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THE RELATIONS OF THE THORACIC AND 
 ABDOMINAL VISCERA, 
 
 THE ANTERIOR THORACIC AND ABDOMINAL WALLS REMOVED. 
 
 A.— Upper bone of the sternum. 
 
 B.B.*— Two first ribs. 
 
 C.C.* — Second pair of ribs. 
 
 D.D.*— Eight and left lungs. 
 
 E. — Pericardium, enveloping the heart— the right ventricle. 
 
 F. — Lower extremity of the sternum. 
 
 G.G.*— Lobes of the liver. 
 
 H.H.* — Right and left halves of the diaphragm, in section ; the 
 
 right half separating the right lung from the liver, 
 
 the left half separating the left lung from the cardiac 
 
 extremity of the stomach. 
 I.I.* — Eighth pair of ribs. 
 K.K.*— Ninth pair of ribs. 
 L.L.* — Tenth pair of ribs. 
 M.M,*^The stomach. 
 N. — The umbilicus. 
 O.O.* — The transverse colon. 
 P.P.*— The omentum, covering the transverse colon and small 
 
 intestines. 
 Q.— The gall-bladder. 
 
 R.R.*— The right and left pectoral prominences. 
 S.S.*— The small intestines. 
 
SAUNDERS' QUESTION COMPENDS, NO. 17. 
 
 ESSENTIALS OF DIAGNOSIS 
 
 ARKANGED IN THE FORM OF 
 
 QUESTIONS AND ANSWERS 
 
 PREPARED ESPECIALLY FOR 
 
 STUDENTS OF MEDICINE. 
 
 BY 
 SOLOMON SOLIS-COHBN, M.D., 
 
 PROFESSOR OF CLINICAL MEDICINE AND APPLIED THERAPEUTICS IN THE 
 
 PHILADELPHIA POLYCLINIC; ONE OF THE PHYSICIANS TO THE 
 
 PHILADELPHIA HOSPITAL, ETC., 
 
 AND 
 
 AUGUSTUS A. ESHNER, M.D., 
 
 INSTRUCTOR IN CLINICAL MEDICINE IN JEFFERSON MEDICAL COLLEGE AND IN 
 
 THE PHILADELPHIA POLYCLINIC j REGISTRAR IN THE NEUROLOGICAL 
 
 DEPARTMENT OF THE PHILADELPHIA HOSPITAL, ETC. 
 
 WITH FIFTY-FIVE ILLUSTRATIONS, 
 
 SOME OF WHICH ARE COLORED, AND A FRONTISPIECE. 
 
 PHILADELPHIA: 
 
 W. B. S AUN DE RS, 
 
 913 Walnut Street. 
 
 1892. 
 
Copyright, 1892. 
 By W. B. SAUNDERS. 
 
TO 
 
 J. M. Da COSTA, M.D., LL.D., 
 
 EMERITUS PROFESSOR OF THE PRACTICE OF MEDICINE AND OF CLINICAL MEDICINE 
 IN JEFFERSON MEDICAL COLLEGE, 
 
 THE MASTER DIAGNOSTICIAN, 
 
 THE BRILLIANT TEACHER, THE DISTINGUISHED CLINICIAN, 
 
 THIS LITTLE BOOK 
 
 IS AFFECTIONATELY INSCRIBED 
 
 TWO GRATEFUL PUPILS. 
 
 (iii) 
 
PREFACE. 
 
 This book is intended to meet a popular demand. While 
 the endeavor has been to make it reliable and helpful, the 
 student is advised not to depend upon it to the exclusion of 
 standard and more elaborate works. It is elementary in 
 character, devoid of detail, and represents but an outline of 
 the subject with which it has to deal. This outline must be 
 filled from observation and further reading. 
 
 Being written especially for students, everything has been 
 sacrificed to accuracy and brevity ; references to authori- 
 ties consulted have been omitted ; and it has been deemed 
 wisest to conform with prevailing views in matters concern- 
 ing which there may be differences of professional opinion. 
 
 In the arrangement of material, systematic classification 
 has often been departed from, to secure the benefit of associa- 
 tion of ideas. 
 
 Diagnosis must be studied from patients, not from books ; 
 even the best of books can only direct the student what to 
 look for at the bedside, and warn him against probable 
 errors. 
 
 If this book facilitates the true methods of study, it will 
 have accomplished its purpose. 
 
 (V) 
 
CONTENTS. 
 
 PAGE 
 
 Introduction . . 17 
 
 Fever . . .27 
 
 Simple Continued Fever — Ephemeral Fever— Febricula . 31 
 
 Ardent Fever 31 
 
 Tliermic Fever — Insolation — Sunstroke .... 32 
 Catarrhal Fever — Influenza — Epidemic Catarrh — La 
 
 Grippe 32 
 
 Typhoid Fever — Enteric Fever 35 
 
 Typhus Fever . ........ 43 
 
 Cerebro-spinal Fever — Epidemic Cerebro-spinal Menin- 
 gitis 45 
 
 Asiatic Cholera — Cholera Infectiosa 49 
 
 Relapsing Fever 51 
 
 Malarial Diseases 52 
 
 Yellow Fever . . .59 
 
 Weil's Disease ......... 62 
 
 The Exanthemata 63 
 
 Morbilli — Measles — Rubeola . . . . .63 
 
 Scarlatina — Scarlet Fever 65 
 
 Rotheln — Roseola — German Measles — French Measles 68 
 
 Yariola— Smallpox 69 
 
 Varicella — Chickenpox 73 
 
 Erysipelas 74 
 
 Dengue— Break-bone Fever 76 
 
 Diphtheria 77 
 
 Glanders — Farcy — Equinia 80 
 
 Anthrax — Wool-sorters' Disease — Charbon — Malignant 
 
 Pustule — Splenic Fever 81 
 
 Actinomycosis 83 
 
 ( vii ) 
 
Vlll dONlENl'g. 
 
 PAGE 
 
 Foot-and-Mouth Disease 84 
 
 Hydatid Disease 84 
 
 Tricliiniasis . . . 85 
 
 Acute Rheumatism — Rheumatic Fever . . . .87 
 
 Gonorrheal Synovitis .88 
 
 Syphilitic Arthritis 89 
 
 Subacute Rlieumatism ....... 89 
 
 Myalgia 90 
 
 Chronic Rheumatism . 90 
 
 Acute Gout 91 
 
 Chronic Gout 92 
 
 Lithemia 93 
 
 Rheumatoid Arthritis — Arthritis Deformans . . . 94 
 
 The Blood . 95 
 
 Anemia 97 
 
 Chlorosis . . 98 
 
 Pernicious Anemia 98 
 
 Leukocytosis 99 
 
 Leukemia ......... 99 
 
 Pseudo-leukemia — Hodgkin's Disease — Lymphatic 
 
 Anemia — Malignant Lymphoma or Lymphadenoma 101 
 
 Infantile Pseudo-leukemic Anemia .... 103 
 
 Scorbutus — Scurvy . 104 
 
 Purpura 105 
 
 Hemophilia . 106 
 
 Addison's Disease 107 
 
 Rachitis 108 
 
 Mollities Ossium ■ . 108 
 
 The Heart 109 
 
 Inspection 109 
 
 Palpation 110 
 
 Percussion 110 
 
 Auscultation ........ 110 
 
 Malformation 115 
 
 Dextrocardia 115 
 
 Functional Disturbance of the Heart . . . . 116 
 
 Tachycardia 116 
 
CONTENTS. IX 
 
 PAGE 
 
 Irritable Heart . .... . . . . 117 
 
 Angina Pectoris . . 118 
 
 Hypertrophy of the Heart . . . . . . 119 
 
 Dilatation of the Heart 120 
 
 Valvular Disease of the Heart . . . . . 121 
 
 Mitral Incompetency — Mitral Regurgitation . . 122 
 
 Mitral Obstruction 123 
 
 Aortic Obstruction 123 
 
 Aortic Incompetency — Aortic Regurgitation . . 124 
 
 Tricuspid Incompetency — Tricuspid Regurgitation . 125 
 
 Tricuspid Obstruction 125 
 
 Pulmonary Obstruction 125 
 
 Pulmonary Incompetency — Pulmonary Regurgitation 125 
 
 Acute Pericarditis .127 
 
 Acute Endocarditis 128 
 
 Mycotic Endocarditis 129 
 
 Myocarditis 130 
 
 Hydropericardium 130 
 
 Heart-clot 130 
 
 Thoracic Aneurism , . 131 
 
 Arterio-Capillary Fibrosis 132 
 
 Symmetrical Gangrene— Local Asphyxia — Raynaud's Dis- 
 ease 133 
 
 The Respiratory System 1,34 
 
 Coryza — Acute I^asal Catarrh 136 
 
 Hay-fever — Hay-asthma — Rag-weed Fever — Au^ 
 tumnal Catarrh — June-cold — Rose-cold — Idiosyn- 
 cratic Coryza — Periodic Vasomotor Coryza . . 137 
 
 Acute Laryngitis 138 
 
 Edema of the Larynx 1,39 
 
 Acute Tuberculous Laryngitis 140 
 
 Laryngismus Stridulus 141 
 
 Laryngeal Vertigo , . . , . . . 142 
 
 Catarrhal Croup — Spasmodic Croup .... 142 
 
 Membranous Croup 143 
 
 Whooping-cough — Pertussis . . , ' . . 145 
 
X CONTENTS. 
 
 PAGE 
 
 Chronic Laryngitis . 146 
 
 Chronic Tuberculosis of the Larynx .... 147 
 
 Physical Diagnosis 147 
 
 Acute Pleurisy 153 
 
 Acute Bronchitis . . 157 
 
 Chronic Bronchitis ....... 158 
 
 Plastic Bronchitis — Fibrinous Bronchitis . . . 159 
 
 Putrid Bronchitis 159 
 
 Bronchiectasis 160 
 
 Capillary Bronchitis 161 
 
 Catarrhal Pneumonia — Broncho-pneumonia — Lobular 
 
 Pneumonia 162 
 
 Acute Croupous Pneumonia — Lobar Pneumonia . 163 
 
 Pulmonary Gangrene .' . 168 
 
 Pulmonary Tuberculosis 169 
 
 Acute Miliar}^ Tuberculosis 177 
 
 Interstitial Pneumonitis 179 
 
 Pulmonar}' Emphysema 179 
 
 Pneumothorax , . . . . . . . 181 
 
 Asthma 183 
 
 The Digestive System— The Mouth 184 
 
 Catarrhal Stomatitis ....... 184 
 
 Aphthous Stomatitis ... .... 184 
 
 Thrush — Muguet — Parasitic Stomatitis . . . 185 
 
 Ulcerative Stomatitis 185 
 
 Mercurial Stomatitis ....... 186 
 
 Gangrenous Stomatitis — Noma— Cancrum Oris . . 186 
 
 The Tongue 187 
 
 Glossitis 187 
 
 Leukoplakia Lingualis — Leukoplakia Buccalis . . 187 
 
 Glossanthrax ........ 187 
 
 ISTigrities — Black Tongue — Hairy Tongue . . . 188 
 
 Mumps— Parotiditis 188 
 
 The Pharynx 188 
 
 Pharyngitis 188 
 
 Tonsillitis 191 
 
CONTENTS, 
 
 XI 
 
 Herpetic Sore-throat— Herpetic Tonsillitis— Herpes of 
 the Pharynx— Common Membranous Sore-throat — 
 
 Ulcero-membranous Angina— Diphtheroid Throat . 192 
 
 Gangrenous Pharyngitis-^Putrid Sore-throat . . 193 
 
 Retro-pharyngeal Abscess 194 
 
 The Esophagus 194 
 
 Stricture of the Esophagus 194 
 
 The Stomach • • • .195 
 
 Gastralgia 196 
 
 Acute Gastritis . .197 
 
 Chronic Gastritis- Chronic Gastric Catarrh . . 198 
 
 Gastric Ulcer 199 
 
 Carcinoma of the Stomach . . . . . . 200 
 
 The Intestines 20.3 
 
 Acute Enteritis 203 
 
 Croupous Enteritis— Membranous Enteritis . . 205 
 
 Cholera Morbus— Cholera Nostras .... 205 
 
 Cholera Infantum 206 
 
 Chronic Enteritis — Chronic Intestinal Catarrh . . 206 
 
 Acute Dysentery 206 
 
 Chronic Dysentery 208 
 
 Typhlitis 208 
 
 Perityphlitis ........ 209 
 
 Intestinal Obstruction 211 
 
 Intussusception— Invagination 212 
 
 Carcinoma of the Intestine 213 
 
 Intestinal Parasites 214 
 
 Tenia Solium ". . 214 
 
 Tenia Mediocanellata 215 
 
 Bothriocephalus Latus 216 
 
 Ascaris Lumbricoides— Round-worms . . . 217 
 Oxyuris Vermicularis— Seat-worms — Thread-worms — 
 
 Spool-worms 218 
 
 Acute Peritonitis 219 
 
 Chronic Peritonitis 221 
 
 Tabes Mesenterica 222 
 
Xll CONTENTS. 
 
 PAGE 
 
 The Liver 222 
 
 Floating Liver 223 
 
 Congestion of the Liver 224 
 
 Acute Hepatitis . . , 225 
 
 Acute Yellow Atrophy of the Liver .... 226 
 
 Abscess of the Liver 228 
 
 Interstitial Hepatitis — Cirrhosis of the Liver . . 229 
 
 Fatty Liver 230 
 
 Amyloid Disease of the Liver 231 
 
 Carcinoma of the Liver 232 
 
 Hydatid Cyst of the Liver 234 
 
 Perihepatitis . . . . . . . . 235 
 
 Cholangitis — Cholecystitis 236 
 
 Biliary Calculi 238 
 
 The Spleen 240 
 
 Floating Spleen 241 
 
 Splenitis 241 
 
 The Pancreas . 241 
 
 Acute Pancreatitis . 241 
 
 The Genito-Urinary Apparatus ...... 242 
 
 Oxaluria 248 
 
 " Pyuria 249 
 
 Albuminuria . . . . . . . . 250 
 
 Chyluria 253 
 
 Lipuria 253 
 
 Hematuria 254 
 
 Hemoglobinuria 254 
 
 Paroxysmal Hemoglobinuria ..... 255 
 
 Endemic Hematuria 256 
 
 Diabetes Insipidus . 256 
 
 Diabetes Mellitus 257 
 
 Cystitis . . 261 
 
 Vesical Calculus 262 
 
 Neoplasms of the Bladder 262 
 
 Pyelitis 263 
 
 Renal Inadequacy 263 
 
 Floating Kidney 264 
 
CONTEN'tS. Xlll 
 
 PAGE 
 
 Benal Calculus 264 
 
 Acute Kephritis 265 
 
 Chronic Parenchymatous Nephritis .... 265 
 
 Amyloid Kidney 266 
 
 Chronic Interstitial Nephritis 266 
 
 Abscess of the Kidney 268 
 
 Perirenal Abscess 269 
 
 Tuberculosis of the Kidney . ... . . 269 
 
 Malignant Disease of the Kidney .... 270 
 
 Hydronephrosis 270 
 
 Hydatid Cyst of the Kidney 271 
 
 The Kervous System 272 
 
 Neuritis . . . . . . . . . 275 
 
 Multiple Neuritis 276 
 
 Sciatica 278 
 
 Paralysis of the Facial Nerve 279 
 
 Paralysis of the Phrenic Nerve . . . . . 281 
 
 Paralysis of the Musculo-Spiral Nerve . . . 281 
 
 Neuromata 282 
 
 Neuralgia 283 
 
 Migraine . . . .... . . 284 
 
 Spinal Meningitis 285 
 
 Cervical Pachymeningitis 286 
 
 Hemorrhage into the Spinal Membranes . . . 286 
 
 Anemia of the Spinal Cord 287 
 
 Hyperemia of the Spinal Cord 287 
 
 Myelitis 288 
 
 Chronic Myelitis ..289 
 
 Acute Anterior Poliomyelitis 290 
 
 Acute Ascending Paralysis 291 
 
 Amyotrophic Lateral Sclerosis — Progressive Muscular 
 
 Atrophy — Glosso-labio-laryngeal Palsy . . . 292 
 
 Acute Bulbar Palsy 296 
 
 Pseudo-bulbar Palsy . 296 
 
 Pseudo-hypertrophic Paralysis 296 
 
 Simple Idiopathic Muscular Atrophy .... 298 
 
 Arthritic Muscular Atrophy 299 
 
XIV CONTENTS. 
 
 PAGE 
 
 Thomsen's Disease — Myotonia Congenita . . , 300 
 Posterior Spinal Sclerosis— Locomotor Ataxia — Tabes 
 
 Dorsalis 300 
 
 Primary Lateral Sclerosis— Spastic Paraplegia . . 302 
 
 Postero-lateral Sclerosis — Ataxic Paraplegia . . 303 
 
 Friedreich's Ataxia — Hereditary Ataxic Paraplegia . 304 
 Cerebro-spinal Sclerosis — Insular Sclerosis— Multiple 
 
 Sclerosis — Disseminated Sclerosis .... 305 
 
 Paralysis Agi tans— Shaking Palsy .... 306 
 
 Spinal Hemorrhage .308 
 
 Spinal Compression 309 
 
 Tumor of the Spinal Cord 310 
 
 Syringomyelia . . . . . .' . . 312 
 
 Morvan's Disease— Analgesic Panaris . . . 312 
 
 Cerebral Meningitis 315 
 
 Hydrocephalus 818 
 
 Hemorrhage into the Cerebral Membranes . . . 818 
 
 Congenital Spastic Paraplegia 319 
 
 Cerebral Anemia 820 
 
 Cerebral Hyperemia 321 
 
 Cerebritis . 821 
 
 Cerebral Abscess . 822 
 
 Cerebral Hemorrhage 828 
 
 Cerebral Softening 827 
 
 Cerebral Embolism 828 
 
 Cerebral Thrombosis . ' 329 
 
 Cerebral Tumor . 830 
 
 Intracranial Aneurism ...... 331 
 
 General Paralysis of the Insane — Paretic Dementia . 332 
 Sunstroke — Heat-stroke — Insolation — Heat-fever — 
 
 Thermic-fever— Heat-exhaustion .... 884 
 
 Delirium Tremens 835 
 
 Plumbism . . . 387 
 
 Torticollis 838 
 
 Occupation-IsTeuroses 339 
 
 Writer's Cramp 889 
 
 Chorea 340 
 
CONTENTS. XV 
 
 PAGE 
 
 Epilepsy 341 
 
 Hysteria 344 
 
 Tetanus 347 
 
 Tetany 349 
 
 Hydrophobia 350 
 
 Aural Vertigo — Labyrinthine Vertigo— Meniere's Dis- 
 ease ..... 351 
 
 Exophthalmic Goiter — Graves's Disease — Basedow's 
 
 Disease 351 
 
 Cretinism . 354 
 
 Myxedema 354 
 
 Akromesalia 355 
 
LIST OF ILLUSTRATIONS. 
 
 Fkontispiece. 
 
 FIG. PAGE 
 
 1. Bacilli of Typhoid Fever (von Jaksch) . . .3(3 
 
 2. Temperature-chart of a case of Typhoid Fever (Wun- 
 
 derlich.) 37 
 
 3. Temperature-chart of a relapse in Typhoid Fever. 
 
 Convalescence from the relapse interrupted by re- 
 crudescence .39 
 
 4. Temperature-chart of a case of Pyemia (Wunderlich) 41 
 
 5. Comma-bacillus of Cholera (Vierordt) ... 49 
 
 6. Spirochetse of Eelapsing Fever (v. Jaksch) . . 51 
 
 7. Organisms of Malaria — Intracorpuscular (Mace) . 58 
 
 8. Organisms of Malaria — Extracorpuscular (Mace) . 53 
 
 9. Temperature-chart of Quotidian Intermittent Fever 
 
 (Wunderlich) 55 
 
 10. Temperature-chart of Tertian Intermittent Fever 
 
 (Wunderlich) .55 
 
 11. Temperature-chart of Measles (Striimpell) ... 64 
 
 12. Temperature-chart of Scarlatina (Striimpell) . . 66 
 
 13. Temperature-chart of Smallpox (Striimpell) . . 69 
 
 14. Anthrax-bacilli in Blood (Vierordt) .... 82 
 
 15. Actinomyces (Ziegler) 83 
 
 16. Tenia Echinococcus — Vesicle, Scolex and Hooks (after 
 
 Heller) 85 
 
 17. Trichina (v. Jaksch) 86 
 
 18. Appearance of the Blood in Leukemia (Funke) . . 100. 
 
 19. Auscultation of the Heart-sounds (Vierordt) . , 113 
 
 20. iSTormal Pulse-tracing (after Eichhorst) . . . 115, 
 
 B ( xvii ) 
 
XVm LIST OF ILLUSTRATIONS. 
 
 FIG. PAGE 
 
 21. Pulse-tracing of Aortic Insufficiency (after Striimpell) 124 
 
 22. Micrococci of Croupous Pneumonia (Vierordt) . . 164 
 
 23. Tubercle-bacilli in Sputum (Ziegler) .... 173 
 
 24. Tenia Solium, magnified (Heller) .... 215 
 
 25. Tenia mediocanellata, magnified (Heller) . . . 216 
 
 26. Bothriocephalus Latus, magnified (Heller) . . . 216 
 
 27. Ascaris Lumbricoides (v. Jaksch) .... 217 
 
 28. Oxyuris Vermicularis, natural size (Vierordt) . . 218 
 
 29. The Relations of the Heart, Lungs, Liver, Stomach 
 
 and Spleen, as seen from the front (Weil) . . 223 
 
 30. Showing the Relations of the Lungs, Liver, Spleen 
 
 and Kidneys, as seen from behind (Weil-Luschka) . 224 
 
 31. Relations of the Spleen (Weil) 240 
 
 32. Uric Acid and Urates (Funke) 244 
 
 33. Calcium Phosphate (Laache) 245 
 
 34. Triple Phosphates and Ammonium Urate (Laache) . 246 
 
 35. Leucin and Tyrosin (Laache) 247 
 
 36. Calcium Oxalate (Laache) 248 
 
 37. Red Blood-corpuscles and a Blood-cast of a Uriniferous 
 
 Tubule (Eichhorst) 251 
 
 38. Epithelial Cast of a Uriniferous Tubule (v. Jaksch) . 251 
 
 39. Grranular Casts of the Uriniferous Tubules (v. Jaksch) 251 
 
 40. Hyaline Casts of the Uriniferous Tubules (Vierordt) . 251 
 
 41. Waxy Casts of the Uriniferous Tubules (v. Jaksch) . 252 
 
 42. Filaria Sanguinis Homiuis (v. Jaksch) . . . 253 
 
 43. Multiple ]Js'euritis — AVrist-drop and Foot-drop (Gowers) 277 
 
 44. Facial Paralysis (Gowers) 280 
 
 45. Progressive Muscular Atrophy (Gowers) . . . 294 
 
 46. Pseudo-hypertrophic Paralysis in two brothers (Gowers) 297 
 
 47. Pseudo-hypertrophic Paralysis. Mode of ri.sing from 
 
 the ground (Gowers) 298 
 
 48. Paralysis Agitans (after St. Leger) .... 307 
 
 49. Appearance of the Hand in Morvan's Disease (after 
 
 Charcot) , . . 313 
 
 50. Cerebral Miliary Aneurisms (Eichhorst) . . . 324 
 
 51. Wrist-drop from Lead-poisoning (Gowers) . . . 337 
 
LIST OF ILLUSTRATIONS. XIX 
 
 FIG. PAGE 
 
 52. Mode of holding the pen favorable to the development 
 
 of Writers' Cramp (Gowers) 340 
 
 Method of holding the pen when writing becomes dif- 
 ficult (Gowers) 340 
 
 53. Exophthalmic Goiter. Defective descent of the upper 
 
 lids on looking down (after Wilks) .... 352 
 
 54. Akromegalia (after Marie) 356 
 
 55. Outline of the Face : 1, In Myxedema ; 2, In Akro- 
 
 megalia ; 3, In Osteitis Deformans (Marie) . . 357 
 
ESSENTIALS OF DIAGNOSIS. 
 
 INTRODUCTION. 
 
 Diagnosis, in medicine, is tlie art and science of observing 
 and of discriminatingly interpreting the phenomena of disease. 
 In its study, a knowledge of the phenomena of health is an 
 essential prerequisite. Unless familiar with the sounds elicited 
 upon percussion of the normal chest, one cannot decide whether 
 or not the sound heard in a given case is indicative of abnormal 
 conditions. Unless one knows the characteristics of normal 
 urine, he cannot h.ope to gain from urinalysis a clue as to the 
 nature of a case of disease. Unless one knows the appearance 
 of a healthy brain, he cannot determine whether the brain seen 
 at a necropsy is or is not the seat of morbid change. Unless 
 one knows the function of a normal joint, he cannot affirm that 
 a joint under investigation has had its function impaired. 
 
 Having learned, by observations upon the healthy, to recog- 
 nize when departures from health have taken place, one must 
 further learn by observation of the sick to appreciate the sig- 
 nificance of such departures. No opportunity should be lost to 
 examine post mortem the organs and tissues that have been 
 altered by disease. 
 
 A knowledge of the effects of drugs upon healthy and un- 
 healthy persons and organs may likewise render easy a diag- 
 nosis that might otherwise be difficult. 
 
 The phenomena indicative of the existence of disease are in a 
 
 general way termed symptoms. These may be either subjective — 
 
 known only to the patient by his sensations ; Or they may be 
 
 objective — capable of investigation by the senses of the observer, 
 
 2 (17) 
 
18 ESSENTIALS OF DIAGNOSIS. 
 
 aided, it may be, by instruments of precision. Thus pain, ver- 
 tigo, nausea, ringing in the ears, are subjective symptoms, while 
 high temperature, vomiting, unsteadiness of motion, loss of 
 voice, are objective symptoms. 
 
 The objective manifestations of disease may be further divided 
 into symptoms (in a restricted sense) and signs. While the two 
 are not rigidly separable, symptoms may be defined as manifesta- 
 tions of disordered function, signs as manifestations of altered 
 structure. Thus, cough is a symptom ; the laryngeal congest- 
 ion discovered by inspection with the mirror, the bronchial 
 rales heard upon auscultation, are signs. DiflSculty in deglu- 
 tition is a symptom ; a pulsating tumor in the chest, indicative 
 of aneurism pressing upon the esophagus, is a sign. Dyspnea 
 is a symptom ; distension of the abdomen with gas (tympanites) 
 or with tluid (ascites), causing pressure upon the diaphragm and 
 restricting its movements, is a sign. 
 
 Thus, signs are in man}- cases directly explanatory of symp- 
 toms, and their discovery is one step further in the diagnosis. 
 It must not be forgotten, however, that signs are not always to 
 be found ; that, when found, a sign may not account in tola for 
 the symptom with which it is associated ; and that even when 
 suflBcient to explain the symptom, the sign itself remains to be 
 explained before the diagnosis is complete. Like all other mor- 
 bid phenomena, signs must, therefore, be considered in relation 
 with all the evidence presented in a given case. 
 
 Certain signs that are not at once manifest, but that require 
 for their study special means of exploration, are termed p%sicoZ 
 signs. In its restricted sense, the term "physical signs" is 
 applied to the phenomena elicited b}- special methods [inspec- 
 tion., mensKralion, palpation, pjercussion, and auscultation), used 
 chiefly in examination of the chest and abdomen, though often 
 applied elsewhere ; while the signs elicited by examination of 
 the blood, the urine, the sputum, the feces, or by laryngoscopy, 
 ophthalmoscop3', cystoscopy and the like, are not given other 
 qualifying designation than the special names describing the 
 respective processes. 
 
 Phenomena corresponding with logical deductions as to the 
 direct results of deranged function, including subjective and 
 
INTRODUCTION. 19 
 
 objective symptoms and signs, are called rationed signs, in con- 
 tradistinction from physical signs, which denote the mechanical 
 condition of the structures examined. Thus, in a case of valvu- 
 lar disease of the heart, weakness, vertigo, shortness of breath, 
 pallor and dropsy would be termed rational signs, while the 
 area of cardiac percussion-duluess and the character of the 
 sounds heard upon auscultation would be termed physical signs. 
 
 Symptoms may also he divided into general or constitutional 
 symptoms and local symptoms. General symptoms are those, 
 like fever, depression, delirium, that may result from unbalancing 
 of the organism as a whole, and are common to affections of many 
 kinds ; while local symptoms are those, like swelling or discol- 
 oration of a part and circumscribed pain or tenderness, that result 
 from localized morbid conditions and are confined to a certain 
 locality, usually that of the organ or tissue diseased. 
 
 Sympioms caused by local disease not at the seat of mani- 
 festation and that are not dependent upon mere mechanical in- 
 fluences or upon interference with related function, but that 
 arise indirectly, as a result of nervous irritation, are termed 
 reflex symptoms. Thus, 'the diflSculty of breathing occasioned by 
 the pressure of a mediastinal tumor upon the trachea is a local 
 symptom, due to a mere mechanical influence ; dyspnea from 
 deranged action of the heart is a symptom dependent upon 
 interference with related function ; while an asthmatoid condi- 
 tion dependent upon disease of the nose is a reflex symptom. 
 It must not be forgotten, however, that the same symptom 
 may at one time be local ; at another time, part of a general 
 process ; at another time, reflex. Thus, vomiting may indicate 
 local disease of the stomach ; or it may be part of the general 
 disturbance caused by certain febrile diseases ; or it maj^ re- 
 flexly indicate disease in the abdomen or in the brain. 
 
 Having, by careful observation and interrogation, ascertained 
 the pi-esent condition of the patient and having, by inquiry, 
 learned his family history (in order to judge of the probable 
 influence of hereditary disease, diathesis or liability) and his 
 previous history (anamnesis) of health or disease (including a 
 knowledge of his mode of life and of his surroundings, as well 
 as the mode of invasion of the disease under investigation and 
 
20 ESSENTIALS OF DIAGNOSIS. 
 
 its course up to the moment of examination), it becomes neces- 
 sary to interpret the information tlius gained — in other words, 
 to mctke a diagnosis. 
 
 In making a diagnosis one lias to consider not only the bear- 
 ing of the signs and symptoms individually and collectively, 
 but also their relations with the phenomena of health and with 
 each other. Further, one has to consider (and this is what 
 may, to some extent, be learned from reading) the historical 
 experience of the medical profession as to the significance of 
 certain symptoms and groups of symptoms, and as to the rela- 
 tion of certain symptoms and groups of symptoms with lesions 
 observed post mortem. 
 
 A diagnosis may thus be made (1) by the inductive method, 
 reasoning, upon anatomical (structural) and physiological (func- 
 tional) data, from the character of the disturbance to the organ 
 affected and the nature of the affection ; (2) by the historical or 
 empirical method, relying upon the recorded experience of other 
 observers and upon one's own experience that certain symp- 
 toms manifested under certain circumstances indicate the 
 existence of a definite malady ; or (3) by the method of pjatho- 
 logical association, which is based upon the fact that when 
 certain symptoms have been observed during life, definite 
 lesions have been discovered after death. By analogy, the les- 
 sons of pathological association may be applied in affections 
 not necessarily of a fatal character. It is obvious, therefore, 
 that a knowledge of the various gross and minute morbid 
 changes occurring in the body generally or in special organs, 
 tissues or cells and of the circumstances under which special 
 changes are likely to occur is essential for precision in diagnosis. 
 The most satisfactory results are to be obtained when all of the 
 methods indicated can be concurrently availed of. 
 
 Diagnosis may further be direct, differential or by exclusion. 
 Diagnosis is said to be direct when one or more of the signs or 
 symptoms, independently of or in relation with other symptoms 
 or with the age, sex, physical and mental characteristics, resi- 
 dence or occupation of the patient, or with his family history, 
 enable direct affirmation to be made of the nature of the malady. 
 Thus, a paroxysm of chill, fever and sweating, in association 
 
INTRODUCTION. 21 
 
 with the presence in the blood of characteristic parasites, per- 
 mits a direct diagnosis of malarial fever to be made. 
 
 Diagnosis is said to be discriminative or differential when the 
 signs or symptoms are suggestive of more than one disease and 
 a decision is reached by comparison and contrast. It is neces- 
 sary to compare the ideal pictures of various diseases in turn 
 with the actual picture presented, in order to establish the 
 resemblance or unlikeness ; finally affirming the nature of the 
 case with more or less certainty, according to the completeness 
 and definiteness of the observations made and the degree 
 of knowledge on the part of the clinician as to the conditions 
 present in the respective affections under review. Diagnosis 
 is usually differential, and as one is often compelled to balance 
 probabilities, with incomplete evidence before him, differential 
 diagnosis calls for the greatest knowledge and skill. ^Numerous 
 examples of differential diagnosis will be found throughout this 
 book. Reference may here be made to malarial fever, in case 
 hematozoa are not demonstrable, and the fever of hepatic sup- 
 puration or of pulmonarj' tuberculosis. Careful observation of 
 the temperature-course and painstaking physical examination 
 may be required to establish the points of difference. 
 
 In diagnosis by exclusion one is unable to affirm the nature of 
 the affection directly ; and even after comparison of the evident 
 phenomena with the phenomena of the respective diseases sug- 
 gested, the points of resemblance are not sufficiently great in 
 number or in character to warrant an affirmative conclusion in 
 any one instance. It then becomes necessary to prove a nega- 
 tive ; to do which, reliance nmst be placed entirely upon points 
 of unlikeness. One endeavors to recall in the ideal picture of a 
 certain malady some symptom or association of symptoms so 
 necessary that its absence from the actual case may warrant a 
 decided negative ; or, on the other hand, to discover in the case 
 before him some symptom or association of symptoms so in- 
 compatible with the ideal picture of the malady under consid- 
 eration as likewise to warrant a negative conclusion. Thus, 
 from the absence of what ought to be present and from the 
 presence of what ought to be absent, one after another of the 
 conditions discussed is set aside, until finally one remains that 
 
22 ESSENTIALS OF DIAGNOSIS. 
 
 cannot be so excluded ; and there is reached a more or less 
 probable diagnosis. 
 
 Diagnosis by exclusion is the least satisfactory, as one can 
 never be sure that he has passed in review and has excluded all 
 of the conditions that ought to be excluded. Nevertheless, it 
 sometimes aflbrds most brilliant results. Thus, paralysis of the 
 left vocal baud, associated with recurring cough and occasional 
 dyspnea and dysphagia, every other suggested cause for which 
 has been excluded, has led to a correct diagnosis of aneurism of 
 the arch of the aorta, not discoverable by the most careful 
 physical exploration. 
 
 As a rule, that diagnosis that best and most readily accounts 
 for all of the symptoms is the most likely to be correct. When 
 any symptom is unaccounted for, the diagnosis is at least in- 
 complete, if not doubtful. Diagnosis of a common disease, 
 other things being equal, is more likely to be correct than diag- 
 nosis of a rare disease. On the other hand, statistics have no 
 beariug upon the individual case ; the rare disease may be 
 present and be overlooked, from want of knowledge or in conse- 
 quence of superficial examination. 
 
 More than one disease may be present in the same patient at 
 the same time ; but certain diseases are held to be antagonistic 
 and thus not likely to coexist. Data bearing on this point are 
 defective and are undergoing revision and correction. Not a 
 few cases have been recorded contradictory of some of the 
 teachings of the past. Hence, in this work, little stress has 
 been laid upon these antagonisms. On the other hand, there 
 are many lesions and morbid processes that are frequently found 
 associated. Such associations are specifically mentioned where- 
 ever it seemed likely that a knowledge of their existence would 
 be of service. 
 
 One disease sometimes strongly predisposes to another. A 
 knowledge of facts of this nature is often of assistance in diag- 
 nosis, as well as in preventive treatment. 
 
 A knowledge of the compUcations and sequelce that ordinarilj' 
 or exceptionally attend or follow certain diseases, independently 
 of its bearing upon therapeutics, is an important equipment 
 for the diagnostician. This can be acquired only by extensive 
 
INTRODUCTION. 23 
 
 reading or by prolonged experience. In anticipation of the latter 
 source of information, tlie former must be sedulously cultivated. 
 In default of such knowledge, the mistake may be made of 
 diagnosticating a single well-marked condition, as, for instance, 
 pleuritis, as the whole of the disease ; when, in reality, the con- 
 dition may be but a comjparatively unimportant complication in 
 the course of typhoid fever or of an hepatic abscess. Similarly, 
 a sequela to some acute disease, remote in time or obscure in 
 symptoms, may be diagnosticated, prognosticated and treated 
 as an independent afiection, often to the grave detriment of the 
 patient. Thus, a temporary loss of knee-jerk following un- 
 recognized diphtheria has led to an incorrect diagnosis of loco- 
 motor ataxia. Sometimes the initial phenomena of disease 
 escape observation (a chancre may be concealed, especially in 
 the female, or scarlatina may occur without eruption or appre- 
 ciable fever, thermometry not being resorted to), and when the 
 later phenomena (such as syphilitic fever or scarlatinal dropsy) 
 develop, the case may be misinterpreted, unless this possibility 
 of masked beginnings be borne in mind. 
 
 The so-called negative signs of disease should not be under- 
 rated. The absence of headache may assist in the exclusion of 
 brain-tumor ; the absence of albumin and casts from the urine, 
 after sufficiently careful and extended observation, may be of 
 great importance in discriminating among the causes of a train 
 of symptoms including vertigo, optic neuritis, vomiting and 
 paroxysmal dyspnea ; the absence of rose-rash and of splenic 
 enlargement may determine the diagnosis between enteric in- 
 fluenza and typhoid fever. In recording cases it is necessary to 
 note negative points in order to show that the inquiry or search 
 has been made. 
 
 No less important is a knowledge of the morbid phenomena 
 that may be caused by certain drugs — not merely by the narcotic 
 agents, opium, belladonna, and the like, but by such poisons as 
 mercury, arsenic and lead, which may produce symptoms 
 closely resembling acute and chronic diseases of common occur- 
 rence or may give rise to nervous and other phenomena puzzling 
 in the extreme. Similarly, common or unusual drug-effects, 
 perhaps due to idiosyncrasy, occurring in the course of treat- 
 
24 ESSENTIALS OF DIAGNOSIS. 
 
 ment, may mask the symptoms of disease, or give rise to addi- 
 tional phenomena that, unless caution be exercised, may lead to 
 error in diagnosis. 
 
 The data for diagnosis are obtained by ofeser'j;aMow and inquiry. 
 
 Inquiry may often have to be made of those about the patient, 
 the latter being unable or incompetent to answer ; and not 
 rarely the same questions will have to be repeated in various 
 ways and be controlled by questions requiring opposite answers, 
 in order that the clinician be not deceived, intentionally or 
 otherwise. 
 
 Ohservaticyti can be made while the questioning is proceeding ; 
 sometimes the manner, method and form of a patient's answers 
 to questions are in themselves part of the data a.cquired by ob- 
 servation. For example, in cases of aphasia, the patient is 
 unable to find words in which to express himself, though he 
 may understand the questions put and may even believe that in 
 his monotonous repetition of certain words and phrases he has 
 given an intelligent answer. 
 
 Observation includes (1) a more or less rapid survey of the 
 general condition of the patient, and (2) a careful examination 
 into the condition of spea'aZ structures^ the performance of special 
 functions and the constitution, chemic and microscopic, of the. 
 blood, the secretions and the excretions, both as to normal and 
 abnormal constituents. 
 
 The whereabouts of the patient may afford information as to 
 the acuteness or severity of the attack. He may be attending 
 to his work as usual, or he may be confined to his house, his 
 room, his bed. 
 
 Position and movement are next noted. Thus, if the patient 
 paces restlessly about, a condition of excitement, of physical or 
 mental causation, is indicated. If, whether seated or recumbent, 
 his position is easy and unconstrained, it indicates that, what- 
 ever the disease may be, the attack is, for the time being, mild 
 and that there is no serious respiratory or circulatory trouble, 
 or inflammation of an important part. If the patient lie pass- 
 ively upon his back, or huddled up in a heap, a prostrating sick- 
 ness, usually an acute infectious disease, is indicated. If he lie 
 persistently on one side, affection of the lung or pleura of that 
 
INTRODUCTION. 25 
 
 side is likely to exist ; because this position restrains the move- 
 ment of tliat side of the thorax, lessens the pain of acute in- 
 flammation and, in addition, permits the healthy lung to better 
 perform its work. Sometimes, however, patients with pneu- 
 monia lie on the sound side, having less pain in that posture. 
 
 If, whether the patient be in an easy-chair, or in bed, the 
 thorax is propped into an upright or semi-upright posture, 
 there is great difficulty in respiration {orthopnea), which may be 
 be due to cardiac or pulmonary disease, to obstruction in the 
 upper air-passages, or to abdominal or general effusions. If the 
 patient lie upon his back with the legs drawn up, there is likely 
 to be peritonitis, and if on the right side with the right leg 
 drawn up, appendicitis should be suspected. 
 
 If the head is retracted, or fixed in opisthotonos, disease of 
 the cerebrum or of the meninges is to be suspected. So, too, 
 deviation of the head to one or the other side, picking at the 
 bedclothes, helplessness of one or more extremities, general 
 restlessness, jactitation, local spasms or general convulsions, 
 incoordination, tremor, temporary or persistent, sometimes 
 throw considerable light on the condition of the nervous system. 
 
 The expression of the countenance should be observed. It may 
 be indicative of comparative comfort or of intense suffering ; it 
 may be dull and apathetic, as in typhus fever ; sunken and 
 anxious, as in cholera ; eager and brilliant, as in some cases of 
 pulmonary tuberculosis ; indeed, a careful study of the physiog- 
 nomy of patients may often directly reveal much, or indirectly 
 serve to lead the attention of the examiner to matters that might 
 otherwise be overlooked. Thus, there is in many cases of chronic 
 nephritis a peculiar pallor that can hardly be mistaken by the 
 experienced observer. Connected with the expression of the 
 face are the general nutrition, the condition of the sMn, and the 
 condition of the mind, all of which must be included in the 
 general examination. 
 
 Concerning the mental condition, without special effort it can 
 be learned whether the patient is interested in his surroundings 
 or is oblivious to them, whether he is conscious or unconscious, 
 whether he is delirious or is aware of his sayings and doings, 
 whether he is able to fix his attention or is continually wander- 
 
26 ESSENTIALS OF DIAGNOSIS. 
 
 ing. To the facts developed on special inquiry no attention is 
 now being paid. 
 
 The skin may be of normal hue, pallid from impoverishment 
 of blood, flushed with fever, discolored by inflammations, bruises, 
 extravasations, eruptions, jaundice, the various cachexias. It 
 may be swollen, or give evidence of swelling or effusion beneath. 
 It may be abnormally smooth or rough, dry or moist, hot or 
 cold. 
 
 The state of the nutrition is usually evident in the preservation 
 of the full, rounded outlines, or in the sharpness and hollows of 
 emaciation. For accuracy and completeness of knowledge the 
 weight should be determined by the scales, 
 
 Ahnorinal prominences of various kinds and situation may in- 
 dicate the existence of tumors^ effusions, articular, osseous, glan- 
 dular and visceral enlargements of inflammatory or other origin, 
 to be determined by further examination. 
 
 Pulsations may be visible that, by their abnormal situation or 
 abnormal character, are indicative of abnormal circulatory con- 
 ditions, or of tumors or collections of fluid external to the heart 
 or vessels. The tortuosity of visible arteries, or the localized or 
 general turgescence of superficial veins, may indicate disease or 
 obstruction in or afffecting the circulatory apparatus. 
 
 The manner in which breathing is performed, the character of 
 the voice, the nature of a cough, afford information as to the con- 
 dition of the respiratory apparatus. 
 
 Examination of the puZse, the tongue, and the temperature, while 
 aflTording general indications, yet mark the transition from 
 general to special examinations. 
 
 Except in a few instances, the plan of this book does not con- 
 template descriptions of methods of special examination, or 
 enumeration of the conditions indicated by special symptoms 
 and signs [semeiology, inductive diagnosis), but rather an account 
 of the observed clinical groupings of signs and symptoms in the 
 recognized and named affections of nosology {historical diagnosis, 
 pKdhological association diagnosis), and an elucidation of the 
 points of contrast between diseases most likely to be confounded 
 {differential diagnosis). 
 
FEVER. 27 
 
 FEVER. 
 
 What is fever ? 
 
 Fever is a complex morbid process, of which the most striking 
 feature is elevation of temperature. Sometimes the term fever 
 is restricted to the abnormal heat, hut this is more correctly 
 termed ipyrexia. In addition to pyrexia, fever is attended with 
 acceleration of the pulse and of the respiration, with thirst and 
 with disturbance of digestion. There are likewise increased 
 and perverted tissue-changes, as manifested by alterations of 
 secretions and excretions, which may be completely arrested or 
 diminished in quantity and changed in quality. As a result of 
 the deprivation of the normal products of metabolism and of the 
 retention in the blood of abnormal products of metabolism, as 
 well as of the waste-products of normal metabolism, other symp- 
 toms are often caused, such as malaise, depression, headache, 
 insomnia, delirium, etc. When fever is long-continued, wasting 
 takes place ; partly as a result of the abnormal heat, both di- 
 rectly and indirectly ; partly from other causes. Many febrile 
 processes are at some period in their course attended with sub- 
 normal temperature. 
 
 What is the average normal temperature of man ? 
 
 The average normal temperature of the adult is 98.4° or 98.6° F. 
 (37° C.) ; in health it may vary from this a little more than a 
 degree ; from 97.3° F. (36.25° C.) to 99.5° F. (37.5° C). It is 
 higher in children than in adults, and in the aged it is some- 
 times a few tenths higher or lower. 
 
 The temperature is increased after meals by the activity of 
 digestion ; it is increased by exertion, and in children and hys- 
 terical persons by emotion. Weather has but slight influence 
 upon the temperature of the healthy; it often has a marked influ- 
 ence upon that of the sick. Thei'e are daily periodic variations. 
 The daily minimum occurs in the early morning between two 
 and five o'clock ; the daily maximum, is reached between five and 
 eight o'clock in the evening. The average difference between 
 maximum and minimum is about 1.5° F. ; it may be much 
 
28 ESSENTIALS OF DIAGNOSIS. 
 
 more. In the tropics the average body-heat is said to be 
 shghtly higher, and tlie daily range greater than in temperate 
 chmates. 
 
 In sickness the diurnal variations (morning remission, evening 
 exacerbation) become quite marked. 
 
 What is subfebrile temperature ? 
 
 The term suhfehrile temperature is not to be confounded with 
 subnormal temperature. It is applied to a moderate morbid ele- 
 vation of temperature not exceeding 100.4° F. (38° C). 
 
 What is the ordinary range of febrile temperature? 
 
 A temperature of from 100.4° F. (38° C.) to 101.2° F. (38.4° C.) 
 is considered an indication of slight fever. 
 
 A temperature of from 101.3° F. (38.5° C.) to 102.2° F. (39° C.) 
 in the morning, and of 103° F. (39.5° C.) in the evening, is in- 
 dicative of moderate fever. 
 
 A temperature of from 103° F. (39.5° C.) to 104° F. (40° C.) 
 in the morning, and of 105° F. (40.5° C.) in the evening, indi- 
 cates high fever. 
 
 What is hyperpyrexia? 
 
 Febrile temperature exhibiting a tendency to remain above 
 107° F. (41.7° C.) is called hyx^erpyrexia. This is ordinarily 
 directly dangerous to life. 
 
 Very high temperatures have been observed in hysterical 
 cases in which, apparently, deception has been guarded against ; 
 a case of injury to the spine, in which recovery took place, is 
 reported to have exhibited on many occasions a temperature of 
 122° F. (50° C). 
 
 What is meant by inverse temperature ? 
 
 Ordinarily the course pursued by morbid temperature is like 
 that of normal temperature in having its maximum towards 
 evening, and its minimum in the early morning. Sometimes, 
 however, the maximum may be much earlier or much later than 
 usual, even at noon or at midnight. Sometimes there are great 
 fluctuations during day and night. When a complete reversal 
 takes place, so that the morning temperature exhibits the maxi- 
 
FEVER. 29 
 
 mum, and the evening temperature the minimum, the concUtiou 
 is said to be one of " inverse temperature." 
 
 Inverse temperature not infrequently occurs in acute tubercu- 
 lous affections. It is of rather rare occurrence in typhoid fever. 
 
 What is the significance of a sudden fall of temperature ? 
 
 A sudden fall of temperature may be part of the usual phe- 
 nomena of a disease, as in intermittent fever ; or it may indi- 
 cate termination by crisis, as in pneumonia ; or when it is not 
 part of the usual course, and is not brought about by obvious 
 loss of blood (as by venesection or menstruation), by drugs or 
 cold applications, or other extraneous influence, it may indicate 
 the development of albuminuria, or the occurrence of internal 
 hemorrhage. 
 
 What is subnormal temperature ? 
 
 A temperature lower than 97.3° F. (36.25° C.) is considered 
 suJinormal. 
 
 The temperature may be subnormal in influenza and in acute 
 yellow atrophy of the liver as part of the essential course of the 
 disease. 
 
 Subnormal temperature occurs, usually associated with pro- 
 fuse perspiration, at periods of critical recovery, as in pneu- 
 monia. There is simultaneous decrease in the frequency of 
 pulse and of respiration and improvement in the general con- 
 dition and sensations of the patient. In many acute diseases 
 that terminate by lysis, such as typhoid fever, the temperature 
 falls below the normal with the setting in of convalescence. 
 
 A subnormal temperature develops abruptly in conditions of 
 collapse. It is then associated with sudden failure of the heart, 
 as indicated by a feeble, rapid and irregular pulse, a fluttering 
 and feeble cardiac impulse, pallor, coldness of the skin, with or 
 without sweating, faintness or syncope, and profound prostra- 
 tion and weakness. The pulse becomes feebler, less rapid, and 
 may finally cease. If recovery take place, the temperature again 
 rises ; or, if the termination be fatal, the temperature may rise 
 post mortem. 
 
 The temperature becomes subnormal in some cases of severe 
 hemorrhage, and at times, temporarily or persistently, in chronic 
 
30 ESSENTIALS OF DIAGNOSIS. 
 
 wasting diseases, such as pulmonary tuberculosis and carci- 
 noma, in chronic Bright's disease and in some diseases of the 
 brain. 
 
 What is an essential fever ? 
 
 An idiopaihic or essential fevei' is one in which the pyrexia and 
 its concomitants do not result secondarily from an anatomical 
 lesion, but arise primarily from the action of a specific poison 
 or a similar cause. Essential fevers may or may not present in- 
 variable lesions as a part of their phenomena. 
 
 What is a symptomatic fever? 
 
 A symptomatic or deutcropathic fever is one that arises second- 
 arily as the result of irritation, intoxication or perverted func- 
 tion, caused by disease or injury of a special organ or tissue. 
 The causative lesion is the essential element ; the fevex is but 
 one of the symptoms. 
 
 What is a specific fever ? 
 
 A spiecific fever is an essential fever due to a specific patho- 
 genetic agent. Typhoid fever and yellow fever are examples of 
 specific fevers. 
 
 What is a continued fever? 
 
 A continued fever is one in which the temperature pursues an 
 uninterrupted course, witliout sudden variation from beginning 
 to end. The diurnal range will not exceed 1.8° F. (1°C.). The 
 first rise may be sudden or gradual ; there may be steady main- 
 tenance of a maximum, or continuous increase ; there may be 
 gradual or sudden final defervescence ; but there is not a decided 
 fall and a renewed rise during the progress of the case. 
 
 What is a remittent fever ? 
 
 A remittent fever is one the course of which is interrupted once 
 or repeatedly by a marked decline in temperature, not reaching 
 the normal, and followed by renewed exacerbation. The daily 
 difi"erence wil exceed 1° C. (1.8^ P.). 
 
 What is an intermittent fever ? 
 
 An intermittent fever is one in the course of whicli a complete 
 intermission takes place once or repeatedly ; that is to say, in 
 
SIMPLE CONTINUED FEVER — ARDENT FEVER. 31 
 
 the progress of the case the temperature becomes normal (or 
 even subnormal), remains normal for an appreciable time, of 
 greater or less duration, and subsequently rises to about its 
 previous level. The maximum may be high. 
 
 Simple Continued Fever. 
 
 What is the clinical course of simple continued fever ? 
 
 Simple continued fever ^ ei^hemeral fever or febricida is a non- 
 specific fever, sometimes apparently idiopathic, but often symp- 
 tomatic of digestive aberration or of some local irritation. It 
 may be caused by error in diet, by fatigue, anxiety, shock, un- 
 usual mental or physical exertion, exposure to cold and damp 
 to a foul atmosphere, or to the sun. 
 
 The disease sets in with a feeling of indisposition, which is 
 followed by chilliness, fever, with heated skin, headache, thirst, 
 anorexia and pain in the back and limbs. The pwZse is acceler- 
 ated. The tongue is coated. There is usually constipation^ less 
 frequently diarrhea. The urine is scanty and high-colored. The 
 pyrexia is slight or moderate ; the diurnal variations are small, 
 the rise rapid, the fall gradual or by critical defervescence, with 
 profuse sweating or watery diarrhea. The duration is commonly 
 less than a week. It may be less than twenty-four hours. Ee- 
 covery is invariable and convalescence is rapid. 
 
 Graver forms of the affection, induced by the graver causes, 
 may be attended with considerable depression, and running a 
 more protracted course, in duration from ten to fourteen days, 
 may simulate typhoid fever. Especially is this resemblance 
 marked in cases of septic intoxication. 
 
 Ardent Fever. 
 
 What is ardent fever ? 
 
 Ardent fever is a non-specific, continued fever, occurring in hot 
 countries, in which the ordinary symptoms of febricula are 
 exaggerated. The temperature reaches or exceeds 103° F. ; there 
 is throbbing of the temporal arteries, with severe headache and 
 
32 ESSENTIALS OF DIAGNOSIS. 
 
 even delirium. The symptoms resemble those of an inflamma- 
 tory fever, so that the utmost care must be observed to avoid 
 error in diascnosis. 
 
 Thermic Fever— Insolation— Sunstroke. 
 
 What is thermic fever ? 
 
 TJiermic fer.er^ or sunstroke, results from exposure to extreme 
 heat. The heat may be excessive and the exposure brief, or 
 the heat may be less intense and the exposure prolonged. The 
 condition is described with affections of the nervous system. 
 
 Catarrhal Fever — Influenza. 
 
 What is catarrhal fever ? 
 
 Catarrhal fever, ejndemic catarrh, influenza or la grippe, now 
 commonly called "grip" in the United States, is an infectious, 
 possibly contagious disease, belonging to the group of specific, 
 essential, continued fevers, that occurs epidemically, endemi- 
 cally or pandemically, more rarely sporadically, and exhibits a 
 protean capability of variation in its symptoms. 
 
 There are four prominent varieties : (1) the catarrhal, in which 
 the predominant features are those of catarrhal inflanmiation of 
 the respiratory tract ; (2) the thoracic, in which, with or without 
 the ordinary catarrhal manifestations, there are symptoms of 
 profound involvement of the thoracic viscera ; (3) the abdominal 
 or gastro-intestinal, in which disturbances of the digestive tract 
 are most marked ; (4) the nervous or cerebral, in which neural 
 phenomena attract attention, and in which, as in the abdominal 
 variety, the clinical course of typhoid fever is often closely simu- 
 lated. Much greater refinement in subdivision might be made, 
 as the symptoms of two or more types are frequently associated 
 in one case. Some epidemics are characterized by greater or 
 even exclusive prevalence of one or two types ; but in other 
 epidemics, half a dozen patients in one household may exhibit 
 six varieties of the disease. 
 
CATARRHAL FEV ER^INFLUENZ A . 33 
 
 What is the clinical course of influenza ? 
 
 The invasion of influenza is commonly sudden, sometimes with 
 a chill, usually with more or less irritation or inflammation of the 
 mucous membranes of the nose and throat, often associated with 
 catarrhal conjunctivitis and blepharitis (pink-eye). There is 
 always a feeling of lassitude, ^jassing into unaccountable de- 
 pression, physical and mental, great soreness in the back and 
 limbs, aching of the muscles, more or less stiftness of the neck, 
 cutaneous hyperesthesia, headache, dyspnea and anorexia. 
 
 The temperature is decidedly irregular ; it may rise high ; it is 
 often subnormal for more or less protracted periods, and is sub- 
 ject to extreme fluctuations. Q^he pulse is not much acceler- 
 ated ; it ordinarily is weak, the heart sharing in the general 
 depression. The tongue is coated ; the bowels are often consti- 
 pated ; the urine is scanty and high-colored, or profuse and 
 light-colored. The skin is hot and dr}'^ and very sensitive to the 
 touch. Sometimes there are irregular perspirations. 
 
 In the catarrhal type^ sneezing, coryza, watering of the eyes, 
 odynphagia, painful respiration and a dry, harassing, irritative 
 cough are early and prominent symptoms. The difficulty and 
 distress in breathing are out of all proportion to the phenomena 
 elicited by auscultation and percussion. Later, the cough be- 
 comes freer, and associated with expectoration of a thick, glairy 
 mucus, sometimes blood-streaked or discolored ; the nasal dis- 
 charge becomes thicker and even purulent and hemorrhagic. 
 With recovery, profuse, watery diarrhea occurs. In some cases, 
 symptoms of tonsillitis or of catarrhal pharyngitis are the earliest, 
 those of laryngitis and of bronchitis following. Coryza may be 
 a late manifestation. In some cases, there is a peculiar edema- 
 toid condition of the tonsil, uvula and neighboring structures 
 that has been termed " solid edema," as puncture gives exit 
 not to serum, but to a sanious, stringy, lymphoid material. 
 Su4)purative otitis media, preceded by excruciating earache and 
 usually affecting both ears in succession, may be the only mani- 
 festation in the upper air-tract. This otitis is quite common in 
 children and usually runs through a household. 
 
 In the thoracic type, pleuritis, pericarditis, endocarditis, pneu- 
 monia--catarrhal, croupous or hemorrhagic— or edematous or 
 3 
 
34 ESSENTIALS OF DIAGNOSIS. 
 
 hemorrhagic infillration of the lung may cause grave symptoms 
 or even death. 
 
 In the abdominal or gastro-intesUnal type, vomiting and purging 
 are common, and tliere may be great pain and tenderness in the 
 epigastrium or over the entire abdomen. Catarrhal jaundice 
 may occur. 
 
 In the cerebral or nervous type, the headache is intense ; there 
 may be insomnia, photophobia, tinnitus aurium, talkativeness 
 or even mild delirium. There is decided hyperesthesia ; there 
 may be restlessness, tremor, muscular twitchings or jactitations. 
 
 In the typhoid type, the course of the disease may be pro- 
 tracted, and the temperature may remain continuously elevated. 
 The prostration may be extreme ; the mental phenomena may 
 be characterized by depression. There may be epistaxis, pain 
 in the splenic region, special tenderness in the right iliac fossa 
 and considerable diarrhea. There may be anomalous eruptions 
 — papular, herpetic or erythematous. The action of the heart 
 may be exceedingly feeble. Heart-failure is always a threaten- 
 ing danger. 
 
 The duration of influenza is as variable as are the symptoms. 
 It may be less than forty-eight hours ; it may be several weeks. 
 Commonly, the acute symptoms last from three or four days to 
 a week, but the weakness and depi-ession continue much longer. 
 Convalescence may be tardy, prolonged subnormal temperature 
 and annoying perspiration being notable features. 
 
 In addition to the complications mentioned, there may be 
 hemorrhages from various organs, meningitis— cerebral and 
 spinal — multiple neuritis, arthritis and nephritis. Among the 
 sequelae, are tuberculosis, paralyses of various kinds, hemicrania 
 and melancholia, and other psychoses. Of itself influenza is not 
 often fatal or directly provocative of serious complications or 
 sequelse ; but it aggravates existing lesions or morbid processes, 
 reawakens latent disease or searches out the weak point in the 
 organism and renders this liable to the action of exciting 
 causes. Hence, the great variability in its clinical course, and 
 hence, too, the high mortality it occasions among the previously 
 sick and debilitated, among infants and the aged. 
 
TYPHOID FEVER — ENTERIC FEVER. 35 
 
 With what diseases may influenza be confounded ? 
 
 The diagnosis of influenza may be extremely easy or ex- 
 tremely difficult. According to its type, it may be mistaken for 
 simple catarrhal inflammation of the mucous membrane of the 
 eye, ear, nose, throat, bronchi, stomach or intestines ; for 
 measles ; for cesebro-spinal meningitis ; for acute articular 
 rheumatism ; for dengue ; for ordinary types of pleurisy or 
 pneumonia ; for malarial fever ; for acute tuberculosis ; for 
 typhoid fever. 
 
 Upon what does the discrimination depend? 
 
 In times of prevalence of epidemic influenza, or of the analo- 
 gous epizooty, the knowledge of that fact will cause one to be 
 on the lookout for the disease, and he may, perhaps, even call 
 other affections by its name. Characteristics upon which stress 
 should be placed are the sudden onset, the great depression, 
 the cutaneous hyperesthesia, the lumbar and muscular pains 
 and the excessive respiratory distress. These serve to distin- 
 guish it from indigestion, gastro-intestinal catarrh, bronchitis, 
 coryza and " colds." In contradistinction from typhoid fever or 
 typhus fever, the common occurrence of some form of catarrhal 
 symptoms, the irregularity of the temperature, the shorter dura- 
 tion and the absence of the characteristic symptoms to be de- 
 scribed, are additional discriminating points. The differential 
 diagnosis from the other diseases mentioned will be successively 
 developed. 
 
 Typhoid Fever— Enteric Fever. 
 
 What is typhoid fever ? 
 
 Typhoid or enteric fever is an acute, infectious disease, belonging 
 to the group of essential, continued fevers, dependent upon a 
 specific microorganism, and presenting constant lesions : inflam- 
 mation, swelling, softening and ulceration of Peyer's patches, 
 enlargement and softening of the mesenteric glands and tume- 
 faction of the spleen. It runs a course of about twenty-four 
 days, beginning gradually and terminating by lysis. The dis- 
 ease is most common in young adults and in the autumn. 
 
 The typhoid-bacillus (Fig. 1) is a plump, motile organism, with 
 
36 ESSENTIALS OF DIAGNOSIS. 
 
 rounded extremities. It is about one-tliird as long as tlie diam- 
 eter of a red blood-corpuscle and one-third as wide as it is long. 
 It presents a characteristic growth upon potatoes and does not 
 liquefy gelatin. It is best stained by means of an alkaline solu= 
 
 Fig. 1. 
 
 Bacilli of typhoid fever. (Von Jaksch.) 
 
 tion of methylene-blue or bj'^ carbol-fuchsin or anilin-water 
 fuchsin. It differs from other organisms found in the stools in 
 not generating indol. The bacillus has been found during life 
 in the blood, in the urine and in the stools, and, after death, 
 in the intestinal wall, in the mesenteric glands and in the spleen. 
 
 What is the clinical course of typhoid fever ? 
 
 The 2Jeriod of incubation of enteric fever varies between two 
 and eleven days. The onset is usually insidious, occasionally 
 abrupt, with a chill. The prodromal 'period, is characterized by 
 headache, pains in the back, epistaxis, general malaise, disturbed 
 sleep, loss of appetite and coated tongue. These symptoms be- 
 come aggravated, while to them are added relaxation of the 
 bowels, abdominal tenderness, especially in the right iliac fossa, 
 intestinal gurgling and elevation of temperature. 
 
 The temperature pursues a characteristic course. (Fig. 2.) 
 There is a period of gradual ascent (first week), a period of 
 maintained height (second week and half of third week), and a 
 period of gradual fall (last half of third week and fourth week). 
 
TYPHOID FEVER — ENTERIC FEVER. 37 
 
 For from five to seven days the temperature rises two or three 
 degrees each evening, to recede a degree or a degree and a half 
 on the following morning, until it has reached a level of from 
 102.5° to 104fi F. (in grave cases even higher), at which, with 
 
 Fig. 2. 
 
 37° C. 
 
 Temperature-chart of a case of typhoid fever. (Wunderlich.) 
 
 slight evening remissions and morning exacerbations, it lingers 
 for from ten to fourteen days, then to decline inversely pretty 
 much as it rose, until, with the setting in of convalescence, it 
 may fall below the normal. 
 
 The pulse is accelerated, but not, as a rule, in proportion to 
 the rise of temperature. It may not exceed 90. It is peculiarly 
 soft and rebounding, giving rise to an apparent duplication 
 known as dicrotism. Tlie tongue is coated in the middle, but 
 red at the margins and tip. The coating is thick and, at first, 
 white. The red, uncoated portion at the tip occupies a charac- 
 teristic wedge-shaped area. The lips, gums and teeth become 
 covered with sordes. The patient often exhales a characteristic 
 odor. The im-pils are dilated. A limited flush colors the cheek. 
 
 Toward the end of the first week or early in the second, a 
 varying number of small, slightly elevated, rose-colored spots 
 that disappear upon pressure or upon stretching the skin may 
 be observed upon the trunk — upon the abdomen or chest, ante- 
 riorly or posteriorly. These spots appear in successive crops, 
 each of which lasts for several days. 
 
 The urine presents a characteristic reaction. If to one part 
 
38 ESSENTIALS OP DIAGNOSIS. 
 
 of a (one-half per cent. ) solution of sodium nitrite in distilled 
 water (1 : 40j and forty parts of a saturated solution of sulph- 
 anilic acid in dilute hydrochloric acid (1 : 20) is added an equal 
 bulk of urine and the whole is rendered alkaline with ammonia- 
 water, a deep-red color is produced. 
 
 In classically typical cases, there is diarrhea ; but in almost 
 an equal number, however, the bowels are constipated. The 
 diarrheal stools present a characteristic appearance, being thin 
 and yellowish, "ochrey," or like pea-soup; they have a pecul- 
 iar, fetid odor ; sometimes they contain blood, independently 
 of a formal hemorrhage. Tympanites is common. The area of 
 splenic percussion-dulness is increased. In the second week, if 
 not earlier, mental dulness and listlessness are manifest. The 
 patient pays little heed to his surroundings, but usually re- 
 sponds when spoken to. Deafness and visual disturbances are 
 not uncommon, and there is frequently low delirium. In the 
 third week, the first sound of the heart is observed to.be feeble ; 
 emaciation is decided, and the tongue often becomes dry, fissured 
 and coated with a heavy, brown fur. Intestinal hemorrhage 
 may occur. Perforation of the bowel, with consecutive peri- 
 tonitis, is among the dangers. 
 
 Usually, towards the end of the third or the beginning of the 
 fourth week, progressive improvement is manifested, coinci- 
 dently with the decline of temperature. The morning remissions 
 exceed the evening rises. Commonly by the twenty-fourth day, 
 but often much later, the temperature has fallen to the norm. 
 Convalescence is slow. 
 
 Death may take place in or after the second week, from exhaus- 
 stion, toxemia, fever or the accidents of the disease. 
 
 Other complications and sequelce than those mentioned are bed- 
 sores, phlebitis, thrombosis, endocarditis, parotiditis, edema, 
 inflammation or ulceration of the larynx, bronchitis, pleuritis, 
 pneumonia, pulmonary tuberculosis, osteomyelitis, meningitis, 
 peripheral neuritis, the formation of abscesses and gangrene. 
 
 Sometimes the symptoms are mild, constituting ambulatory 
 or walking typhoid fever. At other times, the attack, while per- 
 haps severe, terminates at the end of a week, or of two weeks, 
 constituting abortive typhoid fever. A few days after convalescence 
 
TYPHOID FEVER — ENTERIC FEVER. 
 
 39 
 
 has set in, the temperature may again rise, and the attack l^e 
 repeated, though curtailed in duration, constituting a relapse. 
 A relapse may likewise interrupt the declining course of the 
 disease. Sometimes, when convalescence is apparently about 
 to set in, the temperature reascends and remains elevated for 
 an uncertain period, constituting a recrudescence. 
 
 What is the distinction between a relapse and a recrudescence 
 in typhoid fever ? 
 A typical relapse in typhoid fever includes a redevelopment 
 of the entire group of morbid phenomena of the primary disease, 
 as indicated by a characteristic temperature-curve, splenic en- 
 largement and rose-rash, though the duration may be shortened. 
 
 Fig. 3. 
 
 104° F. 
 103° F. 
 lo2° F. 
 101° F. 
 100° F. 
 
 99° F. 
 
 98 °F. 
 
 BSBSSSSBSSBif8i'iBSSSS5SBBBSBSSBiiiBMBSS'a5Bini?BSB 
 
 ■ ■■■■PHHHHBBllmiBiaiBIBiBHHBHBBHBBmiiaiHaillBiaHiaraHBIBi 
 
 ■iiiBLiimBaai 
 
 
 Temperature-chart of relapse in typhoid fever. Convalescence from the relapse 
 interrupted by recrudescence. (From a ease at the Philadelphia Hospital.) 
 
 A recrudescence refers only to a reappearance of fever. The tem- 
 perature of recrudescence does not pursue a typical course ; it 
 may fall as suddenly as it rose. A recrudescence may depend 
 upon some complication or some accidental source of irritation, 
 e. (/., peritonitis, or constipation or the premature or injudicious 
 taking of food. A relapse indicates renewed activity of the spe- 
 cific cause of the disease. 
 
40 ESSENTIALS OF DIAGNOSIS. 
 
 How is perforation of the bowel in typhoid fever to be recog- 
 nized? 
 
 Perforation of the bowel in the course of typhoid fever may 
 or may not be preceded by intestinal hemorrhage. When it 
 occurs, the patient experiences a sudden and intense pain, local- 
 ized at one spot in the abdomen, but soon extending. There 
 may also be rigors. Tympanites, if absent, develops ; if present, 
 it increases. Vomiting may occur. There is exquisite abdom- 
 inal tenderness ; the patient lies upon his back, with the legs 
 drawn up ; the face is pale, pinched and anxious ; the inilse is 
 small, hard and rapid ; the breathing is shallow and thoracic. 
 Shock and collajjse are common. With the fall of temperature, 
 the patient's mind may become clear. Death may take place in 
 a few hours ; but more commonly the temperature again rises 
 and the symptoms of pei'itonitis become predominant, death oc- 
 curring in the course of a few days. 
 
 Fatal perforation may, however, occur without decided symp- 
 toms either of shock or of peritonitis ; or there may be a sudden 
 fall or a sudden rise of temperature, a sudden increase in the 
 pulse-rate or in the intensity of the prostration, or there may 
 be sudden vomiting ; or there may be simply persistent and 
 rebellious tympanites, with comparatively slight abdominal ten- 
 derness and, perhaps, marked depression in the general state of 
 the patient. While perforation is usually fatal, recover}^ has 
 occurred in well-authenticated instances. 
 
 How are typhoid fever and pyemia to be differentiated ? 
 
 Pyemia maybe attended with typhoid symptoms, diarrhea and 
 cerebral manifestations. The temperature (Pig. 4), however, 
 pursues a different course from that of typhoid fever ; it is irregu- 
 lar and presents wide variations in range, often declining below 
 the normal. The morning temperature may be normal, that of 
 noon several degrees above normal, that of evening lower than 
 that of noon. There may be great and sudden changes from 
 day to day. In addition, there may be recurrent chills and 
 sweats. The rose-rash is wanting. The detection of a primary 
 focus of suppuration and the results of metastasis point to the 
 cause of the equivocal symptoms. 
 
TYPHOID FEVER ENTERIC FEVER. 
 
 41 
 
 How are typhoid fever and a typhoid condition to be differ- 
 entiated ? 
 
 A condition of asthenia and low vitality developing in the 
 course of certain febrile conditions, surgical affections, seiDtice- 
 mia and pyemia, possibly attended with diarrhea, is to be dis- 
 
 42° 
 41° 
 40° 
 39° 
 38° 
 37° 
 
 Fig. 4. 
 
 mS'iHi.iH'iiHin 
 jHBiiBiiHiiniiiBB 
 
 HmiBiinnniBB 
 ■MBiiHiiiniag 
 BBHiiBiiniiAHiini 
 ■■■■■riniinnifan 
 ■■■■■■■llll'IIDI'MI 
 
 JSIIIHiil 
 
 ■■■niiniHHBtBBS 
 ■■■nianiHvarBHH 
 ■nauiiBMiM^BiS'^ 
 ■■miiBiiiaSB'Bi 
 
 ■■IIIBMIHHB ■! 
 
 ■■IIIBilHB»aiHB 
 IHIIUHMBM 
 
 Temperature-chart of a case of pyemia. (Wunderlieh.) 
 
 tinguished from typhoid fever by the previous history : on the 
 one hand, there are the evidences of some constitutional or local 
 disease ; on the other, epistaxis, headache, continuous fever of 
 gradual invasion. The age of the patient may have w^eight : 
 typhoid fever being infrequent after thirty-five and rare after 
 fifty, while in the aged many diseases, especially pneumonia, 
 commonly assume a typhoid type. A rose-rash is significant 
 of typhoid fever. 
 
 How are typhoid fever and yellow fever to be differentiated ? 
 
 Initial headache and pains in the loins attend both typhoid 
 fever and yellow fever ; but, in the latter, epistaxis and diarrhea 
 are wanting, the onset is abrupt and the symptoms remit on 
 the second or third day. The discoloi'ation of the skin that 
 gives its name to yellow fever is wanting in typhoid. Yellow 
 fever is a disease of hot climates ; typhoid fever, one rather of 
 temperate climates. 
 
42 ESSENTIALS OF DIAGNOSIS. 
 
 How are typhoid fever and variola to be differentiated ? 
 
 For several days it may be impossible to distinguish typhoid 
 fever and variola from one another. Both present headache and 
 pains in the back. Epistaxis and diarrhea may be wanting in 
 typhoid fever. The onset of variola, however, is likely to be 
 abrupt ; that of typhoid fever insidious and gradual. On the 
 third or fourth day, there appears in variola a characteristic 
 eruption ; simultaneously, the temperature declines. The erup- 
 tion of typhoid fever is unlike that of variola and rarely appears 
 before the fifth day. The subsequent course of the two diseases 
 is sufficiently diverse to remove any possibility of confusion. 
 The presence or absence of vaccine protection and the existence 
 of other cases of one or of the other disease may have some 
 weight in the early diagnosis. 
 
 How may one avoid confounding pneumonia with typhoid 
 fever ? 
 
 While pneumonia may present symptoms of a typhoid char- 
 acter and a temperature-course not unlike that of typhoid fever, 
 the respiratory frequency is out of all proportion to the pulse- 
 rate, while careful physical examination will reveal the signs of 
 pulmonary consolidation (dulness on j)ercussion, bronchial 
 breathing, crepitant rales, increased vocal fremitus and vocal 
 resonance) and perhaps the friction-sound of an associated 
 pleurisy. Pleurisy, however, is by no means rare early in the 
 course of typhoid fever. The appearance of rusty sputum 
 clinches the diagnosis of pneumonia. It must, however, be 
 borne in mind that pneumonia may occur as a complication of 
 typhoid fever. In such a case, the association must be recog- 
 nized by the rose-rash, the splenic enlargement, the diarrhea 
 and the protracted course of the disease. 
 
 How are typhoid fever and trichiniasis to be differentiated ? 
 
 Trichiniasis may present many of the manifestations of 
 typhoid fever, but the epistaxis, the severe headache, the en- 
 largement of the spleen, the characteristic stools, the typical 
 temperature-curve and the i-ose-spots are usually wanting. The 
 knowledge that there is such a condition as trichiniasis, with 
 inquiry as to the food taken and the detection of nodules in 
 the painful muscles, ought to be sufficient to prevent mistake. 
 
TYPHUS FEVER. 43 
 
 Typhus Fever. 
 
 What are the symptoms of typhus fever? 
 
 Typhus fever, also called famine-fever, ship fever and jail fever, 
 is an acute, infectious, essential fever, a type of contagious dis- 
 ease. It develops in crowded and unw^holesoiiie places, among 
 the poor and w^retched, but it may be communicated to any. It 
 has a period of incubation of variable duration— from a few hours 
 to two vv'eeks, during w^hich the patient is comparatively com- 
 fortable, or there may be a brief stage of preliminary depression. 
 
 With the onset of the disease there are general malaise, head- 
 ache, perhaps a chill, pains in the back and a heavily coated 
 tongue, perhaps with nausea. The temperature rises to between 
 104° and 106° F. ; the pulse is frequent, at first full, but early 
 becoming feeble. Stupor soon develops. The bowels are 
 usually constipated. The expression is dull. The ccmjunctivce 
 are injected. The pupils are usually contracted. The face 
 appears livid. A musty odor is manifest. The body may be 
 covered by a diffuse, red rash. Between the fourth and the sixth 
 day a coarse, papular eruptimi appears, usually on the trunk and 
 extremities, exceptionally on the face. Intermingled with this 
 are many petechial spots. For two or three days new papules 
 appear, to recede gradually and disappear. 
 
 At the close of the first week or early in the second, low, 
 muttering delirium, or coma-vigil, without great restlessness or 
 with ceaseless tossing, muscular twitching and jactitation, 
 appears ; the mental depression is profound. In the cerebral 
 type there is a wild, fighting delirium, with intolerance of hght 
 and illusions of sight and hearing. Excitement is soon suc- 
 ceeded by weakness and prostration, perhaps by fatal coma. In 
 some cases the respiration is shallow, irregular and noisy, though 
 no change in the lungs can be detected. The heart-sounds are 
 feeble, though the beat may be excited. Often, there develops 
 an endocardial murmur, due to the depraved state of the blood. 
 The tongue is brown and cracked, the teeth and gums covered 
 with sordes. The urine is scanty, high-colored, deficient in 
 chlorides and may contain albumin. 
 
44 ESSENTIALS OF DIAGNOSIS. 
 
 In cases that recover the temperature gradually subsides at 
 the end of the second week, a decided decline taking plaee on 
 the fourteenth or sixteenth day, accompanied, perhaps, with 
 profuse perspiration, diarrhea or a copious discharge of urine. 
 Belapses are rare. An attack confers subsequent immunity. 
 Pulmonary comjMcations are the most common. Others may be 
 meningitis, phlebitis, gangrene, erysipelas, parotiditis, edema of 
 the larynx. During the last stages, or after convalescence, 
 acute tuberculosis may develop. 
 
 How are typhoid fever and typhus fever to be differentiated ? 
 
 Typhus fever is contagious ; typhoid is not. Typhus is the 
 more likely to be epidemic. Prodromata are more common and 
 of longer duration in typhoid. The onset is acute in typhus, 
 insidious in typhoid. Typhus lasts about two weeks ; typhoid 
 not less than thi-ee. The eruption of typhoid consists of small 
 rose-spots, usually confined to the abdomen and chest, and ap- 
 pearing in successive crops •, that of typhus is coarse, maculai 
 and petechial and of more extensive distribution. The skin is 
 usually moist in t^'phoid ; it is dry in typhus. In typhus, the 
 body exhales a characteristic musty odor. The bowels are 
 often loose in typhoid fever ; they are usually constipated in 
 typhus. Nervous prostration is the more profound in typhus. 
 The course of the temperature is different in each. Epistaxis is 
 common in typhoid ; uncommon in typhus. In typhoid fever, 
 one finds on post-mortem examination intestinal ulceration and 
 enlargement of the spleen and of the mesenteric glands ; in 
 typhus, no constant lesions ; though the spleen is likely to be 
 diffluent. Typhoid fever and typhus fever may, though rarely, 
 coexist in the same patient. 
 
 How are variola and typhus fever to be differentiated ? 
 
 Both variola and typhus fever are in a high degree contagious. 
 Should both be simultaneously epidemic, the diagnosis may be 
 difficult during the first few days of the attack. Tlie eruption 
 of variola, however, appears from twenty -four to thirty-six 
 hours earlier than that of typhus. The former is usually situated 
 on the face, as well as on the trunk, and passes successively 
 through the stages of papule, vesicle and pustule, the pustules 
 
CEREBRO-SPINAL FEVER. 45 
 
 rupturing and leaving cicatrices. The eruptionof typhus fever 
 rarely or never appears on the face ; it remains largely papu- 
 lar, though in part it becomes petechial. In typhus fever, the 
 temperature becomes high at the onset and continues high ; in 
 variola, the temperature declines with the appearance of the 
 eruption. Vaccination commonly protects against variola ; it 
 aftbrds no protection from typhus fever. Finally, typhus is a 
 disease of about two weeks' duration ; variola, of quite three. 
 
 Cerebro-spinal Fever— Epidemic Cerebro-spinal 
 Meningitis. 
 
 What are the clinical features of cerebro-spinal fever ? 
 
 Cerebrospinal fever or e^jidemic cerebrospinal meningitis— Si 
 specific, essential fever of continued type, associated with a 
 constant lesion — is an acute and extremely fatal infectious dis- 
 ease, varying much in its clinical manifestations, but usually 
 characterized by decided disturbances of the cerebro-spinal func- 
 tions. In some cases cerebral, in others spinal symptoms pre- 
 dominate. 'Rot infrequently, respiratory phenomena or blood- 
 changes assume great prominence. A characteristic eruption 
 is usually a marked feature. 
 
 The attack may develop gradually, but more often it sets in 
 suddenly, with a rigor followed by fever ; malaise ; nausea ; 
 great thirst and vomiting, often with a clean tongue and no 
 gastric derangement ; vertigo ; excruciating headache, i-emit- 
 ting, but never entirely ceasing, and attended with paroxysmal 
 exacerbations ; rigidity of the head and neck, sometimes passing 
 into opisthotonos ; muscular twitchings or convulsions ; dry- 
 ness of the skin, with hyperesthesia and paresthesia. There 
 may also be photophobia and tinnitus aurium. Prostration 
 soon becomes profound, though restlessness may continue. De- 
 lirium may set in and be followed by stupor and coma. The 
 expression is anxious. The pulse is rapid and extremely irregu- 
 lar. The temperature fluctuates between wide limits. Hyper- 
 pyrexia is not rare. It may develop suddenly and persist until 
 death. The temperature may continue to rise after death. A 
 
46 ESSENTIALS OF DIAGNOSIS. 
 
 sudden fall of temperature may usher in collapse and death. A 
 gradual fall of temperature precedes recovery. The action of 
 the sphincters is often deranged, so that there may be inconti- 
 nence of urine or feces, or retention of urine, or constipation. 
 As a rule, retention is an early, incontinence a late symptom. 
 The urine is often albuminous and contains an excess of urates. 
 
 Between the first and the third day, purpuric spots, or an ery- 
 thematous eruption that quickly becomes petechial, may appear 
 upon the trunk and extremities. The disease is sometimes 
 called "spotted fever," from the character of this eruption. 
 Between the third and the sixth day, herpetic vesicles may ap- 
 pear on the face about the li^s. 
 
 In the further progress of the case, the pwjj'iZs, at first con- 
 tracted, become dilated ; paralysis and anesthesia of irregular 
 distribution appear ; disturbances of sight and hearing, perhaps 
 also blindness and deafness develop. The resxjiration may be 
 profoundly disturbed. As death approaches, the breathing may 
 assume the Cheyne-Stokes type. Short remissions in the general 
 severity or in individual symptoms may occur, to be followed by 
 renewed exacerbations. The duration of the disease is variable. 
 The fastigium is commonly reached on the sixth day. In pro- 
 tracted cases, profound emaciation occurs. Death may take 
 place early or late, in coma, by exhaustion, or by apnea. If 
 recovery ensues, convalescence is tardy, and sometimes protracted, 
 while permanent loss of special senses is common. Pneumonia 
 is a common cmiplication. Palsies, headache and epileptiform 
 convulsions may be additional sequelce. 
 
 In addition to the ordinary type of epidemic cerebro-spinal 
 meningitis, there may he fulminant cases (death occurring within 
 twelve hours), 7nild or abortive cases and inotracted or typhoid 
 cases. Spoi'adic cases are rare. 
 
 Instances of contagion (direct transference from the sick to 
 the well) and of portagion (conveyance by the person or be- 
 longings of those that have been in contact with the sick) of 
 cerebro-spinal fever appear to have been authenticated, but are 
 extremely uncommon. 
 
CEREBRO-SPINAL FEVER. 47 
 
 How are cerebro-spinal fever and tetanus to be differentiated ? 
 
 Cerebro-spinal fever appears in epidemics, while tetanus 
 usually occurs sporadically, as a result of the infection of a 
 wound by soil. Trismus, an early symptom of tetanus, is the less 
 common in cerebro-spinal fever. Opisthotonos, general rigidity 
 and spasm are more marked in tetanus than in cerebro-spinal 
 fever. Recovery from tetanus is exceptional. Death is not the 
 invariable termination of cerebro-spinal fever. 
 
 Tetanus is wanting in the palsies, the eruption, the derange- 
 ment of intellection and sensation and the febrile symptoms of 
 cerebro-spinal fever, though towards the fatal termination the 
 temperature may rise inordinately high. 
 
 How are cerebro-spinal fever and typhus fever to be differ- 
 entiated? 
 
 While both cerebro-spinal fever and typhus' fever occur in 
 epidemics, and both may be sudden in onset and attended with 
 profound nervous phenomena and petechial eruption, cerebro- 
 spinal fever has not the dusky, stupid facies of typhus, while 
 the herpes of the face, the retraction of the head, the fixed 
 spinal pain, the muscular rigidity and the heightened sensi- 
 bility of cerebro-spinal fever are not observed in typhus ; nor is 
 typhus, as a rule, accompanied with the great impairment of spe- 
 cial senses or followed by the paralytic sequelae of cerebro-spinal 
 fever. The general course of the two diseases, the fever and 
 the eruption may be discriminated on careful observation. The 
 greatest difficulty occurs in cases of malignant cerebral typhus. 
 
 How are cerebro-spinal fever and torticollis to be differen- 
 tiated ? 
 The muscular contraction that gives rise to torticollis is usually 
 unilateral and limited, while in cerebro-spinal fever the con- 
 traction is symmetrical and not confined to the muscles of the 
 head and neck. The symptoms of an acute, febrile disease, with 
 disturbances of the sensorium and paralytic concomitants and 
 sequelae, are not present in torticollis, but are characteristic of 
 cerebro-spinal fever. Even mild cases of cerebro-spinal fever, 
 lacking the characteristic febrile course and without eruption, 
 will present severe headache. 
 
48 ESSENTIALS OF DIAGNOSIS. 
 
 What are the distinctions between cerebro-spinal fever and 
 smallpox ? 
 
 Headache, vertigo, nausea, vomiting, pain in the back and 
 fever attend both cerebro-spinal fever and smallpox ; but re- 
 traction of the head, muscular rigidity and paralysis, hyper- 
 esthesia and anesthesia are wanting in smallpox, and the pecu- 
 liar temperature-record and the characteristic eruption of small- 
 pox are not seen in cerebro-spinal fever. 
 
 What are the distinctions between cerebro-spinal fever and 
 yellow fever ? 
 
 Yellow fever is especially a disease of hot climates ; when 
 found elsewhere its importation may be traced. If cerebro-spinal 
 fever display any susceptibility to climatic conditions, it is most 
 common in temperate zones. Characteristic symptoms of motor 
 and sensory derangement, observed in the course of cerebro- 
 spinal fever, are wanting in yellow fever, which is a disease of 
 brief duration, in contrast to cerebro-spinal fever, the duration 
 of which may be protracted. Petechial and herpetic eruptions 
 appear during the progress of cerebro-spinal fever, while yellow 
 fever is characterized by a saffron-yellow color of the skin. The 
 black vomit often seen in yellow fever is entirely wanting in 
 cerebro-spinal fever. Although remissions in the intensity of 
 special symptoms may occur in the course of cerebro-spinal 
 fever, the characteristic " lull" of yellow fever is absent. 
 
 How are cerebro-spinal fever and typhoid fever to be differen- 
 tiated ? 
 
 In cerebro-spinal fever, the onset is usually abrupt ; in 
 typhoid it is insidious. In typhoid fever the temperature pur- 
 sues a typical course ; in cerebro-spinal fever there is no regu- 
 larity. The eruption of cerebro-spinal fever is petechial or 
 herpetic and appears early — before the fourth day ; that of 
 typhoid is roseolous and appears not earlier than the fifth or 
 sixth day. Constipation is the rule in cerebro-spinal fever ; 
 diarrhea often attends typhoid. Nausea and vomiting occur in 
 cerebro-spinal fever, but not usually in typhoid. The retraction 
 of the head, the paresthesise and the paralyses of cerebro-spinal 
 fever are all wanting in typhoid fever. The headache is more 
 
ASIATIC CHOLERA. 49 
 
 intense in cerebro-spinal than in typhoid fever ; in the latter it 
 disappears when dehrium sets in ; in the former, dehrium and 
 headache coexist. The knowledge of an epidemic assists in the 
 diagnosis. The discovery ophthalmoscopically of recent papil- 
 litis (choked disc) or optic neuritis would be diagnostic of cere- 
 bro-spinal meningitis in contradistinction from uncomplicated 
 typhoid fever. In rare cases, typhoid fever is complicated by 
 meningitis. 
 
 Asiatic Cholera. 
 
 What are the symptoms of Asiatic cholera ? 
 
 Asiatic cholera, also called cholera infectiosa, is an acute, infec- 
 tious disease, having its home in tropical climates and occurring 
 in epidemics. It is dependent upon a specific organism, which 
 is found in the alvine discharges of the patient and is principally 
 transmitted by means of milk and drinking-water. 
 
 Fir.. 5. 
 
 
 ^'^'M>'M? ^'^-^ 
 
 Comma-bacillus of cholera. (Vierordt.) 
 
 The disease has a period of incubation of from half a day to 
 three or four days. It may set in suddenly, with a chill, but 
 more usually the attack proper is preceded by a moderate diar- 
 rhea, to which the name cholerine has been given. This con- 
 stitutes the first or premonitory stage. The course of the disease 
 may be arrested at this stage. 
 
 In the second stage [stage of spasm, or sta<]e of serous diarrhea), 
 there occur violent cramps in the abdomen and legs, and the 
 intestinal flux increases in severity. There is often obstinate 
 4 
 
50 ESSENTIALS OF DIAGNOSIS. 
 
 vomiting. The patient complains of thirst, is restless and anxi- 
 ous ; prostration is marked ; the pulse is weak and thready ; the 
 skin is cold and shrunken ; the eyeballs are sunken. The tem- 
 ])erature, taken in the rectum or with a thermometer carefully 
 applied and allowed to remain at least ten minutes in the axilla, 
 will be found to .be elevated. The stools are almost liquid and 
 colorless and contain large quantities of epithelium, constituting 
 the so-called " rice-water" discharges, in which the comma-hacil- 
 lus of Koch (Fig. 5) is to be found. 
 
 Soon, a third or alyid stage, or stage of collapse, sets in. The circu- 
 lation fails, and there is marked depression of the vital powers ; 
 the respiration is shallow and accelerated ; the skin becomes as 
 cold as marble ; the breath may be chilling ; the voice is lost. 
 Suppression of urine often occurs. The urine that is secreted is 
 albuminous and contains casts. 
 
 In this condition of collapse the patient may die, or he may 
 enter upon a fourth stage, or stage of reaction, convalescence set- 
 ting in or a low, typhoid condition developing, with fever and 
 delirium and iDOSsibly with suppression of urine. This stage may 
 terminate in death or in convalescence. Convalescence may be 
 coiyiplicated by ulceration of the cornea and by parotiditis. 
 
 How are cholera nostras and cholera Asiatica to be differ- 
 entiated ? 
 
 Cholera nostras occurs endemically ; cholera Asiatica, epi- 
 demically, and, in Europe and America, by importation. Asiatic 
 cholera is by far the graver affection ; the stools present a charac- 
 teristic "rice-water" appearance, in which a specific bacillus is 
 to be found. If an apparently similar bacillus be found in the 
 stools of cholera nostras, its morphology and culture will prove 
 it to be different. 
 
 How is arsenical poisoning to be distinguished from cholera? 
 
 Poisoning by arsenic occasions vomiting, cramps in the abdo- 
 men and legs, and diarrhea with stools of a "rice-water" char- 
 acter. Local evidences of the ingestion of arsenic may be 
 present in the mouth ; vomiting precedes diarrhea ; the stools 
 are bloody and do not contain the specific comma-bacilli. 
 
RELAPSING FEVER. 51 
 
 Relapsing Fever. 
 
 What are the distinguishing features of relapsing fever? 
 
 Belapsing fever is rare in other tlian certain tropical countries. 
 It is a specific, essential fever, of intermittent type, and is de- 
 pendent upon the presence of a specific organism— the spirocheta 
 Obermeierii — in the blood. (Fig. 6.) 
 
 Fig. 6. 
 Spirochetse of relapsing fever. (V. Jaksch.) 
 
 The growth and development of the parasite give rise to the 
 periodic paroxysms that characterize the disease and give it 
 its name. After a period of incubation, varying from several 
 hours to two weeks, the disease sets in suddenly with a chill, 
 followed by fever, with decided elevation of temperature, mus- 
 cular pains, vertigo, headache, nausea and vomiting. The 
 spleen is enlarged. Often there is jaundice. 
 
 In the course of from five to seven days the attack abates 
 with the suddenness with which it set in, the temperature fall- 
 ing to the normal and profuse diaphoresis occurring. 
 
 For about a week the patient is free from symptoms. At the 
 end of this time, the paroxysm is repeated, to again subside ; 
 and this may happen a number of times. 
 
 Convalescence is tardy and protracted. During the paroxysms, 
 spirochetse in large numbers may be found in the blood. They 
 are not to be found during; the intermissions. 
 
62 ESSENTIALS OF DIAGNOSIS. 
 
 How is relapsing fever to be diagnosticated from typhoid fever ? 
 
 In typhoid fever, both onset and subsidence are gradual ; in 
 relapsing fever, they are sudden. The former is a continued 
 fever ; the latter intermittent and periodic. Relapsing fever 
 does not present the rose-rash of typhoid fever. Jaundice, 
 often present in relapsing fever, does not occur in typhoid fever ; 
 nor are spirochetse found in the blood in typhoid fever. 
 
 How does relapsing fever differ from typhus fever ? 
 
 The course of relapsing fever is interrupted by intermissions, 
 giving rise to a disease of periodic type ; typhus is a continued 
 fever. 
 
 The marked nervous symptoms, as well as the exanthem, of 
 typhus are wanting in relapsing fever. 
 
 Spirochetse are found in the blood only in relapsing fever. 
 
 Upon what does the differential diagnosis between relapsing 
 fever and yellow fever depend ? 
 
 Yellow fever is a disease of not more than three stages ; there 
 may be more or less in relapsing fever. The primary acute 
 stage, as well as the period of intermission or remission, is longer 
 in relapsing fever than in yellow fever. Vomiting occurs late 
 in yellow fever, early, if at all, in relapsing fever. Vertigo is 
 a more marked symptom in relapsing than in yellow fever. The 
 occurrence of one or the other in an epidemic might aftbrd a 
 clue in diagnosis. Spirochetse are present in the blood in re- 
 lapsing fever ; they are not found in yellow fever. 
 
 Malarial Diseases. 
 
 What are the characteristics of malarial disease ? 
 
 The group of diseases known as malarial is characterized by 
 paroxysmal periodicity, enlargement of the spleen and liver, 
 melanemia and the presence in the blood, free or within the red 
 corpuscles, of parasites that exert a deleterious influence upon 
 the red cells. (Fig. 7. ) 
 
 During the paroxysm, the urine is said to be irritant, the pro- 
 portion of both water and solids being increased. 
 
MALARIAL DISEASES. 
 
 53 
 
 Malarial diseases prevail principally iu the lowlands of warm 
 climates, with marshy soils. 
 
 Fig. 7. 
 
 Organisms of malaria — iutracorpuscular. 
 Fig. 8. 
 
 
 £m^ 
 
 % 
 
 Organisms of malaria — extracorpuscular. (Mace.) 
 
 What are the varieties of malarial fever ? 
 
 Malarial fevers are said to be interynittent when between two 
 paroxysms there intervenes a period of freedom from symp- 
 toms, with a restoration of the temperature to the normal ; 
 remittent^ when between two paroxysms the symptoms moder- 
 ate and the temperature falls (but not to the normal level). 
 
 When the paroxysm is repeated daily, the fever is designated 
 quotidian; if repeated on alternate days, tertian; if with an 
 interval of two days, quartan. If two paroxysms occur daily, 
 the fever is called a duplicated quotidian. There may be a 
 
54 ESSENTIALS OF DIAGNOSIS. 
 
 double tertian, iu which occur daily paroxysms, of which only 
 those of alternate days are alike ; a clauble quartan, and other 
 combinations. When the paroxysms succeed one another so 
 closely that the cold stage of one begins before the sweating 
 stage of its predecessor ends, the fever is called suhivtrant. 
 
 Morphologic and biologic differences among the organisms 
 present in the various types of malarial fever have been recorded. 
 
 What are the features of a malarial paroxysm? 
 
 A typical malarial paroxysm consists of a cold stage, a liot stage 
 and a sweating stage. The disease is therefore called " chills and 
 fever," It is also known as ague. 
 
 What are the characteristics of each stage? 
 
 The cold stage or chill sets in with malaise, nausea, vertigo, 
 shivering ; as the rigor becomes more pronounced, the j)atient 
 may be severely shaken ; his teeth chatter ; the skin is cold and 
 rough ; the breathing is shallow and hurried ; the pulse is small 
 and rapid ; the temperature of internal parts, however, is febrile. 
 
 Gradually, the feeling of coldness subsides and gives way to a 
 sense of warmth, the temperature of the rectum or of the mouth 
 continuing to rise ; the surface of the body becomes flushed and 
 the eyes are brilliant. The patient has now subjective sensa- 
 tions of fever. After the lapse of a variable time, a more or less 
 copious persioiration sets in, with a decline in the temperature 
 and an amelioration or disappearance of the symptoms. The 
 paroxysm is at an end. 
 
 What are the clinical features of malarial intermittent fever ? 
 
 In intermittent fever, as the name indicates, there is in the 
 interval between two paroxysms a complete intermission of the 
 symptoms, the temperature becoming normal or subnormal. 
 
 The cold stage lasts from fifteen minutes to an hour, the hot 
 stage and the siceating stage, respectively, a varying number of 
 hours. The beginning of each successive paroxysm anticipates 
 in time of the clock that of the preceding paroxysm. 
 
 Untreated, the paroxysms of intermittent fever lose their 
 regularity. 
 
 The disease may gradually and spontaneously subside, or the 
 
MALARIAL DISEASES. 
 
 65 
 
 paroxysms may become remittent or pass into the malarial 
 cachexia. 
 
 After apparent recovery, a tendency to a return of the parox- 
 ysms on the fifth, seventh, ninth or fourteenth day is sometimes 
 observed. 
 
 Fig. 9. 
 
 Fig. 10. 
 
 BSSBSaiBSSB 
 ^SiSBIBSr — 
 
 ■■•■■■■■I 
 ■■(■■.■■■I 
 
 ■■■■nlBiii 
 
 ISSSBiSBiZL^,. 
 
 isi!::is8:sss 
 
 jiniBIIBniBHBH 
 
 E:»»ii:8!!i^ 
 
 laisasii 
 
 ■■■■— ■■■■■■■B 
 
 bbssbsBbbsbsb 
 
 BSBBBiaSSBBSS 
 
 ■ ■■■ 1IBBSB5B5B9 
 
 iniBBiRiHiiBBnanL, 
 iiB'BHBniniiHini'Aa 
 
 Temperature-chart of quotidian 
 intermittent fever. (Wunder- 
 licli.) 
 
 Temperature-chart of tertian 
 intermittent fever. (Wun- 
 derlich.) 
 
 What are the clinical features of malarial remittent fever ? 
 
 Remittent fever represents a more pi'ofound degree of intoxi- 
 cation than does intermittent fever. 
 
 The chill is usually severe and protracted. In addition, there 
 is gastric irritability, perhaps vomiting, sometimes jaundice. 
 The temperature attains a high degree. The hot stage may last 
 for from six to eighteen hours and is followed by profuse perspi- 
 ration. 
 
 In the interval between two paroxysms, the symptoms moder- 
 ate and the temperature declines, but does not reach the nor- 
 mal. 
 
 After the occurrence of several paroxysms, the chill may be 
 wanting ; or there may be but one— the initial chill. Without 
 medicinal intervention, the remissions may gradually become 
 less decided and a typhoid condition may develop. 
 
56 ESSENTIALS OF DIAGNOSIS. 
 
 What are the symptoms of hemorrhagic malarial fever? 
 
 Hemorrhagic malarial fever is a grave form of malarial intoxi- 
 cation in which the height of the paroxysm is marked by head- 
 ache, severe pain in the back, nausea, vomiting, decided jaun- 
 dice and hemorrhages from various mucous surfaces, jjarticularly 
 from the kidneys. 
 
 What is pernicious malarial fever ? 
 
 In certain localities in which the malarial organisms are ex- 
 ceedingly numerous or virulent, the attack manifests a penuc/oits 
 tendency. The clinical picture depends upon the system that 
 bears the brunt of the disease. There may thus be a cerebral 
 form^ characterized either by delirium and excitement or by 
 coma and depression ; or there may be a ihoracic form, in whicli 
 the respiration is accelerated, and there is an urgent sense of 
 the need of air ; or there may be a gastro-intestinal variety, at- 
 tended with nausea, vomiting, jaundice and diarrhea ; or there 
 may be an asthenic or an algkl variety, in which there is a condi- 
 tion of marked debility and a strikhig coldness of the surface 
 and of the breath. Pernicious malarial fever usuall}' manifests 
 its character only after a preliminary paroxysm of apparently 
 ordinary intermittent or remittent fever. Unless promptly and 
 vigorously treated, it is likely to be fatal. 
 
 What are the symptoms of the malarial cachexia ? 
 
 After i^rotracted residence in a malarious district or following 
 untreated or rebellious intermittent or remittent fever; there 
 may occur irregular chilly sensations, with some tendency to 
 periodicity, an occasional sense of feverishness, headache, men- 
 tal torpor, drowsiness, a sallow complexion, constipation or 
 diarrhea, impaired appetite, enlargement of the spleen and 
 liver— a complex of symptoms that may not yield to medicinal 
 treatment, but which improves on removal to a non-malarious 
 climate. 
 
 What is meant by "Dumb Ague?" 
 
 There is a variety of irregular manifestations of malarial or 
 paludal poisoning, sometimes acute, but more frequently sub- 
 acute or chronic, which do not at any time present the classical 
 picture of chill, fever and sweat. These attacks of "dumb 
 
MALARIAL DISEASES. 57 
 
 ague," "masked malaria," "larval paludism," as they are 
 variously called, comprise chilly sensations, irregular fever, or 
 flushes, or subjective sensations of heat, Joint-pains and muscle- 
 pains, headache and neuralgias of various kinds, cough, with or 
 without bronchial or laryngeal signs, gastric and other visceral 
 disturbances, sometimes taking the form of crises ; in severe or 
 protracted cases, anemia, anasarca and albuminuria, hematu- 
 ria and hemoglobinuria have been observed. A common va- 
 riety is the so-called "brow-ague," a form of frontal headache 
 frequently associated with tenderness of the nerves at the supra- 
 orbital and infra-orbital foramina and sometimes with an in- 
 tensely painful sensation of pressure or constriction referred to 
 the nasal bones ; the manifestations usually exhibiting an irregu- 
 lar periodicity. Appearing in the morning and disappearing at 
 night, or when aggravated by sunlight, it is called "sun-pain." 
 Enlargement of the spleen is sometimes demonstrable. A 
 careful study of the phenomena in these cases will usually elicit 
 some periodicity in their recurrence, or while the prominent 
 symptoms, gastric or neuralgic, or whatever they may be, may 
 not be periodic, careful temperature-observations will show an 
 unsuspected periodic rise. Sometimes, if quinine be adminis- 
 tered for a short time, and then withheld, a distinct periodicity 
 in the symptoms will be developed upon withdrawal of the drug. 
 The discovery of characteristic plasmodia in the blood would 
 establish the diagnosis. The organisms are usually compara- 
 tively few in number and of the crescentic or sickle-shaped variety. 
 
 What is meant by Ague-cake ? 
 
 The enlargement of the spleen in a case of chronic malaria 
 or of malarial cachexia is sometimes quite manifest to ordinary 
 inspection. When not so readily manifest to sight, it may easily 
 be detected by palpation. Its connection with malaria being 
 well known, the enlarged spleen has in vulgar parlance acquired 
 the name of agiie-calce. 
 
 What are the distinctions between malarial fever and the fever 
 of suppuration or of septic infection ? 
 Suppuration and septic infection usually give rise to fever of 
 a remittent or interniittent type. When an obvious cau.se exists, 
 
58 ESSENTIALS OF DIAGNOSIS. 
 
 the recognition of the nature of the fever is easy. When, how- 
 ever, the fever is induced by deep-seated suppuration, as when 
 abscesses form or in case of puhiionary tuberculosis or of occhi- 
 sion of the hepatic or of the common bile-duct, the connection 
 may be obscure. The distinguishing features, however, are that 
 the symptoms of suppurative or of septic fever are rarely of 
 regular periodicity or typical in course ; that they are often un- 
 influenced by the administration of quinine, which acts specifi- 
 cally in the malarial diseases ; and that the hematozoa charac- 
 teristic of malarial fever are wanting. 
 
 With what conditions may pernicious malarial fever be con- 
 founded? 
 
 The gastro-intestinal type of the disease may simulate ordinary 
 gastro-intestinal catarrh, but the one is a grave condition, while 
 the other is not ; the one is febrile the other antifebrile ; the one 
 submits to treatment by quinine, while the other does not ; in 
 the one, the blood contains characteristic hematozoa and blood- 
 pigment, while the other does not ; in the one, the spleen is en- 
 larged, in the other, it is unchanged in size. 
 
 The pulmonary tyioe may be confounded with pleurisy or with 
 pneumonia, but the physical signs and many symptoms will 
 clear up any doubt. In doubtful cases, examination of the blood 
 and treatment with quinine will furnish irrefutable evidence. 
 
 The algid variety resembles cholera, but it does not occur in 
 epidemics, the general symptoms of cholera are wanting, and 
 treatment decides the result. 
 
 Jaundice attends the hemm-rhagic form ; hemorrhages take 
 place from various mucous surfaces and blood is found in the 
 urine. Hemorrhagic malarial fever differs from paroxysmal 
 hemoglobinuria in not being dependent upon exposure to cold, 
 while the urine contains red corpuscles and not merely hemo- 
 globin. Quinine cures the one, but fails to influence the other. 
 
 The cerebral type is to be distinguished from those conditions 
 that give rise to apoplexy and from profound intoxications of 
 various kinds. The essential, distinguishing features are the 
 occurrence of the symptoms in the course of an attack of 
 malarial fever, the absence of palsies and localizing symptoms, 
 
YELLOW FEVBR, 59 
 
 the tendency to recovery under treatment, the enlargement of 
 the spleen, the presence of hematozoa in the blood. 
 
 How are typhoid fever and malarial fever to be differentiated? 
 
 Typical cases of intermittent and remittent fever are not 
 likely to be confounded with typhoid fever, but if an intermit- 
 tent or remittent has existed for some time, uninfluenced by 
 medication, a typhoid condition develops, and the symptoms 
 may occasion some doubt in diagnosis. Under such circum- 
 stances, the previous history must be considered. 
 
 The diarrhea, the rose-spots, the temperature-course of 
 typhoid fever are all different from what is seen in malarial fevers. 
 
 The reaction of the urine to sulphanilic acid and sodium ni- 
 trite, described by Ehrlich, and a characteristic bacillus are not 
 found in malaria. The detection of the plasmodia of malaria 
 in the blood dissipates even the remotest doubt. 
 
 Malarial fever and typhoid fever may coexist as so-called 
 typho-malarial fever. 
 
 How does syphilitic fever differ from malarial fever ? 
 
 When secondary syphilis is marked by fever, the elevation of 
 temperature usually occurs at night and is associated with bone- 
 pains, cutaneous eruption and other evidences of syphilis. Cere- 
 bral and meningeal syphilis may also give rise to febrile move- 
 ment. In many cases, the discovery of the plasmodia in the 
 blood and the results of treatment by quinine on the one hand, 
 and the results of treatment by mercury and iodides on the 
 other hand, must make the diagnosis. 
 
 Yellow Fever. 
 
 What are the characteristics of yellow fever ? 
 
 Yellow fever is a specific, epidemic disease of hot climates, 
 occurring in a single paroxysm of three stages : the first, a 
 febrile stage, lasting from thirty-six to forty-eight hours, which 
 sets in with a chill, followed by fever, with capillary congestion, 
 especially of the face and eyes, pains in the head, the back and 
 the calves of the legs, restlessness and anxiety, irritability of the 
 stomach, vomiting, thirst, constipation ; the second, a .sia^e of 
 
60 ESSENTIALS OF DIAGNOSIS. 
 
 remission or lull, of less than six hours, in which the fever sub- 
 sides and the skin assumes a deep-yellow or bronze hue ; the 
 third, a stage of renewal, in which the symptoms reappear, pros- 
 tration becomes pronounced and hemorrhages take place from 
 various mucous surfaces ; the vomited matters present a charac- 
 teristic black appearance. The urine usually contains albumin 
 and often casts. Suppression of urine may occur. 
 
 The mind is usually clear almost up to the moment of death, 
 but in some cases delirium and stupor develop. 
 
 Death may result from collapse or with convulsions and the 
 symptoms of uremia. If recovery take place, convalescence is 
 often gradual, and may occasionally be interrupted by relapse. 
 Some cases are quite mild, recovery taking place at the end of 
 the first stage. Even grave cases may be so mild in the first 
 stage as to be unrecognized ; the patient walking about, to be 
 suddenly seized with prostration, quickl}' followed by black 
 vomit and death. 
 
 An attack protects against subsequent infection. 
 
 What are the disting-uishing features between yellow fever and 
 malarial remittent fever with jaundice ? 
 
 Yellow fever is epidemic ; remittent fever, endemic. Yellow 
 fever is a disease of a single paroxysm, not lasting more than a 
 week ; remittent fever is a disease of repeated paroxysms, of 
 periodic recurrence, and lasts more than a week. 
 
 In yellow fever, the eyes become injected and watery, the ex- 
 pression anxious or fierce. In remittent fever, there is no espe- 
 cial change in the eyes or in the expression. 
 
 Prostration and muscular pains are decided in yellow fever 
 and are not so prominent in malarial fever. 
 
 Delirium is common in bilious remittent fever, and the mind 
 is always dull. Delirium is not common in yellow fever, and 
 the mind is usually clear. 
 
 The pulse may become very slow in yellow fever ; it is always 
 quick in remittent fever. 
 
 Hemorrhages from mucous surfaces take place in yellow 
 fever ; not in ordinary remittent fever. 
 
 The urine of yellow fever contains albumin, and suppression 
 
YELLOW FEVER. 61 
 
 may take place ; the urine of remittent fever contains no albu- 
 min and suppression does not commonly occur. Bile-pigment 
 gradually disappears from the urine of yellow fever and increases 
 in the urine of bilious remittent fever. 
 
 An attack of yellow fever confers immunity from subsequent 
 inflexion; one attack of remittent fever predisposes to other 
 attacks. Yellow fever is commonly fatal, remittent fever rarely 
 fatal. 
 
 The treatment of yellow fever is uncertain ; remittent fever 
 yields to quinine. 
 
 Plasmodia malarise are never found in the blood in yellow 
 fever ; they are diagnostic of malarial fever. 
 
 How are hemorrhagic malarial fever and yellow fever to be 
 differentiated ? 
 
 Both hemorrhagic malarial fever and yellow fever occur in hot 
 climates and are attended with jaundice, hematemesis and other 
 hemorrhages. 
 
 Yellow fever, however, is epidemic ; hemorrhagic malarial 
 fever, endemic. The former consists of but a single paroxysm, 
 of three stages, including a remission ; tlie latter is marked by a 
 series of paroxysms, each followed by a remission. 
 
 Black vomit is the more characteristic of yellow fever ; hem- 
 orrhage from the kidneys, of hemorrhagic malarial fever. Al- 
 bumin and casts are commonly found in the urine in yellow 
 fever ; not in malarial fever. An attack of yellow fever con- 
 fers immunity from subsequent infection ; an attack of malarial 
 fever predisposes to the occurrence of other attacks. The de- 
 tection of the Plasmodia of malaria in the blood establishes the 
 diagnosis. 
 
 How is yellow fever to be distinguished from acute yellow 
 atrophy of the liver ? 
 
 Yellow fever is epidemic ; acute yellow atrophy is sporadic. 
 In acute yellow atrophy, the area of hepatic dulness becomes 
 rapidly and decidedly diminished ; in yellow fever, there is either 
 enlargement or no demonstrable change. 
 
 Yellow fever is, and acute yellow atrophy is not, attended with 
 
62 ESSENTIALS OF DIAGNOSIS. 
 
 a distinct remission in the severity of the attack. Yellow fever 
 is sometimes followed by recovery ; acute yellow atrophy is not. 
 
 The injection of the eyes, the pains in the back and extremi- 
 ties, found in yellow fever, are wanting in acute yellow atrophy 
 of the liver. 
 
 In acute yellow atrophy, leucin and tyrosin are found in the 
 urine, and while cerebral symptoms are more pronounced than 
 in yellow fever, the temperature never rises so high and may 
 even be subnormal. 
 
 Weil's Disease. 
 
 What are the symptoms of Weil's disease ? 
 
 WeWs disease^ also called acute infective jctiindice^ is an inter- 
 mittent febrile affection, usually exhibiting two periods of 
 activity separated by an uncertain interval ; the first of a little 
 more, the second of a little less,- than a week's duration. The 
 disease may set in abruptly with nausea and vomiting. The 
 temxnrature at once rises to a considerable height, but falls 
 decidedly on about the night of the fifth day ; subsequently 
 declining gradually until the normal level is reached. After an 
 afebrile period of from twenty-four hours to a week, there is a 
 return of fever lasting a few days or a week. 
 
 The attack is characterized by headache, vertigo, malaise, de- 
 bility, somnolence, and, sometimes, nocturnal fever and restless- • 
 ness, hyperesthesia, diarrhea, muscular pains and jaundice. 
 The imlse is small and frequent and sometimes dicrotic. The 
 respiration is accelerated. The areas of splenic and hepatic per- 
 cussion-dulness are increased. The urine passed is diminished 
 in quantity and contains bile-pigment, bile-acids, albumin and 
 casts. Hemorrhages from various mucous surfaces may take 
 place, epistaxis, hematemesis, hemoptysis and intestinal hem- 
 orrhage. Petechial spots may appear in the skin. 
 
 The disease has been observed most commonly in summer 
 and in vigorous young men, butchers and soldiers seeming to 
 display a peculiar proclivity. Similar manifestations have fol- 
 lowed poisoned wounds. In fatal cases, degeneration of the 
 
MORBILLI MEASLES. 63 
 
 liver and kiclne3's and spleen has been found. Parotiditis, 
 pneumonia, iridocyclitis and motor weakness have been sequeloe. 
 In cases that recover, the convalescence is protracted. 
 
 How are Weil's disease and yellow fever to be differentiated ? 
 
 Weil's disease and yellov^r fever probably exhibit a closer re- 
 semblance in description than in actuality. 
 
 Weil's disease shov^rs a special predisposition for young adults, 
 especially butchers and soldiers ; yellow fever occurs in epidem- 
 ics and does not confine itself to any class of individuals. 
 Diarrhea is the rule in Weil's disease ; constipation in yellow 
 fever. The initial stage of yellow fever is of shorter duration ; 
 it is earlier attended with a remission ; the remission is less 
 complete, and both the remission and final stage are shorter 
 than is the case in Weil's disease. Black vomit is not common 
 in Weil's disease ; the injection and excitement are less than in 
 yellow fever. 
 
 The Exanthemata. 
 
 What are the exanthemata ? 
 
 The term exanthemata or eruptive feoers is applied to a group 
 of contagious, epidemic diseases, each depending upon a specific 
 infection and having as prominent signs, fever and specifically 
 characteristic eruptions on the skin and often on the visible 
 mucous membranes. As exanthemata are commonly described 
 scarlatina or scarlet fever ; measles or morbilli ; French measles 
 or Eotheln ; smallpox or variola and its modification varioloid ; 
 vaccinia — the usual consequence of vaccination ; chicken-pox or 
 varicella. Diphtheria and erysipelas might also be included. 
 
 Morbilli — Measles. 
 
 Upon what does the diagnosis of morbilli depend? 
 
 Morbilli or measles, also called rubeola, is an acute, contagious 
 disease, common in children, attended with catai-rhal symptoms 
 (coryza, rhinitis, pharyngitis, laryngitis, bronchitis, conjuncti- 
 
64 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 vitis), febrile elevation of temperature and a characteristic ex- 
 anthem. 
 
 The period of incubation is from seven to fourteen days. The 
 onset is somewhat abrupt, with a quick rise of temperature to from 
 102'^ to 104° r., more or less headache, restlessness, injection 
 and watering of the eyes, sneezing, running from the nose, often 
 swelling of the nose and lip, perhaps cough and slight sore- 
 throat. Digestion is commonly disturbed, and the urine maj^ be 
 scanty. The temperature (Fig. 11) undergoes a considerable ele- 
 
 FlG. 11. 
 3 4 5 
 
 400° 
 
 39 O" 
 
 380« 
 
 37'0' 
 
 iriii 
 
 . mwiWMkmmi 
 
 S ■!!■■■■ ■Mi^iHiVHI 
 n ■■■■■« ■■kwiii 
 ffinHHHVflHHKWI 
 
 ■■■MVjI 
 
 HHBmtJI _ 
 
 IVM V»k^lHBBHH ■■ 
 .»»■!«■■■■■■■■! 
 ■<■!■■ ■■■■■■ ■■!■! 
 
 ■!■■■■■■■ ■■■■IIL, 
 
 !!■■■■■■■ ■■■■■ml 
 
 isaiB 
 
 300° 
 
 ■■■■■■■■■■■■■■■■ 
 
 Temperature-chart of measles. (Strunii-iell.) 
 
 vation with the onset of the attack, declining on the second or 
 third day, to rise again on the fourth, with the appearance of the 
 eruption. This consists of coarse, pink papules, primarily dis- 
 crete, then becoming surrounded by a somewhat paler border and 
 soon coalescing, to form slightly elevated patches arranged in 
 crescentic form, with intervening healthy skin. The eruption 
 first appears upon the face and neck, then upon the body. The 
 fever declines and the eruption begins to disappear between the 
 fifth and the seventh day. Branny desquamation follows as the 
 attack comes to an end on the ninth day. The eruption may 
 
SCAKLATINA SCARLET FEVER. 65 
 
 usually be detected iu the throat a day or two in advance of its 
 appearance on the skin. 
 
 An attack of measles commonly protects against subsequent 
 infection ; though second attacks are not rare and third attacks 
 not remarkable. The disease is ordinarily mild and benign ; 
 sometimes, however, it is malignant and hemorrliagic {black 
 measles). Lobular pneumonia and catarrhal otitis media are not 
 uncommon comijlications. An attack of measles is likely to pre- 
 cipitate the development of tuberculosis in one predisposed and 
 to accelerate the course of the disease when it already exists. 
 
 How does morbilli differ from typhus fever ? 
 
 Typhus fever is of longer duration and decidedly more grave 
 than measles, than which it is relatively less common in chil- 
 dren. While the eruption of measles in some degree resembles 
 that of typhus, it appears earlier and, as a rule, has no tendency 
 to become petechial ; it begins on the face, while iu typhus the 
 face escapes. The catarrhal symptoms of measles are wanting 
 in typhus ; the profound nervous depression of typhus is not 
 seen iu measles. Typhus in Korth America is rare and as a rule 
 imported, most frequently by emigrant-ships. 
 
 Scarlatina — Scarlet Fever. 
 
 What are the symptoms of scarlatina ? 
 
 Scarlatina is an acute, contagious disease, tO'Which children 
 and young persons evince a special predisposition. An attack 
 confers relative immunity from subsequent infection. 
 
 The period of incubation may be short. It varies from twenty- 
 four hours to a week, rarely ten days. The onset is usually 
 abrupt, perhaps attended with vomiting or convulsions. The 
 temperature at once rises to a considerable height (104° or 105° 
 F.) and the pulse attains a striking frequency. In the first 
 twenty-four hours, or sometimes a little later, a diffuse, fine, 
 punctiform, red rash appears, at first on the neck and breast and 
 in the flexures of the joints, soon spreading as a uniform scarlet 
 flush over the greater part of the body. Pressure causes tempo- 
 5 
 
66 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 rary dissipation of the redness. There are intense subjective 
 burning and itching of the skin. 
 
 The throat is usually sore and swallowing is painful. The 
 fauces and palate are reddened, the tonsils and uvula and the 
 adjacent cervical glands are enlarged and there is stiffness of 
 the muscles of the neck. The scarlet discoloration may some- 
 times be detected in the throat, especially on the free border 
 of the soft palate and on the uvula, in advance of its appearance 
 on the skin. The throat-affection is often ulcerative or pseudo- 
 membranous in character. The larynx is rarely invaded. The 
 nose is usually involved and there is more or less serous or sero- 
 purulent discharge. The inflammation may extend into the Eus- 
 tachian tube and involve the auditory appai'atus. Suppurative 
 otitis is not an uncommon complication, and perforation and 
 deafness may result. 
 
 Fig. 12. 
 1. 2 3 4 5 6 7 8 
 
 41 -O' 
 
 iO-O" 
 
 390« 
 
 380» 
 
 37'0» 
 
 111 
 
 "■"■assisssgisaEss 
 
 mm 
 
 SIBI 
 
 Temperature-chart of scarlatina. (Striimpell.) 
 
 The tongue is at first heavily coated, but, in the course of a 
 little while, the dense fur is cast off, exposing the surface of the 
 reddened organ, with its enlarged and prominent papillse— an 
 appearance characteristically described by the designation 
 "strawberry tongue." Thirst is often great. Digresfion is de- 
 ranged. The urine is scanty. 
 
SCARLATINA — SCARLET FEVER. 67 
 
 Severe nervous symptoms may occur, twitchiags or convulsions, 
 restlessness, insomnia, delirium, stupor, fatal coma ; or the ner- 
 vous disturbances may be very mild and cease with the setting 
 in of convalescence. 
 
 In favorable cases, the eruption fades by the fourth or fifth day. 
 The temperature, which has remained high, begins to decline ; 
 defervescence taking place by somewhat rapid lytiis (Fig. 12). 
 At the end of a week or nine days, the skin undergoes a fur- 
 furaceous or membranaceous desquamation, the temperature 
 falls to the normal and convalescence may set in. Persistence 
 of high temperature into the second week is not common and 
 usually denotes a complication. So, too, a sudden recrudescence 
 of pyrexia, after decline has begun, indicates suppuration or 
 other accident. Convalescence may be interrupted by the ap- 
 pearance of symptoms of an acute nephritis. Edema of the 
 face and body, with diminished elimination of a dense, high- 
 colored or smoky-looking urine, containing considerable albumin 
 and blood, as well as blood-casts and epithelial casts of the uri- 
 niferous tubules. Not rarely, albuminuria and other evidences 
 of renal congestion or inflammation may be detected prior to the 
 appearance of edema. With or without suppression of urine, 
 there may occur convulsions, delirium, stupor, coma and death. 
 
 Another rather frequent complication is arthritis, which may 
 involve a single joint or several joints. Sometimes, with or with- 
 out joint-symptoms, there is endocarditis, pericarditis or pleu- 
 ritis. Permanent valvular lesions of the heart may be sequelae. 
 
 Various types of scarlatina are observed in addition to the 
 ordinary form. When throat-symptoms predominate, the attack 
 is called "anginose." Sometimes the disease is mild or abortive. 
 At other times it is malignant in virulence. In malignant cases, 
 the rash may be delayed ; it may be pale and indistinct or dark 
 and livid. Cases in which the rash is wanting may be mild or 
 severe. This form is called "larval" or "scarlatina sine ex- 
 anthemate." In these cases, dropsy or suppression of urine 
 may be the first symptom to attract attention. Anasarca may 
 occur without nephritis, but its dissociated occurrence is not 
 common. Scarlatina is said occasionally to be hemorrhagic. 
 
68 ESSENTIALS OF DIAGNOSIS. 
 
 How are scarlatina and measles to be differentiated ? 
 
 Scarlatina usually sets in with vomiting or convulsions ; 
 measles rarely so begins. Rather severe sore-throat and gland- 
 ular enlargement characterize scarlatina ; catarrhal symptoms 
 are present in measles. The great rapidity of pulse and eleva- 
 tion of temperature commonly observed in scarlatina are want- 
 ing in measles The eruption of scarlatina appears on the first 
 or second day of the disease and is finely punctate, occasioning 
 an appearance of diftuse redness ; the eruption of measles ap- 
 pears not before the third day and is commonly papular, arranged 
 crescenticall}', with areas of intervening healthy skin. After a 
 preliminary elevation, the temperature of measles falls on the 
 second or third day, to rise again with the appearance of the 
 eruption, then to subside rapidly ; the temperature of scarlatina 
 at once mounts high and, after a few days, declines gradually. 
 Nervous symptoms are decided in scarlatina, wanting in measles. 
 
 Rotheln. 
 
 What are the symptoms of Rotheln ? 
 
 Rotheln, also called roseola, German measles, French measles 
 and, incorrectly, rubella or rubeola, is an acute, contagious ex- 
 anthem, presenting an eruption resembling that of morbilli and 
 throat-symptoms like those of scarlatina. An attack protects 
 from subsequent attacks, but not from measles or scarlatina ; 
 neither does an attack of scarlatina or one of measles confer im- 
 munity from Eothela. The period of incubation of Eotheln is said 
 to be about fourteen days. The onset is usually abrupt. The 
 temperature is moderate ; the pulse not very rapid. In the course 
 of a day or two, there appears, first upon the face and then pro- 
 gressively invading the trunk and the extremities, ?in eruptimi o{ 
 small papules usually separated from one another by skin of 
 normal appearance. Sometimes, the intervening skin is erythem- 
 atous. The eruption lasts for from four days to a week, is 
 attended with itching and is sometimes followed by slight 
 desquamation. The throat is usually sore, the fauces reddened 
 and the cervical glands enlarged. Catarrhal syraptoms are com- 
 mon. The course of the disease is usually mild and uncomplicated. 
 
VARIOLA — SMALLPOX. 69 
 
 How are Rotheln and scarlatina to be differentiated ? 
 
 Rotheln is inherently a mild disease ; scarlatina is never with- 
 out gravity. Rotheln lacks the rapid pulse, the high tempera- 
 ture, the "strawberry tongue" and the grave complications of 
 scarlatina. The eruption of Rotheln more nearly resembles 
 that of morbilli than that of scarlatina. Neither Rotheln nor 
 scarlatina is protective against the other. 
 
 How are Rotheln and morbilli to be differentiated ? 
 
 Rotheln resembles morbilli in its rash, in its mildness and in 
 the catarrhal symptoms it presents. The eruption of Rotheln, 
 however, does not show a tendency to crescentic arrangement, 
 while it appears earlier and the individual papules are smaller 
 than is the case in morbilli. Rotheln is milder than morbilli, 
 even as relates to the catarrhal symptoms. An attack of either 
 confers no immunity from the other. 
 
 Variola— Smallpox. 
 
 Upon what does the diagnosis of smallpox depend ? 
 
 Smallpox or variola is an acute, contagious, epidemic disease, 
 setting in with a chill, pains in the back, head and extremities, 
 nausea and vomiting, elevation of temperature to 102° or 103" F., 
 
 Fig. 13. 
 
 Z 3 4 5 T 8 9 10 11 12 13 !4 15 10 17 ]8 
 
 -^■■■■■■■■■■aHHHiaBiBBBgBBgggggHgBi 
 ^•'■■■■■■■■■■■■■^■■■■■■■■■■■■■■■■i 
 
 ■(■■■■■■■■■■■WKA^HHHBHSSBBBSSBSB"! 
 
 ■■■■■■■■■■■■■^^■■■■■■■■■■■■■■■■■i 
 
 ■■■■■■■■■■■■■nSBUiiriAiHaHiiigHgggggggHi 
 
 ■■■IMHH ■■■■■■■ nHHHBHIWriWniBBBHHHHBaHHH 
 
 BHBnuaHBHHHHMIlaHHHH.raVaWBIHniHHBHHaiHB 
 
 ■■■('■'■■■■■■■fAWHaHgHmHSHSiilgnaggggggg 
 
 3BSSSSgsSiBiEESsSBgiEiimBiiBli 
 
 Temperature-chart of smallpox, (rftriimpell.) 
 
 with marked exacerbations, increased rapidity of pulse, and a 
 diffuse, red rash that is followed on the third or fourth day by 
 the appearance of pajndes; when the temperature declines. 
 
70 ESSENTIALS OF DIAGNOSIS. 
 
 The papules commonly appear first on the lips and forehead. 
 The preceding red rash usually appears first on the arms, and in 
 the neighborhood of the groin. The fauces are apt to be red- 
 dened. There may be decided catarrhal symptoms. In the 
 course of the succeeding four or five days, the papules become 
 vesicles and the vesicles, in turn, pustules. The surface of the 
 pustule is depressed at the middle — umbilicaied. Each pustule 
 is surrounded by an area of redness, constituting an areola. 
 On the eighth or ninth day the pustules rupture and discharge 
 their contents, and the temperature again rises (secondarj'^ or 
 pyemic fever). (Fig. 13.) Secondary fever is sometimes an- 
 nounced by rigor, and its temperature-course is remittent. The 
 evening temperature reaches from 103° to 105° F. The period 
 of maturation and discharge lasts from three to five days, when 
 crusts form and the temperature declines ; in the course of a 
 week the scabs fall ofl^, leaving red cicatrices, which in the 
 course of time become whiter and contracted, leaving "pits." 
 
 Ulceration of the larynx and trachea, bronchitis, pneumonia 
 or pleurisy ma}'^ cmnplicate variola. Secondary inflammations are 
 most likely to occur coincidently with the secondary fever. The 
 eye frequently suffers permanent injury as the result of an attack 
 of smallpox. The pjeriod of incubation of variola is about twelve 
 days. 
 
 What are the varieties of smallpox ? 
 
 Smallpox may be simple or discrete., confluent or hemorrhagic; 
 it may assume a malignant character. 
 
 What are the characteristics of discrete smallpox ? 
 
 Discrete smallpox is the mildest type of smallpox ; the erup- 
 tion is least profuse, the pustules occurring isolated.- Sometimes 
 the pustules are in contact at their periphery, when the disease 
 is said to be coherent. 
 
 What are the characteristics of confluent smallpox? 
 
 In confluent smallpox, the pustules are numerous and I'un into 
 one another. The temperature fails to decline with the appear- 
 ance of the eruption and is apt to be decidedly high during the 
 period of maturation. The gravity of the case is greater than 
 
VARIOLA — SMALLPOX. 71 
 
 in discrete smallpox. Typhoid symptoms, delirium, stupor and 
 fatal coma may develop ; or death may be brought about by 
 diarrhea, ulceration of the larynx or trachea, endocarditis or 
 other complication. 
 
 What are the characteristics of hemorrhagic variola ? 
 
 In hemorrhagic variola the exanthem is from the first consti- 
 tuted of ecchymoses, while hemorrhages may take place from 
 any of the mucous membranes. This is the gravest form. Few 
 cases recover. 
 
 What is malignant smallpox ? 
 
 The epithet malignant is sometimes applied to a variety of 
 smallpox, most frequently encountered at the beginning of an 
 epidemic, in which death may occur early in stupor, following 
 delirium, the eruption being ill-defined and perhaps only devel- 
 oped 'post-mmtem. 
 
 What is varioloid ? 
 
 Varioloid is smallpox modified by vaccination or by a previ- 
 ous attack of smallpox. The symptoms of the disease are similar 
 to those of smallpox, but milder in degree and shorter in dura- 
 tion ; secondary fever is absent. The eruption of varioloid com- 
 monly appears on the second or third day ; that of variola on the 
 fourth day. The course of varioloid is completed in about four- 
 teen days ; that of variola in about twenty-one days. 
 
 What is vaccination ? 
 
 Vaccination consists in the introduction of the virus of cow- 
 pock' into the lymphatic system of man, usually through the skin 
 denuded of its epithelium, as a protection against variola. The 
 protective influence continues for a period of about seven years, 
 at the end of which time vaccination should be repeated. 
 
 1 What is meant by humanized virus ? 
 
 Humauized virus is vaccine-lymph that is not taken directly from the 
 cow (or calf), but from the vaccine-pustule of a human being, usually a 
 child, who may have been inoculated with matter obtained from another 
 child, or from the cow. Unless one is sure as to the purity of the ante- 
 cedents of the source of the humanized virus, bovine virus is to be pre- 
 ferred. 
 
72 ESSENTIALS OF DIAGNOSIS. 
 
 What is vaccinia ? 
 
 Vaccinia is the result of the inoculation of cowpock in human 
 beings, and is protective against smallpox. For two or three 
 days following vaccination, little is to be observed, locally or 
 constitutionally. At the end of this time, the site of inoculation 
 presents an appearance of slight redness, which in the next few 
 days becomes intensified, as a vesicle forms and becomes trans- 
 formed into a pustule, umbilicated and surrounded by a distinct 
 areola. This process goes on for four or five days, when the pus- 
 tule ruptures and the intensity of the inflammation gradually 
 subsides. In the course of a week or ten days, the crust falls 
 off and leaves a reddish cicatrix, which subsequently becomes 
 white and depressed. 
 
 How does smallpox differ from measles ? 
 
 The eruption of measles is coarsely papular throughout, with 
 a tendency to crescentic arrangement, and is followed by branny 
 desquamation ; that of smallpox is irregular in arrangement 
 and passes from the papular into a vesicular and then into a 
 pustular stage, sometimes leaving disfiguring cicatrices. In 
 measles, after a previous decline in temperature, the appearance of 
 the emption is attended with renewed elevation ; in smallpox, the tem- 
 perature declines with tlie appearance of the rash and reascends with ■ 
 the occurrence of pustulation. Smallpox is a grave disease, 
 lasting three weeks ; measles is a mild disease, lasting less than 
 two weeks. 
 
 How are variola and scarlatina to be differentiated ? 
 
 Smallpox may be attended with a primary, diffuse red rash, 
 not unlike that of scarlatina, but, at the end of three or four 
 days, papules appear, in turn to be succeeded bj^ vesicles and 
 pustules, finally leaving disfiguring cicatrices. With the ap- 
 pearance of the secondary rash, the temperature declines. The 
 eruption of scarlatina undergoes no change and terminates in 
 desquamation. The temperature is high from the outset and is 
 continuous. Variola is not characterized by the same rapidity 
 of pulse or by the tj'pical "strawberry tongue" of scarlatina. 
 Uncomplicated scarlatina is a disease of less than two weeks' 
 duration ; variola rarely lasts less than three. 
 
VARICELLA — CHICKENPOX. 73 
 
 Varicella — Chickenpox. 
 
 What are the characteristics of varicella ? 
 
 Varicella or chickenpox is a mild, contagious disease of child- 
 hood, attended with moderate elevation of temperature and the 
 appearance on the first or second day of an eruption of papules, 
 which in turn become transformed into vesicles. The erupticm 
 appears on the trunk and extremities, on the scalp and face. It 
 comes out in crops and continues for thi-ee or four days, the 
 vesicles desiccating and falling off, occasionally leaving cicatrices. 
 
 How does varicella differ from smallpox ? 
 
 Varicella is a mild disease ; variola a grave disease. The erup- 
 tion of smallpox appears on the third or fourth day and passes 
 through papular and vesicular stages to become pustular ; that 
 of varicella appears on the first or second day and does not pass 
 beyond a vesicular stage. The appearance of the eruption in 
 smallpox is attended with a fall in the temperature ; in varicella, 
 the temperature, rarely high, is uninfluenced by the appearance 
 of the rash. Yaricella is a disease of scarcely a week ; small- 
 pox is a disease of three weeks. Neither is protective against 
 the other. 
 
 How are varicella and varioloid to be differentiated? 
 
 There may be a close similarity between the manifestations 
 of varicella and those of varioloid. Yaricella is rare in adults 
 because of the immunity conferred by an attack in childhood. 
 Varioloid does not respect age ; it is likely to appear in the course 
 of an epidemic of variola in those that have been protected by 
 vaccination. Varicella is the milder affection, and is of the 
 shorter duration. Varioloid is but an attenuation and abbrevia- 
 tion of variola. Both varicella and varioloid are contagious. 
 The existence of parallel cases may be decisive in diagnosis. 
 An attack of the one does not protect against invasion by the 
 other. 
 
 How are varicella and morbilli to he. differentiated ? 
 
 The eruption of measles is coarsely papular ; it appears on the 
 third or fourth day and displays a special proclivity to invade 
 
74 ESSENTIALS OF DIAGNOSIS. 
 
 the face, with a tendency to crescentic arrangement. The erup- 
 tion of chickenpox is at first papular and subsequently vesicular ; 
 it appears on the first or second day and is rather less than 
 more abundant on the face than on the trunk. The catarrhal 
 symptoms of measles are wanting in varicella. The tempera- 
 ture-course is not characteristic in varicella, as it is in measles. 
 
 Erysipelas. 
 
 What are the symptoms of erysipelas ? 
 
 Mrysipelas is an acute, infectious disease, setting in suddenly 
 with a chill, sometimes with nausea and vomiting, or with con- 
 vulsions, followed by considerable elevation of temper oiure, and 
 the appearance, usually at some part of the face, and in most 
 instances near one or other ear, of an area of red, brawny indura- 
 tion. The redness progressively increases in extent, is definitely 
 circumscribed by an elevated line of demarkation, and is attended 
 with swelling. 
 
 The cviypetite is impaired. The ton/jue is coated. 
 
 The urine is usually albuminous, and often contains tube-casts. 
 
 There is often some soreness of the throat, and in some cases 
 the disease may extend through the nasal passages into the 
 pharynx and larynx, causing grave complications, and, perhaps, 
 fatal edema. Sometimes the disease begins in the throat. 
 
 Involvement of a cerebral sinus may occur, giving rise to 
 severe symptoms and eventually causing death. 
 
 Usually, in the course of a week or ten days, the redness and 
 swelling subside, desquamation sets in, and the temperature 
 graduallj'^ reaches the normal. 
 
 In some cases, the disease displays a migratory tendency, 
 [erysipelas migrans), continuing for a long period of time, and in 
 turn appearing at various parts of the body. In children, ery- 
 sipelas sometimes appears first in the neighborhood of the amis. 
 The disease often attacks wounds. 
 
 What are the differential features between erysipelas and 
 scarlatina ? 
 Scarlatina is especially a disease of childhood. Erysipelas is 
 more common in adults than in children. 
 
ERYSIPELAS. 75 
 
 The temperature is high in both, but the rapidity of the pulse 
 is the more characteristic of scarlatina. 
 
 The rash of erysipelas is circumscribed in extent, limited in 
 area, homogeneous in color ; it usually appears upon the face, 
 and presents a peculiar brawny induration, with well-defined 
 borders ; while the eruption of scarlatina is extensive in distri- 
 bution and punctate in character. 
 
 An attack of scarlatina confers immunity from subsequent 
 attacks ; one attack of erysipelas rather predisposes to the oc- 
 currence of subsequent attacks. 
 
 Of the two, scarlet fever is the longer in duration. 
 
 How does erysipelas differ from simple erythema ? 
 
 Simple erythema presents a diffuse redness, of transitory char- 
 acter, without febrile concomitants or sequelae. 
 
 Erysipelas is a serious affection, with considerable elevation 
 of temperature and characteristic rapidity of pulse. It lasts a 
 week or more, is followed by desquamation, and is intimately 
 related with nephritis. 
 
 How are facial erysipelas and herpes zoster of the forehead and 
 face to be differentiated ? 
 
 Facial erysipelas and herpes zoster of the forehead and face 
 present a number of symptoms in common. That which dis- 
 tinguishes the latter, however, is that the eruption begins as a 
 number of vesicles and does not extend beyond the middle line. 
 The pain is much greater in herpes than in erysipelas. The 
 constitutional symptoms are more profound in erysipelas than 
 . in herpes. 
 
 How are variola and erysipelas to be differentiated ? 
 
 When variola is attended with a ])rimary roseola, the disease 
 may, for several days, simulate erysipelas. The redness of 
 erysipelas, however, is distinctly circumscribed, although it may 
 slowly spread, and is attended with brawny induration, while 
 that of smallpox rapidly spreads from the face to the trunk and 
 extremities. On the third or fourth day, if the disease is 
 variola, papules appear, progi-essively passing through the 
 
76 ESSENTIALS OP DIAGNOSIS. 
 
 stages of vesicles and pustules. The eruption of erysipelas un- 
 dergoes little change, unless large blebs form, until on about the 
 fifth or seventh day, when it may subside with desquamation. 
 
 Dengue, 
 
 What are the symptoms of dengue or " break-bone fever? " 
 
 Dengue is an exanthematous and arthritic disease of hot 
 climates, occurring in epidemics^ and having a period of incit- 
 hation of about four days. It is characterized by severe pains in 
 the muscles and joints, which may be stiff and swollen. The 
 knees are especially prone to be affected, so that, the gait pre- 
 sents a peculiar character. The disease may be gradual in 
 onset, with anorexia, headache, vertigo, drowsiness, or it may 
 set in suddenly with a chill, moderate elevation of temperature 
 and the appearance of an erythematous rash. There are stiffness 
 of the neck and pain along the spine and in the lumbar region. 
 The fefoer reaches its acme within twenty-four hours. The tem- 
 peratuve fluctuates, rising and falling, but in the course of two 
 or three days subsides nearly or quite to the normal ; the erup- 
 tion disappears, though constitutional depression and more or 
 less pain continue. As a rule, nausea and vomiting do not 
 occur at this stage, though the tongue may be heavily coated, 
 and there may be other symptoms of gastric irritability. 
 
 After an intermittence of from forty-eight to seventy -two hours 
 or more, the fever returns and a new eruption appears, as a rule 
 resembling the eruption of scarlatina. Sometimes the eruption 
 is more like that of measles, or it may be urticarious or ves- 
 icular. It is attended with heat and itching. Nausea and 
 vomiting are usuaUy manifested with this renewal of the fever. 
 
 In the course of a few days, desquamation occurs ; conva- 
 lescence sets in, but is tardy and protracted ; there is weak- 
 ness and more or less rheumatoid muscular pain ; lymphatic 
 swellings in the neck, groin or axilla often appear during the 
 febrile period or during convalescence. When the disease 
 invades a community, few escape. 
 
DIPHTHERIA. 77 
 
 How does dengue differ from scarlatina with arthritic mani- 
 festations ? 
 
 In dengue the fever is not continuous and pursues a course 
 different from that of scarlatina ; the arthritic symptoms are of 
 earlier occurrence, and the pain is of a characteristic nature, 
 giving the name "break-bone" fever. The eruption develops 
 much later, and is sometimes quite different in aj^pearance from 
 that of scarlatina. The erythematous rash of the period of in- 
 vasion is slight, inconstant and disappears without desquama- 
 tion when the remission or intermission occurs. Throat-symp- 
 toms are not common. 
 
 In what respect does dengue differ from influenza ? 
 
 Influenza is the graver disease ; its symptoms are the more 
 intense. 
 
 Catarrhal symptoms are frequent in influenza, infrequent in 
 dengue. 
 
 Eruptions are exceptional in influenza, the rule in dengue. 
 
 Joint-pains are more decided in dengue. Hyperesthesia of 
 the cutaneous surface is more common in influenza. 
 
 The course of dengue is interrupted by a remission. The 
 course of influenza is usually though not invariably continuous 
 to its termination. 
 
 Influenza is independent of climate. Dengue prevails only in 
 certain localities. Convalescence is even more tedious and 
 protracted from dengue than from influenza. 
 
 Diphtheria. 
 
 What are the symptoms of diphtheria ? 
 
 Diphtkeria is an acute, infectious disease affecting children 
 especially, but adults as well, and characterized by septic fever 
 with superficial coagulation-necrosis of mucous membranes, 
 especially of those of the pharynx, larynx and nares. 
 
 The attack may begin insidiously, or set in suddenly with a 
 chill, followed by considerable fever. 
 
 Pain in the throat in swallowing may or may not be com- 
 plained of. The fauces will be seen to be livid, the tonsils usually 
 swollen. 
 
78 ESSENTIALS OF DIAGNOSIS. 
 
 Soon, there appear, in greater or less extent and rapidly 
 spreading over the tonsils, the half-arches, the uvula and the 
 posterior wall of the pharynx, grayish or yellowish patches of 
 false membrane, the forcible detachment of which is followed 
 by bleeding. There are enlargement of the submaxillary and 
 cervical glands and tumefaction of the soft tissues of the neck, 
 externally. 
 
 The constitutional disturbance becomes profound. Albumin- 
 uria is common. Prom the pharynx the inflammation and 
 necrosis may extend to the larynx and to the nose, and to the 
 difficulty of swallowing are added croupy cough, aphonia, diffi- 
 culty of breathing and a nasal discharge. The diphtheritic 
 process is sometimes primary in the nose, and may*thus escape 
 detection, unless careful examination be made. From the 
 larynx the false membrane may invade the trachea and bronchi. 
 Pneumonia may occur. The action of the heart becomes weak 
 and often intermittent. Septicemia, heart-failure and suffoca- 
 tion from obstruction of the larynx or bronchi are the common 
 causes of death. 
 
 The fatality of the disease varies in different epidemics. Even 
 in times of grave epidemics, there are many mild cases that 
 become foci of infection. Chronic diphtheria of the throat is not 
 so rare as it is commonly considered to be and is likewise a 
 focus of infection. Paralysis from peripheral neuritis or cere- 
 bral thrombosis may be a sequel. 
 
 The palsy of diphtheria may appear in the course of the dis- 
 ease, but it is more common after the acute attack is at an end. 
 Adults are rather more prone to suffer than children. The 
 most common manifestations ?aie paralysis of the palate^ permit- 
 ting regurgitation of fluids and giving rise to nasal speech ; 
 paralysis of the ciliary muscle (cycloplegia), causing loss of power 
 of accommodation ; loss of knee-jerks. There may be more 
 general palsy, with deranged sensation, ataxia and trophic 
 changes. 
 
 How are diphtheria and scarlatina to be differentiated ? 
 
 At the onset, the diseases may be indistinguishable. Both 
 present the evidences of constitutional disturbance, with local- 
 
DIPHTHERIA. 79 
 
 » 
 
 ized throat-symptoms. Possibly, the pulse may be relatively 
 more rapid iu scarlatina than in diphtheria. In from twenty- 
 four to thirty-six hours, however, the appearance of a scarlet 
 rash, as well as the subsequent course of the disease, dispels 
 all doubt. 
 
 In diphtheria, the symptoms centralize themselves about the 
 throat ; in scarlatina the throat disturbance represents .but a 
 part of the general derangement. The paralyses commonly 
 seen after diphtheria are rare after scarlatina. More common 
 during the course of scarlet fever or subsequently are suppu- 
 rative ear-disease, nephritis and glandular enlai'gement. 
 
 Diphtheria and scarlatina may coexist in the same patient. 
 
 How is tonsillitis to be distinguished from diphtheria ? 
 
 Deposits on the tonsil may appear diphtheritic. They show 
 little or no tendency to spread, however. Extension is charac- 
 teristic of the diphtheritic membrane. In lacunal tonsillitis, 
 the discreteness of the plugs and their situation at the orifices 
 of the ducts are characteristic, and their creamy color is differ- 
 ent from that of the diphtheritic pseudomembrane. Microsco- 
 pically, they will be seen to be made up of desquamated epi- 
 thelium, of sebaceous material and of ordinary fungi. The 
 diphtheritic membrane is constituted of meshes of fibrin con- 
 taining necrotic tissue. In herpetic tonsillitis the eruption first 
 appears as papules that soon become vesicles ; but it is rarely 
 seen at this stage ; when ulcers and fibrinous deposits form and 
 become confluent, the discrimination is difficult. Still, the her- 
 petic patch is quite superficial, and more readily detached, leav- 
 ing less erosion and causing less hemorrhage in its separation 
 than does the diphtheritic patch. The former is usually the less 
 extensive, and here and there, perhaps, the circular form of an 
 isolated ulcer may give evidence of its origin. If necessary, 
 inoculation-experiments and bacteriologic investigation may 
 also help to discriminate. The constitutional symptoms of ton- 
 sillitis are less profound than those of diphtheria ; local subjec- 
 tive symptoms, such as soreness, odynphagia and burning, are 
 usually the more intense in tonsillitis, which is not, as a rule, 
 followed by paralysis of the palate. Albuminuria is not usual. 
 
80 ESSENTIALS OF DIAGNOSIS. 
 
 How is membranous croup to be distinguished from diph- 
 theria ? 
 
 Until the physician acquires sutiicient experience to warrant 
 a personal opinion, he had best consider all cases of membran- 
 ous croup diphtheritic. The discrimination is difficult and 
 disputed. 
 
 How are diphtheria and stomatitis to be differentiated ? 
 
 The deposits in stomatitis are seated upon the mucous surface 
 of the lips and cheeks and upon the tongue, while the mem- 
 brane of diphtheria is usually seated in the pharynx, from 
 which, as a center, it is distributed. The constitutional 
 derangement is not as profound in stomatitis as in diphtheria. 
 Stomatitis readily yields to mild general and local measures, 
 while diphtheria is more rebellious to treatment. The fatality 
 and the severe sequelae of diphtheria are wanting in stomatitis. 
 
 Glanders— Farcy —Equinia. 
 
 What are the clinical features of glanders ? 
 
 Glanders, farcy or equinia is an infectious disease, especially 
 peculiar to horses, asses, and mules, from which it is trans- 
 mitted to man through abrasions of the skin and through the 
 mucous surfaces of those that come in contact with the diseased 
 animals. 
 
 The site of inoculation displays evidence of active inflamma- 
 tion ; especially is this marked in the nasal passages. There are 
 also malaise, headache, elevation of temperature and pains in 
 the limbs ; the urine may be albuminous. Soon there appears 
 a macular eruption, which becomes vesicular, then pustular 
 and finally umbilicated. The pustules may rupture and leave 
 ugly ulcers. In addition, nodules form beneath the skin ; these 
 also soften and may rupture, discharging sanious pus and de- 
 tritus. Another characteristic symptom of glanders is ozena. 
 There is at first a moderate, thin discharge from the nostrils, 
 soon, however, becoming profuse and purulent. The mucous 
 membrane of the nares and contiguous structures is involved 
 in intense inflammation and may become ulcerated. Catarrhal 
 
ANTHRAX — WOOLSORTERS' DISEASE. 81 
 
 pneumonia and purulent arthritis are occaKsional complications. 
 Glanders may be transmitted from man to the lower animals by 
 inoculation. 
 
 How are glanders and variola to be differentiated ? 
 
 In glanders, there may be a history with the local evidences 
 of inoculation with the specitic virus of the disease. The 
 eruption of variola does not appear until the third or fourth 
 day ; with its appearance the temperature falls. The eruption 
 of glanders may appear within the first twenty-four or forty- 
 eight hours of the disease ; it reaches a pustular stage much 
 earlier than that of variola ; there is no decline of temperature 
 with its appearance. The eczema and the subcutaneous nodules 
 of glanders are wanting in variola. 
 
 How are the ozena of glanders and that of syphilitic disease to 
 be differentiated ? 
 Ozena is dependent upon destruction of the nasal structures 
 and putrefactive decomposition of the secretions. It is thus not 
 distinctive of a single disease. Occurring in syphilis, it is a late 
 manifestation, and probably has been preceded by well-defined 
 symptoms. As seen in glanders, it occurs at the height of the 
 disease, and is associated with a pustular eruption and the 
 presence of nodules beneath the skin. The mode of infection 
 differs in the two diseases. 
 
 Anthrax — Wool-sorters' Disease. 
 
 What are the clinical features of anthrax ? 
 
 Anthrax, wool-sorters'' disease, charbon, malignant pustule or 
 splenic fever is an infectious disease, due to inoculation with the 
 bacillus anthracis (Fig. 14.) It develops in butchers, wool-sorters, 
 workers in hides, stevedores and others that, with cut or wounded 
 or abraded hands, manipulate the wool or skins of animals that 
 have died of splenic fever or charbon. The infection some- 
 times gains entrance through a scratch on the cheek or an 
 abrasion of the lips. In butchers, the tongue is sometimes 
 infected from a knife taken between the teeth. In those that 
 carry hides upon their shoulders, the neck may be the site of 
 6 
 
82 ESSENTIALS OF DIAGNOSIS. 
 
 local infection ; these cases are likely to be more than ordinarily 
 dangerous. The disease may apparently result from eating the 
 flesh or from drinking the milk of infected animals. 
 
 Fig. 14. 
 
 Anthrax bacilli in blood. (Vierordt 
 
 At the site of inoculation, a pimple appears ; the skin in its 
 neighborhood becomes red and infiltrated ; the papule becomes 
 vesicular and pustular, with subsequent gangrene ; other vesi- 
 cles or pustules form and also become gangrenous ; there 
 results a characteristic eschar, which presents the appearance 
 of an elevated patch, consisting of a zone of low, whitish vesicles 
 surrounding a depressed brownish, purplish, or black center, 
 with an outer zone of red induration. Beyond this is usually 
 a region of swelling and edema of variable extent. The 
 spleen and the lymphatic glands in communication with the 
 infected regions enlarge. There is often considerable local 
 tenderness. The constitutional symptoms are those of septico- 
 pyemia : malaise, headache, depression, fever. According to 
 the mode of introduction of the poison, or the direction in 
 which infection spreads, other manifestations appear. Some- 
 times the gastro-intestinal tract appears to bear the brunt of the 
 disease and there are nausea, vomiting, abdominal pains and 
 diarrhea, the stools being bloody. Death may take place from 
 exhaustion or from septicemia. At other times, thoracic symp- 
 toms predominate. There are then dyspnea, a sense of oppression 
 
ACTINOMYCOSIS. 83 
 
 of breathing, hemoptysis and cyanosis. Deatli may take place 
 from edema of the larynx or of the mediastinum. Charac- 
 teristic bacilli may often be found in the blood, pus, sputum, 
 feces, or urine. Under proper treatment recovery frequently 
 takes place. 
 
 Actinomycosis. 
 
 What is actinomycosis ? 
 
 Actinomycosis is a condition dependent upon the presence of 
 ray-fungi : actinoniyces bovis. (Fig. 15.) The disease is more fre- 
 
 FiG. 15. 
 
 Actinomyces. (Ziegler, 
 
 quent in drovers and in those that have to do with cattle, from 
 which the parasite, as found in man, is usually derived. The 
 cattle become infected through their food. The fungus gains 
 entrance through a breach in continuity of the surface and, finding 
 its way to a suitable nidus, gives rise to the formation of a sero- 
 purulent collection ; this manifests itself as a tumor that usually 
 finds vent externally. In the matter discharged, yellowish mili- 
 ary nodules, composed of fungi, can be detected. The lower jaw 
 seems to be a favorite seat of the disease, infection taking place 
 through decayed teeth ; sometimes extensive destruction of bone 
 results. At other times, purulent collections form in internal 
 viscera. When the pleura is infected the ribs may suffer 
 severely. 
 
84 ESSENTIALS OF DIAGNOSIS. 
 
 Foot-and-Mouth Disease. 
 
 What is foot-and-mouth disease ? 
 
 Foot-and-mouth disease is a rare affection that occurs in sheep, 
 cows, pigs and horses, and that occasionally seems to be trans- 
 mitted to man. It manifests itself by the appearance of vesicles 
 and bullse in the mouth and on the feet at the margins of the 
 hoofs and, in cows, on the udder and teats. The disease may 
 be transferred directly to man by inoculation — thus to the 
 butcher or to the veterinary surgeon, or it may be conveyed by 
 milk. In man, vesicles form in the mouth, on the face, on the 
 hands and on the feet. In the course of two or three days, 
 the vesicles rupture, discharging opaque, yellowish fluid, and 
 leaving dark-red ulcers. There are also fever, loss of appetite, 
 pain in eating, sw^elling of the tongue, fetor of the breath, 
 salivation and derangement of digestion. ]n children the dis- 
 ease may prove fatal. 
 
 Hydatid Disease. 
 
 What is hydatid disease ? 
 
 An hydatid cyst is a parasitic formation due to ingestion of 
 the ova of the tenia ediinococctis, the tape-worm of dogs, in which 
 it is derived from the flesh of sheep, or pigs, or less frequently, 
 kine, suffering from hydatid disease. 
 
 When the ovum enters the stomach of man, its capsule is 
 dissolved, and the immature embryo or scolex (Fig. 16) is set 
 free to continue its migrations. Arriving at its destination, 
 the irritation to which it gives rise results in the formation of 
 a membranous envelop, in whi(;h the parasite continues its de- 
 velopment. This capsule, and its contents together constitute 
 an hydatid cyst. An hydatid cyst contains within the capsule, a 
 vesicle or mother-sac, consisting of concentric layers of a gelatin- 
 ous material, inclosing the embryo and more or less fluid. 
 The fluid is clear, opalescent, and faintly alkaline. Within 
 this develop other similar sacs, so-called daughter-vesicles, and 
 
TRICHINIASIS, 
 
 85 
 
 within these again, granddaughter-vesicles ; the mother-sac 
 and its investing membrane continue to enlarge, if in a favor- 
 able situation, until ultimately the cyst attains an enormous 
 size. Multiple cysts may form. The daughter-vesicles contain 
 
 Fig. 16. 
 
 ^ 
 
 ^ 
 
 Tenia Echinococciis — vesicle, scolex and hooks. (After Heller.) 
 
 a germinating layer that produces new scolices. These con- 
 sist of a head, four suckers and a row of booklets. The dis- 
 covery of the booklets (Fig. 16) in fluid removed from the cyst 
 is diagnostic. Sterile echinococci or acephalocysts do not produce 
 scolices. 
 
 Hydatids may develop in various viscera, but are most com- 
 mon in the liver. 
 
 Trichiniasis. 
 
 What is trichiniasis ? 
 
 Trichiniasis is a disease set up by the trichina spiralis (Fig. 
 17), a small roundworm that finds its way into the intestine with 
 meat obtained from diseased swine. 
 
 In the intestine the mature female throws off embryos, which 
 pass through the walls of the intestine and into the blood-cur- 
 rent, finding their way into the voluntary muscles in different 
 parts of the body. Here the embryos occasion irritation and 
 inflammation, so that about each a capsule forms in which 
 lime-salts are in time deposited ; in this way the death of the 
 embryo may be brought about. 
 
86 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 Fig. 17. 
 
 What are the symptoms of trichiniasis ? 
 
 The symptoms of trichiniasis present 
 themselves iu three stages. In the first, 
 which lasts about a week, the trichinae are 
 undergoing development in the alimentary 
 canal, as a result of which the symptoms of 
 gastro-intestinal derangement appear. la 
 the second stage, lasting two or three 
 weeks, the embryos pass from the intestine 
 into the muscular tissue. Finally, retro- 
 gressive changes take place in and around 
 the trichinae encapsulated in the muscles. 
 
 In the first stage, the appetite is im- 
 paired ; the tongue is coated, the breath 
 is foul ; there are malaise, nausea, a bad 
 taste, diarrhea, abdominal pain and slight 
 fever. 
 
 In the second stage, there is edema, ap- 
 parent in the face and sometimes extending 
 downwards ; there are also pains in the 
 muscles, which are swollen ; defects of the 
 ocular muscles and of accommodation some- 
 times appear ; the senses and various func- 
 tions may be affected ; sleep is disturbed 
 and there is moderate fever. The muscles 
 are sensitive to touch, which may detect 
 the minute nodules. Death may result from 
 exhaustion, pneumonia or ulceration of the bowel. In favora- 
 ble cases, the symptoms gi'adually subside and the patient enters 
 upon the third stage of the disease. Active symptoms are now 
 in abeyance, but there may be some stiffness of the muscles, 
 while nodules in the muscles may be detectable. 
 
 Ultimately, however, the patient may be restored to a fair 
 degree of health. 
 
 Trichina, a, Male ; 6, 
 Female ; c, Muscle-Tri- 
 china. (V. Jaksch ) 
 
ACUTE RHEUMATISM — RHEUMATIC FEVER. 87 
 
 Acute Rheumatism — Rheumatic Fever. 
 
 What are the symptoms of acute rheumatism ? 
 
 Acute rheumatism or rheumatic fever usually follows ex- 
 posure to cold. An almost identical condition is sometimes 
 observed in the course of puerperal fever and as a sequel of 
 scarlatina. It is thought to be dependent upon the presence 
 of lactic acid in the blood. One of the larger joints becomes 
 painful, enlarged, hot and reddened. It is evidently inflamed ; 
 sometimes the presence of fluid can be detected. Soon, another 
 joint, probably the corresponding joint on the opposite side, or 
 the next contiguous joint, becomes similarly involved ; and in 
 this way the process may extend, until most or all of the large 
 joints are in turn attacked. On account of the pain, the patient 
 is immovably helpless. From the surface of the body exudes 
 an acid sweat. The temperature ordinarily ranges from 102° F. 
 to 104° F., rising with each fresh access of joint-symptoms, and 
 declining gradually with the termination of the disease. The 
 pulse is disproportionately frequent ; it may be full and bound- 
 ing. The urine is scanty, high-colored, and quite acid ; it may 
 contain a trace of albumin. 
 
 In many cases, to the articular manifestations endocarditis is 
 added, as a result of which permanent valvular lesions may be 
 established. Among other complications are inflammations of 
 the pericardium, the pleura, the peritoneum, the kidney and, 
 though rarely, the cerebro-spinal meninges. As a rule, delirium 
 is due to the toxemia and not to meningitis. 
 
 Sometimes the temperature rises even to hyperpyrexia, and 
 there are decided cerebral symptoms — delirium, convulsions, 
 coma, death. 
 
 Untreated, the duration of acute rheumatism is about six 
 weeks ; sometimes much longer. Relapses are not uncommon. 
 An attack predisposes to subsequent attacks. 
 
 Purpura is sometimes seen in the course of rheumatism ; 
 sometimes tuberculated cutaneous nodules. 
 
 In some eases of rheumatism, hereditary influences can be 
 traced. Some authorities consider the disease a dyscrasia, others 
 
88 ESSENTIALS OF DIAGNOSIS. 
 
 a neurosis. There appears to be an indefinable, yet close relation 
 between acute rheumatism and chorea. 
 
 Articular rheumatism not uncommonl}^ accompanies, pre- 
 cedes or follows acute tonsillitis. In such cases, pericarditis and 
 endocarditis may sometimes be detected if carefully searched 
 for. 
 
 How are pyemia and acute rheumatism to be differentiated ? 
 
 Both pyemia and acute rheumatism occasion arthritis, sweats, 
 cardiac complications and cerebral symptoms. Periodicity and 
 rigors, as well as metastatic invasion of internal structures re- 
 mote from the primary seat of disease, which are common in 
 pyemia, are wanting in rheumatism. The constitutional de- 
 pression is more profound in pyemia than in rheumatism. In 
 one, an obvious or obscure focus of suppuration exists ; in the 
 other, there is a history of rather abrupt onset following ex- 
 posure to cold or wet. 
 
 How are acute synovitis and acute rheumatism to be differ- 
 entiated ? 
 
 Acute synovitis usually involves but a single joint ; it is 
 characteristic of acute rheumatism to progressively attack 
 many joints. The constitutional phenomena are more profound 
 in acute rheumatism than in acute synovitis. 
 
 The peculiar, acid sweats, as well as the cardiac complications 
 of rheumatism are not seen in synovitis. 
 
 In duration, synovitis is the shorter disease. 
 
 Gonorrheal Synovitis, 
 
 What is gonorrheal synovitis ? 
 
 Occasionally, in the course of an attack of gonorrhea, a large 
 joint— and usually but one joint, such as the knee, the elbow, 
 the wrist, the ankle or the shoulder, becomes tumid, painful, 
 tender and hot, and the adjacent textures may be edematous. 
 Tlie ui'cthral discharge often ceases with the appearance of the 
 synovitis. In successive attacks of gonorrhea, different joints 
 may be involved. Permanent stiffness and impaired mobility 
 constitute a common sequel. Cardiac complications have been 
 
SUBACUTE RHEUMATISM. 89 
 
 observed in some cases of gonorrheal synovitis. The diagnosis 
 depends upon a knowledge of the existence of a specific ure- 
 thritis. Sometimes, the course of the temperature is suggestive 
 of a pyemic or of a septic condition. 
 
 Syphilitic Arthritis. 
 
 What is syphilitic arthritis ? 
 
 Every now and then, in the course of syphilis, one or more 
 joints become involved in inflammation, with all of the character- 
 istics of an arthritis. The discrimination of the condition de- 
 pends upon a recognition of its association with syphilis. As a 
 rule, cardiac complications are wanting in syphilis, and the 
 arthritis is more strictly limited to one, or at most, two joints, 
 the migratory tendency of acute articular rheumatism being 
 absent. 
 
 Suhacute Rheumatism. 
 
 What is subacute rheumatism ? 
 
 At times, as a result of exposure to cold and wet, muscular 
 movement becomes painful, in consequence of a rheumatic in- 
 volvement of the muscle-sheaths. The patient sometimes mis- 
 takes for paralytic weakness the restraint of motion by pain. 
 The pain is also in some degree spontaneous and influenced by 
 meteorologic conditions. Affecting the muscles of the lumbar 
 region, the condition is termed lumbago. Affecting the muscles 
 of the neck it mnj give rise to torticollis or wry-neck. 
 
 How are subacute rheumatism and neuralgia to be differ- 
 entiated ? 
 
 Both subacute rheumatism and neuralgia occur in paroxysms, 
 superinduced by suitable meteorologic conditions. Rheumatism 
 is more common in men ; neuralgia in women. The pain 
 of the former is rather dull and diffused ; that of the latter 
 sharp and confined to the distribution of an affected nerve, in 
 the course of which may be found several tender points. Rheu- 
 matic pain more commonly than neuralgic pain is aggravated 
 by movement. 
 
90 ESSENTIALS OF DIAGNOSIS. 
 
 How are subacute rheumatism and trichiniasis to be differen- 
 tiated? 
 In trichiniasis, in addition to symptoms simulating those of 
 subacute rheumatism, there are evidences of a cachexia, wasting, 
 debility and symptoms of gastro-intestinal derangement, with 
 a history of the ingestion of diseased meat. At an advanced 
 stage of the disease, it may be possible to detect the nodules to 
 which the encapsulated parasites give rise. 
 
 Myalgia. 
 
 What is myalgia? 
 
 As a result of muscular strain, groups of muscles become 
 painful to touch and on movement, in association with some 
 degree of cutaneous hyperesthesia. 
 
 Chronic Bheumatism. 
 
 What are the symptoms of chronic rheumatism ? 
 
 As a result of an attack or of repeated attacks of acute 
 rheumatism, numerous joints in different parts of the body 
 remain enlarged, stiff and painful. Sometimes the condition 
 is insidious, progressive and chronic from the outset. How- 
 ever produced, the functions of the various joints are impaired ; 
 attacks of pain occur and are apparently influenced by meteor- 
 ologic conditions. Wasting of the muscular structures adja- 
 cent to the diseased joints takes place. 
 
 Chronic rheumatism may affect both joints and muscles, or the 
 muscle sheaths or tendons only (muscular rheumatisin) ^ or it may 
 attack the nerve-sheaths (rheumatic neuralgia^. The principal 
 symptoms of muscular and of nerve-rheumatism are pain, spon- 
 taneous and on motion, with accompanying tenderness, usually 
 Jocalized. 
 
 How are the enlarged joints of chronic rheumatism to be dis- 
 tinguished from those of chronic spinal disease? 
 
 Trophic changes in the large joints — enlargement, effusion, 
 subluxation, arthropathies— take place in the course of some 
 
ACUTE GOUT. 91 
 
 chronic spinal aflfections, notably posterior spinal sclerosis. As 
 a rule, but one or a few joints are involved. In chronic rheu- 
 matism, many joints are involved. In case of disease of the 
 spinal cord ordinary scrutiny should detect the existence of 
 symptoms indicative of such a condition. 
 
 Acute Gout. 
 
 What are the symptoms of acute gout ? 
 
 Acute gout is a recurrent paroxysmal affection thought to be 
 dependent upon the presence of an excess of uric acid in the 
 blood. It occurs chiefly in those of a sedentary or inactive mode 
 of life, who indulge excessively in the luxuries of the table, more 
 especially in meats, sweets, sweet wines and malt liquors. Those 
 that have been active in out-door sports and afterwards, while 
 diminishing their exercise, maintain the heavy diet formerly 
 appropriate, are extremely liable to gout. The tendency to gout 
 is distinctly hereditary, and in some cases of marked gouty di- 
 athesis the attacks may occur despite personal abstemiousness. 
 
 The paroxysm may be brought on bj'^ an unusual excess, by a 
 fit of anger, by worry or anxiety or by exhaustion. Its advent 
 is sometimes unannounced ; at other times, it is preceded by 
 symptoms of indigestion, by mental irritability or depression. 
 The attack usually sets in suddenly at night, the patient being 
 awakened by intense pain most commonly referred to the meta- 
 tarso-phalangeal joint of the great toe. There is fever in pro- 
 portion to the intensity of the local affection. The pain mode- 
 rates somewhat towards morning, when the patient falls into a 
 gentle perspiration and is again able to sleep. Towards night 
 the pain returns. The joint is now noticed to be tender, red, 
 swollen and edematous ; finally desquamation takes place. 
 Other joints are successively involved, the morbid process show- 
 ing an affinity for the smaller articulations. The attack gradu- 
 ally subsides, leaving the affected joints a little stiffened and 
 swollen. At the height of the attack the proportion of uric 
 acid in the blood is increased, while that excreted in the urine 
 is diminished. When the paroxysm is over the quantity of uric 
 acid in the urine is increased. In an attack of acute gout, the 
 
92 ESSENTIALS OF DIAaNOSIS. 
 
 joint-symptoms may suddenly subside, and gastric, cardiac or 
 even cerebro-spinal symptoms be substituted. 
 
 Sometimes the attack is manifested from the first by visceral 
 rather than by articular crises. Visceral crises are more likely 
 to occur late in the history of the case than early in its course, 
 and they sometimes prove fatal. 
 
 Chronic Gout. 
 
 How are acute riieumatism and acute gout to be differentiated ? 
 
 Gout is an hereditary aflfection, occurring in paroxysms, in 
 which the first metatarso-phalangeal articulation and other small 
 joints are involved. In acute rheumatism, a history of heredity 
 is frequently wanting ; the large joints are especially involved. 
 The duration of an attack of rheumatism is many weeks ; an 
 attack of gout subsides in the course of a week or two. The 
 uratic deposits of gout are wanting in rheumatism. The 
 sweats of rheumatism are absent from gout. Cardiac complica- 
 tions are common in acute rheumatism ; gout never occasions 
 endocarditis, but chronic interstitial nephritis is a common 
 sequel. 
 
 What is chronic gout ? 
 
 In those that have had a number of paroxysms of acute gout, 
 or sometimes chronically from the first, deposits of urates take 
 place around the diseased joints, in the articular cartilages and 
 elsewhere, as in the lobe of the ear, in the kidneys and in the 
 spleen. As a result there is painful thickening of the affected 
 articulations, which are stiff" and finally become deformed. 
 Sometimes distinct " chalk-stones" may be felt, and in extreme 
 cases these may cause ulceration and appear externally. Gout 
 is a potent cause of arterio-capillary fibrosis. An excess of 
 fibrous tissue develops in the viscera and in the walls of the blood- 
 vessels, with secondary contraction. Chronic interstitial ne- 
 phritis is a common sequel. 
 
 Lead-poisoning may give rise to lesions exactly resembling 
 those of chronic or of subacute srout. 
 
LITHEMIA. 93 
 
 Lithemia. 
 
 What are the clinical features of lithemia ? 
 
 Lithemia is modified gout — a manifestation of the uric-acid 
 diathesis. It is caused by defective oxidation within the body 
 and is dependent upon imperfect tissue-metabolism. 
 
 Lithemia manifests itself by varied symptoms, among which 
 are sallowness or abnormal redness of complexion, impaired or 
 perverted appetite, a metallic taste, deranged digestion, consti- 
 pation, headache, vertigo, irritability of temper, a tendency to 
 melancholia, abnormal drowsiness or sleeplessness, palpitation 
 of the heart, irritative cough, disturbances of vision, noises in 
 the ears, anomalous cutaneous eruptions, transient localized 
 edema, and cramps in the calves of the legs. Micturition is fre- 
 quent and burning, the urine usually being diminished in quan- 
 tity and containing an excess of uric acid and urates ; phosphate^ 
 and calcium oxalate are likewise frequently in excess ; in cases 
 attended with paroxysmal flushing red blood-corpuscles and al- 
 bumin are occasionally found ; sometimes a small number of 
 tube-casts. Chronic catarrhal hepatitis and functional inac- 
 tivity of the liver are frequently — perhaps causally — associated 
 with lithemia. Fibrous degeneration of the kidneys and of 
 the walls of the smaller arteries, with cardiac hypertrophy, may 
 be an ultimate sequel. 
 
 For what affections may lithemia be mistaken? 
 
 Unless in a given case one bears in mind the possibility of the 
 existence of lithemia, and is on the alert for its detection, the 
 condition may be mistaken for almost any functional disorder,, 
 or even for serious organic disease of the heart, brain, stomach, 
 intestine, or other organ. 
 
 The discrimination depends partly upon the exclusion of vis- 
 ceral lesions, and partly upon the results of urinalysis : the 
 finding of an excess of urates or free uric acid pointing to the 
 existence of lithemia. An hereditary tendency to gout or rheu- 
 matism, or the existence of gout, rheumatism, or diabetes in 
 other members of the patient's family, or the fact that the 
 patient's habits of life are such as are likely to lead to the de- 
 
94 ESSENTIALS OF DIAGNOSIS. 
 
 velopment of gout, should direct attention to the probability of 
 the existence of litheraia. 
 
 It must not be forgotten that fibroid changes in the blood- 
 vessels and kidneys are frequent concomitants of the uric-acid 
 diathesis. 
 
 Bheumatoid Arthritis — Arthritis Deformans. 
 
 What are the clinical features of rheumatoid arthritis ? 
 
 Bheumatoid arthritis, arthritis deformans, often incorrectly 
 called rheumatic gout, is a morbid condition in which destructive 
 changes take place in many joints of the body, resulting in thick- 
 ening, impairment of mobility, deformity and pain. The ar- 
 ticular cartilages undergo softening and absorption ; the ends 
 of the bones become enlarged and sclerotic, while the apposed 
 surfaces become smooth from mutual pressure ; the subjacent 
 bone, however, becomes rarefied and brittle ; lime-salts are de- 
 posited in the remains of the articular cartilages. A peculiar 
 crepitus due to the apposition of roughened surfaces can often 
 be elicited on manipulation of the affected joint. At a later 
 stage, eburnation takes place, and the apposed bony surfaces 
 slide over one another with abnormal facility. 
 
 The disease manifests a tendency to symmetrical involvement. 
 When the hands are involved, a peculiar deformity results — the 
 fingers being deflected towards the ulnar side. Occasionally, 
 hard fibrous nodules are found in the muscles at a short distance 
 from the affected joints. 
 
 The onset of the disease is usually insidious ; occasionally it is 
 acute and attended with febrile symptoms, with pain, with 
 swelling and with redness of the affected joints. 
 
 Arthritis deformans occurs in those exposed to unfavorable 
 hygienic influences, in the weak and ill-fed, in those exhausted 
 by frequent childbearing, by prolonged lactation, by grief or by 
 anxiety. 
 
 The disease is not directly fatal. It occasions no cardiac com- 
 plication. "When the larger joints (especially the hip, knees and 
 elbows) are involved there often results decided muscular atrophy. 
 
THE BLOOD. 95 
 
 How are chronic rheumatism and rheumatoid arthritis to be 
 differentiated ? 
 
 In rheumatism, the larger joints of the body are especially in- 
 volved ; rheumatoid arthritis involves the smaller joints as well. 
 The deformity of rheumatism is essentially dependent upon a 
 hyperplasia of the fibrous structures that enter into the forma- 
 tion of the articulation ; the joint-lesions of rheumatoid arthritis 
 are partly destructive in character and occasion peculiar de- 
 formities of the hands and feet, while irregular exostoses form 
 on the articular extremities of the bones. The tendency to 
 symmetrical invasion is more conspicuous in rheumatoid arthritis 
 than in chronic rheumatism. The latter is usually a disease of 
 advanced life ; the former may appear in early adult life. 
 
 How are gout and rheumatoid arthritis to be differentiated ? 
 
 Rheumatoid arthritis lacks the paroxysmal character of gout. 
 Unlike gout, it is observed in the underfed rather than in the 
 overfed. In rheumatoid arthritis the deposits of uric acid and 
 of urates in various structures, characteristic of gout, are want- 
 ing. Gout never presents the peculiar deformities of the hands 
 and feet seen in rheumatoid arthritis. The latter does not lead 
 to the fibroid condition of the kidneys, heart and vessels to which 
 gout gives rise. 
 
 THE BLOOD. 
 
 What are the methods of studying the constitution of the blood ? 
 
 For purposes of diagnosis especially, the blood is frequently 
 examined as to its corpuscular richness, as to the proportion of 
 hemoglohin it contains, and as to the presence of abnormal 
 bodies. 
 
 The corpuscular richness of the blood is determined by means of 
 an instrument called a hemocytometer or blood-cell counter, which 
 consists of a shallow cell of known capacity, mounted on a glass 
 slide, in microscopic divisions of which the numbers of red and 
 white blood-corpuscles contained in a centesimal dilution of 
 blood are respectively counted. In healthy men, the blood 
 
96 ESSENTIALS OF DIAGNOSIS. 
 
 contains about five million red corpuscles to the cubic milli- 
 meter ; in women, about four and a half millions. The number 
 of white cells is held not to permanently exceed under normal 
 conditions, 10,000 per cubic millimeter. The normal ratio of 
 white cells to red cells varies between 1 : 400 and 1 : 800. 
 
 The -proportion of hemoglobin in the blood is determined by 
 comparing the color of the diluted blood with a standard, called 
 a he7noglobinometer, the result being expressed in percentages. 
 
 The percentage of hemoglobin is sometimes spoken of as ab- 
 solute or total ; sometunes a.s relative. By the term absolute ^per- 
 centage is meant the comparative richness in hemoglobin of the 
 whole volume of blood, as shown by the direct reading of the 
 hemoglobinometer scale. By relative percentage is meant the 
 relation or ratio of the absolute hemoglobin percentage to the 
 percentage of red corpuscles. Thus, if in a given case, the 
 number of red corpuscles to the cubic millimeter is estimated at 
 3,000,000, or 60 fo (5,000,000 being taken as the standard or 100 
 per cent.), and the hemiglobinometer reading is 54 per cent., the 
 latter figure (54%) would represent the absolute hemoglobin per- 
 centage, while the relative hemoglobin percentage would be f *- 
 or 90 per cent. 
 
 Deficiency of blood is known as anemia or oligemia ; deficiency 
 of corpuscles, as oligocythemia; deficiency of hemoglobin, as oligo- 
 chromemia; deficiency in solid constituents of the plasma, 
 especially albumin, as hydremia; temporary excess of white cor- 
 puscles, as leukocytosis; persistent excess of white corpuscles, 
 as leukemia or leukocythemia. The normal diameter of the red 
 blood-corpuscle is l/x. Srflaller red corpuscles are called micro- 
 cytes ; larger, megalocytes. Irregularly-shaped red corpuscles are 
 called poikilocytes. Certain white cells that readily absorb the 
 staining material called eosin are from this fact termed eosino- 
 phile cells. 
 
 The blood sometimes contains j;io?-asiies, such as the hematozoa 
 of malaria, the spirilla of relapsing fever, the bacilli of anthrax, 
 the embryos of filaria sanguinis hominis, etc. 
 
ANEMIA. 97 
 
 Anemia. 
 
 What are the symptoms of anemia ? 
 
 Simple anemia may be a result of hemorrhage, of long-con- 
 tinued discharges, of syphilis, malaria, fevers and wasting dis- 
 eases, of mal-assimilatiou, of impaired nutrition, of the presence 
 of parasites or of poisons in the system. 
 
 The blood is deficient in quantity and in quality. The actual 
 volume of the circulating fluid, as well as its corpuscular rich- 
 ness, is diminished. The number of red cells and the number of 
 lohite cells are less than normal ; so is the absolute quantity of 
 Jiemoglobin^ while the relative proportion per corpuscle may be 
 scarcely altered. Some of the red cells are ill-shaped and 
 diminutive. 
 
 Anemia long continued gives rise to fatty degeneration of 
 various structures, notably of the walls of the bloodvessels, of 
 the heart and of other viscera. 
 
 The countenance and visible mucous membranes are usually 
 pale ; though in exceptional instances of great vascularity of the 
 face the complexion may be rosy. The eyeball has a bluish tint. 
 There are shortness of breath, an undue readiness of fatigue, 
 and a disinclination to mental or physical effort. The j^atient 
 complains of neuralgia, of headache, of vertigo and of sleep- 
 lessness. The appetite and digestion are impaired ; constipation 
 is the rule. The urine is pale and may be of low specific gravity, 
 from diminution in urea. Emaciation is not always evident. 
 The action of the heart is enfeebled. Palpitation is common. 
 The pulse is soft, compressible, and usually small. A soft, blow- 
 ing murmur is often to be heard at the base of the heart and 
 in the vessels of the neck ; in the arteries less constantly than in 
 the veins (venous hum, '■'■bruit de diabW''). Edema ultimately 
 develops and hemorrhages from various surfaces may take place. 
 
 When anemia is associated with enlargement of the spleen it 
 is termed splenic anemia. By some authorities splenic anemia 
 is considered to be a variety of pseudo-leukemia. In the yellow, 
 waxen countenance of its subjects, in its clinical course, which 
 is sometimes remittent or intermittent, in its intensity and its 
 fatality, the disease closely resembles pernicious anemia. Un- 
 
98 ESSENTIALS OF DIAGNOSIS. 
 
 like the latter affection, splenic anemia presents a definite visce- 
 ral lesion, a relative increase of white cells, and a diminution in 
 the relative percentage of hemoglobin. 
 
 Chlorosis. 
 
 What are the symptoms of chlorosis ? 
 
 Clilcnvsis or green-sickness is a depraved condition of the 
 blood, seen especially at about the time of puberty in young 
 women, with derangement of menstruation. In addition to 
 tlie symptoms of simple anemia^ the complexion and the con- 
 junctivae present a yellowish-green hue. The number of red 
 corpuscles is not diminished in the same degree as is the per- 
 centage of hemoglobin, while the number of leukocytes is not 
 appreciably altered. 
 
 Pernicious Anemia. 
 
 What are the symptoms of pernicious or idiopathic anemia ? 
 
 There is a form of anemia in which the impoverishment of 
 the blood is marked, and which pursues a progressive and usually 
 fatal course. It is more common in women than in men. No 
 constant visceral lesion has been found associated with the 
 disease. In some instances, there has been atrophy of the gas- 
 tric glands ; in others, disease of the medulla of the bones ; in 
 others, increase of iron-containing pigment in the liver ; in still 
 others, no lesion except that of the blood has been detected. 
 The disease sometimes appears in connection with pregnanc3% 
 
 The sympt07ns are those of intense anemia, with irregular out- 
 breaks of febrile temperature. The complexion is pallid and 
 often assumes a strikingly yellowish (lemon) hue. The lips and 
 palpebral conjunctivae may be white. The bones, especially the 
 sternum, exhibit tenderness on pressure. The ])ulse is usually 
 rapid. The urine may be notably dark-colored, and contains an 
 excess of nitrogenous matters. 
 
 Sometimes deceptive remissions in the symptoms occur. The 
 layer of subcutaneous fat is often well-preserved. Hemorrhages 
 take place from the mucous surfaces, beneath the skin, into the 
 
LEUKOCYTOSIS — LEUKEMIA. 99 
 
 retina and elsewhere, as a result of fatty degeneration of the 
 coats of the arteries. The heart is also likely to undergo fatty 
 degeneration. 
 
 The volume of blood is small ; the number of red corpuscles 
 is considerably diminished (less than 2,000,000 per c. mm.), as 
 is necessarily the absolute quantity of hemoglobiyi^ of which, 
 however, the relative proportion per corpuscle is increased. 
 The red corpuscles are poorly developed and ill-shaped. Mega- 
 locytes preponderate ; microcytes and poikilocytes are likewise 
 found. In some cases minute, highly-colored globules resem- 
 bling " small red-tinged, fat globules" are seen. The number 
 of white corpuscles may remain unaltered ; in some cases, it has 
 has been increased ; in others, diminished. 
 
 What special precautions must be taken in arriving at a 
 diagnosis of the various forms of anemia ? 
 When a condition of anemia is discovered, a searching in- 
 quiry' into the history and symptoms and a careful physical 
 examination must be made, to determine whether or not there 
 be a coexistent morbid condition, such as carcinoma, tuber- 
 culosis, hemorrhoids or other source of hemorrhage, nephritis, 
 malarial infection, intestinal parasites, defective or insuflficient 
 nutrition, mal-assimilation, arsenical, plumbic, mercurial or 
 other form of poisoning, and conditions that occasion jaundice. 
 
 Leukocytosis. 
 
 What is leukocytosis ? 
 
 Leukocytosis is a condition of the blood in which, without 
 alteration in the number of red corpuscles, without enlargement 
 of the spleen, of the liver or of the lymphatic glands, the num- 
 ber of white corpuscles undergoes an intermittent or transitory 
 increase. It may be physiologic^ as when it occurs after meals, 
 or it may be a transitional stage of leukemia or pseudo-leukemia. 
 
 Leukemia. 
 
 What is leukemia or leukocythemia ? 
 
 Leukemia is a morbid condition in which, in association with 
 enlargement of the spleen, of the liver, of lymphatic glands, or 
 
100 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 with alterations in the medulla of bones, the blood contains a 
 permanent excess of leukocytes and is deficient in red cells 
 (Fig. 18). 
 
 Fig. 18. 
 
 Appearance of the blood in leukemia. (Funke.) 
 
 Three varieties of leukemia are recognized: Uenal, lyynphatic 
 and raedullary, as the spleen and liver, the lymphatic system, 
 and the medulla of bones, respectively, are involved. 
 
 Early in the course of the disease, the spleen becomes con- 
 spicuously enlarged ; sometimes friction-fremitus may be de- 
 tected on palpation, and a blowing murmur on auscultation ; 
 ascites may develop. In the further course of the disease, the 
 liver and the lymphatic glands may also become enlarged ; the 
 bones may be painful and tender ; changes in the kidneys and in 
 the intestinal glands are sometimes noted. 
 
 The number of ivhite corpuscles in the blood is increased 
 beyond 10,000 to the cubic millimeter, sometimes in extraordi- 
 nary degree. The number of red cells and the quantity ofliemo- 
 globin are diminished. Through increase in the number of the 
 white, and diminution in that of the red, there ensues a great 
 change in the ratio of white cells to red cells. The ratio is, as a 
 rule, not less than 1 : 50, and may reach or exceed 1 : 1. Masses of 
 leukocytes may occasion infarcts in the spleen or lungs. It is 
 
PSEUDO-LEUKEMIA. lOl 
 
 said that in lienal leukemia large leukocytes predominate ; in 
 lymphatic leukemia, small leukocytes ; and in myelogenous leu- 
 kemia, large leukocytes, having large nuclei, together with 
 transition-types and many eosinophils cells. 
 
 The depravity of the blood occasions dyspnea and edema ; 
 conjoined w^ith the secondary changes in the bloodvessels, it 
 predisposes to extravasation of the blood. There are thus 
 breathlessness on exertion, epistaxis and other hemorrhages 
 from mucous surfaces and into the retina and subcutaneous 
 connective tissue. Diarrhea is common. The urine contains 
 an excess of uric acid. Earely, disturbances of vision occur — 
 as a result of hemorrhage, of leukemic deposit, or of leukemic 
 retinitis. From time to time febrile periods, lasting from a few 
 days to a week, in which the temperature may rise to 102° F., 
 ai'e observed. Remissions in all of the symptoms sometimes 
 take place during the progress of the case. 
 
 Leukemia is most common between the ages of twenty and 
 fifty ; it is more common in men than in women. It is usually 
 insidious in onset, the early clinical phenomena being those of 
 anemia in general. Epistaxis is often the first significant symp- 
 tom. The etiology of leukemia is obscure. In some cases there 
 has been a history of antecedent malarial infection ; in others, 
 of traumatism of the spleen ; in others, of traumatism of bones. 
 Privation and exposure are cited among predisposing and ex- 
 citing causes. 
 
 Pseudo-leukemia. 
 
 What is pseudo-leukemia ? 
 
 Pseudo-leukemia, Hodgkin^s disease^ lymphatic anemia, malig- 
 nant lymplioma or lympliadenoma, is an affection characterized by 
 hyperplasia of adenoid tissues, and especially by enlargement of 
 the lymphatic glands in various parts of the body, and by 
 changes in the blood. Anemia prevails, the number of red cor- 
 puscles and the relative proportion of hemoglobin being dimin- 
 ished, the number of white corpuscles remaining unchanged or 
 not uncommonly being slightly inci-eased. An apparent excess 
 
102 ESSENTIALS OF DIAGNOSIS. 
 
 of white cells, due to decrease in the number of red cells, with 
 consequent moderate elevation of the ratio, must not be mis- 
 taken for an actual increase in the number of leukocytes. 
 The superficial glands, especially those of the neck and axilla, 
 are usually chiefly involved. Sometimes the glandular enlarge- 
 ment is first noticed in the groin. The spleen and other viscera 
 may also be enlarged. In addition to the symptoms of anemia 
 and malnutrition, pressure-phenomena are observed. Enlarge- 
 ment of the tonsils, of the lingual, postnasal, cervical, peri- 
 tracheal and peri-bronchial glands gives rise to cough, dyspnea 
 and dysphagia. The cerebral circulation may be impeded from 
 pressure upon the vessels of the neck. Pressure upon nerves 
 may cause paralysis, pain or edema. Jaundice and ascites are 
 sometimes observed. There are, in addition, a tendency to 
 effusions, hemorrhages and j)etechi8e, and from time to time 
 febrile periods. 
 
 How are leukemia and pseudo-leukemia to be differentiated? 
 
 It is possible that leukemia and pseudo-leukemia represent 
 stages of a single condition. Individual cases present symp- 
 toms of both affections. The differentiation of well-marked 
 cases, however, is not difficult. 
 
 In leukemia, the spleen enlarges early ; the lymph-glands 
 are not necessarily involved ; when they are, however, it is late 
 in the disease. In pseudo-leukemia, the lymph-glands are 
 primarily enlarged ; the spleen and liver may escape entirely ; 
 should they become involved, it is late in the disease. In leuke- 
 mia, the number of white blood-cells is always increased — 
 often in decided degree. The alteration of relation of white 
 cells to red cells in pseudo-leukemia is due to decrease in the 
 number of the red cells ; actual excess of white cells constitutes 
 no essential part of the disease ; though not rarely observed, 
 it never reaches the high figures of leukemia. 
 
 How are tuberculosis of the lymph-glands ("scrofula") and 
 pseudo-leukemia to be differentiated ? 
 
 The lymphatic glands over a wide distribution may become 
 tuberculous. Such a condition will also be associated with 
 anemia — so that a clinical picture will be presented simulating 
 
INFANTILE PSEUDO-LEUKEMIC ANEMIA. 103 
 
 that of pseudo-leukemia. Microscopic examination of a portion 
 of one of the growths will disclose the presence of tubercle- 
 bacilli in the one instance and a condition of simple hyper- 
 plasia in the other. 
 
 In pseudo-leukemia the enlarged glands are not inflamed, 
 and do not give rise to inflammation in the surrounding con- 
 nective tissue. They are not hot or tender to the touch ; they 
 are not adherent to the skin, and are, as a rule, freely movable 
 upon each other. Tuberculous glands are usually adherent to 
 the skin, and to each other, and manifest a tendency to chronic 
 inflammation, with caseation and suppuration. There are usu- 
 ally other evidences of tuberculosis present, in the bones, joints, 
 or elsewhere ; and the fades is often significant. Glandular 
 tuberculosis and pseudo-leukemia may, however, coexist ; or 
 inflammatory changes may be set up by traumatism in the 
 glands of pseudo-leukemia. 
 
 Infantile Pseudo-leukemic Anemia. 
 
 What is infantile pseudo-leukemic anemia ? 
 
 Jaksch has described in infants a form of anemia in tUe last 
 stage of which there are a deficiency of red corpuscles, a defi- 
 ciency of hemoglobin, and an increased number of white corpuscles. 
 
 The condition differs from leukemia in that the increase of 
 white corpuscles is not so great, that eosinophile leukocytes are 
 never present, that, while the spleeii is enlarged, the liver is 
 not, and that the prognosis is favorable. 
 
104 
 
 ESSENTIALS OF DIAGNOSIS, 
 
 Table showing alterations in the constitution of the blood 
 in disease. 
 
 
 Number 
 of 
 
 red cells. 
 
 Number 
 
 of 
 
 white cells. 
 
 Proportion of hemoglobin. 
 
 
 Total. 
 
 Per red cell. 
 
 Anemia 
 
 Diminished. 
 
 Normal or 
 .diminished. 
 
 Diminished. 
 
 Normal or 
 diminished. 
 
 Chlorosis 
 
 Diminished. 
 
 Normal or 
 diminished. 
 
 Diminished. 
 
 Diminished. 
 
 Pernicious anemia 
 
 Greatly 
 diminished. 
 
 Variable. 
 
 Greatly 
 diminished. 
 
 Increased. 
 
 Splenic anemia . 
 
 Diminished. 
 
 Increased. 
 
 Diminished. 
 
 Diminished. 
 
 Psevido-leukemia 
 
 Diminished. 
 
 Normal or 
 increased. 
 
 Diminished. 
 
 Normal or 
 diminished. 
 
 Leukocytosis 
 
 Normal. 
 
 Increased. 
 
 Normal. 
 
 Normal. 
 
 Leukemia 
 
 Diminished. 
 
 Greatly 
 increased. 
 
 Diminished. 
 
 Normal or 
 diminished. 
 
 Scorbutus. 
 
 What are the symptoms of scorbutus ? 
 
 Scorbutus or scurvy is a disease dependent upon deficiency in 
 the diet, of certain substances usually contained in the juices of 
 fresh vegetables and iruits. It was formerly common at sea, 
 and in jails and poorhouses. Outbreaks still occasionally 
 occur. Isolated cases sometiaies appear under unexpected 
 circumstances. 
 
 The disease is characterized by a depraved condition of the 
 blood, with degeneration of the walls of the vessels and conse- 
 quent hemorrhages. The gums are soft and spongy, and bleed 
 on slight provocation or spontaneously. The breath is defiled 
 by the fetor of the decomposing necrotic tissue. Hemorrhages 
 take place from other mucous surfaces, while inflammation of 
 serous membranes, with hemorrhagic efltusions, may occur. Ex- 
 travasations of blood take place into the subcutaneous tissues, 
 especially in the course of the superficial veins of the dependent 
 parts of the body, giving a mottled, bluish or purplish appear- 
 
PURPURA. 105 
 
 auce to the skin in more or less extensive areas. The discolor- 
 ation frequently resembles that of a bruise, and, as it slowly 
 fades, assumes a greenish tint. It is often quite persistent. 
 Extravasation into the muscles may likewise occur. With 
 this, edema is often associated. Brawny induration of the 
 connective tissue in various parts of the body may develop. 
 Diffuse, dull pains are felt. The skin is dry and rough. There 
 is mental apathy, with a sense of lassitude and an undue 
 readiness of fatigue. Fungated hemorrhagic ulcers form. Ex- 
 isting ulcers assume an unhealthy, spongy appearance. Frac- 
 tured bones fail to unite, while the union of broken bones may 
 be dissolved. The complexion is sallow ; anemia becomes evi- 
 dent, with shortness of breath and rapidity and feebleness of 
 pulse. In some epidemics, dysenterj- has been a complication. 
 Sometimes hemeralopia or night-blindness has been observed. 
 Without proper treatment death takes place. With proper 
 treatment recovery is slow. 
 
 Purpura. 
 
 What are the clinical features of purpura? 
 
 Purpura is a manifestation of a deteriorated condition of the 
 blood and vessels, as a result of which petechise form, and hem- 
 orrhages from the mucous membranes take place. Sometimes 
 blood is extravasated into the serous cavities ; and occasionally 
 intracranial hemorrhage occurs. The disease sometimes devel- 
 ops in the midst of apparent health ; at other times, in the 
 course of nephritis, the exanthemata, hepatic disease, and rheu- 
 matism. Occasionally, transient febrile periods are observed. 
 Sometimes the disease begins acutely, with a chill followed b}' 
 pain in the back or limbs, but without fever. The purpuric 
 spots may be large or small, of limited or of extensive distribu- 
 tion. Usually they ajjpear in successive crops. At fii-st red- 
 dish, they soon become of a deep purple, gradually fading to 
 brown, and then to yellow, as they disappear. 
 
 The varieties of purpura commonly recognized are purpura 
 simplex, purpmra hemorrhagica and ptirpicra rheumatica. The 
 names are sufficiently descriptive. 
 
106 ESSENTIALS OF DIAGNOSIS. 
 
 How are scorbutus and purpura to be differentiated? 
 
 Scorbutus occurs among those that are massed together and 
 are insufficiently supplied with fresh vegetables ; purpura may 
 develop amid circumstances apparently the most favorable and 
 in the face of an abundant supply of fruits and vegetables. 
 The gums may bleed in purpura, but they are wanting in the 
 sponginess and livid ity of scorbutus. The breath is fetid in 
 scurvy, not necessarily so in purpura. The petechise of scor- 
 butus usually develop about the hair-follicles ; those of purpura 
 are indifferent in distribution. The individual discolored patches 
 are more extensive in scorbutus than in purpura. In the latter, 
 large blotches can usually be resolved into a number of smaller 
 spots aggregated. The hue in the two cases differs to the ex- 
 perienced eye. 
 
 How is purpura to be distinguished from measles? 
 
 The eruption of purpura has in certain instances presented 
 sufficient superficial resemblance to that of morbilli to occasion 
 mistake— the youth of the patients and the coincidence of febrile 
 symptoms increasing the difficulty. The course of the eruption 
 is, however, quite different in the two affections. The distribu- 
 tion of the purpuric spots is not so general as is that of the erup- 
 tion of measles. The spots of purpura often appear first on the 
 legs, while in measles the rash begins on the face and trunk. 
 The purpuric spots change color and fade, new spots appearing 
 while others are receding ; no such phenomenon occurs in 
 measles. Catarrhal symptoms do not occur in purpura ; hem- 
 orrhages are not usual in measles. The characteristic tempera- 
 ture-curve of measles is absent from the course of purpura. 
 
 Hemophilia. 
 
 What are the clinical features of hemophilia ? 
 
 HemcypMUa is a morbid condition manifested by an abnormal 
 tendency to the occurrence of hemorrhages, spontaneously or 
 upon slight provocation. Individuals so affected are called 
 "bleeders." The disease occurs in families; it is much the 
 more common in males, but is mostly transmitted through 
 
Addison's disease. 107 
 
 females, in whom, when it occurs, its manifestations are always 
 mild. Slight wounds, a scratch, the extraction of a tooth, may 
 be followed by alarming or even fatal hemorrhage. Petechise 
 form, while sometimes large extravasations of blood take place 
 into the subcutaneous textures and into the joints. The dis- 
 ease usually first makes its appearance early in life. Tlie 
 diagnosis depends essentially upon tbe history of hei'editar}' 
 transmission, the unusual proneness to the occurrence of 
 alarming hemorrhage, the formation of petechiee, the develop- 
 ment of subcutaneous and articular extravasations of blood, 
 and the appearance of the first symptoms early in life. 
 
 Addison's Disease. 
 
 What are the clinical features of Addison's disease? 
 
 Addison observed that in certain cases, in which after death 
 the supra-renal bodies were found tuberculous, there had existed 
 during life a peculiar pigmentation of the skin, with remark- 
 able asthenia and nausea and vomiting. The discoloration is 
 usually of a brownish hue, like that which develops in one 
 exposed to a tropical sun ; it resembles the pigmentation of the 
 dark-skinned races. It occurs in plaques, on exposed surfaces, 
 at parts that have been compressed or constricted, in the 
 flexures of joints, and about the genitalia and the nipples. 
 The mucous membrane of the mouth and tongue may be pig- 
 mented. Progressive weakness is manifested ; and prostration 
 finally develops. The subcutaneous fat, however, may be 
 preserved. The hearVs action is feeble ; the pitZse is small and 
 compressible. The appetite is impaired ; nausea and vomiting 
 are common ; there may be diarrhea or constipation. Death 
 may take place gradually, from exhaustion, or with unexpected 
 suddenness. 
 
 Tuberculous disease of the supra-renal bodies has been found 
 when there was no bronzing of the skin. In such cases it has 
 been thought that the disease had not progressed sufliciently 
 to have occasioned symptoms. In other cases the skin has been 
 pigmented, but no changes were found in the supra-renal bodies. 
 Pigmentation of the skin may, however, be a result of other 
 
108 ESSENTIALS OF DIAGNOSIS. 
 
 conditions than supra-renal disease. By some, Addison's dis- 
 ease is thought to depend upon changes in the semilunar 
 ganglia and branches of the sympathetic system of nerves, 
 
 Kachitis. 
 
 What are the clinical features of rachitis ? 
 
 Bacliitis is a disease dependent upon defective and perverted 
 development of the osseous structures of growing children, 
 probably as a consequence of fault}' nutrition. There is doubt- 
 less congenital predisposition to its occurrence. The hones are 
 soft and yielding, and wanting in their natural firmness and 
 stability, so that various deformities result. The sides of the 
 chest become flattened, and the sternum projects, giving rise to 
 the " pigeon-breast." ^Nodules or " beads" form at the junction 
 ot the ribs and their cartilages. The long, supporting bones 
 become bent and their epiphyseal extremities enlarged. The 
 soft and deformed bones are especially liable to green-stick frac- 
 tures. The lower jcm is narrow and dentition is delayed. The 
 teeth may decay and fall out soon after their appearance. The 
 head appears large ; its summit is flat ; the fontanels close late. 
 The deformities are maintained by the ultimate hardening of 
 the affected bones. 
 
 Rachitic children present a pasty complexion and pearly con- 
 junctivae ; they are undersized and poorly resist disease. They 
 are restless, and display a tendency to excessive sweating of the 
 head. Digestion is impaired ; the abdomen is often protuberant. 
 Laryngismus stridulus and convulsions are common occurrences. 
 Internal viscera may be enlarged as a result of hyperplasia of 
 the interstitial connective tissue. 
 
 MoUities Ossium. 
 
 What are the clinical manifestations of mollities ossium? 
 
 MoUities ossium is a morbid condition that develops in adults 
 amid unfavorable hygienic surroundings and in women that 
 have borne many children. It manifests itself by both soften- 
 
THE HEART. 109 
 
 ing and rarefaction of the bones, so that progression is impos- 
 sible, and fractures are common. Occasionally febrile symptoms 
 are present. Death is the common result, either from exhaus- 
 tion, or from mechanical interference with respiration. 
 
 How are rachitis and mollities ossium to be differentiated ? 
 
 Mollities ossium is a disease of adult life, attended by changes 
 in developed bone, and usually of fatal termination. Rachitis 
 is essentially a disease of childhood, dependent upon abnormali- 
 ties in developing bone, and from which recovery usually takes 
 place, only the sequels of the disease remaining, 
 
 THE HEART. 
 
 Inspection. 
 
 What can be learned of the heart by inspection? 
 
 On inspecting the normal chest, one perceives in the left fifth 
 intercostal space, two inches below and an inch within the nip- 
 ple, in an area of perhaps an inch in diameter, a gentle rise 
 and fall — the cardiac impulse or apex-heat. It is less distinctly 
 visible in fat than in lean persons. 
 
 The position of the apex-beat varies slightly with the respira- 
 tory movements, with posture, and with the state of the 
 abdominal viscera. It may be displaced, as to the left by an 
 effusion in the right pleural cavity, or by adhesions of the left 
 pleura ; or to the right by an cfllision in the left pleural cavity, 
 or by adhesions of the right pleura. It may be increased in 
 extent, as when the heart is enlarged, or when the pei'icardium 
 is distended with fluid. Under varying conditions an impulse 
 is seen in the epigastrium. 
 
 The impulse may be strong, as in cases of caixliac hypertrophy ; 
 feeble, as in cases of dilatation ; ivavy, as when the pericardial 
 cavity is occupied by fluid ; when the pericardium is adherent 
 "systolic dimpling" occurs. 
 
110 ESSENTIALS OF DIAGNOSIS. 
 
 Palpation. 
 
 What is to be learned of the heart by palpation ? 
 
 PaliMtion confirms aud reinforces what is learned by inspec- 
 tion. An impulse that cannot be seen can sometimes be felt. 
 A feeble impulse indicates that the action of the heart has been 
 enfeebled by disease or by an eftusion in the pericardial cavity ; 
 a strong impulse is indicative of strength, of hypertrophy. A 
 pericardial friction-rub may sometimes be felt. In most cases 
 of mitral valvular obstruction, a imrring treriwr is perceived on 
 palpation. 
 
 Percussion. 
 
 What is to be learned of the heart by percussion ? 
 
 By percussion— which is best practised with the patient re- 
 cumbent—the approximate size of the heart can be learned. A 
 considerable portion of the organ is covered by lung-tissue. By 
 superficial percussion of a normal chest the cardiac dulness is 
 found to be represented by a triangle included between a point 
 at the lower margin of the fourth left costal cartilage at its 
 iunction with the sternum, another at the apex-beat, and a third 
 at the lower extremity of the sternum at its left border. Deep 
 pjercussion defines a somewhat more extended area. 
 
 The area of cardiac percussion-duluess is increased when the 
 heart is enlarged, or the pericardial sac is distended by fluid, 
 when the heart is uncovered by retraction of the lung, or in full 
 expiration. The area is diminished when the heart is covered 
 by emphysematous lung-tissue, or by the lungs in full inspira- 
 tion. 
 
 Auscultation. 
 
 What is to be learned of the heart by auscultation? 
 
 Auscidtation constitutes the most important method of physi- 
 cal examination of the heart. It reveals the frequency, the 
 rhythm, the quality, and the purity of the heart-sounds. 
 
 In health, the heart of an adult at rest beats about seventy- 
 two times to the minute. The frequency of action varies with 
 
AUSCULTATION. Ill 
 
 the degree of bodily exertion, and witli posture. It is increased 
 by exertion and by excitement, after meals, in febrile affections 
 and in many diseases of the heart ; it is greater in the upright 
 than in the horizontal posture ; it is diminished by rest and by 
 jaundice ; in aortic obstruction in fatty degeneration, and dur- 
 ing convalescence from acute disease. It is affected by various 
 drugs and by nervous influences. 
 
 The action of the heart in health is rhythmical and regular. 
 There is a prolonged, dull, first souncZ, and a shorter, 
 sharper second sound, follovired by an interval of silence— with 
 rhythmical repetitions. Occasionally a cycle is omitted — the 
 heart intermits. A normal first sound may be followed by two 
 second sounds — duplication. The first sound may also be dupli- 
 cated. The normal rhythm of the heart may be disturbed by 
 organic disease of the heart, such as degeneration, and by de- 
 rangement of other organs, as of the stomach. 
 
 The _^rsi sound of the normal adult heart is a dull, but well- 
 defined thud ; the second is a shorter, sharper, snapping or ring- 
 ing sound ; it is followed by an interval of silence.^ 
 
 Three elements enter into the production of the first sound, 
 which is synchronous with the contraction of the ventricles 
 (systole) and the closure of the auriculo-ventricular {mitral and 
 tricuspid) valves. These are : the closure of the valves, the mus ■ 
 cular contraction, and the impact of the heart against the chest- 
 wall. The second sound, which is synchronous with the be- 
 ginning of the diastole, is valvular ; it is due to the quick approxi- 
 mation of the semilunar flaps, preventing return of blood through 
 the arterial {aortic and pulmonary) orifices. 
 
 The first sound of the heart may be altered in volume, in tone, 
 in duration and in strength. These are usually increased when 
 the heart is hypertrophied, temporarily under excitement and 
 after the administration of certain drugs ; and diminished when 
 from any cause the action of the heart is enfeebled— among 
 
 ' There can likewise be detected by the trained ear a short interval of 
 silence between the first and second sounds. The fact is mentioned here 
 to avoid misleading the student in his further studies ; but for practical 
 purposes this " minor silence," as it is called, may be entirely ignored. 
 
112 ESSENTIALS OF DIAGNOSIS. 
 
 such causes are dilatation, degeneration, pericardial effusion. 
 The character of the second sound is largely dependent upon 
 the tension in the arteries ; the higher the tension the sharper 
 the sound. 
 
 The ]jurity of the heart-sounds depends upon the condition of 
 the heart-muscle, upon the state of the blood and upon the 
 functional efficiency of the various valves and orifices. 
 
 The functional efficiency of the valves and orifices of the heart 
 can be determined by a study of the sounds of the heart as 
 heard over the respective parts ; but these are so close together 
 that points in the course of the blood-stream are selected for 
 auscultation. That for the mitral sound corresponds to the 
 situation of the apex-beat ; that for the aortic, to the junction 
 of the right second costal cartilage with the sternum ; that for 
 the tricuspid, to the ensiform cartilage ; and that for the pulmo- 
 nary, to the left second intercostal space close to the sternum. 
 
 Alteration of the structure and derangement of the function 
 of the valves and orifices of the heart are revealed by adven- 
 titious sounds, called murmurs, that accompany or replace the 
 normal sounds, or occur in the interval between them. Mur- 
 murs are often blowing ; sometimes they are soft, sometimes 
 harsh, sometimes musical. 
 
 The first sound occupies the ventricular systole; the diastole 
 is taken up by the second sound and the period of silence. During 
 the systole, the blood pases from the ventricles into the aorta 
 and pv;lmonary artery ; the arterial valves should be freely open ; 
 the auriculo-ventricular valves should be perfectly closed : mur- 
 murs generated at the arterial orifices indicate obstruction to 
 the outflow of blood from the ventricles ; murmurs generated at 
 the auriculo-ventricular orifices indicate reflux of blood into the 
 auricles. 
 
 At the conclusion of the systole, there is a brief pause, fol- 
 lowed by the diastole, during which the blood flows from the 
 auricles into the ventricles ; the auriculo-ventricular valves 
 should be freely open ; the arterial valves should be perfectly 
 closed : murmurs generated at the auriculo-ventricular orifices 
 indicate obstruction to the onflow of blood into the ventricles ; 
 
AUSCULTATION. 
 
 113 
 
 murmurs generated at the arterial orifices indicate reflux of 
 blood from the arteries. 
 
 Incompetency or insufficiency of a valve permits of regurgita- 
 tion. 
 
 Constriction or occlusion of an orifice occasions obstruction. 
 
 The seat and character of an endocardial murmur are deter- 
 mined from the 2)lace at which it is best heard (site of maximum 
 intensity), in association with the time of its occurrence and the 
 direction in which it is transmitted. 
 
 Analogous conditions of the right and left heart necessarily give 
 rise to murmurs at the same time ; analogous conditions of the 
 auriculo-ventricular and arterial valves give rise to murmurs at 
 different times ; and conversely. Thus, for example, the mur- 
 murs of mitral insufficiency and of tricuspid insufficiency coin- 
 cide in time with each other and with the murmurs of aortic 
 obstruction and of pulmonary obstruction. Mitral and tricuspid 
 regurgitant murmurs and aortic and pulmonary obstructive 
 murmurs are heard during the systole— with or in place of 
 
 Fig. 19. 
 
 Auscultation of the heart-sounds. The small letters indicate the situation of the 
 valves; the large letters, the points for auscultation, a^, aortic; mit/, mitral; tT, 
 tricuspid ; pP, pulmonary. (Vierordt.) 
 
 the first sound. Mitral and tricuspid obtructive murmurs and 
 aortic and pulmonary regurgitant murmurs are heard during 
 the diastole ; the latter two with or in place of the second sound ; 
 
114 ESSENTIALS OF DIAGNOSIS. 
 
 the first two, however, in what is normally the period of silence 
 immediately preceding the first sound— hence presystolic. 
 
 JMitral rtgurgitant murmurs are heard best at the apex of the 
 heart ; they are transmitted in the course of the fifth and sixth 
 ribs to the axilla, and may be heard below the posterior inferior 
 angle of the scapula. Mitral obstructive murmurs are best heard 
 at the apex of the heart, or a little above the apex ; they are 
 but feebl}^ transmitted. Aortic rtgurgitant and aortic obstructive 
 murmurs are most distinctly heard at the junction of the second 
 costal cartilage on the right with the sternum ; the former are 
 transmitted downwards in the course of the sternum, the latter 
 upwards in the course of the great vessels, especially the 
 carotid. Murmurs generated at the orifices and by the valves 
 of the right side of the heart are exceedingly rare. Tricusidd 
 regurgitant and obstructive murmurs are best heard at the ensi- 
 form cartilage, or a little farther to the right. Fuhwmary mur- 
 murs should be best heard in the second intercostal space on the 
 left, close to the margin of the sternum. In anemia, soft blow- 
 ing murmurs, dependent upon the condition of the blood, are 
 heard in the same situation. 
 
 All murmurs heard in the precordial region are not endo- 
 cardial. Auscultation reveals as well the sounds of pericardial 
 friction as of adjacent pleural friction. 
 
 How are murmurs due to organic disease to be distinguished 
 from so-called functional murmurs? 
 
 In addition to adventitious sounds generated at the orifices 
 of the heart as a result of structural changes, murmurs are 
 heard when the condition of the blood is deteriorated, or when, 
 from disturbed action of the heart or other cause, abnormal 
 currents are generated in the blood-stream. These so-called 
 functional murmurs are distinguished by their inconstancy and 
 their softness ; they are usually heard only at the base of the 
 heart and over the body of the organ ; they are not transmitted ; 
 they are intensified by pressure with the stethoscope ; and they 
 disappear with the removal of the conditions upon which they 
 depend. Organic murmurs are usually harsher, more constant, 
 and vary comparatively little in character and intensity. 
 
MALFORMATION — DEXTROCARDIA. 115 
 
 What is the sphygmograph? 
 
 The sphygmograph is an instrument by which an artery is 
 made to record certain of the characters of its pulsation. The 
 sphygmogrum (Fig. 20) is an important aid in diagnosis, but 
 
 Fig. 20. 
 
 Normal pulse-tracing. (After Eichhorst.) 
 
 cannot be reUed upon apart from the ordinary rational and 
 physical signs. The use of the sphygmograph and the signifi- 
 cance of its tracings must be learned by experience. 
 
 Malformation. 
 
 What are the most common malformations of the heart ? 
 
 The most common malformations of the heart consist in an 
 imperforate interventricular septum and a failure of the foramen 
 ovale to close. i 
 
 To what symptoms do malformations of the heart give rise ? 
 
 Individuals in whom there exist serious abnormal communica- 
 tions between the lateral halves of the heart rarely reach adult 
 life. Cyanosis is the most common symptom. vSystolic mur- 
 murs are heard practically indistinguishable from those oc- 
 casioned by valvular derangement. 
 
 Dextrocardia. 
 
 What is dextrocardia ? 
 
 Dextrocardia is a congenital displacement of the heart on the 
 right side, commonly associated with displacement of the liver 
 on the left and of the spleen on the right. 
 
116 ESSENTIALS OF DIAGNOSIS. 
 
 How is dextrocardia to be recognized ? 
 
 In case of dextrocardia the impulse of the heart is wanting 
 in its usual situation, and is seen to the right of the sternum. 
 The area of cardiac percussion-dulness occupies on the right an 
 extent corresponding to that which it normally occupies on the 
 left. The sounds of the heart are heard on the right side instead 
 of on the left. The hepatic percussion-dulness is not found in 
 its usual situation, hut in a corresponding position on the left. 
 The splenic dulness is found on the right instead of on the left. 
 
 Functional Disturbance of the Heart. 
 
 What is meant by functional disturbance of the heart? 
 
 Under various conditions, as when the nutrition is impaired 
 or the digestion is deranged, as a result of overwork, or of 
 dissipation, or of the excessive use of tobacco, or tea, or coffee, 
 and in connection with gout or lithemia, with hysteria or hypo- 
 chondriasis, the action of the heart may be deranged without 
 recognizable structural change. There will be present such 
 symptoms as pain, palpitation, anxiety, headache, vertigo and 
 breathlessness, sometimes with irregularity and increased 
 frequency of the heart's action. The diagnosis depends upon 
 the recognition of the primary condition and upon the absence 
 of the physical signs of a cardiac lesion. Functional disorder, 
 great in degree and long continued, may lead to structural 
 change. 
 
 Tachycardia. 
 
 What is tachycardia? 
 
 Tachycardia is a term applied to a somewhat rare condition of 
 excessive rapidity of the action of the heart, accompanied with 
 palpitation, the rhythm of the heart sometimes remaining un- 
 affected. The pulse may exceed 200 beats a minute. Occurring 
 in paroxysms, the qualification 'paroxysmal is applied. When no 
 etiologic lesion is discoverable, the condition is termed essential 
 paroxysmal tachycardia. The paroxysm usually begins suddenly, 
 
IRRITABLE HEART. 117 
 
 with or without warning ; at times without apparent exciting 
 cause ; at other times seeming to result from some such con- 
 dition as overdistention of the stomach. Tachycardia may be 
 due to temporary paralysis of the vagus or stimulation of the 
 cardiac accelerator nerve. Increased cardiac dulness and indefi- 
 nite murmurs may be observed during the attack, and disappear 
 with subsidence of the symptoms. The condition may be un- 
 attended with other symptoms, and ordinarily does not shorten 
 life. It may be a part of other neuroses. It has been observed 
 in women at the menopause. 
 
 How does tachycardia differ from angina pectoris? 
 
 Tachycardia is wanting in the threatening symi3toras of an- 
 gina pectoris — the anxiety, the pain, the cardiac failure. Ra- 
 pidity of the heart's action and palpitation are the essential 
 features of tachycardia ; while in angina pectoris the pulse is 
 of variable frequency. 
 
 How does tachycardia differ from exophthalmic goiter? 
 
 Palpitation of the heart and increased frequency of the pulse 
 are among the earliest phenomena of exophthalmic goiter. Be- 
 fore the thyroid gland has become enlarged or the eyeballs pro- 
 trude, the distinction from tachycardia is not possible. There 
 is no difficulty in the diagnosis, however, when not only the 
 exophthalmos and the goiter, but the array of other symptoms 
 that characterize exophthalmic goiter, have also developed. 
 
 Irritable Heart. 
 
 What are the phenomena of irritable heart ? 
 
 Irritable heart is a condition originally observed in soldiers in 
 active service, in which there are in addition to increased fre- 
 quency of the action of the heart, often with disturbed rhythm, 
 recurring attacks of palpitation and pain in the precordia. 
 There are usually headache and vertigo, especially during the 
 paroxysms. The general health may suffer little or not at all. 
 The first sound may be short and sharp or may be barely 
 audible ; the second sound is accentuated. There is no constant 
 murmur. The pulse is compressible and easily influenced by 
 
118 ESSENTIALS OF DIAGNOSIS. 
 
 position. Eespiration is. but little if at all accelerated. A simi- 
 lar condition may develop in civil life in those unaccustomed to 
 arduous labor called upon to perform unusual tasks. It has also 
 been found in athletes and others who have committed excesses 
 in physical exertion, and in masturbators. Under proper regi- 
 men, restoration to the normal results ; under other circum- 
 stances, hypertrophy of the heart develops. 
 
 How does irritable heart differ from tachycardia ? 
 
 Irritable heart results from well-recognized causes that are 
 not concerned in tachycardia. In irritable heart the frequency 
 is less than in tachycardia, and is habitual ; in tachycardia the 
 increased frequency is extraordinary and usually occurs in 
 paroxj'sms. It is pain and palpitation rather than increased 
 frequency of action that marks the paroxysmal seizures of 
 irritable heart. Tachycardia is also wanting in the distressing 
 subjective sensations and the grave issue of irritable heart. 
 
 Angina Pectoris. 
 
 What are the characteristics of angina pectoris? 
 
 Angina 2')e(^oris is a paroxysmal disorder for which no definite 
 structural lesion has been found. Perhaps the most common 
 condition associated with it is atheroma of the coronary 
 arteries. 
 
 The attack sets in suddenl}-, with a sense of oppression, dys- 
 pnea, and pain in the precordia, rising to a high pitch of inten- 
 sity, and attended with a sense of impending dissolution — and 
 not uncommonly death does occur in the parox3sm. There is 
 often a sensation as of throttling. The pain in the heart is de- 
 scribed as " clutching," " squeezing," and " tearing." The pain 
 radiates in various directions from the heart, especially to the 
 left shoulder, and extends down the left arm. The face is pale, 
 the features drawn, the pulse variable. The attacks may occur 
 spontaneously, but are usually brought on b}^ excitement or 
 exertion, or by gastro-intestinal derangement. They recur with 
 varying frequency, sometimes over a long period of j'ears. 
 
HYPERTROPHY. 119 
 
 How does intercostal neuralgia differ from angina pectoris? 
 
 The pain of intercostal neuralgia never attains the intensity 
 or presents the peculiar character of that of angina pectoris ; nor 
 are the general manifestations ever so portentous. The tender 
 points of Yalleix, found in intercostal neuralgia, are absent in 
 angina pectoris. An herpetic eruption on the chest, follow^ing 
 the course of an intercostal nerve, is diagnostic of neuralgia. 
 
 Hypertrophy. 
 
 What are the symptoms of hypertrophy of the heart? 
 
 The size of the heart is proportionate to the demands made 
 upon it, or to the stimulation that it receives. Valvular disease 
 and other conditions impeding the circulation may cause one or 
 all of the cardiac chambers to enlarge and the walls to thicken. 
 Hypertrophy, uncomplicated by valvular disease, results when 
 the heart is called upon to perform excessive labor, or is stimu- 
 lated by abnormal nervous influences. Symptoms arise only 
 when the action of the heart is in excess of the requirements of 
 the system. Under such conditions there will be a sense of dis- 
 comfort in the precordial region, palpitation, paroxysmal cough, 
 shortness of breath, headache, vertigo, ringing in the ears, dis- 
 turbed sleep, deranged digestion, a florid complexion, and a 
 tendency to hemorrhage. 
 
 "What are the physical signs of hypertrophy of the heart? 
 
 When the heart is hypertrophied, its impulse is decided and ex- 
 tended, and usually displaced to the left. The area of per- 
 mssion-dulness is increased. As the enlargement, in most cases, 
 principally involves the left ventricle, the area of dulness in- 
 creases to the left, though enlargement of the left ventricle is 
 likely to be followed in turn by hypertrophy of the remaining 
 cavities. Owing to the position of the heart in the chest, the 
 left ventricle may be moderately enlarged without giving rise 
 to appreciable percutory abnormality. Enlargement of the 
 right heart may be the first cause of extension of the area of dul- 
 ness. The action of the heart is moderately accelerated, regular 
 and rhythmical. The first sound is strong and booming, the secmid 
 accentuated. The pidse is correspondingly full and strong. 
 
120 ESSENTIALS OF DIAGNOSIS, 
 
 Dilatation. 
 
 What are the symptoms of dilatation of the heart ? 
 
 Dilatation of the heart occurs under pretty much the same con- 
 ditions as give rise to hypertrophy, except that the organ is 
 unable to meet the demands made upon it. Dilatation may 
 thus be a sequel of hypertrophy. As dilatation is frequentl}^ 
 an ultimate result of obstruction to the pulmonary circulation, 
 the right heart usually suffers the more. The symptoms are 
 those of failing circulation : precordial anxiety, palpitation, head- 
 ache, vertigo, syncope, i^allor, cough, dyspnea, venous conges- 
 tion, and dropsy. 
 
 What are the physical signs of dilatation of the heart ? 
 
 The cardiac impulse is feeble and diffused, and usually dis- 
 placed to the left. The area of cardiac percussion-d.ulness is in- 
 creased. The first sound is weakened in correspondence with 
 the disproportion between the enlargement of the cardiac cham- 
 bers and the thickness of their walls; the second is little changed. 
 If the dilatation has been great enough to so enlarge the orifices 
 or weaken the muscles that the valves are no longer competent 
 to efiect complete closure, regui'gitant murmurs may be devel- 
 oped, even in the absence of structural alterations in the valves. 
 Such murmurs are usually rather soft and may be inconstant. 
 The action of the heart may be rapid and irregular. The pidse 
 is small and soft. 
 
 What are the distinctions between hypertrophy and dilatation 
 of the heart ? 
 
 HTPERTROPHT. DILATATION. 
 
 Face florid ; ringing in ears ; rush- Face pallid ; tendencj* to sj-ncope ; 
 
 ing of blood to the head. dropsy. 
 
 Cardiac impulse strong, extensive. Impulse feeble, diffused, often ■wavy. 
 
 Increased area of percussion-dul- Increased area of percussion-dul- 
 
 ness. ness. 
 
 Action rapid, regular, rhythmical. Action rapid, irregular. 
 
 First sound strong. First sound relatively enfeebled. 
 
 Pulse full, strong. Pulse small, yielding. 
 
VALVULAR DISEASE. 121 
 
 How does dilatation of the heart differ from fatty degeneration 
 of the heart ? 
 
 Tatty degeneration of the heart may be recognized when the 
 skin has a peculiar, greasy appearance, when an arcus seniHs is 
 present, when the sounds of a heart not enlarged are exceed- 
 ingly feeble, and attended with the symptoms of a failing 
 circulation. It differs from dilatation in the unchanged or 
 diminished size of the heart and the association with such 
 other evidences of fatty degeneration as may be present. The 
 pulse is usually, but not invariably, slow in fatty degeneration, 
 while it is rapid in dilatation. 
 
 How is a pericardial effusion to be distinguished from dilata- 
 tion of the heart ? 
 
 Fluid may collect in the pericardium in connection with 
 pericarditis, or as a part of a general dropsy. In dilatation of 
 the heart the cardiac impulse is feeble and diffuse, but not as 
 feeble or as wavy as in effusion. When dilatation exists, the 
 percussion-dulness in the precordia is not as extensive as when 
 there is an effusion, nor is it peculiarly triangular in outline. 
 While the sounds of the heart are enfeebled over the organ 
 when dilatation exists, they are almost obliterated in case of 
 effusion, except at the base, where, in case of peiicarditis, 
 friction-sounds may likewise be detected. The recognition of 
 a condition that gives rise to pericardial effusion is an aid in 
 diagnosis. 
 
 Valvular Disease. 
 
 What are the symptoms common to valvular lesions of the 
 heart ? 
 
 The functional deficiency of a diseased heart-valve may be 
 compensated for by an improved condition of the heart-muscle. 
 The presence or absence of rational signs will depend upon the 
 extent and constancy of the structural and functional alteration 
 of the muscle. If the alteration be too great, the symptoms 
 will be those of an hypertrophied or ovei'acting heart. If it be 
 too little, the symptoms will be those of an enfeebled heart. If 
 it be inconstant, symptoms of excitement, of overaction or of 
 
122 ESSENTIALS OF DIAGNOSIS. 
 
 enfeeblement may appear in paroxysms, or for prolonged pe- 
 riods at irregular intervals. Even when the compensatory 
 change is apparently constant and sufficient, there may be at 
 times or continuously, with or without pallor and weakness, a 
 sense of precordial discomfort, palpitation of the heart, short- 
 ness of breath, perhaps headache and vertigo — all aggravated 
 by exertion. Often, when compensation is but slightly imper- 
 fect, there are evidences of gastric and intestinal derangement, 
 and a sense of fulness in the hypochondria. Should the heart 
 fail, and compensation be disturbed, the condition becomes vir- 
 tually or actually that of dilatation of the heart ; the phenomena 
 are those of insufficient vis a tergo in the circulation. As a re- 
 sult of the stagnation of blood in the veins, there is engorge- 
 ment of various organs, especially of the lungs, liver, kidneys and 
 spleen ; the existing symptoms become intensified, and in addi- 
 tion there appears dropsy, first manifesting itself in the lower 
 extremities, and extending upwards. 
 
 When two or more lesions coexist, the compensation is less 
 readily established and more easily ruptured than in the case 
 of single lesions. Pulmonary congestion and hemoptysis occur 
 not infrequently. 
 
 Mitral Incompetency — Mitral Regurgitation. 
 
 What are the signs of incompetency of the mitral valve 
 (mitral regurgitation) ? 
 
 As a result of endocarditis, or of fibrous or calcareous degen- 
 eration, the bicuspid leaflets, or the chordae tendinea, become 
 thickened and contracted, interfering with the accurate apposi- 
 tion of the segments of the mitral valve during the systole. In 
 consequence, blood is abuormallj' diverted backward through 
 the mitral orifice, giving rise to a blowing (systolic) sound, 
 heard with greatest distinctness at the apex, and transmitted, 
 in the course of the fifth and sixth ribs, to the axilla and to the 
 inferior angle of the scapula. The heart is usually enlarged — 
 under favorable conditions, hypertrophied ; under unfavorable 
 conditions, dilated. 
 
AORTIC OBSTRUCTION. 123 
 
 Mitral Obstruction. 
 
 What are the physical signs of obstruction at the mitral 
 orifice ? 
 
 The mitral orifice becomes contracted as a result of endocar- 
 ditis or of degenerative changes in the segments of the valve. 
 The characteristics of mitral obstruction are : a rumbling 
 murmur heard just before the systole, with greatest intensity 
 over the left ventricle, and a purring tremor or thrill perceived 
 by the hand placed over the precordia. The left ventricle 
 diminishes in size, while the left auricle becomes enormously 
 enlarged. In turn the right side of the heart becomes enlarged. 
 The pulse is small and feeble. Not rarely mitral incompetency 
 is associated with obstruction. 
 
 Aortic Obstruction. 
 
 What are the physical signs of aortic obstruction ? 
 
 Aortic obstruction is a result of structural changes in the 
 semilunar valves or in the aorta, induced by inflammation or 
 degeneration. Aortic obstruction and incompetency are often 
 associated. The action of the heart is strong ; the left ventricle 
 becomes hypertrophied ; the pulse may be full and strong or 
 small and tardy. At midsternum and on the right side over 
 the junction of the second costal cartilage with the sternum, a 
 coarse, blowing, systolic murmur is heard, transmitted into the 
 great vessels. The murmur of aortic obstruction is sometimes 
 to be heard over the right carotid artery when at midsternum 
 and at the aortic cartilage, merely an obscuration of the first 
 sound can be detected. 
 
 Aortic obstruction, apart from insufficiency, is one of the less 
 common lesions. A systolic murmur heard at the aortic carti- 
 lage and transmitted into the neck may be due to dilatation oi 
 roughening of the aorta, without valvular or^'orificial change, 
 and may give rise to no circulatory disturbance. 
 
124 
 
 ESSENTIALS OP DIAGNOSIS, 
 
 Aortic Incompetency— Aortic Regurgitation. 
 
 What are the physical signs of incompetency of the aortic 
 valve (aortic regurgitation) ? 
 Aortic incompetency arises from conditions similar to those 
 tliat give rise to imperfections at tlie otlier orifices of the heart. 
 It is often associated with aortic obstruction. It is character- 
 ized by a blowing, diastolic murmur, replacing or accompanying 
 the second sound of the heart, heard with greatest intensity at 
 the aortic cartilage, and transmitted downwards in the course 
 of the sternum. Tlie action of the heart is powerful ; the left 
 ventricle becomes enormously hypertrophied ; vascular pulsa- 
 tion is common and may be evident even in parts remote from 
 the center of circulation ; the pulsation in the cai'otids may be 
 so strong that the head is shaken ; the pulse comes up well 
 with the systole of the heart, but immediatel}'^ recedes — consti- 
 tuting the gaseous pulse, the watei'-hammer pulse, or the pulse 
 of Corrigan. This character is well shown in the sphygmo- 
 graphic tracing. (Fig. 21.) 
 
 Fig. 21. 
 
 Pulse-tracing of aortic insufficiency. (After Striimpell. 
 
PULMONARY INCOMPETENCY. 125 
 
 Tricuspid Incompetency — Tricuspid 
 Regurgitation. 
 
 What are the signs of tricuspid regurgitation (incompetency 
 of the tricuspid valve) ? 
 
 Lesions of the valves and orifices of tlie riglit side of the 
 heart are uncommon. 
 
 If the tricuspid valve is incompetent, blood regurgitates with 
 the contraction of the ventricle ; in coiisequcnce, a blowing 
 systolic murmur is heard at the ensiform cartilage, and systolic 
 pulsation is visible in the veins of the neck. In some cases the 
 liver is seen to pulsate. 
 
 Tricuspid Obstruction. 
 
 What are the signs of obstruction at the tricuspid orifice ? 
 
 When the tricuspid orifice is obstructed the blood must 
 accumulate in the peripheral veins ; a presystolic murmur is 
 heard at the ensiform cartilage. 
 
 Pulmonary Obstruction. 
 
 What are the signs of obstruction at the pulmonary orifice ? 
 
 When the pulmonary orifice is obstructed a systolic murmur 
 is heard in the third intercostal space on the left, close to the 
 sternum. 
 
 Pulmonary Incompetency — Pulmonary Regur- 
 gitation. 
 
 What are the signs of incompetency of the pulmonary valve 
 (pulmonary regurgitation) ? 
 When the pulmonary valve is incompetent regurgitation occurs 
 with the dilatation of the ventricle ; as a result a diastolic mur- 
 mur is heard at the junction of the third costal cartilage on the 
 left with the sternum ; the murmur may be transmitted down- 
 wards in the course of the sternum. 
 
126 
 
 ESSENTIALS OF DIAGNOSIS. 
 
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ACUTE PERICARDITIS. 127 
 
 Acute Pericarditis. 
 
 What are the distinguishing features of acute pericarditis ? 
 
 Acute ^pericarditis may develop in association with rheuma- 
 tism, infectious diseases, nephritis, or pleurisy, endocarditis, or 
 other adjacent disease; it may also result from exposure to cold 
 or from hlows upon the chest. It is attended with pain in the 
 precordial region, and sometimes in the epigastrium ; consider- 
 able elevation of temperature and other febrile symptoms ; a 
 sense of anxiety ; dyspnea ; irregularity and increased rapidity 
 of the heart ; irritable cough ; possibly headache, vertigo, deli- 
 rium, nausea, and vomiting. The gastric phenomena may ob- 
 scure the actual condition, or the cerebral symptoms may sug- 
 gest meningitis ; careful inquiry and examination will, however, 
 reveal the inflammation of the pericardium. 
 
 What are the physical signs of acute pericarditis ? 
 
 In the first stage, the characteristic sign is a rubbing friction- 
 sound heard close to the ear at one or more points in the pre- 
 cordia, synchronously with one or both sounds of the heart. 
 The sound is to be distinguished from an endocardial murmur 
 by its quality, its superficiality and by increase of distinctness 
 caused by pressure with the stethoscope. 
 
 In the second stage— that of effusion, a murmur is no longer 
 heard, except j^erhaps above the fluid at the origin of the great 
 vessels. The cardiac impulse is feeble, extended and wavy. 
 The area of percussion-dxdness is increased, and presents a pecu- 
 liar outline — being triangular, with the base below. At the apex 
 and over the body of the heart, the sounds are heard but feebly 
 or not at all, while at the base they may be heard with ordinary 
 distinctness. 
 
 In the third stage, the fluid has disappeared, and murmurs 
 may again be heard. In the course of time, however, the 
 opposite surfaces of the inflamed membrane become adherent, 
 so that the pericardial cavity is in whole, or in part, obliterated. 
 Adhesions to the chest-wall give rise to localized retraction, 
 and to systolic dimpling. The heart in turn becomes enlarged. 
 
128 ESSENTIALS OF DIAGNOSIS. 
 
 How are acute pericarditis and acute pleurisy to be differ- 
 entiated ? 
 Pericarditis and pleuritis arise under similar conditions. 
 The two may be associated. The physical phenomena of both 
 are analogous, differing, however, in degree, extent and situa- 
 tion. The friction-sound of pleurisy is heard synchronously 
 with the respiratory movements, that of pericarditis synchron- 
 ously with the cardiac movements — the latter is thus the more 
 frequent. If doubt arise, the breathing should be suspended 
 for a short time : a pleural friction disappears. The percussion- 
 dulness occasioned by an eflfusion into the pericardium is situ- 
 ated in the precordia, and has a characteristic triangular out- 
 line ; the percussion-dulness of an effusion into the pleural cavity 
 involves the lateral and posterior aspects, as well as the anterior 
 aspect of the chest. 
 
 Acute Endocarditis. 
 
 What are the characteristics of acute endocarditis ? 
 
 Acute endocarditis develops in the course of infectious diseases 
 and of nephritis and chorea, but more especially in connection 
 with acute rheumatism. It is characterized by a sense of dis- 
 tress in the precordia, palpitation and increased frequency of 
 action of the heart, sometimes with irregularity, elevation of 
 temperature, dyspnea, slight cough and an anxious expression. 
 In addition, the face may be flushed ; there may be chills, 
 headache, vertigo, delirium, icterus, irritability of the stomach, 
 and diarrhea. The characteristic sign of acute endocarditis is 
 a soft, blowing, systolic murmur, though it is possible for endo- 
 carditis to exist without the detection of a murmur. 
 
 How is the murmur of an acute endocarditis to be distinguished 
 from a murmur the result of a past endocarditis ? 
 
 The murmur of acute endocarditis is soft, inconstant in its 
 seat, unattended with enlargement of the heart and associated 
 with the fever, precordial anxiety and other symptoms of acute 
 endocarditis ; a murmur dependent upon a past endocarditis is 
 harsher, fixed in seat, unattended with fever, but associated 
 
MYCOTIC ENDOCARDITIS. 129 
 
 Avith cardiac enlargement and a history of one of the conditions 
 that may cause endocarditis or of a remote attack of endo- 
 carditis. 
 
 ACUTE ENDOCARDITIS. CHRONIC VALVULAR DISEASE. 
 
 The murmur is soft and inconstant The murmur is harsher, fixed in 
 
 in seat and occurrence. seat and constant in occurrence. 
 
 Unattended with enlargement of Attended with enlargement of the 
 
 the heart. heart. 
 
 Associated with fever, precordial Not associated with fever or other 
 
 anxiety and other symptoms of symptoms of an acute condi- 
 
 acute endocarditis. tion. 
 
 No history of a remote acute endo- Remote history of acute endocar- 
 
 carditis. ditis. 
 
 Associated with rheumatism or Absence of an -immediate cause of 
 
 other cause of acute endocar- acute endocarditis. 
 
 ditis. 
 
 How is acute endocarditis to be distinguished from acute peri- 
 carditis ? 
 
 The pain of pericarditis is likely to be more severe than that of 
 endocarditis. The murmur of pericarditis appears closer to the 
 ear than that of endocarditis ; the former is a friction-sound, 
 diastolic as well as systolic ; the latter is blowing in character 
 and only systolic. When a pericardial effusion exists, it presents 
 a peculiar area of dulness on percussion, the heart-sounds at the 
 apex are enfeebled or they may be absent, and there is a dif- 
 used, feeble and wavy impulse, not found in endocarditis. 
 
 Mycotic Endocarditis. 
 
 What are the symptoms of mycotic or ulcerative endocarditis? 
 
 In addition to the ordinary symptoms of acute endocarditis, 
 the mycotic form is marked by high temperature with decided 
 oscillations, chills, sweats, the evidences of septic infection, 
 ecchymoses, prostration, a typhoid condition and albuminuria. 
 Mycotic endocarditis is usually engrafted upon preexisting val- 
 vular disease. Septic vegetations may form and ulceration and 
 perforation occur. Embolism is among the threatening dangers. 
 9 
 
130 ESSENTIALS OF DIAGNOSIS. 
 
 Myocarditis. 
 
 What are the symptoms of myocarditis ? 
 
 Some degree of myocarditis necessarily attends pei'icarditis 
 and endocarditis. Inflanwiaticni of the muscular structure of the 
 heart may occur in the course of rheumatism or in association 
 witli septicemia or pyemia. The condition does not give rise to 
 definite signs or symptoms apart from those of the inflamn)ation 
 of the pericardium or endocardium witli which it is commonly 
 associated. 
 
 What are the features of interstitial myocarditis ? 
 
 Interstitial myocarditis may be a result of acute inflammation 
 of the heart or form part of a general fibroid degeneration. 
 
 The action of a heart so aftected is likely to be irregular and 
 intermittent ; one or both sounds may be duplicated, while the 
 second is likely to be accentuated. 
 
 Hydropericardium. 
 
 What are the characteristics of hydropericardium ? 
 
 When not the result of pericarditis, an effusion into the pericar- 
 dium is usually part of a general dropsy. It presents physical 
 phenomena indistinguishable from those of pericarditis in the 
 stage of effusion, but lacks the febrile symptoms as well as the 
 friction-murmurs of the first or of the third stage. Evidences 
 of general dropsy, such as edema, pleural and peritoneal effu- 
 sions, and symptoms or signs of the causative disease — nephritis, 
 for example — will be found if looked for. 
 
 Heart-Clot. 
 
 What are the symptoms of heart-clot ? 
 
 The blood may coagulate in the cavities of the heart in the 
 course of endocarditis, of diseases in which the coagulability of 
 the blood is increased, such as pneumonia, and when from any 
 cause the action of the heart has become enfeebled. Under such 
 circumstances the surface of the body becomes cold and livid, 
 
THORACIC ANEURISM. 131 
 
 there is intense dyspnea, the action of the heart becomes rapid, 
 feeble and irregular, a faint murmur may be heard over the 
 organ and the area of cardiac percussion-dulness is increased. 
 There is great anxiety, nausea, vomiting, nervous excitement, 
 delirium, venous turgidity and attacks of syncope. 
 
 Thoracic Aneurism. 
 
 What are the symptoms of thoracic aneurism ? 
 
 The symptoms and physical signs of thoracic aneurism vary 
 with the location of the aneurism. Aneurisms of the aorta are 
 the most common. The frequency of aneurisms of the aorta 
 diminishes with the distance from the heart. The characteristic 
 manifestations of an aneurism are the existence in the course 
 of a bloodvessel of a imlsating expansile tumor, attended with a 
 thrill and hruit; on percussion, a circumscribed area of dulness will 
 be found to correspond with the area of expansile pulsation, 
 over which a thrill can be perceived with the palpating hand, 
 and a systolic bruit can be heard on auscultation. Other symjj- 
 toms depend upon the compression of adjacent structures. There 
 may thus be a peculiar metallic cough, with or without expec- 
 toration ; dyspnea ; dysphagia ; irregularity of the action of the 
 heart ; venous stagnation and edema ; manifestations of de- 
 rangement of the cerebral circulation ; localized sweating ; dila- 
 tation or contraction of one pupil ; paralysis of one or both 
 vocal bands ; enfeeblement of respiratory murmur over certain 
 areas, from obstruction of a large bronchus ; inequality of the 
 radial pulses ; neuralgic pain and erosion of bone. 
 
 How is an intra-thoracic tumor to be distinguished from an 
 aortic aneurism ? 
 
 An aneurism develops only in the course of a bloodvessl ; a 
 tumor of any other sort is not so restricted. The former presents 
 pulsation, expansion, and usually thrill and bruit ; the latter 
 may rise and fall if seated over an artery, but does not expand 
 or present a thrill or bruit. The sphygmographic tracing (taken 
 in loco) of a solid tumor situated above a normal artery is that 
 of the normal artery ; the curve given by an aneurism is abnor- 
 
132 ESSENTIALS OF DIAGNOSIS. 
 
 mal and often characteristic. Intra-thoracic tumors are usually 
 either secondary or give rise to metastases. If the tumor were 
 a gumma, the diagnosis would depeud upon a history of syphilis 
 or upon other manifestations of syphilis, together with a reces- 
 sion of the symptoms on appropriate treatment. Tuberculosis 
 of the mediastinal glands would be but one manifestation of a 
 general tuberculosis. 
 
 How is an abscess of the mediastmum to be distinguished from 
 an aneurism of the aorta ? 
 
 In addition to the features that distinguish all other thoracic 
 tumors from aneurism, an abscess presents fluctuation if acces- 
 sible, rigors, elevation of temperature, and sweating. There is a 
 history of traumatism or of pyemia. 
 
 How is incompetency of the aortic valve to be distinguished 
 from an aneurism of the aorta ? 
 
 Incompetency of the aortic valve may be attended with 
 marked pulsation in the course of the aorta, with a thrill and 
 bruit, but the evidences of tumor and the consequences of com- 
 pression are wanting ; the radial pulses are of the Corrigan or 
 water-hammer type, but are equal ; while the second sound of 
 the heart at the base is accompanied or replaced by a murmur 
 transmitted downwards in the course of the sternum. 
 
 How is a dilated auricle to be distinguished from an aortic 
 aneurism ? 
 An enlarged auricle ma}' give rise to pulsation at the base of 
 the heart, but not to the compression-phenomena of an aneur- 
 ism, not to the thrill or bruit, be3'ond the sounds generated in 
 the heart itself as a result of the lesion that has led to the 
 enlargement of the auricle : usually obstruction at the mitral 
 orifice with a presystolic murmur. 
 
 Arterio- Capillary Fibrosis. 
 
 What is arterio-capillary fibrosis ? 
 
 Arterio-capiUary fibrosis is a degenerative process of the walls 
 of the smaller bloodvessels, due to the long-continued circulation 
 in the blood of irritants, such as alcohol, lead, the poisons of 
 
SYMMETRICAL GANGRENE. 133 
 
 syphilis, of gout, of rheumatism, and of infectious diseases. 
 Yaso-motor spasm and hyperplasia of the connective tissue of 
 the arteries and of the intercelkilar elements of parenchymatous 
 organs take place. The coats of the vessels become thickened 
 and the size of organs becomes increased. From secondary con- 
 traction of the newly-formed fibrous tissue, the lumen of the 
 arteries becomes narrowed and the organs become reduced in 
 size. The circulation is curtailed and nutritive processes are 
 interfered with ; atrophy may result ; thrombi may form in situ. 
 Sclerotic vessels are prone to rujiture, in the brain, in the retina, 
 and elsewhere. 
 
 What are the symptoms of arterio-capillary fibrosis ? 
 
 The diagnostic symptoms of arterio-capillary fibrosis or arterio- 
 sclerosis are those of vascular spasm, impeded circulation, and 
 impaired nutrition : shortness of breath, vertigo, mental impair- 
 ment, nervous derangement, irregularity of cardiac action, 
 resistant radial arteries, prominent, tortuous temporals, in- 
 creased arterial tension. Edema may be present. The urine 
 becomes increased in quantity and may contain a trace of albu- 
 min and an occasional tube-cast. Numbness and coldness of the 
 extremities are common. The nails are sometimes bluish from 
 impeded circulation. The knee-jerk is often exaggerated. Tran- 
 sient local palsies sometimes occur. Angina pectoris and pseudo- 
 angina are not uncommon. The action of the heart may be 
 arhythmical, the sounds duplicated ; the second or arterial 
 sound is usually accentuated. An hypertrophied left ventricle, 
 without valvular disease of the heart, should be suggestive of 
 the existence of vascular disease. Chronic interstitial nephritis 
 is a frequent result of arterio-capillary fibrosis, or of the same 
 causes that give rise to the vascular changes. Cerebral and 
 retinal thrombosis or hemorrhage may be complviations. 
 
 Symmetrical Gangrene— Local Asphyxia. 
 
 What are the symptoms of symmetrical gangrene ? 
 
 RaynaxuVs disease, local asphyxia, or symmetrical gangrene is an 
 aftection in which the fingers or toes on both sides of the body 
 
134 ESSENTIALS OF DIAGNOSIS. 
 
 become cyanotic, edematous and numb ; they may even undergo 
 spontaneous gangrene. The patholog}- of the disease is not 
 known ; it is considered a vaso-motor neurosis, the persistent 
 contraction of the peripheral capiharies giving rise to the 
 symptoms. 
 
 The afiection sometimes appears after exposure to severe 
 cold. Its onset is occasionall}' marked by the occurrence of 
 hematuria. 
 
 How are the symptoms of Raynaud's disease and those resulting 
 from frost-bite to be differentiated ? 
 The appearances presented by Raynaud's disease and those 
 presented bj^ frost-bite may be almost indistinguishable. Frost- 
 bite is not likel}', however, to exhibit the symmetrj- of distribu- 
 tion observed in cases of Raynaud's disease. The symptoms of 
 frost-bite, moreover, usually recede when cold weather departs, 
 while the manifestations of Raynaud's disease persist, though, 
 perhaps, also aggravated by cold. Raynaud's disease is not 
 necessarilj- dependent upon severe cold as a cause ; while frost- 
 bite is essentially so dependent. 
 
 THE RESPIRATORY SYSTEM. 
 
 How are affections of the upper air-passages (nose, pharynx, 
 larynx and trachea) to be diagnosticated ? 
 
 The diagnosis of affections of the upper air-passages is based, 
 in part, upon the symptoms ; but the only certain methods are 
 those of direct inspection, or of indirect inspection by means of a 
 suitable mirror. For both direct and indirect inspection, 
 proper illumination is necessary. When direct daylight does 
 not suffice, a reflector is employed, either with daylight or with 
 artificial light. There are also apparatus for direct illumination 
 b}' artificial light. Palpation with probe or finger is sometimes 
 additionally necessary. 
 
 It is sometimes necessar}' to remove from the line of vision, 
 by means of suitable retractors, certain structures, as the an- 
 terior palatine folds, the uvula, soft palate or epiglottis. 
 
 By transhimination, or transmission of light through the tis- 
 
THE RESPIRATORY SYSTEM. 135 
 
 sues, information is sometimes gained as to the comparative 
 density of structure. 
 
 Direct inspection of the nasal passages by means of a specu- 
 lum inserted by way of the nostrils is called anterior rhinoscopy. 
 
 Indirect inspection of the nasal passages by means of a 
 mirror so placed in the pharynx, behind and below the soft 
 palate, as to reflect au image of the posterior choanEe and 
 neighboring structures, is called x>^sterior rhinoscopy. The 
 vault of the pharynx and the mouths of the Eustachian tubes 
 are examined by the methods of posterior rhinoscopy. 
 
 Direct inspection of the pharynx is termed direct pharyngo- 
 scopy. To carry it out, only light to illuminate and a spatula 
 to depress the tongue are required. Those parts of the pharynx 
 inaccessible to direct inspection are examined by means of a 
 mirror appropriately placed {indirect jyharynyoscopy). 
 
 The laryngeal structures are rarely accessible to direct inspec- 
 tion. Sometimes a part of the epiglottis^ may be seen, and in 
 exceptional instances a glimpse of the supra-arytenoid struc- 
 tures has been obtained. 
 
 Laryngoscopy is practised by means of a mirror so placed in 
 the pharynx, with the uvula lifted out of the way upon the 
 back of the mirror, as to reflect an image of the deeper parts. 
 In favorable cases, the interior of the trachea, to its bifurcation, 
 may be seen. When the patient phonates, the superior face of 
 the vocal bands and the structures above are reflected. When 
 the patient inspires deeply, the internal face of the vocal bands 
 and the structures below are additionally revealed. One 
 endeavors to observe the contour, the color and the motility of 
 the various parts, and to determine the presence or absence of 
 secretion, ulceration, cicatrices, abnormal growths or foreign 
 bodies. 
 
 To what conditions may difficulty of nasal respiration be due ? 
 
 Difficidty of nasal respAration may be dependent upon enlarge- 
 ment, engorgement or distortion of the septum or of the turbi- 
 
 1 A very long epiglottis, visible on direct inspection, when the patient 
 "gagged," has been mistaken by physicians for a red worm, and one 
 hysterical patient, feeling the epiglottis with her finger, thought, because 
 it was broad and hard, that it was a tapeworm. 
 
136 ESSENTIALS OV DIAGNOSIS. 
 
 nate bodies, upon the presence of foreign bodies, or of pol3'pi 
 or other neopla^^ms, or, especially in children, upon overgrowth 
 of the glands of the vault of the pharynx (adenoid vegetations). 
 The diagnosis can be made only by rhinoscopj-, anterior and 
 posterior, sometimes in conjunction with palpation. 
 
 What symptoms other than those directly referable to the nose 
 may arise from the conditions that occasion difficulty in 
 nasal respiration ? 
 
 In addition to the local S3'mptoms, the conditions that occa- 
 sion difficulty of nasal respiration may be attended by anemia 
 from deficient oxygenation, together with persistent cough, facial 
 tic, headache, asthmatoid seizures, epileptiform convulsions, 
 chorea, exopthalmic goiter, or various other reflex disturbances. 
 The diagnosis is to be based upon a careful study of all of the 
 phenomena and conditions, general and local. 
 
 What is a frequent, unsuspected cause of epistaxis ? 
 
 An ulceration or erosion of the mucous membrane of the nasal 
 septum, usually situated near the anterior inferior angle of the 
 triangular cartilage, is a not uncommon cause of epistaxis. 
 Malignant growth, especialh' sarcoma, which may involve the 
 frontal sinuses and even be hidden from rliinoscopy is another 
 condition worthy of mention. The bleeding may be insignifi- 
 cant in quantity, and might easily be considered of little 
 moment. 
 
 Coryza — Acute Nasal Catarrh. 
 
 What is coryza? 
 
 Coryza or acute nasal catarrh is a superficial inflammation of 
 the nasal mucous membrane, attended b}' sneezing and a pro- 
 fuse watery discharge from the nostrils. There is usually head- 
 ache and sometimes more or less fever. The swollen membrane 
 and more especially the engorged turbinate bodies impede res- 
 piration and modify articulation. In the course of a few daj'^s, 
 the discharge becomes more viscid, often muco-purulent. Usu- 
 ally the attack subsides completely in a week. Conjunctivitis, 
 
HAY-FEVER. 137 
 
 pharyngitis, laryngitis, bronchitis and otitis media are among 
 the complications and sequelce sometimes manifested. 
 
 How is coryza to be differentiated from influenza? 
 
 Some authorities refuse to make a distinction between coryza 
 and influenza. Coryza, with conjunctivitis or bronchitis, is 
 sometimes epidemic. From fully-developed influenza, simple 
 coryza, whether due to cold, to non-specific irritation or to in- 
 fection, differs by the absence of the constitutional symptoms 
 and of the profound depression characterizing the former disease. 
 
 Hay-Fever. 
 
 What is hay-fever? 
 
 Hay-fever, hay-asthma^ rag-weed fever ^ autumnal catarrh, June 
 cold, rose-cold, idiosyncratic coryza, periodic vasomotor coryza, are 
 names applied to a group of symptoms developed in susceptible 
 individuals as the effect of special irritants upon the mucous 
 membranes of the eyes and air-passages, more especially of the 
 nose. The manifestations vary much in severity and in con- 
 stancy in diff'erent individuals, and in the same individual at 
 different times, and comprise conjunctivitis, coryza, pharyngitis, 
 laryngitis, bronchitis, asthma and gastric, enteric and renal 
 crises. There is commonly intolerable itching of the eyelids 
 and of the palate. Fever is not common ; but when it occurs, 
 it is irregular. 
 
 In some individuals the syndrome occurs when any irritating 
 substance gains entrance to the nasal passages. In others the 
 powder of certain drugs, such as ipecacuanha, or the pollen of 
 certain plants, such as grasses, rag-weed, roses, is the exciting 
 cause. The 2jredisposing cause is usually a neurotic constitution, 
 perhaps induced by excessive mental exertion or by undue in- 
 dulgences ; sometimes the presence of nasal abnormalities ag- 
 gravates the symptoms. 
 
 In those in whom the attacks depend on special pollens, the 
 manifestations necessarily recnv periodically. In North America 
 tlie rag-weed is the most common provocative agent, and with 
 most sufferers the attacks begin about the middle of August, and 
 
138 ESSENTIALS OF DIAaNOSIS. 
 
 last until the cause has disappeared, June-colds are dependent 
 on hay and roses. 
 
 How is hay-fever to be distingnished from simple coryza? 
 
 The distinguishing features ot hay-fever are the invariability 
 of its causation, and the severity and association of its 
 symptoms ; together with the rapid disappearance of symptoms 
 on removal to a locality (usually the mountains or the seashore) 
 where the provocative agency is not present. 
 
 Acute Laryngitis. 
 
 What are the symptoms of acute laryngitis ? 
 
 Acute laryngitis usually results from exposure to cold, or from 
 the inhalation of irritating fumes. It occurs deuteropathically 
 in the course of many inflammatory and infectious diseases, 
 whether general or of the respiratory or digestive organs. With 
 great variations in the degree of severity, it manifests itself by 
 laryngeal irritation, hoarseness or painful aphonia, painful deglu- 
 tition, dyspnea and slight hawking cough, with mucous expec- 
 toration. 
 
 There may also be slight elevation of temperature. 
 
 Laryngoscopicallij, the laryngeal structures will be seen to be 
 more or less reddened and swollen. If edema occur, the breath- 
 ing will be labored and stridulous, and, as a result of the im- 
 pediment to respiration, cyanosis may develop. Laryngoscopy 
 or palpation will reveal the cause. 
 
 How is laryngitis to be distinguished from pharyngitis? 
 
 The only reliable method of discrimination is by inspection, 
 both directly and by means of the mirror, as symptoms are very 
 likely to be misleading, and the two aftections not infrequently 
 coexist. 
 
 In pharyngitis the alteration in voice — aphonia or hoarse- 
 ness, of laryngitis is wanting. The difficulty and pain of swal- 
 lowing are likely to be the less in laryngitis, and inspection will 
 reveal the seat of the inflammation. 
 
EDEMA OF THE LARYNX. 139 
 
 How does parotiditis differ from laryngitis ? 
 
 In parotiditis the voice remains unaffected. In laryngitis 
 there is no swelling about the face. 
 
 How does tonsillitis differ from laryngitis ? 
 
 Inspection discloses the swelling of the tonsils and the absence 
 of involvement of the larynx. 
 
 In tonsillitis the voice ma}'^ be nasal, but it is not hoarse or 
 lost ; cough and expectoration ax'e absent, while the difficult}^ of 
 breathing may be great. 
 
 The difficulty and pain of swallowing are greater in tonsillitis 
 than in laryngitis. 
 
 How does hysterical aphonia differ from acute laryngitis ? 
 
 Hysterical aphonia, as a rule, sets in more or less suddenly ; 
 often in association with emotional disturbance, in a person, 
 usually a female, presenting other manifestations of hysteria ; 
 and is unattended with pain, ditficulty of breathing or elevation 
 of temperature. Laryngoscopic examination will reveal the 
 motor impairment of the vocal bands, and the non-existence of 
 an inflammatory process. Recovery may take place as suddenly 
 as did the onset. The attack is likely to be repeated. 
 
 Edema of the Larynx. 
 
 What are the symptoms of acute edema of the larynx ? 
 
 Acute edema of the larynx may occur so insidiously as to pro- 
 duce death without giving rise to appreciable symptoms, or 
 the symptoms may be sudden and overwhelming. 
 
 When edema of the larynx occurs in the course of other 
 affections, or as a sequel, there may be the usual prodromes of 
 inflammatory fever, but as a rule the onset is sudden, and the 
 severity of the attack rapidly increases. There are local ten- 
 derness, dryness and heat in the throat, with a sensation as 
 of the presence of a foreign body ; more or less inefffectual 
 cough ; muffling or extinction of voice ; difficulty of swallowing ; 
 difficulty of inspiration, with harsh stridor, occurring in par- 
 oxysms that increase in frequency and severity, and unless re- 
 lief be afforded, result in expiratory difficulty and apnea. 
 
140 ESSENTIALS OF DTAGNOSTS. 
 
 Bespiration is hurried and spasmodic ; tlie pu^se is small, fre- 
 quent and irregular ; the temperature is elevated ; the eyes are 
 prominent ; the face is flushed and anxious, finally cyanotic. 
 
 When dependent upon acute disease, the suffocative attacks 
 will be abrupt and violent, and will recur at intervals of a feAv 
 hours. 
 
 When dependent upon chronic disease, the paroxysms mny 
 pass off, to recur irregularly, at progressively shorter intervals. 
 Fever is absent, unless the underlying disease itself be febrile. 
 
 Simple inspection of the pharynx may reveal the swollen 
 epiglottis projecting up behind the base of the tongue. Palpa- 
 tion with the finger may detect a soft, elastic, bladder-like swell- 
 ing of the epiglottis, or of the aiy-epiglottic folds ; but unless 
 cautiously practised it may induce a pai'oxysm of suffocation 
 from the additional obstacle or irritation. Laryngoscopic ex- 
 amination at once reveals the cause of the symptoms. 
 
 What are the symptoms of chronic edema of the larynx ? 
 
 Chronic edema of the larynx may be due to laryngeal disease, 
 or to the usual causes of effusions. It gives rise eventually to 
 progressive difficulty of breathing, paroxysmally aggravated, 
 with perhaps some impairment of voice, and pain or difficulty 
 in swallowing. The diagnosis is only to be made by laryngo- 
 scopy, in default of which palpation may perhaps be of service. 
 
 How is chronic edema of the larynx to be distinguished from 
 asthma ? 
 
 Principally by laryngoscopic examination. The paroxysms 
 may exactly simulate asthmatic attacks. Suffocative parox- 
 ysms, due to laryngeal neoplasm, may likewise be mistaken for 
 asthma if laryngoscopic examination be not made. Before the 
 days of laryngoscopy many cases of sudden death were found to 
 be due to laryngeal neoplasm. 
 
 Acute Tuberculous Laryngitis. 
 
 What are the characteristics of acute tuberculous laryngitis? 
 
 Acute tuberculous laryngitis is characterized by the constitutional 
 symptoms of acute miliary tuberculosis, and locally by great 
 
LARYNGISMUS STRIDULUS. 141 
 
 pain in swallowing, by cough, dysphonia or hoarseness, and 
 sometimes pain in respiration. Laryngoscopic ms2jecti(yn reveals 
 peculiar thickenings of the epiglottis and other laryngeal struc- 
 tures, which are quickly followed by ulceration ; or there may 
 be ulceration from the first. Tubercle-bacilli are sometimes to 
 be detected in the secretions or in the debris of ulcers. 
 
 Laryngeal manifestations are sometimes observed before evi- 
 dences of pulmonary tuberculosis can be detected ; but the lat- 
 ter, sooner or later, become manifest. A somewhat rapid fatal 
 termination is the rule, but recognized instances of recovery 
 are multiplying. 
 
 Laryngismus Stridulus. 
 
 What is laryngismus stridulus ? 
 
 Laryngismus stridulus is a spasmodic affection characterized 
 b}' contraction of the constrictor muscles of the larynx, giving 
 rise to dyspnea, inspiratory stridor and a ringing, croupy cough. 
 It occurs most frequently in rachitic children. The attacks are 
 paroxysmal and usually nocturnal. The child may be awakened 
 from sleep with a sense of suffocation and an appearance of 
 lividity. The paroxysm lasts for a few minutes and terminates 
 with a deep inspiration, attended with a crowing sound. Occa- 
 sionally death results in the paroxysm ; perhaps, from incarce- 
 ration of the epiglottis. 
 
 How does laryngismus stridulus differ from asthma ? 
 
 Laryngismus stridulus is a disease of childhood ; asthma is 
 rare in children. 
 
 Eickets predisposes to laryngismus stridulus ; asthma may be 
 apparently idiopathic, or some recognized ii'ritation, direct or 
 reflex, may be discoverable. The wheezing and rales of asthma 
 differ from the cough and stridor of laryngismus. 
 
 The asthmatic paroxysm terminates in abundant expectora- 
 tion ; laryngismus stridulus subsides without critical pheno- 
 menon. 
 
142 ESSENTIALS OF DIAGNOSIS. 
 
 Laryngeal Vertigo. 
 
 What is laryngeal vertigo ? 
 
 The name laryngeal vertigo is applied to a group of symptoms 
 of rare occurrence that may appear in connection with recog- 
 nized nervous diseases, as posterior spinal sclerosis or epilepsy, 
 or without obvious explanation. The symptoms are not always 
 the same, but the essential elements in association are pain 
 or spasm of the larynx, vertigo and perhaps syncope. The oc- 
 currence of laryngeal vertigo should lead to careful search for 
 symptoms or signs of the causative disorder. 
 
 Catarrhal Croup — Spasmodic Croup. 
 
 What is catarrhal or spasmodic croup? 
 
 Catarrhal or spasmodic croup is essentially a catarrhal laryn- 
 gitis, associated with a tendency to spasm of the constrictor 
 muscles of the larynx, causing paroxysms of suffocation. It is 
 almost exclusively a disease of children. It xwBiy follow exposure, 
 may be simultaneous with the prevalence of epidemics of influ- 
 enza, of measles or of scarlatina. It may tegin insidiously with 
 slight hoarseness, or suddenly, with chill. It usually attracts 
 attention at first toward evening ; the voice will be hoarse, with 
 a slight cough. In the middle of the night, the child will sud- 
 denly awaken, with crying and paroxysms of suffocation, and 
 with a peculiar, ringing, metallic cough, which is termed croupy. 
 The spasm may quickly pass away, or it may be repeated 
 several times during the night and for three or four successive 
 nights, the symptoms of ordinary laryngeal or laryngo-bi'on- 
 chial catarrh being manifested during the day. Becxwery may 
 take place, or high fever may set in with a firm, bounding 
 pulse, flushing of the cheek, abnormal brilliance of the eye, 
 and development of the obstructive symptoms of pseudo-mem- 
 branous laryngitis. 
 
 How does catarrhal croup differ from laryngismus stridulus ? 
 
 Laryngismus stridulus is a disorder of repeated occurrence, 
 and comparatively chronic duration, occurring in rachitic chil- 
 
MEMBRANOUS GROUP. 143 
 
 dren, and not associated with fever, cougli or other symptom 
 of inflammation. Spasmodic croup begins acutely, is of sliort 
 duration, attacks healthy as well as rachitic children, and is 
 associated with slight fever, cough and symptoms of catarrhal 
 inflammation. 
 
 How are croup and edema of the larynx to be distinguished ? 
 
 Apart from the revelations of laryngoscopy, croup is a disease 
 of childhood principally — edema usually occurs in adults. In 
 febrile cases the history of exposure to irritating fumes, or of 
 other exciting cause of acute edema, the pain in swallowing, 
 and the local tenderness ; in other cases the absence of fever, 
 and the knowledge of the existence of causative conditions ; 
 together with the absence of the croupal cough, and the purely 
 inspiratory character of the stridor, are additional discrimina- 
 tive features of edema. 
 
 Membranous Group. 
 
 "What are the symptoms of membranous croup ? 
 
 Membranous croup or pseudo-membranous laryngitis, whether an 
 idiopathic disease or due to the extension or original formation 
 of diphtheritic membrane in the larynx and trachea, is mani- 
 fested by symptoms of mechanical and s]>asmodic or paralytic 
 obstruction of the larynx and trachea, associated with more or 
 less fever and the constitutional symptoms of diphtheria, if that 
 disease be present. In some instances, the palate, tonsils and 
 pharynx are involved in simple, exudative or diphtheritic in- 
 flammation. In severe cases, the process extends into the 
 bronchi, and in some cases there is pneumonitis. There is a 
 peculiar ringing cough, which gradually becomes muflled, with 
 progressive muffling or extinction of the voice ; and great diffi- 
 culty in breathing, intensified in pai'oxysms, which may pro- 
 gress to suffocation. Evidences of the severity of the obstruc- 
 tion are the recession upon inspiration of the soft tissues above 
 and below the sternum and the use by the child of the 
 auxiliary muscles of respiration, in its efforts to obtain breath. 
 There is extreme restlessness and agitation, with paroxysmal 
 
144 ESSENTIALS OF DIAGNOSIS. 
 
 exacerbations,' attended by protrusion of the eyeballs, distention 
 of the nostrils, flushing of the cheek, grasping at supports. 
 
 Sometimes a child will sit up straight in bed and clutch at its 
 neck, as if trying to pull away some obstruction. 
 
 Suffocative paroxysms, being parti}' spasmodic, are sometimes 
 relaxed by the effects of the resulting carbonic acid poisoning, 
 and with the production of cyanosis there comes a deep sighing 
 expiration, followed by a deep inspiration, and a period of com- 
 parative quiet. 
 
 Flakes of membrane or even membranous casts of the trachea 
 and bronchi may be expectorated. The duration may be short, 
 from twenty-four to forty-eight hours ; it may be prolonged to 
 two or three weeks ; usually, however, asphyxia or recover}' oc- 
 curs in from five to eight days. Convulsions often precede death. 
 
 How are membranous croup and retropharyngeal abscess to be 
 distinguished ? 
 
 Retropharyngeal abscess may be detected by inspection and 
 palpation. The evidence of tuberculosis or syphilis, the histoiy 
 of previous infectious disease, may be suggestive of abscess. The 
 voice is toneless but distinct in croup ; in abscess it is nasal and 
 indistinct. In abscess there are pain and difficulty in swallowing ; 
 these symptoms are absent from croup. In abscess there is stiff- 
 ness of the neck, with tumefaction and pain on pressure exter- 
 nally ; this is not the case in croup. In croup there is a pe- 
 culiar cough and sometimes expectoration of false membrane ; 
 these are not present in abscess. 
 
 How do membranous croup and catarrhal croup differ 1 
 
 In catarrhal croup fever and constitutional symptoms are 
 slight. In membranous croup, fever is severe ; and in diph- 
 theria, toxemic symptoms are evident. 
 
 In catarrhal croup the obstruction to breathing is purely spas- 
 modic, and disappears with relaxation of the spasm. 
 
 In membranous croup there is mechanical obstruction, con- 
 tinuing when the spasm has passed. 
 
 In catarrhal croup the voice remains clear, or at most becomes 
 hoarse ; the cough preserves its ringing, " croupal" chai-acter. 
 In membranous croup voice and cough become toneless. 
 
WHOOPING-COUGH — PERTUSSIS. 145 
 
 In membi-anous croup shreds of membrane or casts may be 
 expectorated, and diphtheritic membrane is sometimes visible 
 in the pharynx. Laryngoscopic inspection, when possible, will 
 settle the diagnosis. 
 
 How is obstruction of the larynx, trachea or a bronchus by a 
 foreign body to be distinguished from croup ? 
 
 In the absence of the history, which would at once prevent 
 error, the lack of fever and its concomitants, the absence of 
 the peculiar cough, the variation in the symptoms, and finally 
 laryngoscopic examination or the evidences of bronchial obstruc- 
 tion discovered on auscultation and percussion, permit the diag- 
 nosis of foreign body to be made. 
 
 Whooping-Cough — Pertussis. 
 
 What are the symptoms of whooping-cough ? 
 
 Pertussis, or whooping-cough, is a contagious disease of child- 
 hood, attended with catarrhal symptoms, to which is added a 
 peculiar cough, occurring in paroxysms and attended with a 
 characteristic whoop. For several days there is coryza, accom- 
 panied with an acrid discharge, conjunctivitis, laryngitis and 
 bronchitis. The cough then becomes paroxysmally explosive, 
 a series of expiratory eftbrts being followed by a peculiar, ring- 
 ing, inspiratory whoop. During these attacks the child may 
 become livid and appear as if about to suftbcate ; sometimes 
 vomiting is induced. The violence of the cough may cause ul- 
 ceration of the under surface of the tongue on either side of the 
 frenum ; or there may be hemoptysis or epistaxis. The parox- 
 ysms are repeated with variable frequency. The disease may 
 last many weeks, the severity and number of attacks progress- 
 ively diminishing. It may be complicated by catarrhal pneu- 
 monia, which sometimes proves fatal. Bronchitis may long per- 
 sist as a sequel. 
 
 What are points of discrimination between membranous croup 
 and whooping-cough? 
 
 In whooping-cough there is little or no fever, no continuous 
 dyspnea, no alteration of voice, and the child is usually up and 
 10 
 
146 ESSENTIALS OF DIAGNOSIS. 
 
 about, unless there is pulmonary complication. In croup there 
 is not the characteristic whoop. 
 
 What are the differential features of laryngismus stridulus and 
 whooping-cough ? 
 
 Laryngismus stridulus is a paroxysmal neurosis, most com- 
 mon in rickety children ; whooping-cough is a contagious dis- 
 ease that attacks all children alike. 
 
 The cough of laryngismus stridulus is croupy ; that of whoop- 
 ing-cough occurs as a series of explosive expiratory sounds, fol- 
 lowed by a distinctive inspiratory whoop. During the intervals 
 of freedom, whooping-cough presents the symptoms of bron- 
 chitis ; laryngismus stridulus does not. 
 
 Chronic Laryngitis. 
 
 What are the symptoms of chronic laryngitis ? 
 
 Chronic laryngitis may be a result of repeated attacks of acute 
 laryngitis ; it may depend on nasal disease, gastric catarrh, 
 dilated heart, constipation, or kidney disease, or other near or 
 remote affection. It is common in those who use tlieir voices 
 improperly or immoderately, and in those who smoke to excess. 
 It is characterized by hoarseness, persistent, irritable cough 
 and discomfort in phonation and deglutition. Laryngoscopicall}' 
 the structures within the larynx are seen to be thickened, con- 
 gested, covered by tough secretion ; the vocal bands have lost 
 their pearly, glistening appearance, and their motility may be 
 impaired. In many cases chronic lai'yngitis is of tuberculous 
 or of syphilitic origin. 
 
 How is chronic laryngitis to be distinguished from laryngeal 
 neoplasms ? 
 
 The only safe method of diagnosis is by means of laryngo- 
 'scopy, and its neglect is criminal. 
 
PHYSICAL DIAGNOSIS. 147 
 
 Chronic Tuberculosis of the Larynx. 
 
 What are the characteristics of chronic tuberculosis of the 
 larynx ? 
 
 In case of chronic tuherctdosis of the larynx the subjective and 
 objective symptoms may be simply those of ordinary chronic 
 laryngitis, or there may be characteristic tumefactions, ulcera- 
 tions or vegetations in the larynx, or all combined ; with more 
 or less pain and difficulty in swallowing and in respiration, and 
 alteration of the voice. The signs of pulmonary tuberculosis 
 are usually well advanced. Cases of recovery from the local 
 disease in the larynx, or of its prolonged abeyance, are not rare. 
 
 How are paralyses, ulcerations, abscess, stricture and other 
 conditions affecting the larynx and trachea, and giving 
 rise to alterations in voice and difficulty in respiration, 
 to be diagnosticated ? 
 
 The only reliable method is laryngoscopy. 
 
 PHYSICAL DIAGNOSIS. 
 
 What are the methods of physical exploration ? 
 
 In a physical exploratimi, systematically conducted, five 
 means of investigation are employed : inspection, mensuration, 
 palpation, percussion and auscultation. 
 
 What does physical exploration teach ? 
 
 By physical exploration information is gained of physical or 
 mechanical conditions, so far as these may influence the size, con- 
 tour, 'movement, temperature, density, elasticity and acoustic 
 relations of the structures examined. The nature of patho- 
 logic conditions cannot be directly determined from physical 
 signs, but is to be inferred from the latter in association with 
 all other phenomena in a given case. 
 
 What is to be learned by inspection ? 
 
 By inspection the general appearance of an individual is 
 noted— the height, the apparent relative nutrition, the color. 
 
148 ESSENTIALS OF DIAGNOSIS. 
 
 the configuration, the movement, the state of the pupils, the 
 expression. 
 
 Examhiing tlie chest more especially, its symmetry or asym- 
 metry, its fulness or retraction ; the frequency and character 
 of the respiratory movements ; the extent of the respiratory 
 excursion ; the situation, extent and vigor of the cardiac im- 
 pulse are observed, and abnormal manifestations are looked for. 
 
 The chest is distended symmetrically in emphysema and 
 usually in case of hydrothorax ; pleural effusions and pneumo- 
 thorax commonly occasion unilateral bulging. 
 
 The chest is retracted when the parietal and visceral pleurae 
 are adherent, and M^ien the lung is shrunken, as in interstitial 
 pneumonitis. The retraction is well marked after some forms 
 of operative treatment of empyema, and when the lung is col- 
 lapsed from any cause, 
 
 A healthy adult breathes from eighteen to twenty times in 
 the minute. The normal respiratory excursion is curtailed and 
 the frequency of respiratory action is accelerated by almost all 
 diseases of the lung and pleura and also in case of peritonitis. 
 The respiratory frequency is also accelerated when the pulse 
 is quickened, as in febrile conditions. In case of pleurisy, the 
 patient lies on the affected side, so as to reduce to a minimum 
 functional movement of that side. Rapidity of breathing may 
 be hysterical. Women breathe mostly with the upper portion 
 of the chest ; men with the lower. 
 
 What is to be learned by mensuration? 
 
 Mensuration determines with precision what inspection does 
 approximately : the size, configuration, symmetry or asym- 
 metry and respiratory excursion of the chest. 
 
 What is to be learned by palpation ? 
 
 By touch ov palpation one distinguishes elasticity from rigidity 
 and resistance, investigates the existence of pain or tenderness, 
 of edema, of moisture or dryness, of heat or cold. When the 
 palm of the hand is applied to the chest of a speaking person a 
 diffuse, vibratory sensation is perceived, usually slightly greater 
 in intensity on the right side than on the left. This is known 
 as the vocal or tactile fremitus. 
 
PHYSICAL DIAGNOSIS. 149 
 
 It is increased in conditions of condensation of tlie lung or 
 thickening and adliesion of tlie surfaces of the pleura. It is dimi- 
 minished or lost over collections of fluid in the pleura. Variations 
 in vocal fremitus correspond pretty closely with variations in 
 vocal resonance. Sometimes a pleuritic friction-ruh can be felt. 
 
 How is percussion performed? 
 
 Percussion may be immediate or mediate. In the former a 
 sharp blow is struck with the tips of the fingers bunched together, 
 or with the palmar surface of the extended fingers. 
 
 Mediate percussion is performed by means of a thin, flat plate 
 of ivory or of hard rubber (called a pleximeter), applied over the 
 part to be examined, and a small rubber-tipped hammer (called 
 a plexor). 
 
 For many purposes it is preferable to use the extended finger 
 of one hand as a pleximeter, and the index or middle finger (or 
 both) of the other hand as a plexor. Percussion is said to be 
 weak or strong^ superficial or deep, according to the energy of the 
 blow of the plexor. 
 
 What is to be learned by percussion ? 
 
 Percussion gives information as to the relative distribution of 
 gases (usually air), fluids and solids in the structures examined. 
 Attention is paid to the quality (or timbre)^ the pitch and the 
 intensity of sounds. 
 
 Percussion of the healthy chest elicits a sound called clear^ 
 representing the normal^ pulmonary^ vesicular resonance. This 
 may be impaired by increased density of the pulmonary tissues 
 or of superjacent structures — as in interstitial pneumonitis, in 
 pleural thickening or when the chest-wall is thickened. 
 
 Percussion-dulness is dependent upon a high degree of conden- 
 sation — as in the solidification of pneumonia, or at the late stage 
 of tubercle-formation. 
 
 The sound elicited over solid viscera, as the liver, heart or 
 spleen, or over serous efl'usions — as in hydrothorax or hydro- 
 pericardium, or in ascites, is flat. 
 
 The sound occasioned by air (or gas) in inclosed spaces larger 
 than the alveoli of the noriiial lung may be hyper-resonant or 
 tympanitic— as in vesicular emphysema or over the intestines. 
 
150 ESSENTIALS OF DIAGNOSIS. 
 
 An amphoric or metallic sound is elicited by percussion over 
 large closed cavities, with tense walls, containing air— as a dis- 
 tended stomach or a large vomica in the lungs, 
 
 A cracked-pot or cracked-metal sound is occasioned by per- 
 cussing over a cavity of some size, with a small opening, through 
 which air escapes — as in the case of a pulmonary cavity com- 
 municating with a bronchial tube. 
 
 The percussion-sounds may display alterations in degree or 
 pitchy and in intensity or volume. 
 
 Increased density gives heightened pitch^ — hence a dull sound 
 is higher in pitch than a clear one. The pitch of tympanitic 
 sounds varies. As a rule, it is higher than that of the normal 
 pulmonary resonance. Other things being equal, the greater 
 the volume of matter set in vibration the greater the intensity 
 of the sound. 
 
 By mediate percussion with the fingers a sense of elasticity, 
 or of resistance, can be appreciated. 
 
 Sometimes auscultation is practised by one while a second at 
 the same time practises percussion— so-called anscidtatm-y per- 
 cussion. 
 
 The percussion sounds elicited during full-held inspiration 
 diflFer from those elicited during full expiration — so-called respAra- 
 tory percussion. 
 
 How is auscultation practised? 
 
 Auscultation, like percussion, may be immediate or mediate. 
 In the former, the ear is directly applied to the part to be 
 auscultated ; in the latter, auscultation is performed through 
 the mediation of a stethoscope. Stethoscopes are monaural or 
 binaural. Each has its advantages. The student should 
 become familiar with all of the methods of auscultation. 
 
 What is to be learned by auscultation ? 
 
 Auscultation gives information as to the movement of air and 
 fluids, as to the comparative calibers and lengths of the tubes 
 through which the air passes, and as to the presence in the path 
 of the air-current of matters capable of acting the part of reeds 
 in the production of musical tones. 
 
 Listening to the normal respiratory sounds one hears a soft. 
 
PHYSICAL DIAGNOSIS. 151 
 
 breezy inspiration — the normal vesicular murmur^ followed by a 
 scarcely audible, briefer expiration. 
 
 These sounds may be exaggerated — as they normally are in 
 children ; hence they are then called imerile. 
 
 The respiratory sounds are also intensified in a lung, or in a 
 portion of lung, performing an excess of function— as after 
 violent exercise, or, compensatorily, when the function of the 
 other lung, or of a portion of the same lung, is interfered with ' 
 by condensation or compression. 
 
 The respiratory murmur is enfeebled or wanting when there 
 is an obstruction to the circulation of air in the lung — as in 
 incipient pulmonary tuberculosis, and in occlusion of the air- 
 passages— as by intrathoracic aneurism, or when the air vesicles 
 have lost their elasticity— as in emphysema. 
 
 The respiratory murmur is rendered harsh and is heightened in 
 pitch when the bronchial tubes are thickened, and their caliber 
 is narrowed— as in bronchitis. Under similar conditions, rhonchi 
 or dry rdles may be heurd— sibilant, if generated in the small 
 tubes ; sonorous, if generated in the large tubes. Sometimes the 
 sounds are high-pitched and wheezing. 
 
 If the vesicular murmur is but partially obliterated, the 
 breathing is called vesiculo-bronchial ; or if the bronchial element 
 predominates, broncho-vesicular. When occlusion of the alveoli 
 entirely obliterates the vesicular quality, the breathing is said 
 to be bronchial or tubular or blowing ; these terms respectively 
 indicating progressive encroachment upon the integrity of the 
 smaller air-tubes. In case of a cavity in the lung, the breathing 
 may be cavernous; if the cavity have a tense wall and a small 
 orifice of communication with a bronchus, the sound transmitted 
 to the ear is amphoric. 
 
 The presence of secretion in the bronchial tubes occasions 
 rdles, usually qualified as moist : subcrepitant, if in the smaller 
 tubes, mucous if in the larger. 
 
 The presence of fluid in a vomica may give rise to bubbling 
 or gurgling. 
 
 The separation of the adherent surfaces of pulmonary alveoli 
 lined by viscid secretion, as in pneumonia, gives rise to the 
 crepitant rdle. When isolated softening of pulmonary tubercles 
 
152 ESSENTIALS OF DIAGNOSIS. 
 
 takes place, a sound is generated comparable to that produced 
 when salt is thrown upon fire, or when a few hairs are rubbed 
 together between the fingers — so-called crackling. 
 
 When moist rales are heard through solidified pulmonar}- 
 tissues they are transmitted with a peculiar clearness and with 
 a sort of ringing character. Thej^ are then called consonating. 
 
 In the first stage of pleurisy, before effusion has taken place, 
 and in the third stage, after the fluid poured out has been 
 absorbed, a coarse crackling, or creaking, or rasping sound of 
 pleural /cicf ion may be heard. 
 
 In case of pneumothorax resulting from the perforation of a 
 pulmonary vomica into the pleural cavity, vibration of the fluid 
 that has been effused sometimes gives rise to metallic tinkling. 
 Under similar conditions, or in case of a large vomica contain- 
 ing considerable fluid, vigorous shaking of the patient, with the 
 ear applied to the chest, may elicit the sound of splashing — the 
 so-called Hippocratic succussion sound. 
 
 When the ear is applied to the normal chest of a speaking in- 
 dividual a confused sound is heard — the vocal resonance. 
 
 If fluid is effused into the pleural cavity the transmission of 
 the voice is intercepted below the upper level of the fluid. If 
 the pulmonary tissues are solidified, as in pneumonia and tuber- 
 culosis, the resonance is increased, constituting hronchopJiony. 
 When spoken language and whispers can be distinguished, the 
 phenomena are termed pectoriloquy and whispering pjectoo-iloquy 
 respectively. The latter, if circumscribed, is usually indicative 
 of the existence of a cavity in the lung. 
 
 When, in the course of pleurisy, a small quantity of fluid has 
 been poured out the voice is transmitted above the level of the 
 fluid with a peculiar bleating character, constituting egophony. 
 
 Not only may the character of the breath-sounds be altered, 
 but their rhythm may deviate from the normal. Thus, expiration 
 may be prolonged, as when, as in emphysema, the elasticity of 
 the walls of the alveoli is diminished ; or the expiratory sound 
 may be prolonged or jerking, as when, as in the early stages of 
 pulmonary tuberculosis, there is some obstruction to the exit 
 of air. 
 
ACUTE PLEURISY. 153 
 
 Acute Pleurisy. 
 
 What are the symptoms of acute pleurisy ? 
 
 Acute pleurisy may set in with a chill and shai'p pain in the 
 side, aggravated by the respiratory movements. The dyspnea 
 may be slight or considerable. The teinperature rises moderately 
 high ; the breathing is feeble, shallow and rapid. There is slight 
 irritative cough, and scanty, frothy expectoration. In the course 
 of a few days the symptoms subside, and at the end of a week or 
 ten days the patient ,is well. Acute pleurisy may occur as a 
 jirimary condition. It may follow traumatism or exposure to 
 cold. Quite commonly it is secondary to inflammation of adja- 
 cent structures, especially of the lungs. It also occurs in the 
 course of various infectious diseases of nephritis and of rheuma- 
 tism. Pleurisy may be " dry" or attended with effusion. Effu- 
 sion gives rise to respiratory and circulatory embarrassment 
 proportionate to the volume of fluid poured out. 
 
 The fluid poured out may not be readily absorbed. On the 
 contrary, it may remain obstinately persistent. In the course 
 of time, it may become purulent ; under other circumstances, it 
 is purulent from the outset ; in either case the condition is 
 known as empyema. More commonly, the fluid is absorbed and 
 the two layers of the pleura become adherent, with obliteration 
 of the pleural cavity ; in the progress of the case considerable 
 thickening takes place, followed in turn by retraction of the 
 chest. When the effusion is purulent there are repeated rigors, 
 fever, sweats and emaciation ; otherwise the health may be 
 preserved, unless the chronic pleurisy is tuberculous. By the 
 action of the heart, pulsation may be imparted to a collection 
 of fluid in the left pleural cavity, so that an aneurism, may be 
 simulated. When the collection is purulent, the condition is 
 designated pulsatory emi)yema. 
 
 What are the physical signs of acute pleurisy ? 
 
 For convenience of study, the physical signs of acute pleurisy 
 may be considered in three stages. In the first, or pjlastic stage, 
 as the surfaces of the two layers of the pleura, roughened by 
 exudation, slide over one another in inspiration and expiration, 
 
154 ESSENTIALS OF DIAGNOSIS, 
 
 a harsh, creaking sound is heard, the vibration occasioning 
 which may sometimes also be appreciable on palpation — the 
 so-called friction-sound or nib. The breathing is shallow, feeble 
 and rapid ; the movements of the affected side being restrained 
 in the greater degree in order to mitigate the pain. 
 
 In the second stage, or stage of effusion, serum in variable 
 quantity, possibly mixed with blood, is poured out into the 
 pleural cavity. The corresponding lung is pushed upward and 
 backward, and the heart, liver, spleen and diaphragm may be 
 displaced. One side of the chest appears larger than the other, 
 and the interspaces corresponding to the situation of the 
 effusion are abnormally prominent. The cardiac impulse is 
 visibly displaced. The respiratory excursion is limited. Below 
 the upper level of the fluid the percussion-note is fiat ; above, it 
 is subtympanitic. Through the eflfusion the breath-sounds are 
 heard feebly and indistinctly ; the voice-vibrations are not trans- 
 mitted to the palpating hand ; nor, as a rule, to the auscultating 
 ear, though exceptionally bronchophony may exist. To the ear 
 applied to the chest above the level of the fluid the voice may 
 be transmitted with a peculiar bleating quality — constituting 
 egophony. 
 
 In the thi7'd stage, the eflfusion has been absorbed and the 
 apposed layers of pleura again come in contact. The friction- 
 sound of the first stage returns. Ultimately the pleura may 
 be restored to its original condition or its apposed surfaces 
 may become adherent and thickened, giving rise to retraction 
 of the chest and percussion-dulness. 
 
 How does acute pleurisy differ from croupous pneumonia ? 
 
 Pleurisy usually accompanies pneumonia. The signs of the 
 former, however, should not be permitted to obscure the exist- 
 ence of the latter. Neither the local nor the general symptoms 
 of pleurisy are so profound as those of pneumonia. While 
 pneumonia may then present the symptoms of pleurisy, pleurisy 
 does not present the blood-streaked expectoration, the crepitant 
 rale, the blowing breathing, the deficiency of the chlorides in 
 the urine, or the critical termination of pneumonia. 
 
 The percussion-note of pneumonia is dull ; that of pleurisy, 
 when an effusion exists, is fiat. The dulness of pneumonia is 
 
ACUTE PLEURISY. 155 
 
 usually over a lower lobe ; that of pleurisy is universally at the 
 base. In pleurisy, the breath-sounds are heard feebly, or not 
 at all, througli the effusion ; in pneumonia the breathing is 
 bronchial. Vocal resonance and fremitus are increased in 
 pneumonia ; they are diminished or absent in pleural effusion ; 
 above the fluid, however, a bleating sound is transmitted to the 
 auscultating ear. Simple, uncomplicated pneumonia is un- 
 attended with friction-sounds and occasions no displacement of 
 adjacent viscera. 
 
 How are intercostal neuralgia and acute pleurisy to be dif- 
 ferentiated ? 
 
 The pain of intercostal neuralgia may simulate that of acute 
 pleurisy, and give rise to rapid, shallow, feeble respiratory 
 movements. Intercostal neuralgia is paroxysmal and unat- 
 tended with friction-sound, dulness on percussion or fever ; 
 it occurs in anemic individuals with neurotic tendencies, and 
 may be attended with a unilateral herpetic eruption in the 
 course of the nerve affected. In addition there are a number of 
 tender points. 
 
 How are a pleuritic effusion and an hydatid cyst of the liver 
 to be differentiated ? 
 When an hydatid cyst of the liver attains proportions suf- 
 ficient to give rise to definite physical phenomena, these will 
 appear in a region beyond that in which the signs of a pleuritic 
 effusion on the right side are found. The history of an acute 
 attack is wanting, while it is present in pleuritic effusion. 
 Neither in case of pleuritic effusion, nor in case of hydatid of 
 the liver, is the percussion-dulness confined to the right hypo- 
 chondrium ; in the one it extends rather upwards, in the other 
 downwards ; in the latter it is associated with fluctuation. In 
 a case of hydatid cyst it may by percussion be possible to elicit 
 the characteristic thrill or fremitus. In a case of pleuritic 
 effusion the breath-sounds and the vibrations of the voice are 
 feebly transmitted ; breath-sounds, vocal resonance, and fremitus 
 are unaltered in hydatid cyst of the liver. Egophony is char- 
 acteristic of the presence of fluid in the pleura ; it is thus 
 not present in case of hydatid cyst of the liver. Exploratory 
 
156 ESSENTIALS OF DIAGNOSIS. 
 
 puncture may determine the presence of hydatid hooklets, the 
 detection of which places the diagnosis beyond doubt. 
 
 How are a pleuritic effusion and abscess of the liver to be differ- 
 entiated ? 
 Symptoms of respiratory interference are naturally less con- 
 spicuous in case of abscess of the liver than in case of pleuritic 
 effusion. Hepatic abscess may occasion tumefaction in the 
 right hypochondrium ; pleural effusion renders the chest asym- 
 metrical from unilateral bulging. Pleuritic effusion impairs 
 the transmission of the breath-sounds and of the vibrations of the 
 voice, which is unaltered by an hepatic abscess. Egophony may 
 be elicited in case of pleuritic effusion, but not in case of hepatic 
 abscess. Rigors commonly attend an abscess of the liver ; they 
 only take place in cases of pleuritic effusion when suppuration 
 has occurred. In case of hepatic abscess, there is usuall}-^ a 
 history of gallstone, of ulceration of the bowel or of pyemia ; 
 in case of pleuritic effusion, there is a history of an acute attack 
 of pleurisy. Hepatic abscess and perihepatitis may, however, 
 give rise to pleural effusion by extension. 
 
 How are pleuritic effusion and abscess of the spleen to be differ- 
 entiated ? 
 
 Abscess of the spleen is most common as a manifestation of py- 
 emia ; pleuritic effusion is a sequel of an acute pleurisy. The 
 symptoms of respiratory derangement, a necessary part of pleu- 
 ritic effusion, are subordinate in case of splenic abscess. Re- 
 peated rigors occur in abscess of the spleen ; rigors occur 
 in case of empyema, but not when the effusion is not purulent. 
 Egophony may be developed when fluid is present in the pleu- 
 ral cavity, but not in case of splenic abscess. 
 
 How is an intra-thoracic tumor to be distinguished from 
 chronic pleurisy ? 
 Tumors in the chest may arise from the pleura or from the 
 lung ; they may develop in the mediastinum ; or they may 
 be aneurismal. Malignant tumors are secondary to growths 
 elsewhere — an element in diagnosis. They give rise to circum- 
 scribed areas of dulness on percussion, not necessarily limited 
 to one side ; to enfeebled breathing and perhaps friction-sounds ; 
 
ACUTE BRONCHITIS. 167 
 
 in their physical signs, tliey more closely resemble encysted 
 pleurisy than ordinary chronic pleurisy. When actually com- 
 plicated by pleurisy, the diagnosis may not be possible. Aneu- 
 risms occur in the course of the aorta and large vessels, and, in 
 addition to the evidences of tumor, are accompanied by thrill, 
 bruit and pulsation. 
 
 How are a pleuritic effusion and hydrothorax to be differ- 
 entiated ? 
 
 Hydrothorax occurs as a result of cardiac insufficiency or as a 
 part of a general dropsy, from nephritis for instance. 
 
 In contradistinction from pleuritic effusion, the effusion of hy- 
 drothorax is bilateral. In the former there has been an antece- 
 dent pleurisy ; in the latter there are other evidences of cardiac 
 failure or of a general dropsy. 
 
 How is a pericardial effusion to be distinguished from a pleural 
 effusion ? 
 
 A pericardial effiision occurs under circumstances similar to 
 those that give rise to a pleural effusion— as a result of in- 
 flammation or as a part of a general dropsy. The position and 
 outline of the percussion-dulness to which a pericardial efiusion 
 gives rise, however, are entirely different from what is found in 
 a case of pleural effusion ; nor are the breath-sounds notably in- 
 terfered with, while the circulation is embarrassed and the 
 heart-sounds are almost obliterated at the cardiac apex. 
 
 Acute Bronchitis. 
 
 What are the symptoms of acute bronchitis ? 
 
 Acute bronchitis results from exposure to cold, the inhalation 
 of irritating fumes, or as a secondary disorder in the course of 
 fevers, rheumatism or heart-disease. There is irritative cough, 
 and, at fii-st, scanty mucous expectoration, which subsequently 
 becomes more copious and muco-purulent ; slight elevation of 
 temperature ; increased frequency of respiration ; some dyspnea ; 
 retro-sternal pain, and mild constitutional symptoms. 
 
 What are the physical signs of acute bronchitis ? 
 
 The chest is not deformed and expands well. The percussion- 
 resonance is vesicular. The breathing is harsh at first ; dry rales, 
 
158 ESSENTIALS OF DIAGNOSIS. 
 
 sonorous and sibilant, are heard ; subsequently large and small 
 moist rales. Vocal resonance and fremitus are not perceptibly 
 altered. 
 
 How does acute bronchitis differ from acute miliary tubercu- 
 losis ? 
 In acute miliary tuberculosis the dyspnea is greater, the tem- 
 perature is higher, with greater oscillations, the breathing is 
 more rapid, and the symptoms are more profound than in acute 
 bronchitis. The further progress of the case clears up any pos- 
 sible doubt. Recovery from acute bronchitis is the invariable 
 rule. Pulmonary consolidation aud softening, percussion-dul- 
 ness and fine moist rales, emaciation, hectic fever, gradual fail- 
 ure of the vital powers and ultimately death mark the usual 
 course of acute miliary tuberculosis. 
 
 Chronic Bronchitis. 
 
 What are the symptoms of chronic bronchitis ? 
 
 Chronic hronchitis is usually a result of repeated attacks of 
 acute bronchitis ; it may manifest itself as a special suscepti- 
 bility to acute bronchitis ; at first it appears as a winter cough, 
 subsequently becoming continuous. It may obstinately resist 
 treatment ; it is attended with a good deal of cough, copious 
 muco-purulent expectoration, marked shortness of breath, and 
 may in time give rise to emphysema, or to bronchiectasis. It is 
 often attended with loss of flesh and strength. 
 
 What are the physical signs of chronic bronchitis ? 
 
 If emphysema coexists the chest may be enlarged ; otherwise 
 it is not abnormal in size or form ; the respirato^-y excursion is 
 somewhat diminished ; the percussion-resonance is little or not 
 at all impaired ; the hreaihing is harsh and may be feeble, the 
 bronchial element preponderating. Coarse rales, moist and 
 dry, are heard at all parts of the chest. Vocal fremitus and 
 resonatice are rather increased. 
 
PLASTIC BRONCHITIS — PUTRID BRONCHITIS. 159 
 
 How is chronic bronchitis to be distinguished from interstitial 
 pneumonitis ? 
 
 A certain degree of bronchitis commonly attends interstitial 
 pneumonitis ; but the chest is likely to undergo retraction, which 
 is not the case in bronchitis. If impairment of resonance attend 
 chronic bronchitis, it is general and not well defined, while the 
 dulness of interstitial pneumonitis is the more circumscribed 
 and the more decided. 
 
 How does chronic bronchitis differ from pulmonary tuber- 
 culosis ? 
 
 While chronic bronchitis may be attended with obstinate 
 cough, muco-purulent, sometimes blood-streaked, expectoration, 
 loss of flesh and strength, the physical signs are general in their 
 distribution and not localized as in tuberculosis. The impair- 
 ment of resonance is not so great in chronic bronchitis as it is in 
 tuberculosis. The elevation of temperature observed in tuber- 
 culosis is wanting in bronchitis. Tubercle-bacilli are not found 
 in the sputum of cases of simple chronic bronchitis. 
 
 Plastic Bronchitis — Fibrinous Bronchitis, 
 
 "What are the characteristics of plastic or fibrinous bronchitis ? 
 
 In addition to the phenomena of ordinary broncliitis, there 
 are present in plastic bronchitis decided dyspnea and cyanosis, 
 together with the expectoration of tough, fibrinous casts of the 
 smaller bronchial tubes ; there occur lancinating pains in the 
 chest-, and there may be bleeding from the nose and mouth. 
 
 Putrid Bronchitis. 
 
 What are the clinical features of putrid bronchitis ? 
 
 In case of bronchitis with bronchial dilatation, accumulation 
 of secretion may take place, with ulceration and inflammation 
 of the bronchial mucous membrane, as a consequence of which 
 expectoration is augmented, the breath and sputa possessing an 
 offensive, fetid odor. To these phenomena fever and a typhoid 
 condition may be added— and even pulmonary gangrene may 
 supervene. 
 
160 ESSENTIALS OF DIAGNOSIS, 
 
 Bronchiectasis^ 
 
 What is bronchiectasis'? 
 
 Bronchiectasis consists in a cylindrical or saccular dilatation 
 of the bronchial tubes, usually developed in the course of some 
 condition attended with powerful or sustained expiratory' 
 efforts— such as chronic bronchitis. It may also result from 
 contraction of the peribronchial tissues. In addition to the 
 symptoms of the causative aftection, the characteristic feature 
 of bronchiectasis is the periodical occurrence of jDaroxysms of 
 cough, attended with the expectoration of large quantities of 
 muco-purulent secretion of ofi'ensive odor. The tubes filled with 
 fluid may give rise in small areas of irregular distribution to 
 l^ercussion-dulness that disappears with the evacuation of the 
 fluid. On auscultation large, coarse, moist rales and gurgling 
 may be heard. If of moderately large size, bronchiectatic cavi- 
 ties may yield a hyper-resonant percussion-note, with blowing 
 breathing and whispering pectoriloquy. 
 
 How does bronchiectasis differ from pulmonary gangrene? 
 
 The grave constitutional symptoms of gangrene are lacking 
 in bronchiectasis. The expectoration of both is offensive, but 
 that in gangrene is actualh' fetid. The sputum of gangrene 
 contains shreds of pulmonary structure ; that of bronchiectasis 
 does not. 
 
 How does bronchiectasis differ from pulmonary abscess ? 
 
 A sacculated dilatation of a bronchial tube containing fluid 
 fulfils the physical conditions of an abscess communicating with 
 a bronchial tube. The expectoration of a case of bronchial dila- 
 tation, however, has an offensive odor not present in abscess. 
 The fever and sweats of abscess are wanting in bronchiectasis. 
 
 How are bronchiectasis and catarrhal pneumonia to be differ- 
 entiated ? 
 
 In the small areas of dulness of irregular distribution, bron- 
 chiectasis may simulate catarrhal pneumonia, but the former is 
 wanting in the febrile phenomena and the constitutional depres- 
 sion of the latter disease. The association of bronchiectasis with 
 
CAPILLARY BRONCHITIS, 161 
 
 chronic bronchitis is different from the occurrence of catarrhal 
 pneumonia in children. The ofleusive sputa of the former are 
 entirely wanting in the latter. 
 
 Capillary Bronchitis. 
 
 What are the symptoms of capillary bronchitis ? 
 
 Capillary bronchitis, sometimes called suffocative catarrh, is an 
 inflammation of the smallest or '' capillary" bronchi, most com- 
 mon in children and in old persons, and usually secondary to 
 bronchitis of the larger tubes. In addition to the symptoms 
 of the latter affection, capillary bronchitis is attended with de- 
 cided constitutional depression ; the dyspnea is more profound, 
 and cyanosis may be marked. 
 
 Cough is severe, while expectoration is scanty ; the pulse is 
 rapid, the respirations hurried, the countenance discolored, the 
 expression anxious ; fever is moderately high. 
 
 What are the physical signs of capillary bronchitis? 
 
 The chest is symmetrical. The breathing is rapid and shallow. 
 The percussion-resonance is vesicular, though in spots it may be 
 slightly impaired. When it exists, the impairment of resonance 
 does not depend upon exudation, but upon atelectasis. The 
 phenomenon may, therefore, be inconstant, and its location 
 shifting. The breath-sounds are harsh, and in many places in 
 both lungs small, mucous rales may be heard. 
 
 Vocal resonance and /remitws are slightly increased. The de- 
 viations from the normal are most marked at the bases of the 
 lungs posteriorly. 
 
 How are capillary bronchitis and acute miliary tuberculosis 
 to be differentiated ? 
 
 Capillary bronchitis is a quite brief disease of the very young 
 and the very old ; acute miliary tuberculosis is a more prolonged 
 disease of the young and of adults. Dyspnea, cyanosis and 
 constitutional depression are earlv more decided in capillary 
 bronchitis than in acute miliary tuberculosis. The fever of 
 tuberculosis is more intense and vacillating than that of bron- 
 chitis. Localized areas of persistent percussion-dulness, followed 
 11 
 
162 ESSENTIALS OF DIAGNOSIS. 
 
 by the moist rales of softening, may develop in the course of 
 acute miliary tuberculosis, which is progressively fatal ; recovery 
 from capillary bronchitis is not uncommon. 
 
 Catarrhal Pneumonia — Broncho-pneumonia. 
 
 What are the symptoms of catarrhal pneumonia ? 
 
 Catarrhal pyieimionia, also called lobular pneumonia, or brmicJw- 
 pneumonilis, may be apparently primar}-, but is often secondary 
 to capillary bronchitis, as also to measles, influenza and other 
 constitutional affections ; it ma}' result from the inspiration of 
 infectious material, whether contained in the food or from 
 septic surfaces in the respiratory tract. 
 
 It is attended with cough, muco-purulent expectoration, in- 
 creased frequency of respiration, decided febrile phenomena that 
 may be hectic, and constitutional depression. The course of the 
 disease may be protracted. 
 
 What are the physical signs of catarrhal pneumonia ? 
 
 The chest is symmetrical ; respiration is shallow. 
 The range of movement is sometimes curtailed on one side. 
 Small, irregularly distributed patches of jjera<,ssio»-d«Z>ie5S 
 may be found here and there over both sides of the chest, an- 
 teriorly and posteriorly ; the hreathirtg is harsh ; fine and large 
 moist rales may be heard ; the vocal resonance and fremitus ai'e 
 intensified in patches corresponding, as a rule, to the areas of 
 percussion-dulness. 
 
 How does catarrhal pneumonia differ from capillary bron- 
 chitis? 
 The gravity of the symptoms in both depends upon the extent 
 of the disease. Other things being equal, capillary bronchitis 
 is the more acutely dangerous affection, the depression some- 
 times being profound. The duration of catarrhal pneumonia is 
 the longer. Its febrile phenomena are the more decided, and 
 its temperature-range is marked by great oscillations. The 
 impairment of percussion-resonance is more decided in catar- 
 rhal pneumonia than in capillary bronchitis ; it is constant, and 
 does not change its seat. 
 
ACUTE CROUPOUS PNEUMONIA. 163 
 
 What are the means of distinguishing atelectasis from catar- 
 rhal pneumonia? 
 
 Atelectasis is the pre-natal condition of the lungs, before they 
 have been inflated with air. It uia}' also arise in the course of 
 affections attended with inspiratory obstruction of the bronchial 
 tubes, as in whooping-cough or capillary bronchitis, for instance, 
 a plug of mucus acting as a ball-valve, allowing the expiration 
 of air but preventing inspiration. It is said also to occur in 
 parts of the lung functionally inactive. The condition is not 
 an inflammatory one and is not necessarily attended with eleva- 
 tion of temperature, as is catarrhal pneumonia. The collapse 
 is not persistent, but may successively involve diflerent parts of 
 the lung ; so that the physical signs are not constant, but tran- 
 sitory as well as migratory. 
 
 How does catarrhal pneumonia differ from pulmonary infarc- 
 tion? 
 
 Catarrhal pneumonia does not set in with the acuteness and 
 the severe pain of pulmonary infarction ; nor is the expectora- 
 tion as persistently blood-streaked in the former as in the latter. 
 Catarrhal pneumonia is attended with decided febrile manifes- 
 tations and is of considerable duration, while pulmonary infarc- 
 tion scarcely occasions fever and its symptoms soon subside. 
 The detection of a source of an embolus would be strongly in 
 favor of the existence of infarction. 
 
 Acute Croupous Pneumonia. 
 
 What are the symptoms of croupous pneumonia? 
 
 Croupous pneumonia, also called Johar pneumonia^ and at one 
 time lung fever, is an acute, infectious disease dependent upon 
 the invasion of microorganisms (Fig. 22), often following ex- 
 posure to cold, settinij in suddenly with a chill, sometimes with 
 convulsions, the temperature rising at once to 103° or 104° P., the 
 respiratory frequency reaching 35, 40, 50 or more, M^iile the jjwfee 
 is not proportionately accelerated. 
 
 There is at first slight cough, with scanty expectoration of a 
 viscid sputum, which soon becomes blood-streaked (rusty). 
 
164 ESSENTIALS OF DIAGNOSIS. 
 
 There is considerable dyspnea ; the alee nasi are retracted in 
 breathing ; and one or both cheeks are flushed. 
 
 The cough increases ; the expectoration becomes more free, 
 more hemorrhagic, less viscid, and presents the appearance of 
 prune-juice. There is pain in the chest, often referred to the 
 nipple of the affected side ; usually Involving the lateral or axil- 
 lary region in addition. The pain is increased on attempting to 
 make prolonged inspiration. The lijjs and cheeks may be cya- 
 
 FiG. 22. 
 
 M 
 
 Micrococci of croupous pneumonia. (Yierordt.) 
 
 notic. The tongue, is coated ; the cqypetite is lost ; thirst is in- 
 creased ; there may be jaundice, and, at the height of the attack, 
 delirium. 
 
 Between the second and fifth daA's, herpes of the lips may 
 appear. The symptoms continue for from five to seven or nine 
 days, to subside by cmis. Profuse perspiration occurs ; the 
 temperature declines ; and convalescence sets in. 
 
 The cough is still free ; the expectoration copious and muco- 
 purulent. During the attack the urine is deficient or wanting 
 in chlorides, which return as resolution proceeds. Resolution 
 may fail to take place, or it may be but partial ; so that suppura- 
 tion may ensue or chronic induration be a sequel. Death hap- 
 pens in a variable proportion of cases, not rarely from heart- 
 clot or heart-failui'e. 
 
 Pleurisy is a common accompaniment of pneumonia. Occa- 
 sionally large effusions are poured into the pleural cavity. 
 
ACUTE CROUPOUS PNEUMONIA. 165 
 
 What are the physical signs of croupous pneumonia? 
 
 For convenience of description, pneumonia is divided into 
 three stages : a stage of congestion, a stage of exudation, a stage 
 of resolution. 
 
 What are the physical signs of the first stage of pneumonia, 
 or the stage of congestion ? 
 
 The aspect of the chest is unchanged. 
 
 The breathing is accelerated, becoming shallovsr and labored. 
 
 The percussion-resonance is little or not at all impaired. 
 
 The respiratory murmur is roughened over a cii'cumscribed 
 area, usually corresponding to a low^er lobe. At the end of in- 
 spiration a fine, moist, crepitating rale may be heard. 
 
 Vocal resonance and fremitus are not perceptibly altered. 
 
 What are the physical signs of the second stage of pneumonia, 
 or the stage of exudation ? 
 
 The respiratory excursion is curtailed ; the breathing is hurried. 
 
 The lower part of the chest on one side, corresponding to the 
 lower lobe of the lung, may be a little fuller than elsewhere. 
 Here the percussion-note is dull. Above, the note is hyper-reso- 
 nant. 
 
 At the dull area, the breathing is bronchial in character. At 
 other parts of the chest the breathing is puerile. The crepitant 
 rale has disappeared. 
 
 Vocal resonance and fremitus are increased at the area of per- 
 cussion-dulness. A pleuritic friction-sound may be heard and 
 the signs of effusion may develop. 
 
 What are the physical signs of the third stage of pneumonia, or 
 the stage of resolution ? 
 
 The localized fulness of the chest may remain. 
 
 The respiratory excursion and the expansion have somewhat 
 augmented. 
 
 Some degree of impairment of the percussion-resonance persists. 
 
 The breathing is yet bronchial, though not in the same degree 
 as it was. The crepitant rale, which for a time had disappeared, 
 can again be heard — the crepitus redux; other moist rales also 
 now become discernible. 
 
 Vocal resonance and fremitus are still increased. 
 
166 ESSENTIALS OF DIAGNOSIS. 
 
 How is edema of the lungs to be distinguished from pneu- 
 monia ? 
 
 Pulmonary edema may develop in the course of heart-disease, 
 if the compensation be disturbed ; in the course of nephritis or in 
 the course of general asthenia ; in subjects of these affections, 
 it may follow exposure. It is not confined to one lung, hut 
 involves both alike throughout their entire extent. 
 
 Pulmonary edema may be uiTcomplicated, but is likely to be 
 associated with eifusions into the serous cavities and dropsy 
 elsewhere. The sputum is frothy and abundant, but not rusty 
 or like prune-juice. The cheeks are flushed in pneumonia; 
 the face is pale or livid in pulmonary edema. Edema usually 
 does not present febrile symptoms ; the percussion-resonance 
 scarcely suffers ; large and small moist rales are heard all over 
 the chest ; the proportion of chlorides in the urine remains un- 
 altered ; while the brief duration of the condition, speedily 
 terminating, as it does, in recovery or in death, and the knowl- 
 ledge of the existence of a condition that may occasion it, make 
 the diagnosis clear. 
 
 In what respects do catarrhal and croupous pneumonia differ ? 
 
 Croupous pneumonia is sudden in onset ; catarrhal pneu- 
 monia is rather commonly secondary to some other condition. 
 Lobar pneumonia usually attacks robust adults ; broncho-pneu- 
 monia, children, the aged, the debilitated. The sputum of 
 catarrhal pneumonia is not blood-streaked, as is that of croupous 
 pneumonia. Croupous pneumonia terminates in the course of 
 seven or nine days by crisis ; catarrhal pneumonia is a disease 
 of long duration, with tardy convalescence. The physical signs 
 of croupous pneumonia are well-defined, usually limited to one 
 lung and to a lower lobe ; the signs of catarrhal pneumonia are 
 ill-defined, and irregularly disseminated. 
 
 How is passive or hypostatic congestion of the lungs to be 
 distinguished from pneumonia? 
 
 Passive or hypostatic congestion of the lungs may develop in 
 the course of acute or chronic debilitating diseases or as a re- 
 sult of heart-disease ; it usually affects the bases and most de- 
 pendent portions of the lungs. It is attended with increased 
 
ACUTE CROUPOUS PNEUMONIA. 167 
 
 frequency of breatliing, impaired percussion-resonance, and the 
 presence of fine rales. It differs from pneumonia in its associa- 
 tion with the conditions that give rise to it ; in the absence of 
 fever, unless arising in the course of a febrile disorder ; in its 
 bilateral distribution ; in theabsenceofblow^ing breathing ; in its 
 course and in its submission to appropriate management. If ex- 
 pectoration attend congestion of the lungs it is not hemorrhagic. 
 
 How is pulmonary infarction to be distinguished from pneu- 
 monia ? 
 
 Coagulation of the circulating blood may take place in the 
 right side of the heart as a result of increased coagulability or 
 of retarded circulation, or a thrombus may form in a distant 
 vein, and detached fragments of clot be swept into the lungs. 
 The occurrence is attended with pain in the chest, dyspnea, and 
 blood-streaked expectoration. Small areas of dulness on per- 
 cussion can be detected, with enfeebled or bronchial breathing. 
 There may be slight fever, from secondary inflammation. The 
 condition differs from pneumonia in being secondary to a pre- 
 existent condition, in the circumscribed distribution of the 
 physical phenomena on the part of the lungs, in the comparative 
 absence of fever, and in the course of the disease. Pulmonary 
 infarction is not of itself fatal. The danger is from the condition 
 of which the infarction is but one result. 
 
 How is pulmonary infarction to be distinguished from pul- 
 monary abscess ? 
 Pulmonary embolism may result in either infarction or ab- 
 scess. The outcome depends upon the presence or absence 
 of pyogenic microorganisms. The immediate phenomena are 
 the same in both instances. If suppuration take place, how- 
 ever, there are repeated chills, decided fever, with purulent 
 expectoration. Pulmonary abscess is obviously the graver con- 
 dition. The existence of disseminated suppuration is an aid in 
 the diagnosis. 
 
 How is pneumonia to be discriminated from pulmonary tuber- 
 culosis ? 
 
 Pneumonia is an acute disease, terminating by crisis in from 
 five to nine days ; the tendency of pulmonary tuberculosis is to 
 
168 ESSENTIALS OF DIAGNOSIS. 
 
 be chronic ; its duration is indefinite. Tlie sputum of pneu- 
 monia ma}^ be profuse!}' admixed with blood, but actual 
 hemorrhage does not occur except in the peculiar form of pneu- 
 monia associated with influenza. The emaciation, the anemia, 
 the sweats of pulmonary tuberculosis are not present in uncom- 
 plicated croupous pneumonia. The temperature of tuberculosis 
 commonly displays wide variations ; the temperature of pneu- 
 monia is of a continued type. Tuberculosis usually involves the 
 upper portion of the lung, successively invading the remainder 
 of the lung, and the opposite lung as well ; pneumonia is 
 usually unilateral and situated in a lower lobe. The physical 
 signs differ in accordance with this peculiarit}- of distribution. 
 It is not uncommon for pneumonia to be superadded to pul- 
 monary tuberculosis. 
 
 Pulmonary Gangrene. 
 
 What are the clinical features of pulmonary gangrene ? 
 
 Gangrene of the lung may result in the course of pulmonary 
 tuberculosis, or of pneumonia ; it may depend upon ulcerative 
 communication of the lung with an adjacent septic process ; it 
 may be occasioned by the inspiration of septic matters from 
 some portion of the respirator}- tract ; finally it may have its 
 origin in a septic embolus. The sj'mptom characteristic of 
 pulmonary gangrene is the expectoration of a horribl}- offensive, 
 stinking sputum, in association with a typhoid condition. Un- 
 less cavitation occurs, the physical signs are obscure ; at best, 
 they may be masked by those of the primary condition. 
 
 How is pulmonary gangrene to be distinguished from pulmo- 
 nary abscess ? 
 The physical signs and the local phenomena of pulmonary 
 gangrene and of pulmonary abscess may be similar ; but tbe ex- 
 pectoration in a case of abscess is copious and purulent, while 
 that of a case of gangrene is brownish and horribly offensive and 
 more likely to contain fragments of pulmonary structure. The 
 signs of a cavity are more likely to attend abscess than to attend 
 gangrene. Gangrene is more nearl}- certain than abscess to be 
 fatal 
 
PULMONARY TUBERCULOSIS. 169 
 
 How are pulmonary tuberculosis and pulmonary gangrene to 
 be differentiated ? 
 
 Gangrene may complicate tuberculosis of the lung. It differs 
 from uncomplicated tuberculosis by the characteristic odor of 
 the breath and sputum and the absence of tubercle-bacilli from 
 the matters expectorated. 
 
 Pulmonary Tuberculosis. 
 
 What are the varieties of pulmonary tuberculosis ? 
 
 In the present state of knowledge pulmonary tuberculosis 
 may, for practical purposes, be considered under two forms : 
 confluent and disseminated. The lesion in both is essentially the 
 same, the process in the one instance having a tendency to 
 localization and chronicity, with slow extension ; in the other to 
 diffusion and acuteness. The first is commonly known as pulmo- 
 nary phthisis, the second as acute miliary tuberculosis. Acute 
 miliary tuberculosis most frequently involves several organs 
 from the first, and is comparable, in many respects, to an acute 
 infectious fever, such as one of the exanthemata. Localized 
 tuberculosis may undergo retrogression and cicatrization by 
 fibroid substitution, sometimes associated with calcareous de- 
 posits. On the other hand, it may terminate by softening 
 (cheesy necrosis or caseation) leading to excavation, or the 
 formation of vomicee. Calcification, however, may occur, even 
 after caseation has taken place. 
 
 Galloping consumption or florid phthisis is either an extremely 
 rapid form of confluent tuberculosis, or a rapidly caseating sub- 
 acute or chronic broncho-pneumonitis, on which tuberculosis 
 has supervened. 
 
 Fibroid phthisis is a slow, localized tuberculosis in which cica- 
 trization keeps almost even pace with tuberculous ulceration. 
 
 The fibroid conditions of the lungs found in miners, in steel- 
 grinders, and in others exposed to the inhalation of fine parti- 
 cles of dust, will be considered as forms of interstitial pneumo- 
 nitis, comparable to interstitial hepatitis and interstitial ne- 
 phritis. Tuberculosis may supervene, running then the ordi- 
 narjr course. 
 
170 ESSENTIALS OF DIAGNOSIS. 
 
 What are the symptoms of pulmonary tuberculosis ? 
 
 The course of ordinary chronic pulmonary tuberculosis may 
 pathologically be divided into three stages : a first or incipient 
 stage, in which the formation of tubercles begins ; isolated, mili- 
 ary nodules are localized at some part of the lung, most com- 
 monly at an apex ; a second stage, of cmtsolidcition, in which the 
 formation of tubercles has increased in number and density, but 
 not correspondingly in extent, the tendency to localization con- 
 tinuing ; and a third stage, of softening, in which, as a result of 
 caseation and breaking down of the older tuberculous forma- 
 tions, cavities develop ; while at the same time invasion of new 
 areas takes place. 
 
 The p^iysical signs in the different stages differ in accordance 
 with the lesions. The symptoms of one stage, however, pass by 
 imperceptible gradations into those of another. 
 
 The on^et of the disease is usually insidious. The individual 
 complains of a sense of lassitude and of an unusual readiness of 
 fatigue. Exertion induces shortness of breath. There is a 
 gradual failure of nutrition. The color fades ; the digestion is 
 deranged. Perhaps now a slight, irritating cough, attended 
 with little or no expectoration, sets in. Sometimes, however, the 
 first symptoms are observed after a neglected " cold," or super- 
 vene upon an attack of catarrhal pneumonia (so-called caseous 
 phthisis). An occasional sense of chilliness in the back may be 
 perceived. The body-weight diminishes. Perhaps at this time, 
 unprovoked, the patient feels a tickling in the throat, perceives 
 a salty taste, and before he realizes what is about to transpire 
 he ejects a mouthful of bright-red, frothy blood. The hemor- 
 rhage may be repeated ; at this stage it is not likely to be fatal. 
 The cough becomes more aggravated ; it occurs in paroxysms, 
 the severity of which may induce vomiting. The simtum is 
 abundant and muco-purulent ; it contains elastic fibers and 
 tubercle-bacilli. The dyspnea has become decided. Emacia- 
 tion progresses ; evening fever appears ; debilitating night- 
 sweats occur. Hemorrhages "become more common and more 
 profuse. The cheek is flushed, the eye bright, the intelligence 
 quickened, the mind hopeful. The hair becomes straiglit and 
 prematurely gray. Digestion fails. Diarrhea becomes trouble- 
 
PULMONARY TUBERCULOSIS. 171 
 
 some. Atrocious pains in various parts of the cliest indicate the 
 existence of accompanying pleuritic processes. The ends of the 
 fingers become enlarged and bulbous, the nails incurvated. The 
 anemia is profound ; the lower extremities become edematous. 
 The patient must take to his bed. In the last stages of the 
 disease, the patient may suddenly be seized with agonizing pain 
 in the side, increased dyspnea, and a sense of impending death. 
 One side of the chest becomes enlarged ; the percussion-reso- 
 nance is tympanitic ; the breathing is but feebly transmitted ; 
 and metallic tinkling may be developed. Pneumothorax has oc- 
 curred. 
 
 Death ultimately results from exhaustion, and is frequently 
 preceded by the supervention of disseminated tuberculosis, 
 giving rise to the febrile and toxemic symptoms of that condition. 
 Occasionally a large hemorrhage brings about a fatal issue by 
 suffocation, from inspiration of a portion of the fluid. 
 
 Pulmonary tuberculosis is not rarely complicated by or asso- 
 ciated with other tuberculous afi'ections, especially laryngeal 
 tuberculosis and intestinal tuberculosis, the symptoms of which 
 are then superadded. 
 
 What are the physical signs of the first stage of pulmonary 
 tuberculosis ? 
 
 The chest may be full and symmetrical. The respiratory excur- 
 sion may be sufficient ; perhaps, by standing behind the patient 
 and placing the hands on the front of his chest, a slight defi- 
 ciency of expansion at an apex may be detected. The percus- 
 sion-resonance is vesicular, except over a small area at the upper- 
 most portion of one lung, where there is slight relative 
 impairment. At this point, too, the vesicular murmur is 
 altered. The inspiratory murmur is less soft and breezy than 
 normal, while expiration is prolonged and heard more distinctly 
 than usual ; or inspiration is jerking and arhythmical. Careful 
 auscultation by an acute observer may detect fine moist rales at 
 the end of inspiration. Vocal resonance send fremitus are slightly 
 increased. If there is any expectoration, careful search may 
 detect a small number of tubercle-bacilli in the sputum. 
 
172 ESSENTIALS OF DIAGNOSIS. 
 
 What are the physical signs of the second stage of pulmonary 
 tuberculosis ? 
 
 The respiratory frequency is slightly accelerated. The upper 
 part of the chest is less full on one side than on the other, and 
 the expansion in this area is deficient. The resonance here is 
 impaired ; the percussion-note may be dull. The vesicular ele- 
 ment of the respiratory murmur is wanting. Inspiration is 
 harsh ; expiration is prolonged and blowing ; the breathing may 
 be bronchial. Fine crackling sounds are heard. Vocal reso- 
 nance and fremitus are notably increased. Blowing sounds may 
 be heard on stethoscopic auscultation over the subclavian ves- 
 sels. The sputum contains many bacilli. 
 
 What are the physical signs of the third stage of pulmonary 
 tuberculosis ? 
 
 The general emaciation is striking. Decided depressions exist 
 above and below the clavicle, on one or on both sides. The 
 ribs are prominent, the interspaces narrowed. The cliest appears 
 rigid ; it may heave, but it scarcely expands in respiration. 
 The percussion-dulness is marked, perhaps in different degree 
 over the upper lobes of the two sides. Here and there, in irreg- 
 ular areas, are heard the dull sounds of a thickened pleura. In 
 the midst of the dulness a tympanitic or amphoric or cracked-jjot 
 sound is elicited. Coarse and fine rales, gurgling, bronchial or 
 cavernous breathing are heard. Bronchophon}^ or whispering 
 pectoriloquy are present. Tactile fremitus is increased. The 
 sputum contains bacilli and elastic fibers. 
 
 What are the best methods for detecting the presence of 
 tubercle-bacilli in sputum ? 
 
 In all bacteriologic investigations, the instruments and 
 appliances used must be rigidly sterile. Sputa for examination 
 should be collected in glass or poi'celain vessels that have been 
 made clean by boiling, and finally washed with a 1 : 1000 solu- 
 tion of mercuric chloride. The examination should not be too- 
 long deferred. In the interval the vessel should be covered. 
 
 The sputum should be poured from its receptacle on a steril- 
 ized plate of glass having a black background. With a plati- 
 num wire, first heated to redness in the flame of a lamp or 
 
PULMONARY TUBERCULOSIS. 173 
 
 Bunsen burner and permitted to cool, a small quantity of 
 purulent matter is taken up and spread in a thin layer upon a 
 cover-glass that has been washed with alcohol, ether, and bi- 
 chloride solution and carefully wiped dry. The thin layer of 
 sputum is permitted to dry at ordinary temperature, or the pro- 
 cess is accelerated by gentle heat. When perfectly dry, the 
 cover-glass preparation is drawn three or four times through the 
 flame so as to fix the albuminoid matters. 
 
 The preparation is now ready to be stained. For the staining, 
 a filtered solution composed of one part of fuchsin (or gentian 
 violet) , four of carbolic acid, ten of alcohol and one hundred of 
 sterihzed distilled water, may be used ; or ten or fifteen drops 
 of anilin oil and about a dram of sterilized distilled water are 
 shaken together and filtered, and then sufficient of a saturated 
 alcoholic solution of gentian-violet (or fuchsin) addded until a 
 deep coloration is produced. 
 
 The cover-glass preparation may now be floated on the sur- 
 face of one of the solutions indicated, for twenty-four hours, at 
 the ordinary temperature, or the process may be accomplished in 
 
 Fig. 23, 
 
 M- 
 
 Tubercle-bacilli in sputum. (Ziegler.) 
 
 fifteen minutes by the application of moderate heat until the 
 vapor of steam arises ; or face upward, a few drops of either of 
 the solutions indicated are placed upon the surface of the cover- 
 glass preparation, which is gently heated until the vapors of 
 steam arise. 
 
174 ESSENTIALS OF DIAGNOSIS 
 
 The excess of free stain is removed with water. The prep- 
 aration is decolorized iu a solution of nitric acid (1 : 3), or in 
 one of sulphuric acid (1 : 4). It is then briefly passed through 
 seventy per cent, alcohol. It may at once be dried and 
 mounted and examined, but it is better to stain again with an 
 aqueous solution of a color complementary to that first used — 
 fuchsin and methylene-blue, gentian-violet and vesuvin or Bis- 
 marck-brown. 
 
 The search for bacilli in sputum may be facilitated by adding 
 to a])Out four ounces of sputum, one ounce of sterilized distilled 
 water, and from four to eight drops of liquor sodse and heating ; 
 from two to three ounces more of water are added and the 
 mixture is ijut aside in a conical glass for from twenty-four to 
 forty-eight hours, when the supernatant fluid is decanted and 
 cover-glass preparations made from the sediment. 
 
 What is the clinical course of " galloping consumption" ? 
 
 The rapid form of confluent pulmonary tuberculosis, known 
 as "quick consumption" or phthisis jiorida^ as distinguished 
 from the infectious fever known as acute miliary tuberculosis, 
 not infrequentl}' supervenes upon a neglected "cold," com- 
 monly a catarrhal pneumonia of the apex ; or it may suddenly 
 become manifest after localized tuberculosis of the apex, so 
 slight as to be unsuspected, has existed for a longer or shorter 
 time ; it may closely or remotely follow an attack of influenza ; 
 or its immediate antecedents may be untraceable. Frequently, 
 the subjects of phthisis florida present an hereditary liability to 
 tuberculosis. 
 
 Clinically the disease is marked by high temperature of a 
 continued or, more frequently, a remittent type ; profuse night- 
 sweats ; profound digestive and circulatory disturbance ; rapid 
 wasting, with accompan3'ing weakness ; and pulmonary symp- 
 toms of progressive severity, with corresponding physical signs. 
 Pathologically it is characterized by rapid caseation, with for- 
 mation of extensive cavities : severe laryngeal and intestinal 
 complications are frequent. It may apparently begin as an 
 acute laryngitis of ordinary or of tuberculous type. Sometimes 
 persistent diarrhea is the earliest symptom to attract attention. 
 
PULMONARY TUBERCULOSIS. 175 
 
 The duration of the disease is from a few weeks to about eighteen 
 months. 
 
 How is a pulmonary hemorrhage to be discriminated from a 
 gastric hemorrhage? 
 
 The blood of pulmonary hemorrhage has a sweetish or saltish 
 taste, is usually fluid, bright-red, and more or less frothy. In 
 gastric hemorrhage the blood is usually dark and clotted ; its 
 taste is masked as a result of admixture with the contents of 
 the stomach ; the stools that follow are tarry. 
 
 Pulmonary hemorrhage may occur with or without cough, and 
 is not provoked by taking food. Gastric hemorrhage usually 
 occurs with vomiting, and is provoked by taking food. 
 
 How is the distinction to be made between pulmonary tuber- 
 culosis and chronic pleurisy ? 
 
 Pleural adhesion and thickening are extremely common. 
 They occasion retraction of the chest-wall, often more or less 
 displacement of the heart, and give rise to dulness on percus- 
 sion, enfeebled transmission of the breath-sounds, and increased 
 vocal resonance and fremitus ; but they are not associated with 
 the auscultatory and constitutional phenomena of pulmonary 
 tuberculosis, or with the presence of tubercle-bacilli in the 
 sputum. If a pleural effusion is present, there are bulging of 
 the lower part of the chest, flatness on percussion, feebleness 
 or absence of breath-sounds, and diminished vocal resonance and 
 fremitus. If the fluid is purulent, there are chills, fever, sweats 
 and emaciation. 
 
 How is pulmonary carcinoma to be distinguished from pulmon- 
 ary tuberculosis ? 
 
 Carcinoma of the lung is a secondary affection. The meta- 
 static growths give rise to irregularly distributed, multiple 
 areas of percussion-dulness, without corresponding change in 
 the auscultatory phenomena. The temperature is likely to be 
 sub-normal rather than febrile, unless inflammation of the lung 
 or pleura is excited. The duration of pulmonary carcinoma is 
 limited ; pulmonary tuberculosis may be indefinitely protracted. 
 Tubercle-bacilli are not found in the sputum in pulmonary 
 
176 ESSENTIALS OF DIAGNOSIS. 
 
 carcinoma. The presence of carcinomatous new-growths else- 
 where is signiiicant in doubtful cases. 
 
 How is pulmonary syphilis to be distinguished from pulmon- 
 ary tuberculosis ? 
 
 Sj'^philis of the lung appears either in the form of gummata 
 or as fibroid induration. It is to be distinguished from tuber- 
 "culosis by the absence of bacilli from the sputum, by the involve- 
 ment of the middle and lower parts rather than the upper part of 
 the lung, by the diftuse and irregular rather than concentrated 
 localization of physical signs, by the absence of the constitu- 
 tional phenomena of tuberculosis, and by the history or the 
 knowledge of the existence of other syphilitic manifestations. 
 The therapeutic test is sometimes available, but should be 
 cautiously applied, as cases of tuberculosis are usually injured 
 by potassium iodide. 
 
 Syphilis and tuberculosis may coexist. 
 
 How are bronchiectasis and pulmonary tuberculosis to be dif- 
 ferentiated ? 
 
 Bronchiectasis is attended with copious muco-purulent 
 expectoration, and perhaps with decided emaciation ; the pul- 
 monary resonance may be impaired, and large, moist rales may 
 be heard ; but the pliysical phenomena are usually bilateral in 
 distribution and most decided at the bases of the lungs ; pulmo- 
 nary tuberculosis usually begins at the apex of one lung, whence 
 it extends. Bronchiectasis is slowly if at all progressive ; tuber- 
 culosis less commonly stops short of a fatal termination. The 
 sputam of a case of bronchiectasis does not contain tubercle- 
 bacilli. 
 
 How is an abscess of the lung to be diagnosticated from pul- 
 monary tuberculosis ? 
 An abscess of the lung may develop in the course of a pneu- 
 monia or an empyema, as a result of traumatism, or it may con- 
 stitute a manifestation of a general pyemia. It is to be distin- 
 guished from tuberculosis by a knowledge of its possible origin, 
 by the appearance of the phenomena in a lower rather than in 
 an upper lobe and upon one side only. The condition is acute 
 
ACUTE MILIARY TUBERCULOSIS. 177 
 
 rather than chror\ic, and the sputum does not contain tubercle- 
 bacilli. The physical phenomena are peculiarly circumscribed. 
 
 By what means are malarial fever and pulmonary tuberculosis 
 to be differentiated ? 
 
 When caseation and suppuration are taking place in a lung, 
 the temperature is high in the evening, declining towards 
 morning. In addition, however, there are persistent dyspnea, 
 increased frequency of breathing, cough, expectoration contain- 
 ing tubercle-bacilli, loss of flesh, night-sweats, dulness on per- 
 cussion, and mucous rales on auscultation. The symptoms last 
 enumerated are wanting in intermittent fever, while the Plas- 
 modia of malaria are wanting in the blood in pulmonary tuber- 
 culosis. Possible mistakes in diagnosis are to be avoided by a 
 physical examination. 
 
 How does tuberculosis of the bronchial glands differ from 
 whooping-cough ? 
 
 Whooping-cough is a self-limited disease ; tuberculosis is 
 not. Grave constitutional symptoms attend the latter ; re- 
 covery from whooping-cough is comparatively rapid. While 
 the cough induced by tuberculosis of the bronchial glands is 
 ringing, it does not possess the peculiar character of the cough 
 of pertussis. Cases of whooping-cough do not occur isolated. 
 By pressure on adjacent structures, enlarged bronchial glands 
 may occasion dyspnea, cough and cyanosis, and edema of the 
 face and neck. 
 
 Acute Miliary Tuberculosis. 
 
 What are the symptoms of acute miliary tuberculosis ? 
 
 A(Mte miliary tuberculosis sets in insidiously. The victim 
 may be a member of a tuberculous family. He is taken ill with 
 slight cough, scanty or no expectoration, marked dyspnea, ele- 
 vation of temperature, rapidity of pulse, delirium, and other 
 symptoms of a grave intoxication. Tuberculous involvement 
 of the bowel will cause diarrhea ; of the cerebral meninges, the 
 signs of meningitis. The course of the disease may be rapid 
 or protracted. Death may take place from exhaustion, or, in. 
 12 
 
178 ESSENTIALS OF DIAGNOSIS. 
 
 rarer instauces, the acute symptoms subside, and those of 
 chronic tuberculosis appear. 
 
 What are the physical signs of acute miliary tuberculosis ? 
 
 The physical signs of acute miliary tuberculosis are at first 
 practically those of an acute bronchitis : a full chest ; rapid 
 breathing ; unaltered percussion-resonance ; harsh, vesiculo- 
 bronchial respirator}- sounds ; unchanged vocal resonance and 
 fremitus. Later, dulness at one apex or at both apices, or jutt 
 below, and fine crackling rales are heard ; and still later, evi- 
 dences of caseation are found on auscultation and percussion. 
 The detection of tubercle-bacilli may be very late. Some cases 
 early develop indications of apex-pneumonia. 
 
 How are acute miliary tuberculosis and typhoid fever to be dis- 
 tinguished from one another ? 
 
 The prostration and the general condition are much alike in 
 both ; but in acute miliary tuberculosis the epistaxis, the rose- 
 spots, the characteristic temperature-course, and the peculiar 
 stools of typhoid fever are wanting. The temperature of acute 
 miliary tuberculosis presents considerable oscillations on the 
 same day ; without therapeutic interference, it may be normal, 
 subnormal and very high. Bronchitis may attend typhoid fever, 
 but the dyspnea is never so marked as it is in acute miliary tuber- 
 culosis. The progress of the case determines the diagnosis. 
 Not only do the marked physical signs of destructive change in 
 the lungs develop in the one disease, and not in the other, but 
 typhoid fever is a self-limited disease of known duration, with a 
 tendency to recovery, while acute miliary tuberculosis is a dis- 
 ease of uncertain duration, and sooner or later almost inva- 
 riably fatal. 
 
 Tubercle-bacilli may sometimes be discovered in the sputum 
 of acute miliary tuberculosis. 
 
 The knowledge of previous scrofulous or tuberculous disease 
 in the patient, or a family history of scrofula or tuberculosis, 
 should excite suspicion of acute tuberculosis ; and in susceptible 
 subjects the latter disease may even quickly follow typhoid fever. 
 
PULMONAKY EMPHYSEMA. 179 
 
 Interstitial Pneumonitis. 
 
 What are the characteristics of interstitial pneumonitis ? 
 
 As a result of the irritation occasioned by the constant 
 inhalation of fine particles of dust by miners and grinders, and 
 others, a chronic bronchitis with hyperplasia of the interstitial 
 pulmonary tissue develops. The two layers of pleura are often 
 adherent and thickened. As time progresses, contraction takes 
 place, terminating in condensation of the lung and dilatation 
 of the bronchial tubes. Interstitial pneumonitis may develop 
 as a part of a general fibroid degeneration. 
 
 In coal miners the condition is known as anthracosis ; in iron- 
 workers as siderosis ; in grinders as chalicosis. 
 
 What are the symptoms of interstitial pneumonitis ? 
 
 There is obstinate cough and abundant muco-purulent expec- 
 toration, which sometimes contains pai'ticles of the dust inhaled. 
 There may be considerable wasting and dyspnea. 
 
 What are the physical signs of interstitial pneumonitis ? 
 
 The chest is diminished in size, rather flattened anteriorly, 
 from retraction. The respiratory excursion is small, the chest 
 expanding but little in inspiration. The percussion-resonance is 
 impaired over a large area of pulmonary surface. The breath- 
 ing is bronchial. Large moist and dry rales are heard. The 
 vocal resonance and fremitus are increased. 
 
 How does interstitial pneumonitis differ from chronic pleurisy? 
 
 Interstitial pneumonitis and chronic adhesive pleurisy are 
 allied conditions and are often associated. Occurring alone 
 the former is wider in its distribution and is more likely than 
 the latter to be bilateral. Blowing breathing, rales, cough and 
 expectoration attend the pulmonary, but not the pleural, con- 
 dition. 
 
 Pulmonary Emphysema. 
 
 What are the characteristics of pulmonary emphysema? 
 
 Pulmonary emphysema is usually a result of long-continued ex- 
 cessive expiratory effort with closed glottis— as in protracted 
 
180 ESSENTIALS OF DIAGNOSIS. 
 
 cough or in the habitual blowing of wind instruments. It is 
 often associated with chronic bronchitis. The air-vesicles be- 
 come dilated into large sacs, and the bloodvessels in the inter- 
 lobular septa are obliterated. The increased work thrown upon 
 the right heart in turn gives rise to dilatation. 
 
 Emphj'sema manifests itself by dyspnea, expiratory in char- 
 acter ; shortness of breath, aggravated in paroxysms, and at- 
 tended with distressing cough and scanty expectoration. The 
 cardiac insufficiency adds to the dyspnea and may be the cause 
 of dropsy. 
 
 What are the physical signs of emphysema ? 
 
 The chest is large, " barrel-shaped ;" the circumference being 
 increased in greater degree than the vertical diameter. The 
 respirator}/ excursio)i is slight and may be scarcely visible ; al- 
 though the chest may rise and fall as a whole, the ribs being 
 fixed in the position of full inspiration. The percussion-resonance 
 is heightened, almost tympanitic. The hreath-sounds are feeble, 
 being almost continuous and without intermission, expiration 
 being prolonged and attended with a succession of puffs. The 
 vocal resonance and fremitus are diminished. The area of super- 
 ficial cardiac dulness is diminished, but deep percussion will 
 reveal enlargement of the right ventricle. 
 
 How is emphysema to be distinguished from pneumothorax ? 
 
 Pneumothorax usually results from the breaking through the 
 pleura of a destructive process in the lung, such as the casea- 
 tion and suppuration of tuberculosis. The symptoms to which 
 it gives rise are abrupt in onset and distressing in character. 
 The patient perceives a sudden, severe pain in the side, and is 
 seized with great dyspnea and a sense of impending death. 
 The chest is seen to be enlarged, the breathing rapid and shal- 
 low, the respiratory excursion small ; the percussion-resonance 
 is tympanitic and the breath-sounds are feeble. In pneumo- 
 thorax, the dilatation of the chest and the tympany are, however, 
 unilateral ; in emphysema, the}^ are symmetrical. In pneumo- 
 thorax, an amphoric blowing sound is heard on inspiration, and 
 if pleurisy with effusion have set in, metallic tinkling, succussion 
 sounds and egophony as well. The recognition of a condition 
 
PNEUMOTHORAX. 181 
 
 that may give rise to perforation and pneumothorax aids in the 
 diagnosis. 
 
 How is emphysema to be distinguished from a pleural effusion? 
 
 An effusion into the pleura may take place in the course of a 
 pleurisy, or as a result of disease of the heart or kidney. Ad- 
 jacent organs are displaced in proportion to the quantity of 
 fluid poured out. If the percussion-note be hyper-resonant at 
 the upper part of the chest, above the level of the fluid, it is 
 flat below. Pleuritic effusions are usually unilateral ; when the 
 eff"usion is part of a general dropsy it is usually bilateral. Em- 
 physema is rarely unilateral. In emphysema, the breath-sounds 
 are everywhere feebly heard ; in pleural effusion the breathing- 
 may be puerile, or even bronchial, above the level of the fluid, 
 but the breath-sounds are not well heard through the fluid. Yocal 
 resonance and fremitus are diminished in emphysema ; absent 
 below the level of a pleural effusion. If the effusion becomes puru- 
 lent, rigors, hectic fever, sweats and marked emaciation occur. 
 
 Pneumothorax. 
 
 What are the clinical features of pneumothorax ? 
 
 Pneimiothorax may result from traumatism that causes fracture 
 of a rib and perforation of the lung ;. from the rupture of an 
 emphysematous pulmonary alveolus ; from communication be- 
 tween the pleural cavity and an adjacent hollow viscus ; from 
 the softening of a septic infarct or of an area of pneumonic con- 
 solidation ; but the most common cause is ulcerative perforation 
 of a tuberculous cavity in the lung. The phenomenon usuall}' 
 sets m suddenly, with sharp pain in the side, intense dyspnea 
 and a sense of great oppression. The breathing is hurried and 
 shallow. The chest on the affected side becomes bulging ; the 
 percussion-note is tympanitic ; the breath-sounds are enfeebled or 
 distant, perhaps amphoric ; as fluid is poured out, metallic 
 tinkling may be heard, and by shaking the patient, with the ear 
 applied to his chest, a succussion-sound may be elicited ; the 
 voice-sounds and vibrations are poorly transmitted. The heart, 
 as well as other viscera, may be displaced. 
 
182 ESSENTIALS OF DIAGNOSIS. 
 
 How are pneumothorax and diaphragmatic hernia to be 
 differentiated ? 
 
 The stomach may be dragged upwards beneath the ribs by a 
 contracting lung, or the stomach or the large intestine may 
 bulge through a yielding portion of the diaphragm, so that 
 there may be unilateral percussion-tympauy, with displacement 
 of the heart ; vibrations of the fluid in the hollow viscus may give 
 rise to metallic tinkling, whicb, however, occurs independently 
 of respiration and is associated with rumbling sounds peculiar 
 to the gastro-intestinal tract. The interference with the respi- 
 ratory functions that results is, moreover, not only acute in on- 
 set, as it is in pneumothorax (of which the etiologic elements are'', 
 wanting), but it may be equally sudden in disappearance. Dia- 
 phragmatic hernia may have a history dating from birth ; it 
 bodes no danger unless strangulation occurs, of which the symp- 
 toms are characteristic. The outcome of pneumothorax is in 
 the nature of things often rapidly fatal. 
 
 How are pneumothorax and a pulmonary cavity to be 
 differentiated? 
 
 A large cavity in the lung may yield a tympanitic percussion- 
 sound, amphoric respiration, metallic rales or tinkling, and suc- 
 cussion-sounds, but the phenomena are usually circumscribed ; 
 there is no bulging, no acute exacerbation of pain, dyspnea 
 and oppression, and the percussion-flatness of an eflusion into 
 the pleural sac is wanting. 
 
 How is pneumothorax to be distinguished from a pleural 
 effusion ? 
 
 Pneumothorax sets in suddenly, with acute pain and dyspnea. 
 A pleural effusion usually takes place insidiously. Pleurisy 
 with effusion usually attends pneumothorax, so that the signs of 
 both may be present ; but when the pneumotliorax is the 
 primary condition, the percussion-note above the level of the 
 effusion is more pronouncedly tympanitic and the voice more 
 distinctly egophonic. Succussion-phenomena and tinkling are 
 not heard unless both air and fluid are present in the pleural 
 sac. Finally, the recognition of a condition that gives rise to 
 pneumothorax may decide the diagnosis. 
 
ASTHMA. 183 
 
 Asthma. 
 
 What are the symptoms of asthma ? 
 
 Asthma is a paroxysmal affection, the symptoms of which are 
 probably dependent upon spasmodic narrowing of the smaller 
 bronchial tubes. The attacks recur at irregular intervals, with 
 or without apparent exciting cause. Among provocative con- 
 ditions are changes of climate and weather, overeating,. indiges- 
 tion, emanations from feathers and sexual excitement. 
 
 The seizure is sudden in onset, usually occurring at night. The 
 patient is awakened with a sense of oppression and distressing 
 dyspnea, inspiratory in character. Orthopnea is common. Dur- 
 ing the jjaroxysm, which may last for several hours, the chest 
 heaves spasmodically, but the pulmonary expansion is slight ; the 
 face is pale or livid, and the distress is evident. Loud, wheezing 
 sounds are heard. On auscultation, the breath-sounds are feeble, 
 or the vesicular murmur may be obscured by the wheezing or 
 replaced by sonorous and sibilant rales. The percutory phenO' 
 mena are unaltered. The crisis takes place with a profuse ex- 
 pectoration of mucus, perhaps, also, with a copious discharge of 
 limpid urine. This may terminate the attack, or the same phe- 
 nomena may be repeated on several successive nights or even in- 
 vade the day. 
 
 Asthma may be primary or secondary. It may result from 
 reflex influences, such as disease of the nose. It may apparently 
 replace the convulsive seizure of epilepsy, Asthmatoid seizures 
 are common accompaniments of chronic bronchitis and emphy- 
 sema, of cardiac insufficiency, and of chronic nephritis. 
 
 How is asthma to be distinguished from an asthmatoid con- 
 dition ? 
 In true asthma, no cause for the disease may be found or else 
 some local or reflex irritation may be discovered. When so- 
 called asthmatoid attacks occur, their discrimination depends 
 upon the recognition of an organic pulmonary affection, such 
 as emphysema or bronchitis, or of cardiac incompetency or of 
 chronic nephritis. Such attacks do not pursue the typical 
 course of true asthmatic seizures and do not terminate suddenly 
 with profuse expectpration. 
 
184 ESSENTIALS OF DIAGNOSIS. 
 
 How does asthma differ from whooping-cough ? 
 
 Whooping-cough is a disease of children ; asthma, a disease 
 of adults. The characteristic wlioop of pertussis is wanting in 
 asthma. An attack of whooping-cough does not last more than 
 a couple of months, at most ; asthma may continue indefinitely. 
 
 What are the points of differentiation between asthma and 
 paralysis of the diaphragm ? 
 
 The dyspnea resulting from paralysis of the diaphragm is not 
 paroxysmal, as is that of asthma. Paralysis of the diaphragm 
 is not characterized by an absence of the breath-sounds, followed 
 by wheezing and high-pitched rales. When the diaphragm 
 is paralyzed, inspiration is attended with expansion of the 
 chest and depression of the abdominal wall ; in expiration the 
 chest collapses and the abdominal wall is elevated ; stimulation 
 of the phrenic nerves restores the normal harmony of action ; 
 attempts at bearing down are futile or ineffective. 
 
 THE DIGESTIVE SYSTEM— THE MOUTH. 
 
 Catarrhal Stomatitis. 
 
 What are the clinical characteristics of catarrhal stomatitis ? 
 
 Catarrhal inflammation of the r)utcous menihrane of the month 
 may result from the ingestion of irritating substances, from the 
 presence of carious teeth, or by extension from adjacent dis- 
 ease ; it may also develop in conjunction with morbid dentition, 
 or derangement of digestion, or in the course of the exanthe- 
 mata. It manifests itself by redness, tumidity, and increased 
 heat of the structures within the mouth, and by increased 
 secretion. The taking of food is attended with discomfort or 
 with pain ; taste is impaired ; and the breath is offensive. As a 
 rule, there is little or no constitutional disturbance. 
 
 Aphthous Stomatitis. 
 
 What are the clinical features of aphthous stomatitis ? 
 
 In individuals exposed to unfavorable hygienic conditions, 
 and in those debilitated by disease, small discrete or confluent. 
 
THRUSH — ULCERATIVE STOMATITIS. 185 
 
 grayish or whitish masses of degenerated epithelium accumu- 
 late at various parts of the mucous meuibrane of the mouth ; 
 the desquamation of the masses exposes subjacent ulceration. 
 Mastication in adults and nursing in infants are difficult and 
 painful ; the secretions of the mouth are increased ; the appetite 
 may be impaired ; digestion may be deranged ; and there may 
 be diarrhea. 
 
 Thrush. 
 
 What are the clinical manifestations of thrush? 
 
 Thrush, muguet or parasitic stomatitis is a mycotic inflamma- 
 tion of the mucous membrane of the mouth and throat, to 
 which children are especially prone. It is dependent upon the 
 presence of a fungus, termed the mycoderma (or didiiim) albicans. 
 An acid reaction of the secretions of the mouth is an essential 
 condition for the development of the affection. The growth of 
 the fungus and the resulting irritation give rise to the formation 
 of minute curd-like masses upon various parts of the mucous 
 membrane. Forcible detachment of the masses occasions bleed- 
 ing. The symptoms are those of the ordinary form of stomatitis, 
 plus the flaky deposits containing the characteristic fungus. 
 There may also be diarrhea and a varying degree of constitu- 
 tional disturbance. In nurslings, the inability to suckle may 
 result in inanition and death. 
 
 Ulcerative Stomatitis. 
 
 What are the symptoms of ulcerative stomatitis ? 
 
 Ulcerative stomatitis is an aggravated form of inflammation of 
 the mouth, attended with ulceration, which it is stated is 
 usually unilateral. The affection arises amid conditions of 
 crowding and filth, and in those supplied with insufficient and 
 inappropriate food ; it may also be a sequel of other forms of 
 stomatitis, of caries of the teeth, or of the maxillary bones. 
 It is manifested by impaired appetite, fetid breath, increased 
 salivation, pain in eating, and constitutional symptoms of 
 varying intensity. Sometimes adjacent lymphatic glands under- 
 go enlaroremeut. 
 
186 ESSENTIALS OF DIAGNOSIS. 
 
 Mercurial Stomatitis. 
 
 What are tlie clinical manifestations of mercurial stomatitis ? 
 
 Stomatitis sometimes results from the medicinal iugestion of 
 large quantities of mercury, or of small quantities by persons 
 possessing an idiosyncrasy, or as a manifestation of mercurial 
 intoxication by means of articles of food or drink, or from ex- 
 posure to the metal in certain occupations. The symptoms vary 
 greatly in severity. The gums especially become swollen, red- 
 dened, tender, and sometimes ulcerated. The teeth may fall out, 
 and the maxillary bones become carious. The breath is fetid. The 
 salkxi contains mercury ; its secretion and discharge are inordi- 
 uatel}- increased, giving rise to the term "salivation,"" as 
 descriptive of the affection. 
 
 Gangrenous Stomatitis — Noma. 
 
 What are the clinical features of gangrenous stomatitis ? 
 
 Gangrenous stomatitis, noma or cancrum oris is essential!}* an 
 affection of childhood, rare, and almost invariably fatal, which 
 OAvelojjs in those of depraved constitution, often at the termina- 
 tion of one of the exanthemata, particularly measles. The 
 disorder is manifested by a brawny induration of one cheek, the 
 structures of which undergo disintegration, with resulting 
 ulceration of the mucous and cutaneous surfaces, and, not 
 rarely, perforation. Adjacent portions of the gums may by 
 contiguity become involved in the process. The teeth may fall 
 out and the maxillary bones become carious. The early 
 symptoms may be obscured by those of the antecedent condi- 
 tion. Soon, however, the breath becomes fetid, and, in addition 
 to the local manifestations, the symptoms of septic intoxication 
 mav appear, in the midst of which the child may die. Hecovery 
 may take place, with hideous deformity of the face. Pneu- 
 monia, pulmonary gangrene, and entero-colitis ma,j he compli- 
 cations. 
 
GLOSSANTHRAX. 187 
 
 THE TONGUE. 
 
 Glossitis. 
 
 What are the symptoms of glossitis ? 
 
 When the tongue is inflamed, from whatever cause, the organ 
 becomes enlarged, tumid, reddened, painful; speech, degluti- 
 tion and mastication, sometimes respiration, are interfered 
 with, and the secretions of the mouth are increased. The 
 swelling may be so great that sulfocation results, unless relief 
 be given by incision. Glossitis may be superficial or parenchy- 
 matous, acute or chronic; the intensity and character of the symp- 
 toms being modified accordingly. It may be due to erysipelas, 
 either primarily or secondarily. Epidemics of erysipelatous 
 glossitis have occurred, and the name "black tongue" has been 
 applied to this afteetion. Parenchymatous glossitis sometimes 
 proceeds to suppuration. 
 
 Leukoplakia Lingualis. 
 
 What is leukoplakia of the tongue ? 
 
 Leukoplakia lingualis, or leukoplakia buccalis^ is a name applied 
 to a peculiar chronic affection of the tongue or of the tongue 
 and buccal mucous membrane, characterized by the formation 
 of persistent, horny, whitish patches upon the surface, some- 
 times extending entirely through the epithelial layer. Untreated, 
 it is said to lead at limes to the development of carcinoma. 
 Sometimes it appears to be related with gout. 
 
 Glossanthrax. 
 
 What is glossanthrax ? 
 
 Glossanthrax is a term applied to the localization of malignant 
 pustule upon the tongue. It is to be differentiated from carci- 
 noma, tuberculosis, syphilis and other affections leading to 
 suppuration or ulceration. The local and constitutional symp- 
 
188 ESSENTIALS OF DIAGNOSIS. 
 
 toms are those of anthrax in general. The appearance of the 
 eschar is characteristic and the presence of anthrax-bacilli is 
 diagnostic. 
 
 Nigrities. 
 
 What is nigrities ? 
 
 Nigrities, also called blach tongue and hairy tongue, is an affec- 
 tion of the filiform papillee of the tongue, supposed to be due to 
 the irritation of a special fungus. The papillae in various situa- 
 tions become discolored, thickened, and elongated, giving the 
 appearance of a scattered or compact hairy growth upon the 
 dorsum of the tongue. Desquamation takes place, after which 
 the tongue may remain comparatively clean for a longer or 
 shorter period ; then the growth recurs. The aflfectiou is to be 
 differentiated from staining of the tongue by tobacco, medicines, 
 and the like. 
 
 MUMPS— PAROTIDITIS. 
 
 What are the symptoms of parotiditis ? 
 
 Parotiditis or -mumps may be primary or secondary in the 
 course of infectious diseases. It is characterized by pain at the 
 angle of the jaw, followed by tumefaction of the parotid gland, 
 at first on one side and then on the other. Movement of the 
 jaw, as in mastication, is difficult and painful. Deglutition is 
 not interfered with ; hearing may be deranged. The secretion 
 of saliva is usually excessive. There are febrile manifestations 
 of moderate severity. 
 
 Orchitis or ovaritis is a peculiar complication of parotiditis. 
 It is likely to occur as the parotid swelling subsides. 
 
 THE PHARYNX. 
 
 Pharyngitis. 
 
 What are the symptoms of pharyngitis ? 
 
 In acute catarrhal pharyngitis, or angina, the symptoms vary 
 with the intensity and extent of involvement. Ordinarily, there 
 
PHARYNGITIS. 189 
 
 are "sore throat," irritable cough, pain or difficulty in deglu- 
 tition, interference with respiration, enlargement of the tonsils 
 and of the glands of the neck. On inspection, the soft palate, the 
 uvula, the tonsils, the posterior and lateral walls of the pharynx, 
 or the palatine arches may, one or more, be seen to be reddened 
 and tumefied, and often coated with glairy mucus. A moderate 
 degree of fever attends acute pharyngitis. 
 
 Acute phlegmonous pharyngitis is a much more serious affection, 
 involving not only the mucous membrane, but also the sub- 
 mucous connective tissues and even at times the sheaths of the 
 muscles. The constitutional symptoms are in accordance with 
 the severity of the process, and may be those of pyemia. The 
 pus may gravitate to the cellular tissues of the neck, manifesting 
 as an external swelling and causing dyspnea or even suffocation 
 from compression of the trachea. The inflamed tissues of the 
 throat, especially the soft palate and uvula, may be greatly 
 swollen and edematous. 
 
 What is acute tuberculous pharyngitis ? 
 
 Acute tuberculous pjharyngitis is a form of acute miliary tuber- 
 culosis, apparently beginning in the pharynx. 
 
 The constitutional manifestations are those of an acute febrile 
 process of grave type, sometimes simulating typhoid fever. 
 
 Locally, deposits of tubercle may be observed beneath the 
 mucous membrane as little semi-transparent, grayish nodules, 
 resembling in size and form vermicelli-seeds or fish-eggs. These 
 are collected into little patches more or less confluent, which 
 eventually undergo ulceration. 
 
 The uvula is sometimes thickened into a somewhat character- 
 istic gelatinous-looking, reddened, club-shaped mass. This ge- 
 latinous thickening may likewise take place in other portions 
 of the pharynx. 
 
 The disease may extend to the epiglottis, tongue, and larynx, 
 or to the vault of the pharynx and the nasal passages. 
 
 The ulcerative process usually begins on a palatine fold or 
 on a lateral wall of the pharynx, whence it rapidly extends. 
 Ulceration may penetrate the submucous tissues, and the 
 muscles may undergo tuberculous or fatty degeneration. Pus 
 
190 ESSENTIALS OF DIAGNOSIS. 
 
 is usually absent from the surface of the ulcers and the bacillus 
 tuberculosis is sometimes found in the detritus. 
 
 The chief and most distinctive local suhjective symptom is in- 
 tense pain in swallowing, often more than can be accounted for 
 by the extent of visible disease. The pain may extend into the 
 ears. 
 
 As the disease progresses, cough is superadded, emaciation 
 becomes rapid, and signs of pulmonary disease, and perhaps of 
 other complications, become manifest. 
 
 Death may result within a few weeks, and is rarely postponed 
 beyond two or three months. 
 
 Recovery is the exception. 
 
 How is tuberculous pharyngitis to be distinguished from 
 syphilitic sore-throat ? 
 
 The intense pain in swallowing, the characteristic deposit and 
 gelatinous infiltration, the absence of pus from the ulcers, the 
 histor}'^ of the attack, the personal histor}', the family history of 
 the patient, and the febrile symptoms ; the discovery of the 
 tubercle-bacillus in the detritus of the ulcers, or in the sputum, 
 together with the detection of the evidence of pulmonary tuber- 
 culosis as the case proceeds, are the points upon which the diag- 
 nosis from syphilis must depend. 
 
 Syphilitic and tuberculous disease may, however, coexist. 
 
 The supervention of typhoid symptoms in a case of supposed 
 syphilitic ulceration of the throat should excite suspicion of 
 the existence of tuberculosis. 
 
 How is tuberculous pharyngitis to be distinguished from typhoid 
 fever ? 
 Typhoid fever is sometimes accompanied by ulcerative phar- 
 yngitis and laryngitis, though the cases in which this occurs are 
 nuich rarer in North America than they appear to be in Europe. 
 The characteristic fish-egg-looking infiltration of tuberculosis 
 and the non-purulent character of the ulceration would make 
 the discrimination locally ; while, constitutional!}', there would 
 be absence of the characteristic temperature-course, of the rose- 
 spots, and of the peculiar stools of tj^phoid fever. Discovery of 
 the tubercle-bacillus would be conclusive. 
 
TONSILLITIS. 191 
 
 Tonsillitis. 
 
 What are the symptoms of tonsillitis ? 
 
 When the tonsils are inflamed, adjacent parts usually partici- 
 pate in the process. Parenchijmatous tonsillitis or quinsy may be 
 primary or secondary to various infectious diseases. It sometimes 
 sets in suddenly, with a chill, followed by decided elevation of 
 temperature and other febrile manifestations. Usually, one tonsil 
 only is affected, or first one and then the other, but bilateral in- 
 volvement may occur and the glands become so intensely swollen 
 as to meet in the middle line, practically obstructing deglutition 
 and respiration. In such cases the voice is nasal, and fluids at- 
 tempted to be swallowed may return through the nose. There 
 is always some interference with swallowing. The pain is 
 atrocious, and may extend into the ear on the affected side. 
 There is increased secretion of saliva ; swallowing is increased 
 in frequency, and aggravates the pain. Sometimes the patient 
 lies with open mouth, making labored and noisy efforts at respi- 
 ration, while the saliva dribbles. On examination, the tonsils 
 are seen to be enlarged and angry, adjacent parts in some degree 
 participating in the inflammatory process. 
 
 The enlargement of the glands can, sometimes, be distinctly 
 detected from without. Tenderness on pressure beneath the 
 angle of the jaw is common. 
 
 An inflamed tonsil or the peritonsillar tissues may suppurate, 
 and grave complications, such as ulceration into the carotid 
 artery, have occurred. 
 
 Lacunal ov follicular tonsillitis is a much less serious affection. 
 The process is superficial, the lining membrane of the lacuna; or 
 ducts being involved rather than the substance of the gland. 
 Scattered o.ver the surface of the inflamed and enlarged tonsils 
 are a number of yellowish points or patches, indicative of ac- 
 cumulations of sebaceous matter, desquamated epithelium and 
 fungi, at the orifices of the ducts. These plugs may be readily 
 removed by means of a scoop, sometimes by syringing — a point 
 of some importance in the discrimination from diphtheria. 
 Parenchymatous tonsillitis sometimes follows lacunal tonsillitis, 
 
192 ESSENTIALS OF DIAGNOSIS. 
 
 and tonsillar or peritonsillar abscess may then develop. Un- 
 treated, the duration of tonsillitis is from two to ten days or 
 more. 
 
 Some cases of tonsillitis are associated with pain and other 
 rheumatic manifestations in the muscles or joints, and endo- 
 carditis and pericarditis have been noted. An endocardial 
 murmur is not uncommon. Swelling of the joints may appear 
 in apparent metastasis as a tonsillar inflammation declines. 
 
 Anomalous eruptions and albuminuria are among the less 
 common concomitants of tonsillitis. Paralyses are rare sequelse> 
 
 Herpetic Sore-Throat. 
 
 What is herpetic sore-throat ? 
 
 Herpetic sm-e-ihroat, herpetic tonsillitis, herpes of the phary)ix, 
 common membranous sore-throat, ulcer o-memhranous angina, diph- 
 theroid throat, are names applied to a disease often mistaken for 
 diphtheria, but which is, in reality, a form of inflammation of 
 the mucous membrane of the palate, tonsils, uvula and pharynx, 
 characterized by the eruption of herpetic vesicles. Avhich soon 
 rupture, leaving little circular ulcers that coalesce and become 
 covered with a tibrinous exudation. It is sometimes associated 
 with herpes of the lips. 
 
 Constitutional symptoms may be absent, but, when present, are 
 usually of a mild febrile type. There may, however, be high 
 fever, preceded by malaise or chill. 
 
 The pain in deglutition (odynphagia), and the dryness and 
 heat of the throat are often much greater than in ordinary 
 forms of pharyngitis. In rare instances, in children, the false 
 membrane has extended into the larynx, causing suffocation. 
 Usually the disease terminates in recovery in about a week or 
 ten days. 
 
 Chronic or recurrent herpes of the throat is encountered in rare 
 instances. 
 
 How is common membranous sore-throat to be distinguished 
 from diphtheria ? 
 
 The diagnosis is sometimes very difficult, and, when in doubt, 
 the safer plan is to consider the case one of diphtheria. As a 
 
GANGRENOUS PHARYNGITIS. 193 
 
 rule, however, the islet-like distribution of the patches of fibrinous 
 exudation covering the ulcers left by rupture of the vesicles of 
 herpes is quite different from the appearance presented by the 
 coherent, continuous mass of thick, yellowish or grayish mem- 
 brane observed in diphtheria. Herpes is more frequent upon 
 the palate and tonsils. Diphtheria usually involves the phar- 
 ynx extensively. The constitutional symptoms of diphtheria 
 are, as a rule, much more profound than those of herpetic 
 sore-throat. Herpes of the lips often coexists with herpetic 
 sore-throat, very rarely with diphtheria. Diphtheria is con- 
 tagious. Herpes is non-contagious. 
 
 Gangrenous Pharyngitis. 
 
 What is gangrenous pharyngitis ? 
 
 Gangrenous pharyngitis, or putrid sore-throat, may originate 
 independently of any other malady or may follow ordinary 
 forms of pharyngitis, or the sore-throat of the exanthemata, or 
 of dysentery, or of typhus or of typhoid fever. It sometimes 
 occurs in cases of tuberculosis. Constitutional symp)toms are 
 typhoid in type. The local symptoms are those of violent inflam- 
 mation of the mucous membrane of the tonsils, palatine folds, 
 and walls of the pharynx, which soon become covered with 
 gangrenous patches. The destructive process rapidly extends, 
 sometimes into the esophagus, the larynx, and the nares. 
 Sometimes the process is extremely limited, as to the tonsils. 
 Erosion of blood-vessels may cause fatal hemorrhage. 
 
 How is gangrenous sore-throat to be distinguished from diph- 
 theria ? 
 
 In gangrene, the patches are grayish-black in color from the 
 outset, while the pseudo-membrane of diphtheria becomes dark 
 only as the disease progresses. 
 
 Swelling of the cervical glands is unusual in putrid sore throat, 
 and the characteristic odor of gangrene is almost unmistakable. 
 
 13 
 
194 ESSENTIALS OF DIAGNOSIS. 
 
 Retro-pharyngeal Abscess. 
 
 What are the symptoms of retro-pharyngeal abscess ? 
 
 Suppuration in the retro-pharyngeal tissues is most commonly 
 a result of destructive disease of the cervical vertebrae ; it may 
 also be due to inflammation of the lymphatic glands or of the 
 connective tissues, resulting from traumatism or developed in 
 the course of infectious disease, or by extension from adjacent 
 disease. The affection is more common in children than in 
 adults, and in tuberculous or syphilitic than in other subjects. 
 There may be an initial chill, with nausea and vomiting, fol- 
 lowed by considerable elevation of temperature and acceleration 
 of pulse. 
 
 There are soreness of the throat, with pain and difficulty of 
 swallowing ; orthopnea ; suffocative parox3fsms ; and noisy 
 breathing ; the voice is muffled or nasal. The head is often 
 thrown back. There is little or no cough. 
 
 The neck may be swollen and tender to touch, especially be- 
 hind the angle of the jaw, in front of the sterno-mastoid muscle. 
 The submaxillary glands may suppurate and fluctuation become 
 evident. 
 
 On inspection of the throat the posterior wall of the pharynx 
 ma}' appear tumid, or a distinctly circum&cril)ed projection may 
 be seen, the mucous membrane over and around the swelling 
 being reddened, perhaps ecchymotic. 
 
 The abscess may be so hidden that the use of the mirror may 
 be necessary for its detection. 
 
 On palpation fluctuation may be elicited. 
 
 THE ESOPHAGUS. 
 
 Stricture of the Esophagus. 
 
 What are the symptoms of stricture of the esophagus ? 
 
 Tlie esophagus may be narrowed by new-growths in its walls, 
 by cicatrices resulting from previous syphilitic or tuberculous 
 disease or from the ingestion of corrosive substances, by pressure 
 
THE STOMACH. 195 
 
 from without, as by an aneurism or a new-growth, or as a con- 
 genital malformation. Deglutition is interfered with, so that it 
 may be possible to swallow only liquids. If the narrowing is 
 decided, a pouch forms above the seat of constriction, in which 
 considerable quantities of food accumulate, to be periodically 
 rejected. Esophageal growths, if favorably situated, can some- 
 times be detected by the methods of laryngoscopy. Esopliago- 
 scopy has not yet been sufiSciently developed for diagnostic pur- 
 poses. Conclusive evidence of the existence of a stricture of the 
 esophagus is furnished by the resistance encountered in the in- 
 troduction and withdrawal of a bulbous bougie ; if aneurism be 
 suspected, this means of exploration is not permissible. 
 
 How are functional and organic strictures of the esophagus to 
 be differentiated ? 
 
 Spasmodic contraction of the esophagus is apt to result from 
 the presence of a foreign body, as a bougie, in the gullet. Spasm 
 of the esophagus {esophayismus)^ in a degree sufficient to give 
 rise to symptoms, sometimes occurs in hysterical persons. Under 
 the conditions last named, food may be obstinately rejected and 
 a considerable degree of emaciation result. The introduction 
 of a bougie may be met with some resistance, which, however, 
 slowly yields to gentle pressure. Careful observation will dis- 
 close the fact that not all the food taken is rejected. A powerful 
 impression, judiciously made, may at once cause the disappear- 
 ance of the symptoms,which occur, without discoverable cause, 
 in a person with other hysterical attributes. 
 
 THE STOMACH. 
 
 How may the duration of digestion be tested ? 
 
 An experimental meal, consisting of gruel, an ordinary piece 
 of beefsteak, and white bread, is given ; after which nothing is 
 to be taken until the examination is concluded. Seven hours 
 after eating, the stomach is to be washed out by siphonage with 
 a soft-rubber esophageal catheter. If digestion is normal the 
 washings should contain no remains of the food, or at most but a 
 few particles. 
 
196 ESSENTIALS OF DIAGNOSIS. 
 
 What are the tests for free hydrochloric acid in the gastric 
 contents ? 
 
 Many tests have been proposed, none of which is absokxtely 
 free from fallacy. For practical purposes, Congo-red and phloro- 
 gluciu-vanillin seem to be the most available. 
 
 1. Strips of filter-paper saturated with Congo-red become blue 
 if dipped in fluid containing fi'ee hydrochloric acid ; organic acids 
 likewise discolor Congo-red, but do not produce the same blue 
 tint. 
 
 2. One or two drops of a solution consisting of phloroglucin, 
 two parts ; vanillin, one part ; absolute alcohol, thirty parts, 
 are placed in a shallow, porcelain capsule, with an equal volume 
 of the filtrate obtained from the stomach-contents, and gently 
 heated. If free hydrochloric acid is present in a proportion of 
 0.05 or more per thousand, a bright-red deposit will form. If no 
 hydrochloric acid be present, the deposit is brownish-red or 
 brown. The presence of sulphuretted hydrogen is said to be the 
 only source of error. 
 
 How is the solvent power of the gastric juice tested 
 
 By the administration, on an empty stomach or one hour after 
 a trial-breakfast of tea and toast, of potassium iodide in rubber 
 capsules fastened with fibrin, and examination of the saliva for 
 iodine-reaction by means of starch-paper and the fumes of strong 
 nitro-hydrochloric acid. I^ormally the reaction should be de- 
 monstrable in from six to eleven minutes after the ingestion of 
 the capsules. 
 
 Gastralgia. 
 
 What is gastralgia or gastrodynia? 
 
 Gastric pain is usually symptomatic of inflammation, ulcera- 
 tion or neoplasm. It may, however, occur independently of 
 recognizable structural disease, and is then considered a neu- 
 rosis—neuralgia of the stomach. ' The pain of neuralgia is spas- 
 modic, of a cutting character, usually rather brief in duration, 
 shooting and shifting in seat, and occurs spontaneously or im- 
 mediately after the ingestion of food. It may induce and be 
 relieved by vomiting or eructation. It is relieved by heat or 
 
ACUTE GASTRITIS. 197 
 
 pressure. It is not accompanied by vomiting of blood or by the 
 usual manifestations of disordered digestion. Other neurotic 
 symptoms may coexist. 
 
 Acute Gastritis. 
 
 What are the symptoms of acute gastritis ? 
 
 Acute gastritis results from the entrance of irritating matters 
 into the stomach. It varies in degree in accordance with the 
 intensity of the causative irritant. The milder attacks are 
 sometimes called '"'•acute gastric catarrlV or '•'■acute indigestion.'''' 
 Acute gastric catarrh may complicate infectious diseases, or its 
 exciting cause may escape detection. 
 
 The symptoms are anorexia, nausea, vomiting, often epigastric 
 pain and tenderness ; in a severe attack, the face is pale and 
 anxious, the %)ulse small and firm ; the skin may be cold and 
 clammy ; there may be moderate elevation of temioerature ; syn- 
 cope and collapse may occur. The vomited matters consist of 
 the contents of the stomach, mucus, perhaps bile, and sometimes 
 blood. There is often violent retching, without expulsion of the 
 contents of the stomach, or occurring when the organ is empty. 
 In addition there are commonly headache and thirst. The 
 tongue may be red and angry. Perforation of the walls of the 
 stomach may take place. Peritonitis may develop. The intes- 
 tines are not likely to entirely escape. 
 
 How are the gastric symptoms occurring at the onset of acute 
 febrile disorders or in the course of cerebral disease to 
 be distinguished from the symptoms of acute gastritis? 
 
 The vomiting of acute, febrile disorders, or of cerebral dis- 
 ease, is not dependent upon the ingestion of food ; nor is it 
 necessarily attended with nausea, coated tongue, or pain in the 
 epigastrium. Tenderness is not common. If symptoms indicative 
 of a constitutional affection have not been obtrusive, careful 
 investigation will succeed in detecting them at once, or after the 
 lapse of a variable period. No single symptom, but an associa- 
 tion of symptoms establishes the diagnosis. 
 
198 ESSENTIALS OF DIAGNOSIS. 
 
 How are acute gastritis and intestinal obstruction to be differ- 
 entiated ? 
 
 The vomiting of intestinal obstruction usually, but not 
 invariably, becomes fecal ; the rolling of the obstructed intes- 
 tines may be apparent through the abdominal walls. The 
 matter vomited in acute gastritis consists largely of mucus, 
 perhaps of some blood, and shreds of mucous membrane ; while 
 there is a history of irritation, poisoning, or indiscretion in 
 diet. Obstinate constipation attends obstruction ; acute gas- 
 tritis is rather likely to be associated with diarrhea. If an 
 obstruction of the bowel be not speedily removed, death results. 
 Recovery from the milder forms of acute gastritis may take place 
 spontaneously. 
 
 Chronic Gastritis. 
 
 What are the symptoms of chronic gastritis ? 
 
 Chronic gastritis or chrome gastric catarrh is the principai 
 factor in the production of dyspepsia. The symptoms differ 
 from those of acute gastritis not only in degree, but also in 
 character. There are many varieties of the affection but the 
 general phenomena are the same in all. The more or less per- 
 sistent ingestion of food or drink, improper in quality or exces- 
 sive in quantity, is the principal cause of chronic gastric catarrh. 
 The disorder manifests itself by nausea, vomiting, impaired 
 appetite, coated tongue, epigastric discomfort, aggravated by 
 the ingestion of food, flatulence, eructations, pyrosis, acidity, 
 bad taste, offensive breath, and palpitation of the heart. There 
 is dull, diffuse abdominal pain, relieved by vomiting. There 
 is also diffuse epigastric tenderness. The vomiting, as a rule, 
 takes place from one-and-a-half to two hours after the ingestion 
 of food. Constipation is common. Usually there is increased 
 thirst. The complexion is often sallow. Headache is frequent 
 and vertigo not uncommon. There may be loss of flesh and 
 emaciation. Mental operations are in many cases temporarily 
 sluggish, depression (" blues"), not rare, and sleeplessness or dis- 
 turbed sleep and disquieting dreams quite common. 
 
 If much accumulation of undigested and decomposing food 
 
GASTRIC ULCER. 199 
 
 takes place, or impairment of the motor activity of the stomach 
 becomes decided, dilatation of the viscus {gasirectasia) may re- 
 sult. A succession of meals may be taken before vomiting occurs ; 
 when it does, astounding quantities of liquid, containing the 
 macerated and fermenting remains of food, and various fungi 
 (especially the yeast-fungi and sarcinse), are ejected. The quan- 
 tity of hydrochloric acid in the gastric juice may or may not be 
 changed. Organic acids of fermentation are usually present. 
 
 What are the physical signs of dilatation of the stomach ? 
 
 Dilatation of the stomach gives rise to abnormal prominence 
 of the upper portion of the abdomen, with extension of the area 
 of gastric percussion-tympany when the organ is empty, and of 
 percussion-dulness when it is filled. When partially filled (the 
 ordinary condition), succussion-splashing is easily elicited, the 
 stethoscope being placed over the pyloric region while sudden 
 motion is imparted to the left hypochondrium and lumbar region. 
 If so late as thirty-six hours after the administration of salol, 
 salicylic acid can still be detected in the urine by a purplish or 
 purplish-brown precipitate on the addition of tincture of ferric 
 chloride, the delay in the propulsion of the stomach-contents 
 into the duodenum is considered sufficient to warrant the diag- 
 nosis of gastrectasia. 
 
 Gastric Ulcer. 
 
 What are the symptoms of gastric ulcer ? 
 
 Destruction of the mucous coat of the stomach may be a 
 result of acute gastritis. More commonly, however, gastric 
 ulceration develops in the course of chronic gastric catarrh, 
 especially in anemic women with impaired nutrition. In some 
 cases, ulcers of the stomach result from occlusion or obstruction 
 of gastric vessels. Gastric ulcer is not infrequent in cases of cir- 
 rhosis of the liver. The symptoms are sometimes obscure, and 
 the disease may go unrecognized until suddenly perforation and 
 death result. Symptoms of gastric catarrh are usually present, 
 with vomiting, impaired appetite, discomfort after meals, flatu- 
 lence, acidity, coated tongue. There are acute pain and marked 
 
200 ESSENTIALS OF DIAGNOSIS, 
 
 tenderness in the epigastrium or hypochondrium, also sometimes 
 in the lower dorsal or upper lumbar region. Pain and tender- 
 ness over or near the spinal column opposite the site of epigastric 
 pain is quite characteristic of gastric ulcer. The pain and accom- 
 panying tenderness, anteriorly as well as posteriorly, are most 
 frequently distinctly circumscribed. Pain is aggravated by the 
 ingestion of food, especially solid food, and relieved by vomiting, 
 which usually occurs soon after food is taken. The vomited 
 matters are often blood-streaked ; or a considerable quantity of 
 blood, bright-red in hue, or discolored by the gastric juice, is 
 vomited. PoUovving hematemesis the stools contain more or 
 less black, tarry matter. Anemia is a common attendant upon 
 gastric ulcei'. Dyspnea and palpitation are its concomitants. 
 There are often great emaciation and profound prostration. 
 Occasionally perforation of the walls of the stomach results ; if 
 adhesive inflammation have occurred, adjacent structures, as 
 liver or pancreas, may constitute the floor of the ulcer ; other- 
 wise fatal peritonitis ensues. 
 
 How is chronic gastritis to be distinguished from gastric ulcer ? 
 
 The difference is one of degree. With ulceration of the 
 stomach are associated the symptoms of chronic gastritis, but 
 in addition there are the exquisite localized epigastric pain and 
 tenderness, which diff"er from the diffuse soreness of simple 
 gastritis. Hematemesis is usual in ulcer of the stomach and less 
 usual in chronic gastritis of other than alcoholic origin ; and the 
 blood in the latter case is not likely to be bright in color or of 
 frequent appearance in the vomit. In gastritis vomiting occurs 
 not only after taking food, but not uncommonly on an empt}- 
 stomach as well. The vomiting of ulceration is usually brought 
 on by eating. Chronic gastritis responds more readily than 
 gastric ulcer to judicious treatment. The age and sex of the 
 patient sometimes help the diagnosis, as ulcer is most frequent 
 in young persons and especially in anemic girls. 
 
 Carcinoma of the Stomach. 
 
 What are the symptoms of carcinoma of the stomach? 
 
 Otrcinoma of the stomach appears principally in two forms. 
 In the one the cellular element predominates ; in the other the 
 
CARCINOMA OF THE STOMACH. 201 
 
 tibrous. The former involves the coats of the body of the 
 stomach ; the latter almost exclusively the pylorus. The symp- 
 toms occasioned differ in each case. When the body of the 
 stomach is involved the symptoms are those of an aggravated 
 chronic gastritis : impaired appetite, pain after meals, sometimes 
 vomiting, with slow emaciation. As time goes on, ulceration 
 takes place in the neoplasm, with the addition of the symptoms 
 of this condition : severe, deep-seated pain in the region of the 
 epigastrium, aggravated by the ingestion of food, vomiting of 
 blood-streaked matters and of discolored blood presenting an 
 appearance of coftee-grounds. The stools contain tarry matters, 
 from disorganized' blood. With the infiltration of the walls of 
 the stomach, adhesions are formed with adjacent organs, which 
 may be progressively invaded. 
 
 When the new-growth involves the pylorus, a characteristic 
 feature is dilatation of the stomach. The organ may be con- 
 siderably displaced by the weight of the tumor. Emaciation 
 ensues ; while the development of the carcinomatous cachexia 
 is of diagnostic significance. The feature without the establish- 
 ment of which the diagnosis of carcinoma of the stomach is 
 doubtful is the presence of a tumor in the epigastrium. In 
 scirrhus of the pylorus death results from exhaustion, as a 
 result of inanition ; in cellular carcinoma metastasis plays a 
 prominent part in determining a fatal issue. 
 
 How are carcinoma and ulceration of the stomach to be differ- 
 entiated ? 
 
 The similitude between the symptoms of ulcer of the stomach 
 and those of carcinoma of the stomach is sometimes so great 
 that the diagnosis is extremely difficult. The detection of a 
 tumor in the area occupied by the stomach is convincing. In 
 its absence, a cachexia or the detection of enlarged glands or 
 new-growths at other parts of the body may afford corrobora- 
 tive evidence. While the symptoms of ulceration may set in 
 acutely, and rapidly assume a grave aspect, they may on the 
 other hand be comparatively mild ; recovery is the rule. The 
 symptoms of carcinoma are more slowly developed, more per- 
 sistent and more profound than those of ulcer, and the pro- 
 
2Q2 ESSENTIALS OF DIAGNOSIS. 
 
 gress of the case reveals its malignancy. If the pylorus is in- 
 volved, vomiting does not take place for some time after food 
 has been taken, while both in ulceration and in ceilylar carci- 
 noma of the body of the stomach vomiting, when it occurs, takes 
 place early. Obstruction of the pylorus by carcinoma occasions 
 dilatation of the stomach. Before the fortieth year of life ulcera- 
 tion is the more common ; after forty, carcinoma. In ulcer, the 
 gastric hydrochloric acid is said to be excessive ; in carcinoma, 
 to be Avanting. In simple ulcer, sudden, more or less profuse 
 hemorrhages occur ; hence the blood is often bright, and when 
 discolored it is a viscid fluid or coagulated in coherent clots. In 
 carcinomatous ulcer there is a slight but more or less continuous 
 oozing; hence vomiting of blood rai'ely occurs apart from the 
 admixture with food of the disorganized " cofiee-grounds" sedi- 
 ment. 
 
 How is carcinoma or sarcoma of the omentum to be distin- 
 guished from carcinoma of the stomach ? 
 
 The detection of a tumor in the region of the epigastrium is 
 not exclusively indicative of carcinoma of the stomach. The 
 omentum may be the seat of carcinoma or sarcoma. In such a 
 case the symptoms of gastritis are not necessarily present ; in 
 particular the vomiting of matter resembling coffee-grounds is 
 wanting. 
 
 How is carcinoma of the stomach to he distinguished from carci- 
 noma of the pancreas ? 
 It may be impossible to decide from anatomic considerations, 
 especially in view of the displacement that often occurs, whether 
 a tumor in the epigastrium is gastric or pancreatic. If the 
 former, definite symptoms of gastric derangement are present ; 
 the visceral sjnnptoms of the latter are ill-defined. The exist- 
 ence of diabetes and the imperfect digestion of fats would point 
 to involvement of the pancreas. Jaundice sometimes accom- 
 panies carcinoma of the pancreas from pressure upon the bile- 
 ducts. In gastric carcinoma without hepatic complication this 
 does not occur. 
 
THE INTESTINES. 203 
 
 How is chronic gastritis to be distinguished from carcinoma of 
 the stomach ? 
 
 It is not sufficient to make a diagnosis of chronic gastritis. 
 The existence of carcinoma should, if possible, always be ex- 
 cluded. If, in addition to the symptoms of gastritis, there is 
 severe and persistent pain in the epigastrium, or pain increased 
 or developed after eating, with vomiting shortly after meals or 
 after a variable interval, the ejected matters resembling coffee- 
 grounds ; if there exist cachexia, new-growths in various parts 
 of the body^ and a tumor can be detected in the region of the 
 epigastrium, the gastritis is but a concomitant of the mahgnant 
 disease, which, in the course of a year or eighteen months, is 
 almost necessarily fatal. Carcinoma is uncommon before forty ; 
 gastritis may occur at any time of life. The gastric juice is 
 said to contain free hydrochloric acid in nearly all cases of 
 chronic gastritis, but to contain none in cases of gastric carci- 
 noma. While the persistent absence of free hydrochloric acid 
 should excite suspicion of the existence of malignant disease, it 
 is not conclusive evidence. 
 
 THE INTESTINES. 
 
 Acute Enteritis. 
 
 What are the symptoms of acute enteritis ? 
 
 Acute inflammation of the small intestine may vary greatly in 
 severity, from a simple catarrh of the mucous lining to an in- 
 tense inflammation involving the submucous and muscular 
 tunics and even the peritoneal investment. 
 
 Acute intestinal catarrh or mucous enteritis is, in most cases, de- 
 pendent upon the presence of irritating matters in the bowel. 
 As a result, there occur diarrhea, with colicky pains, and often 
 considerable tenderness in the abdomen, and febrile and other 
 constitutional manifestations of varying intensity. The stools 
 may number from three to six or more in twenty-four hours ; 
 they are thin and liquid, containing undigested food and conside- 
 rable mucus, and may be streaked with blood. The stomach is 
 
204 ESSENTIALS OP DIAGNOSIS. 
 
 likely to share in the inflammatory process, and the symptoms 
 of a more or less intense gastritis are superadded. 
 
 When gastro-enteritis is due to the ingestion of corrosive and 
 poisonous substances or to the ingestion or development of 
 ptomaines, the symptoms become more severe, and collapse and 
 death may occur. 
 
 In the severe cases of acute enteritis, involving the serous, mus- 
 cular and submucous coats, constipation, or constipation alter- 
 nating with slight, irritative diarrhea, is the rule ; actual ob- 
 struction of the bowel, from inflammation, paralysis, or in- 
 carceration by bands of lymph, is not uncommon. The consti- 
 tutional and local symptoms are correspondingly intense. There 
 may be an initial chill. While the pain may be colicky at fii'st, 
 it soon becomes constant, subject, however, to paroxysmal ex- 
 acerbations. It is increased by pressure, tenderness at times be- 
 ing exquisite. As in peritonitis, the patient lies upon his back 
 with flexed thighs, to relax the abdominal muscles. There is not 
 uncommonly a marked and distressing pulsation to the right of 
 the umbilicus. Thirst, nausea, vomiting and retching may be 
 decided, even in the absence of gastric involvement. The fever 
 becomes high and does not remit, as it does in intestinal catarrh. 
 The 2mlse is^ rapid ; at first tense and full ; afterward, small and 
 wiry. Following a copious stool, amelioration and recovery may 
 ensue ; or symptoms of failing circulation, with distention of the 
 abdomen, hiccough, incessant retching, sweating, anuria and 
 exhaustion, may precede death. 
 
 How are acute catarrhal enteritis and typhoid fever to be 
 differentiated ? 
 
 Some degree of inflammation of the small intestine necessa- 
 rily attends typhoid fever. Occurring as an independent aftec- 
 tion, however, enteritis is wanting in the epistaxis, the severe 
 headache, the rose-spots, the characteristic temperature-curve, 
 the peculiar character of the stools, the gravity and the 
 typical course and duration of the general infectious disease. 
 
CROUPOUS ENTERITIS CHOLERA MORBUS. 205 
 
 Croupous Enteritis, 
 
 What is croupous enteritis ? 
 
 Croupous or membranous enteritis is a somewhat rare disease, 
 characterized by the discharge of fibrinous casts of the bowel, 
 or of flakes of false membrane. 
 
 These are usually expelled, after paroxysms of colic, with 
 painful straining, in watery stools containing mucus, sometimes 
 blood, but little fecal matter. The paroxysms are often pre- 
 ceded by constipation, and associated with or followed by diar- 
 rhea. The aifection is obstinately recurrent. It occurs chiefly, 
 if not exclusively, in hysterical or hypochondriacal subjects in 
 early adult or middle life. 
 
 Cholera Morbus. 
 
 What are the symptoms of cholera morbus or cholera nostras ? 
 
 Cholera marhus ov cholera nostras is an acute disease, most 
 prevalent during the summer months and characterized by 
 inflammation of the stomach and intestines. It is commonly a 
 result of the ingestion of unsuitable and irritating articles 
 of diet. The affection is manifested by colicky pains in the 
 abdomen, by nausea, vomiting and diarrhea, by cramps in the 
 legs, by increased thirst, by headache, vertigo and debility, by 
 coldness of the extremities, by prostration and rapid wasting. 
 Despite the severity of the symptoms, recovery is almost 
 invariable. 
 
 How are cholera morbus and cholera Asiatica to be differen- 
 ^ tiated ? 
 
 The symptoms of cholera morbus and those of cholera Asiatica 
 differ principally in degree. Cholera Asiatica, however, occurs 
 in epidemics ; isolated cases are rare. Cholera morbus, on the 
 other hand, is not an epidemic disease. The mortality from 
 cholera Asiatica is high ; recovery from cholera morbus is the 
 rule. The detection of characteristic comma bacilli in the feces 
 or in the vomit confirms a diagnosis of cholera Asiatica. 
 
206 ESSENTIALS OF DIAGNOSIS. 
 
 Cholera Infantum. 
 
 What are the symptoms of cholera infantum? 
 
 Cholera infantum is practically gastro-enteritis in children. 
 It is a disease of the summer mouths, and is intimately related 
 with heat, foul air, uncleanliness and fermentation of food. It 
 is manifested by vomiting, profuse watery, often fetid diarrhea, 
 fever, rapid Avasting, depressed fontanel, convulsions and coma. 
 Among the poor the fatality of the disease is great. 
 
 Chronic Enteritis. 
 
 What are the symptoms of chronic enteritis? 
 
 As chronic tnteritis or intestinal catarrh most frequently results 
 from persistent errors in diet, the symptoms depend upon 
 retarded and defective intestinal digestion. Pain and oppres- 
 sion occur at a time after the ingestion of food that varies with 
 the seat of the morbid process. In duodenal catarrh the s^'mp- 
 toms appear earlier than when the jejunum or ileum is involved. 
 When the lower portion of the intestine is affected, colicky pains 
 are frequent. There may be persistent diarrhea, obstinate con- 
 stipation, or diarrhea alternating with constipation. The stools 
 are slimy and may contain undigested food. The aMomen is 
 distended ; flatulence and belching are usual. The cmajjlexion 
 is sallow. The nutrition is impaired. Headache is common. 
 Sleep is disturbed by dreams, while there is unusual drowsiness. 
 
 Acute Dysentery. 
 
 What are the symptoms of acute dysentery ? 
 
 Acute dysentery is practically an inflammation of the large in- 
 testine, probably dependent upon a specific infection ; rarely 
 the lower portion of the small intestine is involved. The in- 
 flammation may be of varying intensit}'. It may be catarrhal, 
 ulcerative or diphtheritic. There are slight fever, abdominal 
 pains of a griping character (tormina), terminating with fre- 
 quent, small, slim}' stools, streaked with blood, each evacuation 
 
ACUTE DYSENTERY. 207 
 
 being attended with bearing-down, burning pain and muscular 
 spasm (tenesmus). The stools sometimes contain pus, sometimes 
 shreds of membrane ; in many cases the ameba coli is found. 
 In addition there are headache, vertigo, weakness, thirst and 
 perhaps nausea and vomiting. Dysentery is a prolific source 
 of hepatic abscess. Death may result from exhaustion, or from 
 perforation of the bowel. 
 
 How are intussusception of the bowel and acute dysentery to 
 be differentiated ? 
 
 In cases of intussusception of the bowel the stools may be 
 small, frequent, mucous, blood-streaked, and attended with 
 tenesmus. Inquiry, howevei", will elicit a history of abrupt 
 onset ; examination will disclose the presence of a sausage- 
 shaped abdominal tumor, perhaps also protrusion of the bowel 
 at the anus. Intussusception is the more common in children ; 
 dysentery, the more common in adults. 
 
 How are acute enteritis and acute dysentery to be differen- 
 tiated? 
 
 The pain of acute intestinal catarrh is colicky, but the pecu- 
 liar tormina and tenesmus of dysentery are wanting. The 
 stools of dysentery are more frequent than those of enteritis, 
 are smaller in quantity, contain more blood, and are in less 
 degree fecal. Dysentery is more likely than is enteritis to be 
 epidemic. 
 
 How are acute dysentery and typhoid fever to be differen- 
 tiated? 
 
 While both acute dysentery and typhoid fever are attended 
 with diarrhea, the stools of dysentery are frequent and small, 
 perhaps ineffectual, and are composed principally of blood- 
 streaked mucus ; the stools of typhoid iever are not necessarily 
 frequent, are larger, often thin and like pea-soup. The epis- 
 taxis, the rose-spots and the characteristic temperature-curve of 
 typhoid fever are wanting in acute dysentery. The duration of 
 dysentery is briefer than that of typhoid fever. 
 
208 ESSENTIALS OF DIAGNOSIS, 
 
 Chronic Dysentery. 
 
 What are the symptoms of chronic dysentery ? 
 
 Dysentery may from the outset manifest a tendency to chron- 
 icity ; or an acute dysentery may become chronic. The symp- 
 toms of chronic dysentery differ Uttle from those of the acute 
 disease. Febrile symptoms, however, are wanting ; intermis- 
 sions occur ; wasting takes place ; anemia develops ; the com- 
 plexion becomes sallow ; hepatic abscess may form. 
 
 Typhlitis. 
 
 What are the symptoms of typhlitis? 
 
 Inflammation takes place in the cecum or vermiform ap- 
 pendix as a result of the accumulation and impaction of fecal 
 matters ; or from irritation by a calculus, the nucleus of which 
 may be inspissated mucus from catarrh of the appendix ; or by 
 a foreign body, such as a cherry-stone or a grape-seed. Trau- 
 matism and straining are occasional exciting causes. The pro- 
 cess may be catarrhal, ulcerative or gangrenous. The pre- 
 monitory symptoms are vague and are frequently mistaken for 
 simple colic. Diarrhea may alternate with constipation, still 
 further misleading the inattentive observer. If the cecum be 
 involved, it becomes paralyzed and distended with accumulated 
 feces ; thus, the condition declares itself primarily by the symp- 
 toms of intestinal obstruction, by pain, often severe, and in- 
 creased by motion, in the right iliac fossa and right hip, with 
 tenderness, a sense of doughy induration, and dulness on per- 
 cussion. The tumor is superficial and sausage-shaped, its long 
 axis pointing inwards and downwards. It is slightly movable ; 
 gurgling may sometimes be developed. The pain may be parox- 
 ysmal or paroxysmally aggravated, and is frequently of an 
 agonizing character. There is usually some fever, and at times 
 the temperature may reach from 102° to 104° F. Peritonitis may 
 develop, even without ulceration and perforation of the bowel, 
 and its symptoms then predominate. It may remain localized 
 or become difiused. With relief to the obstruction, recovery 
 
PERITYPHLITIS. 209 
 
 may ensue, or collapse may suddenly occur, recovery or death 
 following. 
 
 If appendicitis alone exists there may be no interference with 
 the passage of the intestinal contents, and the evidences of a 
 tumor in the iliac fossa are wanting, unless the appendix have 
 undergone great distention. In ulcerative appendicitis, per- 
 foration not rarely results, giving rise to a general or localized 
 purulent peritonitis. This event may be announced by sudden 
 pain, shock, chill and rise of temperature, followed by the de- 
 velopment of a fluctuating tumor indicative of abscess ; or the 
 condition may develop insidiously and be difficult of recogni- 
 tion. Sometimes, after initial shock and pain, deceptive im- 
 provement is njanifested. Surgical exploration may be a diag- 
 nostic necessity. Attacks of typhlitis are prone to be repeated. 
 
 Perityphlitis. 
 
 What are the symptoms of perityphlitis ? 
 
 Perityphlitis, or inflammation of the tissues surrounding the 
 cecum and its appendix, usually occurs in the course of typhlitis 
 or of appendicitis. The fibrous structures and the peritoneum 
 are involved alone or in association. If perforation takes place 
 an abscess may form, or general peritonitis result, or both com- 
 plications may be present. As a rule, the pus is shut off from the 
 general peritoneal cavity by a capsule. The symptoms vary with 
 the pathologic association. To those of the primary condition are 
 added an acute exacerbation of pain and tenderness, as well as of 
 the general symptoms, perhaps preceded by a chill. The pain is 
 deep-seated and is increased by flexing the right thigh upon the 
 abdomen. Sometimes the patient is unable to lift the right leg. 
 He usually lies upon the right side, with the thigh semiflexed. 
 If an abscess forms, there may be repeated rigors and a fluctu- 
 ating tumor in the right iliac fossa. The tumor is not super- 
 ficial and sausage-shaped like that of cecitis, but is deep-seated 
 and irregular. A pericecal abscess may sometimes be detected 
 by rectal exploration. If peritonitis develop, death may ensue, 
 from septicemia or gradual exhaustion, or suddenly, with mani- 
 festations of collapse. 
 14 
 
210 ESSENTIALS OF DIAGNOSIS. 
 
 With what conditions may appendicitis or perityphlitis be con- 
 founded ? 
 
 Inflammations of the cecum and its appendix or inflamma- 
 tion and abscess of the surrounding tissue have been mistaken 
 for typlioid fever, and for " idiopathic peritonitis." 
 
 Tlie mistake is more likely to be made when the inflammation 
 of the appendix has been slow and the symptoms indistinct, 
 until perhaps perforation occurs, causing a limited abscess or a 
 general septic peritonitis. Deep-seated but limited abscess may 
 for a time be concealed from other than surgical exploration, 
 and through septic poisoning give rise to the "typhoid state." 
 
 Before localizing symptoms, such as induration, or the pres- 
 ence of a fluctuating tumor in the iliac fossa, render the case 
 clear, the occurrence of one or more rigors, the absence of dis- 
 tinctive characteristic symptoms of typhoid fever, the course of 
 the temperature, and sometimes the location of the tenderness, 
 should prevent mistake. The location of the pain and tender- 
 ness, however, may be misleading, as the appendix varies greatly 
 in its position ; and appendicitis has even been known to simu- 
 late hepatic disease. Sometimes only an exploratory incision 
 can settle the diagnosis. 
 
 The exploring needle or aspirator should never be used. 
 
 How are perityphlitis and typhlitis to be distinguished from a 
 lumbar abscess? 
 
 Destructive disease of a lumbar vertebra is usually followed 
 by suppuration, the pus following in the course of the psoas 
 muscle and seeking exit below Poupart's ligament. A collec- 
 tion of pus forming in this way differs from typhlitis or peri- 
 typhlitis by the absence of symptoms of intestinal derangement. 
 The situation of the tumor is different in each case. In the one 
 case, examination will reveal a deformity of the spinal column, 
 with pain and tenderness in the lumbar region. The symptoms 
 are slow and progressive. They may be associated with visceral 
 tuberculosis. 
 
 How are typhlitis and perityphlitis in a woman to be distin- 
 guished from an abscess of the right ovary ? 
 
 An abscess of the right ovary is situated nearer the middle line 
 than is the swelling of typhlitis or perityphlitis. With typhlitis 
 
INTESTINAL OBSTRUCTION. 211 
 
 or perityphlitis is associated gastro-intestinal derangement ; 
 with abscess of the ovary, uterine and menstrual derangement. 
 Vaginal and rectal examination may clear up any doubt. 
 
 How are typhlitis and perityphlitis to be distinguished from 
 carcinoma of the cecum ? 
 
 The symptoms of typhlitis and perityphlitis are likely to 
 appear suddenly ; those of carcinoma insidiously and progress- 
 ively. Typhlitis and perityphlitis are affections of compara- 
 tively brief duration ; carcinoma of the cecum will probably 
 continue for a number of months after its detection. The inflam- 
 matory processes are usually attended with fever ; carcinoma 
 is not. When typhlitis or perityphlitis has existed for some 
 time, fluctuation — indicative of the occurrence of suppuration 
 —can be detected in the tumor ; the carcinomatous new-growth 
 retains its original density. Perityphlitis or typhlitis may be 
 attended with emaciation and sallowness of skin, but not with 
 the cachexia of carcinoma. When the cecum is the seat of 
 carcinoma, like new-growths are usually found in other parts of 
 the body. 
 
 Intestinal Obstruction. 
 
 What are the symptoms of intestinal obstruction? 
 
 The lumen of the bowel may be obliterated by an accumula- 
 tion of feces, by a large gall-stone, by an intestinal calculus 
 (enterolith) or other foreign body, by organic narrowing of the 
 bowel, by stricture or neoplasm, by a twist or volvulus, by 
 external constriction and by strangulated hernia, internal or 
 external. 
 
 The condition may arise in a subject of habitual constipation 
 or of hernia. It may follow a violent physical effort. It may be 
 due to acute enteritis. From the onset, or after a variable 
 period during which no stool has been passed, abdominal pain 
 and rumbling set in. Vomiting ensues ; at first of the contents 
 of the stomach, then of yellowish-green fluid and mucus ; 
 finally the vomiting becomes stercoraceous. The apparent con- 
 stipation does not submit to ordinary measures. The abdomen 
 becomes distended. The expression of the face is drawn and 
 
212 ESSENTIALS OF DIAGNOSIS. 
 
 anxious, the pulse small, rapid and feeble, the surface cold and 
 clammy, and if the condition be not relieved by medicine or 
 operative intervention, death is the inevitable result. 
 
 When the obstruction is not complete, as in some cases of 
 fecal impaction, there may be more or less frequent passages of 
 liquid matters somewhat fecal, vphich the patient will de- 
 scribe as diarrhea. Inspection of the stools, and the evidences 
 given by palpation and percussion, of the presence of a hard 
 mass in the course of the bowel, usually in the transverse or 
 descending colon, will prevent error. The nature of the obstruc- 
 tion in any case is to be determined principally by physical ex- 
 amination. In cases of strangulated hernia the knowledge of 
 the existence of hernia may assist the diagnosis. In the absence 
 of such history, examination must none the less be made, if only 
 to exclude that condition from among the possibilities in the case. 
 
 Intussusception. 
 
 What are the symptoms of invagination or intussusception of 
 the bowel ? 
 Under certain circumstances, not definitely recognized, one 
 portion of the bowel becomes invaginated in' another portion. 
 The small intestine or the large intestine, respectively, may be 
 alone involved ; but most commonly the small intestine enters 
 the large at the ileo-cecal orifice. The occurrence of the acci- 
 dent is announced by a sudden attack of pain, repeated in 
 paroxysms, followed by the presence of a sausage-shaped 
 tumor in the abdomen, and stools of a dysenteric character. 
 Sometimes no fecal matter is passed, and there are frequent 
 discharges of blood-stained mucus. The pain is intense, and the 
 child (for the affection is most common in children) often draws 
 up its legs close to the belly. Pressure and manipulation relieve 
 the pain, and quiet the excruciating cries of agony. In the 
 course of a variable period of time, blood is passed by the bowel, 
 the pain becomes continuous and vomiting occurs, with the 
 symptoms of intestinal obstruction. The invaginated bowel 
 may be accessible to rectal examination ; it may even protrude 
 from the anus ; it may slough and be detached, and recovery 
 ensue ; or it may occasion stenosis of the bowel. Intussuscep- 
 
CARCINOMA OF THE INTESTINE. 218 
 
 tion is more common in children than in adults, and in boys 
 than in girls. 
 
 How are intussusception and obstruction of the bowel to be 
 differentiated ? 
 
 Intussusception is the more common in children ; obstruc- 
 tion, in adults. The symptoms of intussusception appear 
 abruptly ; those of obstruction are often abrupt in onset, 
 though sometimes of long standing. A sausage-shaped tumor 
 is characteristic of intussusception ; certain varieties of ob- 
 struction are attended with abdominal tumors of irregular 
 shape. Constipation is not so absolute in intussusception as in 
 obstruction ; and stercoraceous vomiting is less common in 
 the former than in the latter. A discharge of blood and the 
 protrusion of a portion of bowel from the anus are diagnostic 
 of intussusception. Digital exploration of the rectum will often 
 assist in discrimination. 
 
 How are typhlitis and intussusception of the bowel to be differ- 
 entiated ? 
 Both typhlitis and intussusception may present a sausage- 
 shaped tumor in the right iliac fossa and be attended with 
 severe pain and the evidences of intestinal obstruction ; but 
 intussusception, unlike typhlitis, is sudden in onset, is uncommon 
 in adults, is usually afebrile, is likely to be attended with 
 ineffectual or bloody stools, and perhaps to be accompanied 
 by protrusion of the bowel at the anus. The tumor of intus- 
 susception is not necessarily confined to the right iliac fossa. 
 
 Carcinoma of the Intestine. 
 
 What are the clinical manifestations of carcinoma of the 
 intestine ? 
 Carcinoma of the intestine is most commonly situated in the 
 rectum, the sigmoid flexure, the cecum, the vermiform appendix 
 or the duodenum. When in the duodenum, the papilla of the 
 pancreatic duct and common bile-duct is usually involved and 
 jaundice is apt to result. When other parts of the bowel are 
 involved, in addition to the pain and constitutional phenomena 
 occasioned by the malignant growth, symptoms of partial intes- 
 
214 ESSENTIALS OF DIAQNOSIS. 
 
 tinal obstruction develop. There is obstinate constipation, and 
 when the bowels are moved, the stools appear as thin, flat 
 bands, often streaked with pus and blood. On physical exam- 
 ination a tumor may be detected. 
 
 Intestinal Parasites. 
 
 What are the most common varieties of intestinal parasites ? 
 
 The most common intestinal parasites belong to the order of 
 vermes, of which there are two important classes — cestodes, or 
 tape-worms, and nematodes, or round-worms. 
 
 Of the former the more important are the tenia solium, the 
 tenia mediocanellata, and the hothrioce^jhahis lotus. 
 
 Of round-worms the most common are the ascaris lumiricoides, 
 the oxyuris vermicularis, and the trichina spiralis. 
 
 The oxyuris vermicularis inhabits the large intestine, the tape- 
 worms and the lumbricoides the small intestine ; the trichina 
 migrates from the stomach and small intestines into the muscles, 
 setting up an irritative fever with special symptoms, the condi- 
 tion being known as trichiniasis. 
 
 What symptoms are occasioned by the presence of animal 
 parasites in the intestinal canal? 
 
 The presence of worms in the intestinal canal of an otherwise 
 healthy individual may occasion no appreciable disturbance. In 
 other cases, however, there are evidences of gastro-intestinal 
 derangement, capricious appetite, abdominal uneasiness, colicky 
 pains, possibly diarrhea, nausea, vomiting, loss of flesh, debility, 
 cachexia, irregular fever, disturbed sleep, gritting of the teeth, 
 itching of the nose and anus, nervous manifestations, even epi- 
 leptiform convulsions. 
 
 The diagnosis of intestinal worms depends upon the discovery 
 of the parasites or of their ova in the stools. 
 
 Tenia Solium. 
 
 What are the characteristics of the tenia solium ? 
 
 The tenia solium (Fig. 24] is a tape-worm having a small head, 
 or scolex, and a slender neck. The head is of the size of a pin- 
 
TENIA MEDIOCANELLATA. 
 
 215 
 
 head, and is surmounted by a circle of twenty-six booklets, 
 around wlucli are four suckers. From the neck pass off segments, 
 or proglottides, that progressively increase in size. The entire 
 worm, or strobila, may be from seven to ten feet long and com- 
 posed of from four hundred to six hundred segments. The tenia 
 
 Head. 
 
 Mature segment. 
 Tenia Solium, magnified (Heller). 
 
 Ovum. 
 
 solium usually develops in man from the ingestion of " measly" 
 pork or the flesh obtained from swine infected with the cysticercus 
 cellulosae, which in turn develops in animals that have swal- 
 lowed the ova of the tenia solium. 
 
 Tenia Mediocanellata. 
 
 What are the characteristics of the tenia mediocanellata ? 
 
 The tenia mediocanellata, or unarmed tape-worm (Fig. 25) differs 
 from the tenia solium in that the head, though surmounted by 
 four suckers, is without booklets. The tenia mediocanellata may 
 attain a length of from ten to twenty feet, and be composed of 
 from eight hundred to more than one thousand segments, which 
 are longer and broader than those of the tenia solium 
 
 The tenia mediocanellata is transmitted to man by the raw 
 flesh of sheep or cows, in which hosts the larvae develop from 
 the ova of the tenia mediocanellata. 
 
 Tape-worms are usually present in small numbers ; there is 
 often but a single worm ; sometimes there are two or three. 
 
216 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 About three mouths are requisite for the development of a 
 tape-worm. 
 
 Fig. 25. 
 
 Head. 
 
 Mature segment. 
 Tenia mediocanellata, magnified (Heller). 
 
 Ovum, 
 
 Bothriocephalus Latus. 
 
 What are the characteristics of the bothriocephalus latus ? 
 
 The bothriocephalus laius (Fig. 26) sometimes called the tenia 
 lata, is a cestode worm, with a club-shaped head and a filament- 
 
 FiG. 26. 
 
 Mature segment. Ovum. 
 
 Bothriocephalus latus, magnified (Heller). 
 
 Ovum : embryo 
 developed. 
 
ASCARIS LUMBRICOIDES. 
 
 21T 
 
 ous neck. On either side of the head is a longitudinal sucker. 
 The mature segments present a characteristic stellate appear- 
 ance, dependent upon the distention of the uterus with ova. 
 The worm may be from fifteen to twenty-five feet in length, 
 and constituted of from three thousand to four thousand seg- 
 ments. It is thought to be derived from fish or fresh-water 
 molluscs. 
 
 Ascaris Lumbricoides. 
 
 What the characteristics of the ascaris lumbricoides? 
 
 Lumbricoid or round worms inhabit the small intestine. 
 Small worms, embryos, or ova, are supposed to gain access 
 
 Fig, 27. 
 
 a, natural size ; 6, head, magnified ; c, ovum, magnified. 
 Ascaris lumbricoides (v. Jakseh). 
 
 to the alimentary canal of man through drinking water, and in 
 some instances to be conveyed by the fingers to the mouths of 
 
218 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 those engaged in cleansing privies or otherwise handling excre- 
 ment, but the exact history of their development is unknown. 
 
 Mature worms are from eight to fifteen inches in length, are 
 attenuated at both extremities, and resemble common earth- 
 worms. Lumbricoid worms may be present in varying numbers, 
 from one to a dozen or more. They are usually multiple, and 
 in rare instances may "be so multitudinous as to occlude the in- 
 testine. The worms may find their way into the stomach, and 
 be expelled by vomiting. They may pass from the esophagus 
 into the larynx and trachea. They have in this way caused 
 suffocation in children. They may cause occlusion of the bile- 
 duct or pancreatic duct, and, though rarely, suppuration of the 
 liver or of the pancreas. They may also leave the intestine by 
 way of a perforation, causing peritonitis or fecal abscess. 
 
 Oxyuris Vermicularis, 
 
 What are the characteristics of the oxyuris vermicularis ? 
 
 Oxyures vermicular es^ seat-worms^ thread-worms, or spool-worms, 
 are from one-eighth to one-half of an inch long. They infest 
 the large intestine, especially the rectum. The worms find 
 their way out of the anus, and give rise to intense itching. 
 
 Fig. 28. 
 
 1, Female ; 2, males. Ovum, magnified. 
 
 Oxyuris vermicularis, natural size (Vierordt). 
 
 Sometimes they gain access to the vagina, and occasion un- 
 pleasant symptoms. The parasites may be present in the 
 bowel in large numbers ; they are often found in the stools in 
 tangled masses, resembling bunches of thread. 
 
ACUTE PERITONITIS. 219 
 
 Acute Peritonitis. 
 
 What are the symptoms of acute peritonitis ? 
 
 Acute peritonitis may result from the entrance of noxious mat- 
 ters into the peritoneal cavity, either through the blood, by 
 extension from adjacent disease, by intestinal perforation, or by 
 injury of the abdominal walls. Thus, among its causes may be 
 chronic nephritis, acute rheumatism, typhoid fever, dysentery, 
 typhlitis, appendicitis, disease of the uterus and oviducts, tuber- 
 culosis, infectious diseases and traumatism. 
 
 Acute peritonitis may be local or general; it may be simple^ 
 purulent^ or putrid. It is attended with acute abdominal pain, 
 tympanites, nausea, vomiting, constipation, considerable eleva- 
 tion of temperature and other febrile manifestations. The 
 pulse is small, rapid and tense—" wiry. " The /ace is drawn ; the 
 expression anxious. 
 
 The breathing is shallow, rapid, and thoracic. The abdominal 
 pain and tenderness are so intense that the patient shrinks from 
 the slightest movement, and complains of the lightest covering. 
 The legs and thighs are drawn up in flexion, to relax the ab- 
 dominal parietes. The surface of the body may be covered 
 with a cold sweat and collapse may ensue. Effusion may take 
 place or adhesions form among the structures in the peritoneal 
 cavity. Should pus form, there are repeated rigors and hectic 
 fever. If the inflammation is putrid, death speedily takes place 
 amid the symptoms of profound intoxication. 
 
 How are acute gastritis and acute peritonitis to he distin- 
 guished from one another ? 
 
 JS'ausea, vomiting, constipation, headache, abdominal pain 
 and tenderness, and febrile symptoms attend both acute gastritis 
 and acute peritonitis. In the former, however, the vomiting 
 occurs earlier and is more aggravated than in the latter, and 
 the vomited matter may contain blood. In peritonitis, the ab- 
 dominal pain and tenderness are not confined to the epigastrium, 
 but are more extensive and more intense than in gastritis, while 
 abdominal distention is more decided. A cause will be obvious 
 for an acute gastritis sufficiently intense to simulate peritonitis, 
 the symptoms of which are relatively the more profound. 
 
220 ESSENTIALS OF DIAGNOSIS. 
 
 How are acute peritonitis and acute enteritis to be differ- 
 entiated ? 
 
 The pain of enteritis is colicky ; that of peritonitis, lancinat- 
 ing. Tenderness is greater and more general in peritonitis than 
 in enteritis. Diarrhea is common in enteritis ; constipation is 
 the rule in peritonitis. !N'ausea and vomiting are more decided 
 in peritonitis than in enteritis. Effusion occurs in peritonitis, 
 not in enteritis. The constitutional disturbance of peritonitis 
 is comparatively more profound than that of enteritis. Rigors 
 and tiuctuating temperature are suggestive of peritonitis. The 
 cause of peritonitis is sometimes obvious in the history of the 
 case, or discoverable upon vaginal or other examination. 
 
 How are acute intestinal obstruction and acute peritonitis to 
 be differentiated ? 
 
 Constipation attends both acute peritonitis and acute in- 
 testinal obstruction ; it may yield in the one, but it is insuperable 
 in the other. Prior to the acute symptoms of obstruction there 
 may have been small, liquid evacuations, but, when the symp- 
 toms of obstruction have set in, constipation is absolute. The 
 vomiting of acute peritonitis does not present any unusual feat- 
 ures ; that of intestinal obstruction soon becomes stercoraceous. 
 The pain of obstruction is colicky ; that of peritonitis is sharp 
 and lancinating. The exquisite abdominal tenderness of peri- 
 tonitis is not encountered in obstruction. When obstruction 
 exists, the rolling of the intestines may be apparent to the e3'e 
 or to the palpating hand. Peritonitis occasions paralysis of the 
 bowel. The febrile symptoms of peritonitis are wanting in un- 
 complicated obstruction. 
 
 Inquiry and physical examination may elicit one of the known 
 causes of peritonitis or of obstruction respectively. 
 
 How are acute peritonitis and intestinal colic to be differenti- 
 ated? 
 
 Acute peritonitis and intestinal colic have pain in common ; 
 the latter, however, is unattended with febrile manifestations. 
 
 The pain of colic is inconstant and is relieved b}^ frictions ; 
 in peritonitis the pain persists and is intensified by the slightest 
 touch. 
 
CHRONIC PERITONITIS. 221 
 
 Colic, as a rule, is symptomatic, and its cause is to be ascer- 
 tained upon careful -search. A blue line on the gums would 
 indicate lead-poisoning. 
 
 How is subacute rheumatism involving the muscles of the wall 
 of the abdomen to be distinguished from acute peri- 
 tonitis ? 
 
 The pain of i-heumatism is not so severe as that of peritonitis ; 
 nor is it as constant ; nor does it give rise to symptoms of gastro- 
 intestinal derangement ; and it is not attended with febrile 
 manifestations ; while in addition there are other evidences 
 and a history of exposure to influences productive of subacute 
 rheumatism. 
 
 Chronic Peritonitis. 
 
 What are the symptoms of chronic peritonitis ? 
 
 Clironic inflammation of the peritoneum may be the sequel of an 
 acute attack ; it may be insidious in development. It is com- 
 monly a result of persistent irritation, such as may depend upon 
 the presence of new-growths, carcinomatous, sarcomatous or 
 tuberculous, or upon chronic inflammation of the abdominal or 
 pelvic viscera. 
 
 Adhesions form between adjacent viscera and fluid collects in 
 the abdominal cavity. Paroxysmal attacks of pain occur. The 
 abdomen is distended. There may be nausea and vomiting. 
 
 The action of the intestines is interfered with and constipa- 
 tion usually results. In tuberculous cases, with concomitant 
 ulceration of the intestine, there may be intercurrent or con- 
 tinuous diarrhea. In proportion to the chronicity of the attack 
 the omentum is found indurated and rolled up close to its attach- 
 ment to the stomach, the mesentery is shortened and the lumen 
 of the bowel is narrowed, producing visible and palpable distor- 
 tions and prominences. 
 
 There is commonly more or less fever, sometimes hectic, espe- 
 cially if the eflTusion be purulent. Sometimes, particularly in 
 tuberculous disease, there are recurrent febrile exacerbations. 
 In any case there occur gradual emaciation and loss of strength. 
 
222 ESSENTIALS OF DIAGNOSIS. 
 
 breathlessness, edema of the lower extremities ; spontaneous 
 recovery sometimes happens, but as a rule, unless relief be 
 given, surgically or medicinally, death ensues. The cases are 
 often protracted. 
 
 Malignant disease and tuberculosis of the peritoneum are most 
 frequently associated with similar conditions in other structures. 
 
 How are chronic peritonitis and malignant disease of the liver 
 to be differentiated ? 
 
 Malignant disease of the liver, like chronic peritonitis, may 
 give rise to a tumor in the upper portion of the abdomen, and 
 to ascites ; but the physical signs of enlargement fuse with 
 those that normally belong to the liver ; while the percusslon- 
 dulness dependent upon an omentum rolled up and contracted 
 by chronic disease is separated from the hepatic dulness b}'^ an 
 area ol tympanitic resonance. 
 
 Tabes Mesenterica. 
 
 What are the symptoms of tabes mesenterica ? 
 
 In predisposed children the glands of the mesentery some- 
 times become tuberculous, and there occur derangement of 
 health, anemia, and wasting. On palpation it may be possible to 
 detect the enlarged glands. In other respects, the symptoms are 
 like those of subacute peritonitis and chronic enteritis. There is 
 much confusion and dispute concerning the existence of a non- 
 tuberculous tabes mesenterica, of which the principal objective 
 symptom is the tumid abdomen. 
 
 THE LIVER. 
 
 What are the normal limits of the liver as determined by 
 physical examination ? 
 
 Under normal conditions the area of hepatic percussion-dul- 
 ness (Figs. 29 and 30) is included between the sixth rib on the 
 right, in the nipple line, the lower margin of the sixth rib 
 on the right in the axilla, and the tenth rib posteriorly on the 
 right, on the one hand, and the inferior border of the right 
 
FLOATING LIVER. 
 
 Fig, 29. 
 
 223 
 
 The relations of the heart, hings, liver, stomach and spleen, as seen from the 
 front (Weil). The deeply-shaded areas represent the portions of the heart, liver 
 and spleen not covered by the lungs ; the lightly-shaded areas represent portions 
 covered by the lungs, b, c,d, boundary between lung and heart ; e /, lower bound- 
 aries of lungs ; (/ /), upper boundaries of lungs ; I, lower limit of hepatic dulness ; 
 m, area of splenic dulness; ?i, greater curvature of stomach; ^, upper limit of 
 deep hepatic dulness. 
 
 costal arch on the other. The left lobe extends into the left 
 hypochondrium and the dulness to which it gives rise is practi- 
 cally inseparable from the cardiac percussion-dulness. 
 
 Floating Liver. 
 
 To what symptoms does a floating liver give rise ? 
 
 Occasionally the coronary ligament of the liver becomes length- 
 ened and the organ acquires an abnormal freedom of movement. 
 
224 ESSENTIALS OF DIAGNOSIS. 
 
 FiP. 30. 
 
 Sho-sving the relations of the kings, liver, spleen and kidneys, as seen from behind 
 (Weil-Liischka). ' The deeply-shaded areas represent portions of the liver and 
 spleen not covered by the lungs ; the lightly-shaded areas represent portions 
 covered by the lungs, a b, lower border of the lungs; e d, boundaries of comple- 
 mentary pleural spaces ; f/jr, divisions bet-sveen lobes of lungs ; ;', lower margin 
 of liver. 
 
 That such an unusual tumor in the abdomen is the liver is de- 
 termined by the size and conformation of the organ, by the per- 
 cussion-resonance in the normal region of the liver and by the 
 absence of the phenomena of malignant disease. 
 
 Congestion of the Liver. 
 
 What are the symptoms of congestion of the liver ? 
 
 Coiujestion of the liver results from derangement of the circula- 
 tion dependent upon disease of the heart or lungs, or upon com- 
 
ACUTE HEPATITIS. 225 
 
 pressioii of the hepatic vessels ; it may result from constant irri- 
 tation of the hepatic cells by improper, and especially stimulating, 
 articles of diet ; it is wont to occur in those of inactive and seden- 
 tary habits. The condition is manifested by a sense of weight 
 and dull pain in the right hypochondrium, pain at the right 
 shoulder, headache and vertigo. The cqjpeiite is impaired; the 
 tongue is coated ; there are nausea and vomiting ; the digestion 
 is deranged ; the bowels are constipated ; the sA-mand conjunctiva 
 may present a yellowish tinge ; hemorrhoids frequently develop ; 
 there is, sometimes, mental depression or irritability of tem- 
 per ; the heart may be irritable, as manifested by palpitation. 
 The urine may contain bile-pigment and an excess of urates. 
 
 Acute Hepatitis. 
 
 What are the symptoms of acute hepatitis ? 
 
 Acute hepatitis is essentially a disease of tropical climates. 
 It may also occur in association with dysentery and other in- 
 fectious diseases. 
 
 It is manifested by pain in the right hypochondrium, febrile 
 symptoms and possibly slight Jaundice. The appetite is im- 
 paired, and there may be nausea and vomiting. Abscess is 
 a not uncommon sequel of inflammation of the liver. 
 
 How is the malarial cachexia to be distinguished from acute 
 hepatitis ? 
 As a sequel of chronic malarial poisoning, the liver and the 
 spleen become crowded with pigment and undergo enlarge- 
 ment. There may be slight intermittent fever ; the fever of 
 hepatitis is continuous and not periodic. In the malarial 
 cachexia the complexion is sallow, not jaundiced, as it may be 
 in hepatitis. In the malarial cachexia, too, plasmodia are to 
 be found in the blood. 
 
 How are acute hepatitis and portal phlebitis to be differentiated? 
 
 Portal phlebitis may develop in the course of infectious dis- 
 eases or of pyemia ; it may also result by extension from 
 adjacent disease. It is attended by pain in the right hypo- 
 chondrium, by enlargement of the liver, by distention of the 
 15 
 
226 ESSENTIALS OF DIAGNOSIS. 
 
 veins of the abdominal wall, by ascites, b}^ enlargement of the 
 spleen and by diarrhea. Gastric or intestinal hemorrhage may 
 occur. AVhen suppuration takes place, there are recurring 
 chills and fever, with wasting and debility. Enlargement of 
 the spleen, distention of the abdominal veins and gastric and 
 intestinal hemorrhage are not a part of acute hepatitis. 
 
 Acute Yellow Atrophy of the Liver. 
 
 What are the symptoms of acute yellow atrophy of the liver ? 
 
 The etiology of acute yelloic atrophy of the liver is obscure. 
 The disease is more common in females than in males, and in 
 young adults than in others ; it sometimes appears in the 
 course of pregnancy •, at other times, in conjunction with pro- 
 found emotion. After death, the liver is found to be much re- 
 duced in size and weight ; in places it presents areas of reddish, 
 purplish and yellowish discoloration, in the midst of w^hich the 
 hepatic cells are replaced by granules and oil-globules. By 
 some the condition is said to be a parenchymatous inflammation 
 of the liver. 
 
 The onset of the more grave symptoms may, for a few days 
 or weeks, have been preceded by jaundice. This has even been 
 associated in rare instances with enlargement of the area of 
 hepatic percussion-flatness. Commonly, there are soon added 
 headache, intolerance of light, delirium, stupor, convulsions 
 and coma. The tongue is dr}' and coated ; there are nausea 
 and vomiting. Hemorrhages from the mucous surfaces often 
 occur, and subcutaneous petechiae appear. The area of hepatic 
 percussion-dulness progressively diminishes; the abdomen be- 
 comes distended. The urine may be scarcely discolored ; it 
 contains leucin and tyrosin, and sometimes albumin ; it is defi- 
 cient in urea, uric acid, chlorides, phosphates and sulphates. 
 There may be chills and irregular fever, sometimes high ; but 
 usuallj' there is but slight elevation of temperature ; and in most 
 cases the temperature is at some time subnormal. The disease 
 rarely lasts longer than a week ; it usually terminates fatally. 
 
ACUTE YELLOW ATROPHY OF THE LIVER. 227 
 
 How are acute yellow atrophy of the liver and typhoid fever to 
 be differentiated ? 
 
 Typhoid fever is a disease lasting three or four weeks ; re- 
 covery is common. The active stage of acute yellow atrophy 
 rarely lasts longer than a week ; the termination is usually fatal. 
 There is but slight or very irregular fever in acute yellow atrophy 
 and nearly always a tendency to subnormal temperature ; the 
 course of typhoid fever is decidedly febrile and typical. Diar- 
 rhea is common in typhoid fever ; constipation, in acute yellow 
 atrophy. The size of the liver becomes much reduced in acute 
 atrophy ; it is unchanged or increased in typhoid fever. Rose- 
 spots are wanting in acute atrophy, in which there may be pe- 
 techise. Jaundice is invariable in acute atrophy ; rare in 
 typhoid fever. The cerebral symptoms are more decided in the 
 hepatic disease than in the infective fevei\ The presence of 
 leucin and tyrosin and the deficiency of urea, uric acid, chlo- 
 rides, phosphates and sulphates in the urine are characteristic 
 of acute yellow atrophy. 
 
 How are acute yellow atrophy of the liver and phosphorus- 
 poisoning to be differentiated ? 
 
 The symptoms occasioned by poisoning with phosphorus 
 closely resemble those of acute yellow atrophy of tlie liver. 
 Phosphorus-poisoning, however, usually sets in with vomiting 
 and purging, to which the subsequent manifestations succeed ; 
 there is sometimes necrotic disease of the inferior maxillary 
 bone. The first symptom of acute yellow atrophy of the liver 
 is jaundice. In phosphorus-poisoning the liver is enlarged 
 prior to becoming smaller ; the diminution in the size of tlie 
 liver in acute j'ellow atrophy is progressive from the outset of 
 active symptoms, though the organ may have been enlarged 
 previously. Colicky abdominal pains usually attend phosphorus- 
 poisoning, of which it may be possible to elicit a history. The 
 anatomic lesion of acute yellow atrophy is a parenchymatous 
 hepatitis ; of phosphorus-poisoning, a fatty degeneration of the 
 liver. 
 
228 ESSENTIALS OF DIAGNOSIS. 
 
 Abscess of the Liver. 
 
 What are the symptoms of ahscess of the liver ? 
 
 Abscess of the liver ina}^ follow acute hepatitis ; it may result 
 from the activit}- of pyogenic organisms introduced into the 
 structure of the organ in the course of ulcerative processes in 
 the distribution of the tributaries of the portal vein or as a part 
 of a general pyemia. When the suppuration is dependent upon 
 hepatitis or ulceration, but a single abscess usually develops ; in 
 cases of pyemia, there may be multiple abscesses, not only in the 
 liver, but also elsewhere. Dysentery is a prolific cause of hepatic 
 abscess. When the two are associated, the ameba coli may be 
 found both in the stools and in the abscess or its walls. As a 
 result of the inflammation associated wath the development of an 
 abscess, the liver becomes enlarged and tender, the enlargement 
 being detectable by palpation and percussion. There is pain 
 over the liver and at the right shoulder. The right hypochon- 
 drium may be exquisitely tender. Repeated rigors may occur ; 
 there may be periodic exacerbations of temperature, followed by 
 copious sweats. Slight jaundice may develop, but it is often 
 absent. There may be nausea, vomiting and diarrhea. Hic- 
 cough, cough and dyspnea may result from pressure upon the 
 diaphragm, and pleuris}', with the symptoms and physical signs 
 denoting a rapid eftusiou, may result from extension of the 
 inflammation or convej^ance of the infection. If the abscess is 
 superficial, a fluctuating tumor may be detectable in the right 
 hypochondrium. The abscess may rupture into the pleural 
 cavity or into the peritoneum, with a fatal termination ; or the 
 pus may make its exit through the abdominal wall, or even into 
 the intestines. An hepatic abscess may be evacuated through 
 the bronchial tubes. Death may result from septic poisoning or 
 from exhaustion. 
 
 How are abscess of the liver and occlusion of the hiliary pas- 
 sages to he differentiated ? 
 If the common bile-duct is obstructed, bile accumulates in 
 the gall-bladder and in the radicles of the hepatic ducts, tlie 
 liver becomes enlarged, and jaundice, rigors, fever and sweats 
 appear. The stools are pale. 
 
INTERSTITIAL HEPATITIS. 229 
 
 If the cystic duct is occluded, there is do jaundice and the 
 stools are not discolored. In both instances, the gall-bladder 
 becomes distended with fluid and constitutes a fluctuating 
 tumor, which may simulate an abscess. Tlie dift'erentiation 
 depends upon the fact of the tumor occupying the situation of 
 the gall-bladder, upon a knowledge of the existence of a cause 
 of biliary obstruction, such as a calculus or a neoplasm, and 
 upon the absence of a cause of abscess ; nor is an abscess likely 
 to occasion jaundice. 
 
 How are abscess of the liver and carcinoma of the liver to be 
 differentiated ? 
 
 Medullary carcinoma may give rise to a sort of fluctuation 
 on palpation, but beyond this and the enlargement of the liver, 
 the symptoms differ radically from those of abscess. In cases 
 of carcinoma, chills, fever and sweats do not occur ; but there 
 is distinct cachexia, perhaps with nodules in other situations. 
 
 How is actinomycosis of the liver to be distinguished from 
 abscess of the liver ? 
 
 Actinomycosis is dependent upon the presence of a special 
 fungus, which usually gains entrance through an abrasion of 
 the surface, and may be disseminated by the blood-stream. 
 
 The irritation caused by the presence of the fungus, or per- 
 haps by some product of its metabolifTm, is followed by inflamma- 
 tion and suppuration, so that the conditions of abscess are repro- 
 duced, and in that sense there is no discrimination to be made. 
 
 The diagnosis depends upon a knowledge of infection or of 
 the existence of the disease at the original site of entrance, or 
 the discovery of the ray-fungus (actinomyces) in the pus. 
 
 Interstitial Hepatitis — Cirrhosis of the Liver. 
 
 What are the symptoms of interstitial hepatitis, also called 
 sclerosis or cirrhosis of the liver ? 
 When irritating matters are in constant circulation in the 
 blood-current, especially in the portal stream, the interstitial 
 connective-tissue of the liver slowly undergoes hyperplasia, to 
 the consequent detriment of the parenchymatous structures. 
 
230 ESSENTIALS OF DIAGNOSIS. 
 
 The rapidity of the process depends upon the intensity of the 
 irritation. When tlie increase of connective tissue has reached 
 its heiglit, contraction sets in and tlie liver-cells sufler still more. 
 The organ, at first irregularly, perhaps nodularl}', enlarged, now 
 becomes diminished in size. This is the condition of cirrhosis. 
 The different stages are sometimes respectively called h/pertro- 
 phic cirrhosis and atropMc cirrhosis. In many cases the enlarge- 
 ment persists, notwithstanding extensive destruction of the 
 secreting structures. In other cases the hepatic percussion- 
 dulaess and palpation-area are apparently diminished from the 
 first. In the earl}' stages of the disease the symptoms are in- 
 conspicuous ; there may be mauifestations of derangement of 
 the gastro-intestinal S3\stem. As the contraction becomes more 
 marked, however, there appear evidences of interference with 
 the functions of the liver. Ascites develops ; the superficial 
 veins of the abdomen become enlarged and prominent ; this 
 may be especially marked in the ueighl)orhood of the umbilicus, 
 giving rise to the so-called Caput Ileduscc; small networks of 
 venules appear at various parts of the surface of the bod}' ; 
 hemorrhoids form ; hemorrhages may take place from the nose 
 and stomach ; the skin assumes a pallid, clayey hue ; and ulti- 
 mately jaundice appears. Yertigo is not rare. Late in the dis- 
 ease, drowsiness and coma may develop. Excessive indulgence 
 in alcohol is the most prolific cause of cirrhosis of the liver. 
 
 Fatty Liver. 
 
 What are the symptoms of fatty liver ? 
 
 The liver may undergo /aHy injiltration or fatty metammphosis. 
 A temporary accumulation of fat in the liver occurs under 
 normal conditions after the ingestion of food rich in hydrocar- 
 bons. When, from any cause, oxidation becomes deficient, this 
 fatty infiltration may become permanent and excessive, the 
 more especially if, at the same time, immoderate eating or 
 drinking is indulged in. Thus the condition is found in the 
 indolent, in gourmands, in the obese, in the subjects of pul- 
 monary tuberculosis and in drunkards. 
 
 Drunkards,, however, are more liable to true fatty metarnor- 
 
AMYLOID DISEASE OF THE LIVER. 231 
 
 pilosis, the liver-cells in circumscribed or extensive areas un- 
 dergoing oily degeneration, a condition that may likewise occur 
 in wasting diseases, or as an apparent result of protracted dis- 
 charges, or of blood-changes, in pyemia, infectious diseases, or 
 other morbid states accompanied by protracted high tempera- 
 ture. It is sometimes a part of the degenerative processes of 
 old age. It may accompany carcinoma, cirrhosis and amyloid 
 degeneration of the liver. 
 
 The symptoms are not early obtrusive. The area of hepatic 
 percussion-dulness is increased, and to palpation the organ 
 seems smooth and rounded, perhaps soft and doughy. The 
 skin may feel greasy or velvety, and is sometimes smooth and 
 glistening ; it may be pale or flushed. Jaundice is uncommon ; 
 tliere is no pain ; ascites is rare. Diarrhea is the most con- 
 stant symptom, and the least indiscretion in diet may provoke 
 gastro-intestinal catarrh. In the more advanced stages anemia, 
 hydremia, dyspnea and patent signs of failure of hepatic function 
 appear. 
 
 Amyloid Disease of the Liver. 
 
 What are the symptoms of amyloid, waxy or lardaceous disease 
 of the liver ? 
 When the liver undergoes amyloid degeneration, other organs, 
 such as the spleen, the kidneys, perhaps, also, the stomach and 
 the intestines, are likewise involved, either simultaneously 
 or consecutively. The liver is smoothly and often enormously 
 enlarged ; digestion is impaired ; there may be persistent diar- 
 rhea. Pain, jaundice and ascites are uncommon. Isolated dis- 
 ease of the liver usually escapes detection. The process is 
 chronic. Amyloid degeneration is a sequel of syphilis, of tuber- 
 culosis, of suppuration, of bone-disease. 
 
 How are amyloid disease and cirrhosis of the liver to be differ- 
 entiated ? 
 
 The liver is enlarged in both amyloid disease and cirrhosis of 
 the liver ; the enlargement is persistent in the one, replaced by 
 contraction in the other. The amyloid liver is smooth, the cir- 
 
232 ESSENTIALS OF DIAGNOSIS. 
 
 rhotic liver usually irregular. Cirrhosis is attended with ascites 
 and jaundice, while amyloid disease, as a rule, is not. In amy- 
 loid disease, there is a history of syphilis, of tuberculosis, of 
 suppuration or of bone-disease ; in cirrhosis, there is in most 
 cases a history of alcoholism. With amyloid disease of the liver 
 is usually associated amyloid disease of the kidney, occasioning 
 the presence of albumin and tube-casts in the urine. The tube- 
 casts will sometimes give a characteristic reaction with iodine. 
 
 Carcinoma of the Liver. 
 
 What are the symptoms of carcinoma of the liver ? 
 
 The liver is a frequent seat of carcinoma, which may be 
 primary or secondary. Primary carcinoma of the hver is 
 usually diffuse, the organ becoming greatly increased in size ; 
 secondary carcinoma is usually nodular. In its incipiency 
 carcinoma of the liver may escape detection. Soon, however, 
 there is unaccountable loss of tlesh, with the development of 
 the characteristic cachexia. The liver is noted to be enlarged, 
 and on palpation adventitious nodules may be felt through the 
 abdominal wall, in the region of the right hypochondrium. 
 Jaundice is uncommon, unless the biliary passages are com- 
 pressed. The abdomen becomes distended and fluid collects in 
 the peritoneal cavity. The digestive derangement becomes 
 marked. Emaciation progresses and the patient becomes re- 
 duced to the lowest degree. There is often excruciating, lan- 
 cinating pain. Tenderness in the right bypochondrium is a 
 fairly constant attendant of carcinoma of the liver. 
 
 How is carcinoma of the liver to be distinguished from amyloid 
 disease of the liver ? 
 Emaciation and anemia attend both carcinoma and amyloid 
 disease of the liver ; but the straw-colored appearance presented 
 by a patient with the carciilomatous cachexia is wanting in the 
 conditions tbat give rise to amyloid disease. Cases of carcinoma 
 do not present the peculiar distribution of amyloid disease in 
 liver, spleen, kidneys and gastro-intestinal tract. . The liver is 
 often nodulated when carcinomatous ; an amyloid liver is 
 
CARCINOMA OP THE LIVER. 233 
 
 always smooth. Pain is present in carcinoma, absent in amyloid 
 disease. A history of congenital, or of acquired syphilis, of 
 tuberculoiss, or the presence of a suppurating focus anywhere 
 in the body would weigh in favor of amyloid disease. Amyloid 
 disease itself is not immediately fatal. Life is not likely to be 
 prolonged for more than a year after carcinoma of the liver has 
 been discovered. 
 
 How are carcinoma of the omentum and carcinoma of the liver 
 to be differentiated. 
 
 When carcinoma develops in the omentum, this structure 
 becomes shortened and rolled up beneath its attachments. As 
 a consequence, there is dulness on percussion, and evidences of 
 a new-growth on palpation, not alone in the right hypochon- 
 drium, but in the epigastric and umbilical regions, and in the 
 left hypochondrium. 
 
 Carcinoma of the omentum is more commonly than carcinoma 
 of the liver associated with ascites. In carcinoma of the omen- 
 tum the symptoms of derangement of the functions of the liver 
 are wanting. A new-growth of the liver rises and falls with this 
 organ in expiration and inspiration ; when the omentum is 
 involved the mass is fixed. 
 
 How are carcinoma of the stomach and carcinoma of the 
 liver to be differentiated? 
 Carcinoma of the stomach and carcinoma of the liver pre- 
 sent many symptoms in common : a tumor in the right hypo- 
 chondrium, progressive emaciation, cachexia and secondary 
 growths ; but when the stomach alone is involved there is obsti- 
 nate vomiting, with absence of evidence of hepatic derangement'; 
 while if the liver only is involved ascites is common, and vomit- 
 ing of coffee-ground material is lacking. A new-growth of the 
 liver will rise and fall with this organ in respiration ; a gastric 
 tumor is more fixed. The percussion-dulness yielded by a 
 tumor of the liver merges with the dulness of the liver ; while 
 the dulness of a tumor of the stomach may be separated from 
 the hepatic dulness by an interval of tympanitic resonance. 
 Hepatic and gastric carcinoma not infrequently coexist. 
 
234 ESSENTIALS OF DIAGNOSIS. 
 
 Hydatid Cyst of the Liver. 
 
 To what symptoms does an hydatid cyst of the liver give rise ? 
 
 A small, deeply-seated hydatid cyst of the liver, not iuterfering 
 with the function of other parts, may give no sign. When the 
 liver is the seat of an hydatid cyst in an accessible situation, the 
 condition may be recognized by the presence of a soft, elastic, 
 resistant, fluctuating tumor, the viscid contents of which 
 may, on percussion and palpation, transmit a peculiar thrill or 
 fremitus. This " purring tremor," recalling the trembling of a 
 bowl of jelly, is present in about one-half of the cases. In 
 addition, there may be pain in the right hypochondrium. The 
 presence of such a new-growth, together with the absence of 
 symptoms of profound constitutional disturbance, distinguishes 
 an hydatid cyst from a malignant growth in the liver and its 
 neighborhood. 
 
 Pressure-signs vary with the location of the tumor. A cyst 
 situated near the hepatic duct or common bile-duct may cause 
 obstruction and fatal jaundice ; jiressure on the portal vein 
 may cause ascites ; jaundice and dropsy, however, are not usual. 
 If on the upper surface of the right lobe, the cyst will push up 
 the diaphragm, giving rise to dyspnea and cough. The heart 
 may be displaced. If the enlargement takes a different direc- 
 tion, the abdominal viscera may be encroached upon. There 
 may be multiple cysts. 
 
 Retrogressive changes may take place in an hydatid cyst, 
 attended with a diminution in size. The contents of the cyst 
 may be evacuated through the stomach, bowel, bronchial tubes 
 or abdominal wall,^ or into the abdominal or pleural cavity. 
 
 Spontaneous evacuation may lead to recovery or it may cause 
 inflammation and suppuration of the invaded organ and death 
 result. Sudden death may happen from invasion of the vena 
 cava or of the pericardium. When retrogression or evacuation 
 is not brought about, spontaneouslyor therapeutically, gradual 
 failure and death may occur from exhaustion, or from septi- 
 cemia. 
 
PERIHEPATITIS. 235 
 
 How are abscess of the liver and hydatid cyst of the liver 
 to be differentiated? 
 
 An hydatid cyst of the liver is ordinarily wanting in the 
 constitutional phenomena of hepatic abscess : rigors, fever, 
 sweats, emaciation. Should suppuration take place an abscess 
 virtually results. Hydatid cysts are insidious in onset, slow in 
 development, protracted in duration, and may undergo sponta- 
 neous disappearance ; when accessible they occasion extensive 
 percussion-dulness and a peculiar thrill on palpation. An he- 
 patic abscess may be insidious in onset, but it soon gives rise 
 to decided symptoms ; spontaneous resolution never occurs, and 
 thrill or fremitus is wanting. The detection of echinococcus 
 booklets in the contents of an hydatid cyst, and of amebse coli 
 in the pus from an hepatic abscess may in each case be regarded 
 as diagnostic. 
 
 There is a growing tendency to regard exploratory puncture 
 as inconclusive and dangerous, and to substitute exploratory 
 incision— the latter to be followed if necessary by immediate 
 operation. 
 
 How are an hydatid cyst of the liver and a distended gall- 
 bladder to be differentiated ? 
 
 Distention of the gall-bladder is usually dependent upon 
 occlusion of the common bile-duct, or of the cystic duct, and is 
 commonly associated with intense jaundice and clay-colored 
 stools. Jaundice is exceptional in the case of an hydatid cyst, 
 and the action of the bowels is not necessarily deranged. A 
 distended gall-bladder occupies a definite situation ; an hydatid 
 cyst may be seated in any part of the liver. The "purring 
 tremor" is not given by a distended gall-blader. 
 
 Perihepatitis. 
 
 What are the clinical features of chronic inflammation of the 
 capsule of the liver, or perihepatitis ? 
 The capsule of the liver may become thickened as a result of 
 contiguous inflammatory processes, such as pleuritis and hepa- 
 titis, or as may be occasioned by a gastric ulcer. Perihepatitis 
 
236 ESSENTIALS OF DIAGNOSIS. 
 
 may also be but a part of a chronic peritonitis. The liver itself 
 is deformed, but otherwise not altered in size. The symptoms 
 are ill-defined. Pain and tenderness in the region of the liver 
 are usually present. Ascites develops. The kidneys are said 
 usuallj^ to be diseased, so that the urine contains albumin. 
 
 How are chronic perihepatitis and cirrhosis of the liver to be 
 differentiated ? 
 
 Cirrhosis of the liver and perihepatitis may be associated. 
 Occurring independently,, the enlargement or the diminution in 
 the size of the liver and the jaundice of cirrhosis are likely to be 
 wanting in perihepatitis ; while the presence of albumin in the 
 urine points to the existence of perihepatitis. 
 
 Cholangitis — Cholecystitis. 
 
 What are the symptoms of inflammation of the bile-ducts and 
 gall-bladder ? 
 
 Inflammation or catarrh of the bile-ducts and gall-bladder, the 
 most common cause of jaundice, is a result of the extension of 
 inflammation or catarrh or of the invasion of microbes from the 
 duodenum or of the presence of biliary calculi. 
 
 In consequence of the swelling of the mucous membrane, the 
 flow of bile is interfered with and jaundice results. The sur- 
 face of the body and the visible mucous membranes assume a 
 yellowish or greenish hue ; the urine is similarly discolored ; the 
 stools become scanty and claj'-colored. The saliva may be 
 discolored. 
 
 There is pain in the right hypochondrium ; the liver is en- 
 larged. The action of the heart is retarded. There is itching 
 of the skin. The appetite is usually impaired ; the tongue is 
 coated ; digestion is enfeebled ; the bowels are constipated. 
 Chills and irregular fever or transient rise of temperature may 
 occur. 
 
 How is catarrhal jaundice to be distinguished from other 
 forms of jaundice? 
 
 Many conditions occasion jaundice. In some, as in catarrhal 
 jaundice, there is an interference with the discharge of bile into 
 
CHOLANGITIS — CHOLECYSTITIS. 237 
 
 the intestine ; in others, no such obstruction can be detected. 
 In the first group of cases belong sucli conditions as occlusion 
 of the common bile-duct by gall-stones, compression of the 
 common bile-duct by enlarged glands or by neoplasms or as a 
 result of inflammation and thrombosis of the portal vein. In 
 the second group belong yellow fever, the intense forms of ma- 
 larial fever, acute yellow atrophy of the liver and cirrhosis 
 of the liver. 
 
 When the common bile-duct is occluded by a calculus, repeated 
 attacks of colic are apt to occur, attended with excruciating 
 pain, referred to the right hypochondrium ; and occasionally 
 one or more calculi are expelled into and from the intestine, so 
 as to be found in the stools. If the calculus is large, or if more 
 than one is present, it or they may be detected by palpation. 
 Colic and severe pain are wanting in catarrhal jaundice, the 
 icterus of which is apt to be less intense and less protracted than 
 that of obstructive disease. 
 
 In compression of the common bile-duct, the portal vein is 
 likely also to be compressed, so that ascites develops. When 
 such compression is dependent upon an enlarged gland this may 
 be palpable from without. 
 
 Pykplilehitis is likely to be associated with an ulcerative process 
 in the stomach or bowel, or with a suppurating hydatid cyst 
 and may be attended with rigors and decided febrile mani- 
 festations. 
 
 Malignant disease may involve the biliary passages or the sur- 
 rounding structures. A malignant growth occasions emaciation 
 and a peculiar cachexia manifested by a straw-colored com- 
 plexion. Ascites, tumor, repeated rigors, decided fever, ema- 
 ciation and cachexia are wanting in catarrhal jaundice. 
 
 Yellow fever is an epidemic, infectious disease, characterized 
 by a train of grave symptoms, including headache, pains, fever, 
 vomiting and prostration, that is wanting in catarrhal jaundice. 
 
 When malarial fever is attended with jaundice, there are com- 
 monly, in addition, chills, fever, sweats and perhaps hematuria. 
 
 The symptoms of acute yellow atrophy of the liver may super- 
 vene upon those of an apparently catarrhal jaundice. In such 
 a case the area of hepatic percussion-dulness rapidly becomes 
 
238 ESSENTIALS OF DIAGNOSIS. 
 
 diminished, cerebral symptoms appear, the urine contains 
 leucin and tyrosiu, and is deficient in urea, uric acid, chlorides, 
 phosphates and sulphates, and death is the usual issue. 
 
 When jaundice attends cirrhosis of the li>:er, the discoloration 
 is gradual in onset and slight in degree. There are, besides, 
 enlargement or shrinkage of the liver and ascites. 
 
 Biliary Calculi. 
 
 What are the clinical manifestations of biliary calculi ? 
 
 Biliary calculi are more common in women than in men, and 
 late in life than early. They result from the precipitation and 
 agglomeration of the less soluble elements of the bile. They 
 may be single or multiple. They occasion symptoms when 
 they give rise to obstruction. 
 
 The passage of a gall-stone through the common bile-duct is 
 attended with excruciating colicky pain in the right hypochon- 
 drium, with shivering, nausea, vomiting and hiccough. The 
 face is pale and the surface of the body is covered with a cold 
 sweat. Jaundice soon develops — transient, if the calculus 
 passes into the bowel ; persistent, if the calculus remains 
 impacted in the common duct. 
 
 By ulceration and perforation an impacted gall-stone may 
 find its way into the stomach, the bowel or the peritoneal 
 cavity, or it may be evacuated externally through the walls of 
 the abdomen. 
 
 Attacks of hepatic colic are prone to be repeated. Occlusion 
 of the common or of the hepatic duct is followed by stagnation 
 of bile, increased secretion of mucus, and ultimately by the 
 formation of pus. The gall-bladder may become distended into 
 a great sac, and the accumulation advance into the biliary 
 radicles. Under such circumstances, jaundice persists and a 
 type of fever develops that has been designated hepatic inter- 
 mittent. Periodic elevations of temjjerature occur, preceded 
 by rigors and followed by sweats. Unless relief is afforded, 
 death ultimately results from cholemia or from acholia. 
 
 Biliary calculi and carcinoma of the biliary passages are not 
 rarely associated. 
 
BILIARY CALCULI. 239 
 
 How are hepatic intermittent fever and malarial intermittent 
 fever to be differentiated ? 
 
 The interniitteut fever that occurs as a result of obstruction 
 of the biliary passages, with subsequent suppuration, closely 
 resembles malarial intermittent fever ; but in the former, there 
 is jaundice, intense and persistent ; the distended gall-bladder 
 or the obstructing calculi may be detectable by palpation ; 
 parasites are not present in the blood ; and the fever does not 
 yield to quinine. 
 
 How are hepatic colic, renal colic and intestinal colic to be 
 differentiated ? 
 The pain of hepatic colic is referred especiall}' to the right 
 hypochondrium, whence it may radiate to the right shoulder ; 
 that of renal colic is referred to one loin, not necessarily the 
 right, whence it radiates in the course of the corresponding 
 ureter ; the pain of intestinal colic is especially umbilical, 
 whence it may radiate over the entire abdomen. Hepatic colic 
 is soon followed by jaundice ; the urine contains biliary pig- 
 ment, and is greenish or brownish in color. In cases of renal 
 colic, the urine may contain pus-corpuscles, blood-corpuscles and 
 crystalline matters ; jaundice is wanting. Intestinal colic de- 
 pends upon intestinal derangement, sometimes upon lead-poison- 
 ing ; the urine remains unaltered ; there is no jaundice. 
 
 How are carcinoma of the biliary passages and obstruction 
 of the bile-duct by calculi to be differentiated? 
 
 Obstruction of the biliary passages either by gall-stones or by 
 carcinoma occasions persistent and intense jaundice ; but in 
 case of malignant disease there is also progressive emaciation, 
 death usually occurring within a year of the discovery of the 
 existence of the disease. Attacks of hepatic colic attend the 
 l)resence of gall-stones in the biliary passages. 
 
 The obstruction dependent upon calculi may be overcome, 
 spontaneously or therapeutically. Unrelieved, death ultimately 
 results from acholia or cholemia. 
 
 The diagnosis is often extremely difficult. The uncertainty 
 is increased by the fact that calcular obstruction and malignant 
 disease are sometimes associated. The detection of primary 
 
240 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 carcinoma elsewhere, or of metastatic nodules, indicates the 
 existence of malignant disease. It was at one time thought 
 that fever was wanting in malignant disease, but this is not an 
 invariable rule. 
 
 THE SPLEEN. 
 
 What is the normal situation of the spleen, as determinable by 
 physical examination ? 
 
 The spleen (Fig. 31) is placed obliquely beneath the ribs, from 
 
 Fig. 31. 
 
 C JS A Se 
 
 Se M 
 
 Relations of the spleen (Weil). M, middle line of back ; A, B, C, axillary lines; 
 Sn, line of scapula ; abed, limits of spleen ; abc' d, limits of rhomboidal spleen ; 
 efg, limits of kidney ; Ibc, angle between lung and spleen ; dhg, angle between 
 spleen and kidney ; » m, lower margin of liver. 
 
 the ninth to the twelfth, on the left side below the axilla. The 
 organ is about four inches long by three inches wide ; its axis 
 
THE PANCREAS. 241 
 
 passes downwards and forwards. Posteriorly, the dulness of 
 the spleen jjierges with that of the left kidney.. 
 
 Floating Spleen. 
 
 To what symptoms does a floating spleen give rise? 
 
 The attachments of the spleen may become relaxed and pro- 
 longed, so that the mobility of the organ is abnormally 
 increased, and its displacement is facilitated. The essential 
 points in the recognition of a floating spleen are the presence 
 of a solid body in an unusual situation, the absence of the 
 spleen from its normal seat, the possible facilit}' of replacement 
 and the absence of pronounced symptoms. . 
 
 Splenitis. 
 
 What are the symptoms of splenitis ? 
 
 Inflammation of the spleen is a condition clinically obscure. 
 It may occur in the course of infectious diseases or may be set 
 up by emboli swept into the splenic vessels. It has in cases 
 been attributed to traumatism. Under such circumstances the 
 organ becomes enlarged. There are pain and tenderness in the 
 left hypochondrium, or rather at the lower lateral aspect of the left 
 chest, aggravated by respiration ; there are also nausea, vomit- 
 ing and elevation of temperature. Inflammation of the spleen 
 may terminate in suppuration. Then chills, fever and sweats 
 are superadded. The greatest danger is from the rupture of an 
 abscess into the peritoneal cavity. 
 
 THE PANCREAS. 
 
 Acute Pancreatitis. 
 
 What are the symptoms of acute pancreatitis ? 
 
 The frequency of acute pancreatitis is not known, as the con- 
 dition is difficult of recognition. It may result from extension 
 of adjacent inflammation, from the irritation of matters con- 
 16 
 
242 ESSENTIALS OF DIAGNOSIS. 
 
 tained in the blood, from traumatism and from hemorrhage 
 into the pancreas. It is characterized by acute, deeply-seated 
 pain and tenderness in the epigastric region, or perhaps colicky 
 pain, shooting to the back and shoulders ; by anorexia, thirst, 
 nausea, vomiting of a thin viscid liquid, sometimes of bile ; 
 by dyspnea, restlessness, anxiety and depression ; by febrile 
 symptoms ; and usually by constipation— phenomena similar to 
 those presented ])y peritonitis. In some cases there is diarrhea, 
 the stools being thin, watery, and resembling saliva. ' Death is 
 the usual termination. It may be sudden, with the phenomena 
 of collapse. 
 
 THE GENITO-URINARY APPARATUS. 
 
 Examination of the urine is important not only when disease in 
 the genito-urinary tract is suspected, but also in many other 
 varied conditions. 
 
 The constitution of the. urine may be quantitatively or qualita- 
 tively altered. The proportions of normal ingredients may be 
 increased or diminished. Substances not normally found in 
 the urine may under certain conditions be present. 
 
 The quantity of urine excreted by a healthy adult in twenty- 
 four hours varies between forty and fift}' ounces. The quantity 
 is physiologically increasecZ after the ingestion of large quantities 
 of fluid and when the cutaneous, pulmonary and intestinal 
 transpiration is diminished. The quantity is physiologically 
 diminished under the reverse conditions. 
 
 The quantity of urine excreted is altered in many conditions 
 of disease. It is increased in diabetes insipidus and diabetes 
 mellitus, in chronic nephritis and, temporarily, in emotional 
 states, including hysteria. The quantity of urine is diminished 
 in acute nephritis, in the last stages of chronic nephritis, in 
 lithemia, in renal insufficiency, in CQnditions characterized by 
 feebleness of the heart, in Asiatic cholera, in yellow fever, in 
 acute intestinal obstruction and in febrile conditions generally. 
 
 Urine is normall}' clear, transi)arent, of an amber color, with- 
 out obtrusive odor, of acid reaction and a specific gravity varying 
 from 1010 to 1030. The color is paler or darker, and the specific 
 
THE GENITO-URINARY APPARATUS. 243 
 
 gravity lower or higher, as the quantity is increased or dimin- 
 ished. 
 
 The transparency of the urine is interfered with by the presence 
 of matters rendered insoluble by an altered reaction of the 
 urine (such as phosphates), or by a change of temperature (such 
 as urates) ; by the presence of matters foreign to normal urine 
 (such as pus, chyle or blood) ; and sometimes as a result of the 
 action of bacteria. 
 
 The color of urine is intensified when the quantity is dimin- 
 ished, as in fevers, or when the action of the skin is increased. 
 The color is altered by the ingestion of some medicaments and 
 foods and by the presence of other abnormal ingredients. Thus, 
 rhubarb imparts a gamboge-yellow color to acid urine, a violet-red 
 to alkaline urine ; santonin imparts a golden-yellow to acid urine, 
 an orange-yellow to alkaline urine ; senna imparts a brownish, 
 logwood a reddish, carbolic and gallic acids each a blackish 
 tinge. Urates may color the urine orange-red. The presence 
 of blood gives rise to a smoky, reddish or chocolate color ; the 
 presence of biliary pigment to a brownish or greenish hue ; the 
 presence of chyle to a milky appearance. In cases of melanotic 
 tumors the urine may be dark or black ; the color is likewise 
 dark in some cases of pernicious anemia. The urine is pale 
 when it is excreted in excess, as in hysteria, in diabetes and in 
 chronic nephritis. 
 
 The odor of normal urine is typical, but not obtrusive. When 
 fermentation takes place the urine becomes ammoniacal. The 
 ingestion of turpentine imparts to the urine an odor of violets. 
 Other aromatic oils impart odors abnormal to urine. The urine 
 of diabetes mellitus has a sweetish odor. If it contain acetone, 
 the odor resembles that of chloroform. 
 
 The total twenty-four hours' urine of a healthy person is of 
 acid reaction. The urine may be alkaline from fixed alkali a 
 few hours after a meal, especially if large quantities of alkalies 
 have been taken ; in cases in which the stomach is washed out ; 
 and in cases of obstinate vomiting. The urine is alkaline from 
 volatile alkali when ammoniacal fermentation has taken place. 
 
 The average specific gravity of normal urine is 1018 or 1020. 
 Except in diabetes mellitus, the specific gravity bears in gen- 
 
244 
 
 ESSENTIALS OF DIAGNOSIS, 
 
 eral an inverse relation to tlie quantity of urine. It is height- 
 ened after the ingestion of large quantities of nitrogenous food, 
 in diabetes mellitus and in acute nephritis and other febrile 
 conditions. It is lowered in diabetes insipidus, in chronic 
 nephritis, in hysteria, when the activity of the skin is lowered 
 and after the ingestion of large quantities of fluid. 
 
 The normal average quantity of urea excreted in twenty-four 
 hours is about five hundred grains. The excretion of urea is 
 increased on a generous nitrogenous diet and in fevers in 
 which the urine is not suppressed. The quantity of urea in 
 the urine is diminished on a vegetable diet ; when oxidation 
 is interfered with, as in pulmonary or cardiac disease ; in cases of 
 grave hepatic disease, renal insufficiency or suppression of urine ; 
 and when the urea is retained in the circulation. 
 
 If urine or any fluid containing urea be concentrated to a 
 syrupy consistence, by evaporation in a water-bath, and nitric 
 
 Fig. 32. 
 
 Uric acid and urates. (Funke.) 
 
 acid be added, a crystalline precipitate of the rhombic plates of 
 urea nitrate will be thrown down. 
 
 The quantity of uric acid excreted in the urine in twenty-four 
 hours varies from eight to sixteen grains. It is increased when 
 the diet is nitrogenous ; when oxidation is defective, as in pul- 
 
THE GENITO-URINARY APPARATUS. 
 
 245 
 
 monary or cardiac disease ; after an attack of gout or lithema ; 
 and in febrile processes. It is diminished on a diet of carbo- 
 liydrates ; in chronic diseases after hemorrhage ; during an 
 attack of gout or lithema. 
 
 If ten parts of h3'drochloric acid be added to one hundred 
 parts of urine and the mixture be permitted to stand for forty- 
 eight hours, a sediment of fine, red crystals of uric acid will form. 
 
 The quantity of hipimrk, acid excreted in the urine in twenty- 
 four hours is between eight and thirty grains. It is increased on 
 a vegetable, and diminished on an animal diet. It is only pre- 
 cipitated from acid urine, when it appears as rhombic crystals. 
 
 The quantity of sodium chloride excreted in the urine in 
 twenty-four hours is about half an ounce. It depends upon 
 the quantity ingested. The excretion of chlorides is dimin- 
 ished in febrile disorders, and especially when exudation or 
 transudation occurs. 
 
 The presence of chlorides in the urine may be determined by 
 first acidulating t^he urine with nitric acid, and then adding a 
 solution of silver nitrate. If the precipitate that forms is dense 
 
 Fig. 33. 
 
 Calcium phosphate. (Laache.) 
 
 and curdy, the quantity of chlorides is normal ; if the precipitate 
 is milky, the chlorides are diminished. 
 
246 
 
 ESSENTIALS OF DIAGNOSIS, 
 
 Between thirty and eighty grains of xJ^osphoric acid are 
 eUminated in tlie urine in twenty-four hours, two-thirds as 
 alkaline (acid sodium and potassium) phosphates, and one- 
 third as earthy (calcium and magnesium) phosphates. The 
 quantity of phosphates excreted is diminished at the beginning 
 of febrile processes, and increases with defervescence and con- 
 valescence. 
 
 Fig. 34. 
 
 Triple phosphates and ammonium urate. (Laaehe.) 
 
 The earthy phosphates are precipitated when the reaction of 
 the urine is alkaline. The alkaline phosphates are precipitated 
 by the addition of a solution containing one part each of mag- 
 nesium sulphate, ammonium chloride and liquor ammonise, and 
 eight parts of distilled water. 
 
 About thirty grains of sulphuric acid are eliminated as sul- 
 phates in the urine in twenty-four hours. The quantity varies 
 with the character of the food and the degree of activity. 
 
 The presence of sulphates in the urine is determined by the 
 addition of a solution of barium chloride, which gives a cloudy 
 precipitate, insoluble in water or acids. 
 
 Biliari/ coloring matter appears in the urine when jaundice 
 exists. The urine is yellowish, greenish or olive-brown in 
 
THE GENITO-URTNARY APPARATUS. 
 
 2n 
 
 color, and stains the linen. When the jaundice is not due to 
 biliary obstruction it is said that the biliary acids are not found 
 in the urine. 
 
 The presence of biliary coloring matter in the urine may be 
 detected by overlaying nitric acid in a test-tube with urine, 
 or by permitting the fusion of a drop each of nitric acid and of 
 urine on a white plate. A play of color from green, blue, 
 violet, red to yellow, results. 
 
 To detect the presence of the biliary acids in the urine a small 
 quantity of cane-sugar is added to the urine, which is introduced 
 into a test-tube, so as to overlay some sulphuric acid. A purple 
 color is formed at the line of contact. If a bit of filter-paper is 
 dipped in the saccharated urine and touched with a drop of 
 sulphuric acid a purple color results. 
 What are leucin and tyrosin ? 
 
 Leiicin and tyrosin are products of the destructive meta- 
 morphosis of proteids, and are among the waste-products of 
 
 Fig. 35. 
 
 Leucin and tyrosin. (Laache.) 
 
 pancreatic digestion. They do not occur in normal urine, but 
 are found in the urine in cases of phosphorus-poisoning and of 
 acute yellow atrophy of the liver, for which they may have 
 diagnostic significance. They have also been exceptionally 
 
248 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 noted in variola, typhus, pernicious anemia, and in a case of 
 obstructive jaundice caused by hydatid cyst of the gall-duct. 
 
 To obtain leucin and tyrosin in the sediment, the urine should 
 be evaporated in a water-bath to syrupy consistence, or a drop 
 may be boiled down on an object-glass. Leucin appears in the 
 form of faintly shining spheres of variable size, the larger ones 
 sometimes exhibiting radiation or concentric rings. Tyrosin 
 crystallizes in very fine needles, commonly aggregated into 
 sheaves or bundles. 
 
 Oxaluria. 
 
 What is oxaluria ? 
 
 The presence of oxalates in the urine is sometimes associated 
 with a complex of sj'mptoms, to which the designation oxaluria 
 has been applied. Individuals so affected complain of languor, 
 of dull pains in the loins, are irritable or dejected, have boils or 
 
 Fig. 36. 
 
 Calcium oxalate. (Laache. 
 
 carbuncles ; and their nutrition is impaired. The in-ine, the 
 specific gravity of which is increased, contains an excess of urea 
 and of oxalates, and occasionally a trace of albumin. The con- 
 dition has been observed in persons in whom the nervous system 
 has been severely put to task. 
 
PYURIA. 249 
 
 Pyuria. 
 
 What is pyuria ? 
 
 The presence of pus in the urine constitutes pyuria. Pus 
 appears in the urine when there is suppuration in any portion 
 of the genito-urinary tract, as in urethritis, cystitis, ureteritis or 
 pyelitis. Rupture of an abscess into the genito-urinary pas- 
 sages gives rise to the sudden discharge of a large quantity of 
 pus. When, in women, leucorrhea exists, some of the pus may 
 find its way into the receptacle for urine. The addition of 
 caustic alkalies converts pus into a gelatinous viscid mass. Hy- 
 drogen dioxide gives a characteristic foaminess, from libera- 
 tion of oxygen. The microscope is the most certain test. 
 Urine containing pus responds to chemic tests for albumin. 
 
 When xiretliritis exists, micturition is burning. The first 
 urine passed is turbid ; that which follows may be clear. The 
 reaction of the urine remains unchanged. In the vast majority 
 of cases, urethritis is gonorrheal. 
 
 When there is cystitis, there may be vesical tenesmus, with 
 frequent passage of small quantities of urine that is usually 
 of alkaline reaction. Cystitis may be secondary to urethritis ; 
 it may be a result of obstruction, as from stricture of the urethra 
 or an enlarged prostate ; it may be associated with a calculus 
 in the bladder ; it may have been caused by the introduction of 
 septic matters into the bladder in the course of some surgical 
 procedure, such as the employment of an unclean catheter, 
 sound or bougie ; it may be tuberculosis ; it is often seen in asso- 
 ciation with diseases of the brain and spinal cord. The urine is 
 not only turbid, but it is usually also alkaline in reaction and 
 offensive in odor, ft-om ammoniacal fermentation. 
 
 Ureteritis and pyelitis are usually associated. Both are com- 
 monly secondary to cystitis, though they may result from the 
 presence of calculi. In uncomplicated cases the urine is acid 
 in reaction. 
 
 When an abscess ruptures into the genito-urinary tract, a 
 certain sense of relief of tension is perceived, followed by the 
 evacuation of a large quantity of pus in the urine, which had 
 previously presented no abnormal characters. 
 
250 ESSENTIALS OF DIAGNOSIS. 
 
 Albuminuria. 
 
 What is albuminuria ? 
 
 Albumin is foiiud in the urine under many varied conditions ; 
 thus, urine containing pus or blood will respond to the tests for 
 albumin. Under other circumstances, however, the albumin is 
 derived directly from the circulating blood, as a result of the 
 defective action of the epithelium of the secretory tubes of the 
 kidney. Such a condition is present in the various morbid 
 states of the kidney, in the course of fevers and infectious pro- 
 cesses and in association with violent convulsions, obstructive 
 disease of the heart, and interference with the respiratory func- 
 tion. The ordinary form of albumin found in the urine is serum- 
 albumin ; less commonly paraglobulin is present. 
 
 How is the presence of albumin in the urine to be determined ? 
 
 The best test for the detection of albumin in the urine is that 
 by heat. The urine should be clear and of acid reaction. If 
 not clear, it should be filtered. If not acid, a drop or two of 
 acetic acid— sufficient to impart an acid reaction, should be 
 added. The upper half of the urine, in a test-tube, is heated. 
 A resulting cloudiness is due to the presence of albumin or of 
 phosphates. If the urine have been acid, the cloudiness is not 
 likely to be due to phosphates. The addition of a few drops of 
 acetic acid removes any doubt ; if the cloudiness is dependent 
 upon the presence of phosphates, it at once clears ; if due to 
 the presence of albumin, it persists. 
 
 A simpler test for the presence of albumin consists in over- 
 laying a quantity of nitric acid in a test-tube with the urine. 
 A white ring at the line of contact of the two fluids is indicative 
 of the presence of albumin. A faint ring of urates that forms 
 above the line of contact is dissipated by the application of heat. 
 
 A saturated solution of picric acid used by the contact-method 
 in the same way as nitric acid, the urine, however, being over- 
 laid by the acid, constitutes a most delicate test for the detec- 
 tion of albumin in the urine, but it is equivocal, as it reacts with 
 peptones, urates and with the alkaloids. Heat, it is true, dissi- 
 
ALBUMINURIA. 
 
 251 
 
 pates the ring formed with these, but it may also cause a diftu- 
 sion of the turbidity produced by albumin, so that the latter 
 may escape detection. 
 
 What is the significance of the presence of tube-casts in the 
 urine ? 
 The i^resence in the urine of casts of the uriniferous tubules is 
 
 
 m 
 
 Red blood-corpuscles and a blood-cast 
 of a uriniferous tubule. (Eichhorst.) 
 
 Fig. 39. 
 
 .m 
 
 Epithelial cast of a 
 uriniferous tubule. 
 (V. Jaksch;) 
 
 Granular casts of the uriniferous 
 tubules. (V. Jaksch.) 
 
 Hyaline casts of the uriniferous 
 tubules. (Vierordt.) 
 
 indicative of nephritis. The presence of albumin is usually 
 associated with that of tube-casts. 
 
252 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 The character of the casts varies according to the form of 
 nephritis. Blood-casts and epithelial casts are indicative of an 
 acute process ; granular casts of a chronic process ; hyaline casts 
 may be present in many conditions. Fatty casts bespeak the 
 
 Fig. 41. 
 
 Waxy easts of the uriniferous tubules, a, a waxy cast containing crystals of 
 calcium oxalate. (V. Jakseh.) 
 
 late stage of a chronic parenchymatous nephritis— fatty kidney ; 
 waxy casts may be found in acute and chronic nephritis and in 
 amyloid disease of the kidney. 
 
CHYLURIA. 253 
 
 Chyluria. 
 
 What ischyluria? 
 
 The presence in the urine of chyle or its molecular base, fat, 
 constitutes chyluria. The urine presents a whitish, milky ap- 
 pearance and displays a tendency to spontaneous coagulation. 
 Albumin is present ; in cases due to filaria, blood may be found. 
 Under the microscope lymph-corpuscles and a finely granular 
 basis are recognized. Chyle finds its way into the urine as a 
 result of abnormal communication between the lymphatic sys- 
 tem and the genito-urinary tract, in consequence of rupture 
 following obstruction in the lymph-channels, most commonly 
 
 Fig. 42. 
 
 Filaria sanguinis hominis. (V. Jaksch.) 
 
 hy filaria sanguinis hominis. The scrotum and the lower ex- 
 tremities are sometimes infiltrated, and may be enlarged so as 
 to create a resemblance to elephantiasis. Filariosis is a chronic 
 affection, as a rule irregularly intermittent in its manifestations. 
 When fllarise are present, ova or embryos should be discovered 
 in the urine or in the blood obtained during the period of sleep 
 or rest. 
 
 Lipuria. 
 
 What is lipuria ? 
 
 The presence of fat in the urine constitutes lipuria. It may 
 occur in health after excessive ingestion of fatty food. It has 
 been observed in connection with fatt}'^ degeneration of the 
 kidney, pyonephrosis, diabetes mellitus, phosphorus-poisoning 
 and pregnancy. Urine containing chyle responds to the tests 
 for fat. The condition may be recognized by the addition to 
 
254 ESSENTIALS OF DIAGNOSIS. 
 
 the urine of a small quantity of potassium hydrate and then 
 shaking with ether. The ether is permitted to evaporate and 
 the fat collects as glohules. 
 
 Hematuria. 
 
 What is hematuria ? 
 
 The presence of blood in the urine constitutes hematuria. 
 The urine is turbid and darker in color than normal ; the specitic 
 gravity is increased ; and albumin is present in considerable 
 quantity. With the microscope there is no difficulty in distin- 
 guishing the red corpuscles. 
 
 Blood may be present in the urine as a result of hemorrhage 
 from traumatism or ulcerative processes ; in the course of acute 
 inflammations in the genito-urinary tract ; as a symptom of cer- 
 tain nervous diseases ; as a manifestation of a hemorrhagic dia- 
 thesis, as in leukemia, scurvy, purpura, hemophilia, exophthal- 
 mic goiter, and the like ; as a manifestation of influenza or ma- 
 laria, or as the result of drug-action. Like chyluria, hematuria 
 may be due to Filaria sanguinis hominis. Distoina liematrMura 
 and strongylus gigas are additional parasites that may cause 
 hematuria. 
 
 It may sometimes be important to determine whether the blood 
 present in urine comes from the bladder or from the kidneys. A 
 comparatively small quantity of blood ; its uniform admixture 
 with the urine ; the presence of blood-casts of the tubules, or 
 of the ureter ; small size, discoloration, or so-called "ringing" 
 of the blood-cells, point to renal hemorrhage. The passage of 
 pure blood or of clots unmixed with urine, or with but slight 
 admixtvire, or only at the beginning or close of urination, points 
 to hemorrhage from the bladder or urethra. Exploration or cys- 
 toscopic examination ma}* detect the source of hemorrhage and 
 perhaps its cause, as a calculus or a neoplasm. 
 
 Hemoglobinuria. 
 
 What is hemoglobinuria ? 
 
 When the coloring-matter of the blood appears in the urine 
 the condition is designated /if moyZo6i7U<Ha. The coloring-matter 
 of the blood may appear free in the urine as a result of con- 
 
PAROXYSMAL HEMOGLOBINURIA. 255 
 
 ditions attended with disorganization of the blood, such as 
 scurvy, purpura, pyemia, typhus, insolation, extensive burns, 
 and poisoning by potassium chlorate, hydrogen arsenide, phos- 
 phorus, carbolic acid and chloral. Spontaneous hemoglobin- 
 uria has been observed in the new-born infant. 
 
 The urine is dark-red or chocolate-brown in color, of high spe- 
 cific gravity, and contains considerable albumin. Microscopic- 
 ally, few or no blood-cells are found. A drop of such urine 
 treated on a slide with sodium chloride, acetic acid, and 
 heat yields microscopically the flat, rhombic, prismatic tables 
 known as Teichmann's crystals. The addition of a few drops 
 of fresh tincture of guaiac to a small quantity of the same urine 
 gives rise to a whitish or greenish coloration ; shaken well, the 
 addition of a few drops of a solution of hydrogen dioxide or of 
 old oil of turpentine causes a change of color to blue. Spectro- 
 scopic examination reveals characteristic striae. 
 
 The attack sets in with a rigor, to which succeed vomiting, 
 diarrhea, collapse, cyanosis, stupor, and, usually, a fatal issue. 
 
 Paroxysmal Hemoglobinuria. 
 
 What is paroxysmal hemoglobinuria? 
 
 Hemoglobinuria may be intermittent and paroxysmal. In some 
 cases no cause for the condition can be elicited ; in most, how- 
 ever, the exciting factor has been exposure to unusual cold. 
 Attacks may be induced by mental or physical exhaustion. The 
 disease is most common in young adult males. The onset of a 
 paroxysm is indicated by a sense of languor and fatigue, to 
 which is soon added a feeling of chilliness. The fingers and 
 toes and tips of the ears become numb, cold and cyanotic. The 
 paroxysm ends by the restoration of a comfortable sense of 
 warmth. During the attack, or a short time subsequently, the 
 symptom that gives the disease its name appears. The urine, 
 however, soon assumes a normal condition. 
 
 How are paroxysmal hemoglobinuria and malarial hematuria 
 to be diiFerentiated ? 
 
 Paroxysmal hemoglobinuria is not known to be related to 
 malarial infection ; other possible manifestations of malaria are 
 
256 ESSENTIALS OF DIAGNOSIS. 
 
 wanting ; the periodicity of tlie attack is not rhythmical ; ma- 
 larial hematuria is a manifestation of profound malarial intoxi- 
 cation, associated with other distinct characteristics of malaria. 
 In hematuria, with the microscope, many red blood-corpuscles 
 are to be seen in the urine ; the absence of blood-corpuscles in 
 the urine is characteristic of hemoglobinuria. The one condi- 
 tion yields to treatment with quinine ; the other does not. Ex- 
 amination of the blood in a case of paroxysmal hemoglobinuria 
 discloses nothing characteristic ; an examination of the blood in 
 cases of malarial hematuria reveals the presence of characteristic 
 parasites. 
 
 Endemic Hematuria. 
 
 What is endemic hematuria? 
 
 In tropical climates the presence of a nematode worm, the 
 distoma hematobium or Bilharzia hematohia, in the veins about 
 the bladder, occasions the appearance of blood in the urine. 
 The ova of the parasite find their way into the genito-urinary 
 passages and there give rise to irritation and inflammation and 
 extravasation of blood. The disease is most common in 3'outh ; 
 il shows a tendency to subside after the age of puberty. The 
 condition predisposes to the development of urinary calculi. 
 The diagnosis depends upon the endemic character of the affec- 
 tion and the detection of ova, which are often concealed in 
 shreds of tissue contained in the urine. 
 
 Diabetes Insipidus. 
 
 What are the clinical features of diabetes insipidus or poly- 
 uria? 
 
 Diabetes insipidus or polyuria is a morbid condition character- 
 ized by the elimination of an excessive quantity of feebly acid 
 urine, of low specific gravity, containing neither albumin nor 
 sugar. There is increased thirst; an abnormal quantity of 
 fluids may be ingested, than which, however, the quantity of 
 urine excreted is usually in excess. The skin and visible 
 mucous membranes may be rough and dry. In some cases the 
 
DIABETES MELLITUS. 257 
 
 appetite is excessive. The general nutrition may be maintained, 
 but is rather more likely to suffer deterioration, as manifested 
 by wasting and debility. Diabetes insipidus is not directly fatal. 
 Its etiology and pathology are obscure. In many cases, there is 
 a history of injury to the head, or disease of the brain is found 
 post-mortem. It may depend upon disease of the pancreas. 
 Several cases have been found in a single family ; in other in- 
 stances, some members of a family present diabetes insipidus, 
 others diabetes mellitus. 
 
 How are diabetes insipidus and chronic interstitial nephritis 
 to be differentiated ? 
 In cases of chronic interstitial nephritis the quantity of urine 
 eliminated may be abnormally large, but it does not attain the 
 proportions encountered in diabetes insipidus ; in addition, 
 careful investigation will detect the presence of albumin and 
 casts in the urine, as well as the existence of other symptoms 
 indicating a degenerative lesion of the kidney : heightened arte- 
 rial tension, hypertrophy of the heart, breathlessness, edema, 
 headache, diarrhea. 
 
 How are hysterical polyuria and diabetes insipidus to be 
 differentiated ? 
 
 The excessive discharge of urine that is sometimes observed 
 in hysterical patients is paroxysmal rather than persistent ; 
 and does not constitute the essential feature of the disease, but 
 is rather an incidental symptom of a malady of protean feature. 
 
 Diabetes Mellitus. 
 
 What are the clinical features of diabetes mellitus ? 
 
 Diabetes mellitus^ glycosuria, or mellituria, is a morbid condition 
 attended by the discharge of large quantities of urine charac- 
 terized by the persistent presence of a varying quantity of glu- 
 cose. It is sometimes observed in connection with cerebral 
 disease, sometimes in connection with disease of the pancreas 
 or of the liver, sometimes in women at the menopause, but is 
 commonly unassociated with any evident disease. In many 
 17 
 
258 ESSENTIALS OF DIAGNOSIS, 
 
 cases there is a racial or family predisposition or a gouty or 
 rheumatic diathesis. lu not a few instances its advent has 
 been preceded by grief, anxiety or profound emotion. 
 
 Among the earliest symijtoms is a gradual failure of health, 
 with a sense of fatigue disproportionately great. It may be 
 observed that the patient is passing an excessive quantity of 
 urine, examination of which shows it to be pale in color, of a 
 sweetish, fragrant odor, of high specific gravity, and chemic- 
 ally containing glucose. The proportion of sugar varies, being 
 increased by indulgence in and diminished by abstinence from 
 sugars and starches. At the same time, there is increased 
 thirst, together with the ingestion of large quantities of fluids. 
 The tqjijetite is also wont to be excessive and large quantities of 
 food are taken. Constipation is the rule, though exhausting 
 diarrhea may occur. The skin, mouth and throat are dry. A 
 sweetish taste is perceived. The breath may exhale a fragrant, 
 a balsamic, an ethereal odor, or an odor of chloroform. The teeth 
 become carious, the gums spongy and loose. Boils and carbuncles 
 are common. Persistent furunculosis, without obvious cause, 
 should always awaken a suspicion of diabetes. In women, pru- 
 ritus vulvse, and, in men, excoriations about the meatus urina- 
 rius have been observed. Failure of sexual vigor is sometimes 
 an early symptom. Emaciation and debility may ultimately be- 
 come extreme. Exceptionally an appearance of perfect health 
 is preserved. Some have distinguished two groups of cases, 
 those with a tendency to emaciation, and those with a tendency 
 to obesity. 
 
 Sometimes, there is sense of chilliness and the temperature is 
 subnormal. Gangrene from vascular occlusion may result and 
 bring about a fatal issue. After death the bladder is often 
 found hypertrophied. Cataract not rarely develops in the 
 course of diabetes. Nephritis is sometimes superadded. Death 
 commonly results from an intercurrent affection, such as pul- 
 monary tuberculosis or pneumonia. Sometimes coma appears, 
 with or without delirium and convulsions. Coma is in many 
 cases preceded for a few days by the appearance in the urine of 
 acetone and diacetic acid, concurrently, it maybe, with diminu- 
 tion of the percentage of sugar, 
 
DIABETES MELLITUS. 259 
 
 What is Moore's test for the presence of glucose in the urine ? 
 
 The simplest test for the presence of sugar in the urine is 
 Moore's test. To a moderate quantity of urine in a test-tube 
 half as raucli hquor potassee is added. The mixture is heated. 
 If sugar be present in greater proportion than 0.3 per cent., a 
 sherry-wine color results. If a drop or two of nitric acid be 
 added, the brownish color disappears and the odor of molasses 
 becomes perceptible. Other substances than sugar respond 
 similarly in color ; so that the test cannot be infallibly relied 
 upon. 
 
 What is Boettger's test ? 
 
 To a small quantity of urine in a test-tube-is added about an 
 equal quantity of liquor potassse, and then a small pinch of bis- 
 muth subnitrate. The mixture is heated ; if sugar be present a 
 black precipitate of metallic bismuth is thrown down. Sulphur 
 compounds precipitate black sulphides, so that albumin, if pre- 
 sent, should first be removed by precipitation and filtration. If 
 the reaction fails to take place, the presence of sugar in signifi- 
 cant quantity can safely be excluded. 
 
 What is Trommer's test ? 
 
 To a moderate quantity of urine in a test-tube a smaller 
 quantity of liquor potasste, and then a few drops of a ten per 
 cent, solution of cupric sulphate are added. If heat be applied, 
 an orange-red precipitate of cuprous oxide is thrown down if 
 sugar be present. 
 
 What is Fehling's test? 
 
 Two solutions are used. One consists of an ounce of cupric 
 sulphate and sufficient water to make fifteen ounces ; the other 
 of five ounces of crystallized Rochelle salts, three ounces of a 
 solution of sodium hydrate having a specific gravity of 1.34, and 
 sutficient water to make fifteen ounces. When the test is to be 
 made, equal quantities of the two test-solutions are heated in a 
 test-tube. The urine is then slowly added. Should no orange- 
 red precipitate result, the presence of sugar can be excluded. 
 
 Fehling's test can be applied for quantitative analysis by em- 
 ploying solutions of which a known volume will be reduced by 
 a definite quantity of glucose. 
 
260 ESSENTIALS OF DIAGNOSIS. 
 
 What is the fermentation-test? 
 
 If a bit of baker's yeast be added to uriue containing sugar, 
 fermentation takes place, carbon dioxide and alcohol being gen- 
 erated. In making a quantitative examination the specific 
 gravity is taken and recorded ; eight ounces of urine are intro- 
 duced into a pint bottle, a piece of compressed yeast about the 
 size of a walnut fi^ded, and the bottle closed by a perforated 
 cork, and placed in a vsrarm place (from 86° to 90° ¥.) for four 
 or five hours or longer. The urine is then permitted to cool, 
 and its specific gravity is again taken. Each degree of loss of 
 specific gravity represents about one grain of sugar to the ounce, 
 or the total number of degrees lost multiplied by 0.23 will give 
 the percentage of sugar. 
 
 What are the tests for acetone? 
 
 1. To the urine is added a small quantity of yellow precipi- 
 tate (mercuric oxide), freshly prepared by mixing an alcoholic 
 solution of potassic hydrate with mercuric chloride. If acetone 
 is present some of the mercurial will be dissolved. The urine is 
 then filtered and the filtrate overlaid with ammonium sulphide. 
 A black ring of mercuric sulphide shows that the reagent has 
 been dissolved, and thus indicates acetone. Or, 2. About 4 c.c. 
 (1 dram) of solution of potassic hydrate, containing 1 gram (15 
 grains) of jDotassium iodide, are placed in a test-tube and boiled. 
 An equal volume of urine is then cautiously poured in, so as to 
 float on the surface of the alkaline liquid. At the point of con- 
 tact a ring of phosphates will form, which, if acetone be present, 
 will in a few minutes be colored yellow and studded with 
 crystals of iodoform. 
 
 What is a convenient test for diacetic acid? 
 
 Solution' of ferric chloride is slowly added to the urine ; the 
 phosphates thus precipitated are removed by filtration, and 
 more ferric chloride is added. If glacial acetic acid is present, 
 the urine becomes wine-red. The test must then be repeated 
 with urine previously boiled. If the boiled urine gives no reac- 
 tion with the iron solution, or only a slight coloration, and if 
 acetone is likewise found to be present, it may be concluded that 
 diaceturia, a forerunner of diabetic coma, exists. 
 
CYSTITIS. 261 
 
 How are diabetes insipidus and diabetes mellitus to be differ- 
 entiated ? 
 The diagnostic distinction between diabetes mellitus and 
 diabetes insipidus is the presence or absence of sugar in the 
 urine, of which the specific gravity is lower in the latter than 
 in the former. The occurrence of boils, of itching of the skin, 
 of cataract and of gangrene, the presence of a sweetish taste 
 and of a fragrant breath, encountered in saccharine diabetes, 
 are wanting in insipid diabetes. The prognosis in the case of 
 diabetes insipidus is more favorable than in that of diabetes 
 mellitus. 
 
 Cystitis. 
 
 What are the symptoms of cystitis? 
 
 The mucous membrane of the bladder may undergo in- 
 flammation in the course of constitutional disorders, or as the 
 result of local irritation or infection. Cystitis gives rise to 
 pain in the hypogastriuin, a frequent desire to urinate, followed 
 by the evacuation of small quantities of urine, attended with 
 burning pain. The last drops of urine passed are opaque and 
 viscid. The quantity of urine voided does not in the aggregate 
 exceed the normal. When the cystitis is acute the reaction of 
 the secretion is acid ; in chronic cystitis the urine is alkaline ; the 
 urine is turbid and precipitates a dense, copious sediment ; it is 
 albuminous in a degree proportionate to the quantity of pus con- 
 tained. Examined microscopically the sediment is found to be 
 made up of pus-corpuscles, pavement epithelial cells and mucus. 
 In the earliest stages of acute cystitis the urine may contain 
 blood ; in chronic cystitis, crystals of the triple aramonio-mag- 
 nesium phosphate may be found. The walls of the bladder be- 
 come thickened, its cavity reduced in size, its lining membrane 
 ribbed. The dangerous sequelae of cystitis are ureteritis, pye- 
 litis, hydronephrosis and suppurative nephritis, dependent upon 
 extension of the inflammatory process. 
 
 How are cystitis and nephritis to be differentiated? 
 
 Pain in the hypogastrium is a feature when there is acute 
 cystitis. If pain attend acute nephritis, it is referred to the 
 
262 ESSENTIALS OF DIAGNOSIS. 
 
 loins, Uriue is passed less frequentlj- and in smaller quantities 
 when acute nephritis exists than is the case in acute cystitis. 
 The urine of cystitis is the more distinctly purulent ; tliat of 
 nephritis, the more distinctly albuminous. In cases of nephritis, 
 the urine contains casts of the uriniferous tubules. The urine 
 of simple cystitis never contains tube-casts, • The alkalinity of 
 the urine, the presence of pus, and the absence of tube-casts, 
 in addition to the absence of other phenomena, such as edema, 
 dyspnea, anemia, cardiac hypertrophj-, distinguish chronic cys- 
 titis from chronic nephritis. 
 
 Vesical Calculus, 
 
 To what symptoms does a vesical calculus give rise ? 
 
 The presence of a calculus in the bladder gives rise to irrita- 
 tion and inflammation. In addition to the signs of cystitis — 
 frequent, burning discharge of small quantities of urine of alka- 
 line or acid reaction — there occur attacks of vesical tenesmus, 
 with complete obstruction to the discharge of urine, with pain 
 referred to the glans penis, followed by the presence of blood in 
 the urine. Careful examination, by means of a sound or the 
 cystoscope, may furnish conclusive evidence. A vesical calcu- 
 lus may not onh^ excite cj'stitis, but it ma}'' also give rise to 
 inflammation and dilatation of the ureters and pelves gf the kid- 
 neys and to hydronephrosis. 
 
 Neoplasms of the Bladder, 
 
 To what symptoms do neoplasms of the bladder give rise ? 
 
 "When the lining of the bladder is the seat of new-growths, 
 hemorrhage is of frequent occun-ence, together with paroxj'sms 
 of vesical tenesmus. The urine usually contains cellular evi- 
 dence of the presence of a neoplasm, while cystoscopic exami- 
 nation may afford ocular demonstration of the fact. 
 
PYELITIS — RENAL INADEQUACY. 263 
 
 Pyelitis. 
 
 What are the symptoms of pyelitis ? 
 
 Inflammation of the mucous membrane of the pelvis of the 
 kidney may arise in the course of acute infectious diseases, may 
 result by extension from the urethra, through tlie bladder and 
 ureters, or from the presence of a calculus or a new-growth. 
 Pyelitis may be tuberculous. There is pain in the loin. The 
 ?«rme, the reaction of whicli remains acid, precipitates a copious 
 sediment principally constituted of pus, with some epithelial 
 cells. From time to time the urine may contain blood. 
 
 In cases of tuberculosis, tubercle-bacilli may be found in the 
 urine, and there may be evidences of tuberculous disease else- 
 where. It is said that bacilli morphologically indistinguishable 
 from tubercle-bacilli and presenting the same color-reactions are 
 sometimes found in the urine of healthy persons. The numbers 
 are smaller, and the organisms are less constantly present than 
 in cases of tuberculosis, and the inoculation-test proves them 
 to be innocuous. 
 
 How are pyelitis and cystitis to be differentiated ? 
 
 The pain of pyelitis is referred to the lumbar region ; that of 
 cystitis to the hypogastric region. Small quantities of urine are 
 frequently evacuated in case of cystitis ; neither quantity nor 
 frequency are altei-ed in vmcomplicated pyelitis. When there is 
 cystitis, the urine is most likely to be alkaline in reaction ; when 
 there is pyelitis, it is usually acid. 
 
 Renal Inadequacy. 
 
 What is renal inadequacy ? 
 
 Some individuals never pass more than a normal or slightly 
 less than normal quantity of urine of Ioav specific gravity and 
 containing abnormally little urea, even though they should 
 partake of an excess of fluids. The condition has been termed 
 renal inadequacy. The symptoms are vague and indefinite. 
 There is a sense of ill-being, an undue readiness of fatigue, and 
 
264 ESSENTIALS OF DIAGNOSIS. 
 
 a lowered resistance to disease. Patieuts so affected bear opera- 
 tive iuterfereuce badly. Thepe may be slight edema, but the 
 urine contains neither albumin nor casts. 
 
 I 
 
 ' Floating Kidney. 
 
 What are the symptoms of a floating kidney ? 
 
 The kidney ma}^ be furnished with a mesentery, attached to 
 which it may find its wa,y into the abdominal cavitj-, without 
 necessarily giving rise to significaot symptoms. The condition 
 is to be recognized by the mobility, the possibility of replacement, 
 a void in the usual situation of the kidney, and the fact of the 
 remaining viscera occupying their proper positions. By twisting 
 of the ureter, urine may accumulate in the renal pelvis, to be 
 evacuated when the quantity has reached a certain limit. In 
 addition, there may be a sense of weight and dragging in the 
 abdomen, with pain usually dull, but occasionally acute and 
 associated with tenderness. Sometimes the distress is more 
 aggravated, and nausea and vomiting occur. Floating kidney 
 is more common in females than in males ; the right kidney is 
 more frequently aflfected than the left. 
 
 Benal Calculus. 
 
 To what symptoms does a renal calculus give rise ? 
 
 A calculus in the pelvis of the kidney occasions constant dull 
 pain in the loin, aggravated into great intensity in paroxysms, 
 superinduced by active physical exercise or by concussion. 
 Following the paroxysm the urine contains blood. In the in- 
 terval the urine contains pus. If the calculus enter the ureter, 
 efforts at its expulsion give rise to excruciating pain in the 
 course of the ureter, with retraction of the corresponding tes- 
 ticle, numbness of the thigh, nausea and vomiting. When a 
 renal calculus is a cause of obstruction to the flow of urine, 
 hydronephrosis or atrophy of the kidney may result. 
 
CHRONIC PARENCHYMATOUS NEPHRITIS. 265 
 
 Acute Nephritis. 
 
 What are the clinical features of acute nephritis ? 
 
 Acute inflammation of the kidney is common in association 
 with acute infectious diseases— especially scarlatina, erysipelas, 
 small-pox and yellow fever. It may follow exposure to cold. 
 It sometimes develops in the course of pregnancy. The kid- 
 neys are large and smooth and reddened. The inflammation 
 particularly involves the parenchyma of the organs. The 
 occurrence of acute nephritis may be manifested by a chill, 
 which is followed by fever, hj pains in the loins, by headache, 
 perhaps with nausea, vomiting and diarrhea. The face (nota- 
 bly the eyelids) is pufly ; the extremities are swollen and 
 edematous. The excretion of urine is diminished to a mini- 
 mum ; there may be actual suppression. The urine presents a 
 smoky, reddish, turbid aspect ; its specific gravity is high ; it is 
 deficient in urea, but it contains a decided quantity of albumin 
 and hyaline and epithelial casts, and blood-casts, as well as 
 free blood-corpuscles. The symptoms of uremia may super- 
 vene ; to the headache, nausea and vomiting, are added derange- 
 ment of vision, delirium, convulsions and coma. In the course 
 of several weeks, the symptoms gradually subside, though the 
 accompanying anemia yields but obstinat'^ly, while the urine 
 may continue albuminous for a long time, perhaps permanently. 
 Inflammations of the serous membranes are frequent in the 
 course of acute nephritis. 
 r 
 
 Chronic Parenchymatous Nephritis. 
 
 What are the symptoms of chronic parenchymatous nephritis ? 
 
 Recovery from acute inflammation of the kidney may be 
 imperfect ; repeated attacks may leave a permanently damaged 
 organ ; finally an inflammation of the parenchyma of the kidney 
 may be insidious and essentially chronic from the outset. 
 However produced, the symptoms are variable. The essential 
 characteristic is the persistent presence of a considerable 
 quantity of albumin in the urine, together with granular, hyaline 
 
266 ESSENTIALS OF DIAGNOSIS. 
 
 or fatty tube-casts. The quantity of urine may scarcely deviate 
 from the normal. A characteristic variety of retinitis may be 
 detected with the ophthalmoscope. Edema of the face and 
 extremities occurs, anemia is manifest, assimilation is im- 
 paired, the arterial tension is heightened, and the heart becomes 
 enlarged. Ascites is common. Edema of the larj-nx or lungs, 
 or etfusions into the pleurce or pericardium may take place sud- 
 denly or gradually. Headache, impaired vision, somnolence, 
 convulsions and coma, from uremia, may develop. Individuals 
 affected with chronic parenchymatous nephritis badly resist dis- 
 ease. The probabilities are that the so-called fatty kidney is 
 but a modification of the kidne}- of chronic parenchymatous 
 nephritis, dependent upon secondary degeneration. The symp- 
 toms of both conditions are much alike. In the secondary 
 degeneration, the presence of fatty casts and of oil-globules is 
 characteristic. 
 
 Amyloid Kidney. 
 
 What are the clinical features of amyloid disease of the kidney ? 
 
 Amyloid., lardaceous or waxy disease of the kidney depends upon 
 a peculiar hyaline degeneration of the coats of the renal capil- 
 laries, which is often associated with some degree of chronic 
 parenchymatous nephritis, and with amyloid degeneration in 
 other organs, such as the liver, the spleen and the intestine. 
 The symptovis are practically those of the associated condition. 
 In addition to edema, albuminuria, the presence of tube-casts 
 in the urine, heightened arterial tension and cardiac hyper- 
 troph3\ there may be a peculiarly waxy complexion, diarrhea, 
 and painless enlargement of the liver, without ascites and .Ifiun- 
 dice. Amyloid degeneration i-esults usuall}- in consequence of 
 protracted suppuration or ulceration, or of syphilis. 
 
 Chronic Interstitial Nephritis. 
 
 What are the symptoms of chronic interstitial nephritis ? 
 
 The interstitial structure of the kidney participitates, in some 
 degree, in ever}- inflammation of the organ. The involvement 
 
CHRONIC INTERSTITIAL NEPHRITIS. 267 
 
 becomes especially obvious in the late stages of all forms of 
 nephritis. In some cases, however, the interstitial connective 
 tissue undergoes hyperplasia from the outset, ultimately con- 
 tracting and giving rise to a diminution in the size of the organ, 
 which becomes small, red, granular ; the capsule is thickened ; 
 on attempting to remove it the adherent cortex tears. This 
 chronic interstitial nephritis is often but one part of a widely 
 distributed arterio-capillary fibrosis. The principal symptom re- 
 ferable to the kidneys is frequent micturition, the urine being 
 considerably increased in quantity, of a low specific gravity, and 
 containing a trace of albumin and hyaline and granular tube- 
 casts. Albumin and casts are sometimes only to be found by 
 repeated, careful examination. There is little or no edema, 
 unless dilatation of the heart develop. There is shortness of 
 breath. The arterial tension is high and the heart is hypertro- 
 phied. The second sound of the heart is accentuated. There 
 is sometimes persistent diarrhea. Retinitis, papillitis, and he- 
 morrhages may occur. Death usually results from uremia or 
 cerebral hemorrhage. The commonest causes of chronic inter- 
 stitial nephritis are alcoholism, gout and lead-poisoning. 
 
 What are the symptoms of uremia ? 
 
 Uremia is an auto-intoxication, which sometimes arises in the 
 course of disease of the kidneys and is dependent upon the reten- 
 tion in the fluids of the body of certain products that it is the 
 function of the kidneys to remove. Uremia gives rise to head- 
 ache, vertigo, nausea, vomiting, diarrhea, dilatation of the pupil, 
 altered vision, delirium, somnolence, convulsions and coma. 
 , Eflfusions frequently accompany the condition. The tempera- 
 ture may be subnormal. It has exceptionally been observed 
 to be* febrile. The body and breath exhale a musty odor. 
 Uremia is one of the gravest complications of disease of the 
 kidneys. 
 
 How are a uremic seizure and a paroxysm of epilepsy to be 
 
 differentiated ? 
 
 Probably dependent upon analogous conditions of irritation, 
 
 there is little diflerence between the convulsions. The onset of 
 
 an epileptic attack is sudden, attended with a cry and biting of 
 
268 ESSENTIALS OF DIAGNOSIS. 
 
 the tongue, and possibly preceded by an aura •, the convulsions 
 of uremia are usually preceded by headache, vertigo and nausea, 
 and occur without sound or injury to the tongue. The urine 
 may contain albumin during or after an epileptic paroxysm, but 
 casts are present as well when the convulsions are uremic. Epi- 
 leptic seizures are far more likel}' than uremic convulsions to 
 have been and to be repeated. A knowledge of the previous 
 history of the case simplifies the diagnosis. 
 
 How are uremia and insolation to be differentiated ? 
 
 The failure on the part of the skin as well as on the part of 
 the kidneys to eliminate certain excrementitious products ma}' 
 in cases of insolation give rise to phenomena resembling those 
 presented by uremia ; but in the former the temperature attains 
 a height never seen in the latter, while the season of the year 
 at which the accident happens, as well as the attendant circum- 
 stances, makes the diagnosis clear. 
 
 Abscess of the Kidney. 
 
 What are the symptoms of abscess of the kidney ? 
 
 Suppuration may take place in the kidney as the result of an 
 acute infectious nephritis, as a part of a general pyemia, or in 
 consequence of traumatism. When pus has formed, the fiymjj- 
 tottis occasioned are those to which imprisoned pus usually gives 
 rise : rigors, hectic fever, sweats, emaciation. The urinary 
 secretion will be altered in accordance with the intensitj' and 
 extent of the causative or associated nephritis. In the urine 
 may be found albumin, pus, tube-casts and blood- corpuscles. 
 There ma}^ be pain and tenderness in the region of the kidne}-. 
 If the accumulation of pus attains considerable proportions it 
 may give rise to a palpable tumor, with fluctuation, in the loin. 
 The abscess may rupture into the pelvis of the kidney, into an 
 adjacent viscus, into the abdominal cavity ; or the pus may 
 make its way out through the abdominal wall. 
 
TUBERCULOSIS OF THE KIDNEY. 269 
 
 Perirenal Abscess. 
 
 What are the clinical features of perirenal abscess ? 
 
 Suppuration may take place in the perirenal connective 
 tissue as a result of an extension of inflammation in tlie pelvis 
 or in the structure of the kidney or as a result of blows or 
 injuries. The condition is to be recognized by the existence 
 of pain and tenderness in connection vi^ith a boggy, fluctu- 
 ating tumor in the loin, associated with chills, fever, sweats 
 and emaciation. The tumor is not movable, and cannot be 
 separated from the kidney. Exploratory puncture may detect 
 the presence of pus. Such an abscess may burrow and find 
 an exit above or below Poupart's ligament, in the loin, into the 
 kidney, ureter or bladder, into the peritoneum, intestines or 
 into a lung. 
 
 How are a perinephric and a renal abscess to be differentiated ? 
 
 An abscess in the loin developing in the course of pyemia is 
 more likely to be renal than perinephric ; an abscess following 
 traumatism is more likely to be perinephric than renal ; while 
 disease of the pelvis or of the kidney may give rise to one or the 
 other. The pus of a perinephric abscess is more likely than that 
 of a renal abscess to burrow and point at some distant spot. In 
 cases of renal abscess evidences of disease are likely to appear 
 in the urine ; there may be pus with albumin and tube-casts. 
 
 Tuberculosis of the Kidney. 
 
 What are the clinical features of tuberculosis of the kidney ? 
 
 Miliaiy tubercles may be developed in the kidneys in common 
 with other organs, as a part of an acute miliary tuberculosis. 
 More usually, when the kidney is tuberculous, the foci are more 
 extensive, and exhibit a tendency to undergo caseation. The 
 kidney is rarely the exclusive seat of tuberculosis. As a rule, 
 other portions of the genito-urinary tract are likewise involved, 
 and not uncommonly the lungs as well. Miliary tuberculosis of 
 the kidney does not give rise to symptoms apart from those of 
 
270 ESSENTIALS OF DIAGNOSIS. 
 
 the general condition of which it is but an incident. In the more 
 localized lesion, the symptoms are vague. There may be pain 
 in the loin, with tenderness ; exceptionally a tumor is discover- 
 able on physical examination ; the urine may contain pus and 
 detritus, in which tubercle-bacilli can, perhaps, be found ; some- 
 times there is hematuria ; there may be hectic fever. Ulti- 
 mately emaciation sets in, exhausting sweats take place and 
 the vitality fails. Tuberculosis of the kidney is more frequent- 
 in the young than in the old, in males than in females. 
 
 Malignant Disease of the Kidney. 
 
 What are the clinical manifestations of malignant disease of 
 the kidney ? 
 
 Malignant disease of the kidney is sarcomatous or carcino- 
 matous. Sarcoma may be congenital or it may appear during 
 childhood. Carcinoma rarely develops before forty. The 
 classical symptoms are tumor, pain and hematuria. 
 
 The swelling occupies one of the loins, and is separated from 
 the anterior abdominal wall by the large intestine. The pain is 
 dull and heavy, with acute exacerbations. Hematuria is not 
 constant. Its absence is of less significance, than would be its 
 presence. In addition, the appetite fails ; there may be nausea 
 or vomiting, constipation or diarrhea ; emaciation sets in ; and 
 cachexia develops. Edema of the lower extremities and ascites 
 may result from pressure on the veins. 
 
 Hydronephrosis. 
 
 What is hydronephrosis ? 
 
 When there exists at any part of the genito-urinary tract an 
 obstruction to the flow of urine, such as may be occasioned by a 
 calculus, a neoplasm, an enlarged prostate gland, a kink or a 
 twist in, or pressure from without upon, a ureter, fluid accumu- 
 lates behind the point of obstruction, and causes dilatation. 
 The condition is designated hydronephrosis. It may be uni- 
 lateral or bilateral. If it be the urethra or the orifice of the 
 bladder that is obstructed, the bladder, ureters, and pelves of 
 
HYDATID CYST OF THE KIDNEY. 271 
 
 the kidneys all become thickened and dilated. If but one ureter 
 is obstructed the corresponding pelvis suffers. The dilatation 
 of the pelvis gives rise to compression and atrophy of the renal 
 parenchyma. Sometimes the fluid resembles pale urine of low 
 specific gravity ; at other times it contains pus. In the latter 
 case the condition is designated pyonephrosis. The symptoms 
 are ill-defined. There may be dull pain, a sense of fulness, and 
 a fluctuant tumor in one or the other loin, attended perhaps 
 with the periodic discharge of large quantities of urine, as the 
 obstruction is temporarily relieved, with a corresponding reces- 
 sion of the symptoms. There may, in addition, be rigors, hectic 
 fever, sweats and emaciation. Constipation due to pressure 
 upon the bowel, is not uncommon in cases of hydronephrosis. 
 The urine may be normal, except at such times as the periodic 
 copious discharges take place, when pus or other matters may 
 be found present. In cases of double hydronephrosis there is 
 great liability to the sudden development of uremia. 
 
 Hydatid Cyst of the Kidney. 
 
 What are the symptoms occasioned by an hydatid cyst of the 
 kidney ? 
 
 The kidneys are relatively a common seat of hydatid cysts. 
 Such a cyst in connection with the kidney may give rise to a 
 fluctuating tumor in the loin or in the lateral region of the 
 abdomen, yielding the characteristic thrill on percussion, and 
 occasioning symptoms dependent upon pressure ; or prior to 
 surgical exploration, it may not give rise to definite symptoms 
 and may elude physical exploration. Under any circumstances 
 a diagnosis may not be possible, unless the contents of the cyst 
 find their way into the genito-urinary tract and are evacuated ; 
 when the detection of the booklets in the urine leaves no room 
 for doubt. The recognition of an additional cyst in another 
 situation may facilitate the diagnosis. 
 
 How are an hydatid cyst of the kidney and hydronephrosis 
 to be differentiated ? 
 
 An hydatid cyst of the kidney and hydronephrosis both 
 occasion a fluctuating renal tumor, but the peculiar thrill on 
 
272 ESSENTIALS OF DIAGNOSIS. 
 
 percussion that characterizes many hydatid cysts is wanting in 
 all cases of water-logged kidney. Ilydruuephrosis is dependent 
 upon some form of genito-urinary obstruction ; such a condition 
 bears no relation to the development of an hydatid cyst. The 
 periodic discharge of a large quantity of fluid, with a temporary 
 disappearance of the tumor, is characteristic of hydronephrosis ; 
 should a discharge of fluid take place, in connection with an 
 hydatid cyst, microscopic examination will reveal the character- 
 istic hooklets in the urine. 
 
 THE NERVOUS SYSTEM. 
 
 How is a study of diseases of the nervous system to be ap- 
 proached ? 
 By an investigation of motion, sensation, reflex action, nutri- 
 tion, electric reaction and cerebral functions. 
 
 How may motion be affected ? 
 
 The power of muscular movement may be impaired or lost ; 
 motility may be exaggerated ; or coordination may be impaired. 
 Complete loss of muscular power is called parcdysts; partial 
 loss, imresis. Motor over-action is seen in spasm and con- 
 vulsion. Incoordination gives rise to ataxia. 
 
 The power of voluntary motion is impaired or lost in destruc- 
 tive disease at any part of the motor tract, from the cerebral 
 cortex to the end-plates. Movement may be interfered with by 
 disease of the muscle itself, or of an adjacent joint ; or abstained 
 from on account of the pain that it causes in a joint or muscles. 
 
 Loss of motor power confined to one side of the body is called 
 hemiplegia; if bilateral, diplegia; limited to the lower extremities, 
 parapjlegia; localized to a member, monoplegia. 
 
 Hemiplegia is usually dependent upon a unilateral cerebral 
 lesion ; it may possibly be caused by a unilateral lesion seated 
 in the upper portion of the cord. 
 
 Diplegia may be a result of symmetrical bilateral cerebral 
 lesions, or of a lesion in a situation where the motor tracts are 
 close together ; like hemiplegia, it may possibly be caused by a 
 lesion in the upper portion of the spinal cord. 
 
THE NERVOUS SYSTEM. 273 
 
 Paraplegia is invariably a result of disease of the cord. 
 
 Monoplegia is a result of a circumscribed lesion of the brain, 
 usually in or near the motor cortex. Any form of paralysis 
 may be simulated by hysteria. 
 
 Spasm or convulsion is indicative of irritation at any part 
 of the motor tract. It may occur in acute disease, cerebral 
 (hemorrhage, embolism, thrombosis) or constitutional (tetanus, 
 hydrophobia) ; in chronic irritative disease (cortical softening, 
 tumor) ; or it may be a symptom of nutritional disease (epilepsy), 
 or of functional disease (hysteria) ; it may also occur in disease 
 not strictly nervous (uremia). 
 
 Ataxia is the result of derangement of the conducting fibers 
 or the coordinating centers in the cord or cerebellum. Loss of 
 tactile sensation also gives rise to ataxia. Defective equilibra- 
 tion may result from disease of the internal auditory apparatus. 
 
 What are the varieties of sensation ? 
 
 Common or tactile sensibility, the pain-sense, the tempera- 
 ture-sense, the muscular-sense ; special sensation : smell, vision, 
 taste and hearing. 
 
 How may sensation be affected? 
 
 Sensation may be impaired, retarded, lost, perverted or 
 heightened. Impairment of sensation is hypjesthesia ; loss of sen- 
 sation is anesthesia; heightening of sensation, hyperesthesia; 
 perversion of sensation, paresthesia. Alterations in sensation 
 are dependent upon derangement in the course of the sensory 
 path. As the lesion may be destructive or irritative, so may 
 the symptoms be those of diminished sensation, of supersensi- 
 bility, or of perverted sensation. One or the other variety of 
 sensation may be affected without involvement of all. 
 
 What are the varieties of reflexes ? 
 
 Superticial or cutaneous, and muscular or deep. 
 
 What are the principal superficial reflexes 
 
 The plantar, the gluteal, the cremasteric, the abdominal, 
 the epigastric, the conjunctival, the reaction of the iris to light, 
 and to cutaneous irritation. 
 18 
 
274 ESSENTIALS OF DIAGNOSIS. 
 
 What are the principal varieties of deep reflexes ? 
 
 The knee-jerk, ankle-clonus and the elbow-jerk. 
 
 How are the reflexes altered in disease ? 
 
 They may be exaggerated, enfeebled or entirely lost. 
 
 The superficial reflexes are exaggerated when the influence of 
 the inhibitory apparatus is removed, or when the activity of 
 the reflex apparatus of the spinal cord is heightened ; the deep 
 reflexes are exaggerated under similar conditions, and likewise 
 when degeneration has taken place in the ccrebro-spinal motor 
 tract. Both superficial and deep reflexes are lost when the 
 reflex arc is interrupted at any point in its course — sensory 
 nerve, reflex center in the cord, and motor nerve. 
 
 How is the nutrition affected by disease of the nervous system ? 
 
 Trophic changes often attend disease of the nervous system. 
 Bedsores sometimes form. Muscles may waste. A paralyzed 
 limb is edematous and its temperature is subnormal ; in chil- 
 dren the growth of paralyzed parts is retarded. Decided altera- 
 tions in joints may take place. The skin sometimes becomes 
 glossy. Trophic changes are most marked in degenerative dis- 
 ease of the nerves and of the gray matter of the cord, especially 
 of the anterior horns. The nutrition of a palsied member slowly 
 suffers. 
 
 How are the electric reactions affected by disease ? 
 
 The normal response of muscle and nerve to both the voltaic 
 and faradic currents may be enfeebled or exaggerated—a quan- 
 titative change ; or the response of nerve to both fiiradism and 
 voltaism, and of muscle to faradism may be enfeebled or lost, 
 while the response of muscle to voltaism persists and may be 
 exaggerated and is altered in its polar relations — a qualitative 
 change^ the reaction of degeneration. 
 
 Normally, the response of muscle to voltaic stimulation is 
 most ready upon application of the kathode and making (closure) 
 of the current ; least ready upon application of the kathode and 
 breaking (opening) of the current. Response upon anodal clo- 
 sure and anodal opening is less ready than that of kathodal 
 closure, more ready than that of kathodal opening. 
 
 The sequence: (1) K.Cl.C. ; (2) ^^^-^^uj '• ^^^ K.O.C. ; is 
 
NEURITIS. 275 
 
 called the normal foriiuila. A deviation from this sequence 
 gives a formula expressive of the reaction of degeneration — a 
 qualitative change. Quantitative changes take place in simple 
 wasting dependent upon disuse or disease of the muscle or of an 
 adjacent joint, or upon interruption in the motor path betw^een 
 the cerebral cortex and the ganglion-cells of the anterior horns 
 of the spinal cord ; qualitative changes take place in degenera- 
 tive muscular wasting dependent upon lesions of nerve or cord, 
 between the motor end-plates and the ganglion-cells of the ante- 
 rior horns inclusive. 
 
 How are the cerebral functions affected by disease of the 
 nervous system ? 
 Delirium, headache and vertigo may appear. Vision, hear- 
 ing, taste or smell may be perverted, excessively acute, im- 
 paired or lost ; memory may be enfeebled ; speech may be 
 altered or lost ; articulation may be defective ; the emotions 
 may be affected ; consciousness may be deranged ; the higher 
 mental powers may suffer deterioration. 
 
 Neuritis. 
 
 How may neuritis be classified ? 
 
 Into perineuritis, interstitial neuritis and parenchymatous 
 neuritis. Neuritis may be acute or chronic ; it may affect one 
 nerve or many. 
 
 What are the causes of neuritis? 
 
 Inflammation of a nerve may result from local injury or com- 
 pression, from adjacent inflammation, from exposure to cold, 
 or from the influence of irritating matters circulating in the blood. 
 Injury, compression, adjacent inflammation and exposure to 
 cold give rise to circumscribed neuritis ; irritants in the blood 
 to multiple neuritis. 
 
 What are the symptoms of neuritis ? 
 
 When a nerve is inflamed, hyperesthesia, paresthesia and 
 anesthesia, pain, tingling, numbness in the peripheral distribu- 
 tion and tenderness in the coui'se of the nerve-trunk in turn 
 appear, with impairment or loss of motion. If the exciting con- 
 
276 ESSENTIALS OF DIAGNOSIS. 
 
 ditions be maintained, nerves degenerate and muscles waste 
 and the skin becomes glossy. Exposure to cold is a cause of 
 inflammation of the facial nerve ; rheumatism, of inflammation 
 of the sciatic ; lead-poisoning, of inflammation of branches of 
 the radial, median and ulnar ; pressure, of inflammation of the 
 musculo-spiral ; syphilis and alcoholism, of inflammation of the 
 peripheral nerves of the extremities. Obstinate neuralgias are 
 sometimes dependent upon neuritis. Acute neuritis is attended 
 with fever and other constitutional phenomena. 
 
 With what conditions may neuritis be confused ? 
 
 With subacute rheumatism, with neuralgia and with disease 
 of bone. The pain occurring in the course of diseases of the 
 spinal cord may be mistaken for an evidence of neuritis. 
 
 How is the diagnosis of neuritis to be made? 
 
 The sjniiptoms are limited to the distribution of one or more 
 nerves and there is tenderness on pressure. When neuralgia is 
 not dependent on neuritis, there are certain tender points, the 
 pain shoots and intermits, and loss of sensation does not result. 
 Pain of spinal origin is not local in distribution or associated 
 with tenderness. 
 
 Multiple Neuritis. 
 
 What are the causes of multiple neuritis? 
 
 Multix>le or disseminated neuritis, or polyneuritis, may be a com- 
 plication or a sequel of infectious diseases, such as sj'philis, 
 diphtheria and influenza ; it may develop in the course of 
 posterior spinal sclerosis or it may appear as a part of anes- 
 thetic leprosy ; it may be due to lead-poisoning ; it may occur 
 endemically, as in the disease known as Jcak-ke or beri-beri; 
 the most common causes, however, are chronic alcoholism and 
 exposure to wet and cold. 
 
 What are the symptoms of multiple neuritis ? 
 
 If multiple neuritis set in suddenly, it may present rigor, 
 elevation of temperature and other febrile symptoms. 
 
 It is attended with numbness, tingling, pain, tenderness and 
 loss of power in the distribution of the nerves aflected, usually 
 
MULTIPLE NEURITIS. 
 
 277 
 
 those of the extremities. Paralysis, wasting and impairment 
 of sensation soon follow. There may be wrist-drop, foot-drop, 
 abolition of reflexes and ataxia. 
 
 Trophic changes occur in the skin, nails and hair. Edema 
 is not uncommon. The wasted muscles present reactions of 
 degenei-ation. Secondary contractions may take place in the 
 unopposed muscles. 
 
 Fig. 43. 
 
 Multiple neuritis, wrist-drop and foot drop. (Gowers ) 
 
 Involvement of spinal nerves, such as the phrenic, the vagus 
 or the third, gives rise to symptoms referable to the distribution 
 of those nerves. 
 
 How are spinal pachymeningitis and multiple neuritis to be 
 differentiated? 
 
 Spinal pachymeningitis is usually cervical ; the symptoms are 
 thus especially referable to the upper extremities. There is also 
 an absence of tenderness in the course of the nerves, while pain 
 radiating from the spinal column is the rule. 
 
 How does acute myelitis differ from multiple neuritis ? 
 
 Myelitis usually involves a limited area of tlie spinal cord in 
 the dorsal or lumbar region. The symptoms are thus mani- 
 fested in the lower half of the body and constitute the type of 
 paraplegia. The action of the sphincters is impaired. There 
 is anesthesia, with a zone of hyperesthesia and but little pain. 
 The paralyzed muscles waste rapidly. The reflexes are mostly 
 exaggerated in the parts supplied by the nerves that arise below 
 the affected area of the cord. 
 
278 ESSENTIALS OF DIAGNOSIS. 
 
 Sciatica. 
 
 What are the causes of sciatica? 
 
 Sciatica is usually dependent upon inflammation of the sciatic 
 nerve. 
 
 It is more common in males than in females and in middle 
 life than at any other period. It may be primary, developing 
 in gouty or rheumatic persons or after exposure to wet and 
 cold, or following injury, or as the result of pressure from sitting 
 on the edge of a chair ; or secondary in consequence of com- 
 pression by tumors in the course of the nerve, within or with- 
 out the pelvis, or as a result of extension froiu adjacent disease, 
 as of the hip-joint. 
 
 What are the symptoms of sciatica? 
 
 Sciatica is attended with pain and tenderness in the coui'se 
 and distribution of the sciatic nerve, increased by movement. 
 There are certain tender points : 1, at the posterior inferior 
 spine of the ilium ; 2, at the sciatic notch ; 3, at the middle of 
 the thigh ; 4, on the posterior aspect of the knee ; o, below the 
 head of the fibula ; 6, behind the external malleolus ; and 7, on 
 the dorsum of tlie foot. There are also paresthesia, tingling, 
 formication and numbness. 
 
 In aggravated cases, the affected muscles waste and present 
 degenerative reactions. There ma)^ also be fibrillary contrac- 
 tions and muscular cramps. 
 
 Primary sciatica is rarely bilateral. 
 
 With what conditions may sciatica he confounded ? 
 
 With sciatic neuralgia, with disease of the hip-joint, and with 
 disease of the spinal cord or cauda equina. 
 How is the differential diagnosis to be made ? 
 
 Sciatic neuralgia occurs in debilitated and anemic persons, 
 with neuralgia elsewhere ; the pain is intermittent, and in the 
 distribution rather than in the course of the nerve ; it may be 
 induced by movement, but is not otherwise aggravated thereby ; 
 there is spontaneous pain rather than tenderness. 
 
 Disease of the hip-joint may give rise to pain about the hip- 
 
PARALYSIS OF THE FACIAL NERVE. 279 
 
 joint and knee ; but there is no tenderness in the course of the 
 nerve ; and investigation will disclose the obvious cause of the 
 symptoms. 
 
 The pain to which disease of the spinal cord or of the cauda 
 equina gives rise is bilateral in distribution ; it is not attended 
 with tenderness in the course of the nerve ; but it is associated 
 with additional symptoms indicative of its origin. 
 
 How are primary and secondary sciatica to be differentiated? 
 
 The pain and tenderness in the course of the nerve in primary 
 sciatica are wanting when the sciatica is secondary ; the pain 
 is then rather in the distribution of the nerve ; other symptoms, 
 and careful examination per rectum, if need be, may lead to the 
 detection of an adequate cause for the pain. 
 
 Paralysis of the Facial Nerve. 
 
 What are the causes of paralysis of the facial nerve? 
 
 The facial nerve may be paralyzed by lesions above its nucleus 
 (supra-nuclear), by lesions of the nucleus (nuclear), or by lesions 
 in the course of the nerve (infra-nuclear). The first is repre- 
 sented by the paralysis of hemiplegia. The nucleus and the 
 root-fibers may be damaged as a result of hemorrhage, softening, 
 degeneration, or inflammation, or by a new-growth. The nerve 
 may sutfer from compression by tumors, from traumatism, from 
 neuritis (primary or secondary). The most common cause of 
 facial paralysis is exposure to cold. 
 
 What are the symptoms of paralysis of the facial nerve ? 
 
 In facial paralysis of nuclear or infra-nuclear origin all of 
 the muscles of one side of the face are paralyzed ; the face is 
 rendered asymmetrical by the unantagonized action of the 
 muscles of the opposite side ; the eye upon one side remains 
 open audcannot be closed ; the lower lid is relaxed and epiphora 
 results ; the forehead on that side is smooth and cannot be 
 wrinkled ; the angle of the mouth droops ; saliva dribbles from 
 the corner of the mouth ; the normal furrows are obliterated ; 
 the lips cannot be puckered, as in whistling, nor elevated, as in 
 displaying the teeth ; associated and emotional movements are 
 
280 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 wanting on the paralyzed side. ISTunibness and tingling indi- 
 cate involvement of filaments of the fifth nerve. 
 
 The affected muscles waste and reactions of degeneration 
 develop. If complete recovery do not occur, secondary contrac- 
 tion in the paralyzed and wasted muscles takes place. 
 
 Fig. 44. 
 
 Facial paralysis. 
 
 The figure on the right represents an attempt to close the eyes. 
 (Gowefs.) 
 
 If the seventh nerve is injured between the geniculate gan- 
 o-lion and the origin of the chorda tympani, the sense of taste is 
 lost in the anterior portion of the tongue. 
 
 How are facial palsy of supra-nuclear origin and that of 
 nuclear or infra-nuclear origin to be differentiated? 
 
 Facial palsy of supra-nuclear origin is but part of a hemi- 
 plegia, of which other manifestations will be evident ; unlike 
 what takes place in nuclear and infra-nuclear disease, the orbi- 
 cularis palpebrarum and the occipito-frontal muscles escape. In 
 nuclear and infra-nuclear palsy, muscular wasting takes place, 
 with degenerative reaction, which is not the case in palsy of 
 supra-nuclear origin. In supra-nuclear paralysis, associated and 
 emotional movements of the face are symmetrically performed ; 
 in nuclear or infra-nuclear palsy, they are not. 
 
PARALYSIS OP MUSCULO-SPIRAL NERVE. 281 
 
 Paralysis of the Phrenic Nerve. 
 
 What are the causes of paralysis of the phrenic nerve ? 
 
 The function of the phrenic nerve may be interfered with by 
 disease of the spinal cord or of the vertebroe, by the pressure 
 of a tumor or of an aneurism, as a result of a neuritis or of a 
 deep wound of the neck. 
 
 To what symptoms does paralysis of the phrenic nerve give 
 rise? 
 
 When the phrenic nerve is paralyzed, the movements of the 
 diaphragm are enfeebled or abolished. If the nerve on one side 
 is affected, the loss of power is not marked ; but if both are par- 
 alyzed, the diaphragm does not actively descend in inspiration ; 
 instead of the protusion of the upper portion of the abdominal 
 wall, there is retraction ; dyspnea is induced by exertion ; 
 cough becomes difficult. 
 
 From what conditions is paralysis of the phrenic nerves to 
 be differentiated? 
 
 From superior intercostal breathing, from inflammation of the 
 diaphragm and from degeneration of the diaphragm. In the 
 first condition, inspiratory contraction of the diaphragm must 
 be carefully looked for ; in the second, there has been an adja- 
 cent inflammation, most probably of the pleura or peritoneum ; 
 the third has only been recognized after death. 
 
 If the paralysis of the phrenic nerves is dependent upon dis- 
 ease of the cord, there are present other symptoms than inac- 
 tivity of the diaphragm. 
 
 Paralysis of the Musculo-spiral Nerve. 
 
 What are the causes of paralysis of the musculo-spiral nerve ? 
 
 The musculo-spiral nerve may be paralyzed as a result of 
 traumatism, as from a blow or when the humerus is fractured ; 
 the nerve may be compressed by calkis, by contraction of the 
 triceps muscle, or by the head of a crutch in the axilla ; neuritis 
 may result from exposure to cold. The most common cause of 
 
282 ESSENTIALS OF DIAGNOSIS. 
 
 musculo-spiral paralysis is pressure by the head on the arm 
 during sleep. 
 
 How is paralysis of the musculo-spiral nerve to be recognized ? 
 
 The characteristic sj'mptom of paralysis of the musculo-spiral 
 nerve is loss of power in the extensors of the elbow and 
 wrist, in the long extensors of the fingers and thumb, and in the 
 supinators. There is wrist-drop and the fingers and thumb 
 cannot be extended. From the want of antagonism the power 
 of flexion is also enfeebled. Subsequentl}^, the palsied muscles 
 may present reactions of degeneration. 
 
 How does the neuritis of lead-poisoning differ from the neu- 
 ritis of the musculo-spiral nerve resulting from compres- 
 sion or traumatism? 
 
 Both are attended by wrist-drop, which in lead-poisoning is 
 bilateral, in compression-neuritis unilateral. In the former, the 
 onset is slow and gradual and the action of the supinators is 
 unimpaired ; in the latter, the onset is acute and supination 
 cannot be performed. A blue line on the gums attends lead- 
 poisoning ; careful chemic examination during the administra- 
 tion of potassium iodide may detect lead in the urine ; while 
 in musculo-spiral palsy a cause of a different kind is readily 
 ascertainable. 
 
 Neuromata. 
 
 To what symptoms do neuromata give rise? 
 
 Tumors in the course of nerves may be composed of nervous 
 structure or be heterologous. They may be hereditary, con- 
 genital, or a result of traumatism ; they are not uncommonly 
 seen on the stumps of .amputated members. The symptoms 
 that such growths occasion necessarily depend upon their 
 situation. At first they give rise to irritation and heightened 
 function, as evidenced by pain and spasm ; subsequently they 
 cause abolition of function and paralysis. 
 
 Upon what does the diagnosis of neuromata depend ? 
 
 Upon the detection of a tumor and the obstinacy of symptoms 
 referable to the distribution of one or more nerves. 
 
NEURALGIA. 283 
 
 Neuralgia. 
 
 What are the clinical features of neuralgia ? 
 
 Pain in the course of a nerve, independent of neuritis, appears 
 most commonly in adult life, in anemic and ill-nourished women 
 of emotional temperament. In some instances, an hereditary 
 predisposition can be traced. Among the causes of neuralgia 
 are exposure to cold, rheumatism, gout, malaria, alcoholism, 
 plumbism, traumatism and peripheral irritation. 
 
 The pain occurs in paroxysms, in the intervals between which 
 some sensitiveness persists. In the course of the nerve are cer- 
 tain tender points — points douloureux of Yalleix. Muscular 
 spasm sometimes takes place in the distribution of the motor 
 nerve corresponding to the sensory nerve involved. The i^ar- 
 oxysm is sometimes attended with vomiting. Vaso-motor de- 
 rangement and trophic changes may manifest themselves in the 
 course of the disease. ISTeuralgia may be localized to a single 
 nerve ; it may progress in a radiating manner, or it may char.ge 
 its seat from nerve to nerve. 
 
 How are neuritis and neuralgia to be differentiated ? 
 
 The pain of neuralgia is intermittent and paroxysmal ; that 
 of neuritis is continuous ; in neuritis there is, in addition, ten- 
 derness in the course of the nerve, with swelling. Neuritis is 
 riot limited to sensory nerves ; in consequence, muscular weak- 
 ness and, later, wasting and alterations in the electrical reac- 
 tions are manifest. 
 
 What are the symptoms of trigeminal neuralgia ? 
 
 The symptoms of neuralgia of the fifth nerve, trigeminal or tri- 
 facial neuralgia, or tic douloureux, depend upon its distribution. 
 One or several branches of the nerve may be involved. 
 
 Of the first division, the supra-orbital branch is most com- 
 monly affected. Pain is felt on the forehead, on the ej'elid, in 
 the eye and on the side of the nose. There are supra-orbital, 
 palpebral, nasal and ocular tender points. 
 
 Of the second division of the fifth nerve, the infra-orbital 
 branch is most commonly attacked by neuralgia. Pain is 
 referred to the cheek and ala nasi, between the orbit and the 
 
284 ESSENTIALS OF DIAGNOSIS. 
 
 mouth. There are infra-orbital, nasal, malar and gingival 
 tender points. 
 
 The pain of neuralgia of the inferior maxillary nerve is referred 
 to the parietal eminence, the temple, the lower jaw, the ear and 
 the tongue. There are inferior dental, temporal and parietal 
 tender points. Sometimes the inferior dental and the auriculo- 
 temporal branches are alone involved. 
 
 Migraine. 
 
 What are the clinical features of migraine ? 
 
 Migraine^ hemicrania or sicTc headache is a paroxysmal neurosis 
 characterized by unilateral headache, associated with nausea, 
 vomiting and derangement of vision and sensation. It is more 
 common in females than in males and in the first half of life 
 than at any other time. Frequently a neurotic heredity can be 
 traced, some members of the same family presenting migraine, 
 epilepsy, neuralgia, insanity or some other neurosis. 
 
 The paroxysm often begins with some sensory disturbance, 
 such as tingling or numbness ; or with a perversion of vision, 
 such as the appearance of a luminous or brightly colored object ; 
 or with an impairment of vision usuallj^ presenting the char- 
 acters of hemianopia or with auditory manifestations, such as 
 tinnitus or a sudden explosive sound. "When the headache 
 reaches a considerable degree of intensity nausea and vomiting 
 occur. In extreme cases motor weakness and aphasia are 
 present. The headache, at the beginning of the disease uni- 
 lateral, may subsequently become bilateral. It is often periodic, 
 and not rarely in some fixed relation with menstruation, which 
 it may accompany, or precede or follow at a certain interval. 
 
 It may sometimes be traced to reflex influences, such as may 
 arise from gastric disturbance or eye-strain. These, however, 
 are to be regarded merely as excitants, acting upon a predis- 
 posed nervous system, and would not alone be effective. 
 
 How are migraine and ordinary headache to be differentiated? 
 
 Headache may arise from a multiplicity of conditions — among 
 others from neuralgia, from rheumatism, from gastro-intestinal 
 
SPINAL MENINGITIS. 285 
 
 derangement, from toxemia, from eye-strain, from anemia, from 
 hyperemia and from organic disease of the brain. It is un- 
 associated with other subjective or with visual manifestations ; 
 it is bilateral ; it is not paroxysmal ; it is dependent upon other 
 influences than is migraine. 
 
 Spinal Meningitis. 
 
 What are the varieties of spinal meningitis ? 
 
 Spinal meningitis may be acute or chranic; it may involve the 
 dura, arachnoid or pia, giving rise respectively io pachymenin- 
 gitis^ arachnitis or leptomeningitis; it may be simpde^ pwulent, 
 tuberculous or hemorrhagic. 
 
 What are the causes of spinal meningitis ? 
 
 Inflammation of the spinal meninges may result from an ex- 
 tension of adjacent inflammation, from traumatism, from ex- 
 posure to cold and wet ; it may develop in the course of infec- 
 tious diseases, or as a manifestation of syphilis, of tuberculosis, 
 of pyemia or of alcoholism. 
 
 What are the symptoms of acute spinal meningitis ? 
 
 Meningitis may set in abruptly with a chill, followed by ele- 
 vation of temperature, pain in the back and radiating in the course 
 of the nerves, hyperesthesia, stiffness and spasmodic contrac- 
 tion of various muscles, exaggerated reflexes, retention of urine 
 and constipation. The pain is intensified in paroxysms. The 
 muscular spasms are induced by efforts at movement. The 
 finger drawn over the skin leaves a red streak. 
 
 With the subsidence of the acute symptoms, the pain may 
 yet- remain, but the manifestations of irritation give way to 
 those of paralysis : muscular weakness and wasting, anesthesia, 
 abolition of reflexes and enfeeblement of the sphincters. The 
 extent and distribution of the symptoms depend upon the seat 
 of the meningeal inflammation. 
 
 How are rheumatism of the muscles of the back and spinal 
 meningitis to be differentiated ? 
 Pain may accompany dorsal or lumbar rheumatism, but it is 
 not radiating, nor is it attended with muscular rigidity, or fol- 
 lowed by anesthesia, loss of power and wasting. 
 
286 ESSENTIALS OF DIAGNOSIS. 
 
 Cervical Pachymeningitis. 
 
 What are the symptoms of cervical pachymeningitis ? 
 
 Intlaiiiniatiou of the dura mater in the cervical region is 
 recognized by pain and stiffness in that region, with shoot- 
 ing pains in the arms, and numbness, and impaired sensibiUty, 
 and loss of power, and wasting. The over-extension of the 
 hand, with flexion of the fingers, that results from the paralysis 
 of the long flexors of the wrist and fingers, and of the intei"- 
 ossei gives rise to characteristic deformity. There may also be 
 weakness of the lower extremities. 
 
 How is cervical pachymeningitis to be distinguished from 
 progressive muscular atrophy and subacute anterior 
 poliomyelitis ? 
 
 All three may give rise to wasting and weakness in the 
 upper extremities, and weakness in the lower ; but in pachy- 
 meningitis sensation is deranged, the wasting is irregular in 
 distribution, and there have at some time been stifiiiess in the 
 muscles of the neck, and pains in the back and radiating down 
 the arms ; while spasm and sensory symptoms are wanting in 
 progressive muscular atrophy and poliomyelitis. 
 
 Hemorrhage into the Spinal Membranes. 
 
 What are the varieties of hemorrhage into the spinal men- 
 inges? 
 Hemorrhage may take place between the dura and the ver- 
 tebrse, being then extrameningeal ; or within the dura, being then 
 intrameningeal. Intrameningeal hemorrhage may take place 
 between the dura and the arachnoid, being then subdural; or 
 between the arachnoid and the pia, being then subarachnoid. 
 
 What are the causes of hemorrhage into the spinal meninges? 
 
 Hemorrhage into the membranes of the cord is usually a result 
 of traumatism, as from falls or blows, or of violent muscular 
 activity, as during convulsions or labor ; it may occur in the 
 course of acute infectious diseases or as a manifestation of a 
 
HYPEREMIA OF THE SPINAL CORD. 287 
 
 hemorrhagic diathesis ; or an aneurism that has eroded the 
 vertebrae may rupture and empty its contents into the spinal 
 canal. 
 
 What are the symptoms to which hemorrhage into the spinal 
 membranes give rise? 
 Hemorrhage into the spinal meninges is marked by sudden, 
 severe pain in the back, to which are soon added rigidity, mus- 
 cular spasm, radiating pains, hyperesthesia, retention of urine 
 and constipation ; sliould death not occur, these symptoms in 
 turn give way to muscular weakness, anesthesia and derange- 
 ment of the sphincters. 
 
 How are spinal meningitis and hemorrhage into the spinal 
 meninges to be differentiated ? 
 
 The onset of liemorrhage is sudden, that of meningitis gradual. 
 Meningitis is from the outset attended with elevation of tem- 
 perature ; in hemorrhage, the temperature rises only when men- 
 ingitis sets in. 
 
 Anemia of the Spinal Cord. 
 
 What are the manifestations of anemia of the spinal cord ? 
 
 Anemia of the spinal cord may be part of a general anemia. 
 There is no definite symptom by which it can be recognized. 
 Whatever the symptoms to which it may give rise, they are 
 comprised in those of the condition of which the spinal anemia 
 is a part. There is aching in the legs and the patient fatigues 
 readily. There may be wasting of the extremities and para- 
 plegia. 
 
 Hyperemia of the Spinal Cord. 
 
 What are the symptoms of hyperemia of the spinal cord ? 
 
 The clinical recognition of hyperemia, other than as a condition 
 antecedent to inflammation of the spinal cord, is as doubtful as 
 is that of spinal anemia. A diagnosis of hyperemia is justifiable 
 when symptoms apparently indicative of a beginning myelitis 
 disappear in the course of a few days. 
 
288 ESSENTIALS OF DIAGNOSIS. 
 
 Myelitis. 
 
 What are the varieties of myelitis ? 
 
 Myelitis may be acute^ subacute or chronic; it may be transr 
 verse, focal, disseminated, diffuse or central; or it may involve 
 only the anterior horns of the gray matter. 
 
 What are the causes of myelitis ? 
 
 Myelitis is more common in males than in females. It may 
 result from traumatism, from exposure to cold and wet, from 
 compression, by extension from adjacent disease and in the 
 course of acute infectious diseases ; syphilis may be a cause of 
 myelitis. 
 
 What are the symptoms of acute myelitis? 
 
 The symptoms of acute myelitis set in with variable abrupt- 
 ness and with febrile manifestations. There may at first be 
 pains of moderate severity in the back. Soon, there is loss of 
 motion and sensation in the parts supplied by the nerves 
 arising from the cord below the level of the inflammation, with 
 a girdle-sensation and a zone of hyperesthesia corresponding 
 to the distribution of the nerves given off at the upper Umit of 
 the inflammation. Grave trophic changes, as wasting and the 
 formation of bed-sores, may take place, with the development 
 of the reactions of degeneration. The reflexes within the dis- 
 tribution of the nerves arising from the inflamed area are lost ; 
 those below are exaggerated. Control of the sphincters is 
 lost. 
 
 After the subsidence of the acute symptoms, some improve- 
 ment slowly takes place, greater in respect to sensation than in 
 respect to motion. Cystitis and consecutive pyelonephritis may 
 develop. Contractures may take place. The inflammation of 
 the cord may extend. 
 
 How are acute spinal meningitis and acute myelitis to be 
 distinguished from one another? 
 
 The two are likely to be associated ; the symptoms of the one 
 or the other, however, predominating. Pain, hyperesthesia 
 and muscular spasm, followed by anesthesia and palsy, char- 
 
CHRONIC MYELITIS. 289 
 
 acterize acute meningitis. In myelitis, pain and hyperesthesia 
 are sHght, transient and circumscribed ; muscular spasm is want- 
 ing ; and wasting, palsy, anesthesia and derangement of the 
 sphincters appear early. 
 
 How are acute myelitis and spinal hemorrhage to be differen- 
 tiated ? 
 The onset of hemorrhage is more abrupt than that of myelitis. 
 Initial fever indicates myelitis rather than hemorrhage. Hem- 
 orrhage into the spinal cord is soon followed by myelitis, and the 
 differentiation then becomes impossible. 
 
 Chronic Myelitis 
 
 What are the causes of chronic myelitis? 
 
 Chronic myelitis is more common in males than in females, 
 and in early and middle adult life than at any other period. The 
 same causes tliat occasion acute mj'elitis may also give rise to 
 chronic myelitis. Thus chronic myelitis may follow syphilis, 
 repeated exposure to cold and wet, repeated over-exertion, com- 
 pression of the cord, chronic alcoholism and lead-poisoning. 
 Chronic myelitis may be a sequel of acute myelitis or of chronic 
 meningitis. 
 
 What are the symptoms of chronic myelitis? 
 
 The symptoms of chronic myelitis vary in distribution with 
 the localization of the disease. There is at first an undue readi- 
 ness of muscular fatigue, soon progressing to weakness and fol- 
 lowed by actual palsy. Sensation is deranged ; paresthesiae are 
 common ; girdle-pain may appear. The reflexes are exaggerated. 
 A tendency to spasm develops. The musdes waste and present 
 quantitatively altered electric reactions, which, in the later 
 stages of the disease, suffer qualitative change. The sphincters 
 usually participate in the loss of motor power. 
 
 How does chronic differ from acute myelitis ? 
 
 The symptoms of chronic myelitis, unlike those of acute mye- 
 litis, are slow and gradual in onset, progressive in course, irreg- 
 ular in distribution and unattended with febrile reaction. 
 19 
 
290 ESSENTIALS OF DIAGNOSIS. 
 
 What are the distinctions between chronic myelitis and pro- 
 gressive muscular atrophy? 
 
 The symptoms of chronic myelitis are irregular in distribu- 
 tion ; the manifestations of progressive muscular atrophy ap- 
 pear somewhat symmetrically. Sensory symptoms constitute a 
 distinctive feature of chronic myelitis, but are inconsiderable or 
 wanting in j)rogressive muscular atrophy. Exaggeration of re- 
 flexes and spasm characterize myelitis rather than muscular 
 atrophy. ribrillary muscular contractions and heightened 
 mechanical irritability mark progressive muscular atrophy. 
 
 In wh3,t respects does chronic myelitis differ from lateral 
 sclerosis ? 
 
 In lateral sclerosis, sensation is not deranged ; there is no 
 girdle-sensation ; and the action of the sphincters remains 
 unimpaired. 
 
 What is the distinction between chronic myelitis and spinal 
 pachymeningitis ? 
 Spinal pachymeningitis is most commonly cervical and the 
 symptoms are limited to the upper extremities ; myelitis ir- 
 regularly involves all four extremities. Pain is a more constant 
 manifestation of pach^^meningitis than of myelitis. 
 
 Acute Anterior Poliomyelitis. 
 
 What are the causes of acute anterior poliomyelitis ? 
 
 Acute inflammation of the anterior horns of the gray matter 
 of the spinal cord is more conunon in males than in females, 
 in late infancy than at any other period of life, and in summer 
 than in winter. It follows sudden chilling of the heated body ; 
 injuries to the spine ; acute infectious diseases ; over-exertion. 
 
 What are the symptoms of acute anterior poliomyelitis ? 
 
 Acute anterior poliomyelitvi may set in abruptly, with convul- 
 sions, delirium, headache, dull, heavy pains in the back and in 
 the extremities, and febrile symptoms. Soon, extensive palsy 
 appears, followed, after a variable period, by wasting of certain 
 groups of muscles. There may have been incontinence of urine 
 and of feces. 
 
ACUTE ASCENDING PARALYSIS. 291 
 
 In the course of several weeks the original extent of paralysis 
 gradually diminishes, until ultimately the loss of power and the 
 wasting are limited to certain parts that remain permanently 
 deficient in nutrition, growth and function. 
 
 Degenerative reactions of nerve and muscle develop and the 
 reflexes are enfeebled or lost. 
 
 What are the distinctions between myelitis and poliomyelitis ? 
 
 The permanent palsy is more extensive in myelitis than in 
 poliomyelitis. In the former the reflexes are exaggerated ; in 
 the latter, enfeebled or lost. Sensory symptoms characterize 
 myelitis ; not poliomyelitis. Bedsores are common in the 
 former ; not in the latter. 
 
 How are the paralysis of poliomyelitis and that of cerebral 
 origin to be differentiated? 
 
 The paralysis of poliomyelitis may be limited to one side ; but 
 it is not characteristically hemiplegic. It is attended with 
 wasting and the reaction of degeneration ; cerebral paralysis 
 may be attended with wasting, but not with the reaction of de- 
 generation. Athetoid movements appear in the course of palsy of 
 cerebral origin ; not in the course of the palsy of poliomyelitis. 
 The reflexes are exaggerated in cerebral disease ; enfeebled or 
 lost in poliomyelitis. 
 
 How are multiple neuritis and anterior poliomyelitis to be dif- 
 ferentiated ? 
 
 Sensory symptoms — tingling, pain, tenderness, numbness and 
 anesthesia — as seen in neuritis, are wanting in poliomyelitis. 
 Multiple neuritis is rather symmetrical, poliomyelitis irregular 
 in distribution. The one is the more common in adults ; the 
 other, in children. 
 
 Acute Ascending Paralysis. 
 
 What are the symptoms of acute ascending paralysis or 
 
 Landry's paralysis ? 
 
 The nature of acute ascending paralysis is not yet known. 
 
 The disease is thought to depend upon a toxic influence exerted 
 
 upon the nervous system. It arises under conditions similar to 
 
292 ESSENTIALS OF DIAGNOSIS. 
 
 those that precede acute mj'elitis. It is characterized by pro- 
 gressive motor paralysis, beginning in the lower extremities and 
 gradually extending upwards. The power of movement is lost ; 
 respiration, deglutition, and articulation are interfered with. 
 Numbness and tingling are sometimes present at the onset and 
 followed by impairment of sensation. The reflexes are en- 
 feebled. Trophic changes are wanting. The sphincters are 
 usually involved. The spleen is enlarged. Most cases termi- 
 nate fatally. 
 
 How are acute myelitis and acute ascending paralysis to be 
 differentiated ? 
 
 Febrile symptoms, anesthesia, trophic changes and involve- 
 ment of the sphincters do not attend acute ascending paralysis 
 (Landry's disease). Recovery from acute ascending paralysis 
 is less common than is recovery from myelitis. 
 
 How is acute ascending paralysis to be distinguished from 
 multiple neuritis ? 
 
 The view has been expressed that acute ascending paralysis 
 is dependent upon multiple neuritis. Acute ascending paraly- 
 sis, however, does not appear in all four extremities at once, and 
 is said not to present the alterations of sensation, the muscular 
 wasting and the elevation of temperature of multiple neuritis. 
 
 What is the distinction between acute ascending paralysis and 
 anterior poliomyelitis ? 
 
 The onset of acute anterior poliomyelitis is, while that of acute 
 ascending paralysis is not, attended with febrile manifestations. 
 In poliomyelitis, the paralyzed muscles waste ; in ascending 
 paralysis, they do not. Poliomyelitis is rarely fatal ; ascending 
 paralysis is usually fatal. 
 
 Amyotrophic Lateral Sclerosis — Progressive 
 Muscular Atrophy— Glosso-Labio-Laryngeal 
 Palsy. 
 
 There are three afiections intimately related to one another : 
 amyotrophic lateral sclerosis, progressive rtmscular atrophy and 
 
AMYOTROPHIC LATERAL SCLEROSIS. 293 
 
 glosso-labio-laryngedl palsy. The pathologic lesions are similar 
 in all : a degenerative process in the gray matter and in the 
 conducting paths. The symptoms of the three aftections differ 
 according to the situation of the disease in the gray matter, 
 and according to whether the change begins first in the graj'- 
 matter and then involves the white or vice versa. 
 
 If the white matter of the lateral columns is first involved, 
 with partial or with subsequent invasion of the gray matter of 
 the anterior horns, amyotrophic lateral sclerosis results. If the 
 gray matter of the cord be first involved, the symptoms of pro- 
 gressive muscular atrophy appear ; while if the process extend 
 to or originate in the gray matter of the medulla the symptoms 
 are those of bulbar palsy, superadded or occurring isolated. 
 
 What are the causes of amyotrophic lateral sclerosis, progres- 
 sive muscular atrophy and chronic bulbar palsy ? 
 In many cases, no cause can be determined ; in others the 
 symptoms have been preceded by mental strain, by exposure to 
 cold and wet, by concussion, by syphilis, by lead-poisoning, and 
 by acute diseases ; in some there is an indirect neurotic heredity. 
 All three affections are more common in males than in females, 
 and in middle life than at any other period. 
 
 What are the symptoms of amyotrophic lateral sclerosis ? 
 
 Amyotropliic lateral sclerosis begins with symptoms of lateral 
 sclerosis : weakness ; a stiff, awkward, spastic gait ; muscular 
 spasm ; exaggerated reflexes ; spinal epilepsy ; to which in 
 turn may be superadded the symptoms of degeneration of the 
 anterior horns of the gx'ay matter : muscular wasting, paralysis, 
 loss of reflexes, reaction of degeneration. 
 
 What are the symptoms of progressive muscular atrophy ? 
 
 Progressive muscular atrophy is usually insidious in onset ; some- 
 times slow, sometimes rapid, but always progressive in course. 
 Muscular wasting, preceded by pain, is first observed in one por- 
 tion of the body, usually in an upper extremity, and followed 
 by weakness ; both wasting and weakness in turn successively 
 invade all four extremities and the trunk as well ; respiration 
 
294 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 may be embarrassed. If the duration of the ease be long enough, 
 symptoms of bulbar paralysis are superadded. 
 
 Fig. 45. 
 
 
 Progressive Muscular Atrophy. (Gowers.) 
 
 1. Wasting of the muscles of the back and arms. 
 
 2. Wasting of the trapezii and deltoids. 
 
 3. Wasting of the muscles of the neck ; a, habitual posture of the head ; B, posi- 
 tion into which the head falls if it be not inclined backward. 
 
 The wasting is especially manifest in the thenar and hypo- 
 thenar eminences and in the interosseous spaces ; as a result, a 
 
AMYOTROPHIC LATERAL SCLEROSIS, 295 
 
 peculiar deformity — tlie claw-like hand — develops. The wasting 
 muscles are the seat of spontaneous fibrillary contractions. Me- 
 chanical muscular irritability is heightened. The deep reflexes 
 are enfeebled in a degree proportional to the muscular wasting. 
 The electric reactions are also dependent upon the nutrition of 
 the muscles and nerves. At first, they present quantitative, 
 subsequently qualitative changes. 
 
 What are the symptoms of chronic or progressive bulbar 
 paralysis— glosso-labio-laryngeal palsy ? 
 The symptoms of glosso-labio-laryngeal paralysis are analogous 
 to those of progressive muscular atrophy, the degenerative pro- 
 cess, however, involving the nuclei of the cerebral rather than 
 those of the spinal nerves, especially the facial, glosso-pharyn- 
 geal, pneumogastric, spinal accessory and hypoglossal. The 
 disease is marked by difficulty in mastication, in deglutition, in 
 respiration, in phonation and articulation, and by wasting of the 
 muscles concerned in these functions. The affected muscles dis- 
 play spontaneous fibrillary contractions. Speech becomes pro- 
 gressively more difficult and indistinct and finally nasal. Swallow- 
 ing is difficult and fluids regurgitate through the nose. Saliva 
 dribbles from the mouth. Food may find its way into the larynx. 
 Keflex action in the throat may be lost. Earely the ocular and 
 the facial muscles participate in the palsy. 
 
 How is progressive muscular atrophy to be distinguished from 
 acute anterior poliomyelitis ? 
 
 Progressive muscular atrophy is especially a disease of adult 
 life. It is usually gradual in onset and progressive in course, 
 while acute anterior poliomyelitis is especially a disease of child- 
 hood, and is acute in onset and retrogressive in course. Febrile 
 symptoms attend acute poliomyelitis, but not progressive atro- 
 phy. The fibrillaiy tvi^itching of the latter is not present in the 
 former. Terminal bulbar symptoms attend progressive muscu- 
 lar atrophy, but not acute poliomyelitis. 
 
296 ESSEiiTTlALS OF DIAGNOSIS. 
 
 Acute Bulbar Palsy. 
 
 What is acute bulbar palsy ? 
 
 Symptoms almost identical with those of progressive glosso- 
 labio-laryngeal paralysis may set in acutely. They may subse- 
 quently undergo some iuiprovement and then remain stationarj-. 
 The condition is dependent upon an acute lesion — softening or 
 hemorrhage or inflammation of the medulla, involving the nuclei 
 of the glosso-pharyngeal, pneumogastric, spinal accessory and 
 hypoglossal nerves or the fibers passing to or from them. 
 
 How is acute to be distinguished from chronic bulbar palsy ? 
 
 The symptoms of chronic bulbar palsy are gradual in onset, 
 progressive in course and symmetrical in distribution ; those 
 of acute bulbar palsy are sudden in onset, regressive or sta- 
 tionary and are apt to display slight irregularities of distribu- 
 tion. 
 
 Pseudo-Bulbar Palsy. 
 
 What is pseudo-bulbar palsy? 
 
 A bilateral lesion, such as softening or hemorrhage, involving 
 the lower portion of the ascending frontal convolution of both 
 hemispheres, or the corresponding motor tracts in symmetrical 
 situations, will give rise to the symptoms of bulbar palsy: para- 
 l3'sis of the lips, tongue and throat. 
 
 How is pseudo-bulbar palsy to be distinguished from true bul- 
 bar palsy ? 
 Pseudo-bulbar palsy, in contradistinction to true bulbar 
 palsy, is likely to be characterized by two distinct attacks, by 
 slight asymmetry of distribution of the syniiDtoms, and by the 
 absence of wasting. 
 
 Pseudo-Hypertrophic Paralysis. 
 
 What are the symptoms of pseudo-hypertrophic paralysis ? 
 
 Pseudo-hypertr opine paralysis is a congenital family-affection, 
 transmitted through females but occurring more commonly in 
 
l^SEUBO-HYPERTROPllrC PARALYSIS. 
 
 297 
 
 males, usually appearing in childhood, and characterized by 
 weakness and enlarged muscles, the fibers of which undergo 
 atrophy, while the interstitial tissue increases. The muscles of 
 the calves and the infra-spinati usually participate in the en- 
 
 FiG. 46. 
 
 Pseudo-hypertrophic paralysis in two brothers. (Gowers.) 
 
 largement in striking degree. Wasting of the latissimus dorsi 
 and of the lower portion of the pectoralis major is characteristic. 
 The gait has a peculiar oscillating character ; ascending 
 stairs is difficult, and the manner of rising from the floor is 
 characteristic (Fig. 47) : the patient first gets on his hands and 
 knees ; then extending the legs he stands upon his feet ; finally, 
 by supporting his hands upon his thiglis he manages to reach 
 the erect posture. Ultimately the muscles become reduced in 
 size ; the electric reactions suffer quantitative changes, indica- 
 
298 
 
 ESSENTIALS OF DIAGNOSIS. 
 Fig. 47. 
 
 Pseudo-hypertrophie paralysis. Mode of rising from the ground. (Gowers 
 
 tive of diminished excitability ; the deep reflexes are enfeebled 
 and lost. Talipes equinus, spinal curvature and muscular con- 
 tractions occur at a late stage of the disease. 
 
 Simple Idiopathic Muscular Atrophy. 
 
 What is simple idiopathic muscular atrophy ? 
 
 There is a condition, allied to pseudo-hypertrophic paralysis, 
 in which the muscles atrophy, but do not become enlarged by 
 interstitial deposit. The affection occurs in families, is as com- 
 mon in females as in males, and usually appears in early adult 
 life. 
 
 What are the symptoms of simple idiopathic muscular 
 atrophy ? 
 
 Sinijile idictpathic muscular atrophy sets in graduallj^, with 
 weakness and wasting in the face, arms or legs and extension 
 to the rest of the body. The deep reflexes become enfeebled, 
 deformities result and the electric reactions are quantitatively 
 changed. Among other muscles, the latissimus dorsi, the 
 
ARTHRITIC MUSCULAR ATROPHY. 299 
 
 infraspinati, the zygomatic! and the orbicularis oris show a 
 special proueuess to undergo wasting and palsy. 
 
 What are the distinctions between pseudo-hypertrophic 
 muscular paralysis and simple idiopathic muscular 
 atrophy ? 
 
 PSEUDO-HYPERTROPHIC MUSCULAR SIMPLE IDIOPATHIC MUSCULAR 
 
 PARALYSIS. PARALYSIS. 
 
 More common in males. Equally common in the two sexes. 
 
 Some muscles enlarged ; gastroc- Muscles usually wasted, especially 
 
 nemii and infraspinati especi- the orbicularis and the zygomatici. 
 
 ally prone to enlargement. 
 
 Face not involved as a rule. Involvement of face characteristic. 
 
 Notable increase of interstitial tis- Slight or no increase of interstitial 
 
 sue in muscles. tissue in muscles. 
 
 Other cases, typical of one or of the other form of idiopathic 
 muscular atrophy, will be found among the members of the 
 family of either, respectively. 
 
 What are the distinctions between progressive muscular 
 atrophy and simple idiopathic muscular atrophy? 
 
 Simple idiopathic muscular atrophy is a disease that occurs 
 in families, appearing in childhood, the muscles of the face, 
 especially the orbicularis oris and the zygomatici, being in- 
 volved. 
 
 Progressive muscular atrophy is a disease independent of 
 family influences, appearing in adult life, the wasting often be- 
 ginning in the hands, while the face remains uninvolved. 
 
 Arthritic Muscular Atrophy. 
 
 What is arthritic muscular atrophy 
 
 It has been observed that in the course of inflammation of a 
 joint, acute or chronic, spontaneous or traumatic, the related 
 muscles, especially the extensors, undergo a varying degree of 
 atrophy. With the disappearance of the arthritis, the affected 
 muscles gradually return to their normal condition. If the 
 joint-disorder continue for a long period, the deep i-eflexes in 
 
300 ESSENTIALS OF DIAGNOSIS. 
 
 the region involved are heightened and the muscles present 
 quantitative electrical changes ; contracture of the opponent 
 muscles may also occur. 
 
 Thomsen's Disease — Myotonia Congenita. 
 
 What are the symptoms of myotonia congenita— Thomsen's 
 disease ? 
 
 The disorder described by Thomsen is one that occurs as a 
 congenital affection in families. It is characterized by tonic 
 muscular spasm on voluntary movement following a period of 
 rest. If movement is persevered in, the spasm relaxes. The 
 spasm is intensified by emotion or by the fear of its occurrence. 
 Muscular hypertrophy is the ultimate result. A peculiar elec- 
 tric reaction, myotonia electrica^ is developed. 
 
 Posterior Spinal Sclerosis — Locomotor Ataxia. 
 
 What are the causes of posterior spinal sclerosis ? 
 
 Posterior spinal sclerosis^ loco^iwtor ataxia, or tabes dorsalis is 
 more common in males than in females, and in middle adult life 
 than at any other period. Its most common cause is syphilis ; 
 other causes are exposure to cold and wet, concussion, over- 
 exertion and sexual and alcoholic excesses ; the disease has 
 been observed to follow acute infectious diseases ; it is some- 
 times secondary to other forms of spinal disease ; in some cases 
 an hereditary neurotic influence can be traced. It has been 
 attributed to metallic poisoning. The etiology is sometimes 
 obscure. 
 
 What are the symptoms of posterior spinal sclerosis ? 
 
 Posterior spinal sclerosis is characterized by impairment of 
 coordination, giving rise to difficulty in performing delicate 
 movements, to unsteadiness of gait and of station, particularly 
 when the guidance of vision is removed ; by shooting pains in 
 the extremities ; by a girdle-sensation ; by other abnormalities 
 of sensation, particularly anesthesia, and especially in the soles 
 of the feet ; by abolition of the deep reflexes ; by primary ex- 
 
POSTERIOR SPINAL SCLEROSIS. 301 
 
 aggeration and secondary loss of the superficial reflexes ; by 
 primary increase of the sexual propensity and secondary impair- 
 ment of the sexual power ; by derangement of the sphincters, 
 manifested by retention or incontinence ; by narrow pupils that 
 act in accommodation, but do not respond to the stimulus of 
 light ; by paralysis of ocular muscles, giving rise to strabismus 
 and diplopia ; by atrophy of the optic and auditory nerves, occa- 
 sioning loss of vision and of hearing ; by laryngeal, gastric, in- 
 testinal and other visceral crises, manifested by paroxysms of 
 intense distress ; by trophic changes in the joints, giving rise to 
 enlargement and subluxation, rendering the bones brittle and 
 liable to spontaneous fracture ; by perforating ulcers of the 
 foot ; and in the last stages by muscular wasting. 
 
 How is multiple neuritis to be distinguished from posterior 
 spinal sclerosis ? 
 
 If abolition of tlie reflexes, unsteady gait and station, loss of 
 sensation and sharp pains attend neuritis, they may recede and 
 ultimately disappear ; once present in the course of posterior 
 spinal sclerosis they persist. Posterior sclerosis is progressive 
 in course, and unyielding in treatment. With appropriate 
 treatment neuritis is retrogressive. The girdle-sensation of 
 sclerosis is wanting in neuritis. In neuritis, the muscles 
 undergo degeneration and waste ; there is palsy ; the electric 
 reactions are qualitatively changed. In sclerosis, muscular 
 wasting and weakness result only after long-continued inactivity ; 
 if the electric reactions undergo any change, it is quantitative. 
 In neuritis there are pains and points of special tenderness in 
 the course and in the peripheral distribution of various nerves ; 
 in posterior sclerosis the muscles are not tender. 
 
 How are lumbar pachymeningitis and posterior spinal sclerosis 
 to be differentiated ? 
 Pachymeningitis in the lumbar region may be attended with 
 shooting pains in the thighs and with abolition of the knee- 
 jerks, but not with manifestations indicative of involvement of 
 cerebral nerves. In meningitis the muscles waste early ; in 
 posterior sclerosis, not at all or only late. Impairment of co- 
 ordination characterizes posterior sclerosis. 
 
302 ESSENTIALS OF DIAGNOSIS. 
 
 What are the distinctions between posterior spinal sclerosis 
 and cerebellar tumor 1 
 A tumor in or compressing tlie middle lobe of the cerebellum 
 may give rise to incobrdinatiou, to a staggering gait and to 
 abolition of the knee-jerks ; it gives rise in addition to occipital 
 headache, to vertigo, vomiting, nystagmus, optic neuritis and 
 to other evidences of compression ; while lightning-pains and 
 alteration of sensation are wanting. 
 
 Primary Lateral Sclerosis — Spastic Paraplegia. 
 
 What are the causes of primary lateral sclerosis ? 
 
 Primary lateral sclerosis or spastic paraiilegia occurs with equal 
 frequency in both sexes, and a little earlier in life than posterior 
 sclerosis. 
 
 In many cases, no etiologic element can be discovered ; in 
 others, there is a history of concussion, of exposure to cold and 
 wet, of syphilis, of excesses or of neurotic heredity. 
 
 What are the symptoms of primary lateral sclerosis ? 
 
 Primary lateral sclerosis, or spastic paraplegia, is character- 
 ized by muscular weakness and spasm ; the latter usually 
 involves the extensors of the lower extremities occasioning a 
 peculiar spastic gait and so-called " clasp-knife" rigidity ; at- 
 tacks of " spinal epilepsy" occur ; the reflexes are exaggerated ; 
 ankle-clonus is present. There is usually muscular wasting, 
 occasionally hypertrophy. The arms are affected less commonly 
 and in less degree than the legs. There may be abnormal sen- 
 sations, but no anesthesia. The sphincters may be involved. 
 
 The electric reactions undergo quantitative changes. 
 
 How is lateral sclerosis to be distinguished from myelitis? 
 
 While lateral sclerosis presents the symptoms of degeneration 
 of the lateral columns, as seen in myelitis, it is always gradual 
 in onset and unattended with febrile manifestations, with girdle- 
 pain, or with impairment of sensation. Typical paraplegia, 
 with muscular wasting and degeneration and impairment of the 
 sphincters is less characteristic of lateral sclerosis than of 
 myelitis. 
 
POSTERO-LATERAL SCLEROSIS. 303 
 
 How may lateral sclerosis simulate and be distinguished from 
 cerebral hemiplegia? 
 
 The manifestations of primary lateral sclerosis may be uni- 
 lateral ; but the face is not involved, as it usually is in hemi- 
 plegia of cerebral origin ; and careful examination will detect 
 exaggeration of the reflexes of the upper as well as of the lower 
 extremity on the apparently uninvolyed side, unlike what is 
 found in cerebral hemiplegia. 
 
 Postero-lateral Sclerosis — Ataxic Paraplegia. 
 
 What are the causes of ataxic paraplegia or postero-lateral 
 sclerosis ? 
 
 Postero-lateral sclerosis, or ataxic paraplegia, is more common 
 in males than in females and in middle adult life than at any 
 other period. Its etiology is often obscure. In some cases a 
 neurotic heredity can be traced ; in others there has been ex- 
 posure to cold and wet ; in still others concussion seems to have 
 been the cause ; a history of syphilis is uncommon. 
 
 What are the symptoms of postero-lateral sclerosis, or ataxic 
 paraplegia ? 
 
 The symptoms of ataxic paraplegia are dependent upon 
 sclerosis of the posterior and lateral columns of the spinal cord. 
 The disease is gradual in onset and marked by muscular weak- 
 ness, spasm and incoordination. There may be pain in the 
 sacral region, but lightning-pains are absent. Articulation may 
 be defective. Tremor of the muscles of the face may occur. The 
 deep reflexes are exaggerated. The iris usually reacts to light. 
 Atrophy of the optic nerve is rare. Sexual power may be lost. 
 The sphincters become enfeebled. Ultimately, contractures 
 develop. 
 
 How is posterior spinal sclerosis to be distinguished from 
 postero-lateral sclerosis ? 
 
 POSTERIOR SCLEROSIS. POSTERO-LATERAL SCLEROSIS. 
 
 Syphilis a common cause. Syphilis a rare cause. 
 
 Weakness a late symptom. Weakness an early sj'mptom. 
 
 Knee-jerk lost early. Knee-jerk exaggerated. 
 
304 ESSENTIALS OF DIAGNOSIS. 
 
 POSTERIOR SCLEROSIS. POSTERO-LATERAL SCLEROSIS. 
 
 No ankle-clonus. Ankle-clonus. 
 
 Never muscular spasm. Characteristic muscular spasm. 
 
 Argyll- Robertson pupil. Pupil responds to light. 
 
 Lightning-pains. Dull sacral pains. 
 
 Sensory impairment. Sensation unimpaired. 
 
 Girdle-sensation. No girdle-sensation. 
 
 Optic-nerve atrophy common. Optic-nerve atrophy rare. 
 
 Visceral crises. No crises. 
 
 How is postero-lateral sclerosis to be distinguished from 
 primary lateral sclerosis? 
 Ataxic paraplegia is to be distinguished from spastic para- 
 plegia by tlie presence of symptoms of muscular incoordination, 
 dependent upon involvement of the posterior columns of the 
 cord. 
 
 What are the distinctions between a tumor of the cerebellum 
 and postero-lateral sclerosis ? 
 A growth involving the middle lobe of the cerebellum may 
 give rise to vreakness, ataxia, spasm, and heightened reflexes ; 
 there are, besides, occipital headache, optic neuritis, vertigo, 
 vomiting and nystagmus ; other evidences of pressure may be 
 present. 
 
 -Friedreich's Ataxia— Hereditary Ataxic 
 Paraplegia. 
 
 "What are the symptoms of Friedreich's ataxia ? 
 
 The symptoms of Friedreich''s ataxia are dependent upon 
 sclerosis of the lateral and posterior columns of the spinal cord. 
 The disease occurs in families and appears early in life ; it 
 attacks both sexes alike. It is attended with an ataxic gait, 
 impairment of coordination and equilibration, muscular weak- 
 ness, abolition of knee-jerks, nystagmus and defective speech ; 
 sensation is usually unimpaired. 
 
 What are the distinctions between Friedreich's ataxia and 
 ataxic paraplegia? 
 
 The eai-ly period of life at which the symptoms appear, its 
 occurrence in families, the absence of knee-jerks and of ankle- 
 
CEREBRO-SPINAL SCLEROSIS. 305 
 
 clonus and the presence of nystagmus distinguish Friedreich's 
 disease from ataxic paraplegia. 
 
 Cerebro-Spinal Sclerosis — Insular Sclerosis. 
 
 What are the causes of cerebro-spinal sclerosis? 
 
 The more commonly-recognized causes of disseminated^ mul- 
 tiple, insular, or cerehro-spinal sclerosis are exposure to cold and 
 wet, traumatism, nervous shock and acute febrile diseases. Oc- 
 casionally a neuropathic heredity can be traced. 
 
 What are the symptoms of cerebro-spinal sclerosis ? 
 
 The symptoms of disseminated, multiple, insular, or cerebro- 
 spinal sclerosis vary with the distribution of the islets of sclerosis. 
 As a rule, there is a peculiar jerky incoordination or tremor, most 
 marked in the upper extremities, and sometimes involving the 
 head and the tongue, aggravated by effort, emotion or observa- 
 tion ; there is commonly nystagmus, usually lateral, sometimes 
 vertical, sometimes rotatory ; speech is often slow, scanning, 
 syllabic, parts of words being dropped ; the reflexes are usually 
 exaggerated. In addition there are certain mental changes, 
 often manifested by a sense of complacency, contentment and 
 self-satisfaction, quite at variance with the patient's condition. 
 Evidences of muscular weakness are not rarely present. There 
 may also be headache, vertigo and optic neuritis. 
 
 How is cerebro-spinal sclerosis to be distinguished from postero- 
 lateral sclerosis ? 
 There may sometimes be considerable difficulty in differentia- 
 ting cerebro-spinal sclerosis and postero-lateral sclerosis (ataxic 
 paraplegia) and Triederich's (hereditary) ataxia. In postero- 
 lateral sclerosis, the defect of coordination involves the lower 
 extremities primarily ; in multiple sclerosis, there is coarse 
 tremor rather than true incoordination, and the upper extremi- 
 ties are especially involved. Nystagmus occurs in Friedreich's 
 ataxia and in multiple sclerosis, but not in ataxic paraplegia. 
 The knee-jerks are exaggerated in multiple sclerosis and in ataxic 
 paraplegia, but are wanting in Friedreich's ataxia. Friedreich's 
 ataxia is a family-disease and appears early in life. Multiple 
 20 - . 
 
306 ESSENTIALS OF DIAGNOSIS. 
 
 sclerosis and ataxic paraplegia appear in middle life. Cerebral 
 symptoms and mental phenomena belong to multiple sclerosis 
 rather than to postero-latei'al sclerosis. Speech is slow and 
 scanning in cerebro-spinal sclerosis ; in Friedreich's ataxia 
 there are merely elision and occasional separation of syllables. 
 
 Paralysis Agitans — Shaking Palsy. 
 
 What conditions favor the development of paralysis agitans ? 
 
 Paralysis agitans or shaking palsy begins most commonly at 
 about fifty years of age. It is more common in males than in 
 females. In some cases, an hereditary influence can be traced 
 in an etiologic connection. In others, the onset of the disease 
 has been preceded by decided emotional disturbance, by phys- 
 ical injury or by acute disease. . 
 
 What are the symptoms of paralysis agitans ? 
 
 Paralysis agitans, shaMng ][jalsy or Parhinsmi''s disease is char- 
 acterized by tremor, -weakness and rigidity. Tremor is usually 
 first observed ; weakness and rigidity subsequently. The mani- 
 festations first appear in one extremity, and gradually extend 
 to the others. The tremor is fine and rhythmical ; in its in- 
 cipiency it may be absent during rest and induced by movement : 
 in its characteristic form, it is constant during the waking hours. 
 As a rule, the head does not participate in the tremor ; excep- 
 tionally it does. The expression of the face is fixed and immo- 
 bile. The shoulders are bent forward, giving rise to the phe- 
 nomena of propulsion— a tendency to run forward. Occasionally 
 there is retropulsion, or there may be a tendency to lateral 
 movement. The hands assume a peculiar, semi-flexed attitude, 
 the fingers performing movements as if rolling a small object 
 between their tips ; or the fingers are held as if grasping a pen. 
 The voice is monotonous ; words are uttered rapidly, with a 
 tendency to confluence of syllables. The reflexes are usually 
 unaltered ; exceptionally the knee-jerks are exaggerated and an 
 ankle-clonus can be elicited. A sensation of abnormal heat, 
 sometimes with perspiration, is often present. 
 
PARALYSIS AGITANS. 
 
 307 
 
 What are the differential features between paralysis agitans 
 and cerebro-spinal sclerosis ? 
 
 The diagnosis between tliese two conditions, ordinarily simple, 
 may under some circumstances be extremely difficult. The 
 tremor of cerebro-spinal sclerosis is coarse and irregular, and is 
 
 Fig. 48. 
 
 ^^:--.^;l 
 
 Paralysis agitans. (After St. Leger.) 
 
 induced and aggravated by voluntary effort, by emotion and by 
 observation ; that of paralysis agitans is fine and regular, and 
 is constant, at least during the waking hours. In cerebro-spinal 
 sclerosis, the head participates in the movements ; in paralysis 
 agitans, on the contrary, the face is fixed, immobile, expression- 
 less. Paralysis agitans does not present the slow, scanning 
 speech and nystagmus of multiple sclerosis ; while the latter does 
 not present the tendency to forward or backward or even lateral 
 movement of the former. The characteristic attitude of the 
 hand, as if holding a pen in writing, or as if rolling pills between 
 the fingers, seen in paralysis agitans, is not seen in multiple scle- 
 rosis. 
 
308 ESSENTIALS OF DIAGNOSIS. 
 
 Spinal Hemorrhage. 
 
 What are the causes of hemorrhage into the spinal cord? 
 
 Spinal hemorrhage is more common in males than in females, 
 and in adult life than at any other period. It may he primary, 
 dependent upon disease of the bloodvessels, or as a result of 
 exposure to cold, or of over-exertion, or of sexual excess ; second- 
 ary, in the course of inflammation, tumors and cavities in the 
 cord ; accessory, occurring towards the close of convulsive dis- 
 orders ; and traumatic following blows, falls and other injuries. 
 
 What are the symptoms of hemorrhage into the spinal cord ? 
 
 The occurrence of hemorrhage into the spinal cord is indicated 
 by sudden, severe pain in the back, with loss of motion and 
 sensation. Consciousness may be lost, but is likely to be pre- 
 served. A girdle-sensation exists at the level of the lesion, and 
 loss of motion and sensation below, on alternate sides, or on 
 both sides of the body, according to the seat of the lesion. The 
 sphincters are likely to be deranged and trophic changes to 
 occur. Bespiration will be interfered with if the lesion is in the 
 cervical or dorsal region of the cord. 
 
 Some degree of myelitis and meningitis are usually developed 
 in the progress of the case, giving rise to fever and irritative 
 symptoms. Subsequently, the symptoms become paralytic in 
 type. Some degree of paraplegia remains permanently. The 
 paralyzed muscles waste. The deep reflexes are exaggerated. 
 
 What are the distinctions between spinal hemorrhage and 
 spinal meningitis ? 
 The abruptness of onset is more decided in hemorrhage than 
 in meningitis. Febrile manifestations attend meningitis from 
 the beginning ; they only appear in hemorrhage when myelitis 
 is established. Motor and sensory impairment is more decided 
 in hemorrhage than in meningitis ; in the latter, there is a 
 preliminary stage of spasm and pain. 
 
 How are hemorrhage into the cord and hemorrhage into the 
 meninges to be distinguished from one another ? 
 
 Both the local and the radiating pains are less severe in 
 spinal than in meningeal hemorrhage, while the subsequent 
 
SPINAL COMPRESSION. 309 
 
 anesthesia is more decided in the former than in the latter. 
 In the case of spinal hemorrhage the paralytic symptoms are 
 more decided from the outset ; while in meningeal hemorrhage 
 these are preceded by muscular spasm. Trophic changes char- 
 acterize spinal hemorrhage, and are wanting in meningeal 
 hemorrhage. 
 
 Spinal Compression. 
 
 What are the causes of compression of the spinal cord? 
 
 The cord may be compressed by tumors of the spinal canal ; 
 by dislocation of the vertebrse, independently, or as a result of 
 caries, or of fracture ; by an exostosis ; by an aneurism that has 
 eroded the bones ; or by an hydatid cyst. 
 
 How can the causes of spinal compression be diflferentiated ? 
 
 The recognition of a tumor in the spinal canal depends upon 
 its detection from without, or the detection of new-growths in 
 other parts of the body. 
 
 Simple dislocation and fracture of the vertebriB follow trau- 
 matism ; the symptoms to which dislocation gives rise set in 
 suddenly and are profound in degree ; a deformity of the spinal 
 column may be detectable. 
 
 The diagnosis of caries depends upon the knowledge of a 
 history of syphilis or of tuberculosis and the detection of a 
 painful deformity in the back. 
 
 An hydatid cyst of the spinal canal may be diagnosticated by 
 the detection externally of a fluctuating tumor, upon puncture 
 of which the characteristic booklets may be found. 
 
 It may be impossible to diagnosticate the cause of compres- 
 sion of the cord dependent upon an exostosis or upon an aneu- 
 rism. 
 
 To what symptoms does compression of the spinal cord give 
 rise? 
 
 The rapidity with which the symptoms of compression appear 
 depends somewhat upon the cause. Dislocation is apt to occa* 
 sion manifestations of immediate gravity. In other cases, the 
 symptoms are gradual in appearance and px'ogressive in course. 
 
310 ESSENTIALS OF DIAGNOSIS. 
 
 Compression gives rise to two groups of phenomena, referable 
 to the nerve- roots and to the cord, respectively. There is local 
 pain in the back, aggravated by movement, as well as pains of 
 a radiating character, with girdle-sensation ; ultimately anes- 
 thesia develops. There is loss, of motion in the parts supplied 
 by the nerves from the cord below the seat of compression ; 
 with exaggerated reflexes and involvement of the sphincters. 
 The palsied muscles slowly waste and degenerative reactions 
 set in. Contractures may develop. 
 
 How is compression-myelitis to be distinguished from hemor- 
 rhage into the spinal cord ? 
 When a vertebra softened by destructive disease suddenly 
 gives way, the resulting displacement may be followed by com- 
 pression of the cord, occasioning symptoms with which those 
 jiroduced by hemorrhage into the cord may be identical. The 
 symptoms of compression, however, are usually more extensive 
 and more absolute than those of hemorrhage ; the existence of 
 a deformity of the spine makes the diagnosis certain. 
 
 What are the distinctions between compression of the cord and 
 chronic myelitis ? 
 
 Symptoms of irritation referable to the nerve-roots are want- 
 ing in myelitis. The recognition of a cause of compression 
 determines the diagnosis. 
 
 Tumor of the Spinal Cord. 
 
 What are the symptoms of tumor of the spinal cord ? 
 
 Tumors of the spinal canal may be situated without or within 
 the dura mater, or within the structure of the cord itself. They 
 are most diverse in character. The symptoms will depend upon 
 the situation of the tumor and upon the degree of mechanical 
 interference with the functions of the cord that it occasions. 
 Pressure on the nerve-roots gives rise to pain, to abnormal sen- 
 sations, to girdle-pain and to muscular spasm and rigidity. 
 Pressure on the cord or myelitis occasions anesthesia, paralysis 
 and exaggerated reflexes below the level of the lesion and 
 
TUMOR OF THE SPINAL CORD. 311 
 
 abolition of tlie reflexes wilhin the area innervated from the 
 seat of tlie growth. Involvement of the anterior horns of the 
 gray matter is attended witli wasting and other trophic dis- 
 orders ; involvement of the lumbar enlargement causes abolition 
 of the knee-jerk, loss of control of the sphincters and wasting 
 and palsy in the lower extremities ; involvement of the cervical 
 enlargement occasions wasting and palsy in the upper ex- 
 tremities. The unilateral appearance of symptoms of spinal 
 disease, or evidence of sensory derangement on one side and 
 motor derangement on the other, is strongly suggestive of 
 tumor of the spinal canal. With the growth of the tumor the 
 symptoms become bilateral. 
 
 From what conditions is spinal tumor to be distinguished ? 
 
 The diagnosis of spinal tumor includes the determination of 
 the nature of the tumor and its distinction from other condi- 
 tions presenting similar symptoms. 
 
 In the first connection, a history of syphilis, of tuberculosis, 
 or of tumors situated elsewhere is to be considered. 
 
 The differentiation from caries of the vertebrae depends upon 
 the recognition of disease of the bone, upon the deformity that 
 results and upon the greater degree of pain on movement that 
 attends caries. 
 
 From hypertrophic pachymeningitis spinal tumor differs in 
 course ; being progressive, while symptoms of irritation precede 
 those of paralysis and wasting. The symptoms of pachy- 
 meningitis are more circumscribed in distribution than are 
 those of tumor. 
 
 The symptoms of tumor differ from those of myelitis, in be- 
 ing irritative in character— attended by pain and spasm, rather 
 than paralytic. If tumor give rise to myelitis, the I'ecognition 
 of the condition depends upon a knowledge of the previous 
 symptoms. 
 
 The persistence of obstinate neuralgia, especially if bilateral, 
 should excite suspicion of spinal tumor. 
 
312 ESSENTIALS OF DIAGNOSIS. 
 
 Syringomyelia. 
 
 What are the symptoms of syringomyelia ? 
 
 Cavities in the spinal cord may be a result of defective appo- 
 sition of the lateral halves of the cord in the course of devel- 
 opment ; of occlusion of the central canal, with accumulative 
 distention by cerebro-spinal fluid ; of the disintegration of 
 glioraata ; or Ihey may appear subsequently to myelitis. The 
 course of the disease is slow and chronic, sometimes covering 
 many years. The symptoms vary somewhat with the situation 
 of the cavity. They are usually most conspicuous in the upper 
 extremities. There are muscular wasting and weakness, pre- 
 ceded by alterations of sensation. Common sensibility is usuall}'' 
 preserved, while the perception of pain and of heat and cold is 
 enfeebled or lost. In some cases, severe pains occur. A spastic 
 condition may be present in the lower extremities. The sphinc- 
 ters are often involved. Trophic changes are common. There 
 may be cutaneous eruptions, as eczema or herpes. The skin 
 may be thin and glossy or thick and horny. Yaso-motor dis- 
 turbance may be manifested by coldness and lividity. 
 
 From what conditions is syringomyelia to be differentiated ? 
 
 Myelitis, hypertrophic pachymeningitis and progressive mus- 
 cular atrophy occasion certain symptoms in common with 
 syringomyelia. 
 
 Myelitis is recognized by the much more profound palsy and 
 loss of sensory power, without involvement of the pain-sense 
 and the temperature-sense ; hypertrophic pachymeningitis by 
 the attendant pain and the less extensive anesthesia ; and 
 chronic muscular atrophy by the absence of conspicuous sensory 
 symptoms. 
 
 Morvan's Disease — Analgesic Panaris. 
 
 What are the symptoms of Morvan's disease? 
 
 Under the name of Morvan''s disease has been described a 
 syndrome of symptoms, including the development of a pain- 
 less inflammation at the extremities of the fingers, followed by 
 necrotic sequestration of the phalanges. At the beginning of 
 
mouvan's disease. 
 
 313 
 
 the disease, the affected parts may be the seat of pain. Subse- 
 quently, analgesia develops together with the destructive process 
 
 Appearance of the hand in Morvan's Disease. (After Charcot.) 
 
 in the fingers. In most cases abnormal curvature of the spinal 
 column has been observed. After death, hyperplasia of the 
 connective tissue of the peripheral nerves and in the posterior 
 horns, posterior columns, and the gray matter of the cervical 
 segment of the spinal cord has been found. 
 
 What is the distinction between Morvan's disease and sclero- 
 derma ? 
 
 Scleroderma is a morbid condition in which, as a result of 
 inflammatory changes in the subcutaneous arteries of a varying 
 
314 ESSENTIALS OF DIAGNOSIS. 
 
 distribution, hyperplasia of the connective tissue takes place, 
 with hardness, swelling and fulness, which in turn is succeeded 
 by contraction and atrophy. The condition may be circum- 
 scribed or diffuse. It is sometimes attended with pigmentation 
 and sometimes with desquamation. The etiology of the affec- 
 tion is obscure. 
 
 A condition in which the extremities of the fingers close to 
 nails undergo discoloration, followed by the formation of bullae, 
 with perhaps loss of the nails and shortening of the fingers, has 
 been described as a variety of scleroderma or sclerodactylia. 
 When nose and ears and face, as well as hands and feet, become 
 reduced in size, the name ahromikria has been employed. 
 In scleroderma there may be anesthesia, but there is not 
 analgesia. Trophic changes may take place in the affected 
 parts, but they are not of a necrotic character. The nails may 
 be lost, but there is no exfoliation of bone. 
 
 How are Morvan's disease and anesthetic leprosy to be differ- 
 entiated ? 
 
 In anesthetic leprosy, a destructive process may be set up in 
 the extremities, attended sometimes with the loss of fingers or 
 toes, but the condition is usually to be recognized by the asso- 
 ciation of other definite symptoms of leprosy, such as patches 
 of anesthesia and leprous nodules in various parts of the body. 
 
 From what other conditions is Morvan's disease to be differenti- 
 ated? 
 
 Syringmvjelia may present trophic changes and analgesia ; 
 but there is usually also loss of temperature-sense ; while necro- 
 sis of bone is wanting and common sensibility is preserved. 
 
 J?ayno«c7's disease is attended with cyanosis of the extremities, 
 sometimes terminating in gangrene ; but sensibilit}* remains 
 unimpaired ; and there are other characteristic symptoms. 
 
 Syphilis may occasion a destructive dactylitis. The diagno- 
 sis will depend upon the absence of sensory symptoms and upon 
 a knowledge or a history of infection or of other manifestations. 
 
 Necrosis of bone may attend diabetes, but sensory symptoms 
 are wanting, distinctive symptoms are present and examination 
 of the urine will make clear the clinical association. 
 
CEREBRAL MENINGITIS. 315 
 
 Cerebral Meningitis. 
 
 What are the varieties of inflammation of the membranes 
 of the brain ? 
 
 Inflammation of the dura, pia or arachnoid is known as 
 
 pachymeningitis, leptomeningitvi or arachnitis, respectively ; most 
 commonly the pia and arachnoid are involved togetlier— pta- 
 arachnitis or leptommingitis. Inflammation of the dura mater 
 may be attended with the extravasation of a membranous 
 hemorrhagic exudate— 7ifmo7T/ic<gtc pachymeningitis. Meningitis 
 may especially involve the convexity or the hase ; it may be acute 
 or chronic, primary or secondary ; it may be simple, piurulent, tuber- 
 culous, syphilitic. 
 
 What are the causes of cerebral meningitis ? 
 
 Inflammation of the pia and arachnoid may be a result of 
 traumatism or of contiguous inflammation ; it may develop in 
 the course of infectious disease or of pyemia ; it may depend 
 upon a deposit of tubercles in the membranes. 
 
 What are the symptoms of cerebral meningitis ? 
 
 The symptoms of meningitis vary somewhat, as the base or the 
 convexity of the brain is involved. Tuberculous meningitis is 
 usually basilar. Meningitis dependent upon causes other than 
 tubercles, usually, though not exclusively, affects the convexity. 
 Certain symptoms are common to meningitis in any situation. 
 In addition to those of the associated condition, there are, 
 together with febrile manifestations, headache, delirium, vomit- 
 ing, convulsions, retraction of the head, derangement of the 
 sphincters, palsies, vaso-motor and trophic disturbances, in- 
 equality of the pupils and irregularity of the pulse and respira- 
 tion. When the base is involved, there are optic neuritis 
 followed by atrophy, irritation followed by paralysis of cranial 
 nerves and more decided alteration of pulse and respiration, 
 trophic and vaso-motor disturbances and retraction of the head. 
 When the inflammation is tuberculous, tubercles may, on oph- 
 thalmoscopic examination, be detected in the choroid. 
 
316 ESSENTIALS OF DIAGNOSIS. 
 
 Wliat are the symptoms of cerebral pachymeningitis ? 
 
 Inflammation of the dura mater may be a result of trauma- 
 tism or of adjacent disease. In addition to the symptoms of 
 the primary condition, there may be headache, deUriura, con- 
 vulsions, febrile manifestations. A collection of pus may occa- 
 sion paralysis. 
 
 What are the symptoms of hemorrhagic pachymeningitis ? 
 
 Hemorrhagic pachymeningitis is more common in males than in 
 females, and late in life than at any other period. It is usually 
 preceded by a history of alcoholism, of insolation, of trauma- 
 tism, or of insanity ; it may also develop in the course of blood- 
 diseases. It is attended with headache, contracted pupils, in- 
 tellectual torpor, apoplectiform convulsions, unnatural drowsi- 
 ness and mental wandering. The condition is rather obscure, 
 and the symptoms not well defined. It is often unexpectedly 
 found post mortem. 
 
 How is simple cerebral meningitis to be distinguished from 
 tuberculous meningitis ? 
 
 Ordinary cerebral meningitis sets in rather acutely ; tubercu- 
 lous meningitis usually more insidiously. The ordinary fox-m of 
 inflammation is associated with well-known causes : traumatism, 
 adjacent inflammation, infectious diseases and pyemia ; tuber- 
 culous meningitis is usually secondary to tuberculous processes 
 at other parts of the body. The symptoms of the former espe- 
 cially indicate involvement of the convexity and freedom of 
 the base, while in the latter the conditions are reversed, and 
 choked disc and paralysis of cranial muscles are more common. 
 Tubercles are never found in the choroid in ordinary meningitis. 
 Simple meningitis is not uncommonly attended with recovery ; 
 tuberculous meningitis but rarely. 
 
 How are the cerebral symptoms of acute general disease to be 
 distinguished from the symptoms of cerebral meningitis ? 
 
 Cerebral symptoms may appear at any time in the course of 
 acute general diseases, such as scarlatina, smallpox, yellow 
 fever, typhoid fever, rheumatism, pneumonia and acute miliary 
 
CEREBRAL MENINGITIS. 317 
 
 tuberculosis. Investigation should be directed to the deter- 
 mination of the association, so that the primary condition may 
 not be obscured. Sufficient cause for the symptoms may be 
 found in the high temperature, in the state of inanition, or in 
 the poisoned condition of the blood. When the delirium of 
 febrile affections appears, the headache that has been present 
 disappears. Headache and delirium continue together in menin- 
 gitis. The manifestations of irritation and paralysis of cranial 
 nerves, including optic neuritis and atroj)hy, seen in meningitis, 
 are wanting in simple febrile disorders. 
 
 How is cerebral meningitis to be distinguished from cerebro- 
 spinal fever ? 
 
 The differences are of degree, extent and etiology. When 
 the membranes of the brain are inflamed, the spinal mem- 
 branes are usually in some degree also involved. Cerebro-spinal 
 fever is considered a constitutional affection, cerebral meningitis 
 a local affection. In the former, however, the spinal involve- 
 ment stands boldly out. as evidenced by the tendency to opis- 
 thotonos, the symptoms on the part of the trunk, the sphinc- 
 ters, and the lower extremities ; while the latter is especially 
 marked by the involvement of cerebral structures. Cutaneous 
 eruptions mark cerebro-spinal fever, but are no part of cerebral 
 meningitis. The recognition of a cause of cerebral meningitis, 
 or a knowledge of the existence of other cases of cerebro-spinal 
 fever may determine the diagnosis. 
 
 How is cerebral meningitis to be distinguished from acute 
 mania? 
 
 The mental wandering of meningitis does not usually attain 
 the high degree seen in mania ; and in the former it is attended 
 with febrile manifestations, in the latter not. The symptoms 
 on the part of the cranial nerves, the headache, the convulsions 
 of meningitis are wanting in mania. 
 
318 ESSENTIALS OF DIAGNOSIS. 
 
 Hydrocephalus. 
 
 What are the varieties of hydrocephalus ? 
 
 An excessive accumulation of cerebro-spinal fluid maj' take 
 place in the subdural space or within the ventricles of the 
 brain. The one condition is called external ; the other internal 
 hydrocephalus. Either may be acute or chronic, primary or sec- 
 ondary, congenital or acquired. 
 
 What are the causes of hydrocephalus ? 
 
 Hydrocephalus may be a result of meningitis, of obstruction 
 of the orifices of communication between the ventricles and 
 between the fourth ventricle and the subarachnoid space, or of 
 pressure on the veins of Galen. Occasionally no causative 
 factor is recognizable. 
 
 To what symptoms does hydrocephalus give rise ? 
 
 Occurring in a child prior to the closure of the sutures and 
 the complete ossification of the bones, hydrocephalus causes a 
 separation and a thinning of the cranial bones. When the 
 fluid distends the ventricles, the surrounding cerebral tissue 
 becomes attenuated. Under such conditions the head is en- 
 larged ; the fontanels may be open ; the eye-balls roll ; the men- 
 tal condition is defective ; there is muscular weakness ; there 
 may be convulsions ; and various cranial nerves may be para- 
 lyzed. 
 
 In the more aggravated cases idiocy exists ; there is blindness, 
 with choked discs ; and life may be terminated by convulsions 
 and coma. 
 
 Analogous symptoms also occur when hydrocephalus develops 
 later in life. 
 
 Hemorrhage into the Cerebral Membranes. 
 
 What are the varieties of hemorrhage in the cerebral meninges ? 
 
 The extravasation of blood without the dura mater, between 
 the dura and the bone, constitutes extradural hemorrhage ; 
 hemorrhage within the dura mater, between the dura and arach- 
 
CONGENITAL SPASTIC PARAPLEGIA. 319 
 
 noid is called subdural; and between the arachnoid and pia 
 mater, subarachnoid. 
 
 Under what conditions does hemorrhage into the meninges of 
 the brain occur ? 
 
 Hemorrhage into the cerebral membranes may be a result of 
 traumatism ; of the rupture of an aneurism of a meningeal vessel ; 
 of the rupture of a hemorrhage in the brain ; of the same condi- 
 tions as occasion cerebral hemorrhage ; it may occur in the 
 insane ; rarely it occurs spontaneously. 
 
 To. what symptoms does hemorrhage into the cerebral mem- 
 branes give rise ? 
 
 The symptoms of hemorrhage into the cerebral membranes, 
 depend upon the volume and the extent of the extravasation. 
 The symptoms are those of meningitis, plus those of cerebral 
 hemorrhage, and may be preceded by headache, vertigo and 
 vomiting. 
 
 The infantile meningeal hemorrhages that result during labor 
 occasion the so-called birth-palsies, vv^ith the symptoms of con- 
 genital spastic paraplegia or hemiplegia. 
 
 Congenital Spastic Paraplegia. 
 
 What is infantile or congenital spastic paraplegia? 
 
 When, as a result of injury to the child during birth, bilateral 
 meningeal hemorrhage takes place over the central convolutions, 
 the pyramidal tracts fail to develop or they degenerate. The 
 child is late in learning to walk. It presents the symptoms of 
 spastic paraplegia. The gait is peculiar, one foot being placed 
 over or in front of the other, or a swinging oscillation taking place. 
 Growth and development are retarded. Athetoid movements 
 in the hands are common. Initial convulsions may occur and 
 be repeated, subsequently to cease. Should the hemorrhage be 
 circumscribed or unilateral, the distribution of the symptoms 
 will vary accordingly. There is usually defective mental de- 
 velopment. 
 
320 ESSENTIALS OF DIAGNOSIS. 
 
 What are the distinctions between congenital spastic para- 
 plegia and pseudo-hypertrophic paralysis? 
 The reflexes are exaggerated in congenital spastic paraplegia, 
 enfeebled or lost in pseudo-hypertrophic paralysis. The gait of 
 congenital spastic paraplegia is spastic ; that of pseudo-hyper- 
 trophic paralysis is oscillating ; the manner in which the child 
 rises from the floor in the latter is characteristic. In congenital 
 spastic paraplegia the contractures are yielding ; in pseudo- 
 hypertrophic paralysis unyielding ; the former is retrogressive, 
 the latter progressive. Should there be decided enlargement of 
 some of the muscles, this will constitute a diagnostic feature. 
 
 Cerebral Anemia, 
 
 What are the conditions that lead to cerebral anemia? 
 
 Anemia of the brain may be general : as a part of a systemic 
 anemia, from cardiac insufliciency, from accumulation of blood 
 elsewhere, from pressure on the large vessels to the head, from 
 pressure on the brain ; or partial : from obstruction of the circu- 
 lation by vascular occlusion or by pressure from without. 
 Cerebral anemia ma}^ develop gradually or suddenly. 
 
 To what symptoms does cerebral anemia give rise ? 
 
 General anemia of the brain, suddenly induced, occasions the 
 symptoms of syncope : failure of vision, ringing in the ears, 
 vertigo, nausea, shallow, sighing respiration, contracted pupils, 
 pallor of the face, a cool, moist skin and loss of consciousness. 
 Nystagmus and convulsions may occur. The loss of conscious- 
 ness may pass into coma, and coma into death. 
 
 General anemia of the brain, gradually induced, occasions 
 enfeeblement with irritability of function. There are headache, 
 vertigo, impaired intellection, motor weakness, drowsiness or 
 insomnia, hallucinations, mania or melancholia. The optic 
 disc may be pale. The symptoms are aggravated b}'^ the erect 
 posture and may be mitigated by recumbency or inhalation of 
 amyl nitrite. 
 
 Partial anemia of the brain is followed by impaired nutrition 
 and loss of function ia the affected area. Occurring suddenly, 
 
CEREBRAL HYPEREMIA — CEREBRITIS. 821 
 
 it is attcnclcd with loss of consciousness and convulsions ; when 
 of gradual development, it occasions headache, vertigo, numb- 
 ness, tingling and weakness. 
 
 Cerebral Hyperemia. 
 
 What conditions lead to cerebral hyperemia ? 
 
 Hyperemia of the brain may be active or passive. Active hy- 
 peremia may be caused by an overacting left ventricle ; by sudden 
 contraction of the vessels elsewlierc ; by insolation ; it may be 
 part of a general plethoric condition ; and it occurs as the first 
 stage of the inflammatory process. 
 
 Passive hyperemia is a result of cardiac insufficiency, of venous 
 obstruction as a result of pressure from without or of pulmonary 
 disease. 
 
 To what symptoms does cerebral hyperemia give rise ? 
 
 The symptomatology of cerebral hyperemia is somewhat 
 obscure. The recognition of the condition is not always easy. 
 Usually there are dull headache, a sense of fulness of the head, 
 vertigo, mental torpor, derangement of sleep, a disinclination to 
 activity, flashes of light and tinnitus aurium. The countenance 
 may be flushed ; the vessels of the eyeground injected. There 
 may be transient loss of consciousness. Convulsions are un- 
 common. 
 
 Cerebritis. 
 
 What are the clinical features of cerebritis ? 
 
 Inflammation of the structure of the brain may be acute or 
 chronic. It is usually a result of traumatism, or it may arise 
 by extension from adjacent disease. Some degree of cerebritis 
 is coincident with inflammation of the membranes. The symp- 
 toms are rather obscure ajid ill-defined. There are headache, 
 vertigo, delirium, convulsions and febrile symptoms. Cerebritis 
 may be followed by abscess. 
 21 
 
322 ESSENTIALS OF DIAGNOSIS. 
 
 How is inflammation of the membranes to be distinguished 
 from inflammation of the structure of the brain ? 
 
 luflammation of the membranes and inflammation of the 
 structure of the brain are to some degree always associated, the 
 symptoms of either condition respectively predominating. In- 
 flammation of brain-tissue, however, is usually attended with 
 symptoms more profound and more depressing than are those 
 of meningitis; while the symptoms of meningitis are usuallj' 
 more widely distributed and more irritative in character. 
 
 Cerebral Abscess. 
 
 What are the causes of abscess of the brain ? 
 
 The development of cerebral abscesses is usually dependent 
 upon traumatism, suppurative disease of adjacent structures or 
 pyemia. Distant suppuration may give rise to embolic abscess. 
 luflammation of the brain may terminate in suppuration and 
 the formation of an abscess. Cerebral abscess may be acute or 
 chronic in its course ; it may be single or multiple. 
 
 What are the symptoms of abscess of the brain ? 
 
 The symptoms of abscess of the brain present themselves in 
 three stages : a irnmartj acute stage, in which the symptoms of the 
 associated condition may obscure the cerebral symptoms ; a 
 secondary stage of lull, in which the symptoms are latent and in 
 abeyance ; and a terminal stage, in which rupture of the abscess 
 gives rise to the abrupt appearance of the signs of meningitis, 
 of cerebritis or ofapoplex}-, followed b}' stupor, coma and death. 
 These stages are not always distinct. Commonly the one passes 
 by gradations into the other. 
 
 The more obvious symptoms are fever, recurrent rigors, head- 
 ache (■which may be localized), vertigo, vomiting and optic 
 neuritis (which are most marked in cerebellar abscess), epilep- 
 tiform convulsions and paralysis (when the abscess is seated in 
 the motor area). There may be, in addition, unilateral ptosis, 
 defect of speech, impairment of articulation, difficulty of deglu- 
 tition and mental disturbance. 
 
CEREBRAL HEMORRHAGE, 323 
 
 From what conditions is abscess of the brain to be differen- 
 tiated ? 
 
 Abscess of the brain gives rise to many of the symptoms of 
 tumor of the brain. In the terminal stage it occasions the 
 symptoms of meningitis, of cerebritis or of apoplexy. The dis- 
 tinction from these several conditions depends upon the recog- 
 nition of a cause of abscess, upon the recurrence of chills, upon 
 the presence of febrile symptoms. The headache and optic 
 neuritis of tumor are more intense than those of abscess. In 
 meningitis there is greater involvement of cranial nerves than 
 in abscess. The course of the symptoms of abscess is of longer 
 duration than is the case in cerebritis. Optic neuritis is wanting 
 in apoplexy. The symptoms of the terminal stage of abscess 
 are to be distinguished from meningitis, cerebritis and apoplexy 
 by a knowledge of the previous existence of obscure symptoms 
 of cerebral disease. 
 
 Cerebral Hemorrhage. 
 
 What are the causes of cerebral hemorrhage ? 
 
 The ultimate cause of cerebral hemorrhage, not traumatic 
 in origin, is disease of the bloodvessels. The event may be 
 induced by over-action of the heart. In some cases of cerebral 
 hemorrhage, an hereditary tendency can be elicited. Hemor- 
 rhage in the brain is most common at the degenerative period 
 of life, and its freqency increases with age ; the condition occurs 
 more commonly in males than in females ; in temperate than in 
 tropical climates ; in winter than in summer. The antecedent 
 disease of the vessels may depend upon alcoholism, gout, rheu- 
 matism, syphihs, nephritis, lead-poisoning, infectious diseases 
 and blood-diseases. 
 
 What is the pathology of cerebral hemorrhage ? 
 
 The symptoms that follow the occurrence of cerebral hemor- 
 rhage depend upon laceration of the brain-tissue, and upon tlie 
 compression and irritation of adjacent structure to which the 
 extravasation gives rise. In the course of time, the blood, as 
 well as the products of disintegration, are absorbed, until there 
 
324 ESSENTIALS OF DIAGNOSIS. 
 
 remains to mark the previous hemorrhage nothing but a fibrous 
 cicatrix or a cyst. The conducting motor fibers related to the 
 structures destroyed undergo secondary degeneration. 
 
 Fig. 50. 
 
 Cerebral miliary aneurisms. (Eichhorst.) 
 
 The most frequent seat of cerebral hemorrhage is the region 
 of the central ganglia ; next in frequency is the centrum ovale ; 
 then the cortex, pons and cerebellum. 
 
 What are the symptoms of cerebral hemorrhage? 
 
 The occurrence of hemorrhage in the brain is indicated by 
 sudden, complete loss of consciousness, with general muscular 
 relaxation, and depression of temperature. True prodromata 
 are wanting. The breathing is labored and stertorous ; an 
 initial convulsion may occur ; the pulse is apt to be slow, full 
 and hard ; the pupils unequal ; the reflexes abolished or unequal ; 
 and the head and eyes deviated to one side (conjugate deviation). 
 Urine and feces may be passed involuntarily. The urine may con- 
 tain albumin. Vomiting may occur. As the shock of the seizure 
 passes off, consciousness slowly returns and the evidences of 
 hemiplegia become apparent. The leg, the arm, perhaps the 
 face, are paralyzed on the side opposite to that on which the 
 lesion is situated. The tongue, protruded, deviates to the para- 
 lyzed side. There is difficulty in deglutition, in phonation, in 
 articulation. There may be partial or complete anesthesia of 
 the paralyzed members. Secondary fever appears. Gradual 
 improvement slowly takes place, in greatest degree in those parts 
 
CEREBRAL HEMORRHAGE. 325 
 
 that habitually act in association with corresponding parts of the 
 opposite side. 
 
 , If the hemorrhage occur in the cortex, epileptiform convul- 
 sions take place ; if in the posterior part of the third frontal con- 
 volution of the left side, aphasia results ; if in the posterior part 
 of the first temporal convolution, word-deafness ; if in the 
 angular gyrus and occipital lobe, hemianopsia and word-blind- 
 ness ; if in the anterior part of the uncinate couvolution, loss 
 of the sense of taste. If the hemorrhage is large and extensive 
 the patient may never emerge from the primary coma, but death 
 may speedily or slowly take place. Implication of the pons or 
 medulla is indicated by abnormal elevation of temperature. In 
 most cases the hemorrhage involves the region of the central 
 ganglia and the internal capsule. 
 
 Athetosis, post-hemiplegic chorea and other spasmodic condi- 
 tions may be sequelae of cerebral hemorrhage. The reflexes be- 
 come exaggerated, especially upon the paralyzed side, as a result 
 of descending degeneration of the pyramidal tracts. The memory 
 is impaired. Emotional mobility is increased. Various vaso- 
 motor and trophic changes may take place in the affected parts, 
 which may also become fixed by contractures. 
 
 In what respects do the symptoms of cerebral hemorrhage 
 differ from those of cerebral congestion ? 
 
 Cerebral congestion may be attended with transient loss of 
 consciousness, not so profound, however, as is the case in 
 hemorrhage. The event is prone to be repeated, but the con- 
 dition does not give rise to permanent paralytic manifestations. 
 
 What are the distinctions between the loss of consciousness of 
 syncope and that of cerebral hemorrhage ? 
 
 Syncope is usually a result of cerebral anemia, induced by 
 insufficiency of the circulation ; it may also result from ner- 
 vous influences that stimulate the vagus. The loss of con- 
 sciousness is of but brief duration. The pulse is feeble, the 
 face pale, the breathing shallow and sighing. The reflexes are 
 preserved. The sphincters are continent. The return to con- 
 sciouness is not attended with evidences of paralysis. The 
 attack is prone to be repeated. 
 
326 ESSENTIALS OF DIAGNOSIS. 
 
 How is the coma of cerebral hemorrhage to be distinguished 
 from the coma of alcoholic intoxication ? 
 
 The symptoms of cerebral hemorrhage come on suddeul}' ; 
 those of alcoholic coma, less sudcleuly, as a direct consequence 
 of the imbibition of a toxic quantity of alcohol. The coma of 
 alcoholism is not so profound as that of hemorrhage. It may 
 be possible by appropriate stimuli to rouse an individual over- 
 come by alcohol, but there is no response from the coma of 
 hemorrhage. The odor of alcohol in the breath, and the detec- 
 tion of alcohol in the urine would be doubtful evidence ; but 
 the absence of these conditions would exclude alcoholism. 
 Conjugate deviation of the head and eyes is a common feature 
 of hemorrhage ; alcoholism will not cause it. The pupils are 
 usuall}' dilated in alcoholism, not contracted and unequal as 
 in hemorrhage. The temperature-alterations of hemorrhage 
 are wanting in alcoholic intoxication. On the return of con- 
 sciousness after alcoholic coma, there is no pals}^ ; palsy is 
 characteristic of hemorrhage. 
 
 How is the coma of cerebral hemorrhage to be distinguished 
 from that of opium-poisoning ? 
 
 In the absence of the previous history, cerebral hemorrhage 
 is to be distinguished from opium-poisoning by the primary 
 depression and secondar}- elevation of temperature, by the con- 
 jugate deviation of the head and eyes, by the evidences of par- 
 alysis. 
 
 The small pupils of opium-poisoning are equal ; if hemorrhage 
 causes contraction of the pupils, one is likely to be smaller than 
 the other. The noisy breathing of hemorrhage does not become 
 so infrequent as the breathing in opium-poisoning. 
 
 How is uremia to be distinguished from cerebral hemorrhage ? 
 
 The conditions under which uremia develops predispose to 
 the occurrence of cerebral hemorrhage. The recognition of dis- 
 ease of the kidney does not help in diagnosis. The coma of 
 hemorrhage, however, is likely to set in more suddenly and to 
 be more profound than is tliat of uremia. 
 
 Uremia is more likely than hemorrhage to appear in 3'oung per- 
 sons. The convulsions that attend uremia are general ; unilat- 
 
CEREBRAL SOFTENING. 327 
 
 eral convulsions are indicative of cerebral hemorrhage. The 
 primary depression of temperature is followed by a secondary 
 elevation in hemorrhage, but usually not in uremia. Inequality 
 of the pupils and conjugate deviation of the head and eyes are 
 indicative of hemorrhage, rather than of uremia. 
 
 If loss of muscular power follow uremia, it is circumscribed 
 and transitory ; in hemorrhage, it is usually hemiplegic and 
 permanent. 
 
 In uremia the tongue is dry and covered with a thick brownish 
 fur ; there is often vomiting ; the body exhales a peculiar, musty 
 odor, not observed in hemorrhage. 
 
 How is asphyxia to be distinguished from cerebral hemorrhage? 
 
 When an individual is asphyxiated from whatever cause, the 
 appearance is cyanotic. Respiration is interfered with, but is 
 not noisy. There is no conjugate deviation of the head and 
 eyes. Measures of resuscitation may, in a little while, prove 
 successful, while the paralytic phenomena attendant upon 
 cerebral hemorrhage are absent. 
 
 Cerebral Softening. 
 
 What are the varieties of softening of the brain ? 
 
 Softening of the brain may be acute or chronic. Acute soften- 
 ing of the hrain may be a result of inflammation ; it may follow 
 vascular occlusion, thrombotic or embolic, arterial or venous. 
 
 Chronic softening of the brain is an affection of the degenera- 
 tive period of life. It usually involves the while matter of the 
 hemispheres. The symptoms to which it gives rise are not 
 well defined. There is usually progressive loss of motor power 
 and impairment of sensation, sometimes with I'igidity. Mental 
 deterioration may be slight or considerable. Life may be pro- 
 longed for from two months to two years, death usually result- 
 ing from bedsores, pneumonia, or some other intercurrent 
 malady. 
 
328 ESSENTIALS OF DIAGNOSIS. 
 
 Cerebral Embolism. 
 
 Under what conditions does cerebral embolism occur ? 
 
 A vegetation from a diseased cardiac valve may be washed 
 into one of the vessels of the brain ; or the plug may have its 
 source in a thrombus that has formed in one of the cavities of 
 the heart, or in a calcareous fragment from the wall of an 
 atheromatous aorta. 
 
 To what symptoms does cerebral embolism give rise ? 
 
 The sudden plugging of one of the vessels of the brain is 
 usually manifested by transient loss of consciousness of varying 
 duration, often accompanied by convulsions. On the return to 
 consciousness, the symptoms of hemiplegia are evident, often 
 right-sided, and associated with aphasia. In the course of a 
 few days, secondary fever appears. Unilateral convulsions 
 may be repeated. Choreoid, athetoid, and other disorders of 
 movement are likely to develop. 
 
 How do the symptoms of cerebral hemorrhage differ from 
 ■ those of cerebral embolism ? 
 
 Cerebral embolism is a disease rather of early life ; hemor- 
 rhage is one of advanced life. Hemorrhage occurs in association 
 with disease of the vessels ; embolism with valvular disease of 
 the heart or other source of emboli. Consciousness is invariably 
 lost when hemorrhage takes place ; it is more likely not to be 
 in cases of embolism. Embolism is more likely to be cortical 
 and to give rise to initial and consecutive epileptiform convul- 
 sions, to localized palsies and to aphasia ; hemorrliage is more 
 likely to be central, to be unattended with convulsions, and to 
 present hemiplegia. Both direct (local) and indirect (general) 
 symptoms are more profound and more extensive in hemorrhage 
 than in embolism. The detection of emboli in other organs is 
 an important element in diagnosis. 
 
CEREBRAL THROMBOSIS. 329 
 
 Cerebral Thrombosis. 
 
 Under what conditions does cerebral thrombosis occur? 
 
 The most common cause of cerebral thrombosis is vascular 
 disease, whether atheromatous, syphilitic or fibroid. The blood 
 may also coagulate in the vessels in conditions of lowered 
 vitality and enfeebled circulation. Increased coagulability of 
 the blood predisposes to the occurrence of thrombosis. A 
 thrombus may form from an embolus by extension. 
 
 To what symptoms does cerebral thrombosis give rise? 
 
 The actual occurrence of thrombosis in a cerebral vessel may 
 for a long time be preceded by distressing headache, vertigo, 
 numbness, tingling, muscular weakness, impairment of memory 
 and mental failure. The formation of the thrombus is announced 
 by loss of consciousness, of varying degree and duration, per- 
 haps attended with convulsions or with delirium. In the course 
 of a few days, decided secondary fever may appear. Subse- 
 quently, the evidences of hemiplegia become manifest ; while 
 recurring localized convulsions may take place. As in the case 
 of embolism, involuntary and spasmodic disorders of movement 
 in the affected parts are common. Thrombosis of the sinuses 
 gives rise to localized edema of the face and scalp. 
 
 How are cerebral hemorrhage and cerebral thrombosis to be 
 differentiated ? 
 
 Thrombosis, unlike hemorrhage, is of not rare occurrence in 
 infancy and extreme old age. The symptoms of hemorrhage set 
 in suddenly, with loss of consciousness ; those of thrombosis are 
 preceded by prodromata and develop gradually, with headache, 
 delirium, perhaps convulsions. The convulsions of thrombosis 
 are wont to be localized or unilateral ; if convulsions attend 
 hemorrhage, they are usually general. Hemorrhage is the more 
 likely to occur under conditions of excitement ; thrombosis, amid 
 conditions of depression. In hemorrhage the circulation is 
 active, the arterial tension high ; thrombosis is not uncommonly 
 associated with a stagnant circulation in a debilitated indi- 
 vidual. The symptoms are more profound and extensive in 
 
330 ESSENTIALS OF DIAGNOSIS. 
 
 hemorrhage than in thrombosis. Mobile spasm, athetosis and 
 other disorders of movement more commonly follow thrombosis 
 than hemorrhage. Kecurrent convulsions also point to throm- 
 bosis rather than to hemorrhage. 
 
 Cerebral Tumor. 
 
 What are the more common varieties of tumor of the brain ? 
 
 Cerebral tumors are most commonly gliomata, tuberculomata, 
 sarcomata, gummata, mysomata, carcinomata or psammomata. 
 They may develop in the cerebral mass, in the membranes, or 
 in the bone. 
 
 2sot rarel}', cysticerci or echinococcus cysts develop in the 
 brain, Gliomata sometimes follow injuries to the head. 
 
 Tuberculomata appear in 3'oung persons, and are usuallj'' 
 associated with tuberculosis elsewhere than in brain. Car- 
 cinomata occur later in life, give rise to a cachexia, and are 
 associated with similar growths elsewhere. Gummata are 
 present with other manifestations and a history of syphilis. 
 
 What are the symptoms of tumor of the brain ? 
 
 The symptoms vary somewhat with the size and situation of 
 the new-growth. Certain phenomena, however, characterize 
 the presence of a neoplasm in any part of the brain. There is 
 persistent headache, intensel}^ aggravated in paroxysms ; optic 
 neuritis followed by atrophy ; mental failure ; impaired memory ; 
 emotional mobility ; vomiting ; vertigo ; sometimes forced move- 
 ments ; slowness of speech ; separation of S3'llables ; confluence 
 of articulation ; sometimes aphasia ; paralysis of varying dis- 
 tribution, associated with or followed by contractions ; some- 
 times choreoid or athetoid movements, or a jerky incooordi- 
 nation ; convulsions resembling those of major or of minor 
 epilepsy, or of Jacksonian epilepsy, or attacks of transient 
 convulsions ; alterations of sensation ; palsy of cranial nerves ; 
 sometimes conjugate deviation of the head and eyes ; abnor- 
 malities of the pulse ; interference with the respiration. The 
 quantity of urine evacuated may be increased ; there may be 
 albuminuria or gh'cosuria. Finally, stupor and coma may be 
 the precursors of death. 
 
INTRACRANIAL ANEURISM, 331 
 
 How may chronic nephritis simulate cerebral tumor ; how are 
 the two to be differentiated ? 
 
 Chronic nephritis may be attended with headache, vertigo, 
 vomiting, optic neuritis and convulsions, but the urine con- 
 tains casts as well as albumin, edema exists, the arterial tension 
 is heightened, the heart is hypertrophied, and the palsies of 
 tumor are wanting. 
 
 What symptoms does anemia have in common with tumor of 
 brain, and how are the two to be differentiated ? 
 
 Both anemia and cerebral tumor may occasion headache, 
 vertigo, optic neuritis and albuminuria, but the headache of 
 anemia is not so intense as that of tumor ; the optic neuritis of 
 anemia is more rapid in development than is that of tumor ; 
 while the pallor, the breathlessness, the edema, the submissive- 
 ness to judicious treatment of the one, and the convulsions, the 
 palsies, the x^rogressiveness, and the resistance to treatment of 
 the other are distinctive. 
 
 How are the epileptiform convulsions of cerebral tumor to be 
 distinguished from the convulsions of essential epilepsy ? 
 In themselves the convulsions may be indistinguishable, 
 though those of tumor are the more likely to be local or uni- 
 lateral. Epilepsy, however, fails to present the distinctive 
 symptoms of tumor : headache, vertigo, vomiting, optic neuritis 
 and palsies. 
 
 How may the symptoms of cerebral tumor be mistaken for 
 those of cerebro-spinal sclerosis ; how is the diagnosis to 
 be made ? 
 
 A tumor in the brain may occasion a peculiar jerky incoordi- 
 nation, but it does not occasion the nystagmus, the peculiarity 
 of speech, the exaggeration of reflexes of cerebro-spinal sclerosis, 
 while headache and optic neuritis are more common and more 
 intense. 
 
 Intracranial Aneurism, 
 
 To what symptoms does an intracranial aneurism give rise ? 
 
 Aneurism of the cerebral vessels may develop as a result of 
 vascular disease, syphilitic or otherwise, of traumatism and of 
 embolism. 
 
332 ESSENTIALS OF DIAGNOSIS. 
 
 The symptoms of intracranial aneurism necessarily vary with 
 the situation of the aneurism. The more constant symptoms 
 are those of an intracranial tumor : headache, vertigo, vomiting, 
 convulsions, palsies, optic neuritis. The detection of a bruit or 
 the demonstration of symptoms dependent upon the presence 
 of a tumor in the course of a cerebral vessel would be diagnostic. 
 
 The occurrence of rupture is indicated by the symptoms of 
 cerebral hemorrhage. 
 
 General Paralysis of the Insane. 
 
 What are the symptoms of general paralysis of the insane? 
 
 General ov progressive ijaralysis of the insane, or paretic dementia, 
 is a fatal disease of insidious invasion, occurring in those who 
 have abused their mental and physical energies, and charnc- 
 terized by psychic alteration and failure, with progressive palsy. 
 
 It is much more common in men than in women, and in early 
 middle life than at any other period. 
 
 Among the first symptoms are an alteration of disposition, 
 and a change of character. An individual, previously more or 
 less refined, aflfectionate, attentive, scrupulous, methodical, pre- 
 cise and neat, becomes careless, indifferent, negligent, coarse, 
 indecent, irritable and forgetful. He fails to keep appointments. 
 He makes ill-judged investments and extravagant expenditures. 
 He eats irregularly and hastily, and sometimes eats and drinks 
 excessively, and sleeps poorly. 
 
 The palsy is not of the ordinary type. There is at first loss 
 of coordinating power for delicate tasks, such as writing or 
 painting, while general muscular strength, as for lifting, is but 
 slightly impaii'ed. The paralysis is associated with tremor. 
 The pupils may be contracted, sluggish and unequal. 
 
 To these symptoms are added the so-called delusions of gran- 
 deur, which vary from time to time. The patient believes him- 
 self fabulously wealthy. He projects colossal enterprises, or 
 announces wonderful discoveries. He is, however, contented 
 with his surroundings. In a milder form, the delusions take 
 the less obtrusive shape of an invincible, unreasoning optimism, 
 and may be overlooked. In other cases there are alternations 
 
GENERAL PARALYSIS OF THE INSANE. 333 
 
 of depression and exaltation. Sleeplessness becomes more obsti- 
 nate. Speech becomes defective, indistinct and stuttering. In 
 writing, words, syllables, letters are omitted or misplaced or 
 repeated. There is a peculiar tremor of the lips. The protruded 
 tongue presents both rhythmical tremor and fibrillary contrac- 
 tions. The gait becomes shuffling. Control over the limbs is 
 progressively lost. At this stage, apoplectiform and epileptiform 
 seizures may take place, and paroxysms of rage and fury may 
 occur. Sensibility is not impaired until late, when it may be 
 almost abolished. 
 
 Deceptive lulls and remissions may interrupt the progress of 
 the disease, but finally a condition of terminal dementia is 
 reached. IsTutrition gradually fails. Paralysis, mental and phy- 
 sical, becomes so great that death may result from the entrance 
 of food into the air-passages. Coma, convulsions, painful con- 
 tractions, obstinate diarrhea, pulmonary affections, especially 
 pneumonia, are among the phenomena preceding death. At 
 the autopsy chronic congestive, inflammatory and degenerative 
 changes may be found in the brain and membranes and in the 
 posterior and lateral columns of the spinal cord. 
 
 How are progressive paralysis of the insane and posterior spinal 
 sclerosis to be differentiated? 
 
 As the symptoms of posterior spinal sclerosis may "be super- 
 added to those of progressive paralysis of the insane, the dif- 
 ferentiation of uncomplicated cases from locomotor ataxia, as 
 from cerebro-spinal sclerosis and paral3'sis agitans, essen- 
 tially depends upon a recognition of the presence or absence 
 of those manifestations of central dissolutional processes that 
 characterize progressive paralysis : the changes in character 
 and disposition, the emotional disturbances, the impairment of 
 memory, the maniacal outbursts, the delusions of grandeur, 
 the peculiar tremor of lips and tongue, the inequality of the 
 pupils, the derangement of the language-faculty in speech and 
 writing, the progressive failure of voluntary motion and intel- 
 lection, the epileptiform and apoplectiform attacks. 
 
 Acute development of the peculiar loss of coordinating power, 
 mental and physical, without obvious cause, in a man of middle 
 
334 ESSENTIALS OF DIAGNOSIS. 
 
 life, especially one given to mental, emotional, venereal or alco- 
 holic excess, should at once excite a suspicion of the develop- 
 ment of paretic dementia. 
 
 Sunstroke. 
 
 What are the symptoms of sunstroke ? 
 
 Sunstro'ke, heat-stroke, insolation, of which there are at least 
 two principal varieties, heat-fever or thermic fever and heat-exhaus- 
 tion — is an affection of the heated term. It occurs in persons 
 exposed to intense heat, solar or artificial, in whom the respira- 
 tory and cutaneous transpiration is checked. 
 
 Crowding and defective ventilation predispose to the occur- 
 rence of heat-stroke. The onset may be abrupt or gradual, the 
 symptoms severe or mild (incomplete). While most often com- 
 ing on during active muscular exertion, as in the case of 
 laborers and marching soldiers, the attack not infrequently 
 follows the mid-day meal. It usually but not invariably 
 happens during the period of maximum heat of the day. 
 
 There occur increased frequency of micturition, headache, 
 vertigo, nausea, vomiting, delirium, loss of consciousness, dys- 
 phagia, stertorous breathing and coma, associated in the febrile 
 form with a hot, often flushed, skin, frequent pulse and high tem- 
 perature. The pupils may be dilated or contracted, or contrac- 
 tion and dilatation may be present at different times in the same 
 case. There ma}^ be rectal and vesical incontinence, sometimes 
 partial suppression of urine. The duration of the symptoms 
 varies from a few minutes to several hours. 
 
 Death may occur early or late ; recovery may be speedy or 
 tardy. Persistent headache, vesical irritability, choreoid move- 
 ments of the upper extremities, mental impairment, epileps}', 
 and in rare instances hemiplegia, or other paral5^sis, usually 
 transient, may supervene as sequelae. Anhydrosis, with headache 
 and elevation of temperature, annually recurring near the anni- 
 versary of the attack, has been observed. 
 
 General paralysis of the insane (paretic dementia) has been 
 attributed to sunstroke. 
 
DELIRIUM TREMENS. 335 
 
 What are the principal points of differentiation between heat- 
 exhaustion and heat-fever, or sunstroke proper ? 
 
 In heat-exhaustion the skin is pale, cool or cold, moist or 
 clammy ; the temperature is low, even subnormal ; there is 
 syncope rather than coma ; the pupils are usually dilated ; the 
 pulse is feeble ; convulsions are absent ; and rapid relief foUow^s 
 tile use of warmth and stimulants. 
 
 How does cerebral hemorrhage differ from sunstroke ? 
 
 The coma of sunstroke, unlike that of cerebral hemorrhage, 
 does not set in unannounced ; nor is it as lasting or as profound ; 
 while dysphagia may be greater, stertor is less. 
 
 The symptoms of sunstroke are symmetrical ; the pupils and 
 the reflexes are equal ; hemiplegia is not an ordinary sequel. 
 
 The temperature rises much higher in insolation than at any 
 time in hemorrhage. The pulse is frequent, often feeble ; that 
 of cerebral hemorrhage is commonly slow and full. 
 
 It must, however, not be forgotten that cerebral hemorrhage 
 may occur amid circumstances favorable for the development of 
 sunstroke. 
 
 With what other conditions might sunstroke be confounded ? 
 
 Sunstroke might be mistaken for acute alcoholism, meningitis, 
 uremia or narcotic poisoning. Alcoholic excess may bring on 
 an attack, so that the phenomena of both might be intermingled. 
 The history and the symptoms detailed should prevent error in 
 other cases. 
 
 In uremia, too, convulsions usually precede coma. 
 
 Delirium Tremens. 
 
 What are the symptoms of delirium tremens ? 
 
 The continued ingestion of excessive quantities of alcohol 
 sometimes gives rise to a condition in which with impaired 
 appetite and gastric irritability are associated inability to 
 sleep, tremor and delirium. The temperature is likely to be 
 elevated. The urine may contain albumin. The patient is 
 restless and evinces a tendency to talkativeness ; he is always 
 busily engaged with his delusions. Sometimes the delirium is 
 
336 ESSENTIALS OF DIAGNOSIS. 
 
 more violent. The victim is terror-stricken by hideous illusions 
 and hallucinations. The figures of the wall-paper, and articles 
 of furniture are converted into crawling reptiles ; attendants, 
 into demons. The patient is unable to sleep. Hypnotics may 
 prove futile. There is little desire for food. That which is 
 taken may be rejected. If recovery is to take place, sleep is 
 gradually restored ; else the patient is worn out and succumbs 
 to exhaustion. Pneumonia, especially of the apices, is not an 
 uncommon complication of alcoholism. The use of tobacco 
 during convalescence is sufficient to renew the attack. 
 
 How is delirium tremens to be distinguished from acute 
 mania ? 
 
 The delirium of alcoholic intoxication may be maniacal, 1)ut 
 it is associated with a history of alcoholism, Avhile acute mania 
 usually develops in a person with a psychopathic family history, 
 and has probably been preceded by a prodromal period charac- 
 terized by a change in manner, in disposition or in behavior. 
 The character of the illusions and hallucinations diflers in the 
 two disorders. Delirium tremens usually subsides after sound 
 sleep for a number of hours consecutively, and recovery is 
 complete. Evidences of insanity persist after the attack of 
 acute mania is at an end. 
 
 How are delirium tremens and cerebral meningitis to be differ- 
 entiated ? 
 
 The distinction between delirium tremens and cerebral men- 
 ingitis depends upon a knowledge of the cause, the history, the 
 course, the symptoms and the termination of the two afiections 
 respectively. Delirium tremens is preceded by a history of alco- 
 holism ; meningitis, by a history of traumatism or infection. 
 Delirium tremens lasts from a few days to a week ; meningitis 
 for a much longer time. In meningitis there are, and in deli- 
 rium tremens there are not, muscular spasm, convulsions and 
 sensory disturbance, followed by paralysis. The delirium and 
 tremor of alcoholism are peculiar and characteristic. The tem- 
 perature may be slightly elevated above the normal in delirium 
 tremens, but meningitis is distinctly a febrile disease. 
 
PLUMBISM. 
 
 337 
 
 Plumbism. 
 
 What are the clinical manifestations of lead-poisoning? 
 
 Lead may gain entrance into the system and give rise to 
 toxic manifestations under diverse circumstances. Thus satur- 
 nine intoxication occurs in tliose who work witli the metal, as 
 miners, color-grinders, painters, plumbers, type-founders, com- 
 positors. Lead may also be introduced into the system by 
 means of drinking-water conveyed through lead-pipes, or with 
 food prepared in leaden vessels, or by the use of hair-dyes, of 
 cosmetics, or of snuif packed in lead-paper, or by the medicinal 
 administration of lead in some form. The most common mani- 
 festatiou of plumbism is multiple neuritis. 
 
 Fig. 51. 
 
 Wrist-drop from lead poisoning. (Gowers.) 
 
 The symptoms vary in kind, degree, distribution and acute- 
 ness. The more common and the more characteristic are obsti- 
 nate constipation, abdominal colic, wrist-drop, and a blue line 
 on the gums. In addition, the nutrition is impaired and there 
 
 22 
 
338 ESSENTIALS OF DIAGNOSIS. 
 
 is anemia. Among other symptoms are cramps in the legs, 
 tremor, headache, convulsions, delirium and coma. The par- 
 alysis of the extensors of the wrist and fingers upon which the 
 wrist-drop depends is bilateral, but does not involve the supi- 
 nator longus. Sometimes, the intrinsic muscles of the hand 
 atrophy ; at times, too, the lower extremities are paralyzed. 
 The knee-jerks may be enfeebled or lost ; station may be un- 
 steady ; coordination may be deranged. Occasionally, symptoms 
 of sensory derangement, laryngeal palsy, mental failure, melan- 
 cholia, inequality of the pupils and impairment of vision are 
 observed. The pupils may be small and fail to react to light. 
 The optic nerve may undergo atrophy. Paralyzed muscles 
 display the reaction of degeneration, Cardio-vascular-renal 
 changes ai'e of strikingly common occurrence. Arthritic mani- 
 festations and deposits indistinguishable from those of gout are 
 not rare. If potassium iodide be administered, the urine may 
 respond to chemic tests for lead. 
 
 How may lead- poisoning he confounded with cerebral tumor, 
 and how is the differentiation to be made ? 
 37hen the sj^stem has been impregnated with lead, there may 
 be optic neuritis, headache, convulsions, delirium and palsy ; 
 but there are also a blue line on the gums ; a history of expo- 
 sure to the toxic metal ; of intestinal colic ; of obstinate con- 
 stipation ; and the palsy gives rise to wrist-drop. 
 
 Torticollis. 
 
 What is torticollis ? 
 
 Torticollis or wry-neck is a condition in which, from shortening 
 or from spasm of one or more muscles of the neck, the head is 
 maintained in an abnormal position. 
 
 What are the varieties of torticollis ? 
 
 There are two types of wry-neck. In one, as a result of 
 traumatism, or of defective development, the muscle, usually 
 the sterno-mastoid upon one side, is atrophied and shortened. 
 
 The head is rotated to the side opposite to that of the affected 
 
"WRITERS' CRAMP. 339 
 
 muscle, which is conspicuous for its prominence. In the second 
 variety of wry-neck, tlie muscles involved, most commonly the 
 sterno-mastoid, tlie trapezius and the splenius, are in a state of 
 active contraction, tonic or clonic, or alternately both. As a 
 result, the head may be rotated or inclined to one side or 
 retracted in over-extension, in accordance with the muscle or 
 combination of muscles that participates in the spasm. Not 
 infrequently, with the spasm of the muscles of the neck is also 
 associated spasm of muscles of the arm or of the face. 
 
 Occupation-Neuroses. 
 
 What are the occupation-neuroses ? 
 
 As the result of persistent and long-continued movement of 
 a part in a constrained position, involving the activity of certain 
 groups of muscles, spasmodic interference with the performance 
 of the same movement may develop. 
 
 Thus, as a type of the disease, there is produced writers' 
 cramp or scriveners' palsy. An analogous condition may be 
 produced in telegraphers, shoemakers, piano-players, violinists, 
 zither-players, seamstresses, smiths, painters, turners, watch- 
 makers, knitters, engravers, masons, compositors, cigarette- 
 makers, milkers, money-counters. 
 
 Writers' Cramp. 
 
 What are the symptoms of writers' cramp? 
 
 In those who write much, especially in such a way that the 
 burden of the work falls upon the small muscles concerned, there 
 sometimes develops a condition that renders writing impossible. 
 Under such circumstances, as soon as an attempt to write is 
 made, the fingers contract in spasm that may be painful, so 
 that the act, if possible, is imperfectly accomplished. At 
 other times, there may be tremor, and rarely weakness. In 
 some cases, neuralgic pain is the most conspicuous symptom. 
 In aggravated cases, the manifestations are not confined to the 
 
340 ESSENTIALS OF DIAGNOSIS. 
 
 Fig. 52. 
 
 Mode of holding the pen favorable to 
 the development of writers' cramp. 
 (Gowers.) 
 
 Mode of holding the pen when writ- 
 ing becomes difficult. (Gowers.) 
 
 act of writing, but may appear upon attempts to perform other 
 movements. The onset of the symptoms is usually gradual, 
 but occasionally it is sudden. 
 
 Chorea. 
 
 What are the etiologic elements concerned in the determination 
 of an attack of chorea ? 
 
 Chorea is most common at or about the age of puberty, and 
 more so in girls than in boys. At Philadelphia, attacks are said 
 to be more common in the spring of the year than at any other 
 time. It has been observed that chorea is more common in 
 white than in colored children. In many cases, an hereditary 
 influence can be traced— directly, as chorea, or, more commonly, 
 in the nature of other diseases of the nervous system, as 
 epilepsy or insanity, or of rheumatism. Fright is frequently an 
 exciting cause of the disease. Occasionally traumatism has 
 preceded an attack. An obscure but well-determined causal 
 relation exists between acute rheumatism, heart-disease and 
 pregnancy, on the one hand, and chorea on the other. 
 
 What are the symptoms of chorea ? 
 
 Chorea is a spasmodic neurosis, manifested by irregular, in- 
 voluntary, incoordinated muscular movements, aggravated b}-- 
 excitement or observation. Tlie movements cease during 
 sleep, but they may be sufficiently violent to prevent sleep. 
 
EPILEPSY. 341 
 
 They are often more decided on one side of the body than on 
 the other. Speech is often interfered witli. A shght degree 
 of muscular weakness exists. The electric irritability is usually 
 increased ; sometimes there are slight qualitative changes. 
 Occasionally pain is felt in the parts affected. The tempera- 
 ture is, as a rule, slightly elevated. There is mental irritability 
 or dulness of intellect. Anemia is often present. 
 
 At times, hemic heart-murmurs are heard ; at other times, 
 murmurs dependent upon organic disease, either antecedent or 
 coincident, are heard ; endocarditis is not an uncommon com- 
 plication of chorea. 
 
 Chorea is a self-limited affection, the average duration of 
 which is about ten weeks. It is said sometimes to involve the 
 diaphragm, and to give rise to obstinate hiccough. It is thought 
 that the irregularity of the action of the heart, sometimes ob- 
 served in choreic children, is dependent upon involvement of the 
 cardiac muscle ; chorea of the larynx has also been seen. 
 
 So-called choreoid movement, athetosis, and mobile spasm, are 
 often observed in cases of paralysis of cerebral origin. 
 
 What is hereditary chorea or Huntingdon's chorea ? 
 
 Chorea sometimes appears in families, developing at the mid- 
 dle period of life, and possibly continuing until death, in hasten- 
 ing which it may play some part. The symptoms differ in no 
 essential particular from those of the ordinary form of chorea. 
 
 Epilepsy. 
 
 What is the etiology of epilepsy ? 
 
 Epilepsy is immediately dependent upon an irritable condition 
 of the nervous system that must be referred to changes in the 
 nerve-cells, beyond our present means of recognition. The 
 disease is more common in females than in males. In a con- 
 siderable proportion, a neurotic heredity can be traced. In 
 many cases, no etiologic factor can be determined. The first 
 attack usually occurs in early life, frequently in conjunction 
 with dentition, or in association with rachitis. In other cases, it 
 may be excited by mental influences, especially anxiety, by fails 
 
342 ESSENTIALS OF DIAGNOSIS. 
 
 or blows, by acute disease, by the presence of parasites in the in- 
 testine, by menstrual derangement, by nasal polypi, by phimosis, 
 by cicatrices, and by other sources of peripheral irritation. 
 
 When no source of irritation, direct or reflex, can be found, 
 the disease is designated essential or idiopathic. 
 
 What are the symptoms of epilepsy ? 
 
 Epilepsy is a paroxysmal neurosis, characterized by attacks 
 of varying frequency, duration and severity, which may ap- 
 pear as transient loss of consciousness {2Mit mal, minor epilepsy) 
 or may be preceded by a premonitory sensation or aura, fol- 
 lowed successively by a cry, loss of consciousness, frothing at 
 the mouth, tonic followed b}'^ clonic convulsions, headache, 
 biting of the tongue and somnolence {grand rnal, major e^nlepsy). 
 
 The attacks of petit mal may be so inconspicuous as to 
 escape observation. There may be simply a vertiginous or 
 other abnormal sensation, or an abrupt interruption in speech ; 
 or the grasp of an object held in the hand may be relaxed ; or 
 there may be a twitching of the muscles of the face. 
 
 When the seizure is preceded by an aura, this may be 
 motor, sensory, visceral or psychic. In the attack the face 
 Taecomes at first pallid, then flushed, and finally cyanotic ; the 
 pupil is dilated and insensible to light ; urine and feces may be 
 expelled involuntarily. The urine may contain a trace of 
 albumin. 
 
 Mental deterioration ensues in a degree corresponding to the 
 frequency of the attacks. Paroxysms may be succeeded by 
 transient liemiplegia and aphasia, by the automatic performance 
 of some act or by mania. 
 
 Sometimes a series of convulsions occurs, one attack scarcely 
 ceasing before another begins, constituting the status epilepticus. 
 
 Nothing is known of the pathologic anatomy of epilepsy. 
 
 How are the epileptiform convulsions of cerebral disease to be 
 distinguished from attacks of true epilepsy ? 
 Epileptiform convulsions usually result from lesions involving 
 the cortex cerebri. The most common of these lesions are 
 softening from vascular occlusion, hemorrhage and new- 
 growths. The convulsions occasioned are likely to be local in 
 
EPILEPSY. 343 
 
 character and not at the onset attended with loss of conscious- 
 ness ; while the convulsions of epilepsy are usually general and 
 simultaneous with loss of consciousness. In the intervals be- 
 tween epileptiform convulsions, some evidences of cerebral 
 disease — hemiplegia, athetoid movements, choked discs— are 
 likely to be present. 
 
 What are the distinctions between chorea and epilepsy ? 
 
 Epilepsy occurs in paroxysms with intermissions, and may 
 persist during the greater part of hfe ; chorea is but a temporary, 
 self-hmited condition, the symptoms of which are constant 
 during the continuance of the disease. The movements of 
 chorea do not possess the violence of the convulsions of epilepsy ; 
 nor in chorea is consciousness lost or the tongue bitten. 
 
 How are the attacks of syncope and those of petit mal to be 
 differentiated? 
 
 Syncope occurs under well-known circumstances that occasion 
 temporary cerebral anemia ; the pulse at the wrist is almost 
 obliterated; loss of consciousness is of brief duration; the 
 return to the normal condition takes place slowly. In case of 
 petit mal, there have been previous attacks of a similar character 
 or perhaps of major epilepsy ; the loss of consciousness is sudden 
 and transitory ; the normal condition is soon resumed ; there may 
 have been slight muscular tvvitchings ; or urine may have been 
 passed involuntarily ; or some automatic action is performed. 
 
 How is eclampsia to be distinguished from epilepsy ? 
 
 By eclampsia is meant convulsions occurring incidentally and 
 temporarily, as during dentition, or in connection with preg- 
 nancy and parturition. The relation of eclampsia to epilepsy 
 and epileptiform convulsions is uncertain. The recognition of 
 eclampsia and its distinction from epilepsy and epileptiform 
 convulsions depend upon its incidental and transient occurrence 
 in connection with one of the conditions that give rise to it. 
 
 How are the convulsions of uremia and those of epilepsy to be 
 differentiated ? 
 
 The convulsions of uremia are not unlike those of epilepsy. 
 Their significance, however, depends upon their association 
 
344 ESSENTIALS OF DIAGNOSIS. 
 
 with edema, a peculiar raustiness of the breath, the presence of 
 albumin and tube-casts in the urine, and the existence of degen- 
 erative changes in the retina. If obtainable, the previous his- 
 tory may determine the diagnosis. 
 
 Hysteria. 
 
 What are the symptoms of hysteria ? 
 
 Hysteria is a disease of the nervous system, more common in 
 females than in males, and in early adult life than at any other 
 period. In many cases a neuropathic heredity can be traced. 
 The manifestations of the disease may be induced by mental 
 emotion, anxiety, visceral disease and other disease. As a rule, 
 they are sudden in onset and as sudden in disappearance. They 
 may be dissipated by a profound mental impression. The symp- 
 toms are protean ; some are continuous, others paroxysmal. 
 Among the former are derangements of sensibility and motility, 
 visceral, vaso-motor and cerebral disturbances ; the paroxysmal 
 symptoms include convulsive seizures. That which fundament- 
 ally characterizes the disease is a loss of self-control, a deficiency 
 of will-power, a heightened self-consciousness, a tendency to 
 exaggeration and a morbid desire for sympathy. Tbe patient is 
 moved to laughter or tears with undue readiness and without 
 adequate cause. Duplicity and deception are practised, and 
 there is an irresistible tendency to imitation. Sensation may 
 be lost or heightened, or otherwise abnormal, locally, or upon 
 one-half of the body, or in irregular distribution, with un- 
 steady station and gait when the eyes are closed. Spinal 
 tenderness is common. There is frequently a recurrent sen- 
 sation of obstruction in the throat, as of a ball rising from 
 the stomach, or of a sense of pharyngeal constriction— the 
 so-called globus hysterims. At times, there is a feeling of 
 intense pain in the head, such as might be occasioned by the 
 driving in of a nail— the davits hystericus. The special senses 
 may be variously impaired. Motor palsy of diverse distribution 
 may exist, occasioning paraplegia, hemiplegia or monoplegia, 
 unattended with muscular wasting or alteration in the elec- 
 tric reactions or impairment of activity of the sphincters. 
 
HYSTERIA. 345 
 
 The reflexes are usually unaltered : in a number of cases, they 
 are exaggerated. There may be aphonia, loss of the power of 
 articulation, retention of urine, constipation, stammering. 
 Contractures may take place and give rise to troublesome 
 deformity. Laryngeal spasm may occasion distressing dyspnea, 
 or a peculiar barking cough. Independently of any spasm, there 
 may be increased frequency of respiration, with shortness of 
 breath. Spasm of the pharynx or of the esophagus may entail 
 the rejection of all food ingested. There may in addition be 
 such repugnance to food that little is taken. On the other hand, 
 the appetite may be strangely, even disgustingly perverted. 
 There may be local flushing and perspiration. In females, 
 menstruation may be deranged ; ovarian tenderness is common. 
 The paroxysmal attacks of convulsions are marked by tonic and 
 clonic spasm, without loss of consciousness or biting of the tongue. 
 The arms and legs are wildly thrown about by coordinated mus- 
 cular activity — purposive movement. The patient may shriek 
 and bite the lips. Opisthotonos and trismus may be developed. 
 At times, there are evidences of profound psychic disturbance, 
 as manifested by hallucinations and delusions, perhaps of an 
 •erotic nature. Lethargy and catalepsy are sometimes observed. 
 The temperature may display decided irregularity. 
 
 How are hysterical paralysis and the cerebral paralysis of 
 organic origin to be differentiated ? 
 
 The palsy of hysteria, hemiplegic, paraplegic, diplegic or 
 monoplegic, is usually atypical. 
 
 The face is rarely involved. Sensory derangement is common. 
 The evidences of secondary descending degeneriition : contrac- 
 tures and exaggeration of reflexes, are wanting. There may be 
 constipation and retention of urine, but not incontinence. 
 
 While the onset may have been sudden, it will not have been 
 apoplectic. Other symptoms of hysteria may make the character 
 of the palsy clear, but the mere existence of the symptoms of 
 hysteria should not obscure the possible simultaneous existence 
 of organic disease. 
 
346 ESSENTIALS OF DIAGNOSIS. 
 
 How are the convulsions of hysteria and those of epilepsy to 
 be differentiated ? 
 
 An epileptic paroxysm takes place without special excitation, 
 and sets in abruptly, often with a cry ; an hysterical attack may- 
 be brought on by emotion, sets in gradually, and is attended 
 with screaming. The convulsions of epilepsy pursue a regular 
 sequence, and are associated with cyanosis, biting of the tongue, 
 and insensibility of the iris to Irght ; in the hysterical attack, the 
 members are wildly thrown about, the pupil responds to stimu- 
 lation, while the patient may bite the lips or hands or other 
 persons or things. Involuntary extrusion of urine and feces 
 may take place in epilepsy ; but does not occur in hysteria. 
 
 Loss of consciousness is complete in epilepsy ; consciousness 
 is retained or perverted in hysteria, the paroxysm of which is 
 characterized by talkativeness. 
 
 The epileptic attack lasts but a few minutes ; the hysterical, 
 ten minutes or longer. Opisthotonos is common in hysteria, 
 exceptional in epilepsy. 
 
 An epfleptic seizure may occur at any time and under any 
 circumstances ; hysterical attacks take place only in the presence 
 of a second person. The hysterical patient is careful in the 
 paroxysm to suffer no injury ; the epileptic falls, whatever the 
 attendant dangers, powerless to avert them. 
 
 An hysterical patient may, however, also be epileptic. 
 
 What are the distinctions between spastic paraplegia and 
 hysterical paraplegia ? 
 
 Spastic paraplegia develops at an age when hysteria is com- 
 mon ; but in hysteria the reflexes are not exaggerated and the 
 peculiar muscular spasm of lateral sclerosis does not occur, 
 while sensox-y and emotional symptoms cannot escape ob- 
 servation. 
 
 How are acute myelitis and hysterical paraplegia to be differ- 
 entiated ? 
 
 Myelitis should not be overlooked because it occurs under cir- 
 cumstances amid which hysteria is to be expected. Exaggerated 
 reflexes, trophic changes, wasting, derangement of sphincters 
 and girdle-pain indicate the existence of more than hysteria. 
 
TETANUS. 347 
 
 How are the symptoms of hysteria and those of meningitis to 
 be differentiated ? 
 If symptoms of meningitis appear in fin hysterical individual, 
 their true significance may be overlooked. Convergent strabis- 
 mus may be hysterical ; but divergent strabismus always 
 depends upon organic disease. There may be retention of urine 
 in hysteria, but there is never incontinence. Trophic changes 
 and continued elevation of temperature are evidences of the 
 existence of something more than functional disease. 
 
 How are hysteria and cerebral tumor to be differentiated ? 
 
 Hysteria may present any of the imitable symptoms of cere- 
 bral tumor, but in addition there will alw^ays be indubitable 
 evidence of their nature. Optic neuritis or ptosis, of course, 
 is not to be duplicated. Hysterical manifestations in associa- 
 tion with cerebral symptoms should not be permitted to obscure 
 the existence of organic disease. 
 
 Tetanus. 
 
 What are the symptoms of tetanus ? 
 
 Tetanus is a spasmodic disorder dependent upon a specific 
 infection contained in soil and introduced into the system 
 through wounds or abrasions. It is manifested by painful 
 rigidity of the head and jaw, soon progressing to trismus, and 
 by stiffness of the tongue. In turn, the rigidity involves the 
 muscles of the face (resulting in the risus sardonicus), the mus- 
 cles of the trunk, the respiratory muscles and the diaphragm. 
 To the tonic spasm of the muscles are added frequently recur- 
 ring clonic exacerbations, which may be induced by external 
 irritation. 
 
 The body may be arched in strong extension and supported 
 only on the head and heels, constituting opisthotonos ; it may be 
 strongly arched forward {emprosthotonos), or laterally (pleuros- 
 tlioto^ws), or it may be rigidly straight [orthotonos). The symp- 
 toms of tetanus set in at a variable period after inoculation — 
 from a few hours to several days. The duration of the disease 
 likewise varies from a few days to several weeks. Recovery is 
 
348 ESSENTIALS OF DIAGNOSIS. 
 
 exceptional. Towards the close of life or even after death, the 
 temperature may rise to an extraordinar}' height. 
 
 How are hysterical trismus and opisthotonos to he distinguished 
 from tetanus ? 
 Hysteria is an unruly disease, the symptoms of which are 
 disorderly in appearance, while the symptoms of tetanus appear 
 in fairly regular succession. Should trismus or opisthotonos 
 develop as a manifestation of hysteria, it is likely to bo asso- 
 ciated with other symptoms of hysteria. The paroxysms remit 
 and recur and do not go on to a fatal termination. 
 
 How is strychnine-poisoning to he distinguished from tetanus ? 
 
 Strychnine-poisoning gives rise to some of the manifestations 
 of tetanus. If trismus develops in strychnine-poisoning, it does 
 so late ; in tetanus, it is one of the first symptoms. 
 
 The convulsions of strychnine-poisoning are intermittent, but 
 may be induced by external irritation ; those of tetanus are 
 continuous, with paroxysmal exacerbations : inquiry into the 
 history of the case may elicit important evidence. 
 
 How are hemorrhage into the spinal memhranes and tetanus 
 to he differentiated ? 
 Meningeal hemorrhage is sudden, tetanus gradual, in onset. 
 Pain is a more prominent symptom in hemorrhage than in 
 tetanus. Trismus is wanting in hemorrhage ; it is characteristic 
 of tetanus. Spasm is constant in tetanus, with exacerbations ; 
 intermittent in meningeal hemorrhage. 
 
 How are acute spinal meningitis and tetanus to he differ- 
 entiated ? 
 
 Meningitis sets in abruptly with a chill, followed by elevation 
 of temperature ; tetanus is of gradual development, usually 
 after an injury, and is at the outset unattended with elevation 
 of temperature. Trismus is characteristic of tetanus, but ex- 
 ceptional in meningitis. 
 
 The convulsions of tetanus are excited by slight peripheral 
 irritation ; the muscular contractions of meningitis are induced 
 by efibrts at movement. 
 
 Tetanus is far more commonly fatal than is meningitis. Motor 
 and sensory impairment are common sequelae of meningitis. 
 
TETANY. 349 
 
 Tetany, 
 
 What is the etiology of tetany ? 
 
 Tetany is most common in infancy and early adult life, when 
 males are more prone to the disease than females. Occurring 
 later in life, females are affected in larger proportion. In some 
 cases, an hereditary influence can be made out. In many, 
 diarrhea is an exciting cause. In others, the disease has been 
 preceded by one of the acute infectious diseases. Pregnant or 
 nursing women seem especially predisposed. The disease has 
 been observed to develop in a considerable number of cases fol- 
 lowing removal of the thyroid gland. It has also been seen in 
 association with dilatation of the stomach. In children it is 
 often associated with rachitis, laryngismus stridulus, carpo-pedal 
 spasm and convulsions. Other possible causes are exposure to 
 cold and blows and injuries. Epidemics of the disease have 
 been observed. 
 
 What are the symptoms of tetany? 
 
 Tetany is an affection characterized by muscular spasm, of 
 symmetrical distribution, which usually begins and is most 
 marked in the extremities. 
 
 The spasm may be continuous, remittent or intermittent. 
 
 A paroxysm may be induced by compression of the vessels 
 and nerves of a part. 
 
 At the onset of the attack, there may be headache, vomiting, 
 spinal pain, numbness and tingling. There may be moderate 
 elevation of temperature. 
 
 In the intervals between paroxysms, the mechanical excita- 
 bility and electric irritability of nerve and muscle are height- 
 ened. The disease may continue for a period ranging from a 
 few days to several months. 
 
 Cases in which the spasm is intermittent are longer in dura- 
 tion than those in which the spasm is continuous. 
 
 How are tetany and tetanus to be distinguished ? 
 
 The spasm of tetany is more likely than that of tetanus to 
 be intermittent. Trismus is an early symptom of tetanus ; if 
 
350 ESSENTIALS OF DIAGNOSIS. 
 
 it occurs at all in tetany, it appears late. Tiie participatioH of 
 the extremities in the spasm is a feature of tetany. 
 
 Hydrophobia. 
 
 What are the clinical features of hydrophobia? 
 
 Hydrophobia results from the inoculation of man with rabies 
 of animals. The infection is usually transmitted by the saliva 
 of a rabid beast, as a dog, a cat, a fox, or a wolf, through 
 a bite or a preexisting wound. The period of incubation of 
 hydrophobia is extremely variable, but is on an average from 
 six to ten weeks. During this time, the primary wound may 
 have healed, and no symptom have been present. Local 
 pain may be perceived preceding the development of the dis- 
 ease proper, with the onset of which there are a sense of 
 malaise, mental depression and slight difficulty in swallowing. 
 Sleep is impaired and there may be respiratory spasm. The 
 stomach now becomes intolerant, rejecting everything intro- 
 duced. The muscular spasm extends and cutaneous hyperes- 
 thesia becomes manifest. External stimuli readily induce 
 convulsions. The mental distress becomes intense. The tem- 
 perature is elevated. Priapism may occur. Albumin and 
 sugar are sometimes found in the urine. Ultimately, paralytic 
 phenomena may supervene. Death may result from exhaus- 
 tion, by reason of the inability to retain food, and the violence 
 of the convulsions ; from suffocation, as a result of respiratory 
 spasm ; or from heart-failure. 
 
 How are lyssophobia or pseudo-hydrophobia and true hydro- 
 phobia to be differentiated? 
 
 Persons who have been bitten by animals, rabid or not, 
 develop a state of fear and dread, sometimes difficult to dis- 
 tinguish from true hydrophobia. Usually, however, the laryn- 
 geal and pharyngeal spasm characteristic of hydrophobia is 
 wanting, while judicious moral assurance may cause a dissipa- 
 tion of the symptoms. 
 
EXOPHTHALMIC GOITER.. 351 
 
 How are hydrophobia and tetanus to be differentiated? 
 
 In hydrophobia there is the history of a bite, with a long period 
 of incubation ; in tetanus of wound-infection with earth, and a 
 short period of incubation. In hydrophobia, respiratory and 
 pharyngeal spasm is an early manifestation ; in tetanus, trismus 
 is among the first symptoms. In the former all food is rejected ; 
 in the latter, if food can be introduced into the mouth, there is 
 no difficulty of retention. Tetanus does not present the inten- 
 sity of mental distress and disturbance encountered in hydro- 
 phobia. 
 
 Aural Vertigo— Labyrinthine Vertigo. 
 
 What is aural vertigo ? 
 
 Meniere's disease^ aural or lahyrinlhine vertigo^ is an affection 
 dependent upon a pathologic condition of the terminal fibers 
 of the auditory nerve in the labyrinth. The disease of the 
 labyrinth may be inflammatory, gouty, syphilitic or degenera- 
 tive. The symptoms occasioned are impairment of hearing, 
 tinnitus aurium and vertigo. The last is aggravated in parox- 
 ysms, in which in addition there are nausea and vomiting, with 
 pallor of the face and cold sweats. The patient may fall to 
 the ground and the vertigo be so intense that he is temporarily 
 unable to arise. 
 
 How are epilepsy and aural vertigo to be differentiated ? 
 
 Epilepsy is, and aural vertigo is not, attended with muscular 
 spasms and loss of consciousness. In the intervals between 
 the paroxysms of aural vertigo some degree of dizziness persists 
 and there are also impairment of hearing and tinnitus aurium, 
 which are not accompaniments of epilepsy. 
 
 Exophthalmic Goiter. 
 
 What are the sjrmptoms of exophthalmic goiter ? 
 
 Exophthalmic goiter, also called Graves's disease and Basedow's 
 disease, is an affection characterized by increased frequency of 
 action and palpitation of the heart, protrusion of the eyeballs 
 
352 
 
 ESSENTIALS OF DIAGNOSIS. 
 
 and enlargement of the thyroid gland. Its pathology is not yet 
 established. It is clinically a vaso-motor ataxia, and has long 
 been considered a disease of the sympathetic nervous system, 
 especially of the cervical ganglia. There is growing evidence, 
 however, that the disease is dependent upon a lesion of the floor 
 of the fourth ventricle, with which many of the symptoms would 
 harmonize. 
 
 The disease is more common in females than in males, and 
 in adult life than at any other period. In some cases a neuro- 
 pathic heredity can be traced. The exciting cause is usually 
 mental emotion, shock, grief, anxiety. 
 
 Fig. 53. 
 
 
 
 ft 
 
 
 Exophthalmic Goiter. Defective descent of the upper lids on looking down. 
 (After Wilks.) 
 
 Palpitation of the heart, associated with or independent of 
 an organic lesion, is one of the earliest symptoms. The action 
 
EXOPHTHALMIC GOITEK. 353 
 
 of the heart is increased both in frequency and in energy, and 
 is often extremely irregular. The tachycardia and the palpita- 
 tion may reach a high degree of intensity, the pulse sometimes 
 exceeding 140 in the minute. Tliere may also be evident pulsa- 
 tion in the arteries and a bruit in the vessels of the neck. 
 
 Anemia is often an early symptom. In the progress of the 
 case, the eyes protrude and the thyroid gland becomes enlarged. 
 
 The exophthalmos and the goiter may each be symmetrical 
 or unilateral ; the protrusion and the enlargement, respectively, 
 are not uncommonly greater upon the right side. In some 
 cases, the upper lids are retracted, displaying the sclerotic, and 
 do not follow the eyes when the glance is depressed. This lag- 
 ging of the lids is called " Von Graefe's sign." 
 
 Over the enlarged thyroid gland a blowing systolic bruit is 
 visually to be heard. The goiter frequently pulsates ; it is at first 
 usually elastic ; ultimately it may become firm. The appearance 
 of the goiter may be intermittent ; when permanent, the en- 
 largement may undergo spontaneous variation. 
 
 Among other symptoms are nystagmus, tremor of the ex- 
 tremities, an abnormal sense of heat, flushing and perspiration. 
 It has been stated that the bodily electric resistance is dimin- 
 ished. Various cutaneous affections have been noted. In 
 women, menstruation is commonly deranged. 
 
 In some cases, albuminuria, in others, diabetes has been 
 observed. Hemoptysis, hematuria, hematemesis and other 
 hemorrhages, and sometimes purpura, occur. Mental changes 
 are not uncommon. Mania is an occasional complication. 
 
 Exophthalmic goiter is not directly fatal. Spontaneous re- 
 covery is possible. Temporary exacerbations take place. 
 
 What are the features distinguishing exophthalmic goiter 
 from simple goiter? 
 
 Occasionally, the enlargement of the thyroid gland may be 
 the first symptom of exophthalmic goiter observed. The bruit 
 heard over the gland in exophthalmic goiter is wanting in the 
 simple enlargement. Then, investigation will disclose the exist- 
 ence of palpitation and examination will reveal increased rapidity 
 of the action of the heart, with the development, in the progress 
 23 
 
354 ESSENTIALS OF DIAGNOSIS. 
 
 of the case, of protrusion of the eyes and the other symptoms 
 of exophthahnic goiter. Even before the heart is much dis- 
 turbed, there may be a tendency to flushing of the face, and occa- 
 sionally red blood-cells may be found in the urine. 
 
 Cretinism. 
 
 What is cretinism ? 
 
 Cretinism is a morbid condition, occurring endemically or 
 sporadically and manifested by characteristic mental and phys- 
 ical abnormalities. The body is undersized ; the head is broad, 
 but shallow ; the eyes are far apart and the nose is flat ; the lips 
 are thick ; the tongue is sometimes enlarged ; the hands are 
 broad and spade-like ; the skin is dry, rough and wrinkled ; the 
 aspect is that of age ; the hair is straight and stift"; the intelli- 
 gence is feeble, even to the degree of idiocy ; masses of fat 
 sometimes appear in the posterior triangles of the neck ; the 
 thyroid gland is often enlarged ; it is sometimes wanting. In a 
 number of cases premature ossification of the occipito-sphenoidal 
 suture has been found. Some members of families in which 
 cretinism existed have presented goiters. 
 
 Myxedema. 
 
 What are the clinical features of myxedema ? 
 
 Myxedema is a peculiar condition, apparently more common 
 in women than in men, in which a mucoid substance is found 
 in the subcutaneous tissue in various parts of the body, in asso- 
 ciation with anemia, atrophy of the thyroid gland and mental 
 impairment. The condition has been termed sporadic cretinoid- 
 ism in distinction from sporadic cretinism. 
 
 The patient becomes dull, stupid and irritable ; sjyeech thick 
 and hesitant ; the memory enfeebled. Movement is awkward and 
 clumsy, and there is undue readiness of fatigue. Sendbility is 
 impaired, while abnormal sensations of heat and of chilliness 
 are perceived. There may be visible flushing. 
 
 The heart is slow and feeble, the respiration sluggish, with 
 
AKROMEGALTA. 355 
 
 breathlessness on exertion ; the iemperature is, as a rule, sub- 
 normal ; the appetiteifi impaired, and taste is deranged ; the diges- 
 tion is enfeebled ; the nutrition is poor ; the urine is altered in 
 quantity, and late in the disease may be albuminous. 
 
 The face is pallid and puffy, and of roundish ("full-moon") 
 outline ; the expression is dull and stupid ; the thyroid gland is 
 diminutive or absent. The skin is thickened, dry, rough, some- 
 times scaly, somewhat translucent in appearance, of a doughy 
 consistence, but with a certain degree of elasticity ; there is no 
 edema and no pitting on pressure ; perspiration is diminished. 
 The hands, if affected, become square or "spade-shaped ;" the 
 fingers clubbed ; and the nails brittle and distorted. The hair 
 is dry and harsh and brittle, and may fall out. 
 
 In the progress of the case, mental and physical failure 
 increase, irritability becomes marked, hallucinations develop, 
 stupor sets in and death may take place in coma, from exhaus- 
 tion or from uremia. 
 
 A condition resembling myxedema, occurring in circumscribed 
 areas in various situations— cac/iexm strumipriva, has been in- 
 duced in man and in animals by removal of the thyroid gland. 
 
 How are myxedema and scleroderma to be differentiated? 
 
 In a given case the diagnosis between myxedema and sclero- 
 derma may be exceedingly difficult. In scleroderma, however, 
 the skin is brawny and indurated ; not elastic and doughy, as 
 in myxedema. Jn scleroderma, too, the thyroid gland remains 
 unafiected, while the mental phenomena of myxedema are 
 wanting. The histologic changes in the two conditions differ : 
 in scleroderma, there is hyperplasia of the subcutaneous con- 
 nective tissue ; in myxedema, there is a mucoid deposit or 
 degeneration. 
 
 Akromegalia. 
 
 What is akromegalia ? 
 
 Akromegalia or Marie^s disease is a morbid condition that has 
 been described by Marie, which is especially characterized by 
 hypertrophy of the bones of the hands and feet and face. 
 
356 
 
 ESSENTIALS OP DIAGNOSIS. 
 
 Fig 
 
 Some of the fibro-cartilages, as those of the ear and larynx, also 
 become enlarged. The related soft parts undergo coi'responding 
 
 enlargement. There develop 
 decided weakness and slight 
 muscular atrophy. The inter- 
 osseous spaces become exagger- 
 ated. Owing to the enlarge- 
 ment of the inferior maxillary 
 and the frontal bones, the face 
 assumes a peculiarly elongated, 
 elliptical outline. The hyper- 
 trophy of the nasal bones gives 
 the nose a thickened appearance. 
 The enlargement of the malar 
 bones increases the normal tem- 
 poral fossEe. The enlargement 
 of the frontal sinuses and the 
 projection of the superciliary 
 ridges give the forehead a re- 
 treating appearance. The chin 
 is prominent and the lower teeth 
 project beyond the plane of the 
 upper teeth. The tongue is en- 
 larged and thickened. The lips 
 and ej'elids may also be thick- 
 ened. The enlargement of the 
 hands involves their width more 
 than their length. The nails 
 may present longitudinal stria- 
 tion. There are increased thirst, 
 usuallv polyuria, and sometimes 
 glycosuria. The appearance may 
 be cachectic, the conjunctivEe 
 icteric. There is commonly 
 spinal curvature, usually a cer- 
 vico-dorsal kyphosis, with a 
 compensatory lumbar lordosis. 
 The abdomen may be protuber- 
 
 Akromegalia. (After Marie.) 
 
AKROMEGALIA. 357 
 
 ant. The stature is often increased. The skin maj'- be pig- 
 mented. There may be severe spontaneous pain ; headache is 
 common. Tliere may be somnolence. In some cases, varicose 
 veins and hemorrlioids have been observed. In individual cases, 
 there has been hemianopsia, limitation of the visual fields, blind- 
 ness or deafness. In women, menstruation is usually deranged. 
 The thyroid gland may be atrophied or hypertrophied. The 
 disease appears most commonly in young adults and is chronic 
 in course. 
 
 How does akromegalia differ from osteitis deformans, Paget's 
 disease ? 
 
 The disease called by Sir James Paget osteitis deformans 
 more especially involves the long bones, which, while they 
 become enlarged, also become distorted, with resulting defor- 
 mities ; akromegalia displays a predilection for the small bones 
 of the hands and feet and face, and is unattended with distor- 
 tion and deformity. In osteitis deformans, as a result of the 
 enlargement of the cranial bones, the face presents a triangular out- 
 line, with the base above and the apex below ; in akromegalia 
 the enlargement of the hones of the face occasions a characteristic 
 
 Fig. 55. 
 
 1 2 3 
 
 Outline of the Face, 1, in myxedema; 2, in akromegalia ; 3, in osteitis deformans. 
 
 (Marie.) 
 
 elongated, elliptical outline. In akromegalia there may be an 
 increase in stature ; in osteitis deformans there is more likely to 
 be a diminution. The former appears early, .between fifteen 
 and thirty-five ; the latter, later, after forty. Akromegalia may 
 appear in several members of one family ; osteitis deformans 
 
858 ESSENTIALS OF DIAGNOSIS. 
 
 does not. The invasion of akromegalia is symmetrical ; that of 
 osteitis deformans is indiscriminate. 
 
 How are akromegalia and myxedema to be differentiated? 
 
 The enlargement that appears in myxedema is dependent 
 upon changes in the skin and subcutaneous soft structures ; 
 while the enlargement of akromegalia is due to a hyperplasia 
 of bone. In the latter, the skin is healthy and mobile ; in the 
 former, it is thickened and adherent. In myxedema, in contrast 
 to akromegalia, the hands and feet may be entirely uninvolved. 
 In myxedema the face is almost round, "moon-shaped;" in 
 akromegalia it is elUptical and elongated, with a prominent lower 
 jaw, prominent malar processes and prominent nasal bones. 
 
 How is akromegalia to be discriminated from pulmonary hyper- 
 trophic osteo-arthropathy ? 
 
 Under a name signifying '"'■ IxypertropMc disease of hones and 
 joints in association with pulmonary lesion,''^ Marie has discrimi- 
 nated a group of cases presenting, in connection with empyema, 
 pleurisy, chronic bronchitis, tuberculous disease of the lungs, 
 and possibly other disease of the lungs and their appendages, 
 skeletal changes somewhat resembling those of akromegalia. 
 
 There are kyphosis, enlargement of the distal epiphyses of 
 the bones of the forearm and of the leg, and, most characteristic, 
 an enlargement in all directions of the distal phalanges of both 
 fingers and toes, with the peculiar curvation of the nails that 
 gives rise to the so-called Hippocratic finger. The lower jaw 
 projects, but not so markedly as in akromegalia, and the other 
 facial bones are not enlarged ; on the contrarj^, the features are 
 usually sharpened. 
 
 There is commonly dulness on percussion over the manubrium 
 sterni, supposably dependent upon the persistence of the thymus 
 gland. The thyroid gland may be wanting. 
 
 Akromegalia. Pulmonary osteo- arthropathy. 
 
 Stature heightened. Stature not heightened. 
 
 Cervico-dorsal kyphosis. Dorso-lumhar kyphosis. 
 
 Projection of abdomen. No projection of abdomen. 
 
 Enlargement of face. No enlargement of face, 
 
 Macroglpssia. Tongue not enlarged. 
 
AKROMEGALIA, 
 
 359 
 
 Akromegalia. 
 Hands broadened — spade-like. 
 Digits uniformly enlarged. 
 Nail short, broad, flat, not reach- 
 ing end of finger. 
 
 Epiphyseal enlargements uncom- 
 mon. 
 
 Polyuria and disturbance of special 
 senses. 
 
 Pulmonary osteo-arthropathy. 
 
 Hands lengthened — not spade-like. 
 
 Terminal phalanges enlarged. 
 
 Hippocratic nail — curved, longi- 
 tudinally striated, overlapping 
 finger, " parrot-beak-like." 
 
 Epiphyseal enlargements the rule. 
 
 Intra-thoracic disease. 
 
INDEX. 
 
 A BORTIVE typhoid fever, 38 
 Xi Abscess, cerebral, 322 
 Abscess, cerebral, differentiated 
 from — 
 cerebral meningitis, 323 
 tumor of the brain, 323 
 Abscess, genito-urinary, 249 
 Abscess, lumbar, differentiated 
 from — 
 perityphlitis, 210 
 typhlitis, 210 
 Abscess of the kidney, 268 
 Abscess of the kidney differentiated 
 
 from perirenal abscess, 269 
 Abscess of the liver, 228 
 Abscess of the liver differentiated 
 from — 
 actinomycosis of the liver, 229 
 carcinoma of the liver, 229 
 hydatid cyst of the liver, 235 
 occlusion of thebiliary passages, 
 
 228 
 pleuritic effusion, 156 
 Abscess of the mediastinum differ- 
 entiated from aneurism of the 
 aorta, 132 
 Abscess of the right ovary differen- 
 tiated from — 
 perityphlitis, 210 
 typhlitis, 210 
 Abscess of the spleen differentiated 
 
 from pleuritic effusion, 156 
 Abscess, perirenal, 269 
 Abscess, perirenal, differentiated 
 
 from abscess of the kidney, 269 
 Abscess, pulmonary, differentiated 
 from — 
 bronchiectasis, 160 
 pulmonary gangrene, 168 
 pulmonary infarction, 167 
 pulmonary tuberculosis, 17() 
 Abscess, retro-pharyugeal, 194 
 
 Abscess, retro-pharyngeal, differen- 
 tiated from membranous croup, 
 144 
 
 Acetone in the urine, tests for the 
 presence of, 260 
 
 Acid, hydrochloric, free, in the gas- 
 tric contents, tests for, 196 
 
 Acids, biliary, in the urine, 247 
 
 Actinomycosis, 83 
 
 Actinomycosis of the liver differen- 
 tiated from abscess of the liver, 
 229 
 
 Action of the heart. 111 
 
 Acute alcoholism, 335 
 
 Acute anterior poliomyelitis, 290 
 
 Acute ascending paralysis, 291 
 
 Acute bronchitis, 157 
 
 Acute bulbar palsy, 296 
 
 Acute catarrhal pharyngitis, 188 
 
 Acute croupous pneumonia, 163 
 
 Acute dysentery, 206 
 
 Acute edema of the larynx, 139 
 
 Acute endocarditis, 128 
 
 Acute enteritis, 203, 204 
 
 Acute gastric catarrh, 197 
 
 Acute gastritis, 197 
 
 Acute general disease differentiated 
 from cerebral meningitis, 316 
 
 Acute gout, 91 
 
 Acute hepatitis, 225 
 
 Acute indigestion, 197 
 
 Acute infective jaundice, 62 
 
 Acute intestinal catarrh, 203 
 
 Acute laryngitis, 138 
 
 Acute mania, 317, 336 
 
 Acute miliary tuberculosis, 177 
 
 Acute nasal catarrh, 136 
 
 Acute nephritis, 265 
 
 Acute pancreatitis, 241 
 
 Acute pericarditis, 127 
 
 Acute peritonitis, 219 
 
 Acute phlegmonous pharyngitis, 189 
 (361) 
 
362 
 
 INDEX. 
 
 Acute pleurisy, 153 
 
 Acute rheumatism, 87 
 
 Acute synovitis, b8 
 
 Acute tuberculous laryngitis, 140 
 
 Acute tuberculous pharyngitis, 189 
 
 Acute yellow atrophy of the liver, 
 
 226 
 Addison's disease, 107 
 Ague-cake, 57 
 Ague, dumb, 56 
 
 Air-passages, obstruction of, differ- 
 entiated from croup, 146 
 Akromegalia, 355 
 Akromegalia differentiated from — 
 myxedema, 358 
 osteitis deformans or Paget's 
 
 disease, 357 
 pulmonary hypertrophic osteo- 
 arthropathy, 358 
 Akromikria, 314 
 Albumin in urine, tests for, 250 
 Albuminuria, 250 
 Alcoholic intoxication differentiated 
 
 from cerebral hemorrhage, 326 
 Alcoholism, acute, differentiated 
 
 from sunstroke, 335 
 Ambulatory typhoid fever, 38 
 Amj'loid disease of the liver, 231 
 Amyloid disease of the liver differ- 
 entiated from — 
 carcinoma of the liver, 232 
 cirrhosis of the liver, 231 
 Amj'loid kidney, 266 
 Amyotrophic lateral sclerosis, 292 
 Analgesic panaris, 312 
 Anamnesis, 19 
 Anemia, 86 
 Anemia, cerebral, 320 
 Anemia differentiated from cerebral 
 
 tumor, 331 
 Anemia, idiopathic, 98 
 Anemia, infantile pseudo-leukemic, 
 
 103 
 Anemia, lymphatic, 101 
 Anemia of thespinal cord, 287 
 Anemia, pernicious, 98 
 Anemia, simple, 97 
 Anemia, splenic. 97 
 Anesthesia, 273 ' 
 Anesthetic leprosy, 314 
 Aneurism, intracranial, 331 
 Aneurism of the aorta differentiated 
 
 from abscess of the mediastinum, 
 
 132 
 
 Aneurism of the aorta differentiated 
 from — 
 aortic incompetency, 132 
 dilatation of the auricle, 132 
 intra-thoracic tumor, 131 
 
 Aneurism, thoracic, 131 
 
 Angina, 188 
 
 Angina pectoris, 118 
 
 Angina pectoris differentiated from — 
 intercostal neuralgia, 119 
 tachj'cardia, 117 
 
 Angina, ulcero-membranous, 192 
 
 Anthrax, 81 
 
 Aorta, aneurism of, 131, 132 
 
 Aortic incompetency or regurgita- 
 tion, 124 
 
 Aortic obstruction, 123 
 
 Apex-beat of the heart, 109 
 
 Aphonia, hysterical, 139 
 
 Aphthous stomatitis, 184 
 
 Appendicitis, 209 
 
 Appendicitis, differential diagnosis 
 of, 210 
 
 Arachnitis, 315 
 
 Ardent fever, 31 
 
 Arsenical poisoning differentiated 
 from Asiatic cholera, 50 
 
 Arterio-capillary fibrosis, 132 
 
 Arthritic muscular atrophy, 299 
 
 Arthritis deformans, 94 
 
 Arthritis, rheumatoid, 94 
 
 Arthritis, syphilitic, 89 
 
 Ascaris lumbricoides, 217 
 
 Asiatic cholera, 49 
 
 Asphyxia differentiated from cere- 
 bral hemorrhage, 327 
 
 Asphyxia, local, 133 
 
 Asthma, l83 
 
 Asthma differentiated from — 
 an asthmatoid condition, 183 
 chronic edema of the larynx, 140 
 laryngismus stridulus, 141 
 paralysis of the diaphragm, 184 
 whooping-cough, 184 
 
 Ataxia, 272, 273 
 
 Ataxia, Friedreich's, 304 
 
 Ataxia, locomotor, 300 
 
 Ataxic paraplegia, 303 
 
 Ataxic paraplegia, hereditary, 304 
 
 Atelectasis differentiated from ca- 
 tarrhal pneumonia, 163 
 
 Atrophy, muscular, arthritic, 299 
 
 Atrophy, muscular, progressive, 292, 
 293 
 
INDEX. 
 
 363 
 
 Atrophy, muscular, progressive, dif- 
 ferentiated from — 
 acute anterior poliomyelitis, 
 
 295 
 cervical pachymeningitis, 286 
 chronic myelitis, 290 
 simple idiopathic muscular 
 
 atrophy, 299 
 syringomelia, 312 
 Atrophy, muscular, simple idio- 
 pathic, 298 
 Atrophy, muscular, simple idio- 
 pathic, diflerentiated from — 
 progressive muscular atrophy, 
 
 299 
 pseudo-hypertrophic muscular 
 paralysis, 299 
 Atrophy, yellow, acute, of the liver, 
 
 226 
 Atrophy, yellow, acute, of the liver 
 differentiated from — 
 catarrhal jaundice, 237 
 phosphorus-poisoning, 227 
 typhoid fever, 227 
 yellow fever, 61 
 Aural vertigo, 351 
 Auricle, dilatation of, 120 
 Auscultation, 150 
 Auscultation of the heart-sounds, 
 
 110 
 Auscultatory percussion, 150 
 Autumnal catarrh, 137 
 
 BASEDOW'S disease, 351 
 Beri-heri, 276 
 
 Bile-duct, common, compression of, 
 237 
 
 Biliary acids in the urine, 247 
 
 Biliary calculi, 238 
 
 Biliary passages, carcinoma of, 239 
 
 Biliary passages, occlusion of, 228 
 
 Black tongue, 188 
 
 Bladder, neoplasms of, 262 
 
 Blood, 95 
 
 Blood-casts of the uriniierous 
 tubules, 253 
 
 JJlood in disease, 104 
 
 Boettger's test for the presence of 
 sugar in the urine, 259 
 
 Bone, disease of, differentiated from 
 neuritis, 276 
 
 Bothriocephalus latus, 216 
 
 Bowel, invagination or intussuscep- 
 tion of, 212 
 
 Bowel, perforation of, in typhoid 
 
 fever, 40 
 Break-bone fever, 76 
 Breathing, superior Intercostal, dif- 
 ferentiated from paralysis of the 
 phrenic nerve, 281 
 Bronchial glands, tuberculosis of, 
 
 177 
 Bronchiectasis, 160 
 Bronchiectasis differentiated from — 
 catarrhal pneumonia, 160 
 pulmonary abscess, 160 
 pulmonary gangrene, 160 
 pulmonary tuberculosis, 176 
 Bronchitis, acute, 157 
 Bronchitis, acute, differentiated from 
 
 acute miliary tuberculosis, 158 
 Bronchitis, capillary, 161 
 Bronchitis, capillary, differentiated 
 from — 
 acute miliary tuberculosis, 161 
 catarrhal pneumonia, 162 
 Bronchitis, chronic, 158 
 Bronchitis, chronic, differentiated 
 from — 
 interstitial pneumonitis, 159 
 pulmonary tuberculosis, 159 
 Bronchitis, plastic or fibrinous, 159 
 Bronchitis, putrid, 159 
 Bronchophony, 152 
 Broncho-pneumonia, 162 
 Brow-ague, 57 
 
 pACHEXIA, malarial, 56 
 
 \J Cachexia strumipriva, 355 
 
 Calculi, biliary, 238 
 
 Calculi, biliary, differentiated from — 
 
 carcinoma of the biliary pass- 
 ages, 239 
 
 catarrhal jaundice, 237 
 Calculus, renal, 264 
 Calculus, vesical, 262 
 Cancrum oris, 186 
 Capillary bronchitis, 161 
 Caput Medusas, 230 
 Carcinoma of the biliary passages 
 differentiated from biliary calculi, 
 239 
 Carcinoma of the cecum differenti- 
 ated from — 
 
 perityphlitis, 211 
 
 typhlitis, 211 
 Carcinoma of the intestine, 213 
 Carcinoma of the liver, 233 
 
364 
 
 INDEX. 
 
 Carcinoma of the liver differentiated 
 from — 
 abscess of the liver, 229 
 amyloid disease of the liver, 232 
 carcinoma of the omentum, 233 
 carcinoma of the stomach, 233 
 Carcinoma of the omentum differen- 
 tiated from — 
 carcinoma of the liver, 233 
 carcinoma of the stomach, 202 
 Carcinoma of the stomach, 200 
 Carcinoma of the stomach differ- 
 entiated from — 
 carcinoma of the liver, 233 
 carcinoma of the omentum, 203 
 carcinoma of the pancreas, 202 
 chronic gastritis, 203 
 sarcoma of the omentum, 202 
 ulceration of the stomach, 201 
 Carcinoma, pulmonary, differenti- 
 ated from pulmonary tubercu- 
 losis, 175 
 Cardiac impulse, 109 
 Caries of the vertebrse differentiated 
 from tumor of thespinal cord, 311 
 Casts of the uriniferoue tubules, 251 
 Catarrh, epidemic, 32 
 Catarrh, gastric, acute, 197 
 Catarrh, gastric, chronic, 198 
 Catarrh, gastro-intestinal, differenti- 
 ated from pernicious malarial 
 fever, 58 
 Catarrh, intestinal, acute, 203 
 Catarrh, intestinal, chronic, 206 
 Catarrhal croup, 1+2 
 Catarrhal fever, 32 
 Catarrhal jaundice, 237, 238 
 Catarrhal pharyngitis, acute, 188 
 Catarrhal pneumonia, 162 
 Catarrhal stomatitis, 184 
 Cavity, pulmonary, differentiated 
 
 from pneumothorax, 182 
 Cecum, carcinoma of, 211 
 Cerebellar tumor, 302, 304 
 Cerebral abscess, 322 
 Cerebral anemia, 320 
 Cerebral congestion, 325 
 Cerebral disease differentiated from 
 
 epilepsy, 342 
 Cerebral disease, paralysis of, differ- 
 entiated from the paralysis of hys- 
 teria, 345 
 Cerebral embolism, 328 
 Cerebral functions, alterations in, in 
 disease of the nervous system, 275 
 
 Cerebral hemorrhage, 323 
 
 Cerebral hyperemia, 321 
 
 Cerebral membranes, hemorrhage 
 
 into, 318 
 Cerebral meningitis, 315 
 Cerebral softening, 327 
 Cerebral thrombosis, 329 
 Cerebral tumor, 330 
 Cerebritis, 322 
 
 Cerebritis differentiated from cere- 
 bral meningitis, 322 
 Cerebro-spinal fever, 45 
 Cerebro-spinal fever differentiated 
 from — 
 
 cerebral meningitis, 317 
 
 tetanus, 47 
 
 torticollis, 47 
 
 typhoid fever, 48 
 
 typhus fever, 47 
 
 variola, 48 
 
 yellow fever, 48 
 Cerebro-spinal sclerosis, 305 
 Cervical pachymeningitis, 286 
 Charbon, 81 
 Chickenpox, 73 
 Chickenpox differentiated from — 
 
 measles, 73 
 
 smallpox, 73 
 
 varioloid, 73 
 Chlorosis, 98 
 Cholangitis, 236 
 Cholecystitis, 236 
 Cholera Asiatica, 49 
 Cholera Asiatica differentiated from 
 
 cholera morbus, 50, 205 
 Cholera differentiated from perni- 
 cious malarial fever, 58 
 Cholera infantum, 206 
 Cholera infectiosa, 49 
 Cholera morbus, 205 
 Cholera morbus differentiated from 
 
 cholei-a Asiatica, 60, 205 
 Cholera nostras, 205 
 Chorea, 340 
 Chorea differentiated from epilepsy, 
 
 343 
 Chorea, hereditary, 341 
 Chorea, Huntingdon's, 341 
 Chronic bronchitis, 158 
 Chronic dysentery, 208 
 Chronic edema of the larynx, 140 
 Chronic enteritis, 206 
 Chronic gastric catarrh, 198 
 Chronic gastritis, 198 
 Chronic gout, 92 
 
INDEX. 
 
 365 
 
 Chronic interstitial nephritis, 266 
 
 Chi-onic intestinal catarrh, 206 
 
 Chronic laryngitis, 146 
 
 Chronic myelitis, 289 
 
 Chronic nephritis, 331 
 
 Chronic parenchymatous nephritis, 
 
 265 
 Chronic rheumatism, 90 
 Chronic tuberculosis of the larynx, 
 
 147 
 Chyluria, 253 
 Cirrhosis of the liver, 229 
 Cirrhosis of the liver diflferentiated 
 from — 
 amyloid disease of the liver, 2S1 
 catarrhal jaundice, 238 
 chronic perihepatitis, 236 
 Clavus hystericus, 344 
 Colic, hepatic, intestiual and renal, 
 
 differential diagnosis of, 239 
 Colic, intestinal, differentiated from 
 
 acute peritonitis, 220 
 Color of urine, 243 
 Coloring-matter, biliaiy, in urine, 
 
 246 
 Common membranous sore-throat, 
 
 192 
 Complications in disease, 22 
 Compression- myelitis diflerentiated 
 from hemorrhage into the spinal 
 cord, 310 
 Compression of the common bile- 
 duct differentiated from catarrhal 
 jaundice, 237 
 Compression, spinal, 309 
 Compression, spinal, differentiated 
 
 from chronic myelitis, 310 
 Confluent smallpox, 70 
 Congenital spastic paraplegia, 319 
 Congestion, cerebral, diflferentiated 
 
 from cerebral hemorrhage, 325 
 Congestion of the liver, 224 
 Congestion, pulmonary, differenti- 
 ated from croupous pneumonia, 
 166 
 Constitution of urine, 242 
 Constitutional signs, 19 
 Consumption, galloping, 169, 174 
 Continued fever, 30 
 Convulsion, 273 
 Cord, spinal, anemia of, 287 
 Cord, spinal, hyperemia of, 287 
 Coryza, 136 
 
 Coryza diflTerentiated from — 
 hay-fever, 138 
 intiuenza, 137 
 
 Cramp, writers', 339 
 Cretinism, 354 
 Cretinoidism, sporadic, 354 
 Croup, catarrhal, 142 
 Croup differentiated from obstruc- 
 tion of the air-passages, 145 
 Croup, membranous, 143 
 Croup, membranous, diflferentiated 
 from— 
 
 diphtheria, 80 
 
 retro-pharyngeal abscess, 144 
 
 spasmodic croup, 144 
 
 whooping-cough, 145 
 Croup, spasmodic, 142 
 Croup, . spasmodic, differentiated 
 from — 
 
 edema of the larynx, 143 
 
 laryngismus stridulus, 142 
 
 membranous croup, 144 
 Croupous enteritis, 205 
 Croupous pneumonia, 163 
 Cystitis, 249, 261 
 Cystitis differentiated from — 
 
 nephritis, 261 
 
 pyelitis, 263 
 
 DATA for diagnosis, 24 
 Deep reflexes, 274 
 Degeneration, fatty, of the heart, 
 
 121 
 Degeneration of the diaphragm, 281 
 Degeneration, reaction of, 274 
 Delirium tremens, 335 
 Delirium tremens diflferentiated 
 from — 
 acute mania, 336 
 cerebral meningitis, 336 
 Dengue, 76 
 
 Dengue differentiated from — 
 influenza, 77 
 scarlet fever, 77 
 Dextrocardia, 115 
 Diabetes insipidus, 256 
 Diabetes insipidus diflferentiated 
 from — 
 chronic interstitial nephritis, 257 
 diabetes mellitus, 261 
 hysterical polyuria, 257 
 Diabetes mellitus, 257 
 Diabetes mellitus diflferentiated 
 from — 
 diabetes insipidus, 261 
 Morvan's disease, 314 
 Diacetic acid in the urine, tests for 
 the presence of, 260 
 
366 
 
 INDEX. 
 
 Diaceturia, 260 
 Diagnosis, 17 
 
 Diagnosis by exclusion, 21 
 Diagnosis bj' the historical or em- 
 pirical method, 20 
 Diagnosis by the inductive method, 
 
 20 
 Diagnosis by the method of patho- 
 logical association, 20 
 Diagn,osis, data for, 24 
 Diagnosis, direct, 20 
 Diagnosis, discriminative or diflFer- 
 
 ential, 21 
 Diagnosis, physical, 147 
 Diaphragm, degeneration of, differ- 
 entiated from paralysis of the 
 phrenic nerve, 281 
 Diaphragm, inflammation of, dif- 
 ferentiated from paralysis of tlie 
 phrenic nerve, 281 
 Diaphragm, paralj'sis of, 184 
 Diaphragmatic hernia, 182 
 Differential diagnosis, 21 
 Digestion, duration of, 195 
 Digestive system, 184 
 Dilatation of the auricle differenti- 
 ated from aneurism of the aorta, 
 132 
 Dilatation of the heart, 120 
 Dilatation of the heart differentiated 
 from — 
 fatty degeneration of the heart, 
 
 121 
 hypertrophj' of the heart, 120 
 pericardial effusion, 121 
 Dilatation of the stomach, 199 
 Diphtheria, 77 
 
 Diphtheria differentiated from — 
 common membranous sore- 
 throat, 192 
 gangrenous sore-throat, 193 
 membranous croup, 80 
 scarlet fever, 78 
 stomatitis, 80 
 tonsillitis, 79 
 Diphtheroid throat, 192 
 Diplegia, 272 
 Direct diagnosis, 20 
 Discrete smallpox, 70 
 Discriminative diagnosis, 21 
 Disseminated neuritis, 276 
 Disseminated sclerosis, 305 
 Distention of tbe gall-bladder differ- 
 entiated from hydatid cyst of the 
 liver, 235 
 
 Drug-effects, 23 
 Dumb ague, 56 
 
 Duplication of the heart-sounds, 111 
 Duration of digestion, 195 
 Dysentery, acute, 206 
 Dysentery, acute, differentiated 
 from — 
 
 acute enteritis, 207 
 
 intussusception of the bowel, 207 
 
 typhoid fever, 207 
 Dj'sentery, chronic, 208 
 
 ECLA:MPSIA differentiated from 
 epilepsy, 3-13 
 Edema of the larynx, acute, 139 
 Edema of the larynx, chronic, 140 
 Edema of the larynx differentiated 
 from — 
 asthma, 140 
 spasmodic croup, 143 
 Edema, pulmonary, differentiated 
 
 from pneumonia, 166 
 Efficiency of the heart, 112 
 Effusion, pericardial, differentiated 
 from — 
 dilatation of the heart, 121 
 pleuritic effusion, 157 
 Effusion, pleural, differentiated 
 from — 
 pneumothorax, 182 
 pulmonary emphysema, 181 
 Effusion, pleuritic, differentiated 
 from — 
 abscess of the liver, 156 
 abscess of the spleen, 156 
 hydatid cyst of the liver, 155 
 hydrothorax, 157 
 pericardial effusion, 157 
 Egophony, 152 
 Electric reactions, alterations in, in 
 
 disease, 274 
 Embolism, cerebral, 328 
 Embolism, cerebral, differentiated 
 
 from cerebral hemorrhage, 328 
 Emphysema, pulmonary, 179 
 Emphysema, pulmonary, differenti- 
 ated from — 
 pleural effusion, 181 
 pneumothorax, 180 
 Empirical method, diagnosis by, 20 
 Emprosthotonos, 347 
 Empyema, 153 
 Empyema, pulsatory, 153 
 Endemic hematuria, 256 
 
INDEX. 
 
 ^67 
 
 Endocardial murmurs, 126 
 Endocarditis, 128 
 
 Endocarditis, acute, difi'ereutiated 
 from — 
 
 acute pericarditis, 129 
 
 valvular disease of the heart, 
 128 
 Endocarditis, mycotic, 129 
 Enteric fever, 35 
 Enteritis, acute, differentiated 
 from — 
 
 acute dysentery, 207 
 
 acute peritonitis, 220 
 Enteritis, catarrhal, acute, differen- 
 tiated from typhoid fever, 204 
 Enteritis, chronic, 206 
 Enteritis, croupous, 205 
 Enteritis, membranous, 205 
 Enteritis, mucous, acute, 203 
 Eosinophile leukocytes, 96 
 Ephemeral fever, 31 
 Epidemic catarrh, 32 
 Epidemic cerebro-spinal meningitis, 
 
 45 
 Epilepsy, 341 
 Epilepsy differentiated from — 
 
 aural vertigo, 351 
 
 cerebral disease, 342 
 
 cerebral tumor, 331 
 
 chorea, 343 
 
 eclampsia, 343 
 
 hysteria, 345 
 
 syncope, 343 
 
 uremia, 267, 343 
 Epilepsy, essential, 342 
 Epilepsy, idiopathic, 343 
 Epilepsy, major, 342 
 Epilepsy, minor, 342 
 Epistaxis, 136 
 Epithelial casts of the uriniferous 
 
 tubules, 252 
 Equinia, 80 
 Erysipelas, 74 
 Erysipelas differentiated from — 
 
 erythema, 75 
 
 herpes zoster, 75 
 
 scarlet fever, 74 
 
 smallpox, 75 
 Erythema differentiated from ery- 
 sipelas, 75 
 Esophagismus, 195 
 Esophagus, 194 
 Esophagus, stricture of, 194 
 Essential epilepsy, 342 
 Essential fever, 30 
 
 Examination of urine, 243 
 Exclusion, diagnosis bj", 31 
 Exophthalmic goiter, 351 
 Exophthalmic goiter differentiated 
 from — 
 
 simple goiter, 353 
 
 tachycardia, 117 
 
 1 RACIAL nerve, paralysis of, 279 
 ' Family history, 19 * 
 
 Farcy, 80 
 
 Fatty casts of the uriniferous tubules, 
 253 
 
 Fatty degeneration of the heart dif- 
 ferentiated from dilatation of the 
 heart, 121 
 
 Fatty infiltration of the liver, 230 
 
 Fatty liver, 330 
 
 Fatty metamorphosis of the liver, 
 230 
 
 Febricula, 31 
 
 Febrile temperature, 28 
 
 Fehling's test for the presence of 
 sugar in the urine, 259 
 
 Fermentation-test for the presence 
 of sugar in the urine, 260 
 
 Fever, 27 
 
 Fever, ardent, 31 
 
 Fever, break-bone, 76 
 
 Fever, catarrhal, 33 
 
 Fever, cerebro-spinal, 45 
 
 Fever, continued, 30 
 
 Fever, enteric, 35 
 
 Fever, ephemeral, 31 
 
 Fever, essential, 30 
 
 Fever, hemorrhagic malarial, 56 
 
 Fever, hepatic intermittent, 339 
 
 Fever, intermittent, 30 
 
 Fever, malarial intermittent, 54 
 
 Fever, malarial remittent, 55 
 
 Fever of suppuration, 57 
 
 Fever, pernicious malarial, 56 
 
 Fever, rag-weed, 137 
 
 Fever, relapsing, 51 
 
 Fever, remittent, 30 
 
 Fever, rheumatic, 87 
 
 Fever, scarlet, 65 
 
 Fever, simple continued, 31 
 
 Fever, specific, 30 
 
 Fever, splenic, 81 
 
 Fever, symptomatic, 30 
 
 Fever, syphilitic, 59 
 
 Fever, thermic, 33, 334 
 
 Fever, typhoid, 35 
 
368 
 
 INDEX, 
 
 Fever, typhus, 43 
 
 Fever, yellow, 59 
 
 Fibrinous bronchitis, 159 
 
 Fibroid phthisis, 160 
 
 Fibrosis, arterio-capillary, 133 
 
 Filariosis, 253 
 
 Floating kidney, 264 
 
 Floating liver, 223 
 
 Floating spleen, 241 
 
 Floria phthisis, 169, 174 
 
 Follicular tonsillitis, 191 
 
 Foot-and-mouth disease, 84 
 
 Fremitus, vocal or tactile, 148 
 
 French measles, 68 
 
 Frequency of action of the heart, 110 
 
 Friedreich's ataxia, 304 
 
 Frost-bite differentiated from Ray- 
 naud's disease, 134 
 
 Functional heart-murmurs, 114 
 
 Functional stricture of the esopha- 
 gus, 195 
 
 GALL-BLADDER, distention of, 
 235 
 Galloping consumption, 169, 174 
 Gangrene, pulmonary, 168 
 Gangrene, pulmonary, differentiated 
 from — 
 bronchiectasis, 160 
 pulmonary abscess, 168 
 pulmonary tuberculosis, 169 
 Gangrene, symmetrical, 133 
 Gangrenous pharyngitis, 193 
 Gangrenous stomatitis, 186 
 Gastralgia, 196 
 Gastrectasia, 199 
 Gastric catarrh, acute, 197 
 Gastric catarrh, chronic, 198 
 Gastric contents, free hydrochloric 
 
 acid in, tests for, 196 
 Gastric hemorrhage, 175 
 Gastric ulcer, 199 
 Gastritis, acute, 197 
 Gastritis, acute, differentiated from — 
 acute peritonitis, 219 
 intestinal obstruction, 198 
 the gastric symptoms of acute 
 febrile disease or of cerebral 
 disease, 197 
 Gastritis, chronic, 198 
 Gastritis, chronic, differentiated 
 from — 
 carcinoma of the stomach, 203 
 gastric ulcer, 200 
 
 Gastrodynia, 196 
 Gastro-enteritis, 204 
 Gastro-intestinal catarrh, 58 
 General paralysis of the insane, 332 
 General signs, 19 
 Genito-uriuary apparatus, 242 
 German measles, 68 
 Glanders, 80 
 
 Glanders differentiated from — 
 smallpox, 81 
 syphilis, 81 
 Globus hystericus, 344 
 Glossanthrax, 187 
 Glossitis, 187 
 
 Glosso-labio-laryngeal paralysis, 292 
 Glycosuria, 257 
 Goiter, exophthalmic, 351 
 Goiter, simple, differentiated from 
 
 exophthalmic goiter, 353 
 Gonorrheal synovitis, 88 
 Gout, acute, 91 
 Gout, acute, differentiated from 
 
 acute rheumatism, 92 
 Gout, chronic, 92 
 Gout differentiated from rheumatoid 
 
 arthritis, 95 
 Grand mal, 342 
 Granular casts of the uriniferous 
 
 tubules, 252 
 Graves's disease, 351 
 Green-sickness, 98 
 Grippe, la, 32 
 
 HAIRY tongue, 188 
 Hay-asthma, 137 
 
 Hay-fever, 137 
 
 Hay- fever differentiated from co- 
 ryza, 138 
 
 Headache differentiated from mi- 
 graine, 284 
 
 Headache, sick, 284 
 
 Heart, 109 
 
 Heart, action of. 111 
 
 Heart, action of, intermission of, 111 
 
 Heart, apex-beat of, 109 
 
 Heart-clot, 130 
 
 Heart, dilatation of, 120 
 
 Heart, efficiencj' of, 112 
 
 Heart, fatty degeneration of, 121 
 
 Heart, functional disturbance of, 116 
 
 Heart, hypertrophy of, 119 
 
 Heart, irritable, 117 
 
 Heart, malformation of, 115 
 
 Heart-murmurs, 112 
 
INDEX. 
 
 369 
 
 Ileart-murmurs, organic, diflferenti- 
 
 ated from functional, 114 
 Heart-sounds, auscultation of, 110 
 Heart, valvular disease of, 131 
 Heat-exhaustion, 334 
 Heat-exhaustion diflFerentiated from 
 
 heat-fever or sunstroke, 335 
 Heat^fever, 334 
 Heat-stroke, 334 
 Hematuria, 254 
 Hematuria, endemic, 256 
 Hematuria, malarial, differentiated 
 from paroxysmal hemoglobinuria, 
 255 
 Hemicrania, 284 
 Hemiplegia, 272 
 Hemocytometry, 95 
 Hemoglobinometry, 96 
 Hemoglobinuria, 254 
 Hemoglobinuria, paroxysmal, 255 
 Hemoglobinuria, paroxysmal, dif- 
 ferentiated from malarial hema- 
 turia, 255 
 Hemophilia, 106 
 Hemorrhage, cerebral, 323 
 Hemorrhage, cerebral, differentiated 
 from — 
 alcoholic intoxication, 326 
 asphyxia, 327 
 cerebral congestion, 325 
 cerebral embolism, 328 
 cerebral thrombosis, 329 
 opium-poisoning, 326 
 primary lateral sclerosis, 303 
 sunstroke, 335 
 syncope, 325 
 uremia, 326 
 Hemorrhage, gastric, differentiated 
 from pulmonary hemorrhage, 175 
 Hemorrhage into the cerebral mem- 
 branes, 318 
 Hemorrhage into the spinal mem- 
 branes, 286 
 Hemorrhage into the spinal mem- 
 branes dififerentiated from — 
 spinal hemorrhage, 308 
 spinal meningitis, 287 
 tetanus, 348 
 Hemorrhage, pulmonary, differenti- 
 ated from gastric hemorrhage, 175 
 Hemorrhage, spinal, 308 
 Hemorrhage, spinal, differentiated 
 from — 
 acute myelitis, 289 
 compression-myelitis, 310 
 24 
 
 Hemorrhage, spinal, differentiated 
 from — 
 meningeal hemorrhage, 308 
 spinal meningitis, 308 
 
 Hemorrhagic malarial fever, 56 
 
 Hemorrhagic pachymeningitis, 315 
 
 Hemorrhagic smallpox, 71 
 
 Hepatic colic, 239 
 
 Hepatic intermittent fever differen- 
 tiated from malarial intermittent 
 fever, 239 
 
 Hepatitis, acute, 225 
 
 Hepatitis, acute, differentiated 
 from — 
 malarial cachexia, 225 
 portal phlebitis, 225 
 
 Hepatitis, interstitial, 229 
 
 Hereditary ataxic paraplegia, 304 
 
 Hereditary chorea, 341 
 
 Hernia, diaphragmatic, differenti- 
 ated from pneumothorax, 182 
 
 Herpes of the pharynx, 192 
 
 Herpes zoster differentiated from 
 erysipelas, 75 
 
 Herpetic sore-throat, 192 
 
 Herpetic tonsillitis, 192 
 
 Hip-joint, disease of, differentiated 
 from sciatica, 278 
 
 Hippuric acid in urine, 245 
 
 Historical method, diagnosis by, 
 20 
 
 History, family, 19 
 
 History, previous, 19 
 
 Hodgkin's disease, 101 
 
 Humanized virus, 71 
 
 Huntingdon's chorea, 341 
 
 Hyaline casts of the uriniferous 
 tubules, 252 
 
 Hydatid cyst, 84 
 
 Hydatid cyst of the kidney, 271 
 
 Hydatid cyst of the kidney differen- 
 tiated from hydronephrosis, 271 
 
 Hydatid cyst of the liver, 234 
 
 Hydatid cyst of the liver differenti- 
 ated fi-om — 
 abscess of the liver, 235 
 distention of the gall-bladder, 
 
 235 
 pleuritic effusion, 155 
 
 Hydatid disease, 84 
 
 Hydremia, 96 
 
 Hydrocephalus, 318 
 
 Hydrochloric acid in the gastric 
 contents, 196 
 
 Hydronephrosis, 270 
 
370 
 
 INDEX. 
 
 ITydrouepbrosis differentiated from 
 
 cyst of the kidney, 271 
 Hydropericardium, 130 
 Hydrophobia, 350 
 Hydrophobia differentiated from — 
 pseudo-hydrophobia, 350 
 tetanus, 351 
 Hydrothorax differentiated from 
 
 pleuritic effusion, 157 
 Hyperemia, cerebral, 321 
 Hyperemia of the spinal cord, 287 
 Hyperesthesia, 273 
 Hyperpyrexia, 28 
 Hypertrophic pachymeningitis, 311, 
 
 312 ■ 
 Hypertrophy of the heart, 119 
 Hypertrophy of the heart differenti- 
 ated from dilatation of the heart, 
 120 
 Hypesthesia, 273 
 Hysteria, 344 
 
 Hysteria differentiated from — 
 acute meningitis, 347 
 cerebral tumor, 347 
 epilepsy, 345 
 tetanus, 348 
 Hysterical aphonia differentiated 
 
 from acute laryngitis, 139 
 Hysterical paralysis differentiated 
 from the paralysis of cerebral dis- 
 ease, 345 
 Hysterical paraplegia differentiated 
 from — 
 acute myelitis, 346 
 spastic paraplegia, 346 
 Hysterical polyuria, 257 
 
 IDIOPATHIC anemia, 98 
 1 Idiopathic epilepsy, 342 
 Idiosyncratic coryza, 137 
 Immediate percussion, 149 
 Impulse, cardiac, 109 
 Inadequacy, renal, 263 
 Incompetency, aortic, 124 
 Incompetency, aortic, differentiated 
 
 from aneurism of the aorta, 132 
 Incompetenc}', mitral, 122 
 Incompetency, pulmonary, 125 
 Incompetency, tricuspid, 125 
 Indigestion, acute, 197 
 Inductive method, diagnosis by, 20 
 Infantile pseudo-leukemic anemia, 
 
 103 
 Infantile spastic paraplegia, 319 
 
 Infarction, pulmonary, differenti- 
 ated from — 
 catarrhal pneumonia, 163 
 croupous pneumonia, 167 
 pulmonary abscess, 167 
 
 Inflammation of the diaphragm, 281 
 
 Influenza, 32 
 
 Influenza differentiated from — 
 coryza, 137 
 dengue, 77 
 
 Inquiry, 24 
 
 Insane, general paralysis of, 332 
 
 Insolation, 32, 334 
 
 Inspection, 109, 134, 147 
 
 Insular sclerosis, 305 
 
 Intercostal neuralgia, 119, 155 
 
 Intermission of the heart's action, 
 111 
 
 Intermittent fever, 30 
 
 Intermittent fever, hepatic, 239 
 
 Intermittent fever, malarial, 54 
 
 Interstitial hepatitis, 229 
 
 Interstitial myocarditis, 130 
 
 Interstitial pnemonitis, 179 
 
 Interstitial nephritis, chronic, 266 
 
 Intestinal catarrh, acute, 203 
 
 Intestinal catarrh, chronic, 206 
 
 Intestinal colic, 220, 239 
 
 Intestinal obstruction, 211 
 
 Intestinal parasites, 214 
 
 Intestines, 203 
 
 Intestines, carcinoma of, 213 
 
 Intoxication, alcoholic, 326 
 
 Intracranial aneurism, 331 
 
 Intra-thoracic tumor, 131, 156 
 
 Intussusception of the bowel, 212 
 
 Intussusception of the bowel differ- 
 entiated from — 
 acute dysentery, 207 
 obstruction of the bowel, 213 
 typhlitis, 213 
 
 Invagination of the bowel, 212 
 
 Inverse temperature, 28 
 
 Irritable heart, 117 
 
 Irritable heart differentiated from 
 tachycardia, 118 
 
 JAIL-FEVER, 43 
 d Jaundice, catarrhal, differential 
 
 diagnosis of, 236 
 Jaundice, catarrhal, differentiated 
 
 from — 
 acute yellow atrophy of the liver, 
 
 237 
 
INDEX. 
 
 371 
 
 Jaundice, catarrhal, differentiated 
 from — 
 
 biliary calculus, 237 
 
 cirrhosis of the liver, 288 
 
 compression of the common bile- 
 duct, 237 
 
 malarial fever, 237 
 
 malignant disease, 237 
 
 pylephlebitis, 237 
 
 yelloAV fever, 237 
 June-cold, 137 
 
 KAK-KE, 276 
 Kidney, abscess of, 268 
 Kidney, amyloid, lardaceous or 
 
 waxy, 266 
 Kidney, floating, 264 
 Kidney, hydatid cyst of, 271 
 Kidney, malignant disease of, 270 
 Kidney, tuberculosis of, 269 
 
 LABYRINTHINE vertigo, 351 
 Lacunal tonsillitis, 191 
 Landry's paralysis, 291 
 Lardaceous kidney, 266 
 Larval paludism, 57 
 Laryngeal neoplasms differentiated 
 
 from chronic laryngitis, 146 
 Laryngeal vertigo, 142 
 Laryngismus stridulus, 141 
 Laryngismus stridulus differentiated 
 from — 
 asthma, 141 
 catarrhal croup, 142 
 whooping-cough, 146 
 Laryngitis, acute, 138 
 Laryngitis, acute, differentiated from 
 
 hysterical aphonia, 139 
 Laryngitis, chronic, 146 
 Laryngitis, chronic, differentiated 
 
 from laryngeal neoplasms, 146 
 Laryngitis differentiated from — 
 parotiditis, 139 
 pharyngitis, 138 
 tonsillitis, 139 
 Laryngitis, pseudo-membranous, 143 
 Laryngitis, tuberculous, acute, 140 
 Laryngoscopy, 135 
 Larynx, edema of, 139 
 Larynx, tuberculosis of, chronic, 
 
 147 
 Lateral sclerosis, primary, 302 
 Lead-poisoning, 337 
 
 Lead-poisoning differentiated from 
 cerebral tumor, 338 
 
 Lead-poisoning, neuritis of, differ- 
 entiated from neuritis of the 
 musculo-spiral nerve, 282 
 
 Leprosy, anesthetic, differentiated 
 from Morvan's disease, 314 
 
 Leptomeningitis, 135 
 
 Leucin, 247 
 
 Leukemia, 96, 99 
 
 Leukemia differentiated from pseu- 
 do-leukemia, 102 
 
 Leukocythemia, 96, 99 
 
 Leukocytosis, 96, 99 
 
 Leukoplakia lingualis s. buccalis, 
 187 
 
 Lipuria, 253 
 
 Lithemia, 93 
 
 Liver, 222 
 
 Liver, abscess of, 228 
 
 Liver, actinomycosis of, 229 
 
 Liver, amyloid disease of, 231 
 
 Liver, atrophy of, acute yellow, 226 
 
 Liver, carcinoma of, 232 
 
 Liver, cirrhosis of, 229 
 
 Liver, congestion of, 224 
 
 Liver, fatty, 230 
 
 Liver, floating, 223 
 
 Liver, hydatid cyst of, 234 
 
 Liver, malignant disease of, differ- 
 entiated from chronic peritonitis, 
 222 
 
 Lobar pneumonia, 163 
 
 Lobular pneumonia, 162 
 
 Local asphyxia, 133 
 
 Local signs, 19 
 
 Locomotor ataxia, 300 
 
 Lumbar pachymeningitis, 301 
 
 Lumbricoid worms, 217 
 
 Lymphadenoma, 101 
 
 Lymphatic anemia, 101 
 
 Lymph-glands, tuberculosis of, 102 
 
 Lymphoma, malignant, 101 
 
 Lyssophobia, 350 
 
 MAJOR epilepsy, 342 
 Malaria, masked, 57 
 Malarial cachexia, 56 
 Malarialcachexiadifferentiatedfrom 
 
 chronic hepatitis, 225 
 Malarial diseases, 52 
 Malarial fever differentiated frora-^ 
 catarrhal jaundice, 237 
 pulmonary tuberculosis, 177 
 
372 
 
 INDEX, 
 
 Malarial fever difFerentiated from — 
 
 syphilitic fever, 59 
 
 the fever of suppuration or of 
 septic infection, 57 
 
 typhoid fever, 59 
 Malarial fever, hemorrhagic, 56 
 Malarial fever, hemorrhagic, differ- 
 entiated from — 
 
 paroxysmal hemoglobinuria, 58 
 
 yellow fever, 61 
 Malarial fever, pernicious, 56 
 Malarial fever, varieties of, 53 
 Malarial hematuria, 255 
 Malarial intermittent fever, 54 
 Malarial intermittent fever differen- 
 tiated from hepatic intermittent 
 fever, 239 
 Malarial paroxj'sm, 54 
 Malarial remittent fever, 55 
 Malarial remittent fever differenti- 
 ated from yellow fever, 60 
 Malformation of the heart, 115 
 Malignant disease differentiated 
 
 from catarrhal jaundice, 237 
 Malignant disease of the kidney, 270 
 Malignant disease of the liver, 222 
 Malignant lymphoma, 101 
 Malignant pustule, 81 
 Malignant smallpox, 71 
 Mania, acute, differentiated from — 
 
 cerebral meningitis, 317 
 
 delirium tremens, 336 
 Marie's disease, 355 
 Masked malaria, 57 
 Measles, 63 
 Measles differentiated from — 
 
 chickenpox, 73 
 
 purpura, 106 
 
 Rotheln, 69 
 
 scarlet fever, 68 
 
 smallpox, 72 
 
 typhus fever, 65 
 Mediastinum, abscess of, 132 
 Mediate percussion, 149 
 Megalocytes, 96 
 Meilituria, 257 
 Membranes, spinal, hemorrhage 
 
 into, 286 
 Membranous croup, 143 
 Membranous enteritis, 205 
 Membranous sore-throat, common, 
 
 192 
 Meniere's disease, 351 
 Meningitis, acute, differentiated 
 from hysteria, 347 
 
 Meningitis, acute, differentiated 
 
 from sunstroke, 335 
 Meningitis, cerebral, 315 
 Meningitis, cerebral, differentiated 
 from — 
 acute general disease, 316 
 acute mania, 317 
 cerebral abscess, 323 
 cerebritis, 322 
 cerebro-spinal fever, 317 
 delirium tremens, 336 
 Meningitis, cerebral, simple, differ- 
 entiated from tuberculous menin- 
 gitis, 316 
 Meningitis, spinal, 285 
 Meningitis, spinal, acute, differenti- 
 ated from — 
 acute myelitis, 288 
 tetanus, 348 
 Meningitis, spinal, differentiated 
 from — 
 hemorrhage into the spinal men- 
 inges, 287 
 rheumatism of the muscles of 
 
 the back, 285 
 spinal hemorrhage, 308 
 Meningitis, tuberculous, differenti- 
 ated from simple cerebral menin- 
 gitis, 316 
 Mensuration, 148 
 Mercurial stomatitis, 186 
 Microcytes, 96 
 Migraine, 284 
 
 Migraine differentiated from ordi- 
 nary headache, 284 
 Miliary tuberculosis, acute, 177 
 Minor epilepsy, 342 
 Mitral incompetency or regurgita- 
 tion, 123 
 Mitral obstruction, 123 
 MoUities ossium, 108 
 Mollities ossium differentiated from 
 
 rachitis, 109 
 Monoplegia, 272, 273 
 Moore's test for the presence of sugar 
 
 in the urine, 259 
 Morbilli, 63 
 Morvan's disease, 312 
 Morvan's disease differentiated 
 from — 
 anesthetic leprosy, 314 
 diabetes, 314 
 Raynaud's disease, 314 
 scleroderma, 313 
 syphilis, 314 
 
INDEX. 
 
 373 
 
 Morvan's disease differentiated from 
 syringomyelia, 314 
 
 Motion, 272 
 
 Mouth, 184 
 
 Mucous enteritis, 203 
 
 Muguet, 185 
 
 Multiple neuritis, 276 
 
 Multiple sclerosis, 305 
 
 Mumps, 188 
 
 .Murmurs, endocardial, 126 
 
 Murmurs, organic, differentiated 
 from functional heart-murmurs, 
 114 
 
 Musculo-spiral nerve, paralysis of, 
 281 
 
 Musculo-spiral neuritis differenti- 
 ated from the neuritis of lead- 
 poisoning, 282 
 
 Myalgia, 90 
 
 Mycotic endocarditis, 129 
 
 Myelitis, 288 
 
 Myelitis, acute, differentiated from — 
 acute anterior poliomyelitis, 291 
 acute ascending paralysis, 292 
 acute spinal meningitis, 288 
 chronic myelitis, 287 
 hysterical paraplegia, 346 
 multiple neuritis, 279 
 spinal hemorrhage, 289 
 
 Myelitis, chronic, 289 
 
 Myelitis, chronic, differentiated 
 from — 
 acute myelitis, 289 
 compression of the cord, 310 
 lateral sclerosis, 290 
 primary lateral sclerosis, 302 
 progressive muscular atrophy, 
 
 290 
 spinal pachymeningitis, 290 
 syringomyelia, 312 
 tumor of the spinal cord, 311 
 
 Myocarditis, 130 
 
 Myocarditis, interstitial, 130 
 
 Myotonia congenita, 300 
 
 Myxedema, 354 
 
 Myxedema differentiated from — 
 akromegalia, 358 
 scleroderma, 355 
 
 NASAL catarrh, 136 • 
 Nasal respiration, difficulty of, 
 135 
 Nasal septum, ulceration or erosion 
 of, 136 
 
 Negative signs, 23 
 
 Neoplasms, laryngeal, 146 
 
 Neoplasms of the bladder, 262 
 
 Nephritis, acute, 265 
 
 Nephritis, chronic, differentiated 
 
 from cerebral tumor, 331 
 Nephritis, chronic interstitial, 266 
 Nephritis, chronic interstitial, differ- 
 entiated from diabetes insipidus, 
 257 
 Nephritis, chronic parenchymatous, 
 
 265 
 Nephritis differentiated from cysti- 
 tis, 261 
 Neuralgia, 283 
 
 Neuralgia differentiated from — 
 neuritis, 276, 283 
 subacute rheumatism, 89 
 Neuralgia, intercostal, differentiated 
 from — 
 acute pleurisy, 155 
 angina pectoris, 119 
 Neuralgia of the stomach, 196 
 Neuralgia, sciatic, differentiated 
 
 from sciatica, 278 
 Neuralgia, trifacial or trigeminal, 
 
 283 
 Neuritis, 275 
 
 Neuritis, diagnosis of, 276 
 Neuritis differentiated from — 
 disease of bone, 276 
 neuralgia, 276, 283 
 subacute rheumatism, 276 
 Neuritis, multiple or disseminated, 
 
 276 
 Neuritis, multiple, differentiated 
 from — 
 acute anterior poliomyelitis, 291 
 acute ascending paralysis, 292 
 acute myelitis, 277 
 posterior spinal sclerosis, 301 
 spinal pachymeningitis, 277 
 Neuritis, musculo-spiral, 282 
 Neuromata, 282 
 Neuromata, diagnosis of, 282 
 Nigritie.f , 188 
 No^ma, 186 
 
 Nutrition, alterations in, in disease 
 of the nervous system, 271 
 
 OBJECTIVE symptoms, 17 
 Observation, 24 
 Obstruction, aortic, 123 
 Obstruction, intestinal, 211 
 
374 
 
 INDEX. 
 
 Obstruction, intestinal, acute, dif- 
 ferentiated from acute peritonitis, 
 330 
 
 Obstruction, intestinal, differenti- 
 ated from acute gastritis, 198 
 
 Obstruction, mitra , 123 
 
 (Obstruction of the aii--passages, 146 
 
 Obstruction of the bowel differenti- 
 ated from intussusception, 213 
 
 Obstruction, pulmonary, 125 
 
 Obstruction, tricuspid, 125 
 
 Occlusion of the biliary passages 
 differentiated from abscess of the 
 liver, 328 
 
 Occupation-neuroses, 339 
 
 Odor of urine, 243, 243 
 
 Oligemia, 96 
 
 Oligochromemia, 96 
 
 Oligocythemia, 96 
 
 Omentum, carcinoma of, 203, 333 
 
 Omentum, sarcoma of, 202 
 
 Opisthotonos, 347 
 
 Opium-poisoning differentiated from 
 cerebral hemorrhage, 336 
 
 Organic heart-murmurs, 114 
 
 Organic stricture of the esophagus, 
 195 
 
 Orthotonos, 347 
 
 Osteitis deformans, 357 
 
 Osteo-arthropathy, hypertrophic, 
 pulmonary, 358 
 
 Ovary, right, abscess of, 310 
 
 Oxaluria, 348 
 
 Oxyuris vermicularis, 318 
 
 PACHYMENINGITIS, 315, 316 
 Pachymeningitis, cervical, 386 
 Pachymeningitis, cervical, differen- 
 tiated from — 
 progressive muscular atrophy, 
 
 386 
 subacute anterior poliomyelitis, 
 286 
 Pachvmeningitis, hemorrhagic, 315, 
 
 316 
 Pachymeningitis, hypertrophic, dif- 
 ferentiated from — 
 syringomyelia, 313 
 tumor of the spinal cord, 311 
 Pachymeningitis, lumbar, differen- 
 tiated from posterior spinal scle- 
 rosis, 301 
 Pachymeningitis, spinal, differenti- 
 ated from chronic myelitis, 290 
 
 Pachymeningitis, spinal, differen- 
 tiated from multiple neuritis, 277 
 Paget's disease, 357 
 Palpation, 110, 148 
 Palsy, bulbar, acute, 296 
 Palsy, bulbar, acute, distinguished 
 
 from chronic bulbar palsy, 296 
 Palsy, bulbar, differentiated from 
 
 pseudo-bulbar palsy, 296 
 Palsy, pseudo-bulbar, 396 
 Palsy, pseudo-bulbar, differentiated 
 
 from true bulbar palsy, 296 
 Palsy, shaking, 306 
 Paludism, larval, 57 
 Panaris, analgesic, 313 
 Pancreas, 341 
 Pancreatitis, acute, 341 
 Paralysis, 373 
 Paralysis agitans, 306 
 Paralysis agitans differentiated from 
 
 cerebro-spinal sclerosis, 307 
 Pai-alysis, ascending, acute, 391 
 Paralysis, ascending, acute, differ- 
 entiated from — 
 acute anterior poliomyelitis, 293 
 acute myelitis, 293 
 multiple neuritis, 393 
 Paralysis, bulbar, progressive, 395 
 Paralysis, cerebral, differentiated 
 from acute anterior poliomyeli- 
 tis, 291 
 Paralysis, general, of the insane, 333 
 Paralysis, general, of the insane, dif- 
 ferentiated from posterior spinal 
 sclerosis, 333 
 Paralysis, glosso-labio-laryngeal, 
 
 292, 293 
 Paralysis, hysterical, 346 
 Paralysis, Landry's, 291 
 Paralysis of the diaphragm differen- 
 tiated from — 
 asthma, 184 
 
 paralysis of the phrenic nerve, 
 281 
 Paralysis of the facial nerve, 379 
 Paralysis of the musculo-spiral 
 
 nerve, 281 
 Paralysis of the phrenic nerve, 381 
 Paralysis, pseudo-hypertrophic, 296 
 Paralysis, pseudo-hypertrophic, dif- 
 ferentiated from — 
 congenital spastic paraplegia, 
 
 320 
 simple idiopathic muscular 
 atrophy, 399 
 
INDEX. 
 
 375 
 
 Paraplegia, 273, 273 
 
 Paraplegia, ataxic, 303 
 
 Paraplegia, ataxic, hereditary, 304 
 
 Paraplegia, ataxic, hereditary, dif- 
 ferentiated from postero- lateral 
 sclerosis, 304 
 
 Paraplegia, hysterical, 345 
 
 Paraplegia, spastic, 303 
 
 Pai'aplegia, spastic, congenital, 319 
 
 Paraplegia, spastic, congenital, dif- 
 ferentiated from pseudo-hypertro- 
 phic paralysis, 330 
 
 Paraplegia, spastic, differentiated 
 from hysterical paraplegia, 346 
 
 Parasites, intestinal, 214 
 
 Parasitic stomatitis, 185 
 
 Parenchymatous tonsillitis, 191 
 
 Paresis, 372 
 
 Paresthesia, 273 
 
 Paretic dementia, 333 
 
 Parkinson's disease, 306 
 
 Parotiditis, 188 
 
 Parotiditis differentiated from laryn- 
 gitis, 139 
 
 Paroxysmal hemoglobinuria, 25') 
 
 Paroxysmal hemoglobinuria differ- 
 entiated from hemorrhagic mala- 
 rial fever, 58 
 
 Pathological association, diagnosis 
 by the method of, 20 
 
 Pectoriloquy, 152 
 
 Pectoriloquy, whispering, 153 
 
 Percussion, 110, 149 
 
 Percussion, auscultatory, 150 
 
 Percussion, immediate, 149 
 
 Percussion, mediate, 149 
 
 Percussion, respiratory, 150 
 
 Perforation of the bowel in typhoid 
 fever, 40 
 
 Pericardial effusion dififerentiated 
 from — 
 dilatation of the heart, 121 
 pleuritic effusion, 157 
 
 Pericarditis, acute, 127 
 
 Pericarditis, acute, diflFerentiated 
 from — 
 acute endocarditis, 139 
 acute pleurisy, 138 
 
 Perihepatitis, 335 
 
 Perihepatitis, chronic, differentiated 
 from cirrhosis of the liver, 336 
 
 Periodic vasomotor coryza, 137 
 
 Perirenal abscess, 269 
 
 Peritonitis, acute, 219 
 
 Peritonitis, acute, differentiated 
 from — 
 acute enteritis, 330 
 acute gastritis, 319 
 acute intestinal obstruction, 330 
 intestinal colic, 330 
 subacute rheumatism, 331 
 Peritonitis, chronic, 221 
 Peritonitis, chronic, differentiated 
 from malignant disease of the 
 liver, 232 
 Perityphlitis, 209 
 Perityphlitis, differential diagnosis 
 
 of, 210 
 Perityphlitis differentiated from — 
 abscess of the right ovary, 310 
 carcinoma of the cecum, 311 
 lumbar abscess, 310 
 Pernicious anemia, 98 
 Pernicious malarial fever, 56 
 Pernicious malarial fever, diagnosis 
 
 of, 58 
 Pertussis, 145 
 Petit mal, 342 
 Pharyngitis, 188 
 
 Pharyngitis, acute catarrhal, 188 
 Pharyngitis, acute phlegmonous, 189 
 Pharyngitis, acute tuberculous, 189 
 Pharyngitis differentiated from 
 
 laryngitis, 138 
 Pharyngitis, gangrenous, 193 
 Pharyngitis, tuberculous, differenti- 
 ated from — 
 syphilitic sore-throat, 190 
 typhoid fever, 190 
 Pharyngoscopy, 135 
 Pharynx, 188 
 Pharynx, herpes of, 192 
 Phlebitis, portal, differentiated from 
 
 acute hepatitis, 225 
 Phlegmonous pharyngitis, acute, 189 
 Phosphoric acid in urine, 246 
 Phosphorus-poisoning differentiated 
 from acute yellow atrophy of the 
 liver, 237 
 Phrenic nerve, paralysis of, 281 
 Phrenic nerve, paralysis of, differen- 
 tiated from — 
 degeneration of the diaphragm, 
 
 281 
 inflammation of the diaphragm, 
 
 281 
 superior intercostal breathing, 
 281 
 
376 
 
 INDEX, 
 
 Phthisis, florid, 169, 174 
 
 Physical diagnosis, 147 
 
 Ph^'sieal signs, 18 
 
 Pia-arachnitis, 315 
 
 Plastic bronchitis, 159 
 
 Pleural effusion, 181, 182 
 
 Pleui-isy, acute, 153 
 
 Pleurisy, acute, differentiated from — 
 acute pericarditis, 128 
 acute pneumonia, 154 
 intercostal neuralgia, 155 
 
 Pleurisy, chronic, differentiated 
 from — 
 interstitial pneumonitis, 179 
 intrathoracic tumor, 156 
 pulmonary tuberculosis, 175 
 
 Pleurisy differentiated from perni- 
 cious malarial fever, 58 
 
 Pleuritic effusion, 155, 156, 157 
 
 Pleurosthotonos, 347 
 
 Plumbism, 337 
 
 Pneumonia, acute croupous or lobar, 
 163 
 
 Pneumonia, acute, differentiated 
 from acute pleurisy, 154 
 
 Pneumonia, catarrhal, 162 
 
 Pneumonia, catarrhal, differentiated 
 from — 
 atelectasis, 163 
 bronchiectasis, 160 
 capillary bronchitis, 162 
 croupous pneumonia, 166 
 pulmonary infarction, 163 
 
 Pneumonia, croupous, differentiated 
 from — 
 catarrhal pneumonia, 166 
 pulmonary congestion, 166 
 pulmonary edema, 166 
 pulmonary infarction, 167 
 pulmonarj' tuberculosis, 167 
 
 Pneumonia differentiated from — 
 pernicious malarial fever, 58 
 typhoid fever, 42 
 
 Pneumonia, lobular, 162 
 
 Pneumonitis, interstitial, 179 
 
 Pneumonitis, interstitial, differenti- 
 ated from — 
 chronic bronchitis, 179 
 chronic pleurisy, 179 
 
 Pneumothorax, ISl 
 
 Pneumothorax differentiated from — 
 diaphragmatic hernia, 182 
 pleural efiusion, 182 
 pulmonary cavity, 182 
 pulmonary emphysema, 180 
 
 Poikilocytes, 96 
 Poisoning, arsenical, 50 
 Poisoning, narcotic, differentiated 
 
 from sunstroke, 335 
 Poliomyelitis, anterior, acute, 290 
 Poliomyelitis, anterior, acute, differ- 
 entiated from — 
 acute ascending paralysis, 292 
 acute myelitis, 291 
 cerebral paralysis, 291 
 multiple neuritis, 291 
 progressive muscular atrophy, 
 295 
 Poliomyelitis, anterior, subacute, dif- 
 ferentiated from cervical pachy- 
 meningitis, 286 
 Polyneuritis, 276 
 Polyuria, 256 
 Polyuria, hysterical, differentiated 
 
 from diabetes insipidus, 257 
 Portal phlebitis, 225 
 Posterior spinal sclerosis, 300 
 Postero-lateral sclerosis, 303 
 Previous history, 19 
 Primary lateral sclerosis, 303 
 Primary sciatica, 279 
 Progressive bulbar paralysis, 295 
 Progressive muscular atrophy, 292 
 Progressive paralysis of the insane, 
 
 332 
 Pseudo-bulbar palsy, 296 
 Pseudo-hydrophobia, 350 
 Pseudo-hypertrophic paralysis, 296 
 Pseudo-leukemia, 101 
 Pseudo-leukemia differentiated 
 from — 
 leukemia, 102 
 
 tuberculosis of the lymph- 
 glands, 102 
 Pseudo-leukemic anemia, infantile, 
 
 103 
 Pseudo-membranous laryngitis, 14."J 
 Pulmonary abscess. 160, 167, 168, 
 
 176 
 Pulmonary carcinoma, 175 
 Pulmonaiy cavity, 182 
 Pulmonary- congestion, 166 
 Pulmonary edema, 166 
 Pulmonary emphysema, 179 
 Pulmonary gangrene, 168 
 Pulmonary hemorrhage, 175 
 Pulmonary hypertrophic osteo-ar- 
 
 thropathy, 358 
 Pulmonary incompetency or regur- 
 gitation, 125 
 
INDEX, 
 
 377 
 
 Pulmonary infarction, 163, 167 
 Pulmonary obstruction, 135 
 Pulmonary syphilis, 176 
 Pulmonary tuberculosis, 169 
 Pulsatory empyema, 153 
 Purity of the heart-sounds, 112 
 Purpura, 105 
 Purpura differentiated from — 
 
 measles, 106 
 
 scorbutus, 106 
 Purring tremor, 110 
 Putrid bronchitis, 159 
 Putrid sore-throat, 193 
 Pyelitis, 249, 263 
 Pyelitis differentiated from cystitis, 
 
 263 
 Pyemia differentiated from — 
 
 acute rheumatism, 88 
 
 typhoid fever, 40 
 Pylephlebitis differentiated from ca- 
 tarrhal jaundice, 237 
 Pyonephrosis, 271 
 Pyuria, 249 
 
 QUANTITY of urine, 242 
 Quinsy, 191 
 
 RACHITIS, 108 
 Kachitis differentiated from mol- 
 lifies ossium, 109 
 Rag-weed fever, 137 
 Rales, 151 
 Rational signs, 19 
 Raynaud's disease, 133 
 Raynaud's disease differentiated 
 from — 
 
 frost-bite, 134 
 
 Morvan's disease, 314 
 Reaction of degeneration, 274 
 Reaction of urine, 243 
 Recrudescence in typhoid fever, 39 
 Reflex symptoms, i9 
 Reflexes, 273 
 Reflexes, alterations in, in disease, 
 
 274 
 Reflexes, deep, 274 
 Reflexes, superficial, 273 
 Regurgitation, aortic, 124 
 Regurgitation, mitral, 122 
 Regurgitation, pulmonary, 125 
 Regurgitation, tricuspid, 125 
 Relapse in typhoid fever, 39 
 Relapsing fever, 51 
 
 Relapsing fever differentiated from — 
 
 typhus fever, 53 
 
 yellow fever, 53 
 Remittent fever, 30 
 Remittent fever, malarial, 55 
 Renal calculus, 264 
 Renal colic, 339 
 Renal inadequacy, 263 
 Resonance, vocal, 152 
 Respiratory percussion, 150 
 Respiratory system, 134 
 Retro-pharyngeal abscess, 194 
 Rheumatic fever, 87 
 Rheumatism, 90 
 Rheumatism, acute, 87 
 Rheumatism, acute, differentiated 
 from — 
 
 acute gout, 93 
 
 acute synovitis, 88 
 
 pyemia, 88 
 Rheumatism, chronic, 90 
 Rheumatism, chronic, differentiated 
 
 from rheumatoid arthritis, 95 
 Rheumatism of the muscles of the 
 back differentiated from spinal 
 meningitis, 285 
 Rheumatism, subacute, 89 
 Rheumatism, subacute, differenti- 
 ated from — 
 
 acute peritonitis, 221 
 
 neuralgia, 89 
 
 neuritis, 276 
 
 trichiniasis, 90 
 Rheumatoid arthritis, 94 
 Rheumatoid arthritis differentiated 
 from — 
 
 chronic rheumatism, 95 
 
 gout, 95 
 Rhinoscopy, 135 
 Risus sardonicus, 347 
 Rose-cold, 137 
 Roseola, 68 
 Rotheln, 68 
 Rbtheln differentiated from — 
 
 measles, 69 
 
 scarlet fever, 69 
 Round-worms, 217 
 Rubeola, 63 
 
 SARCOMA of the omentum differ- 
 entiated from carcinoma of the 
 stomach, 202 
 Scarlatina, 65 
 Scarlet fever, 65 
 
378 
 
 INDEX. 
 
 Scarlet fever differentiated from — 
 
 dengue, 77 
 
 diphtheria, 78 
 
 erysipelas, 74 
 
 measles, 68 
 
 Rbtheln, 69 
 
 smallpox, 73 
 Sciatic neuralgia, 278 
 Sciatica, 278 
 Sciatica differentiated from — 
 
 disease of the hip-joint, 278 
 
 sciatic neuralgia, 278 
 Sciatica, primary, differentiated 
 
 from secondary sciatica, 279 
 Sciatica, secondary, differentiated 
 
 from primary sciatica, 279 
 Sclerodactylia, 314 
 Scleroderma differentiated from — 
 
 Morvan's disease, 313 
 
 myxedema, 355 
 Sclerosis, cerebro-spinal, 305 
 Sclerosis, cerebro-spinal, differenti- 
 ated from — 
 
 cerebral tumor, 331 
 
 paralysis agitans, 307 
 
 postero-lateral sclerosis, 305 
 Sclerosis, disseminated, 305 
 Sclerosis, insular, 305 
 Sclerosis, lateral, amyotrophic, 292, 
 
 293 
 Sclerosis, lateral, differentiated from 
 
 chronic myelitis, 290 
 Sclerosis, lateral, primary, 303 
 Sclerosis, lateral, primary, differen 
 tiated from — 
 
 cerebral hemiplegia, 303 
 
 chronic myelitis, 303 
 
 postero-lateral sclerosis, 304 
 Sclerosis, multiple, 305 
 Sclerosis, postero-lateral, 303 
 Sclerosis, postero-lateral, differenti- 
 ated from — 
 
 cerebellar tumor, 304 
 
 cerebro-spinal sclerosis, 305 
 
 hereditarj' ataxic paraplegia, 
 304 
 
 posterior spinal sclerosis, 303 
 
 primary lateral sclerosis, 304 
 Sclerosis, spinal, posterior, 300 
 Sclerosis, spinal, posterior, differen- 
 tiated from — 
 
 cerebellar tumor, 302 
 
 general paralysis of the insane, 
 383 
 
 lumbar pachymeningitis, 501 
 
 Sclerosis, spinal, posterior, differen- 
 tiated from — 
 
 multiple neuritis, 301 
 
 postero-lateral sclerosis, 303 
 Scorbutus, 104 
 
 Scorbutus differentiated from pur- 
 pura, 106 
 Scurvy, 104 
 Seat-worms, 218 
 Secondary sciatica, 279 
 Sensation, 273 
 Septic infection, fever of, dififerenti- 
 
 ated from malarial fever, 57 
 Sequelae, 22 
 Shaking palsy, 306 
 Ship-fever, 43 
 Sick headache, 284 
 Signs, 18 
 
 Signs, general or constitutional, 19 
 Signs, local, 19 
 Signs, negative, 23 
 Signs, physical, 18 
 Signs, rational, 19 
 Simple continued fever, 31 
 Simple idiopathic muscular atrophy, 
 
 298 
 Smallpox, 69 
 Smallpox, confluent, 70 
 Smallpox differentiated from — 
 
 cerebro-spinal fever, 48 
 
 chickenpox, 73 
 
 erysipelas, 75 
 
 glanders, 81 
 
 measles, 72 
 
 scarlet fever, 72 
 
 typhoid fever, 43 
 
 typhus fever, 44 
 Smallpox, discrete, 70 
 Smallpox, hemorrhagic, 71 
 Smallpox, malignant, 71 
 Sodium chloride in urine, 245 
 Softening, cerebral , 327' 
 Solvent power of the gastric juice, 
 
 196 
 Sore-throat, common membranous, 
 
 192 
 Sore-throat, common membranous, 
 differentiated from diphtheria, 192 
 Sore-throat, gangrenous, differenti- 
 ated from diphtheria, 193 
 Sore-throat, herpetic, 192 
 Sore-throat, putrid, 193 
 Sore-throat, syphilitic, diflferentiated 
 from tuberculous pharyngitis, 190 
 Spasm, 373 
 
INDEX. 
 
 379 
 
 Spasmodic croup, 142 
 
 Spastic paraplegia, 302 
 
 Spastic paraplegia, congenital, 319 
 
 Specific fever, 30 
 
 Specific gravity of urine, 243 
 
 Spliygmogram, 115 
 
 Sphygmograph, 115 
 
 Spinal compression, 309 
 
 Spinal hemorrhage, 308 
 
 Spinal membranes, hemorrhage Into, 
 286 
 
 Spinal meningitis, 285 
 
 Spinal pachymeningitis, 277, 290 
 
 Spinal tumor, 310 
 
 Spleen, 240 
 
 Spleen, abscess of, 156 
 
 Spleen, floating, 341 
 
 Splenic fever, 81 
 
 Splenitis, 241 
 
 Spool-worms, 218 
 
 Sporadic cretinism, 354 
 
 Sporadic cretlnoldlsm, 354 
 
 Sputum, tubercle-bacilli in, 172 
 
 Status epllepticus, 342 
 
 Stomach, 195 
 
 Stomach, carcinoma of, 200 
 
 Stomach, dilatation of, 199 
 
 Stomach, neuralgia of, 196 
 
 Stomatitis, aphthous, 184 
 
 Stomatitis, catarrhal, 184 
 
 Stomatitis differentiated from diph- 
 theria, 80 
 
 Stomatitis, gangrenous, 186 
 
 Stomatitis, mercurial, 186 
 
 Stomatitis, parasitic, 185 
 
 Stomatitis, ulcerative, 185 
 
 Stricture, functional, of the esopha- 
 gus differentiated from organic 
 stricture, 195 
 
 Stricture of the esophagus, 194 
 
 Strychnine-poisoning differentiated 
 from tetanus, 348 ~ 
 
 Subacute rheumatism, 89 
 
 Subfebrile temperature, 28 
 
 Subjective symptoms, 17 
 
 Subnormal temperature, 29 
 
 Sugar In the urine, Boettger's test 
 for the presence of, 259 
 
 Sugar in the urine, Fehllng*s test 
 for the presence of, 259 
 
 Sugar In the urine, fermentation-test 
 for the presence of, 260 
 
 Sugar in the urine, Moore's te^t for 
 the presence of, 259 
 
 Sugar in the urine, Trommer's test 
 
 for the presence of, 259 
 Sulphuric acid in urine, 246 
 Sun-pain, 57 
 Sunstroke, 32, 334 
 Sunstroke differentiated from — 
 
 acute alcoholism, 335 
 
 acute meningitis, 335 
 
 cerebral hemorrhage, 335 
 
 heat-exhaustion, 335 
 
 narcotic poisoning, 335 
 
 uremia, 268, 385 
 Superficial reflexes, 273 
 Suppuration, fever of, differentiated 
 
 from malarial fever, 57 
 Supra-renal bodies, tuberculosis of, 
 
 107 
 Symmetrical gangrene, 133 
 Symptomatic fever, 30 
 Symptoms, 17, 18 
 Symptoms, objective, 17 
 Symptoms, reflex, 19 
 Symptoms, subjective, 17 
 Syncope differentiated from — 
 
 cerebral hemorrhage, 325 
 
 epilepsy, 343 
 Synovitis, acute, differentiated from 
 
 acute rheumatism, 88 
 Synovitis, gonorrheal, 88 
 Syphilis differentiated from — 
 
 glanders, 81 
 
 Morvan's disease, 314 
 Syphilis, pulmonary, differentiated 
 from pulmonary tuberculosis, 176 
 Syphilitic arthritis, 89 
 Syphilitic fever differentiated from 
 
 malarial fever, 59 
 Syphilitic sore-throat, 190 
 Syringomyelia, 312 
 Syringomyelia differentiated from — 
 
 chronic myelitis, 312 
 
 hypertrophic pachymeningitis, 
 312 
 
 Morvan's disease, 314 
 
 progressive muscular atrophy, 
 312 
 
 TABES dorsalis, 300 
 Tabes mesenterica, 222 
 Tachycardia, 116 
 Tachycardia differentiated from- 
 angina pectoris, 117 
 exophthalmic goiter, 117 
 
380 
 
 INDEX. 
 
 Tachycardia differentiated from irri- 
 table heart, 118 
 Tactile fremitus, 148 
 Tape-worm, 211 
 Temperature, 27 
 Temperature, febrile, 28 
 Temperature, inverse, 28 
 Temperature, subfebrile, 28 
 Temperature, subnormal, 29 
 Tenia medioeanellata, 215 
 Tenia solium, 214 
 Tetanus, 347 
 Tetanus differentiated from — 
 
 acute spinal meningitis, 348 
 
 cerebro-spinal fever, 47 
 
 hemorrhage Into the spinal 
 membranes, 348 
 
 hydrophobia, 351 
 
 hysteria, 348 
 
 strychnine-poisoning, 348 
 
 tetany, 349 
 Tetany differentiated from tetanus, 
 
 349 
 Thermic fever, 32, 334 
 Thomsen's disease, 300 
 Thoracic aneurism, 131 
 Thread-worms, 218 
 Throat, diphtheroid, 192 
 Thrombosis, cerebral, 329 
 Thrombosis, cerebral, differentiated 
 
 from cerebral hemorrhage, 329 
 Thrush, 185 
 Tic douloureux, 283 
 Tongue, 187 
 
 Tongue, black or hairy, 188 
 Tonsillitis, 191 
 Tonsillitis differentiated from — 
 
 diphtheria, 79 
 
 laryngitis, 139 
 Tonsillitis, herpetic, 192 
 Tonsillitis, lacunal or follicular, 191 
 Tonsillitis, parenchymatous, 191 
 Torticollis, 338 
 
 Torticollis differentiated from cere- 
 bro-spinal fever, 47 
 Touch, 148 
 Translumination, 134 
 Transparencj' of urine, 243 
 Tremor, purring, 110 
 Trichii\iasis, 85, 214 
 Trlchiniasis differentiated from — 
 
 subacute rheumatism, 90 
 
 typhoid fever, 42 
 Tricuspid incompetency or regurgi- 
 tation, 125 
 
 Tricuspid obstruction, 125 
 Trifacial neuralgia, 283 
 Trigeminal neuralgia, 283 
 Trommer's test for the presence of 
 
 sugar in the urine, 259 
 Tube-casts in urine, 251 
 Tubercle-bacilli in sputum, 172 
 Tuberculosis, acute miliary, 177 
 Tuberculosis, acute miliary, differ- 
 entiated from — 
 acute bronchitis, 158 
 capillar}' bronchitis, 161 
 typhoid fever, 178 
 Tuberculosis, chronic, of the larvnx, 
 
 147 
 Tuberculosis of the bronchial glands 
 differentiated from whooping- 
 cough, 177 
 Tuberculosis of the kidney, 269 
 Tuberculosis of the lymph-glands 
 differentiated from pseudo-leuke- 
 mia, 102 
 Tuberculosis of the supra-renal 
 
 bodies, 107 
 Tuberculosis, pulmonary, 169 
 Tuberculosis, pulmonary, differenti- 
 ated from — 
 bronchiectasis, 176 
 chronic bronchitis, 159 
 chronic pleurisy, 175 
 croupous pneumonia, 167 
 malarial fever, 177 
 pulmonary abscess, 176 
 pulmonary carcinoma, 175 
 pulmonary gangrene, 169 
 pulmonary sj'philis, 176 
 Tuberculous laryngitis, acute, 140 
 Tuberculous meningitis, 316 
 Tuberculous pharyngitis, acute, 
 
 189 
 Tumor, cerebellar, differentiated 
 from — 
 posterior spinal sclerosis, 302 
 postero-lateral sclerosis, 304 
 Tumor, cerebral, 330 
 Tumor, cerebral, differentiated 
 from — 
 anemia, 331 
 
 cerebro-spinal sclerosis, 331 
 chronic nephritis, 331 
 epilepsy, 331 
 hysteria, 347 
 lead-poisoning, 338 
 Tumor, intra-thoracic, differentiated 
 from aneurism of the aorta, 131 
 
INDEX. 
 
 381 
 
 Tumor, intra-thoracic, differentiated 
 
 from chronic pleurisy, 156 
 Tumor of the brain differentiated 
 
 from cerebral abscess, 323 
 Tumor of the spinal cord, 310 
 Tumor of the spinal cord differenti- 
 ated from — 
 caries of the vertebrae, 311 
 chronic myelitis, 31 1 
 hypertrophic pachymeningitis, 
 311 
 Typhlitis, 208 
 
 Typhlitis diiferentlated from — 
 abscess of the right ovary, 310 
 carcinoma of the cecum, 211 
 intussusception of the bowel, 
 
 213 
 lumbar abscess, 210 
 Typhoid condition differentiated 
 
 from typhoid fever, 41 
 Typhoid fever, 35 
 Typhoid fever, abortive, 38 
 Typhoid fever, ambulatory or walk- 
 ing, 38 
 Typhoid fever differentiated from — 
 acute catarrhal enteritis, 204 
 acute dysentery, 207 
 acute miliarv tuberculosis, 
 
 178 
 acute yellow atrophy of the liver, 
 
 227 
 a typhoid condition, 41 
 cerebro-spinal fever, 48 
 malarial fever, 59 
 measles, 65 
 pneumonia, 42 
 pyemia, 40 
 relapsing fever, 52 
 trichiniasis, 42 
 tuberculous pharyngitis, 190 
 typhus fever, 44 
 variola, 42 
 yellow fever, 41 
 Typhoid fever, perforation of the 
 
 bowel in, 40 
 Typhoid fever, recrudescence in, 
 
 39 
 Typhoid fever, relapse in, 39 
 Typhus fever, 43 
 
 Typhus fever differentiated from — 
 cerebro-spinal fever, 47 
 typhoid fever, 44 
 variola, 44 
 Ty rosin, 247 
 
 ULCER, gastric, 199 
 Ulcer, gastric, differentiated 
 from chronic gastritis, 200 
 
 Ulceration of the stomach differ- 
 entiated from carcinoma of the 
 stomach, 201 
 
 Ulcerative stomatitis, 185 
 
 Ulcero-membranous angina, 192 
 
 Urea in urine, 244 
 
 Uremia, 267 
 
 Uremia differentiated from — 
 cerebral hemorrhage, 326 
 epilepsy, 267, 343 
 sunstroke, 268, 335 
 
 Ureteritis, 249 
 
 Urethritis, 249 
 
 Uric acid in urine, 244 
 
 Urine, acetone in, tests for the pres- 
 ence of, 260 
 
 Urine, albumin in, 250 
 
 Urine, biliary acids in, 247 
 
 Urine, biliary coloring-matter in , 246 
 
 Urine, color of, 243 
 
 Urine, constitution of, 242 
 
 Urine, diacetic acid in, tests for the 
 presence of, 260 
 
 Urine, examination of, 243 
 
 Urine, hippuric acid in, 245 
 
 Urine, odor of, 242, 243 
 
 Urine, phosphoric acid in, 246 
 
 Urine, quantity of, 343 
 
 Urine, reaction of, 343 
 
 Urine, sodium chloride in, 245 
 
 Urine, specific gravity of, 243 
 
 Urine, sugar in, Boettger's test for 
 the presence of, 259 
 
 Urine, sugar in, Fehliug's test for 
 the presence of, 259 
 
 Urine, sugar in, fermentation-test 
 for the presence of, 260 
 
 Urine, sugar in, Moore's test for the 
 presence of, 259 
 
 Urine, sugar in, Trommer's test for 
 the presence of, 359 
 
 Urine, sulphuric acid in, 246 
 
 Urine, transparency of, 243 
 
 Urine, tube-casts in, 251 
 
 Urine, urea in, 244 
 
 Urine, uric acid in, 344 
 
 VACCINATION, 71 
 Vaccinia, 72 
 Valvular disease of the heart, 121 
 
382 
 
 INDEX, 
 
 Valvular disease of the heart diflfer- 
 
 entiated from acute endocarditis, 
 
 128 
 Varicella, 73 
 Variola, 69 
 Varioloid, 71 
 Varioloid differentiated from chick- 
 
 enpox, 73 
 Vertebrae, caries of, 311 
 Vertigo, aural, 351 
 Vertigo, aural, differentiated from 
 
 epilepsy, 351 
 Vertigo, labyrinthine, 351 
 Vertigo, laryngeal, 142 
 Vesical calculus, 262 
 Virus, humanized, 71 
 Vocal fremitus, 148 
 Vocal resonance, 152 
 
 WALKING typhoid fever, 38 
 Waxy casts of the uriniferous 
 tubules, 252 
 Waxy kidney, 266 
 Weil's disease. 62 
 
 Weil's disease differentiated from 
 yellow fever, 63 
 
 Whispering pectoriloquy, 152 
 
 Whooping-cough, 145 
 
 Whooping-cough differentiated 
 from — 
 asthma, 184 
 
 laryngismus stridulus, 146 
 membranous croup, 145 
 tuberculosis of the bronchial 
 glands, 177 
 
 Wool-sorter's disease, 81 
 
 Writers' cramp, 339 
 
 Wry neck, 338 
 
 YELLLOW fever, 59 
 Yellow fever differentiated 
 
 from — 
 acute yellow atrophy of the liver, 
 
 61 
 catarrhal jaundice, 237 
 cerebro- spinal fever, 48 
 hemorrhagic malarial fever, 61 
 malarial remittent fever, 60 
 relapsing fever, 52 
 typhoid fever, 41 
 Weil's disease, 63 
 
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 Medical Sheep, 2,50 " 
 
 Times and Register, Philadelphia, August 23, 1890.— Nancrede's Anatomy 
 and Dissector— this is a good dissector's manual, with clear type and hand- 
 some cuts. The colored i)latps are e.-pecially commendable. 
 
 The Southern Practitioner, Nashinlle, Tenn., September, 1890.— Nancrede's 
 Anatomy and Dissector— truly a" Vade Mecuin," a "inultum in parvo." The 
 illustrations are marvels of beauty and clearness of illustration. 
 
 7 
 
IN PREPARATION. 
 
 DISEASES OF THE EYE, 
 
 G. E. DE SCHWEINITZ, M.D., 
 
 'Ophthalmic Surgeon to Children's Hospital and to the Philadelphia Hospital : 
 Ophthalmologist to the Orthopaedic Hospital and Infirmary for Ner- 
 vous Diseases ; Lecturer on Medical Ophthalmoscopy, 
 University of Pennsylvania, etc. 
 
 A HAND-BOOK OF OPHTHALMIC PRACTICE, 
 
 Especially useful to the student who has had neither time 
 nor inclination to study the numerous able but more volu- 
 minous text-books. 
 
 The object of this manual is to present to the student who is be- 
 ginning work in the field of ophthahnologj^ a plain description of 
 the optical defects and diseases of the eye. To this end special 
 attention has been paid to the clinical side of the question ; and the 
 methods of examination, the symptomatology leading to a diagnosis, 
 and the treatment of the various ocular defects have been brought 
 into special prominence. Anatomy, physiology, and pathological 
 histology, except in so far as they serve the purpose just stated, 
 have been omitted. The sections devoted to optical principles and 
 the normal and abnormal refraction of the eye in large portion have 
 been written by Dr. James Wallace, Chief of the Eye Dispensary of 
 the University Hospital. The chapter devoted to the application 
 of the shadow-test has been prepared bj' Dr. Edward Jackson. The 
 book will be suitably illustrated by a number of wood-cuts, many of 
 them from cases in the practice of the author, in addition to which 
 there will be several chromo-lithographs. 
 
IN PEEPARATION. 
 
 DISEASES OF WOMEN. 
 
 By henry J. GARRIGUES, A.M., M.D., 
 
 Professor of Obstetrics in the New York Post-Graduate Medical School and 
 Hospital ; Gynaecologist to St. Mark's Hospital in New York City ; Gyne- 
 cologist to the German Dispensary in the City of New York; Con- 
 sulting Obstetrician to the New York Infant Asylum; Obstetric 
 Surgeon to the New York Maternity Hospital ; Fellow of 
 the American Gynaecological Society ; Fellow of the 
 New York Academy of Medicine ; President of the 
 German Medical Society of the City of New 
 York, etc. etc. 
 
 It is the intention of the writer to provide a practical manual on 
 Gynaecology, for the use of students and practitioners, in as concise a 
 manner as is compatible with clearness. 
 
 Syllabus of Obstetrical Lectures 
 
 In the Medical Department, University of Pennsylvania. 
 
 By RICHARD C. NORRIS, A.M., M.D., 
 
 Demonstrator on Obstetrics in the University of Pennsylvania. 
 
 Price, Oloth, Interleaved for Notes . . . $2.00 Net. 
 
 The New York Medical Record of April 19, 1890, referring to this 
 hook, says : " This modest little work is so far superior to others on 
 the same subject that we take pleasure in calling attention briefly to 
 its excellent features. Small as it is, it covers the subject thoroughly, 
 and will prove invaluable to both the student and the practitioner as 
 a means of fixing in a clear and concise form the knowledge derived 
 from a perusal of the larger text-books. The author deserves great 
 credit for the manner in which he has performed his work. He has 
 introduced a number of valuable hints which would only occur to one 
 who was himself an experienced teacher of obstetrics. The subject- 
 matter is clear, forcible, and modern. We are especially pleased with 
 the portion devoted to the practical duties of the accoucheur, care of 
 the child, etc. The paragraphs on antiseptics are admirable ; there 
 is no doubtful tone in the directions given. No details are regarded 
 as unimportant ; no minor matters omitted. We venture to say that 
 even the old practitioner will find useful hints in this direction which 
 he cannot afford to depise." 
 
 9 
 
READY SHORTLY. 
 
 SAUNDERS' 
 
 Pocket Medical Formulary. 
 
 BY 
 
 WILLIAM M. POWELL, M.D., 
 
 Attending Physician to the Mercer House for Invalid Women, at Atlantic 
 
 City, N. J. ; Late Physician to the Clinic for the Disea'ses of Children 
 
 in the Hospital of the University of Pennsylvania and St. Clement's 
 
 Hospital ; Instructor in Physical Diagnosis in the Medical 
 
 Department of the University of Pennsylvania, and 
 
 Chief of the Medical Clinic of the Philadelphia 
 
 Polyclinic. 
 
 Containing about 2000 Formulas, selected from several 
 hundreds of the best-known authorities. 
 
 A concise, clear, and correct record of the many 
 hundreds of famous formulse which are found scattered 
 through th-^, works of the 
 
 Most fiminent Physicians and Surgeons 
 
 of the world; pa^icularly helpful to the student and 
 young practitioner, as it gives him a taste for writing his 
 prescriptions in an elegant and correct manner, thus avoid- 
 ing incompatible and dangerous prescriptions. The use 
 of this worlc is to be recommended even to the older prac- 
 tionar, as through it he becomes acquainted with numerous 
 formuiifi which are not found in the text-books, but have 
 been collected from among the 
 
 Bising Generation of the Profession, College Professors, and 
 
 Hospital Physicians and Surgeons. 
 
 10 
 
NOW BEADY. 
 
 NEW AND REVISED EDITIONS OF 
 
 SAUNDERS' 
 
 QUESTION COMPENDS. 
 
 Arranged in Question and Answer Form, 
 
 The Latest, Cheapest, and Best 
 
 ILLUSTRATED SERIES OF COMPENDS EVER ISSUED. 
 
 THE ADVANTAGES OF QUESTIONS AND 
 ANSWERS. — The usefulness of arranging the subjects in 
 the form of Questions and Answers will be apparent, 
 since the student, in reading the standard works, often is at 
 a loss to discover the important points to be remembered, 
 and is equally puzzled when he attempts to formulate ideas 
 as to the manner in which the Questions could be put 
 in the Examination- Room. 
 
 These small works, which can be conveniently carried in the pocket, 
 contain in a condensed form the teachings of the most popular 
 text books. 
 
 The authors are nearly all connected with the various colleges as 
 Demonstrators or Lecturers, and are therefore thoroughly conver- 
 sant, not only with the wants of the average student, but also with 
 the points that are absolutely necessary to be remembered in 
 the Examination-Room. Tliese books are constantly in the hands 
 of their authors for revision, and are kept well up to the times, their 
 fast sale allowing them to be almost entirely re'written whenever 
 necessary, instead of having to wait for the edition to be sold, as is 
 the case with an ordinary text book. 
 
 11 
 
No. 1. 
 
 ESSENTIALS OE PHYSIOLOGY. 
 
 H. A. HARE, M.D., 
 
 Professor of Tlierapeutics and Materica Medica in tlie Jefferson Medical Col- 
 lege of Philadelphia; Physician to St. Agnes' Hospital and to the 
 Medical Dispensary of the Cliildren's Hosiiital ; Laureate of 
 the Royal Academy of Medicine in Belgium, of the 
 Medical Society of London, etc. ; Secretary 
 of the Convention for the Revision of 
 the Pliarmacopoeia, 1890. 
 
 NUMEROUS ILLUSTRATIONS. 
 Third Edition, Revised and Enlarged. 
 Price, Cloth . . . $1.00 ; Interleaved for Notes . . 
 
 $1.25. 
 
 University Medical Magazine, 
 October, 1888.— " Dr. Hare has 
 admirably succeeded in gather- 
 ing together a series of Ques- 
 tions which are clearly put and 
 1 tersely answered." 
 
 Pacific Medical Journal, Octo- 
 i ber, 1889. — " Hare's Physiology 
 contains the essences of its sub- 
 i ject. No better book has ever 
 been produced, and every stu- 
 dent would do well to possess a 
 1 copy." 
 
 Times and Register, Philadel- 
 I phia, October 5, 1889.—" In the 
 second edition of Hare's Physi- 
 ology all the more difficult points 
 of the study of the nervous sys- 
 1 tern have been elucidated. As 
 the work now appears it cannot 
 fail to merit the appreciation of 
 Specimen of Illustrations. the overworked student." 
 
 Journal of the American Association, November 23, 1889. — " Hare's 
 Physiology — an excellent work ; admirably illustrated ; well calcu- 
 lated to lighten the task of the over-burdened undergraduate." 
 
 12 
 
No. 2. 
 
 ESSENTIALS OF SURGERY. 
 
 CONTAINING, ALSO, 
 
 Venereal Diseases, Surgical Landmarks, Minor and Operative Sur- 
 gery, and a Complete Description, together with full Illustra- 
 tions, of the Handkerchief and Roller Bandage. 
 
 By EDWARD MARTII^, A.M., M.D,, 
 
 Clinical Professor of Genito-Uriuary Diseases, Instructor in Operative Sur- 
 gery, and Lecturer on Minor Surgery, University of Peunsylvaiiia; 
 Surgeon to the Howard Hospital ; Assistant Surgeon to tlie 
 University Hospital, etc. etc. 
 
 PKOFUSEL.Y ILLUSTRATED, 
 
 FOURTH EDITION, 
 Considerably enlarged by an Appendix containing ftill directions 
 and prescriptions for the preparation of tlie various mate- 
 rials used in 4NTISEPTIC SUReERT ; also sey- 
 eral hundred recipes covering the medical 
 treatment of surgical affections. 
 Price, Cloth, $i.oo. Interleaved for Notes, $1.25. 
 
 Medical and Surgical Reporter, 
 February, 1889. — " Martin's Sur- 
 gery contains all necessary essen- 
 tials of modern surgery in a com- 
 paratively small space. Its style 
 is interesting and its illustrations 
 admirable," 
 
 University Medical Magazine, 
 January, ]889. — "Dr. Martin has 
 admirably succeeded in selecting 
 and retaining just what is neces- 
 sary for purposes of examination, 
 and putting it in most e.xcellent 
 shape for reference and memor- 
 izing." 
 
 Kansas City Medical Record. — 
 "Martin's Surgery. — This admir- 
 able compend is well up in the 
 most advanced ideas of modern 
 surgery." 
 
 13 
 
 Specimen of Illustrations. 
 
No. 3. 
 
 ESSENTIALS OF ANATOMY, 
 
 Including: the Anatomy of the Viscera. 
 
 By CHARLES B. N^ANCREDE, M.D., 
 
 Professor of Surgery and Clinical Surgery in the University of Michigan, 
 
 Ann Arbor ; Corresponding Member of the Royal Academy of 
 
 Medicine, Rome, Italy ; Late Surgeon Jefferson 
 
 Medical College, etc. etc. 
 
 ONE HUNDRED AND FORTY FINE WOODCUTS 
 
 THIRD EDITION. 
 
 Enlarged by an Appendix containing over Sixty Illustrations of 
 
 the Osteology of the Human Body. 
 
 The whole based upon the last (eleventh) edition of 
 
 GRAY'S ANATOMY. 
 
 Price, Clothj $1.00. Interleaved for Notes, $1.25. 
 
 Ameiican Practitioner and 
 News, February 16, 18&9. 
 
 " Nancrede'ri Anatomy. — 
 For self-quizziug aiidkeep- 
 ing fresh in mind the 
 knowledge of Anatomy 
 gains at school, it would 
 not be easy to speak of it 
 in terms too favorable." 
 
 Southern Cnlifornian Practi- 
 tioner, January 18, 1889. 
 " Nancrede's Anatomy. — 
 Very accurate and trust- 
 worthy. ' ' 
 
 American Practitioner and 
 News, Louisville, Kentucky. 
 " Nancrede's Anatomy. — 
 Truly such a book as no 
 student can afford to be 
 without." 
 
 Specimen of Illustrations. 
 
 14 
 
No. 4. 
 
 Essentials of Medical Chemistry 
 
 ORGANIC AND INORGANIC. 
 
 CONTAINING, ALSO, 
 
 Questions on Medical Physics, Chemical Physiology, 
 Analytical Processes, Urinalysis, and Toxicology. 
 
 LAWRENCE WOLFF, M.D., 
 
 Demonstrator of Chemistry, Jefferson Medical College ; Visiting Physician 
 
 to German Hospital of Philadelphia ; Member of Philadelphia 
 
 College of Pharmacy, etc. etc. 
 
 SIXTH THOUSAND. 
 
 Price, Cloth, $1.00. Interleaved for Notes, $1.25. 
 
 Cincinnati Medical Neivs, January, 1889. — " AVolff 's Chemistry.- -A little 
 work that can be carried in the pocket, for ready reference in solving difficult 
 problems."' 
 
 St. Joseph's Medical Herald, March, 1889.— "Dr. "Wolff explains most 
 simply the knotty and difficult points in chemistry, and the book is therefore 
 well suited for use in medical schools." 
 
 Medical and Surgical Reporter, November, 1889. — "We could wish that 
 more books like this would be written, in order that medical students might 
 thus early become more interested in what is often a difficult and uninterest- 
 ing branch of medical study." 
 
 Resistered Pharmacist, Chicago, December, 1890. — " Wolff 's Chemistry." 
 — " The author is thoroughly familiar with his subjects. A useful addition to 
 the medical and pharmaceutical library." 
 
 15 
 
No. 5. 
 
 ESSEITIALS OF OBSTSTEICS. 
 
 By W. easterly ASHTOi^, M.D., 
 
 Obstetrician to the Pliilatielpliia HospitaL 
 
 NUMEROUS lULUSTKATIONS. SIXTH THOUSAIfD. 
 
 Price, Cloth, $1.00. Interleaved for Notes, $1.25. 
 
 Specimen of Illustrations. 
 
 SoHtheni Fractitioner, January, 1890. — Ashton's Obstetrics. — An excellent 
 little volume containins- correct and practical knowledge. An admirable com- 
 pend, and the best condensation we have .=een." 
 
 Chicago JMedical Times. — '" Ashton's Obstetrics. — Of extreme value to stu- 
 dents, and an excellent little book to freshen up the memory of the practi- 
 tioner." 
 
 Medical and Surgical Hejiorter, January 26. 1889. — "Ashton's Obstetrics. 
 — A work thoroughly calculated to be of service to students in preparing for 
 examination."' 
 
 IS^ew Yorl- Medical Abstract, April. 1890. — " A.shton's Obstetrics should be 
 consulted by the medical student until he can answer every question at sight. 
 The practitioner would also do well to glance at the book now and then, to 
 prevent his knowledge fromgetting rusty." 
 
 16 
 
No. 6. 
 
 ESSENTIALS 
 
 OF 
 
 Pathology and Morbid Anatomy. 
 
 C. E. ARMAND SEMPLE, B.A., M.B., Cantab., I.S.A., M.R.C.P., lond., 
 
 Physician to the Northeastern Hospital for Children, Harkney ; Pro- 
 fessor of Vocal and Aural Physiology and Examiner in Acous- 
 tics at Trinity College, London, etc. etc. 
 
 ILLUSTRATED. FOURTH THOUSAND. 
 
 Price, Cloth f $1.00, Interleaved for Notes, $1,25. 
 
 From the College and Clinical Record, 
 September, 1889. — " A small work upon 
 Pathology and Morbid Anatomy, that re- 
 duces such complex subjects to the ready 
 comprehension of the student and practi- 
 tioner, is a very acceptable addition to 
 medical literature. All the more modern 
 topics, such as Bacteria and Bacilli, and 
 the most recent views as to Urinary Path- 
 ology, find a place here, and in the hands 
 of a writer and teacher skilled in the art 
 of simplifying abstruse and difficult sub- 
 jects for easy comprehension are rendered 
 thoroughly intelligible. Few physicians 
 do more than refer to the more elaborate 
 works for passing information at the time 
 it is absolutely needed, but a book like this 
 
 of Dr. Scrapie's can be taken up and perused continuously to the profit and 
 instruction of the reader." 
 
 Indiana Medical Jonriial, December. 1889. — " Scrapie's Pathology and 
 Morbid Anatomy. — An excellent corapend of the subject frora the points of 
 view of Green and Payne." 
 
 Cinciyinati Medical Nen-s, November, 1889. — Semple's Pathology and Mor- 
 bid Anatomy. — A valuable little volume — truly a multuni in 'parvo.''' 
 
 17 
 
 Specimen of Illustrations. 
 
No. 7. 
 
 ESSENTIALS 
 
 OF 
 
 Materia Medica, Therapeutics, 
 
 AND 
 
 PRESCRIPTION WRITING. 
 
 HENHY MORRIS, M.D., 
 
 Late Demonstrator, Jefferson Medical College ; Fellow College of Physicians, 
 
 Philadelphia ; Co-editor Biddle's Materia Medica ; Visiting 
 
 Physician to St. Joseph's Hospital, etc. etc. 
 
 SECOND EDITION. FOURTH THOUSAND. 
 
 Price, Cloth, $1.00. Interleaved for Notes, $1.25. 
 
 Medical and Surgical Reporter, October, 1889. 
 "Morris* Materia Medica and Therapeutics. — One of the best compends in 
 this series. Concise, pithy, and clear, well-suited to the purpose for which it 
 is prepared. " 
 
 GrAiLLARD*.s Medical Journal, November, 1889. 
 "Morris' Materia Medica.— The very essence of Materia Medica and Thera- 
 peutics boiled down and presented in a clear and readable style." 
 
 Sanitarium, New York. January, 1890. 
 "Morris' Materia Medica.— A well-arranged quiz-book, comprising the 
 most important recent remedies." 
 
 Buffalo Medical and Surgical Journal, January, 1890. 
 "Morris' Materia Medica. — The subjects are treated in such a unique and 
 attractive manner that they cannot fail to impress the mind and instruct in 
 a lasting manner." 
 
 18 
 
Nos. 8 and 9. 
 
 Essentials of Practice of Medicine. 
 
 By HEKRY MOEEIS, M.D., 
 
 Author of " Essentials o£ Materia Medica," etc. 
 
 With an Appendix on the Clinical and Microscopical 
 Examination of Urine. 
 
 By LAWEENCE WOLFF, M.D., 
 
 Author of " Essentials of Medical Chemistry," etc. 
 
 COLORED (VOGEL) URINE SCALE AND NUMEROUS 
 FINE ILLUSTRATIONS. 
 
 SECOND EDITION, 
 
 Enlarged by some THREE HUNDRED Essential 
 
 Formulae, selected from the writings of the 
 
 most eminent authorities of the 
 
 Medical Profession. 
 
 COLLECTED AND ARRANGED BY 
 
 WILLIAM M. POWELL, M.D., 
 
 Author of "Essentials of Diseases of Children." 
 
 Price, Clotb, $2.00. Medical Slieep, $3.50. 
 
 Southern Practitioner, Nashville, Tenn., January, 1891. 
 "Morris' Practice of Medicine. — Of material aid to the advanced student 
 'in preparing for his degree, and to the young practitioner in diagnosing affec- 
 tions or selecting the proper remedy." 
 
 American Practitioner and News, Louisville, Ky., January, 1891. 
 "Morris' Practice of Medicine. — The teaching is sound, the presentation 
 graphic, matter as full as might be desired, and the style attractive." 
 
 Southern Medical Record, January, 1891. 
 "Morris' Practice of Medicine is presented to the reader in the form of 
 Questions and Answers, thereby calling attention to the most important lead- 
 ing facts, which is not only desirable, but indispensable to an acquaintance 
 with the essentials of medicine. The book is all it pretends to be, and we 
 cheerfully recommend it to medical students." 
 
 19 
 
No. 10. 
 
 ESSENTIALS OF GYNECOLOGY. 
 
 EDWIN B. CRAIGm, M.D., 
 
 Attending Gynaecologist, Roosevelt Hospital, Out-Patients' Department 
 Assistant Surgeon, New York Cancer Hospital, etc. etc. 
 
 58 FINE ILLUSTRATIONS. 
 SIXTH THOUSAND. 
 
 Price, Cloth, $1.00. Interleaved for IS^otes, $1.25. 
 
 Specimen of Illustrations. 
 
 Medical and Surgical Re- 
 porter, April, 1890. — "Craig- 
 gin's Essentials of Gynsecol- 
 ogy. — This is a most excel- 
 lent addition to this series 
 of question compends, and 
 properly used will be of 
 great assistance to the stu- 
 dent in preparing for ex- 
 amination. Dr. Craigin is 
 to be congratulated upon 
 having produced in com- 
 pact form the Essentials of 
 Gynaecology. The style is 
 concise, and at the same 
 time the sentences are well 
 rounded. This renders the 
 book far more easy to read 
 than most compends, and 
 adds distinctly to its value. " 
 College and Clinical Record, 
 April, 1890. — " Craigin's 
 Gynaecology.— Students and 
 practitioners , general or spe- 
 cial, even derive information 
 and benefit from the perusal 
 and study of a carefully 
 written work like this." 
 
 20 
 
No. 11. 
 
 Essentials of Diseases of the Skin. 
 
 By henry W. STELWAGON", M.D., 
 
 Clinical Lecturer on Derinatolojry in the Jefferson Medical College, Philadel- 
 phia; Physician to Philadelphia Dispensary for Skin Diseases; Chief 
 of the Sl?in Disi)ensa7-y in the Hospital of University of Penn- 
 sylvania; Physician to Skin Department of the Howard 
 Hospital ; Lecturer on Dermatology in tlie Women's 
 Medical College, Philadelphia, etc. etc. 
 
 74 ILLUSTRATIONS, many of which are original. 
 
 FOURTH THOUSAND. 
 
 Price, Cloth, $I.OO. Interleaved for Notes, $1.25. 
 
 Specimen of Illustrations. 
 
 New York Medical Journal, May, 1890. — "Stelwagon's Diseases of tho 
 Skin. — We are indebted to Philadelphia for another excellent book on Derma- 
 tology. The little book now before us is well entitled "Essentials of Derma- 
 tol-ogy, " and admirably answers the purpose for which it is written." Tho 
 experience of the reviewer has taught him that just such a book is needed. 
 We are pleased with the handsome appearance of the book, with its clear 
 type, good paper, and fine wood-cuts." 
 
No. 12. 
 
 ESSENTIALS 
 
 Minor Surgery, Bandagmg, and 
 Venereal Diseases. 
 
 By EDWARD MARTIN, A.M., M.D., 
 
 Author of "Essentials of Surgery,'' etc. 
 
 82 ILLUSTRATIONS, mostly specially prepared for this wcrk. 
 
 Price, Cloth, $1.00. Interleaved for Notes, $1.25. 
 
 Medical JYen-s, Phila- 
 delphia, January 10,1891. 
 "Martin's Minor Surgery, 
 Bandaging, and Venereal 
 Diseases. — The best con- 
 densation of the subjects 
 of which it treatsyetplaeed 
 before the profession. The 
 chapter on G enito-Urinary 
 Diseases, though short, is 
 sufficiently complete to 
 make them thoroughly 
 acquainted with the most 
 advanced views on the 
 subject." 
 
 JVaskville Journal of 
 JSIedicineand Surgery, '^o- 
 vember, 1890. — "Martin's 
 Minor Surgery, etc., should 
 be in the* hands of every 
 student, and we shall per- 
 sonally recommend it toour 
 students as the best test- 
 book upon the subject." 
 Pharmaceutical Era, Detroit, Michigan, December 1, 1890. — "Martin's 
 Minor Surgery, etc, — Especially acceptable to the general practitioner, who 
 is often at a loss in cases of emergency as to the proper method of applying a 
 bandage to an injured member."' 
 
 22 
 
 Specimen of Illustrationg. 
 
No. 13. 
 
 ESSENTIALS 
 
 Legal Medicine, Toxicology, 
 
 tlYGHE^'E. 
 
 BY 
 
 C. E.- ARMAND SEMPLE, M.D., 
 
 Author of " Essentials of Pathology and Morbid Anatomy. 
 
 130 ILLUSTRATIONS. 
 
 Price, Cloth $1.00. 
 
 Interleaved for Notes .... l./i5. 
 
 Southern Practitioner, Nashville, May, 1890. 
 
 " Seraple's Legal Medicine, etc. — At tlie present time, when the 
 field of medical science, by reason of rapid progress, becomes so vast, 
 a book which contains tlie essentials of any branch or department of 
 it, in concise, yet readable form, must of necessity be of value. This 
 little brochure, as its title indicates, covers a portion of medical science 
 that is to a great extent too much neglected by the student, by reason 
 of the vastness of the entire field and the voluminous amount of matter 
 pertaining to what he deems more important departments. The lead- 
 ing points, the essentials, are here summed up systematically and 
 clearly." 
 
 Medical Brief, St. Louis, May, 1890. 
 " Semple's Legal Medicine, Toxicology, and Hygiene. — A fair sample 
 of Saunders' valuable compends for the student and practitioner. It 
 is handsomely printed and illustrated, and concise and clear in its 
 teachings." 
 
 23 
 
No. 14. 
 
 ESSENTIALS OF 
 
 Refraction and Diseases of the Eye. 
 
 By EDWAKD JACKSOIvT, A.M., M.D., 
 
 Professor of Diseases of the Eye in the Pliiladelphia Polyclinic and Collejre for 
 Graduates in Medicine; Member of the American Oplithalmological So- 
 ciety; Fellow of tlie College of Pliysicians of Philadelphia; Fel- 
 low of the American Academy of Medicine, etc. etc. 
 
 AND 
 
 Essentials of Diseases of the Nose and Throat. 
 
 By E. BALDWINS' GLEASOX, M.D., 
 
 Assistant in the Nose and Throat Dispensary of the Hospital of the University 
 
 of Pennsylvania ; Assistant in the Nose and Throat Department of the 
 
 Union Dispensary; Member of the German Medical Societj% 
 
 Philadelphia ; Polyclinic Medical Society, etc. etc. 
 
 TWO VOLUMES IN ONE. PROFUSELY ILLUSTRATED, 
 
 Price, Cloth, $1.00. Interleaved for Notes, $1.25. 
 
 TJniversity Medical Mag- 
 azine, Philadelphia, Octo- 
 ber, 1890. — " Jackson and 
 Gleason's Essentials of Dis- 
 eases of the Eye, Kos6, and 
 Throat. — The subjects 
 have been handled with 
 skill, and the student who 
 acquires all that here lays 
 before him will have much 
 more than a foundation for 
 future work." 
 
 New York Medical Rec- 
 ord, November 15, 1890. 
 — "Jackson and Gleason 
 on Diseases of the Eye, 
 Nose, and Throat. — A 
 valuable book to the be- 
 ginner in these branches, 
 to the student, to the busy practitioner, and as an adjunct to more thorough 
 reading. The authors are capable men, and as successful teachers know 
 
 what a student most needs." 
 
 24 
 
 Specimen of Eye Illustrations. 
 
No. 15. 
 
 ESSENTIALS 
 
 DISEASES OF CHILDREN, 
 
 BY 
 
 WILLIAM M. POWELL, M.D., 
 
 Attending Physician to the Mercer House for Invalid Women, at Atlantic 
 City, N. J. ; Late Physician to the Clinic for the Diseases of Chil- 
 dren in the Hospital of the University of Pennsylvania and 
 f St. Clement's Hospital ; Instructor in Physical Diag- 
 nosis in the Medical Department of the Uni- 
 versity of Pennsylvania, and Chief of 
 the Medical Clinic of the Phil- 
 adelphia Polyclinic. 
 
 Price, Cloth $1.00. 
 
 Interleaved for Notes .... 1.25. 
 
 American Pkactitioner and News, Louisville, Ky., December 20, 1890. 
 " Powell's Diseases of Children. — This work is gotten np in the 
 clear and attractive style that characterizes the Saunders' Series. It 
 contains in appropriate form the gist of all the best works in the de- 
 partment to which it relates." 
 
 Southern Practitioner, Nashville, Tennessee, November, 1890. 
 "Dr. Powell's little book is a marvel of condensation. Handsome 
 binding, good paper, and clear type add to its attractiveness." 
 
 Annals of GynjEcology, Philadelphia, December, 1890. 
 " Powell's Diseases of Children, — The book contains a series of im- 
 portant questions and answers, which the student will find of great 
 utility in the examination of children." 
 
 25 
 
No. 16. 
 
 ESSENTIALS 
 
 EXAIIMTIO]^ OF URHE. 
 
 BY 
 
 LAWRENCE WOLFF, M.D., 
 
 Author of "Essentials of Medical Chemistry," etc. 
 
 COLORED (VOGEL) URINE SCALE AND NUMEROUS 
 ILLUSTRATIONS. 
 
 Price, Cloth 
 
 . 75 Cents. 
 
 University Medical Magazine, 
 June, 1890. 
 " Wolff's Examination of the 
 Urine. — A little work of decided 
 valne." 
 
 Medical Recoed, New York, 
 
 Specimen of Illustrations. 
 
 August 23, 1890. 
 "Wolff's Examination of 
 good manual for , 
 well written, and 
 answers, categorically, many- 
 questions beginners are sure 
 to ask." 
 
 Memphis Medical Monthly, Memphis, Tennessee, June, 1890. 
 "Wolff's Examination of Urine. — The book is practical in char- 
 acter, comprehensive as is desirable, and a useful aid to the student 
 
 in his studies." 
 
 26 
 
No. 18. 
 
 ESSENTIALS 
 
 PRACTICE OF PHARMACY. 
 
 BY 
 
 LUCIUS E. SAYRE, 
 
 Professor of Pharmacy and Materia Mediea in the University of Kansas. 
 
 Price, Oloth, $1.00. Interleaved for Notes, $1.25. 
 
 Albany Medical Annals, Albany, N. Y., November, 1890. 
 " Sayre's Essentials of Pharmacy covers a great deal of ground in 
 small compass. The matter is well digested and arranged. The 
 research questions are a valuable feature of the book." 
 
 American Doctoe, Richmond, Va., January, 1891. 
 " Sayre's Essentials of Pharmacy. — This very valuable little manual 
 covers the ground in a most admirable manner. It contains practical 
 pharmacy in a nutshell." 
 
 National Drug Register, St. Louis, Mo., December 1, 1890. 
 " Sayre's Essentials of Pharmacy.— The best quiz on pharmacy we 
 have yet examined." 
 
 Western Drug Record, November 10, 1890. 
 "Sayre's Essentials of Pharmacy.— A book of only 180 pages, but 
 pharmacy in a nut-shell. It is not a quiz-compend compiled to en- 
 able a grocery clerk to ' down' a board of pharmacy ; it is a finger- 
 post guiding a student to a completer knowledge." 
 
 27 
 
Saunders' Question-Compends. 
 
 In Preparation. Ready about September 1, 1891. 
 
 No. 17. 
 
 Essentials of Diagnosis. 
 
 No. 19. 
 
 Essentials of Hygiene. 
 
 ILLUSTRATED. 
 
 By ROBERT P. ROBINS, M.D. 
 
 No. 20. 
 
 Essentials of Bacteriology. 
 
 ILLUSTRATED. 
 
 By M. V. BALL, M.D. 
 
 No. 21. 
 
 Essentials of Nervous Diseases and Insanity. 
 
 ILLUSTRATED. 
 
 By JOHN C. SHAW, M.D. 
 
 No. 92. 
 
 Essentials of Medical Physics. 
 
 ILLUSTRATED. 
 
 By FRED. J. BROCKWAY, M.D. 
 
 No. 23. 
 
 Essentials of Medical Electricity. 
 
 ILLUSTRATED. 
 
 By DAVID D. STEWART, M.D., and EDWARD S. LAWRENCE, M.D. 
 
 OTHERS PREPARING. 
 
 28 
 
The Fiske Fund Prize Essay for 1890. 
 
 THE 
 
 SUEGIOAL TREATMENT 
 
 OF 
 
 Wounds and Obstruction 
 
 OF THE 
 
 INTESTINES. 
 
 BY 
 
 EDWARD MARTIN, A.M., M.D., 
 
 Clinical Professor of Genito-Urinary Diseases, Instructor in Operative Sur- 
 gery, and Lecturer on Minor Surgery, University of Pennsylvania; 
 Surgeon to tlie Howard Hospital ; Assistant Surgeon to tlie 
 University Hospital, etc. etc. 
 
 AKD 
 
 HOBART A. HARE, M.D., 
 
 Professor of Therapeutics, Jefferson Medical College ; Attending Physician 
 to St. Agnes' Hospital. 
 
 ILLUSTRATED. 
 
 Price, Cloth $2.00, Net. 
 
 " In presenting this Essay upon the Surgical Treatment of Wounds 
 and Obstruction of the Intestines to the Trustees of the Fiske Fund, 
 it is proper to outline the scope of our work, and to state briefly the 
 facts and lines of original research upon which our conclusions are 
 based. For over two years we have made experiments in the labo- 
 ratory upon these subjects, and have carried out in every detail all 
 the methods and modifications of operations that have been published 
 or which have occurred to us in the course of our own studies. . . . 
 In addition to the original work involved in studying so important 
 a branch of surgery as the one before us (and which will be found 
 represented, graphically, in part at least by a number of tracings), 
 we have collected and placed before the reader what we believe to be 
 the fullest statistics yet collected upon gunshot wounds of the abdo- 
 men." — Extract from Preface. 
 
 29 
 
INDEX. 
 
 PAGE 
 
 Announcement i 
 
 American Text-Book of Surgery . . . . 2, 3 
 
 ViERORDT AND StU ART'S MeDICAL DIAGNOSIS . . 4 
 
 Keating's New Unabridged Dictionary of Medicine 5 
 Saunders' Pocket Medical Lexicon .... 6 
 Nancrede's Anatomy and Manual of Dissection . 7 
 DeSchweinitz's Diseases of the Eye . . . .8 
 Garrigue's Diseases of Women ..... 9 
 NoRRis' Syllabus of Obstetrical Lectures . . 9 
 Saunders' Pocket Medical Formulary . . .10 
 Saunders' Series of Question Compends . . .11 
 
 Hare's Physiology 12 
 
 Martin's Surgery *. . .13 
 
 Nancrede's Anatomy 14 
 
 Wolff's Chemistry 15 
 
 Ashton's Obstetrics 16 
 
 Semple's Pathology, etc 17 
 
 Morris' Materia Medica 18 
 
 Morris' Practice of Medicine 19 
 
 Cragin's Gynecology 20 
 
 Stelwagen's Diseases of the Skin . . . .21 
 Martin's Minor Surgery, etc. . . . . .22 
 
 Semple's Legal Medicine, etc 23 
 
 Jackson and Gleason's Diseases of Eye, Nose, and 
 
 Throat 24 
 
 Powell's Diseases of Children 25 
 
 W^oLFF's Examination of Urine 26 
 
 Sayre's Practice of Pharmacy 27 
 
 Works in Preparation and in Press . . .28 
 
 Martin and Hare's Wounds and Obstruction of 
 
 THE Intestines 29 
 
 30 
 
^ ..^ i^f^^WSTfta'.^,^ 
 
.MINATIOiN ^ 
 
 "^B OF Pharmacy . 
 
 TON AND IN PkESS 
 
IViAY & li^^li 
 
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