. 

5. Sarcoma not infrequently attacks the upper end of the tibia or 
fibula, producing lesions similar to those described in the femur. 

6. (Edema of the legs 1 is oftenest due to: 

(a) Uncompensated heart lesions, primary or secondary from 
lung disease. 

(6) Nephritis. 

(c) Cirrhotic Liver. 

(d) Anaemia. 

1 It is notable that oedema is usually greatest in the front of the leg and in the back of 
the thigh. 



(e) Neuritis (alcoholic, beri-beri, etc.). 

(/) Varicose veins. 

(g) Obesity, flat-foot, and other causes of deficient local circu- 

In some cases no cause can be found ("angioneurotic" oedema, 
"essential" and "hereditary" oedema). Diagnosis of the cause of 

Fig. 237. — Sporadic elephantiasis. (Non-filarial. 

oedema depends on the history and the examination of the rest of 
the body. 

In one leg oedema may be due to thrombosis of a vein (see page 
427), to pressure of tumors in the pelvis (pregnancy, etc.), to hemi- 
plegia, elephantiasis (see Figs. 237 and 238) 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. 

The Feet. 

i. The varieties of club-foot are: (a) Equinus, the heel drawn 
up. (b) Varus, the ankle bent outward, (c) Valgus, the ankle 
bent inward and the foot outward, (d) Calcaneus, the foot turned 
'outward and upward. 

Fig. 238. — Elephantiasis. 

The affection, which is usually congenital, occasionally the result 
of contractures after paralysis, presents no difficulties in diagnosis. 

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 are usually pain and tenderness near the attachment of the 
ligaments and often higher up on the leg. 

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. 240). 
The other signs of rickets in the child make diagnosis easy. 

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 461). 

6. Epithelioma of the ankle has the characteristics of epithelioma, 

7. Erythromelalgia, or red neuralgia of the extremities, is common- 
est in the feet. The toes (or fingers) are red, hot, tender, and painful. 

Fig. 239. — Flat-foot. (Bradford and Lovett.) 

In Raynaud's disease the digits are cold and painless or anaesthetic. 
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 arteriosclerosis and myocarditis. The patient 
kicks off the bed clothes from his feet at night on account of the burn- 
ing sensations in them. Other evidence of insufficient arterial blood 
supply (e.g., clubbing, intermittent claudication, cramps, gangrene) 
may coexist. 

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 : 

Fig. 240 — Rachitic deformity of leg bones. 

i . Gout, which is especially prone to attack the metatarso-phalan- 
geal joint of the great toe, producing all the classical signs of 

2. Gangrene is usually the result of arteriosclerosis (see Fig. 241) 
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 diseases just mentioned. It is called 
"perforating ulcer" because of its stubborn progression despite a plan 
of treatment that checks ordinary infectious abscesses. Actual per- 
foration is not often seen. 

Fig. 241 — Arteriosclerotic gangrene. 

4. " Tender toes" after typhoid fever result from an infectious 

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. 


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. 

V. Coagulation time, rarely. 

I will now give a brief account of each of these methods and of the 
interpretation of the data obtained by them. 

/. 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. , haemoglobin 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. 
Always saturate at least half a square inch of filter paper with blood 
and allow it to dry until the gloss has disappeared. Do not blot it, and 
do not delay in making the comparison after the humid gloss has disap- 
peared. 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. 242) must be obtained from one of 
the firms recommended by him, 1 else the standard solution is likely to 

1 Holtz or Buchi of Berne. 




be inaccurate in color. To use the instrument we first put a few drops 
of decinormal HC1 solution into the empty tube (Fig. 242, B), so as to 
fill it to the mark 10; then suck up blood with the pipette (Fig. 242, C) , 
until the mark 1 is reached. Wipe the point of the pipette and imme- 
diately 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 trans- 
mitted light. After each addition 
of water close the end of the tube 
B 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 

Fig. 2 4 2.-Sahli's Hsemoglobinometer. B, at a time > and close the e Y es for a 
Diluting tube; C, pipette; D, dropper. few seconds between each two at- 
tempts at reading. When the 
colors in the two tubes seem to be identical, read off the figure cor- 
responding 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 of 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 
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 447). 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 re- 
duction 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 ; so do four million red 
cells with eighty per cent, of haemoglobin, three million and sixty per 
cent, two million and forty per cent, and so on. An example of low 
color index would be four million red cells with forty per cent haemo- 
globin, representing a color index of 0.5; or three million red cells with 
thirty per cent haemoglobin, representing again a color index of 0.5. 

The diagnostic significance of the color index is briefly this: Any 
diminution in hcemoglobin means ancemia, but a diminution in hemoglo- 
bin with a high color index suggests, though it does not prove, pernicious 
ancemia, while a low color index points to chlorosis or secondary ancemia 
of any type. Normal color index, despite anaemia, is most often found 
immediately after hemorrhage. 

II. Study of the Stained Blood Film. 

To recognize the presence and the degree of anaemia one needs only 
the hcemoglobin 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. 

1 . 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 


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. 243, 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 

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. 243.— Method of Spreading Fig. 244.— Proper Method of Holding 

Blood Films. 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. 244, 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 


brethren. Holding a cover glass as in Fig. 244, touch the centre of it 
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, 
leucocytes, and blood parasites, and for clinical work no other stain is 

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 polychromatophilia) refers to abnormal 
staining reactions in the red corpuscles, whereby isolated individuals 
take on a brownish or purplish tint, sharply contrasted with the pink 
or yellow of the corpuscles around. If this brownish or purplish tint 

occurs in all the corpuscles, it has 
no pathological significance, but 
merely means that the staining has 
been incorrectly 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 de- 
scribed are to be found in any of 
the types of severe anaemia, 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. 245). 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, 
gray, or even blue, and sometimes stippled, so that by beginners the 

Fig. 245. — Nucleated Red Cells, m, m, 
Megaloblasts; n, normoblast; s, stippled 



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 by practice. 

2. Leucocytes . — In normal blood four main varieties may be dis- 
tinguished : 

(a) Polynuclears or polymorphonuclear neutrophiles. 

(b) Lymphocytes (large and small). 

(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 
by a pinkish protoplasm studded with spots or granules just large 

Fig. 246. — a, Leucocytosis (40,000); sixteen polynuclears in a field, b, Lymphatic leu- 
kaemia, p, Polynuclear; m, megaloblast; e, eosinophile. Twenty-one lymphocytes 
in this field. 

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. 246, 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 the nucleus occupies much less space relatively, 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 
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 twenty-five to thirty- five per 
cent (or about one-third) of all leucocytes belong to the lymphocyte 
group — classing all sizes together (see Fig. 246, 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 

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. 

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. 



The points most often looked for are : 

i . 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. 

III. Counting the White Corpuscles. 

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 mark point 
.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 1 1 . 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 dilution 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. 248 B) is let down upon it 1 the drop will cover at 

1 To avoid air bubbles lower the cover glass with aid of a needle as in mounting micro- 
scopic specimens. This must be done as quickly as possible after the drop has been 
adjusted on the counting disc. 

Fig. 247. — Indicating an Order in which the 
Squares may be Counted. 


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. 247. 
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 


1 m " m T"^T 1 

Fig. 248. — 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 
35X200 = 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. 

IV. 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 § iv. 

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. 


Interpretation of the Results so Obtained. 
i. 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 
haemoglobin 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: Poikilocytosis, abnormal staining of the red corpuscles, and 
the presence of nuclei either in normal-sized corpuscles (normoblasts) 
or in giant corpuscles (megaloblasts) . The degree of poikilocytosis 
and abnormal staining reaction is proportional to the severity of the 
anaemia. In mild cases we find only normoblasts, and those only after 
a long search; in severe cases we may find megaloblasts as well, but 
almost invariably these cells are fewer than the normoblasts. 

The commonest causes for secondary or symptomatic anaemia 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 glomerulo-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 anaemia, 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 


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 Anaemia. 

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. The stained specimen shows very marked deformities and 
abnormal staining reactions in the red cells, with a tendency to the 
predominance of large forms. Many of the latter contain nuclei 
("megaloblasts"), and a smaller number of normal-sized cells also 
contain nuclei ("normoblasts"). 

The polynuclears are relatively diminished, with a corresponding 
relative increase in the lymphocytes. 

In the remissions which form so important a feature of the course 
of pernicious ansemia, the blood is generally transformed until it is 
almost or quite normal. In the subsequent fall it may take on all the 
features of secondary anaemia or chlorosis, and lead to unavoidable 
errors in diagnosis and prognosis. Fortunately cases are rarely seen 
for the first time at this (non-characteristic) stage. 

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 
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 lympho- 
cytes may reach 60 per cent and yet be well within the normal limits, 
for 60 per cent of 3 ,000 is only 1 ,8co. In this case the apparent lymph- 
ocytosis 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. 

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 toxcemic conditions, such as uraemia, hepatic 
toxaemia, diabetic coma, rickets, and poisoning by illuminating gas. 

3. In a minority of cases of malignant disease, especially sarcoma. 

4. After violent muscular exertion, including parturition, and after 
cold baths or massage. 

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 
forty-eight hours. When taken in connection with the other clinical data, 


a leucocyte chart is often of the greatest value, especially in follow- 
ing the course of any disease; to a less extent in diagnosis. Sondern 
(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 

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. 

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 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 glandular enlargement. 


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. 

There seems to be also some vague connection between eosinophilia 



and diseases of the female genital tract (except cancer and fibre-myoma 
of the uterus) . 


Two forms are distinguished, though the distinction is chiefly a 
clinical one: (a) Myeloid and (b) lymphoid. 

i. 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 anaemia in the earliest stages; later moderate secondary 
anaemia develops. 

The differential count shows an extraordinary variety of types, 
ncluding many not seen in normal blood (see Fig. 249) . 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 in- 
crease of the other forms. Eosino- 
philes are absolutely much in- 
creased, though the percentage is 
not much above normal. Mast cells 
are more numerous than in an} 5 - 
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 rr-ray treat- 
ment the blood may return to normal. 

2. 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- 
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. 

Fig. 249. — Myelogenous Leukaemia. 
m, Myelocytes; p, polynuclear; b, mast 
cell; n, normoblast. 


The blood-film is monotonous in contrast with the wonderful 
variety seen in myelogenous leukaemia (see Fig. 246, b). 

V. 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 1 .10 mixture, 
or if within one hour clumping has taken place in the 1 150 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 

(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 
epidemics about two-thirds of the cases show a positive Widal reaction 
by the time the patient is sick enough to consult a physician. The 
reaction may be absent one day and present on the next, and varies 

Cabot — Physical Diagnosis. 


Fig. i. — Young Tertian Parasites. (Stained with Wright's modification of Leishman's 


Fig. 2. — Mature Tertian Parasites. (Eosin and methylene blue.) 

Fig. 3. — Segmenting Tertian Parasites. (Eosin and methylene blue.) 



greatly in intensity in different cases and at different times with the 
same case. 

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 
that only one who is constantly doing it is reliable. A positive reaction 
done by a reliable expert is very important 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. 

Fig. 250. — Trypanosoma in Human Blood. (By permission of Dr. J. Everett Dutton and 

the London Lancet.) 

VI. Blood Parasites. 
1. 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 ; 
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 aestivo-autumnal 
variety by the following tests: 

Fig. 251. — The Filaria Sanguinis Hominis. The head, curled up, is seen to the right 
of the cut, the tail to the left. Instantaneous photomicrograph. Four hundred diameters 

Fig. 252. — Pratt's Modification of the Brodie-Russell Coagulomeler. R, Brass ring 
soldered to glass slide; C, cover glass; a blood drop on the under side of this, when in place 
on the brass ring, is close to the point of the hollow metal needle which forms the extremity 
of the inflation tube, C. 

(a) Tertian parasites make the corpuscle containing them larger 
than its uninfected neighbors. 

(b) Segmenting forms never occur in the peripheral blood of sestivo- 
autumnal fevers. 

Cabot — Physical Diagnosis 


Fig. i. — Two Young .Fsuvo-autumnal Parasite;. Wright's modification of Iris hm a n 's 


Fig. 2. — .Fsuvo-autumnal Parasites. Ring body at the left: crescent at the right. Stained 

like Fig. i. 

Fig. 5. — Ovoid in .FLstivo- 
autumnal Malaria. 

Fig. 4. — Crescent in .Fstivo-autumnal Malaria. 


(c) "Crescents" (see Plate V.) never occur except in aestivo- 
autumnal fevers. 

2. The Trypanosoma. 

In Central Africa (and presumably in other tropical countries) the 
blood or gland juice of many persons contains the organism shown 
in Fig. 250, 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. 251. 
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 slide and cover and examined with a low-power 
lens (Xo. 5 objective Leitz). 



Examinations of the Joints. 
A. Methods and Data. 

1. By inspection and palpation we detect: 

i. Pain, tenderness, and heat in, near, or at a distance from the 

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. 
(6) Due to muscular spasm. 

(c) Due to thickening or adhesions in the capsular and periarticular 

(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 abscess 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. 



ii. Telescoping of the joint with shortening (limb, toe, finger, or 
trunk) . 

II. By radioscopy we investigate : 

i. 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. 

B. 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 



an otherwise free 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, 
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. 

Fig. 253. — Testing for Psoas Spasm. (Bradford and Lovett.) 

(1) Hip-joint, two forms of spasm are important: (1) 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- 253). 

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. 


Using the sound leg as a standard of comparison, we may then draw 
the knee away from the middle line (abduction) , toward the past and 
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. 254. — 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. 254) . 

(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 


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 rule, 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 

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 x-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 456 
needs no explanation, except the radioscopic technique — a subject 
which I am not competent to discuss. 

C. foint 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). 


3. Hypertrophic arthritis. 

4. Gouty arthritis. 

5. Hemophilic 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 

(a) Slow progress, with gradual enlargement and disabling of the 

(6) Muscular spasm, especially in disease of the hip or vertebrae. 

(c) Evidences of low-grade inflammation (moderate heat, swelling, 
pain, and tenderness) . 

(d) Abscess and sinus formation. 

(e) Malpositions (e.g., shortening of one leg in hip-joint disease, 
angular backward projection in spinal disease, subluxations in the 

(/) 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 55). 

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 458), 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 con- 
traction (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. 231); 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 : 

(a) Hypertrophic arthritis of the spine. 

(b) 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, (b) 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 
lesions 1 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- 
rhceal, 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 pyogenic cocci 
may leave a sound joint, though the general tendency is to crippling 
through fibrous adhesions. On the other hand, arthritis of "rheu- 
matic" (i. e., of unknown) origin may end in suppuration, crippling the 
joint with adhesions, though in most cases it leaves a sound joint. 

All the members of the infectious 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 unknown 
origin ("rheumatic") this complication is especially common. There 
is no bony hypertrophy, bone destruction, 1 sinus formation, or marked 

Exceptionally, virulent infections (especially those due to pneumococci or strepto- 
cocci) may destroy cartilage and bone and end in true bony ankylosis. 



irregularities of contour. A general enlargement (more or less spindle 
shaped, owing to periarticular thickening and muscular atrophy) is 

Fig. 255. — X-ray, showing Hands in Atrophic Arthritis. 

the rule. The joint motions are limited chiefly by pain and effusion; 
muscular spasm is not prominent. 



One or many large or small joints may be affected in any of the 
varieties of infectious arthritis, 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. 

III. Atrophic Arthritis. — Two types must be recognized: (a) A 
monarticular form, secondary usually to tabes or syringomyelia 
("Charcot's joint," "neuropathic joint"), and other diseases of the 

Fig. 256. — a, Charcot's Joint with Loose Bodies; b, Pulmonary Osteo-arthropathy. 

spinal cord, (b) A polyarticular primary form ("rheumatoid ar- 
thritis" or "anchylosing 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. 255). Later 
the disintegration of the joint is usually evident, and is followed by 
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. 256). 



Fig. 257. — Atrophic Arthritis. Early stage. 

Fig. 258. — Atrophic Arthritis. (Goldthwait.) 



(b) 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. 257). 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. 258). 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. 259), 
Pain is not severe until motion is attempted or unless the joint is 
jarred and stirred up by some traumatism. 

Fig. 259. — Atrophic Arthritis. Late stage with constriction ring at the joint line. 


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. 

IV. Hypertrophic Arthritis. — This is a degenerative type of disease 
in which bony enlargement and osteophytic spurs are the distinguish- 
ing feature. The new bone is oftenest deposited round the edges of 
the articular cartilage, forming an irregular fungoid ring ("ring bone" 
in horses) or "lip" near the 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 260). 

(b) The disease may be limited to the hip-joint ("morbus coxae 
senilis") or to any other single joint, producing purely mechanical 

Fig. 260. — 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- 



dylitis deformans," "osteoarthritis"), where a portion of the front 
and side of the vertebral column is "plastered over" with new- 
formed bone (see Fig. 261), which later invades the intervertebral 
cartilage and produces (see Fig. 262) finally either a straight "ramrod" 
spine or a forward curved spine. 

Fig. 261. — Hypertrophic Arthritis of Spine. (Goldthwait.) 

Non-tuberculous disease of the sacro iliac joint has already been 
referred to on page 58. 

In the early stages the disease is recognized by: 


(a) Nerve pain, running round the body or down the legs, 1 as the 
intercostal and spinal nerves are pressed on. 

Fig. 262. — Hypertrophic Arthritis (Spine) of Spine with Ankylosis. (Goldthwait.) 

Fig. 263. — Showing Normal Flexibility of Spine. (Goldthwait.) 

(b) Limitation of Motion. The process is usually unilateral, wholly 
or predominantly; hence the patient can usually bend much better to 
one side (see Figs. 263 and 264) 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. 



well performed as a rule, in sharp contrast with "lumbago," which 
renders forward bending and the subsequent recovery almost 

Fig. 264. — Hypertrophic Arthritis of Spine. Motion to left limited. (Goldthwait.) 

Fig. 265. — 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. 



Fig. 266. — Gouty Arthritis. (Goldthwait.) 

Fig. 267. — -J^-ray of Hand in Gouty Arthritis. (Goldthwait.) 


V. Gouty Arthritis. — The deposits of urate of sodium in the soft 
structures around the joint are, like those in the ear (see Fig. 265), 
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. 
266 and 267). 

VI. Hemophilic Arthritis. — A chronic stiffening and enlargement 
of the joint, resembling in many respects the joint of hypertrophic 
arthritis, but often accompanied by the formation of fibrous adhesions, 
ensues in some cases of haemophilia, presumably as a result of frequent 
hemorrhages and serous oozings in the joint. The diagnosis depends 
on the evidence of haemophilia, the youth of the patient, and the 
absence of infection as a causative factor. 

Relative Frequency of the Various Joint Lesions. 1 — The 
following table was prepared by Dr. Vickery 2 from the records of the 
Massachusetts General Hospital (1893-1903): 

[ Acute rheumatic arthritis 591 \ 

, , ... I Subacute rheumatic arthritis iqs I „ 

Infectious arthritis. < _ , . , . . n . ) 873 

I Gonorrhceal arthritis So 

[ Typhoid arthritis (spine) 3 J 

Hypertrophic and atrophic arthritis 43 

Gout 9 

1 Chronic villous arthritis ("dry joint") is a purely local process and therefore receives 
no further mention here. 

2 Boston Med. and Surg, four., November 17, 1904. 


Examination of the Nervous System. 

The outlines of neurological diagnosis depend on knowledge of : 

1. 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. 

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. 

I. Disorders of Motion. 
i. Gaits. 

2. Paralyses. 

3. Spasms and tremors. 

4. Ataxia. 

1 . 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 

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 paralyses. 




The ataxic 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. 268), and, 
if progress is accelerated by a push 
given from behind, the patient 
may 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. — No 
detailed account can be given here 
of the method of testing individual 
muscles for loss or impairment of 
power. In general, a knowledge 
of the origins and attachments of 
muscles enables us to work out for 
ourselves a series of tests that will 
bring any desired group into con- 
traction. It is convenient to class 
paralyses according to their origin 
as follows : 

(a) Brain paralysis: usually 
hemiplegia (arm and leg on same 
side, with or without the face). 

(b) Cord paralysis: usually par- 
aplegia (both legs, rarely both arms) 
or monoplegia (one extremity). 

(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, oftenest 
monoplegia (one extremity). 

Peripheral nerve paralyses are especially apt to be accompanied by 
sensory symptoms, electrical changes, and wasting. Brain paralyses 
have relatively few sensory symptoms (sometimes paresthesias, see 

Fig. 268. — Altitude Characteristic of 
Paralysis Agitans. 


below, page 477) 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 
alternately 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 strychinine 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 474) are also examples of local tonic 

Athetosis, a special variety of local tonic spasm, has been described 
on page 50. 

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 479). 

(b) Tremor may be defined as a clonic spasm of short excursion. 
Its causes and varieties have already been discussed (see page 45) . 

(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 have already been described 
(page 47) . 

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, 


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 

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 ''Romberg's sign." 

II. Disorders of Sensation. 

The following are the most important types : 

i. Anaesthesia (or insensibility to pain, to touch, to heat and cold, 
and to muscle sensation). 

2. Hyperesthesia (or over sensitiveness) . 

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 anaesthesia 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 as tereo gnosis, 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. 


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. Hemianesthesia 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 anesthesia (with hyperaesthesia and paresthesia) 
usually do not correspond to the distribution of any set of nerves or 
centres, and are distinguished by this fact. 

2. Hyperesthesia 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. Paresthesia 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 paresthesia 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. 

777. 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 1 5 . 

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. 
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 " rein- 
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. 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 
presence of Romberg's symptom (see page 476), 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 

Partial destruction of the cord often increases the reflexes, but total 
division usually abolishes them. 

Increased knee-jerk is found in : 

(a) Cerebral paralyses (infantile, apoplectic, dementia paralytica, 


(b) Spastic paraplegia and the amyotrophic forms of lateral 

(c) Many cord lesions, localized above the lumbar enlargement 
(transverse or 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 usually 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 473) 
and the absence of marked sensory or sphincteric symptoms. Its 
pathology is not known. If marked wasting of the muscles occurs it 
is termed "amyotrophic lateral sclerosis." 

Transverse or diffuse cord lesions above the lumbar enlargement 
produce usually anaesthesia below the level of the lesion and almost 
invariably relaxation of the sphincters. 

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 45), nystagmus (page 16), and staccato speech. In 
atypical cases diagnosis is difficult and cases are often mistaken for 

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. 

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 contraction of the ham-string muscles, 
obtained by flexing the thigh on the trunk at a right angle (as in the 
ordinary sitting position) and then attempting to extend the 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 deep reflexes of the arms (wrist, biceps, and triceps tendon) 
are obtained by snapping these tendons sharply with the finger. 
Decrease in these reflexes we cannot perceive, since they are only 
obtainable when increased. They are increased in practically the 
same diseases which increase the leg reflexes, and also in some 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 modifica- 
tion or reverse of the normal plantar 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 patient's 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. 

The reflex is obtained on the paralyzed side in hemiplegia and 
other lesions involving the motor tract. 

(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 faeces. 
If there is no awareness of fasces 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 and brain lesions rarely affect 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. 

IV. 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 

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. 


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 myeltis, and all severe 
forms of peripheral neuritis. In brain lesions this reaction rarely 

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. 

V. 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 

VI. Trophic or Vasomotor Disorders. 

Trophic lesions of the joints, muscles (atrophy), skin, and nails 
have already been exemplified (pages 464 and 54). 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- 

1 In some left-handed persons the centres are on the right side of the brain. 


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. 

VII. 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. 


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 diagnosis of coma applies 
equally well to the diagnosis of convulsions. Either or both may 
result from : 

i. Apoplexy (including cerebral hemorrhage, embolism, and 
thrombosis) . 

2. Uraemia and hepatic toxaemia. 

3. Diabetes. 

4. Cerebral concussion (stun). 

5. Cerebral compression. 

6. Syncope (fainting). 

7. Opium. 

8. Alcohol. 

9. Hysteria. 

10. Epilepsy. 

1 1 . Gas poisoning. 

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 

(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, long-standing 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 apoplexy, 
meningitis, arteriosclerosis, etc. Convulsions more often precede or 
follow the coma of uraemia than that of apoplexy. Retinal hemor- 
rhages or albuminuric retinitis, if recognized by ophthalmoscopic 
examination, point strongly to uraemia. 

The hepatic toxaemia in which many cases of cirrhosis die is dis- 
tinguishable from uraemia only if the previous history of the case is 
known to us and the signs of liver disease (ascites, jaundice, 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 emacia- 
tion of the patient, the sweetish odor of the breath, the presence of 
sugar, and especially the evidences of acetone and diacetic acid in 
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 without trephining, 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 which precede it and which are usually known to have 
occurred at intervals before. The scars of previous falls may be found 
on the head. 

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 

Sunstroke is recognized by the state of the weather and the presence 
of a very high temperature (106 , i io°, 1 15 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. 


Abdomen*, contour of, 339 

distended and tortuous veins of. 

examination of, 33 B— 342 
free fluid in. 345. 347 
inspection of, 339 
organs palpable in, 341 
palpation of, 340 
projection or levelling of navel 

respiratory movements ::. 340 
rose spots on, 339 
striae of, 339 
tumors of, 343 
tumors of, frequency of, 346 
tumors of, respiratory mobility 

in, 343 
Abdominal distention, 3 7 B 

reflexes, 480 

wall, abscess of. 342 

wall, inflammation of. 343 

wall, lesions of, 346 

wall, movements of. 3 ; _ 

wall, sarcoma of. 3 _ 3 

wall, thickening of, $43 
Abscess, alveolar. 25 

axillary, 40 

cervical, caries in, 29 

cervical in Pott's disease. 3a 

cold. 59. 70 

glandular, 32 

in tuberculous arthritis, 461 

ischiorectal, 414 

of abdominal wall, 342 

of hip -joint. 58 

of liver. 3 _ B 

of lung, breath in, 2 1 

of urethra, 419 

peri -urethral, 416 

perihepatic, 348 

Abscess, perinephritic, 59, 391 

perinephritic, psoas spasm in, 

perisplenic, ;_S 

psoas, 426 

pulmonary, 293, 333 

pulmonary, sputa in, 303 

rerropharyngeal. : S 

subphrenic, ;_^ 

tonsillar. 2 i 

tuberculous, 59 
Acetone breath, 22 
Achilles reflex. 479 
Achromia of red cells in chlorosis, 44 S 
Achylia gastrica, stomach contents in, 

Acne rosacea, nose in, iS 
Acromegalia, S 

arm in. 43 

hands in, 52 

nose in, S, 17 

''whopper jaw" in, S 
Actinomycosis, 59 

of belly- wall, 343 

of neck, 3 5 

of pleura, 330 
Addison's disease, 106 

disease, buccal patches in, 26 
Adenitis, 29, 92, 93 
Adenoid growths, 64 

growths, nose in, iS 
Adenoids, 11 

lips in, 19 
Adherent pericardium, 84, 203, 260 
Agraphia. 4S2 
Albuminuria, 398 

in peritonitis, 347 

significance of, 399 

with nephritis, 400 

without nephritis, 400 




Albumosuria, significance of, 400 
Alcoholism, 364, 478 

breath in, 22 

ccJma in, 485 

face in, 12 

hands in, 44, 45 

in myocarditis, 244 

nose in, 17, 18 

pharyngeal reflexes in, 29 

skin in, 100 

tongue in, 23 
Alkaline urine, 398 
Alopecia areata, patchy baldness in, 

Amoeba coli, 381 

histolytica in feces, 38 1 
Amyloid disease, of liver, 365 

disease, spleen in, 389 
Amytrophic lateral sclerosis, 479 
Anaesthesia, hysterial, 477 

neuritis after, 37 

tests of, 476 
Anatomy of chest, 61 
Anemia, capillary pulsation in, 90 

functional heart murmurs in, 187 

haemoglobin test in, 439 

hypertrophy in, 198 

interpretation of blood count in, 

lips in, 19 

mitral stenosis in, 217 

murmurs in, 225 

nails in, 57 

oedema of legs in, 431 

oedema of lids in, 14 

pallor in, 92 

pernicious, 106, 448 

pulse in, 221 

retinal hemorrhage in, 17 

splenic, 389 

venous murmurs in, 189 

secondary causes of, 447 
Aneurism, 34, 59, 70, 82, 85, 86, 239, 

26 3. 3 2 7- 334 
aortic, 299 
aortic, pupils in, 16 
cardiac, 214 
diagnosis of, 270 
diffuse, 219, 263 

Aneurism, distinguished from aortic 
stenosis, 271 

distinguished from diffuse dilata- 
tion of the arch, without 
rupture of coats, 271 

distinguished from empyema 
necessitatis, 272 

distinguished from mediastinal 
tumors, 272 

location of, 269 

oedema of arm in, 40 

of aorta, 231 

percussion signs in, 264, 266 

pulsation in, 263 

pupils in, 266 

radial pulse in, 266 

radioscopy in, 268 

saccular, 220, 263 

thoracic, 263 
Angina pectoris, 196, 244, 312 
Angioneurotic oedema, 14, 20, 483 

oedema of legs, 432 
Ankle clonus, spasm in, 475 

clonus, test for, 479 
Ankylosis, 460, 466 
Anorexia in local peritonitis, 347 

nervosa, malnutrition in, 2 
Anterior poliomyelitis, 428 

poliomyelitis, acute, paralysis in, 

poliomyelitis, knee-jerk in, 478 

poliomyelitis, reaction of de- 
generation in, 481 
Anus, fistula of, 414 

fissure of, 414 
Aortic aneurism, see Aneurism 

arch, dilatation of, 219, 226 

arch, roughening of, 231, 239 

dilatation, 209, 231 

insufficiency, 216 

obstruction, see Stenosis 

regurgitation, see Regurgitation 

second sound, 173, 174, 175 

stenosis, see Stenosis aortic 

valves, roughening of, 226 
Aortitis, syphilitic, 218 
Apex retraction, 83 
Aphasia, 247, 482 
Aphonia, 258 



Apnoea in Cheyne-Stokes breathing, 

Apoplexy, breathing in, 76 

coma in, 483 

distinguished from uraemia, 484 
Appendicitis, 375 

cause of peritonitis, 345 

diagnosis of, 376 

leucocytosis in, 449 

local and constitutional signs, 


muscular spasm in, 376 

psoas spasm in, 376, 462 

simulated, 376 

tenderness in, 376 

tumor in, 376 
Arcus senilis, 16 
Argyll-Robertson pupil, 16, 478 
Arms, artophy of, 39 

contractures of, 39 

contractures of, in cerebral lesion, 

contractures of, in hysteria, 39 
cyanosis of, 266 
deep reflexes of, 480 
fatty tumors of, 40 
gouty deposits in, 41 
in acromegalia, 43 
in acute anterior poliomyelitis, 

38, 39 
in osteoarthropathy, 43 
in Paget's disease, 42 
in rickets, 42 
oedema of, 266 
oedema of, causes of, 40 
oedema of, in aneurism, 40 
oedema of, in cancer, 40 
oedema of, in Hodgkin's disease, 

oedema of, in nephritis, 40 
oedema of, in sarcoma of medi- 
astinum, 40 
oedema of, in sarcoma of lung, 

oedema of, in thrombosis, 40 
pain in, 35, 266 
paralysis of, 37 
sarcoma of bone of, 40 
tuberculosis of bone of, 41 

Arms, tuberculous lesions of, 41 
Arrhythmia, 213, 222, 247, 250 

causes of, 102 

"nervous," 218 
Arsenic poisoning with conjunctivitis, 


Arterial embolism, 215 
murmurs, 189, 190 
pressure, 107 
tension, 104, 106 
walls, calcification of, 106 
walls, condition of, 105 
walls, stiffening of, 105, 106 
Arteries, calcification of, 105 
changes in, 40 
diseases of, 89 
inspection of, 88 
position of, 105 
pulsation in, see Pulsation 
stiffening of, 89 
Arteriograms, 113 
Arterio-sclerosis, 82, 89, 105, 107, 

cornea in, 16 
gangrene of toes in, 435 
heart sounds in, 174 
hypertrophy in, 198 
pulse in, 103 
Arthritis, 425 

acute infectious, distinguished 

from other types, 462 
acute infectious, endocarditis in, 

atrophic, 54, 464 
atrophic, monarticular form, 464 
atrophic, of sacro-iliac joint, 467 
atrophic, primary polyarticular 

form, 466 
atrophic, symmetrical involve- 
ment of joints in, 466 
atrophic, X-ray of hand in, 464 
gouty, 472 
hsemophilic, 472 
hypertrophic, features of, 466 
hypertrophic, Heberden's nodes 

in, 466 
hyertrophic, limitation of motion 

in, 469 
hypertrophic, nerve pain in, 469 



Arthritis, hypertrophic, of sacro-iliac 
joint, 58 
hypertrophic, psoa sspasm in, 

hypertropic, with kyphosis, 58 
infectious, 461 
spinal, 57 

tuberculous, characteristics of, 
Ascaris lumbricoides, 381, 384 
Ascites, 422 

causes of, 347 
Asphyxia, local, in Raynaud's disease, 

Astereognosis, 476 
Asthma, 277 

breathing in, 153 

bronchial, 276, 300 

bronchial, eosinophilia in, 450 

thymic, 301 
As- Vs interval, 1 14 

-Vs interval, in mitral stenosis, 
Ataxia, 475 

Romberg's sign in, 476 
Atelectasis, 268, 275, 284, 335 

creptant rales in, 160 

pulmonary, 328 
Athetosis, 50 

Atrophic arthritis, see Arthritis 
Atrophy, acute yellow, 368 

following fracture or dislocation, 


of disuse, 39 

in hysteria, 39 

muscular, claw hand in, 5 1 

muscular, reaction of degenera- 
tion in, 482 

optic, 17 

progressive muscular, fibrillary 
twitching in, 475 
Auricle, dilatation of, 202 

hypertrophy of, 202 
Auricular fibrillation, 115 
Auscultation, differences between two 
sides of chest, 154 

importance of, 137 

in pneumohydrothorax, 165 

in aortic regurgitation, 222 

Auscultation in croupous pneumonia, 
in mitral stenosis, 212 
in myocarditis, 245 
mediate versus immediate, 137, 

of heart, 167, 197 
of lungs, 147 
of muscle sounds, 145 
of voice sounds, see Vocal Frem- 
see also Breathing, Murmurs, 

Rales, Heart sounds 
sources of erorr in, 146, 147 
technique of, 137 
Austin Flint murmur, 215, 216, 226 

Babinski reflex, test for, 480 
Bacilli influenza, 305, 307 

pneumococcic, 305 

tubercle, 305, 380 

tubercle, identification of, 380 
Back, 57-60 

aneurism pointing in, 59 

dermoid cyst of, 60 

epithelioma of, 60 

in lumbago, 57 

nodes in, 59 

spina bifida of, 60 

stiffness of, 57 

tumors of, 59, 60 
Balanitis, 416 
Baldness, 7 

patchy, in alopecia areata, 7 
Basedow's disease, 375 
Bathycardia, 84 
Bence-Jones' body, 400 
Biceps, rupture of, 40 
Bigeminal pulse, 119, 215, 249 
Bile ducts, 368 

ducts, incidence of diseases of, 
Bilharzia disease, blood in, 450 

eggs, 385 
Biliary colic, 369, 392 

obstruction, 15 
Bismuth line, 24 

X-ray examination of stomach, 



Bladder disease, incidence of, 410 

disease, percussion in, 410 

disease, urine in, 412 

distention of, 410 

pus in, 396 

stone of, 413 

tuberculosis of, 413 

tumor of, 398 
Blindness, dilatation of pupil in, 16 
Blood, altered, 379 

color, index of, 438 

counting red corpuscles of, 
method of, 446 

counting white corpuscles, 
method of, 445 

cover- glass preparation of, 439 

eosinophilia in, 444, 450 

examination of, 437 

filaria in, 455 

films, appearance of stains, 442 

films, preparation of, 439 

films, staining of, 441 

films, stains used, 441 

haemoglobin test, 437 

in Bilharzia disease, 450 

in chlorosis, 448 

in feces, 379 

in filariasis, 450 

in hydatid disease, 450 

in lymphoid leukaemia, 450, 451 

in myeloid leukaemia, 451 

in pernicious anemia, 448 

in secondary anemia, 447 

interpretation of result of leuco- 
cyte count and differential 
count, 446 

in trichiniasis, 450 

in trypanosomiasis, 450 

in uncinariasis, 450 

in urine, 405 

leucocytes in, 443 

lymphocytes in, 443 

normoblasts distinguished from 
megaloblasts in, 442 

nucleated red cells in, 442 

occult, 380 

parasites in, 453 

plates, 444 

poikilocytosis, 442 

Blood, polychromasia, 442 

polynuclears in, 443 

pressure, see Pressure 

stippled red cells in, 442 

trypanosoma in, 455 

Wassermann reaction, 453 

Widal reaction, 452 

see also Anemia 
Body, as a whole, 1 
Bone, necrosis of, in tuberculous 

arthritis, 461 
Bowel, cancer of, 378 
Bradycardia, 248 
Brain, abscess of, optic neuritis in, 17 

defects, spasms in, 14 

lesions, astereognosis in, 476 

lesions, hemianaesthesia in, 477 

lesions, nystagmus in, 16 

paralysis of, 474 

tumor, optic neuritis in, 17 
Breast, funnel, 65 

pigeon, 65 
Breath, 22 

acetone, 22 

alcoholic, 22 

causes of foul, 22 

in gastric fermentation, 2 2 

in poisoning by illuminating gas, 

in Rigg's disease, 22 

in stomatitis, 22 

in tonsillitis follicular, 22 

in uraemia, 22 
Breathing, amphoric, 158, 292, 310 

asthmatic, 74 

bronchial, 150, 156, 157 

bronchial or tracheal, 150, 151 

broncho-vesicular, 152, 154, 157, 
158, 279, 290 

catchy, 76 

cavernous, 158, 292, 310 

Cheyne-Stokes, 75, 244 

cog-wheel, 152, 153, 286, 287 

compensatory, 155 

differences between two sides of 
chest, 154 

difficult, 72 

emphysematous, 72, 152, 298 

exaggerated vesicular, 155 



Breathing in apoplexy, 76 

in asthma, 72, 153 

in hysteria, 77 

interrupted, 152, 153, 287 

metamorphosing, 154 

normal, 70, 73 

rapid, 72, 73 

shallow, 76 

"sharp," 290 

sighing, 76 

stertorous, 76 

stridulous, 76 

tubular, 143, 157, 258, 279 

types of, 72, 73, 74, 148 

vesicular, 148, 149, 150, 274 

vesicular, diminished, 155 

see also Respiration 
Bronchi, dilatation of, see Bronchiec- 

spasm of, 300 
Bronchial asthma, see Asthma 

breathing, see Breathing 

pneumonia, see Pneumonia 
Bronchiectasis, 277, 293, 302 

sputa in, 303 
Bronchitis, acute, 274, 277, 284 

chronic, 277, 302 

tuberculous, acute, 295 
Bronchophony, 164 
Buccal cavity, see Mouth 
Bulbar paralysis, see Paralysis . 
Bundle of His, 114, 248 
Bursitis, prepatellar, 429 

Cachexia, 273 

of old age, 1 
Calcaneus, 433 
Cancer, 272 

age of patient in, 360 

anemia in, 447 

gastric, advanced, symptoms, 

gastric, bismuth X-ray examina- 
tion in, 358 

gastric, malnutrition in, 2 

gastric, statistics of, 360 

gastric, tumor in, 351 

gastric with absence of hydro- 
chloric acid, 360 

Cancer, glands in, 3 1 

jaundice in, 367 

metastatic, of femur, 426 

oedema of arm in, 40 

of bowel, 378 

of esophagus, 353 

of lip, 20 

of liver, 364 

of pancreas, jaundice in, 371 

of penis, 416 

of peritoneum, 348 

of pleura, 329 

of rectum, 414 

of rectum, stools in, 379 

of sigmoid, 377 

of stomach, 360 

of testis, 417 

of tongue, 22 

of tonsil, 28 

of uterus, 420 

of vertebras, 57 

tongue in, 23 
" Canker sores," 20 
Cardiac compensation, see Compen- 

cycle, see Heart cycle 

disease, diuresis in, 1 

disease, sweating in, 1 

disease, weight in, 1 

disease, see also Heart 

dulness, 133, 212, 250, 275, 288, 

3". 319 

impulse, 94, 95, 185, 198, 220, 

243, 258, 260, 309, 322 
impulse, character of, 79-81 
impulse, displacement of, 62, 68, 

82, 197 
impulse, maximum, 79 
impulse, normal, 79 
impulse, position of, 79 
murmurs, see Murmurs 
neuroses, 81, 246 
space, 129 

Cardio-spasm, 353 

Caries of vertebras, abscess in, 29 

Carphologia, 44 

Casts in urine, 463 

Catarrhal pneumonia, see Pneu- 



Cavity, pulmonary, 292, 302 
Cervical rib, an accessory, 35, 39 
Charcot's joint, atrophic arthritis in, 

Chest, anatomy of, 61 

barrel shaped, 66 

diminished expansion of, 71 

examination of, 61 

flattening of, 68 

in adenoid disease, 65 

increased expansion of, 72 

in phthisis, 65, 66, 67, 68 

inspection of, 64 

landmarks of, 62, 63 

local prominences, 69 

palpation of, 94 

percussion of, 121 

prominence of one side, 69 

rachitic, 65 

shape of, 64 

size of, 64 

tenderness in, 99 

tumor of, 70 

wall, nutrition of, 67 
Cheyne-Stokes breathing, 75, 244 
Children, splenic enlargement in, 

Chill, cause of, 3 

true, cause of, 4 
Chilliness distinguished from chill, 4 
Chlorosis, blood in, 448 

visible pulsation in, 84 
Cholangitis, 365 
Cholecystitis, signs of, 370 

results of, 370 
Chorea, hands in, 47 

leg in, 428 

post-hemiplegic, 49 

spasms in, 13 

Sydenham's, of hands, 47 

true, to differentiate, 14 
Choreiform movements, 47, 49, 50 
Cirrhosis of liver, see Liver 

of lung, see Pneumonia, chronic 

portal, jaundice "in, 367 
Claudication, intermittent, 427 
Club-foot, varieties of, 433 
" Cold sores," 19 

Colic, biliary, 369 

intestinal, 393 

lead, 369 

renal, 369 
Collargol-radiographs in kidney dis- 
ease, 391 
Colon, congenital dilation of, 375 

inflation of, in diagonsis of 
abdominal tumors, 345 

palpation of, fluid in, 345 
Coma, alcoholic, 485 

causes of, 483 

in Stokes-Adams syndrome, 486 

knee-jerk in, 478 

postepileptic, 485 

sphincteric reflexes in, 481 
Compensation, 278 

cardiac, establishment of, 194 

cardiac, failure of, 195 

establishment of, 203 

failing, 205, 207 

tests of, 196 
Compression, coma in, symptoms of, 


of lung, 283 
Concussion, coma in, 484 
Conjunctivitis, causes of, 14, 15 

following arsenic, 15 

following iodide of potash, 15 

with hay fever, 14 

with measles, 14 

with yellow fever, 14 
Constipation, 378 

in intestinal obstruction, 377 

tongue in, 23 
Contractures following atrophic arth- 
ritis, 466 

hemiplegic, hand in, 5 1 

of arm, 39 

of the interossei and lumbricales, 
claw hand in, 51 
Cornea, 16 

Corrigan pulse, 103, 221, 230, 241 
Cough, 161, 196, 207, 258, 274, 283, 

28 5> 2 93. 3° 2 . 3 21 
with sputa, 307 
Cranium, size and shape, 5 
Cremasteric reflex, 480 
Crepitation, atelectatic, 277 



Crepitus in monarticular atrophic 
arthritis, 464 

in perigastritis, 344 

in perihepatitis, 344 

in perisplenitis, 344 

in peritonitis, 344 

peritoneal, 344 
Cretinism, 1 1 

lips in, 19, 21 

teeth in, 22 

tongue in, 24 
"Croup," breathing in, 76 
Curvature of spine, 34, 58, 59, 67 
Cyanosis, 57, 90, 196, 207, 235, 238, 
250, 278, 283 

causes of, 91 

of arm, 266 

of intestinal origin, 19 

of lips, 19 

of tongue, 23 
Cyst, branchial, 34, 35 

hydatid, 365 

of kidney, 389, 390 

of mediastinum, 335 

pancreatic, 371 
Cystitis, 412 

urine in, 396, 397, 398, 408 
Cystoscopy, 396 
Cytodiagnosis, in meningitis, 332 

of pleural effusion, 331 

technique of, 331 

Dactylitis, syphilitic, 55 

tuberculous, 55 
Debility, 285 

fibrillary twitchings in, 475 

mitral stenosis in, 217 

spleen in, 387 
Deformities, congenital, of heart, 250 

of chest, 67 

of hands, 51 
Degeneration, reaction of, 481 
Delirium cordis, 116, 207, 249 
Dementia paralytica, degeneration 
of handwriting in, 482 

paralytica, tongue in, 23 
Dextrocardia, 83 
Diabetes, acetone breath in, 22 

bronzed, 372 

Diabetes, coma in, 484 

dyspnoea in, 73 

gangrene of toe in, 435 

optic neuritis in, 17 

retinal hemorrhage in, 17 

ulcer of toe in, 435 
Diaphragm, movements of, 70, 77-78 
Diarrhoea, causes of, 375 
Diastole, 181 

Dibothriocephalus latus, 380 
Digitalis, 215 
Dilatation, aortic, 231 

cardiac, 199 

of aortic arch, 219, 226 

of heart, 84, 94, 261, 273 
Diphtheria, tonsils in, 27 

with nasal discharge, 18 
Dipping, 344, 363 
Displacement. of apex beat, 220 

of cardiac impulse, see Cardiac 
Distomum, Westermanni, 304 
Diverticulum of esophagus, 353 
"Double shock sound," 213, 215 
Dropsy, 1, 207, 235 

in cardiac disease, 195 

of pericardium, 255 
Drummond's signs, 267 
Ductus arteriosus, persistence of, 251 
Duodenal ulcer, 360 
Dupuytren's contraction, 56 
Duroziez's sign, 224 
Dysentery, chronic, anemia in, 447 
Dyspepsia, clean tongue in, 23 
Dysphagia, 258 

Dyspnoea, 19, 196, 207, 235, 238, 258, 
275, 2 78, 283 

nose in, 18 

varieties of, 72, 73 

see also Breathing 
Dystrophy, muscular lordosis in, 59 

Ear, gouty tophi of, 472 
Echinococcus of pleura, 329 
Egophony, 164, 280, 321 
Electrical reactions, 481 
Electrocardiograms, 113, 247 
Emaciation, 2, 350, 368 
Embolism, 312 



Embolism in mitral stenosis, 215 

septic, 238 
Embryocardia, 176 
Emphysema, 58, 64, 69, 75, 78, 275, 
277, 288, 296, 300 

atrophic (" small- lunged ") , 298 

breathing in, 152 

complementary, 300 

expiration in, 298 

interstitial, 299 

large-lunged, 296 

of lung, 156 

percussion signs in, 297 

sub-cutaneous, see Interstitial 

vicarious, 284 

with asthma, 299 

with bronchitis, 299 

with phthisis, 294 
Empyema, 70, 157 

interlobar, 259, 324, 325 

necessitatis, 272 

post-pneumonic, 281, 325 

sputa in, 303 

tuberculous, 325 
Endaortitis, 231 

Endocarditis, 191, 232, 233, 260, 

acute, 186 

aortic, 230 

chronic, 209 

foetal, 250 

in arthritis, acute infectious, 462 

rheumatic, 116, 218 

septic, 57 
Endometritis, 420 
Endothelioma, 329 
Enteritis, stools in, 379 
Eosinophilia, 450 
Epididymitis, 416 
Epigastric pain, 350 

pulsation, 198 

reflexes, 480 

retraction, 83 
Epigastrium, hernia in, 342 

inspection and palpation of, 350 

tenderness in, 350 

tumor of, 350 
Epilepsy, coma in, 485 

Jacksonian, hands in, 46, 47 

Epiphyses, enlarged in rickets, 434 
Epiphysitis, acute, septic, 425 

chronic, tuberculous, 425 
Epispadias, 415 
Epithelioma, 24 

of ankle, 434 

of back, 59 

of nose, 19, 20 
Epulis, 25 
Equinus, 433 
Eruptions, 92 

of forehead, 7 
Erysipelas, oedema of lids in, 14 
Erythromelalgia, 434 
Esbach's test for albumin, 399 
Esophagus, cancer of, 353 

cardio-spasm with dilatation of, 

dilatation of, 353 
diverticulum of, 353 

Ewald's test meal, 355 

Exophthalmic goitre, see Graves' 

Exostosis of thigh, 426 

Extrasystoles, 118, 249 

Eyes, 14 

circles under, 14 

in aneurism, 266 

in muscle paralysis, 474 

oedema of lids, causes of, 14 

Face, 8-13 

after vomiting, 1 2 

in acromegalia, 8 

in adenoids, n 

in alcoholism, 12 

in cretinism, 1 1 

in Graves' disease, 12 

in leprosy, 12 

in myxcedema, 8, n 

in nephritis, 13 

in paralysis agitans, n, 12 

in phthisis, 12 

"mask-like," n, 12 

cedematous, 13 

spasms of, cause of, 13 

swelling of, 25 
Fallopian tubes, 420 
Faradic reaction in disease, 481 



Fatigue, degeneration of handwriting 

in, 482 
Fatty metamorphosis of heart, 246 
Feces, abnormal ingredients in, 379 

blood in, 379 

color of, 378 

gall-stones in, 380 

microscopic examination of, 383 

mucus in, 379 

odor of, 378 

parasites' eggs in, diagnosis of, 

parasites in types, of, 380 

pus in, 380 

tarry, 379 

weight of, 378 
Feet, hot, in myocarditis in arterio- 
sclerosis, 434 
Fehling's test, 400 
Fermentation in cancer of stomach, 

Fever, 2, 285 

causes of 2, 3 

"continued," 3 

crisis in, 3 

determination of, 3 

dilatation of pupils in, 16 

emaciation in, 2 

in appendicitis, 376 

infectious, nosebleed in, 18 

in intestinal obstruction, 377 

"intermittent," 3 

in tonsillar abscess, 28 

leucocyte count in, 450 

lysis in, 3 

sordes in, 24 

tongue in, 23 

typhoid, see Typhoid fever 

types of, 3 
Fibrillary twitchings, 475 
Fibro-myoma of uterus, 420 
Filariasis, blood in, 455 

parasites in, 455 
Finger-ends, tender, 57 
Fingers, clubbed, 43, 53, 266 

in heart disease, 43 

in lung disease, 43 

in pleural disease, 43 
Fistulae, branchial congenital, 35 

Flipper-hand in atrophic arthritis; 51 
Fluid, free in abdomen, tests for, 345 

in pleurisy, 321 
Fluoroscope, 268, 287 

use of, 329 
Follicular tonsillitis, 427, 428 
Fontanels, 6 

bulging,. 6 

delayed closure of, 6 

depressed, 6 
Forehead, bony nodes of, 8 

eruptions of, 7 

scars of, 7 
Foot, 433 

club-, varieties of, 433 

flat-, 433 
Fremitus, tactile, see Tactile fremitus 
Friction, pericardial 253, 254 

pleural, see Pleural 
Frontal sinusitis, 8 
Funnel breast, 65 

Gait, ataxic, 474 

in paralysis agitans, 474 

spastic, 45, 474 

toe-drop, 474 
Gall bladder, 369 

bladder, adhesions about, 370 

bladder, enlarged, 370 

bladder, incidence of diseases of, 

-stones in feces, 380 
Galvanic reaction in disease, 482 
Gangrene, local, in Raynaud's disease, 


of lung, 293, 33 7, 

of mouth, 26 

of toes, 435 
Gas, poisoning by, coma in, 485 
Gastric cancer, see Cancer 

contents, see Stomach contents 

crises, 370 

diseases, incidence and diagnosis 
of, 360 

disturbances, mitral stenosis in, 

fermentation, breath in, 22 

fermentation, tongue in, 23 

peristalsis, 351 



Gastric stasis, 361 

ulcer, 360 
J ulcer, malnutrition in, 2 

ulcer, tongue in, 23 
Genitals, female, inspection of, 418 

female, lesions of, 418 

female, palpation of, 418 

male, 415 
German measles, glands in, 3 1 
Gland, atrophy of thyroid, 33 

cancer of thyroid, 33 

cervical, in malignant disease, 3 1 

cervical, in syphilis, 30 

cervical, in tuberculosis, 30 

enlarged, causes of, 29, 31, 33, 


enlarged, in mesentery, 349 

in cancer, 3 1 

in German measles, 3 1 

inguinal, in syphilis, 424 

in Hodgkin's disease, 30 

in lymphatic leukaemia, 31 

in mumps, 3 1 

in tonsillitis, 30 

sarcoma of, 31, 33 

see also Adenitis 
Glanders, 59 
Glottis, obstruction of, 74, 76 

spasm of, 301 
Glucosuria, 400 

experimental, 401 

permanent, 401 
Goitre, exophthalmic, see Graves' dis- 

simple, 32 

with exophthalmus, 12 
Gonorrhoea, arthritis in, 461 

balanitis in, 416 

distended bladder in spasm of 
urethra in, 410 

inguinal glands in, 424 

orchitis in, 416 

with epididymitis, 416 

with frequent micturition, 412 
Gout, toes in, 43 5 

tophi in arm, 41, 42 

tophi in ear, 472 

tophi in joints, 458 
Gouty arthritis, 472 

Gouty arthritis, destruction of bone 
in, 472 

arthritis, X-ray of hand in, 472 
Graves' disease, 12, 32, 45, 248 

disease, capillary pulsation in, 90 

disease, expression in, 12 

disease, hands in, 44 

disease, heart sounds in, 173 

disease, hypertrophy in, 198 

disease, pulse in, 221 
Grocco's sign, 319 
Groin, 424 

glands in, 424 • 

hernia in, 424 

psoas abscess in, 425 
Guaiac test of stomach contents, 3 56, 

Gumboil, 25 
Gums, 24 

bismuth line in, 24 

bleeding, 25 

in lead poisoning, 24 

in poisoning by mercury, 24 

in poisoning by potassic iodide, 

in scurvy, 25 

sordes of, 24 

spongy, 25 

suppuration of, 25 
Giinzburg's reagent, 356 

H^ematemesis in portal obstruction, 

Hasmatocele, 417 
Haematoma, infected, of belly wall, 

Hematuria, 385, 397 

causes of, 413 
Haemoglobin, tests for, 19, 437 
Haemopericardium, 256 
Haemophilia, nosebleed in, 18 
Hemophilic arthritis, 472 
Haemoptysis, 196 

causes of, 285, 303, 304 

in mitral stenosis, 215 
Haemorrhage, see Hemorrhage 
Hair, abnormal loss of, 7 

in myxcedema, 8 

in rachitis, 6 



Hair, in syphilis, 7 

parasites in, 7 
Hands, 43 

choreiform, movements of, 47 

deformities of, 51 

evidence of occupation, 43 

examination of, 43, 44 

in alcoholism, 44 

in atrophic arthritis, 54 

in cardiac weakness, 44 

in carphologia, 44 

in chorea, 47 

in contractures following hemi- 
plegia, 51 

in Graves' disease, 44 

in Jacksonian epilepsy, 46, 47 

in myx oedema, 51, 52 

in paralysis of median or ulnar 
nerves, 51 

in progressive muscular atrophy, 

in subsultus tendinum, 44 
in typhoid fever, 44 
moisture of, 44 
spasms of, 47 
temperature of, 44 
tremor of, 45 

Handwriting, degeneration of, 482 

Hang-nails, 56 

Hare-lip, 21 

Harrison's groove, 65 

Hay fever with conjunctivitis, 14 

Head, abnormalities of, 5 
open areas of, 5 
shaking of, 13, 219 

Heart, see also Cardiac, Murmurs, 
Regurgitation, Stenosis, 
action, accelerated, 116 
apex impulse, 79, 80, 81, 94, 95, 
181, 198, 220, 243, 258, 260, 
309, 322 
auscultation of, 167, 197 
beat, alternation of, 119 
beat, coupling of, 119, 215 
beat, "dropped," 114, 115 
beat in mitral stenosis, 213 
beat, irregular, 245 
beat, premature, 118, 119 

Heart, block, 113, 250 

block, "dropped beats," 114, 115 
bradycardia, 248 
characteristics of dilatation, 199, 

chronic dilatation of, 199 
compensation, 194 
congenital malformations, 250 
cycle, systole and diastole, 180, 

dilatation of, 84, 199, 200, 261, 

disease, congestion of liver in, 

3 6 4 
disease, emphysema in, 19 
disease, methaemoglobinasmia, 19 
disease, pneumonia in, 19 
disease, poisoning in, 19 
diseases of, 191 
dislocation of, 309, 319, 323 
enlarged, 70, 129, 204, 207, 217, 

219. 235 
fatty metamorphosis, 246 
hypertrophy of, 81, 82, 219, 252, 

260, 261, 303 
impulse, 79, 81, 95 
in aortic aneurism, 266 
in aortic regurgitation, 218-226 
in combined lesions, 239—242 
in mitral regurgitation, 201—209 
in mitral stenosis, 209-218 
in myocarditis, 243 
in pericarditis, 253 
pleural effusion, 259 
in pneumothorax, 309 
in tricuspid regurgitation, 208 
irregular action of, 213, 222, 247, 

lips in disease of, 19 
mitral insufficiency, 202 
murmurs, see Murmurs 
over-distention of, 86 
palpation of, 81, 197, 200, 221 
palpitation of, 249, 250, see also 

parietal diseases of, 243—247 
rapid, 247 see Tachycardia 
situation of apex impulse, 62, 68 
slow, 248, see Bradycardia 



Heart, sounds, 167, 168, 245, 253-258 
sounds, accentuation of , 172-174 
sounds, arterial, 177 
sounds, doubling of, 176 
sounds, first, 168-170, 171, 175 
sounds, metallic, 176 
sounds, muffled, 176, 177 
sounds, modification in, 170 
sounds, normal, 168 
sounds, qualities of, 169-170 
sounds, reduplication of, 176, 

sounds, second, 168, 171, 172, 

173- 175 

sounds, third, 170 

sounds, weakening of, 174 

stenosis, 191 

tachycardia, 247 

"tobacco," 218 

"valve areas," 62 

valves, position of, 167 

valvular incompetence, 192 

valvular lesions of, 191 

wall, 244, 246 

wall, weakened, 191 

weakness, 243 

weakened, 244 
Heberden's nodes, 54, 457, 467 
Hemianassthesia, 477 
Hemiplegia, 215, 474 

atrophy of arm in, 39 

hands in, 51 

paralysis of leg in, 428 
Hemorrhage, anemia in, 447 

in retina, 17 

pulmonary, 285 

tendency of, in jaundice, 367 
Hemorrhoids, 414 
Hepatic abscess, symptoms in, 348 
Hepatization, 277 
Hernia, epigastric, 342 

of intestine, 312 

of scrotum, 417 

umbilical, 342 
Herpes labialis, 19-20, 482 

zoster, 482 
"Herzenstoss," 81 

Hip-joint, hypertrophic arthritis of. 
5 8 > 467 

Hip-joint, hypertrophic arthritis, 
morbus coxas senilis, 467 

limitation of motion of, 58, 458, 

psoas-spasm of, 458 
Hirschsprung's disease, 375 
Hoarseness, 285 
Hodgkin's disease, 334, 389 

disease, glands in, 30, 93 

disease, oedema of arm in, 40 
Hook-worm, 382 
Housemaid's knee, 429 
Hydatid disease, liver in, 365 
Hydrocele, 417 

of scrotum, 417 
Hydrocephalus, head in, 5 
Hydronephrosis, 390 
Hydropericardium, 255 
Hydrothorax, 155, 308 
Hymen, imperforate, 419 
Hyperacidity, gastric, 361 
Hyperaesthesia, tests of, 477 
Hyperchlorhydria, pain in, 370 
Hypernephroma, 390 
Hyperresonance, 297, 300, 320 
Hypertension, vascular, nosebleed in, 

Hypertrophic arthritis, see Arthritis 
Hypertrophy, cardiac impulse in, 82, 

cardiac, causes of, 196 

cardiac, results, 197 

of heart, 81, 94, 194, 195, 219, 
252, 260, 261, 303 

of left ventricle, 197, 217 

of lung, 308 

of right ventricle, 198, 233, 238 
Hypoacidity of stomach, 361 
Hypostatic penumonia, 337 
Hysteria, 45, 106 

anaesthesia in, 477 

atrophy in, 39 

breathing in, 7 7 

coma in, 485 

contractures of arm in, 39 

hemianaesthesia in, 477 

hyperaesthesia in, 477 

paralysis in, 428, 429, 474 

ptosis in, 16 



Hysteria, spasms in, 14 
temperature in, 2 

Idiocy, mouth in, 19 

Incidence of diseases of the bladder, 
of diseases of gall-bladder and 

bile ducts, 362 
of diseases of the intestine, 373 
of diseases of the kidney, 389 
of diseases of the liver, 361 
of diseases of the pancreas, 372 
of diseases of the stomach, 360 
of joint lesions, 472 
of thigh disease, 425 
of thigh tumors, 426 

Indicanuria, 402 

Indigestion, 285 

Infancy, examination of chest in, 64, 
jaundice in, 15 

Infantile atrophy, malnutrition in, 2 

Infections, 106, 243, 347 
acute chills in, 3 
leucocytosis in, 449 
lymphocytosis in, 449 
pneumococcus, 277 
pulse in, 103 
symptoms, 368 

Influenza, 18, 243, 275 

with conjunctivitis, 14 

Insomnia, 2 

Inspection in aneurism, 263 

in aortic regurgitation, 219 

in croupous pneumonia, 278 

of abnormal thoracic pulsations, 

of apex beat, 79 
of cardiac movements, 7 9 
deformities of chest, 62 
of head and face, 5 
of peripheral vessels, 86 
of respiratory movements, 70 
of skin and mucous membranes, 

of thorax, 64 

Insufficiency, aortic, 216 
mitral, 226, 232 
myocardial, 116 

Interlobar empyema, see Empyema 
Intestinal colic, 393 

contents, examination of, 378 

obstruction, 371 

obstruction, acute and chronic, 

obstruction by gall-stones, 371 
obstruction, causes of, 377 
obstruction, chronic visible peris- 
talsis in, 377 
Obstruction, distention in, 374 
obstruction, physical signs in, 

obstruction, tumor in, 377 
parasites, 380 

parasites, anemia from, 447 
parasites, diagnosis of eggs of, 

parasites, eosinophilia due to, 

parasites, relative frequency of, 

tenderness, 374 
tenesmus, 374 
Intestines, diseases of, 373 

diseases of, constitutional mani- 
festations, 373 
gaseous distention in, 374 
hernia of, 312 
Intussusception, 379 
Iritis with irregular outline Of pupil, 

Ischiorectal abscess, 414 
Itching in jaundice, 15 

Jacksonian epilepsy, 46 

epilepsy, spasms of hand, causes 
Jaundice, 15, 90, 92, 364 

catarrhal, 367 

causes of, 15, 366 

congenital, 368 

diagnosis of cause, 367 

in biliary cirrhosis, 368 

in cancerous obstruction of gall 
duct, 367 

in cholelithiasis, 367 

in portal cirrhosis, 367 

in syphilis, 15, 368 



Jaundice in Weil's disease, 368 

itching in, 15 

mental depression in, 15 

of new-born, 367 

of tongue, 23 

results of, on body, 367 

secondary, in septicemia, 368 

slow pulse in, 15 

with bile, 15 

with hepatic cirrhosis, 15 

with obstruction by stone, 15 

with syphilis, 15 

with toxaemia, 15, 367 

with tumors obstructing bile- 
ducts, 15 
Jaw, in acromegalia, 8 

-jerk, test for, 480 
Joints, ankylosis of, 460 

bony outgrowths, 457 

Charcot's, 464 

chronic diseases of, knee-jerks in, 

creaking in, 456, 460 
crepitus in, 456, 460 
diseases of, 460 
enlarged, 457 
examination of, 456 
excessive motion in, 456, 460 
fluctuation in, 457 
free bodies in, 456, 460 
gouty deposits in, 458 
inspection of, 456 
irregularities of contour, 456 
lesions of, relative frequency of, 

neuropathic, 464 
pain in, 456 
palpation of, 456 
radioscopy of, 457 
sacro-iliac, hypertrophic arthritis 

scaro-iliac, tuberculosis of, 57 
tests of limitation of motion, 456, 

see also Arthritis, Hip- joint 

Keratitis, syphilitic, cornea in, 16 

Kernig's sign, 480 

Kidney, abscess of, 390, 391 

Kidney, contracted, urine in, 409 

cyst of, 389, 390 

cyst of, distinguished from hydro- 
nephrosis, 390 

diseases of, 389—409 

diseases, statistics of, 389 

diseases, urine in, 393 

diseases, vocal and constitutional 
evidence of, 393 

displaced, movable, 392 

floating, 369, 392 

floating, tenderness in, 390 

malignant disease of, 390 

pus in, 396 

tumors of, 390 

see also Renal 
Knee, housemaid's, 429 

tuberculosis of, distinguished 
from sarcoma, 426 

-jerk, 477 

-jerk, absence of, 478 

-jerk, increased, 478 
Knock-knee, 429 
Koplik's spots in measles, 25 
Koranyi's sign, 319 
Korotkoff's method, no 
Kyphosis, 58 

in emphysema, 58 

in hypertrophic arthritis, 58 

in Paget's disease, 58 

in Pott's disease, 58 

in rickets, 58 

Lactic acid in gastric contents, 357 

Lamblia intestinalis, 380 

Lavage of stomach, 355 

Lead colic, pain in, 370 
line, 24 
poisoning, see Plumbism 

Legs, bowed, 429 

chronic ulcers of, 430 
in hysteria, 428 
in multiple sclerosis, 428 
in spastic paraplegia, 428 
in tabes dorsalis, 428 
malpositions of, 460, 461, 462 
oedema of, causes of, 43 1 
osteomyelitis in, 431 
paralysis of, causes of, 428 



Legs, paralysis of, differential diag- 
nosis in, 428 

sarcoma of, 43 1 

syphilitic periostitis of, 430 

tenderness, in neuritis, 432 

tenderness, in trichiniasis, 432 

varicose veins of, 430 
Leprosy, 56 

face in, 12 
Leucocyte chart, 450 

count, 444, 445 

count in general peritonitis, 347 
Leucocytosis, 449 

diagnostic value of, 449 

in appendicitis, 376 

occurrence of, 449 
Leukaemia, 70 

liver in, 365 

lymphatic, blood in, 450, 451 

lymphatic, glands in, 3 1 

myelogenous, blood in, 450, 451 

nosebleed in, 18 

percussion in, 131 

spleen in, 389 
Leukoplakia buccalis, 24 
Line, mid-axillary, 62 
Lineas albicantes, 339 
Lingula pulmonalis, 295 
Lips, 19 

angioneurotic oedema of, 20, 21 

cancer of, 20 

chancre of, 20 

cracks or fissures in, 19 

in cretinism, 19, 21 

in heart disease, 19 

in myxcedema, 19, 21 

pallor of, 19 

parted, 19 
Litmus-test, 398 
Litten's sign, 77, 78, 134, 286, 287, 

2 9 6 > 3°9> 3 2 4 
Liver, 207, 323, 361—369 

abscess of, 348 

abscess of, distinguished from 
syphilis or malignant dis- 
ease, 365 

acute yellow atrophy of, 366 

amyloid, 365 

atrophy of, 365 

Liver, cancer of, 364 

cirrhosis of, 70, 190, 261, 364, 388 
cirrhosis of, anemia in, 447 
cirrhosis of, coma in, 484 
cirrhosis of, oedema of legs in, 

disease, cerebral symptoms in, 

disease, incidence of, 361 
disease, portal obstruction in. 


enlargement, 328, 362 

enlargement, causes of, 363 

fatty, 364 

growth of, in cancer, 364 

hydatid disease of, 365 

in pneumothorax, 309 

leukaemic, 365 

malignant disease of, symptoms 
in, 364 

percussion of, 130 

pulsation in, 234 

syphilis of, distinguished from 
cirrhosis or malignant dis- 
ease, 364 

tumor of, 343 

see also Gall bladder, Jaundice 
Lordosis, 59 

in muscular dystrophy, 59 

in tuberculosis, 59 

with abdominal tumors, 59 

with pregnancy, 59 
Ludwig, angle of , 296 
Lumbago, 57 
Lung, abscess of, 21, 303, 333 

adventitious sounds, see Rdles 

anatomy of, 61 

atelectasis of, 328 

auscultation of, 147 

cancer of, 69, 348 

cirrhosis of, 68, 302 

collapse of, see Atelectasis 

compression of, 283 

condensation of, 268 

congestion of, see CEdema 

consolidation of, see Solidifica- 

diseases of, 274-295 

emphysema of, 156, 296—300 



Lung fever, 283 

fibroid, disease of, 83, 273, 294 

fistula sound, 166 

gangrene of, 22, 293, 333 

hypertrophy of, 308 

malignant disease of, 69, 348 

miliary tuberculosis of, 295 

neoplasms of, 334 

oedema of, 276, 336 

palpation of, 96 

percussion of, 134 

phthisis, 285-295 see also Tuber- 

culosisof the lungs 
pneumonia, 277, 283 
rales, in disease of, 158, 274 
reflex, 336 

reflex in percussion, 136 
resolution of, 281 
retraction of, 84, 273 
Rontgen ray examination of, 

325. 333 

sarcoma of, 40, 334 

solidification of, 277, 279, 283. 
284, 288, 290 

syphilis of, 301 

tuberculosis of, 285-295 
Lupus erythematosus, nose in, 18 
Lymphangiectasis, filarial, 425 
Lymphatic leukaemia, blood in, 450 

leukaemia, glands in, 3 1 . 
Lymphocytosis, 450 

in acute sepsis, 450 

in debility, 450 

in whooping cough, 450 

Mackenzie's polygraph, 115 
Malaria, anemia in, 447 

chills in, 3 

jaundice in, 15, 367 

parasites in, 453 

splenic, enlargement in, 387 
Malignant disease, anemia in, 447 

disease, glands in", 3 r 

disease, toxemia in, 449 

disease, see also Cancer, Epithe- 
lioma, Sarcoma, Myelomata 
Malnutrition, 2 

emaciation in, 2 

in anorexia nervosa, 2 

Malnutrition in chronic diarrhoea, 2 

in chronic dyspepsia, 2 

in diabetes, 2 

in gastric cancer, 2 

in gastric dilatation, 2 

in gastric ulcer, 2 

in infantile atrophies, 2 

in oesophageal stricture, 2 
Massage, leucocytosis in, 449 
Mast cells in blood, 443 
Measles, conjunctivitis in, 14 

German, glands in, 3 1 

Koplik's spots in, 25 

mouth eruption in, 25 

oedema of face in, 10, 14 
Mediastinitis, chronic, 260 

fibrous, 84 
Mediastinum, cysts of, 334 

neoplasms of, 36, 334 

sarcoma of, 334 
Megaloblasts, 442 
Melaena, 379 

Membranes, mucous, inspection of, 90 
Meningitis, bulging of fontanels in, 6 

cytodiagnosis in, 332 

leucocytosis in, 449 

tuberculous, breathing in, 76 

tuberculous, optic neuritis in, 17 
Mensuration, 61 

Mental depression in jaundice, 15 
Meralgia paraesthetica, 427 
Mesentery, enlarged glands of, 349 

thrombosis of, 349 
Metallic tinkle, 165, 310 
Metatarsalgia, 436 
Methaemoglobinaemia, lips in, 19 
Microcephalia, 6 
Migraine, aphasia in, 482 
Mitral disease, 99 

disease, double, 240, 241 

stenosis, see Stenosis, mitral 
Monoplegia, 474 

leg in, 428 
Morbus coxae senilis, 467 
Morton's disease, 436 
Morvan's disease, 56 
Motion, disorders of, 473 
Mouth, eruptions of, 25 

fissures of, 19 



Mouth, gangrene of, 26 

herpes of, 20 

in Addison's disease, 26 

in adenoids, 19 

in cretinism, 19, 21 

in dyspnoea, 19 

in idiocy, 19 

mucous patches in, 25, 26 

pigmentations of, 26 

syphilitic ulcers of, 20 
Movements, respiratory, 70 
Mucus in feces, 379 
Multiple sclerosis, 478 

sclerosis, intestinal tumors of, 45 

sclerosis, knee-jerk in, 479 

sclerosis, nystagmus in, 16, 45 

sclerosis, paraplegia in, 428 

sclerosis, spastic gait in, 45 

sclerosis, speech in, 45 

sclerosis, tremor in, 45 
Mumps, glands in, 3 1 

orchitis in, 416 
Murmurs, aortic, 183, 209 

aortic regurgitant, 179 

arterial, 189, 190 

Austin Flint, 215, 216, 226 

cardiac, 178 

cardio-pulmonary, 225 

cardio-respiratory, 188, 189, 209 

diagnostic interpretation of, 182, 

diastolic, 180, 182, 185, 223 
disappearance of, 186 
functional, 185, 186, 187, 188, 

203, 208, 231, 236, 238, 239 
functional, cause of, 186 
haemic, see Functional 
"hour-glass," 183 
in aortic aneurism, 267 
in mitral regurgitation, 203, 204 
in mitral stenosis, 211, 213, 214 
intensity of, 183, 184 
intracardiac, 255 
in tricuspid stenosis, 237 
length of, 185 
metamorphosis of, 186 
musical, 204 
of Flint, 215, 216, 226 
organic, 186, 188 

Murmurs, position of, 181, 182 

presystolic, 180, 237 

presystolic in tricuspid stenosis, 
215, 216, 217 

quality of, 184 

significance in enlarged heart, 

significance of, 185 

significance of precordial, 239, 

systolic, 180, 182, 187, 203, 251 

systolic, in aortic stenosis, 228, 

terminology of, 178 

time of, 180 

transmission of, 181 

venous, 189 
Muscle sounds, 276, 315 
Muscular dystrophy, lordosis in, 15 
Myelitis, acute, bedsores in, 483 

knee-jerks in, 479 

reaction of degeneration in, 482 

sexual power in, 481 

transverse or diffuse, paraplegia 
in, 428 
Myelomata of skull, 5, 6 
Myocarditis, acute, 243 

auscultation in, 245 

causes of, 245 

chronic heart sounds in, 171 

chronic interstitial, 244 

in acute rheumatism, 244 

hot feet in, 434 
Myoma of uterus, 420 
Myxcedema, 8, n 

face in, 8, 11 

hands in, 51,52 

increase in weight in, 1 

infantile form, 10 

lips in, 19, 2 1 

loss of hair in, 7 

nose in, 17 

tongue in, 24 

Nails, 56 

capillary pulse, 57 
changes, in hemiplegia, 56 
changes, in myxcedema, 56, 
changes, in neuritis, 56 



Nails, changes, in syringomyelia, 56 

grooved, 56 

in anemia, 57 

incurvation of, 57 

indolent sores around, 56 
Neck, 29 

abscess in, 32 

actinomycosis of, 3 5 

diseases of, 29—36 

in emphysema, 29 

in paralysis agitans, 1 1 

oedema of, 36 

scars of, 32 
Necrosis, anaesthetic, in leprosy, 56 

of bone, in tuberculous arthritis, 

of rib, 99 
Nephritis, acute, 397 

acute, urine in, 408 

albuminuria in, 400 

chronic, 106, in 

chronic glomerular, anemia in, 


chronic glomerular, urine in, 408 

coma in, 484 

face in, 13 

glomerular, polyuria in, 394 

heart sounds in, 174 

oedema of legs in, 431 

oedema of lids in, 14 

parenchymatous, 408 

retinal hemorrhage in, 17 
Nervous system, 473—486 
Neuralgia, intercostal, 76 

red, of extremities, 434 
Neurasthenia, fibrillary twitchings in, 

ptosis in, 16 
pulse in, 221 
Neuritis after anaesthesia, 37 
alcoholic, 38 
atrophy of arm in, 39 
due to pressure, 37 
lead, 38 
multiple, 39 
oedema of legs in, 43 1 
obstetrical, paralysis in, 38 
optic, 17 
paralysis of arm in, 37, 38, 39 

Neuritis, paralysis of leg in, 428 

peripheral, knee-jerk in, 478, 479 

postdiphtheritic, pharyngeal re- 
flexes in, 29 

pressure, test for, 3 7 

toxic, paralysis in, 38 
Neuroses, functional, 247 

hysterical, 39 

traumatic, 39 
Nodes, Heberden's, 54, 457, 467 

in back, 59 

in gouty arthritis, 472 

on forehead, 8 

syphilitic, 40 

sino-auricular, 113, 114 
Noma, 26 

Normoblasts in blood, 442 
Nose, 18 

discharge from, 18 

epithelioma of, 19, 20 

falling in of bridge of, 18 

hemorrhage of mucous mem- 
branes, 18 

in acne rosacea, 18 

in acromegalia, 8, 17 

in adenoid growths, 18 

in alcoholism, 17, 18 

in lupus erythematosus, 18 

in myxcedema, 1 7 

in syphilis, 18 

in tuberculosis, 19 

local disease of, 19 

size and shape of, 1 7 
Nosebleed, 18 
Nostrils, 18 
Nystagmus, 16, 45 

Obesity, i 

Obstruction, intestinal, see Intestinal 

laryngeal, 76 

portal, 366 
Ocular motions, 16 
(Edema, 91, 247, 266 

angioneurotic, 14, 432 

angioneurotic of lips, 20 

in anaemia, 43 1 

in deficient local circulation, 432 

in flat-foot, 432 

in heart disease, 195 



OEdema in hemiplegia, 432 
in inflammation, 432 
in nephritis, 43 1 
in neuritis, 432 
in obesity, 432 
in pressure, 432 
in thrombosis, 432 
in uncompensated heart lesions, 

in varicose veins, 432 

of arm, causes of, 40 

of eyelids, causes of, 14 

of face, 13 

of legs, causes of, 43 1 

of lungs, 207, 276, 303, 336 

of neck, 36 
Oliguria, 394 
Opium-poisoning, coma in, 485 

-poisoning, shaking of head in, 13 
Optic atrophy, 17 
Orchitis acute, 416 
Orthopncea, 207 
Osteitis deformans, 5, 427 
Osteoarthritis, 467 
Osteo-arthropathy, 43, 52, 53 

arm in, 43 
Osteoma or exostosis of thigh, 426 
Osteomyelitis, acute, septic, 425 

chronic, tuberculous, 425 

tibia in, 43 1 
Ovarian disease, diagnosis of, 421 
Ovaries, cyst of, with twisted pedicle, 

tumors of, 421 
Ovaritis, 421 
Oxaluria, 407 
Oxyuris vermicularis, 380 

"Pace-maker," 114 
Paget's disease, 5, 58, 427 

disease, arm in, 42 
Pain, epigastric, 350 

hepatic, 348, 362 

in appendicitis, 376 

in arm, 266 

in intestinal disease, 373 

in joints, 456 

in peritonitis, 346 

in sacro-iliac joint, 57, 58 

Pain in thorax, 156 

in tonsillar abscess, 28 

muscular, 320 

nerve, in hypertrophic arthritis, 

over sternum, 274 

precordial, 196 

renal, 392 
Palate, perforation of soft, 29 
Pallor, 92 

causes of, 92 

in phthisis, 12 
Palpation, 94—105 

and dipping, 344 

and friction, 98 

in aneurism, 263 

in aortic regurgitation, 221 

in croupous pneumonia, 278 

in myxcedema, 1 1 

of abdomen, methods of, 338 

of apex beat, 94 

of heart, 81, 197, 200 

of normal abdomen, 341 

of rales, 99 

of the pulse, 100 

of thrills, 95 

of voice vibrations, 96 
Palpitation, 249 
Pancreas, cancer of, diagnosis of, 371 

cyst of, 371 

diseases of, 371 

diseases of, diabetes in, 372 

diseases of, incidence of, 372 

diseases of, stools in, 371 

diseases of, urine in, 371 
Paresthesia, 477 

in neuritis, 38 
Paralysis agitans, 11, 12, 45, 46 

agitans, gait in, 474 

agitans, shaking head in, 13 

bulbar, 23 

cerebral, knee-jerk in, 478, 479 

congenital, choreiform move- 
ments in, 50 

facial, tongue in, 23 

in acute anterior poliomyelitis, 
37. 428 

in chorea, 428 

in diseases of spinal cord, 428 



Paralysis, infantile cerebral, athetosis 

in, 5° 
in hemiplegia, 49, 428 
in hysteria, 39, 428, 429, 474 
in lead-poisoning, 37, 38, 428 
in myelitis, 428 
in neuritis, 37, 428 
in tabes, 428 
in toxic neuritis, 428 
in traumatic neurosis, 37 
of arm, 37 
of brain, 474 
of cord, 474 
of cranial nerve, 474 
of dorsal or abdominal muscles, 


of legs, 428 

of interossei and lumbricales, 
claw -hand in, 51 

of muscles of respiration, 156 

of peripheral nerve, 474 

pharyngeal reflexes in, 29 

pupils in, 16 

serratus, scapula in, 60 

with contraction of pupil, 15 
Paraphimosis, 416 
Paraplegia, 474 

paralysis of leg in, 428 

spastic, 428, 479 
Parasites, animal, diseases due to, 


in feces, 380 

in hair, 7 

intestinal, eggs of, 382 

malarial, 453 
Paravertebral triangle, 319 
Paresis, 474 
Paronychia, 56 
Parotid gland, cancer of, 3 1 

gland, enlargement of, 31 
Parturition, leucocytosis in, 449 
Patella, floating of, test for, 457 
Pectus carinatum, 65 
Pediculi in hair, 7 
Penis, 415 

cancer of, 416 

chancre of, 415 

chancroid of, 416 

discharge from, 415 

Penis, inflammation of glands of, 416 

malformations of, 416 
Peptic ulcer, 360, 369 
Percussion, auscultatory, 126 

dull areas in, 129, 131, 133 

force of, 124, 130 

importance of symmetrical, 132 

in aneurism, 267 

in aortic regurgitation, 222 

in croupous pneumonia, 278, 279 

in enlarged heart, 130 

lung reflex in, 136 

mediate and immediate, 120 

note, modifications of, 133 

of heart, 200 

of lung borders, 134