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Cabot — Physical Diagnosis

ARGYRIA
Silver Nitrate Poisoning, with Slaty Blue Color of Skin

{Painted from Life)

PHYSICAL DIAGNOSIS

RICHARD C. CABOT, M. D.

ASSISTANT PROFESSOR OP MEDICINE IN HARVARD UNIVERSITY

3fiftb JEDition

REVISED AND ENLARGED, WITH 5 PLATES
AND 268 FIGURES IN THE TEXT

NEW YORK

WILLIAM WOOD AND COMPANY

MDCCCCXII

COPYBIGHT, 1912

By WILLIAM WOOD AND COMPANY

y^f=^S>

THE. MAPLE-PRESS. YORK. PA

FREDERICK C. SHATTUCK, M. D.

FORMERLY JACKSON PROFESSOR OF CLINICAL MEDICINE
IN HARVARD UNIVERSITY

IN EVIDENCE OF MY APPRECIATION OF

THE EXAMPLE OF SINCERITY, COMMON SENSE, AND ENTHUSIASM

ESTABLISHED BY HIM IN THE TEACHING AND

THE PRACTICE OF MEDICINE

Digitized by tine internet Archive

in 2011 with funding from

Open Knowledge Commons and Harvard Medical School

http://www.archive.org/details/physicaldiagnosi12cabo

PREFACE TO THE FIFTH EDITION.

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.

vi PREFACE

For the same reason the most important methods of investigat-
ing the stomach have been grouped together without any distinction
of "clinical" and "laboratory" procedure.

For the illustrations I owe many thanks to many persons, espe-
cially to Drs. Frank Billings, A. E. Boycott, E. H. Bradford, E. R.
Carson, J. Everett 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.

TABLE OF CONTENTS.

CHAPTER I.
DATA RELATING TO THE BODY AS A WHOLE.

Page

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

(d) Chills and Their Causes, 3,4

CHAPTER II.

THE HEAD, FACE, AND NECK.

I. The Cranial Vault, 5

1. Size, Shape, 5

2. Fontanels, 6

3. Hair, 6

II. The Forehead, 7

III. The Face as a Whole, 8

IV. Movements of the Head and Face, 13

V. The Eyes, 14

(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

vii

viii TABLE OF CONTENTS

CHAPTER III.
THE ARMS AND HANDS; THE BACK.

Page
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

CHAPTER IV.

THE CHEST.

TECHNIQUE AND GENERAL DIAGNOSIS.

Introduction.

I. Methods of Examining the Thoracic Organs, .61

II. Regional Anatomy of the Chest, 61

INSPECTION.

I. Size, 64

II. Shape, 64

(a) The Rachitic Chest, 65

(b) The Paralytic Chest, 65

III. Deformities, 67

(a) Curvature of the Spine, 67

(6) Flattening of One Side of the Chest 68

(d) Local Prominences, 69

TABLE OF CONTENTS ix

Page

IV. Respiratory Movements, 70

(a) Normal Respiration, 70

(b) Anomalies of Expansion, 71

1. Diminished Expansion, 71

2. Increased Expansion, 72

V. The Respiratory Rhythm, 74

(a) Asthmatic Breathing, 74

(b) Cheyne-Stokes Breathing, 75

(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

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

CHAPTER V.
PALPATION AND STUDY OF THE PULSE.

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

X TABLE OF CONTENTS

Page

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

CHAPTER VI.

ARTERIOGRAMS, PHLEBOGRAMS AND
ELECTROCARDIOGRAMS.

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

CHAPTER VII.

PERCUSSION.

I. Technique, 120

( \ J Mediate Percussion, 1

^ Immediate Percussion, J

(b) Auscultatory Percussion, 126

II. Percussion-Resonance of the Normal Chest, 128

(a) Vesicular Resonance, 128

(b) Dulness and Flatness, 129

(d) Cracked-pot Resonance, 134

(e) Amphoric Resonance, 135

if) The Lung Reflex, 135

III. Sense of Resistance, 136

CHAPTER VIII.
AUSCULTATION.

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

TABLE OF CONTENTS xi

Page

(b) Tubular Breathing, 150

(d) Emphysematous Breathing, 152

(e) Asthmatic Breathing, 153

(/) Cog-wheel Breathing, 153

(g) Amphoric Breathing, 154

(h) Metamorphosing Breathing, •I54

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

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

XI. Phenomena Peculiar to Pneumo-hydrothorax, 165

(a) Succussion, 165

(6) Metallic Tinkle, 165

CHAPTER IX.
AUSCULTATION OF THE HEART.

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

(d) Weakening of the Aortic Second Sound, 174

Second Sounds, 175

xii TABLE OF CONTENTS

Page

(d) Metallic Quality of the Heart Sounds, 176

0) "Muffled" Heart Sounds, 176

4. Sounds Audible Over the Peripheral Vessels, 177

CHAPTER X.

(Auscultation of the Heart, Continued.)

CARDIAC MURMURS.

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

CHAPTER XI.
DISEASES OF THE HEART.

VALVULAR LESIONS.

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

(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

TABLE OF CONTENTS xiii

Page

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

2. Differential Diagnosis, 230

V. Tricuspid Regurgitation, 232

1. (a) The Murmur, 233

(b) Venous Pulsation, 234

(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

CHAPTER XII.

PARIETAL DISEASE AND CARDIAC NEUROSES.

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

CHAPTER XIII.
DISEASES OF THE PERICARDIUM.

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

TABLE OF CONTENTS

Page
(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

CHAPTER XIV.

THORACIC ANEURISM.

x. Inspection and Palpation.

(a) Abnormal Pulsation, 263

(b) Tumor, 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

CHAPTER XV.
DISEASES OF THE LUNGS AND PLEURA.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS.

1. Tracheitis, 274

2. Bronchitis, 274

(a) Physical Signs, 274

(b) Differential Diagnosis, 276

3. Croupous Pneumonia, 277

(a) Inspection, 278

(b) Palpation, 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

(d) Anomalous Forms of Pulmonary Tuberculosis, 294

TABLE OF CONTENTS XV

CHAPTER XVI.

(Diseases of the Lungs, Continued.)

Page

i. Emphysema, 296

(a) Small- Lunged Emphysema, 296

(b) Large- Lunged Emphysema, 296

(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

(d) Microscopic Examination, 305

(e) Description of Commoner Organism, 307

CHAPTER XVII.

DISEASES AFFECTING THE PLEURAL CAVITY.

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

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

xvi TABLE OF CONTENTS

CHAPTER XVIII.

ABSCESS, GANGRENE, AND CANCER OF THE LUNG, PUL-
MONARY ATELECTASIS, (EDEMA, AND HYPOSTATIC
CONGESTION.

Page
i. Abscess and Gangrene of the Lung, 333

2. Cancer of the Lung, 334

3. Atelectasis, 335

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

CHAPTER XIX.

THE ABDOMEN IN GENERAL, THE BELLY WALLS, PERI-
TONEUM, OMENTUM, AND MESENTERY.

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

Ascites,

347

3. Cancer and Tuberculosis, 348

The Mesentery,

349

1. Glands, 349

2. Thrombosis, 349

CHAPTER XX.
THE STOMACH LIVER, AND PANCREAS.

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, 362

(b) Enlargement, 362

(d) Portal Obstruction, 366

(e) Jaundice, 367

(/) Loss of Flesh and Strength, 368

TABLE OF CONTENTS xvii

Page

(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

CHAPTER XXI.
THE INTESTINES, SPLEEN, AND KIDNEY.

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

(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

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

xviii TABLE OF CONTENTS

Page

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

CHAPTER XXII.
THE BLADDER, RECTUM, AND GENITAL ORGANS.

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

CHAPTER XXIII.

THE LEGS AND FEET.

The Legs, 424

I. Hip, 424

II. Groin, 424

III. Thigh, 425

IV. Knee,

429

V. (a) Lower Leg, 430

(b) The Feet, 433

CHAPTER XXIV.
THE BLOOD.

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

TABLE OF CONTENTS xix

Page

(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

CHAPTER XXV.
THE JOINTS.

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

CHAPTER XXVI.

THE NERVOUS SYSTEM.

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

PHYSICAL DIAGNOSIS.

CHAPTER I.

DATA RELATING TO THE BODY AS A WHOLE.

I. WEIGHT.

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

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) .

Under the head of malnutrition come the cases of oesophageal

2 PHYSICAL DIAGNOSIS

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.

II. TEMPERATURE.

The method of taking temperature is too familiar to need expla-
nation, but the student should be aware of the fact that hysterics
and malingerers can and often do raise the mercury in the bulb by
various manoeuvres, unless they are vigilantly watched. Dipping
the bulb into hot water, shaking the mercury upward toward the
higher degrees of the scale, and possibly friction with the tongue (?)
are to be suspected.

In comatose or 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 990 F., has much more diag-
nostic value in adults than in infancy and childhood. In the latter
it is often impossible to make out any pathological condition to
account for a fever. After childhood the vast majority of fevers
are found to be due to :

(a) Infectious disease or inflammation of any type.

(b) Toxaemia without infection — a much less common and less
satisfactory explanation. 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.

TEMPERATURE 3

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.

4 PHYSICAL DIAGNOSIS

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-
plained.

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
especially.

CHAPTER II.

THE HEAD AND FACE; THE NECK.
THE HEAD AND FACE.

Almost all that we can learn about the manifestations of disease
on the head and face is to be learned by the use of our eyes, by inspec-
tion, as the term is. 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.

6 PHYSICAL DIAGNOSIS

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

THE HEAD AND FACE 7

alopecia areata, and occasionally over the painful area in trigeminal
neuralgia.

(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.

:-■

'■■"■"

^'"M

' %

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.) .

8 PHYSICAL DIAGNOSIS

(c) Nodes may be the result of many bumps in childhood or may
be caused by a syphilitic periostitis or neoplasms (see Figs. 3, 4, 5
and 7) . The history must decide.

(d) Evidence of frontal sinusitis may be found (see Fig. 9).

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 ■

jjT

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-

THE HEAD AND FACE

Fig. 6. — Acromegalia.

Fig 7. — Gumma Involving Frontal Bone.

PHYSICAL DIAGNOSIS

? ™^BJ

■HH

^ ^Jm

II ■

• /

( 7>

Fig. 8. — Typical Face in Acromegaly.

Fig. 9. — Frontal Sinusitis.

Fig. 10. — Myxoedema.

THE HEAD AND FACE

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
legs.

(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
deafness.

(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

PHYSICAL DIAGNOSIS

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.

THE HEAD AND FACE

(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-

14 PHYSICAL DIAGNOSIS

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

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

THE HEAD AND FACE 15

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.

16 PHYSICAL DIAGNOSIS

(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
drugs.

(c) Contracted pupils are common in old age and in photophobia
from any cause. Disease high up in the spinal cord (tabes, general
paralysis, etc.) may produce contraction (spinal 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 HEAD AND FACE

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
cause.

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

PHYSICAL DIAGNOSIS

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.

THE HEAD AND FACE 19

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
suffices.

2. Cyanosis, a purplish or slatey-blue color of the lips, occurs in
some healthy persons from simple "weathering." When well marked,
however, it should always suggest: — (a) Heart disease (especially
mitral or congenital lesions) . — (b) Lung diseases (especially 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.)

PHYSICAL DIAGNOSIS

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. Epithelioma1 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
lesions.

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."

THE HEAD AND FACE

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.

22 PHYSICAL DIAGNOSIS

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.

(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
sputa.

Acetone breath has a faintly sweetish odor, which has been com-
pared to that of chloroform, new-mown hay, and rotting apples. It
occurs not only in diabetes, but in various conditions involving
starvation (vomiting, fevers), and especially, but not only, a lack of
carbohydrates.1

In 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.

THE HEAD AND FACE

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

(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.

24 PHYSICAL DIAGNOSIS

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
dots.

(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.

THE HEAD AND FACE

(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,

26 PHYSICAL DIAGNOSIS

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.

THE HEAD AND FACE 27

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.

28 PHYSICAL DIAGNOSIS

(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.

THE NECK 29

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.

XIV. THE NECK

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:

30 PHYSICAL DIAGNOSIS

(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
elsewhere.

(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

THE NECK 31

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
observation.

(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
other.

PHYSICAL DIAGNOSIS

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

THE NECK

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-
recognizable.

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.

Fig.

3i-

-Dislocation of the Cervical Vertebrae.
(Walton.)

34 PHYSICAL DIAGNOSIS

(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.

THE NECK

on the
aspira-

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

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

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-
charge.

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.

PHYSICAL DIAGNOSIS

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.

CHAPTER III.
THE ARMS AND HANDS; THE BACK.
THE ARMS.

Most of the lesions of these parts are joint lesions and are dealt
with in the section on joints. Others fall under the province of the
neurologist or the dermatologist, but must be briefly mentioned here.

/. 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
forearm.

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

PHYSICAL DIAGNOSIS

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
lesions.

Toxic Neuritis. — Lead or alcohol produces usually a weakness of
both forearms, especially the extensors of the wrist ("wrist-drop"),
but one side may be predominantly affected and other muscles are

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

THE ARMS J 39

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.

(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.

40 PHYSICAL DIAGNOSIS

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
tendon.

Fatty tumors are recognized by the history of long duration and
very slow growth, by their superficial position, usually external to the
muscles, and soft, lobulated feel.

Sarcoma forms the only large 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.

THE ARMS

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

Tuberculous lesions1 are much more common on the forearm bones,
but are occasionally seen on the humerus near the epiphyseal ends.
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
present.

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.

PHYSICAL DIAGNOSIS

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.

THE HANDS

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.)

THE HANDS.

I. Evidence of Occupation. — The horny, stiffened hands of
the "son of toil," the stains of paint in house painters, the flattened,
calloused finger-tips of the violinist, the worn fingers of the sewing

PHYSICAL DIAGNOSIS

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
origin.

(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.)

THE HANDS

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.
Hysteria.

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.

PHYSICAL DIAGNOSIS

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-

THE HANDS

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
follow.

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

PHYSICAL DIAGNOSIS

Fig. 44. — Tetany. (Masland.)

Fig. 45. — Tetany. (Masland.)

THE HANDS

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
4

PHYSICAL DIAGNOSIS

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

THE HANDS

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.

PHYSICAL DIAGNOSIS

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 HANDS

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-posterior1 (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.

PHYSICAL DIAGNOSIS

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

THE HANDS

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

PHYSICAL DIAGNOSIS

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
arthritis.

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
Illness.

THE BACK 57

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,
embolic.

THE BACK.

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-
teristic.

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

58 PHYSICAL DIAGNOSIS

ilium are forcibly pressed together, the pain in the joint is much
increased. Abscess formation is often the first distinctive sign. The
motions at the hip-joint are not restricted and the local signs of verte-
bral caries are absent. The duration of the disease, the local reaction
after tuberculin injection and the formation of abscess distinguish it
from other lesions of the sacro-iliac joint.

Goldthwait1 has 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.

THE BACK 59

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) .

60 PHYSICAL DIAGNOSIS

(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.

THE CHEST.

INTRODUCTION.

I. Methods of Examining the Thoracic Organs.

To carry out a thorough examination of the chest we do five
things: i. We look at it; technically called "inspection." 2. We
feel of it; technically called "palpation." 3. We listen to the sounds
produced by striking it; technically called "percussion." 4. We
listen to the sounds produced within it by physiological or pathological
processes; technically called "auscultation."
5. We study pictures thrown on the fluoroscopic
screen or on a photographic plate by the Roentgen
rays as they traverse the chest; technically
called "radioscopy."

Measuring the dimensions or 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.

62 PHYSICAL DIAGNOSIS

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)

INTRODUCTION

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.

Spleen.

Lower lobe.

Upper
lobe.

Middle
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).

CHAPTER IV.

TECHNIQUE AND GENERAL DIAGNOSIS.

INSPECTION.

Much may be learned by a careful inspection of all parts of the
chest, but only in case the clothes are wholly removed. A good light
is essential, 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

INSPECTION

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.
5

Fig. 63. — Funnel Breast.

PHYSICAL DIAGNOSIS

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.)

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

INSPECTION 67

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.

PHYSICAL DIAGNOSIS

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

INSPECTION

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

PHYSICAL DIAGNOSIS

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
outward.

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

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

IV. The Respiratory Movements.
(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.

INSPECTION
(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

PHYSICAL DIAGNOSIS

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.

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.

INSPECTION

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

PHYSICAL DIAGNOSIS

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.

INSPECTION

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

Fig.

wwwww

-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

76 PHYSICAL DIAGNOSIS

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.

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
discomfort.

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

INSPECTION 77

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 contain1 (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.

PHYSICAL DIAGNOSIS

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.

INSPECTION 79

Williams and others, much more easily and cheaply than with the
#-rays.

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
individual.

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.

PHYSICAL DIAGNOSIS

(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

r7<

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

INSPECTION

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
larger.

(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

82 PHYSICAL DIAGNOSIS

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

INSPECTION 83

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.

Summary.

The apex impulse is displaced by:

(a) Hypertrophy and dilatation of the heart,

(b) Pressure from below the diaphragm.

(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.

84 PHYSICAL DIAGNOSIS

(a) In by far the greater number of instances such retraction is
due to negative pressure produced within the chest by the vigorous
contraction of a more or less hypertrophied and dilated heart. In
these cases the retraction is usually balanced by an impulse in the
next interspace so that a "walking beam" appearance or tilting of a
piece of the chest wall results.

(b) In rarer cases several interspaces, both in the precordial
region and in the left lower axilla and back, may be drawn in as a
result of adhesions between the pericardium and the chest wall, such
as form in cases of adherent pericardium and fibrous mediastinitis1
(see below, pages 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.

INSPECTION

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.

86 PHYSICAL DIAGNOSIS

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
contractions.

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

INSPECTION

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.

88 PHYSICAL DIAGNOSIS

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
heart.

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

INSPECTION 89

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.

90 PHYSICAL DIAGNOSIS

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

INSPECTION 91

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.

(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
appearances.

92 PHYSICAL DIAGNOSIS

(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
pigmentation.

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-

INSPECTION

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.

CHAPTER V.

PALPATION AND THE STUDY OF THE PULSE.

I. Palpation.

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

(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
later.

(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).

PALPATION AND THE STUDY OF THE PULSE 95

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.

PHYSICAL DIAGNOSIS

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!?.

PALPATION AND THE STUDY OF THE PULSE

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
7

PHYSICAL DIAGNOSIS

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.

PALPATION AND THE STUDY OF THE PULSE

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.

100 PHYSICAL DIAGNOSIS

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.

PALPATION AND THE STUDY OF THE PULSE. 101

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.

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

102 PHYSICAL DIAGNOSIS

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
pressure).

PALPATION AND THE STUDY OF THE PULSE 103

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

104 PHYSICAL DIAGNOSIS

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).

PALPATION AND THE STUDY OF THE PULSE 105

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
cases.

Not infrequently the nurse reports in alarm that the patient has
no pulse, when in reality the pulse is excellent but the artery mis-
placed so as to be impalpable in the ordinary situation. It may be
simply more deeply set than normal, so that the fingers cannot get
at it, or it may run superficially over the end of the radius toward
the "anatomical snuff box." Other anomalies are less common.
As a rule, the other radial artery is normally placed and can be used
as a standard, but occasionally both radials are anomalous and we
may be compelled to use the temporal or facial instead.

7. The Condition of the Artery Walls.

Arterio-sclerosis1 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.

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.

106 PHYSICAL DIAGNOSIS

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.

PALPATION AND THE STUDY OF THE PULSE 107

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.

108

PHYSICAL DIAGNOSIS

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

K TUBS
K PRESSURE CONTROL

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
manometer.

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.

PALPATION AND THE STUDY OF THE PULSE

109

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.

110 PHYSICAL DIAGNOSIS

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
fragility.

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.

ARTERIAL PRESSURE 111

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.

112 PHYSICAL DIAGNOSIS

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.

CHAPTER VI.

ARTERIOGRAMS, PHLEBOGRAMS, AND
ELECTROCARDIOGRAMS.

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 monograph1 that "the mechanism
of the heart may be identified in the majority of cases in which it is
irregular by a careful examination of the radial pulse tracing alone.''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

114 PHYSICAL DIAGNOSIS

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.

(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

ARTERIOGRAMS, PHLEBOGRAMS, AND ELECTROCARDIOGRAMS 115

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 stethoscope1 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
disease.

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."

116 PHYSICAL DIAGNOSIS

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.

ARTERIOGRAMS, PHLEBOGRAMS, AND ELECTROCARDIOGRAMS 117

A-V JUNCTION

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

A-V JUNCTION

^
^

III

A-V JUNCTION

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.

118 PHYSICAL DIAGNOSIS

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

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.

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.

ARTERIOGRAMS, PHLEBOGRAMS, AND ELECTROCARDIOGRAMS 119

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).

CHAPTER VII.

PERCUSSION.

I. Technique.

There is no other method of physical examination which needs
so much practice as percussion, and none that is so seldom thor-
oughly learned. Many physicians never succeed in acquiring a
facility in the use of it sufficient to make them rely upon their results.
Undoubtedly one of the greatest difficulties arises from the necessity
of being at once active and passive — at once the percussor and the
one who listens to the percussion. Students half unconsciously get
to treat the percussion as an end in itself, and hammer away indus-
triously without realizing that two-thirds of the attention must be
given to listening, while the percussion itself should become semi-
automatic.

It is undoubtedly an advantage to possess a musical ear, but this
is by no means a necessity. Some of the most accurate percussors
that I know possess absolutely no musical ear — no ear, that is, for
pitch — and form their judgments in percussing upon the quality or
intensity of the note, and upon the sense of resistance.

In this country practically all percussion is done with the 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
ringer.

Methods.

Mediate percussion (which is used ninety-nine hundredths of the
time) is performed as follows:

The patient should either lie down or sit with his back against
some support. The reason of this is that for good percussion one
needs to press very firmly with the middle finger of the left hand

120

PERCUSSION 121

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

122

PHYSICAL DIAGNOSIS

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

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

PERCUSSION

123

chest with the second finger of the left hand1 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 finger2 of the right hand upon the second finger of the
left just behind the nail, imitating as far as possible with the right

Fig.

-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
obtained.

(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.

124

PHYSICAL DIAGNOSIS

(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-

PERCUSSION

125

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.

126

PHYSICAL DIAGNOSIS

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.

PERCUSSION 127

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
Stethoscope.

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.

Some German observers use a method of percussion in which
attention is fixed directly or primarily on the amount of resistance

128 PHYSICAL DIAGNOSIS

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
dulness.

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 "</»//"

PERCUSSION

129

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.
9

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

130 PHYSICAL DIAGNOSIS

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.

PERCUSSION 131

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.

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).

132 PHYSICAL DIAGNOSIS

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
side.

The normal resonance of the different parts of the chest can be
considerably modified by the position of the patient, by deep breathing,

PERCUSSION 133

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.

134 PHYSICAL DIAGNOSIS

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.

PERCUSSION 135

(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
space.

(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
areas.

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

136 PHYSICAL DIAGNOSIS

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.

CHAPTER VIII.
AUSCULATION.

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) .

(d) Because it is difficult to localize the different valvular areas
and the sites of cardiac murmurs if immediate auscultation is
employed.

On account of the latter objection the great majority of observers
now use the stethoscope to examine the heart. For the lungs, both
methods are employed by 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

137

138

PHYSICAL DIAGNOSIS

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.

AUSCULTATION

139

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

axilla.

(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.-
Stethoscope.
view.

Fig. 108. — Combination
Bowles' Stethoscope.

140 PHYSICAL DIAGNOSIS

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

AUSCULTATION

141

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
one.

142

PHYSICAL DIAGNOSIS

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
Stethoscope.

Having secured an
instrument which fits
the ears satisfactorily,
the beginner may get a
good deal of practice by
using it upon himself,
especially upon his own
heart. The chief point
to be learned is to dis-
regard various irrelevant
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-

AUSCULTATION 143

tion or concentration upon those sounds which we know to be of
importance.

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

(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

144 PHYSICAL DIAGNOSIS

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

AUSCULTATION 145

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,
10

146 PHYSICAL DIAGNOSIS

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

AUSCULTATION

147

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
need.

As a rule, the patient must be taught how to breathe deeply, which

148 PHYSICAL DIAGNOSIS

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.

AUSCULTATION.

149

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
expiration.

(3) The thickness of the up-stroke as compared with the down-
stroke represents the intensity of the inspiration as compared with
the expiration.

(4) The pitch of inspiration as compared with that of expiration
is represented by the sharpness of the angle which the up-stroke makes
with the perpendicular as compared with that which the down-stroke
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 — ■

150

PHYSICAL DIAGNOSIS

(a) More intense.

(&) Longer.

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
Breathing.

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

AUSCULTATION 15

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
pneumonia.

152

PHYSICAL DIAGNOSIS

(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
Breathing.

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.

AUSCULTATION

153

(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.

154 PHYSICAL DIAGNOSIS

(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.

AUSCULTATION 155

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

156 PHYSICAL DIAGNOSIS

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
chest.

AUSCULTATION 157

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

158 PHYSICAL DIAGNOSIS

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
"who."

VII. RALES.

The term "rales" is applied to sounds produced by the passage of
air through bronchi which contain mucus or pus, or which are narrowed
by swelling of their walls.1 Rales are best classified as follows:

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

(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.)

AUSCULTATION 159

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
bronchi.

In the majority of cases these rales are most numerous during
inspiration and especially during the latter part of this act. Their
relation to respiration may be represented graphically as in Fig. 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 pme 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.

160 PHYSICAL DIAGNOSIS

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.

AUSCULTATION 161

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
varieties.

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

162 PHYSICAL DIAGNOSIS

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

AUSCULTATION 163

around him. F. T. Lord1 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.

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

164 PHYSICAL DIAGNOSIS

(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.

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.

AUSCULTATION 165

XI. Phenomena Peculiar to Pneumohydrothorax and Pneumo-

PYOTHORAX.

(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.

166 PHYSICAL DIAGNOSIS

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
pneumopyothorax.

(3) The Lung-Fistula Sound.

When a perforation of the lung occurs below the level of the fluid
accumulated in the pleural cavity, bubbles of air may be forced out
from the lung and up through the fluid with a sound reminding one of
that made by children when blowing soap-bubbles.

CHAPTER IX.

AUSCULTATION OF THE HEART.

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

167

168 PHYSICAL DIAGNOSIS

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.

AUSCULTATION OF THE HEART 169

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.

170 PHYSICAL DIAGNOSIS

Over the tricuspid area one hears sounds practically indistinguish-
able in quality and in rhythm from those heard at the apex.1

When the chest walls are thick and the cardiac sounds feeble, it
may be difficult to hear them at all. In such cases the heart sounds
may be heard much more distinctly if the patient leans forward and
toward his own left. Such a position of the body also renders it
easier to,map out the outlines of the cardiac dulness by percussion if
we allow for the swing of the heart to the left.

In cardiac neuroses 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.

AUSCULTATION OF THE HEART 171

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.

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-
sclerosis.

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

Heart.

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.

172

PHYSICAL DIAGNOSIS

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

100%-

90%-
80%--
70/o— -

0-9

10-19

20-29

DECADES.
30-39 J40-49

50-59

60-69

70-79

-—100%

— 90%

— 80%

-—00%
—50%
—40%

— - 30*/

JO
O

a
m

30%—

20%-

10%-.

-—20%

—10^

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."

AUSCULTATION OF THE HEART

173

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

100%-
90%--
go*/

0-9

10-19

20-29

DECADES.
30-39 40-49

50-59

60-69

70-79

— Mxtf

—90%
-—-80%

TO%—

— «r.

--60%

-—50%
—-40%
-—30%
-—20%
--10%

33
O

O
m

30%-
20%-
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.

174 PHYSICAL DIAGNOSIS

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

AUSCULTATION OF THE HEART 175

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
significance.

(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

176 PHYSICAL DIAGNOSIS

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
collapse.

(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
breath.

In mitral stenosis the double diastolic sound is also to be heard at
the apex, and in the diagnosis of this disease this "double shock
sound" during diastole may be an important piece of evidence, and
may sometimes be felt and seen as well as heard. Just what its
mechanism is, is disputed. Except in mitral stenosis, it has no
especial clinical significance.

(4) Metallic Heart Sounds.

The presence of air in the immediate vicinity of the heart, as, for
example, in pneumothorax or in gaseous distention of the stomach or
intestine, may impart to the heart sounds a curious metallic quality
such as is not heard under any other conditions.
(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

AUSCULTATION OF THE HEART 177

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.

CHAPTER X.

AUSCULTATION OF THE HEART: CONTINUED.

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
"murmurs."

(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

178

AUSCULTATION OF THE HEART 179

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.)

180 PHYSICAL DIAGNOSIS

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.

AUSCULTATION OF THE HEART 181

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

182 PHYSICAL DIAGNOSIS

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-

AUSCULTATION OF THE HEART

183

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
ventricle.

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

184 PHYSICAL DIAGNOSIS

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

AUSCULTATION OF THE HEART 185

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.

186 PHYSICAL DIAGNOSIS

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
phenomena.

' ' 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.

AUSCULTATION OF THE HEART 187

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.

188 PHYSICAL DIAGNOSIS

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

AUSCULTATION OF THE HEART 189

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.

190 PHYSICAL DIAGNOSIS

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
it.

(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.

CHAPTER XI.
DISEASES OF THE HEART.

VALVULAR LESIONS.

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
wrong.

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").

191

192

PHYSICAL DIAGNOSIS

(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,

VALVULAR LESIONS

193

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.

Papillary
muscle.

Myocardium.

Pericardium.

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

Spalteholz.)

(After

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
itself.

194 PHYSICAL DIAGNOSIS

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.

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

VALVULAR LESIONS 195

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.

196 PHYSICAL DIAGNOSIS

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.

Causes.

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 :

Arterio-sclerosis

Nephritis

Valvular heart disease

Adherent pericardium

Hard work

Tumors

Aneurism

Polycytha;mia

10S

Cases.

Per c

ent.

13-4

VALVULAR LESIONS 197

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.

Results,
(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.

198 PHYSICAL DIAGNOSIS

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
hypertrophy.

Epigastric pulsation gives us no evidence of the existence of
hypertrophy of the right ventricle, despite contrary statements in
many text-books. Such pulsation is frequently to be seen in persons
with normal hearts, and is frequently absent when the right ventricle
is obviously hypertrophied. It is perhaps most often due to an
unusually low position of the whole heart.

VALVULAR LESIONS

199

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,

200 PHYSICAL DIAGNOSIS

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.

VALVULAR LESIONS 201

(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.

"-ZttjeaStrt/JftftaS

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).

202 PHYSICAL DIAGNOSIS

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
ventricle.

(2) The overfilled left auricle cannot receive the blood from the
lungs as readily as it should; hence the blood "backs up" in the lungs
and thereby increases the work which the right ventricle must do in
order to force the blood through them. Thus result oedema of the
lungs, and —

(3) Hypertrophy and dilatation of the right ventricle, which in
turn becomes sooner or later overcrowded so that 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,

VALVULAR LESIONS 203

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

204 PHYSICAL DIAGNOSIS

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:

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

2nd

_L_L

2nd

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

VALVULAR LESIONS 205

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

1st

2nd

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

206

PHYSICAL DIAGNOSIS

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
accented.

Systolic murmur
loudest here.

Fig.

147.

-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.

VALVULAR LESIONS 207

(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.

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

208 PHYSICAL DIAGNOSIS

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

VALVULAR LESIONS 209

sound,1 or any evidences of engorgement of the lungs or general venous
system.

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.
14

210

PHYSICAL DIAGNOSIS

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.

VALVULAR LESIONS

211

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
accented.

" Double-shock "
sound.

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.

212 PHYSICAL DIAGNOSIS

(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
regurgitation.

VALVULAR LESIONS 213

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.

II.

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
individuals.

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.)

214 PHYSICAL DIAGNOSIS

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.

2nd

II. Mil lilllllllllllllllllll I

1st

3rd

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) .

III.

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

VALVULAR LESIONS 215

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.

216 PHYSICAL DIAGNOSIS

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.

VALVULAR LESIONS 217

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

218

PHYSICAL DIAGNOSIS

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

VALVULAR LESIONS 219

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

220 PHYSICAL DIAGNOSIS

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|Fvv/~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

VALVULAR LESIONS 221

inequality in the pressure made by the observer upon the glass slide
or upon the nail. Very slight movements of the observer's fingers,
even such as are caused by his own pulse, may give rise to changes
simulating capillary pulsation. Capillary pulsation of normal tissues
is not often seen in any condition other than aortic1 regurgitation,
yet occasionally one meets with it in diseases which produce very low
tension of the pulse, such as Graves' 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.

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.

222 PHYSICAL DIAGNOSIS

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.

Percussion adds but little to the information obtained by inspec-
tion and palpation, but verifies the results of these methods of investi-
gation respecting the increased size of the heart, and especially of the
left ventricle, which may reach enormous dimensions, especially in
cases occurring in young persons. The heart may be increased to
more than four times its normal weight.

Auscultation.

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.

VALVULAR LESIONS

223

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
heard.

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).

224 PHYSICAL DIAGNOSIS

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

2nd

12nd

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.

VALVULAR LESIONS 225

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.

(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) .

226 PHYSICAL DIAGNOSIS

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.

Complications.

(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.

VALVULAR LESIONS

227

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.

228 PHYSICAL DIAGNOSIS

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.

VALVULAR LESIONS 229

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
222).

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.

230 PHYSICAL DIAGNOSIS

"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.

(d) Functional murmurs.

(e) Pulmonary stenosis.

(/) Open ductus arteriosus, and other congenital lesions.

VALVULAR LESIONS 231

(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

232 PHYSICAL DIAGNOSIS

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.

VALVULAR LESIONS 233

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

234 PHYSICAL DIAGNOSIS

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

VALVULAR LESIONS 235

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.

236 PHYSICAL DIAGNOSIS

(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"

between.

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

VALVULAR LESIONS 237

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 ah. 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.

238 PHYSICAL DIAGNOSIS

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
Steell.

From the diastolic murmur of aortic regurgitation we may dis-
tinguish the diastolic murmur of pulmonary incompetency by the
fact that the latter is best heard over the pulmonary valve, is never
transmitted to the apex of the heart nor to the great vessels, and is
never associated with a Corrigan pulse nor with capillary pulsation.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.

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
lungs.

VALVULAR LESIONS 239

(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
mediastinum.

(/) 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

240 PHYSICAL DIAGNOSIS

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
lesion.

It is a good rule not to multiply causes unnecessarily, and to
explain as many signs as possible under a single hypothesis. In
the above example the mitral leak might be due to an old 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

1st

2nd

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

VALVULAR LESIONS

241

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
visible.

242 PHYSICAL DIAGNOSIS

(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.

CHAPTER XII.

PARIETAL DISEASE.-CARDIAC NEUROSES.-

CONGENITAL MALFORMATIONS OF

THE HEART.

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
dilatation.

1 Henchen's recent monograph on this subject," Ueber die acute Herzdilatation bei
acuten Infectionskrankheiten," Jena, 1899, does not seem to me convincing.

243

244 PHYSICAL DIAGNOSIS

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.

PARIETAL DISEASE 245

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.

Summary.

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.

(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

246 PHYSICAL DIAGNOSIS

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 247

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

248 PHYSICAL DIAGNOSIS

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
character.

Bradycardia (Slow Heart).

In many healthy adults the heart seldom beats over 50 times a
minute.

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
dyspepsia.

(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).

Arrhythmia.

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.

DISTURBANCES OF RHYTHM 249

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.

Palpitation.

Best defined as an "irregular or forcible heart action perceptible
to the individual." The essential point is that the individual becomes

250 PHYSICAL DIAGNOSIS

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.

(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:

CONGENITAL HEART DISEASE 251

(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.

(d) An increased area of cardiac dulness corresponding to the right
ventricle.

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
cases.

(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

252 PHYSICAL DIAGNOSIS

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.

(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.

CHAPTER XIII.
DISEASES OF THE PERICARDIUM.

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

253

254 PHYSICAL DIAGNOSIS

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

DISEASES OF THE PERICARDIUM 255

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.

256

PHYSICAL DIAGNOSIS

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
pulse.

(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

DISEASES OF THE PERICARDIUM

257

patient, but also on the amount of "give" in the pericardium and in
the lungs, as well as on the size of the lingula pulmonalis. Allowing
for these uncertain factors, we may say: (a) One of the most charac-
teristic points is the unusual1 extension of the percussion dulness a
considerable distance to the left of the maximum cardiac impulse.
(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
liver.

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.
17

258 PHYSICAL DIAGNOSIS

In some cases the area of dulness may be modified by change in the
patient's position. After marking out the area of percussion dulness
with the patient in the upright position, let him lie upon his right side.
The right border of the area of dulness will sometimes move consider-
ably farther to the right. A dilated heart can be made to shift in a
similar way, but to a lesser extent. Comparatively little change takes
place if the patient lies on his left side, and no important information
is elicited by placing him flat on his back or by getting him to lean
forward.

Unfortunately, it is only with moderate-sized effusions occurring
in a pericardial sac free from adhesions to the surrounding parts that
this shifting can be made out. Large effusions may not shift appre-
ciably, and less than 150 c.c. of fluid probably cannot be recognized by
this or by any other method. But with large effusions the lateral
extension of the area of dulness may be so great as to be almost dis-
tinctive in itself, i.e., from the middle of the left axilla nearly to the
right nipple.

(2) Feebleness of the heart sounds and of the apex impulse is of
diagnostic importance only when it gradually takes the place of the
normal phenomena as one watches the heart from day to day. Under
these conditions they have some confirmatory value in the diagnosis
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

DISEASES OF THE PERICARDIUM 259

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.

260 PHYSICAL DIAGNOSIS

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
by

(a) A systolic retraction of the chest wall in the region of the apex
impulse, at the base of the left axilla and in the region of the eleventh
and twelfth ribs in the left back (Broadbent's sign). Such retraction
is more marked during a deep inspiration. (It should be remembered
that systolic retraction of the interspaces in the vicinity of the apex
is very commonly seen in cases of cardiac hypertrophy from any cause,
owing to the negative pressure produced within the chest by the
contraction of a powerful heart.) A quick rebound of the cardiac
apex at the time of diastole (the diastolic shock) is said to be character-
istic of pericardial adhesions, but is often absent.

(b) Collapse of the cervical veins during diastole has been noticed
by Friedreich, and the paradoxical pulse, above described, is said to
be more marked in adherent pericardium than in any other known
condition. Most recent writers, however, place no reliance 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.

DISEASES OF THE PERICARDIUM

261

(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.

262 PHYSICAL DIAGNOSIS

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.

(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.

CHAPTER XIV.

THORACIC ANEURISM.

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.

Tumor.

If the aneurism involves the ascending portion of the aortic arch,
it is likely sooner or later to erode the right margin of the sternum and
the adjacent parts of the second or third costal cartilages and appear

263

264

PHYSICAL DIAGNOSIS

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.

Thrill.
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

THORACIC ANEURISM

265

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

266 PHYSICAL DIAGNOSIS

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.

THORACIC ANEURISM 267

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

Aneurismal
dulness.

-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

268

PHYSICAL DIAGNOSIS

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.

Summary.

The most important signs of aneurism are:

1. Abnormal pulsation — visible or palpable

2. Tumor over which a

3. Thrill and a

THORACIC ANEURISM

269

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-

270

PHYSICAL DIAGNOSIS

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

THORACIC ANEURISM

271

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

272

PHYSICAL DIAGNOSIS

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

THORACIC ANEURISM 273

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.

CHAPTER XV.

DISEASES OF THE LUNGS.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS.
I. Tracheitis.

In connection with bronchitis or as a forerunner thereof, inflam-
mation of the trachea is not uncommon. It gives rise to no charac-
teristic physical signs, but is to be suspected when the patient com-
plains of cough with pain over the upper portion of the sternum.

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.

274

BRONCHITIS, PNEUMONIA, TUBERCULOSIS 275

rales are much less often heard than the finer, crackling variety. The
latter are produced in the smallest tubes, the former in the larger
variety.

Simple non-tuberculous bronchitis is almost invariably bilateral
or symmetrical, and affects most often the lower two-thirds of the
lungs, leaving the apices relatively free. It is almost never confined
to an apex. When rales are to be heard on one side of the chest only,
and when they persist in the same spot for days and weeks, tuberculosis
is always to be suspected, especially if the rales are localized at the
summit of one or both lungs. 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.

276

PHYSICAL DIAGNOSIS

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.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS 277

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

278 PHYSICAL DIAGNOSIS

plugged with fibrin and leucocytes, is a relatively rare form of the
disease, but possesses great clinical importance on account of the
marked resemblance between its physical signs and those of pleural
effusion.

The 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.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS 279

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

280

PHYSICAL DIAGNOSIS

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 resolution1 ("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.

Solidification.

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.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS 281

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
axilla.

In examining the posterior lobes, when the patient is too weak
to sit up and is loath even to turn upon the side, the Bowles stetho-
scope is a great convenience, owing to the ease "with which its flattened
extremity may be worked in between the 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.

Summary.

In a typical case one finds (oftenest at the right base behind)

1. Dulness on percussion.

2. Increased tactile fremitus and voice sounds.

3. Tubular breathing and occasionally crepitant rales.

These signs occurring in connection with fever, cough, rusty sputa,
pain in the side, dyspnoea, herpes and leucocytosis are sufficient
for the diagnosis.

But many cases are not typical when first seen. The following
are the commonest anomalies:

(a) There may be tympany instead of dulness, especially in children
or when the solidification is at the left base.

282 PHYSICAL DIAGNOSIS

(6) The breathing may be feeble but vesicular in character, or it
may be absent, in case bronchi are plugged; from the same cause,

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.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS 283

(2) Tuberculosis of the lung causing, as it may, a diffuse solidifica-
tion of the organ, may be indistinguishable from pneumonia if we
take account only of the physical signs, but the two diseases can usually
be distinguished without difficulty by the difference in their symptoms
and course, and by the presence or absence of tubercle bacilli in the
sputum.

(3) Compression of the left lung by a pericardial effusion and of
either lung by some subdiaphragmatic lesion (perinephric abscess,
hepatic abscess) often simulates pneumonia, indeed the physical signs
may be indistinguishable. Diagnosis depends mostly on establishing
the presence or absence of a cause for such compression.

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.

Broncho-Pneumonia.

(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
course.

The solidified lobules may fuse so as to form considerable areas of
hepatized lung, or there may be no lesion larger than a pea.

This is the usual type of " lung fever " in infants, although ordinary
lobar pneumonia is fully as common in older children.

The widespread atelectasis of the lower lobes which is associated

284 PHYSICAL DIAGNOSIS

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
bronchitis.

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-

BRONCHITIS, PNEUMONIA, TUBERCULOSIS 285

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
hemorrhage.

286

PHYSICAL DIAGNOSIS

(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
breathing").

(a) In examining the apices of the lungs for evidence of early
tuberculosis one should secure if possible perfect quiet in the room, and
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.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS 287

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
itself.

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.

288 PHYSICAL DIAGNOSIS

(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. _

Partial
-\~~ 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) .

(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.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS

289

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

290 PHYSICAL DIAGNOSIS

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
resistance.

2. Great increase of voice sounds or of tactile fremitus.

3. Tubular breathing, sometimes loud, sometimes feeble.

4. As a rule, coarse rales, due to breaking down of the caseous
tissue, are also to be heard over the solidified areas. Sometimes these
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
there.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS

291

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
sounds.

Rales.

■ 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

292 PHYSICAL DIAGNOSIS

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.

(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.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS 293

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) .

(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.

294 PHYSICAL DIAGNOSIS

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.

BRONCHITIS, PNEUMONIA, TUBERCULOSIS 295

The summit of the axilla should always be carefully examined, as
tuberculous foci may be so situated as to produce signs only at that
point.

Another point often overlooked in physical examination is the
lingula pulmonalis or tongue-like projection from the anterior margin
of the left lung overlapping the heart. Tuberculosis is sometimes
found further advanced at this point than anywhere else.

As a rule cases in which signs like those of phthisis are found at the
base of the lung turn out to be either empyema, 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.

CHAPTER XVI.

EMPHYSEMA, ASTHMA, PULMONARY
SYPHILIS, ETC.

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
mentioned.

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 Ludwig1 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.

296

EMPHYSEMA, ASTHMA, PULMONARY SYPHILIS, ETC. 297

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

298 PHYSICAL DIAGNOSIS

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- iowering of its pitch (see Fig. 189).

gram o us ra e This type of breathing is like bronchial breath-

Lmphysematous J ■*■ °

Breathing with Musi- 'mS 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.

Summary.

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.

• EMPHYSEMA, ASTHMA, PULMONARY SYPHILIS, ETC. 299

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

300 PHYSICAL DIAGNOSIS

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.

BRONCHIAL ASTHMA.
(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

EMPHYSEMA, ASTHMA, PULMONARY SYPHILIS, ETC. 301

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
asthma.

(b) Spasm of the glottis produces a noisy dyspnoea, but the diffi-
culty is with inspiration, instead of with expiration, and the crowing
or barking sound is not like the long wheeze of asthma. No rales are
to be heard, and the signs in the lungs are those of collapse instead of
the distention characteristic of asthma.

(c) The paroxysmal attacks of dyspnoea, which often occur in
chronic nephritis, 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.

SYPHILIS OF THE LUNG.

The diagnosis cannot be made with certainty from the physical
signs, and rests entirely (in the rare cases in which it is made at all)
on the history, the evidence of syphilis elsewhere in the body, and the
result of treatment. Most cases are mistaken for phthisis.

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.

302 PHYSICAL DIAGNOSIS

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
solidification.

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.

EMPHYSEMA, ASTHMA, PULMONARY SYPHILIS, ETC. 303

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.

EXAMINATION OF SPUTA.

1. Origin. — Probably the majority of all sputa, excepting tobacco
juice, come from the nasopharynx, and are hawked, not coughed up.
It is rarely of value to examine such sputa, although influenza bacilli,
diphtheria bacilli, pneumococci, and other bacteria may be found.

What we want in most cases is sputa coughed up from the primary
bronchi or lower down, and the patient should be accordingly 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.

304 PHYSICAL DIAGNOSIS

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
either

(1) Tawny-yellow or fawn-colored ("rusty"), or

(2) Orange-juice colored (not orange, but pale straw-colored).
These colors, associated with great tenacity, so that the sputum

clings to the lips and does not fall from an inverted sputum-cup, are
almost pathognomonic of pneumonia — though pneumonia often
occurs without any such sputa.

(d) Black or gray sputum is due to carbon, dust, or tobacco smoke
inhaled.

(e) Pure pus — not muco-purulent — is oftenest seen in influenza
and bronchiectasis, occasionally in empyema breaking through the
lung.

(/) 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:

EMPHYSEMA, ASTHMA, PULMONARY SYPHILIS, ETC. 305

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. H2S04.

5. Wash in water and then in ninety-five-per-cent. alcohol for thirty
seconds or until the color ceases to come out.

6. Wash in water and cover with Loffler's methylene blue2 for
about thirty seconds.

7. Wash in water, dry on blotting paper, and mount in Canada
balsam.

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 specimens3 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.
20

306

PHYSICAL DIAGNOSIS

i. Prepare a smear as above directed.

2. Cover it with anikne-oil-gentian-violet solution1 (freshly
made each week) and heat to steaming point.

3. Wash in water and cover with IKI solution2 for thirty seconds.

4. Wash in ninety-five-per-cent. alcohol until the blue color ceases
to come out.

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.

EMPHYSEMA, ASTHMA, PULMONARY SYPHILIS, ETC. 307

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).

CHAPTER XVII.

DISEASES AFFECTING THE PLEURAL CAVITY.

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.

308

DISEASES AFFECTING THE PLEURAL CAVITY 309

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 less 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,

310 PHYSICAL DIAGNOSIS

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's1 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 Emerson2 and
James1 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.

DISEASES AFFECTING THE PLEURAL CAVITY 311

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
stationary.)

Differential Diagnosis.

The distinction between pneumothorax and emphysema has
already been discussed.

312 PHYSICAL DIAGNOSIS

(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

faint

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.

DISEASES AFFECTING THE PLEURAL CAVITY

313

(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.

PLEURISY.

Clinically, we deal with three types:
(a) Dry or plastic pleurisy.
(6) Pleuritic effusion, serous or purulent,
(c) Pleural thickening.

314

PHYSICAL DIAGNOSIS

(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
pain.

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
Heard.

what was there said.

DISEASES AFFECTING THE PLEURAL CAVITY 315

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-

316 PHYSICAL DIAGNOSIS

tion. Since it is usually the results of percussion which first put us on
the right track, I shall take up first

Percussion.

i. A small effusion first shows as an area of dulness

(a) Just below the angle of the scapula.

(b) In the left axilla between the fifth and the eighth rib.

(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

Heart.

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.

DISEASES AFFECTING THE PLEURAL CAVITY

317

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
breathing.

Tympany, voice and ._
fremitus increased.

Flatness, no breath-
ing, voice sounds,
or fremitus.

Zone of condensed
lung above the
fluid.

Exaggerated (com-
pensatory) breath-
ing and reso-
nance.

Fig. 196. — Diagram to Illustrate Physical Signs in Moderate-Sized Effusion in the Left

Pleura.

The pitch changes if the patient opens and closes his mouth while
we percuss ("William's tracheal tone").

The dulness over the lower portions of a large effusion is usually
very marked, and the percussing finger feels a greatly increased 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

318

PHYSICAL DIAGNOSIS

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

DISEASES AFFECTING THE PLEURAL CAVITY 319

or weeks in bed, we should never begin the examination at once, since
it may take some minutes for the lungs and the fluid to accommodate
themselves to the new position. It is well also to get the patient to
cough and to take a number of full breaths before the examination is
begun.

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

320 PHYSICAL DIAGNOSIS

dulness at the right sternal margin from that which may be produced
in right-sided effusions by the fluid itself (see above) .

As mentioned above, a right pleural effusion may very early show
itself as an area of dulness along the right sternal margin. Light
percussion will usually demonstrate that this dulness is continuous
with a narrow strip of flatness at the base of the axilla (ninth and
tenth ribs). Such an effusion is late in creeping up the axilla. It
appears first and 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.

Auscultation.

The auscultatory phenomena vary greatly in different cases, and
in the same case at different times, because the essential conditions

DISEASES AFFECTING THE PLEURAL CAVITY . 321

are subject to similar variations. Whatever sounds are produced in the
lungs or in the bronchi may be heard over the fluid unless interfered
with by inflammatory thickening of the costal pleura. Fluid transmits
sounds well, but there may be no breath sounds produced and hence none
audible over the fluid. Or tubular sounds only may be produced
because only the bronchi remain open, the rest of the lung being
collapsed.

Or again, if rales or friction sounds are produced in the lung, they,
too, may be transmitted to the fluid and may (alas!) deter the timid
"observer" from tapping.

In about two-thirds of all large effusions no breathing at all is
audible over the area of flatness on percussion. In the remaining
third, and especially in children, tubular breathing, sometimes feeble,
sometimes very intense, is to be heard.

In moderate effusions there are often three zones in the back. At
the bottom we hear nothing, in the middle zone distant bronchial or
broncho-vesicular breathing, while at the summit of the chest the
breathing is normal.

The voice sounds correspond. When breath sounds are absent,
the voice sounds are likewise absent. When the breathing is tubular,
the voice, and especially the whisper, is also tubular and intensified.
That is, whenever the bronchi are open, the lung retracted, and
the chest walls thin, the breathing, voice, and whisper will correspond
to the tracheal sounds. Since children have especially thin chest
walls, these 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.
21

322

PHYSICAL DIAGNOSIS

cases the patient should always be made to cough and then breathe
deeply before the examination is completed.

In very large effusions, when only the primary bronchi are open,
there may be signs like those of pulmonary cavity at the site of the
bronchi in front or behind (amphoric breathing, large metallic rales,
etc.). Over the sound lung the breathing is exaggerated and extends
unusually far down in the back and axilla, owing to hypertrophy of the
lung.

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

DISEASES AFFECTING THE PLEURAL CAVITY 323

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
heart.

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.

324 PHYSICAL DIAGNOSIS

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.

DISEASES AFFECTING THE PLEURAL CAVITY

325

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-
ness.

Flatness.
Diminished or absent

breathing.
Diminished or absent

voice.

XtAA1 ^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
diagnosed.

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 :

326 PHYSICAL DIAGNOSIS

(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
made.

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

DISEASES AFFECTING THE PLEURAL CAVITY 327

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
pleura.

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

328

PHYSICAL 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
described.

(2) It is sometimes almost impossible to distinguish small fluid
accumulations in the pleural cavity from pleural thickening with
pulmonary atelectasis. In both conditions one finds dulness, diminu-
tion of the voice sounds, respiration, and tactile fremitus, and absence

Fig. 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

DISEASES AFFECTING THE PLEURAL CAVITY 329

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
are:

1. The presence of bloody fluid with any endothelial sediment.

2. Its rapid and repeated reaccumulation.

3. Metastases (supraclavicular, axillary, pectoral) and along the
needle-track.

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.

330 PHYSICAL DIAGNOSIS

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.

DISEASES AFFECTING THE PLEURAL CAVITY 331

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
drops.

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.

332

PHYSICAL DIAGNOSIS

make up from seventy to ninety-nine per cent — usually over ninety
per cent — of all the cells found in the smear1 (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
sporadic.

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.

CHAPTER XVIII.

ABSCESS, GANGRENE, AND CANCER OF THE

LUNG, PULMONARY ATELECTASIS, (EDEMA,

AND HYPOSTATIC CONGESTION.

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
suspected.

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.

333

334 PHYSICAL DIAGNOSIS

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 Christian1 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.

ATELECTASIS 335

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.

Atelectasis.

(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

336 PHYSICAL DIAGNOSIS

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
intensity.

Dulness on percussion and modification of voice sounds are not
present, unless hydrothorax or hypostatic pneumonia complicate the
oedema.

HYPOSTATIC PNEUMONIA 337

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.

The right lung is apt to be more extensively affected than the left.

Occasionally the breathing is tubular and the voice sounds are in-
creased, making the physical signs identical with those of croupous
pneumonia, but as a rule the bronchi are as much engorged as the alve-
oli to which they lead, and hence no breath sounds are produced.

Rales of oedema or of bronchitis may be present in the adjacent
parts of the lungs. The fact that the dulness is less marked at the
base of the lung than higher up helps to distinguish the condition from
hydrothorax.

The diagnosis is usually easy, owing to the presence of the under-
lying disease. Fever, pain, and cough such as characterize croupous
pneumonia are usually absent.

CHAPTER XIX.

THE ABDOMEN IN GENERAL, THE BELLY

WALLS, PERITONEUM, OMENTUM, AND

MESENTERY.

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.

338

THE ABDOMEN IN GENERAL 339

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.

(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. Richardson1 has shown that they often
contain bunches of typhoid bacilli. The spots are present in about
three-fourths of all cases, and, while they also may occur in any dis-
ease when the blood contains bacteria (e.g., sepsis), they are common-
est in typhoid.

2. Distended and tortuous veins on the abdomen are seen in dis-
eases obstructing the portal circulation (rarely in cirrhotic liver) or
the inferior cava (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..

340 PHYSICAL DIAGNOSIS

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. :

(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.

THE ABDOMEN IN GENERAL 341

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 no0 and 1200 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
felt.

342

PHYSICAL DIAGNOSIS

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

THE ABDOMEN IN GENERAL 343

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
note:

(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,

344

PHYSICAL DIAGNOSIS

while the tumor itself remains motionless or nearly so. Tumors con-
nected with the stomach, omentum, liver or spleen move about two
inches with a forced inspiration. Kidney tumors move less, seldom
as much as an inch. Pancreatic and retroperitoneal tumors have
scarcely any mobility. Those connected with the. intestine vary con-
siderably in respiratory mobility, according to the presence and degree
of adherence to other parts, but their excursion is rarely an inch.

Peritoneal crepitus is a grating, rubbing sensation experienced on
light palpation, and due — supposedly — to the presence of a plastic,
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
palpation.

THE ABDOMEN IN GENERAL 345

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

346 PHYSICAL DIAGNOSIS

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
manifestations.

The pain may be at first diffuse, later localizing itself at the site of
the lesion; or it may be felt first where the peritonitis begins and spread
with the lesion if the general peritoneal cavity becomes involved. The
character and intensity of the pain vary greatly.

1 Some of these were so small as hardly to deserve classification as tumors.

2 Rarely produces a palpable tumor but is here mentioned for convenience.

THE ABDOMEN IN GENERAL 347

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
albumosuria.

The commonest causes of local peritonitis are:

1. Appendicitis.

2. Pus tube.

3. Gall-bladder inflammation.

Less common is cancer or ulcer of the stomach or intestine.

2. General Peritonitis. — The belly may be generally swollen and
tympanitic or retracted and hard. General tenderness is the most im-
portant sign. In advanced cases free fluid in the flanks may be demon-
strated, 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.

348

PHYSICAL DIAGNOSIS

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.

THE ABDOMEN IN GENERAL 349

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.

CHAPTER XX.

THE STOMACH, LIVER, AND PANCREAS.

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.

350

THE STOMACH, LIVER, AND PANCREAS

351

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
finger.

(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

Stomach.

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

352

PHYSICAL DIAGNOSIS

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

THE STOMACH, LIVER, AND PANCREAS 353

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
here.

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
easily.

2. Great and long-continuing relief is obtained by dilating the
stricture a few times with water pressure inside a silk covered rubber
bag.

Radiography of a bismuth meal and the use of the 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
passed.

Diverticulum of the Esophagus. — Most diverticula are so high up in
the gullet that they are easily recognized by radiography and sounding.
The rarer diverticula low down in the 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.
23

54 PHYSICAL DIAGNOSIS

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 meal1
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.

THE STOMACH, LIVER, AND PANCREAS 355

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

356 PHYSICAL DIAGNOSIS

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
water.

Chemical Tests of Gastric Contents.

1 . Dip a piece of blue litmus in the contents; if no reddening occurs,
no further tests need be made.

2. If the contents are acid to litmus, test with Giinzburg's reagent
(phloroglucin, 2 gm.; vanillin, 1 gm.; alcohol, 30 gm.), by mixing two
drops of it with an equal amount of gastric contents (unfiltered) upon
a white porcelain plate or dish, and evaporating slowly over a flame.1
If free HC1 is present, a bright rose pink appears. In the absence of
free HC1, the color is a dirty yellowish-brown.

If this test is positive, we need make no further tests except the
following:

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.

THE STOMACH, LIVER, AND PANCREAS 357

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
contents.

The estimation of combined HCl and of the acid salts is seldom of
importance.

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
contents.

358

PHYSICAL DIAGNOSIS

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

fef^fl

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-

THE STOMACH, LIVER, AND PANCREAS

359

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.

360 PHYSICAL DIAGNOSIS

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

Dyspepsia1 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).

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.

THE STOMACH, LIVER, AND PANCREAS 361

(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

362 PHYSICAL DIAGNOSIS

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-

THE STOMACH, LIVER, AND PANCREAS 363

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 adults2), 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.)

364 PHYSICAL DIAGNOSIS

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 disease1 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.

THE STOMACH, LIVER, AND PANCREAS 365

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) .

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)

366 PHYSICAL DIAGNOSIS

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. Ascites1 (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.

THE STOMACH, LIVER, AND PANCREAS 367

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.

368 PHYSICAL DIAGNOSIS

6. Enlargement of the liver with jaundice lasting for years in
young people is probably due to biliary cirrhosis, or family hemolytic
jaundice.

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.

THE STOMACH, LIVER, ADD PANCREAS 369

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

370 PHYSICAL DIAGNOSIS

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

In the first of these jaundice is rarely present (ten to fifteen per
cent — Riedel2) , and colic with or without palpable tumor is our guide
to diagnosis.

In cancerous obstruction there is intense and permanent jaundice.

In cholecystitis there is usually no jaundice, but all the signs of
local and general infection — pain, tenderness, leucocytosis, and fever —
are present. In acute cases the symptoms, however, may be indis-
tinguishable from those of appendicitis, since the pain may be referred
to the navel or even to the appendix region. Many mistakes of
diagnosis between appendicitis and acute cholecystitis occur, and
must occur until our present diagnostic resources are increased.

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.

THE STOMACH, LIVER, AND PANCREAS 371

(&) 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
structures.

Indirect and uncertain information is afforded by the presence in
the urine of sugar or fat-splitting ferments1 and in the stools by the
appearance of an abnormal amount of muscle fibre or of fat not other-
wise to be accounted for (i.e., in the absence of jaundice, diarrhoea,
tuberculous peritonitis, or large meals of fat) .

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

JThe suspected urine is neutralized with potassium hydroxide and one portion of it
boiled to destroy any ferment that may be present. To this and to the unboiled portion
ethyl butyrate is added. In twenty-four hours an acid reaction may appear in the unboiled
specimen if it contains a ferment, while the other specimen shows no considerable change in
reaction.

372 PHYSICAL DIAGNOSIS

pressure effects, and may be associated with glycosuria and fatty
stools.

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):

Cases

Cancer of the pancreas 35

Acute pancreatitis 13

Chronic pancreatitis 10

Cyst of the pancreas 3

Total 61

CHAPTER XXI.
THE INTESTINE, SPLEEN, KIDNEY.

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
gas.

3. Diarrhoea or constipation.

4. Muscular rigidity of the belly wall protecting an intestinal lesion.

5. Tumor, palpable or visible, and believed to be connected with
the intestines (together with the 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
378).

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-

373

374

PHYSICAL DIAGNOSIS

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.

THE INTESTINE, SPLEEN, KIDNEY 375

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).

(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 important1 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
tumor.

2. The general or constitutional signs are fever, chill, rapid pulse,
vomiting, constipation, frequency or cessation of micturition, and
leucocytosis.

1 Tuberculous enteritis and pericaecal tuberculosis will be briefly referred to later.

376 PHYSICAL DIAGNOSIS

(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
vagina.

(e) The constitutional signs may or may not be marked, according
to the duration of the process, its virulence, and the degree of infection
of the peritoneal cavity. The fever is usually moderate, under 102. 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

THE INTESTINE, SPLEEN, KIDNEY 377

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
constipation.

By physical signs alone I do not believe that general peritonitis
and acute intestinal obstruction can always be distinguished. Fever
is not distinctive of general peritonitis, for it occurred in eighty-four
out of one hundred and twenty-two cases of acute obstruction in the
Massachusetts Hospital records, and in forty- three of these cases free
fluid in the peritoneal cavity was demonstrated as well. Stercoraceous
vomiting may occur in general peritonitis; it was absent in three-
fourths of the Massachusetts Hospital cases of obstruction. Weak,
rapid pulse, cold extremities, and a drawn, anxious face are common
to both diseases. Tenderness is more general and more marked in
general peritonitis than in simple obstruction, yet some tenderness was
complained of in fifty-six out of the one hundred and twenty-two cases
of obstruction just cited.

On the whole, the differential diagnosis of these two diseases seems
to depend far more on the history and the etiology than on physical
signs.

(b) Chronic Obstruction. — Here the diagnosis is simpler. There is
usually a history of increasing constipation sometimes interrupted by
occasional attacks of diarrhoea.1 Tumor is palpable in fifty-eight per
cent of cases. Visible peristalsis was recorded in seventeen per cent,
of the Massachusetts Hospital cases. Distention is gradual and late,
but often persists 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.

378 PHYSICAL DIAGNOSIS

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
chocolate.

(e) Bloody red — if in small amount and fresh, usually due to
hemorrhoids; in large amounts it may also be due to hemorrhoids or
to any of the causes of intestinal ulceration (typhoid, cancer, dysen-
tery, etc.).

3. Odor. — In adults of no great significance. In infants foul stools
suggest albuminoid decomposition, and strongly sour stools suggest
acid fermentation.

1 "Physiological Economy in Nutrition," 1904, p. 42.

THE INTESTINE, SPLEEN, KIDNEY 379

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
mucosa."

(c) Fresh Blood. — Piles are by far the commonest cause of bloody
stools, and the amount of blood may be trifling or may be large enough
to produce in time a severe anaemia.

Enteritis (the mild follicular or the severe ulcerative form) often
produces bloody stools. The associated symptoms, diarrhoea, mucus,
and pain, together with the etiology (dietetic error, typhoid fever,
amoeba 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
diagnosis.

In hemorrhagic diseases (purpura, scurvy, acute leukaemia) blood
may come from the intestine as well as from the other mucous mem-
branes. Other rare causes for blood in stools are a ruptured aneurism,
thrombosed mesenteric artery, rectal syphilis, or fissure.

(d) Altered blood (tarry stools, melaena) follows the pouring out of
blood — a pint or more — in the upper gastro-intestinal tract, and occurs

380 PHYSICAL DIAGNOSIS

in hepatic cirrhosis, gastric or duodenal ulcer, after severe nose-bleed,
and occasionally from other causes. Occult blood, recognizable by
the guaiac test, often occurs in cancer or ulcer of the stomach, and
forms an important link in the chain of evidence on which the diagnosis
of those diseases is based.

(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

latus1) 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.

PLATE I.

Fig. i. — Trichomonas hominis. (Leuckart.)

Fig. 2. — Balantidium coli. (Leuckart.) Magnified about 150 diameters.

Fig. 3. — Lamblia intestinalis. (Leuckart.)

THE INTESTINE, SPLEEN, KIDNEY

381

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 MgS04 has been given. A bit of mucus from
such stools or a little obtained by
passing a rectal tube is put upon a
warmed slide with a drop of water,
covered with a cover glass, and ex-

Fig. 2ir. — a, Head of Taenia saginata, much magnified; b, uterine canal of same,
twenty branches on each side.

About

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.

382

PHYSICAL DIAGNOSIS

The other parasites are identified, as a rule, by the finding of their
eggs in the stools. The technique of this operation is described below,
as exemplified in the search for the egg of uncinaria — at present the egg
most important for Americans to recognize.

Eggs of parasites catch the eye in the examination of stools, first
of all, by the clean-cut, mathematical symmetry of their oval, when com-
pared with the irregular, shapeless masses which usually appear in
slide and cover preparations from the faeces.

Secondly, the size of parasitic eggs is
greater than that of most of the objects
seen in the faeces; and, thirdly, they are for
the most part dark brown, stained with bile
(the uncinaria is an exception) .

Fig. 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
catalogued.

The Uncinaria americana or its European equivalent (Anchylos-
toma duodenale) is recognized most easily by the identification of its
eggs in the stools. These eggs are characteristic (see Plate II.), and
' the only thing liable to be confounded with them is the ovum of
Ascaris lumbricoides stripped of its heavy, bile-stained outer shell
(see Plate II.) ; but this has a double contour and contains a shapeless
mass of granular matter not differentiated" (as most uncinaria eggs

Cabot — Physical Diagnosis.

PLATE II.

' '.

jilfe

Ti f'Tiff

k *

Distoma buski.

Ascaris lumbricoides.

Uncinaria americana.

Anchylostoma duodenale.

..jCV<-..r.

• "-*■

i •.••>,"'^_j

<-;.,*

■ ;>q £^Z

JU %$

-■'~(m&

Pr.

■*imm

W T'-»*

■ "i®^(

*BL ■/■?

WA/> «i

YF. i J

v ■**^$»*:

y<*r ■

>^V ;Jpr

^'k

Trichuris trichiura. Dibothriocephalus latus. Taenia solium.

EGGS OF INTESTINAL PARASITES.
All are magnified 250 diameters.

Taenia saginata.

THE INTESTINE, SPLEEN, KIDNEY

383

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.

384

PHYSICAL DIAGNOSIS

diaphragm. If too much light is admitted the delicate ovum will be
passed over."

The following interesting table (from the studies of Ashford, King,
and Igaravidez in Porto Rico) shows, roughly, the relative frequency
(in a tropical climate) of the common intestinal parasites recognizable

Fig. 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.

PLATE III.

Heterophyes
heterophyes.

Distoma
sinense.

Fasciola hepatica.

Distoma buski.

Distoma
felineum.

Dictocoelium
lanceolatum.

Taenia solium

Taenia
saginata

Bilharzia Diplogonoporus Bilharzia Dibothrio- Bilharzia

haematobium. grandis. haematobium, cephalus latus. haematobium.

Ascaris Oxyur's

lumbricoides. vermicularis.

Paragonimus
westermani.

Taenia nana.

Ascaris
lumbricoides.

Anchylostoma
duodenale.

Uncinaria
americana

Strongyloides
stercoralis.

DRAWINGS OF EGGS OF INTESTINAL PARASITES.
All are magnified 250. (After Looss).

THE INTESTINE, SPLEEN, KIDNEY

385

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
examinations.

Splenic enlargement is detected chiefly by
palpation. Percussion plays a minor role in the
determination of the organ's size, and should
never be relied on in the absence of palpable
evidence. Palpation is easy, provided the organ
is enlarged sufficiently to project beyond the
ribs without forced respiration, but much prac-
tice is needed when the enlargement is slight, as
in, for example, most cases of typhoid fever.

■ ■

.,"•'; Kill

. ^K%Jb*>

I!!

H/^H

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

386

PHYSICAL DIAGNOSIS

toward the expectant finger-tips of the right hand; (b) at the same
time the left hand should slide the skin and subcutaneous tissues
over the ribs and toward the right hand (see Fig. 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 INTESTINE, SPLEEN, KIDNEY

387

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

388 PHYSICAL DIAGNOSIS

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
Enlargement.

In children splenic enlargement without fever or leukaemic blood
changes is to be classed as a manifestation of general debility. It
has no special connection with any type of anaemia, though anaemia
is often seen with it.

In typhoid the fever with the Widal reaction and blood culture are
generally sufficient to make clear the cause of the splenic enlargement ;
in active malaria the blood parasites are always demonstrable, and in
chronic cases the history and the locality are significant.

Hepatic cirrhosis (and Banti's disease) should show evidences "1
portal stasis (ascites, jaundice, haematemesis) .

THE INTESTINE, SPLEEN, KIDNEY 389

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 2501

Amyloid nephritis 9

Floating kidney 227

Stone in the kidney 145

Malignant disease 42

Tuberculous kidney 41

Pyonephrosis and abscess 542

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.

390 PHYSICAL DIAGNOSIS

peculiar sensitiveness to pressure, which differs from ordinary
tenderness.

(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

THE INTESTINE, SPLEEN, KIDNEY

391

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
more.

(d) Abscess of the kidney, including tuberculous, suppurating kid-
neys and pyonephrosis, usually produces a smooth, round tumor in

Fig. 218. — Left Hydronephrosis.

392 PHYSICAL DIAGNOSIS

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

THE INTESTINE, SPLEEN, KIDNEY 393

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.

394 PHYSICAL DIAGNOSIS

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.

THE INTESTINE, SPLEEN, KIDNEY 395

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.

396 PHYSICAL DIAGNOSIS

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
necessary.

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

THE INTESTINE, SPLEEN, KIDNEY 397

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

398 PHYSICAL DIAGNOSIS

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.

THE INTESTINE, SPLEEN, KIDNEY

399

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 reagent1 up to the mark "R." The
tube is then corked, inverted about half a dozen times,
and set aside for twenty-four hours. A precipitate
falls and the amount per mille is then read off on the
scale etched upon the tube. If the urine is not acid
it must be made so with dilute acetic acid, and unless
its specific gravity is already very low it should be
diluted once or twice with water so as to bring the
gravity below 1.008. After such a dilution we must, of
course, multiply the result obtained by a figure 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-
ature.

** if

777. Significance of Albuminuria. FlG- 2I9- —

Esbach's Albu-
It is important to realize that albuminuria very menometer.

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.

400 PHYSICAL DIAGNOSIS

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 sulphate1 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.

THE INTESTINE, SPLEEX, EXDXEY 401

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
reading;.

402 PHYSICAL DIAGNOSIS

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 INTESTINE, SPLEEN, KIDNEY 403

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.

404

PHYSICAL DIAGNOSIS

Fig. 22i. — Casts, i, Hyaline casts; 2 and 3,
hyaline casts with cells and blood adherent; 4,
"cylindroids."

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-
iphery.

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.

THE INTESTINE, SPLEEN, Klt>NEY

405

Fig. 223.
Spermatozoa.

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' 0 (
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-
nition.

(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
shape.

Fig. 224. — Crystals of Triple Phosphate
(prisms) and Ammonium Urate (small
spheres with spines.)

406

PHYSICAL DIAGNOSIS

Fig. 225. — Crystals of Uric Acid
stone-shaped) with Calcic Oxalate
octahedral) and Amorphous Urates.

(whet-
(small

(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
oxalate.

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
urine.

Uric-acid crystals, if present in great numbers in the urine

Calcic Oxalate Crystals.

THE INTESTINE, SPLEEN, KIDNEY

407

when passed, suggest the search for macroscopic masses (gravel)
and for other evidence of renal stone, but as a rule they are of no
importance.

The same may be said of calcium oxalate. Oxaluria is one of the
most persistent bugbears of the medical profession, but it is utterly

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).

408

PHYSICAL DIAGNOSIS

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.

(O'Neil.)

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

THE INTESTINE, SPLEEN, KIDNEY 409

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
impossible.

This disease should be borne in mind :

(a) In all cases of unexplained fever without obvious local cause — ■
especially in girl babies and in women a short time before or after
parturition (subacute or chronic renal infection).

(b) In acute abdominal emergencies when appendicitis, chole-
cystitis, intestinal obstruction, perforating peptic ulcer, and pan-
creatitis are being considered. With these consider also acute infection
of the kidney, for in some cases the pain is in the right hypochondrium
and no complaints suggesting the kidney are uttered.

CHAPTER XXII.

THE BLADDER, RECTUM, AND GENITAL

ORGANS

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.

Data.

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
trouble.

/. 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

410

THE BLADDER, RECTUM, AND GENITAL ORGANS 411

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,

412 PHYSICAL DIAGNOSIS

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.

(d) Paralysis of the bladder (see above) .

THE BLADDER, RECTUM, AND GENITAL ORGANS 413

(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").

(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.

Methods.

For most examinations the finger suffices. It should be covered
by a thin, rubber finger-cot, greased with vaseline, and should be

414 PHYSICAL DIAGNOSIS

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,

THE BLADDER, RECTUM, AND GENITAL ORGANS 415

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
recognize.

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.

(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).

(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-

416 PHYSICAL DIAGNOSIS

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.

THE BLADDER, RECTUM, AND GENITAL ORGANS 417

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.

418 PHYSICAL DIAGNOSIS

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.

Methods.

Inspection of the external genitals is easy if the parts are properly
exposed by a satisfactory position and a good light. Intravaginal
inspection needs a speculum (Sims' or bivalve) and usually an assistant
to hold it.

Palpation should always be bimanual, the left forefinger in the
vagina (or in the rectum if the hymen is narrow), the right hand
above the symphysis pubis. The proper co-operation of the hands
is hard to describe and depends on practice. The pressure 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.

Lesions.

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.

THE BLADDER, RECTUM, AND GENITAL ORGANS 419

(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.

420 PHYSICAL DIAGNOSIS

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

THE BLADDER, RECTUM, AND GENITAL ORGANS 421

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
uterus.

Ovaritis, enlargement, and tenderness of one or both ovaries is
usually part of tubal disease and not sharply to be distinguished
from it before operation. In other cases it is associated with cyst for-
mation, and the cysts may be palpated bimanually. Abscess of the
ovary is not commonly diagnosed, but is met with in operations for
pus tubes.

Ovarian Tumors.

(a) Small Tumor. — In their earlier stages these growths pro-
duce symptoms only when complications arise, i.e., suppuration or
twisting of the pedicle. Small, suppurating cysts give practically
the same signs as those of a pus tube, and are recognized only at
operation or autopsy.

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.

422

PHYSICAL DIAGNOSIS

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.

THE BLADDER, RECTUM, AND GENITAL ORGANS 423

Vaginal examination may exclude fibroid by showing that the
uterus is not directly connected with the tumor and by demonstrating
with a uterine sound that the uterine canal is not elongated.

Solid tumors of the ovary, carcinoma, sarcoma, or fibroma are
rarely recognizable before operation and are often mistaken for pedun-
culated uterine fibroids. They are apt to be associated with ascites.

CHAPTER XXIII.
THE LEGS AND FEET.

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
inflammation.

2. Hernia and hydrocele of the cord.

3. Psoas abscess.
Less common are :

4. Retained testis.

5. Filarial lymphatic varix.

1. Inguinal Glands. — Two sets of inguinal glands are distin-
guished— one arranged along the lower half of Poupart's ligament;
the other lower down, around the saphenous opening.

(a) The "Poupart's group" are acutely enlarged in lesions of
the genitals ("bubo" 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
too.

1 The bubo of gonorrhoea often suppurates; that of syphilis rarely. Hence a scar in the
in guinal region suggests an old gonorrhoea.

424

THE LEGS AND FEET

425

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.)

(Bradford

426

PHYSICAL DIAGNOSIS

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,
but

(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.

THE LEGS AND FEET

427

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 ... ^

0 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,

428 PHYSICAL DIAGNOSIS

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).

Paralyses.

(i) Paralysis of one leg, occurring in children, is usually due to
anterior poliomyelitis ; in adults it usually forms part of a hemiplegia or
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
disease.

(3) Partial paralysis of both legs is oftenest due to neuritis, resulting
from the causes mentioned above. The extensors of the foot are
especially affected and toe-drop results, so that in walking "the entire
foot is slapped upon the ground like a flail" (Osier).

Differential Diagnosis. — (a) In diffuse or transverse myelitis,
whether or not the trouble be due to pressure, there are increased
reflexes, anaesthesia, usually loss of control of the sphincters (involun-
tary urine and 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.

THE LEGS AND FEET

429

(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 \

■k^^i

V\J

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.

430

PHYSICAL DIAGNOSIS

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

THE LEGS AND FEET

431

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 legs1 is oftenest due to:

(a) Uncompensated heart lesions, primary or secondary from
lung disease.

(6) Nephritis.

(d) Anaemia.

1 It is notable that oedema is usually greatest in the front of the leg and in the back of
the thigh.

432

PHYSICAL DIAGNOSIS

(e) Neuritis (alcoholic, beri-beri, etc.).

(/) Varicose veins.

(g) Obesity, flat-foot, and other causes of deficient local circu-
lation.

In some cases no cause can be found ("angioneurotic" oedema,
"essential" and "hereditary" oedema). Diagnosis of the cause of

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

THE LEGS AND FEET

433

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.

434

PHYSICAL DIAGNOSIS

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,
elsewhere.

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,

THE LEGS AND FEET

435

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
inflammation.

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

436

PHYSICAL DIAGNOSIS

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
neuritis.

5. "Morton's disease" (metatarsalgia) means pain in the tarsus at
a small spot near the distal end of one of the three outer toes, always
associated with compression of the foot by tight boots and probably
due to pinching of the external plantar nerves between the metatarsal
bones. It is relieved by proper shoes.

CHAPTER XXIV.
THE BLOOD.

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.

437

438

PHYSICAL DIAGNOSIS

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. 242.-Sahli's Hsemoglobinometer. B, at a time> and close the eYes 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 BLOOD 439

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

440 PHYSICAL DIAGNOSIS

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
stain.

The cover-glass method requires a much greater degree of cleanliness
and manual dexterity than the slide method. Cover glasses must be
washed in water and then thoroughly polished with a silk (not cotton

te>verjf/t?fs^

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

THE BLOOD 441

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

442

PHYSICAL DIAGNOSIS

widely applicable. It brings out all the minutiae of the red corpuscles,
leucocytes, and blood parasites, and for clinical work no other stain is
needed.

Appearance of Films so Stained. — i. The normal red corpuscles
appear as round discs with pale centres. Their color depends upon
the length of time that we continue the washing with clear water after
the staining mixture has been poured off, and varies from brown
through pink to golden yellow.

(a) Poikilocytosis means the appearance in the blood of red cells
variously deformed, sausage shaped, battledore shaped, oblong, pear
shaped, etc. It is always associated with abnormalities in the size of
the corpuscles, so that dwarf forms and giant forms appear.

(b) Polychromasia (or 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.

THE BLOOD

443

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).

(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

444 PHYSICAL DIAGNOSIS

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
leucocytes.

Other varieties of leucocytes which appear in the blood only in
disease will be mentioned later.

3. Blood Plates. — In the normal blood film, stained as directed
above, one finds, beside the red corpuscles and the different varieties
of leucocytes, a varying number of bodies, usually about one-third the
diameter of a red corpuscle, irregularly oval in shape, staining dark red
or blue and tending to cohere in bunches. Occasionally larger forms
occur, and in these a vague network and some hints of a nucleus may
be traced.

These bodies which are probably derived from one or more species
of leucocytes have at present no considerable importance in medicine,
although they not infrequently lead to mistakes, because, when lying
on top of a red corpuscle, they bear a slight resemblance to a malarial
parasite. They are usually increased in secondary anaemia and dimin-
ished in pernicious anaemia.

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 BLOOD

445

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 it1 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.

446 PHYSICAL DIAGNOSIS

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

T7gmT7M^WMk

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.

THE BLOOD 447

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.

(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
present.

448 PHYSICAL DIAGNOSIS

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

THE BLOOD 449

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,
29

450 PHYSICAL DIAGNOSIS

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
diagnosis.

Certain exceptions to the rules above given must be remembered:

1. Quiescent, thickly encapsulated collections of pus, in which the
bacteria have died or lost their virulence, usually produce no leucocyto-
sis. In this group come some of the abscesses of the liver or about the
kidney, and a few cases of appendicitis.

2. The most virulent and overwhelming infections are apt not to be
accompanied by leucocytosis . Thus, for example, the most virulent
cases of pneumonia, diphtheria, or general peritonitis often run their
course without leucocytosis.

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.

Eosinophilia.

The eosinophiles are increased chiefly in:

1. Bronchial asthma.

2. Chronic skin diseases.

3. Diseases due to animal parasites (trichiniasis, uncinariasis,
filariasis, hydatid disease, Bilharzia disease, trypanosomiasis, and with
most of the intestinal worms).

4. Myelogenous leukaemia.

There seems to be also some vague connection between eosinophilia

THE BLOOD

451

and diseases of the female genital tract (except cancer and fibre-myoma
of the uterus) .

Leukemia.

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.

452 PHYSICAL DIAGNOSIS

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
itself.

(b) Interpretation. A positive reaction occurs at some period in
the course of ninety-five per cent of all cases of typhoid fever, but the
proportion of cases in which the reaction occurs early enough to be of
diagnostic value varies greatly in different epidemics. In most
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.

PLATE IV.

Fig. i. — Young Tertian Parasites. (Stained with Wright's modification of Leishman's

stain.)

Fig. 2. — Mature Tertian Parasites. (Eosin and methylene blue.)

Fig. 3. — Segmenting Tertian Parasites. (Eosin and methylene blue.)

THE BLOOD

453

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

454

PHYSICAL DIAGNOSIS

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
magnification.

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

PLATE V.

Fig. i. — Two Young .Fsuvo-autumnal Parasite;. Wright's modification of Irishman's

stain.)

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.

THE BLOOD 455

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).

CHAPTER XXV.

THE JOINTS.

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
joint.

2. Enlargement:

(a) Hard, probably bony.

(b) Boggy, probably infiltration or thickening of capsule and
periarticular structures.

3. Irregularities in contour:

(a) Osteophytes or "lipping" (attached to the bone).

(b) Gouty tophi (not attached to the bone) .

(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.

(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.

456

THE JOINTS 457

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.

(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

458

PHYSICAL DIAGNOSIS

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.

THE JOINTS 459

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

460 PHYSICAL DIAGNOSIS

spasm, on the contrary, checks motion a little from the outset, the
resistance and pain gradually increasing until our efforts are arrested
at some point, vaguely determined by our strength and hard-hearted-
ness and by the patient's ability to bear the pain.

Motions limited by capsular thickening and adhesions are not, as
a 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
limitation.

In true ankylosis, there is no motility whatever.

(g) Excessive motion in a joint is recognized simply by contrast
with the limits furnished us by our knowledge of anatomy and of the
physiology of joint motion at different ages. When the bone and
cartilage appear normal or are not grossly injured, we call the excessive
motility of the joint a subluxation, but excessive motility may also be
due (as in Charcot's joint) to destruction of bone and other essentials
of the joint.

(h) To detect crepitus and creaking we simply rest one hand on the
suspected joint, and with the other put it through its normal motions,
while the patient remains passive.

(i) Most free joint bodies are not palpable externally, and are rec-
ognized only by their symptoms, by the 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).

THE JOINTS 461

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
are:

(a) Slow progress, with gradual enlargement and disabling of the
joint.

(6) Muscular spasm, especially in disease of the hip or vertebrae.

(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
knee-joint).

(/) Bone necrosis, as shown by x-ray.

The order of frequency in the different joints is as follows: spine,
hip, knee, wrist, shoulder (tuberculous dactylitis is described on
page 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

462 PHYSICAL DIAGNOSIS

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.

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
lesions1 in most cases, (b) The tendency to recovery in the great
majority of cases.

The milder forms, whose cause is unknown, we have hitherto
designated as "rheumatism." The others are distinguished as gonor-
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.

THE JOINTS

463

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.

464

PHYSICAL DIAGNOSIS

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).

THE JOINTS

465

Fig. 257. — Atrophic Arthritis. Early stage.

Fig. 258. — Atrophic Arthritis. (Goldthwait.)

466 PHYSICAL DIAGNOSIS

(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.

(Goldthwait.)

The changes progress slowly and attack new and larger joints,
moving centrally from the periphery. At any stage the process may
become arrested, but usually not until ankylosis or contractures have
occurred in one or many joints. Some of the "ossified men" of dime
museums are in the ankylosed stage of this terrible malady. Flexion
of fingers with hyperextension of the terminal joints and deflection to
the ulnar side are common deformities.

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

THE JOINTS

467

(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-

468

PHYSICAL DIAGNOSIS

dylitis deformans," "osteoarthritis"), where a portion of the front
and side of the vertebral column is "plastered over" with new-
formed bone (see Fig. 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:

THE JOINTS 469

(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.

470

PHYSICAL DIAGNOSIS

well performed as a rule, in sharp contrast with "lumbago," which
renders forward bending and the subsequent recovery almost
impossible.

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.

THE JOINTS

471

Fig. 266. — Gouty Arthritis. (Goldthwait.)

Fig. 267. — -J^-ray of Hand in Gouty Arthritis. (Goldthwait.)

472 PHYSICAL DIAGNOSIS

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. Vickery2 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.

CHAPTER XXVI.
THE NERVOUS SYSTEM.

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.

(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.

473

474

PHYSICAL DIAGNOSIS

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).

(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.

THE NERVOUS SYSTEM 475

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
spasms.

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,

476 PHYSICAL DIAGNOSIS

and it is also exemplified in the gait of tabes dorsalis. There is no lack
of muscular contraction — often too much — but it is disorderly and
ill-directed.

Deficiency in the power to balance in standing or walking is perhaps
the commonest type of ataxia, and may be due not only to the causes
just mentioned, but also to cerebellar disease and ear disease. In these
types there is often a tendency to stagger in one particular direction,
e.g., to the right, and the ataxia is associated with vertigo and with
other evidences of brain tumor or of ear disease.

In tabes dorsalis and other diseases we test the power to balance
by asking the patient to bring his feet together (toe to toe and heel to
heel) and to close his eyes. If he is unable to preserve his balance his
failure is known as ''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.

THE NERVOUS SYSTEM 477

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

478 PHYSICAL DIAGNOSIS

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.

(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
lost.

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,
etc.).

THE NERVOUS SYSTEM 479

(b) Spastic paraplegia and the amyotrophic forms of lateral
sclerosis.

(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
hysteria.

Almost any chronic joint disease, except tuberculosis, may be
associated with increased reflexes. Diagnosis depends on the absence
of other causes for the increase.

Other Deep Reflexes. — The Achilles reflex is best obtained by
having the patient kneel on the seat of a well-padded chair, with
his feet unsupported, while we strike the Achilles tendon. The
significance of its absence or increase is practically the same as that
just given for the knee-jerk, but, since it represents a slightly lower
position in the spinal cord, it may be affected earlier than the knee-
jerk in any cord disease which begins at the bottom of the cord and
travels up. Thus in tabes I have known the Achilles reflex absent
when the knee-jerk still persisted.

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

480 PHYSICAL DIAGNOSIS

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.

THE NERVOUS SYSTEM 481

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.
31

482 PHYSICAL DIAGNOSIS

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
occurs.

In prognosis a reaction of degeneration persisting after six to
twelve weeks is unfavorable for recovery of the use of the muscles
in which it occurs. If reaction of degeneration is absent or partial
from the start, the prognosis is for relatively speedy recovery, i.e., in
weeks rather than months.

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
states.

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.

THE NERVOUS SYSTEM 483

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.

Coma.

The causes of coma are nearly identical with the causes of con-
vulsions. Almost every disease which causes the one may cause the
other; hence all that is here said on the 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

484 PHYSICAL DIAGNOSIS

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.

(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

THE NERVOUS SYSTEM 485

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
hours.

Sunstroke is recognized by the state of the weather and the presence
of a very high temperature (1060, i io°, 1 150 F., or even more) . There

486 PHYSICAL DIAGNOSIS

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.

INDEX

Abdomen*, contour of, 339

distended and tortuous veins of.

339
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

339
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,
462

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,

361
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

4S7

488

INDEX

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,

7
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,
448

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,

263. 327- 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,
38

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

IXDEX

489

Apnoea in Cheyne-Stokes breathing,

75
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,

376

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,

39
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,

40
oedema of, in nephritis, 40
oedema of, in sarcoma of medi-
astinum, 40
oedema of, in sarcoma of lung,

40
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,

in
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,

462
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

490

INDEX

Arthritis, hypertrophic, of sacro-iliac
joint, 58
hypertrophic, psoa sspasm in,

462
hypertropic, with kyphosis, 58
infectious, 461
spinal, 57

tuberculous, characteristics of,
461
Ascaris lumbricoides, 381, 384
Ascites, 422

causes of, 347
Asphyxia, local, in Raynaud's disease,

55
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,
213
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,
279
in mitral stenosis, 212
in myocarditis, 245
mediate versus immediate, 137,

138
of heart, 167, 197
of lungs, 147
of muscle sounds, 145
of voice sounds, see Vocal Frem-
itus
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,
362
Bilharzia disease, blood in, 450

eggs, 385
Biliary colic, 369, 392

obstruction, 15
Bismuth line, 24

X-ray examination of stomach,
358

INDEX

491

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,
22

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

492

INDEX

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-
tasis

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,
360

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-
sation

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-
monia

INDEX

493

Cavity, pulmonary, 292, 302
Cervical rib, an accessory, 35, 39
Charcot's joint, atrophic arthritis in,

462
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,

388
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
interstitial

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,

485

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,

285> 293. 3°2. 321
with sputa, 307
Cranium, size and shape, 5
Cremasteric reflex, 480
Crepitation, atelectatic, 277

494

INDEX

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
impulse
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, 278, 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

INDEX

495

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,
278

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,

353
dilatation of, 353
diverticulum of, 353

Ewald's test meal, 355

Exophthalmic goitre, see Graves'
disease

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

496

INDEX

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,
382

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,

360
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,
362

-stones in feces, 380
Galvanic reaction in disease, 482
Gangrene, local, in Raynaud's disease,

of lung, 293, 337,

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,
217

fermentation, breath in, 22

fermentation, tongue in, 23

peristalsis, 351

INDEX

497

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-
ease

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
32

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,

380
Gumboil, 25
Gums, 24

bismuth line in, 24

bleeding, 25

in lead poisoning, 24

in poisoning by mercury, 24

in poisoning by potassic iodide,
24

in scurvy, 25

sordes of, 24

spongy, 25

suppuration of, 25
Giinzburg's reagent, 356

H^ematemesis in portal obstruction,

366
Hasmatocele, 417
Haematoma, infected, of belly wall,

342
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

498

INDEX

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,

5i
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,
Breathing
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,

200
chronic dilatation of, 199
compensation, 194
congenital malformations, 250
cycle, systole and diastole, 180,

181
dilatation of, 84, 199, 200, 261,

273
disease, congestion of liver in,

364
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,

250
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

Arrhythmia
parietal diseases of, 243—247
rapid, 247 see Tachycardia
situation of apex impulse, 62, 68
slow, 248, see Bradycardia

INDEX

499

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,

213
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.
58> 467

Hip-joint, hypertrophic arthritis,
morbus coxas senilis, 467

limitation of motion of, 58, 458,
461

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,

18
Hypertrophic arthritis, see Arthritis
Hypertrophy, cardiac impulse in, 82,
84

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

500

INDEX

Hysteria, spasms in, 14
temperature in, 2

Idiocy, mouth in, 19

Incidence of diseases of the bladder,
410
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,
65
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,

64
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,

90
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,

377
obstruction by gall-stones, 371
obstruction, causes of, 377
obstruction, chronic visible peris-
talsis in, 377
Obstruction, distention in, 374
obstruction, physical signs in,

377
obstruction, tumor in, 377
parasites, 380

parasites, anemia from, 447
parasites, diagnosis of eggs of,

382
parasites, eosinophilia due to,

45°
parasites, relative frequency of,

384
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,

16
Ischiorectal abscess, 414
Itching in jaundice, 15

Jacksonian epilepsy, 46

epilepsy, spasms of hand, causes
46
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

INDEX

501

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,

477
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,

472
neuropathic, 464
pain in, 456
palpation of, 456
radioscopy of, 457
sacro-iliac, hypertrophic arthritis

of,_57
scaro-iliac, tuberculosis of, 57
tests of limitation of motion, 456,

458
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

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